Pain Management: A Practical Guide for Clinicians, 6th edition

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PAIN MANAGEMENT A Practical Guide for Clinicians SIXth Edition

PAIN MANAGEMENT A Practical Guide for Clinicians SIXth Edition Editor Richard S. Weiner

AMERICAN ACADEMY OF PAIN MANAGEMENT

CRC PR E S S Boca Raton London New York Washington, D.C.

The publishers, the authors, and the American Academy of Pain Management cannot assume responsibility for the validity of all materials contained in this book or for the consequences of their use. Some of the content represents an emerging area of study. As new information becomes available, changes in treatment and in the use of drugs may be necessary. The reader is advised to consult his or her healthcare practitioner before changing, adding, or eliminating any treatment. The reader is also advised to carefully consult the instruction and information material included in the package insert of each drug or therapeutic agent before administration. The publisher, authors, and the American Academy of Pain Management disclaim any liability, loss, injury, or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents of this volume.

Library of Congress Cataloging-in-Publication Data Pain management : a practical guide for clinicians / executive editor, Richard S. Weiner.—6th ed. p. ; cm. Includes bibliographical references and index. ISBN 0-8493-0926-3 (alk. paper) 1. Pain—Treatment. 2. Analgesia. I. Weiner, Richard S., Ph.D. [DNLM: 1. Pain—therapy. 2. Chronic Disease—therapy. 3. Disability Evaluation. 4. Pain—diagnosis. 5. Patient Care Management. WL 704 P14656 2001] RB127 .P33233 2001 616′.0472—dc21

2001037442

This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. Neither this book nor any part may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, microfilming, and recording, or by any information storage or retrieval system, without prior permission in writing fromlisher. the pub All rights reserved. Authorization to photocopy items for internal or personal use, or the personal or internal use of specific clients, may be granted by CRC Press LLC, provided that $.50 per page photocopied is paid directly to Copyright clearance Center, 222 Rosewood Drive, Danvers, MA 01923 USA. The fee code for users of the Transactional Reporting Service is ISBN 0-8493-0926-3/02/$0.00+$1.50. The fee is subject to change without notice. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. The consent of CRC Press LLC does not extend to copying for general distribution, for promotion, for creating new works, or for resale. Specific permission must be obtained in writing from CRC Press LLC for such copying. Direct all inquiries to CRC Press LLC, 2000 N.W. Corporate Blvd., Boca Raton, Florida 33431. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation, without intent to infringe.

Visit the CRC Press Web site at www.crcpress.com © 2002 by CRC Press LLC No claim to original U.S. Government works International Standard Book Number 0-8493-0926-3 Library of Congress Card Number 2001037442 Printed in the United States of America 1 2 3 4 5 6 7 8 9 0 Printed on acid-free paper

Remembering Richard S. Weiner, Ph.D. While standing upon the shoulders of giants certainly helped many advances to occur, the genius of Richard S. Weiner, Ph.D. was more accurately due to the fact that he could see the finished puzzle within the constituent pieces. He could take pre-existing parts and ideas that others had ignored or overlooked, pull them together in slightly altered ways and create new results. He created harmony from the same puzzle pieces in which others only perceived chaos. He did more than talk about the developing field of pain management; he walked the walk and co-founded the American Academy of Pain Management with Kathryn A. Weiner, Ph.D. Together, the Weiners created a new organization that finally met the needs of its pain practitioner members through pain-related education, practitioner credentialing, pain program accreditation, outcome measurement, and many other offerings. Bringing together leaders in the field of pain management to create the American Academy of Pain Management’s textbook, Pain Management: A Practical Guide for Clinicians was one of his greatest accomplishments and was a continuing source of pride for Richard. Revising six editions became proof not only of his commitment to the advancement of the pain management profession, but also his stamina. For Richard, editing a textbook was a challenging process that required more than a year of preparation. Richard weathered this process six times in 12 years to make certain that the American Academy of Pain Management’s textbook was clinically useful, current, and the best source for multidisciplinary information about the assessment, evaluation, and treatment of pain. For Richard, this was his labor of love and he gave his very best to this process. Many might say that authoring textbooks is just too much work. It is far more effort than most people would ever willingly take upon themselves. Richard never saw the textbook as too much work for himself. He looked forward to the revision process and the updating of the chapters with each new edition. He enthusiastically called authors, new and old alike, to talk with them about their submissions, suggested points to discuss, and then called others to tell them about what he had learned in the new chapters when he received them. No matter how many hours or how many authors were involved, he treated each of the authors with consideration, excitement, and respect. He asked more of the authors than some knew they had within themselves, but always knew what they could accomplish if properly motivated. Richard was the consummate manager, who not only managed ideas, but the people bringing the ideas to fruition. Knowing that he was quite seriously ill in 2001, Richard began to consider future goals for the American Academy of Pain Management. He knew that in another couple of years the seventh edition of the textbook would need to be written to maintain the currency associated with the book. In his own amazing way, and in his attempt to find goodness and humor even in the worst of circumstances, he speculated that he wouldn’t have to edit any more textbooks if he didn’t respond to his anti-cancer therapies. He even tried to cheer up those who were so concerned about him by telling us that the chemotherapy was easier than editing the textbook. Before his death in May 2002, he helped identify a worthy successor as the next editor for the seventh edition of the textbook. Practitioners fortunate enough to have personally known Richard continue to mourn his passing. His hundreds of personal friends and members of his immediate family remember all that he gave to our evolving profession. Always the gentleman in his dealings with others, he shall best be remembered as the man who gathered together the many disciplines that constitute the modern field of pain management to improve the treatment of pain for so many unfortunate sufferers he never met. He never wanted special recognition, but wanted the profession to mature and to see the “mainstreaming” of pain management services. I miss Richard. Never a day goes by when I do not think about something he said to me, some lesson he taught me, or some opportunity he created for all of us who now follow in his footsteps. Few men pass through our lives and have as significant an impact as he did for me personally and for so many of my colleagues. While his life was far too short, his accomplishments more than filled his lifetime and left a permanent legacy for all of us. It is only fitting that this Sixth Edition be dedicated to the outstanding work of Dr. Richard S. Weiner. B. Eliot Cole, M.D., M.P.A. Director, Education and Special Projects American Academy of Pain Management Sonora, CA 95370

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Table of Contents Dedication..........................................................................................................................................................................xv Preface .............................................................................................................................................................................xvii Editor’s Note .................................................................................................................. ..................................................xxi Editorial Advisory Board ...............................................................................................................................................xxiii List of Contributors ........................................................................................................... ..............................................xxv Chapter Consultants ............................................................................................................ ...........................................xxxi

SECTION I

Pain in Perspective..................................................................... 1

Chapter 1 Pain and Its Magnitude......................................................................................................... .........................3 Barry Fox Chapter 2 Historical Perspective of Pain Management ...................................................................................... ...........9 C. Norman Shealy and Roger K. Cady

SECTION II Elements of Multidisciplinary Pain Management .................... 17 Chapter 3 Implementing a Pain Management Program......................................................................................... ......19 Anne Marie Kelly Chapter 4 The Classification of Pain ...................................................................................................... .....................27 Ole Thienhaus and B. Eliot Cole Chapter 5 Starting a Pain Clinic ......................................................................................................... .........................37 Clayton A. Varga Chapter 6 Multidisciplinary Pain Clinics.....................................................................................................................45 C. Norman Shealy and Roger K. Cady Chapter 7 Columbia Medical Plan Pain Management Group Manual........................................................................55 Clark Brill, Juliet Scotti Post, Thomas Ferguson, Harry Shabsin, Jane Tenberg, Kathleen Wooding, Marilyn Lauffer, Robin Thomas, and Mary Ann Buchmeier

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SECTION III Treatment of Commonly Occurring Pain Syndromes............. 75 Chapter 8 Clinical Diagnosis of Heel Pain ................................................................................................ ..................77 Paula Lizak Gilchrist Chapter 9 Cervicogenic Processes: The Results of Injury .................................................................................. ........85 Alfred V. Anderson Chapter 10 Thyroid and Parathyroid Diseases and Pain ...................................................................................... .........91 Stuart A. Dorow and Gretajo Northrop Chapter 11 Posttraumatic Headache: Pathophysiology, Diagnosis, and Treatment....................................................103 Gary W. Jay Chapter 12 Posttraumatic Headache: Practical Interdisciplinary Approaches to Diagnosis and Treatment ...............125 Nathan D. Zasler and Michael F. Martelli Chapter 13 Orofacial Pain and Temporomandibular Disorders................................................................................. ..139 Gary M. Heir Chapter 14 Chinese Medicine and Acupuncture for Pain Management in HIV/AIDS ..............................................149 Misha R. Cohen Chapter 15 Mild Traumatic Brain Injury and Pain........................................................................................... ...........155 Gary W. Jay Chapter 16 Trauma and Soft Tissue Injuries: Clinic and Courtroom.......................................................................... 169 Thomas J. Romano Chapter 17 Neuropathic Pain: Mechanisms and Management .................................................................................... 181 Mark V. Boswell, Samuel K. Rosenberg, and Thomas C. Chelimsky Chapter 18 Primary Headache Disorders..................................................................................................... ................195 R. Michael Gallagher Chapter 19 Muscular Parafunction of the Masticatory System: Headache, Face, Jaw, and Sinus Pain (Temporomandibular Disorders).................................................................................................. ..............207 James P. Boyd Chapter 20 Complex Regional Pain Syndrome, Types I and II...................................................................................213 Nelson Hendler

ix Chapter 21 Treatment of Myofascial Pain Syndromes................................................................................................235 Robert D. Gerwin and Jan Dommerholt Chapter 22 Chronic Pelvic Pain ............................................................................................................ .......................251 Andrea J. Rapkin and Julie Jolin

SECTION IV Specialty Approaches to Pain Management through Team Management ................................................................. 269 Chapter 23 Pain Medicine and the Primary Care Physician .......................................................................................271 Uday S. Uthaman and Pierre L. LeRoy Chapter 24 The Impact of Pain on Families................................................................................................. ...............279 James H. Ballard Chapter 25 The Impact of Nursing on Pain Management....................................................................................... ....285 Chris L. Algren and Mary Romelfanger Chapter 26 The Psychiatrist’s Role in Pain Diagnosis and Management ...................................................................295 Nelson Hendler Chapter 27 A Rheumatologist’s Perspective on Pain Management.............................................................................309 Thomas J. Romano Chapter 28 The Role of the Neurologist in a Multidisciplinary Pain Clinic..............................................................329 Jacob Green

SECTION V Approaches to Chronic and Acute Pain................................. 339 Chapter 29 Epidural Steroid Injection: A Review of Indications, Techniques, and Interpretation of Results............341 W. David Leak and A. Elizabeth Ansel Chapter 30 Myofascial Trigger Point Injection ............................................................................................. ..............351 Hal S. Blatman Chapter 31 The Role of Cannabis and Cannabinoids in Pain Management ...............................................................357 Ethan B. Russo Chapter 32 Nutrition for Pain Management .................................................................................................. ..............377 Hal S. Blatman

x Chapter 33 Pain Management with Regenerative Injection Therapy (RIT)................................................................381 Felix S. Linetsky, Rafael Miguel, and Lloyd Saberski Chapter 34 Prescription NSAIDs: Choices in Therapy ........................................................................................ .......403 Linda L. Norton Chapter 35 Chronic Pain Management with a Focus on the Role of Newer Antidepressants and Centrally Acting Agents .....................................................................................................................415 Robert L. Barkin, Jan Fawcett, and Stacy J. Barkin Chapter 36 Drug Management of Pain ........................................................................................................ ................435 Robert B. Supernaw Chapter 37 The Role of Neural Blockade in the Management of Common Pain Syndromes...................................449 Steven D. Waldman Chapter 38 Myths and Misconceptions about Chronic Pain: The Problem of Mind–Body Dualism........................465 Keith Nicholson, Michael F. Martelli, and Nathan D. Zasler

SECTION VI Specialty Concerns ............................................................... 475 Chapter 39 Management of Procedural and Perioperative Pain in Children ..............................................................477 John T. Algren and Chris L. Algren Chapter 40 Pain Management in Geriatrics .................................................................................................. ...............491 Samuel K. Rosenberg and Mark V. Boswell Chapter 41 Sleep and Weight Problems Associated with Pain....................................................................................503 Arnold Fox and Barry Fox Chapter 42 Hospice, Cancer Pain Management, and Symptom Control ....................................................................517 Samira Kanaan Beckwith and B. Eliot Cole

SECTION VII Work Disability and Return to Work................................... 539 Chapter 43 Postinjury: The Return-to-Work Challenge ....................................................................................... .......541 Stephen A. Lawson Chapter 44 Neuro-Orthopedic Impairment Rating ............................................................................................. .........549 Gabriel E. Sella

xi Chapter 45 Ergonomics for the Pain Practitioner ........................................................................................... .............563 Hal S. Blatman

SECTION VIII Physical Therapy, Manual Medicine, Imaging, Electromedicine, and Oriental Medicine............................. 569 Chapter 46 Axiologic Disorders – The Missing Outcome Dimension: Innovations in Pain Management................571 Richard S. Materson and C. Stephen Byrum Chapter 47 Surface Electromyography in the Assessment and Treatment of Muscle Impairment Syndromes in Pain Management ...............................................................................................................587 Jeffrey R. Cram Chapter 48 Six Diverse Acupuncture Techniques Useful in Pain Management .........................................................603 William D. Skelton Chapter 49 Tai Chi Chuan for Pain Management .............................................................................................. .........615 Richard A. Peck and Iva Lim Peck Chapter 50 Energetic Medicine............................................................................................................. .......................619 Diane H. Polasky Chapter 51 Qigong: A Paradigm Shift Tool for Pain Management.............................................................................637 Linda C. Hole Chapter 52 Koryo Hand Therapy: Modern Pain Management ....................................................................................651 Daniel C. Lobash Chapter 53 Koryo Hand Therapy for Pain Relief............................................................................................. ...........659 Linda C. Hole Chapter 54 ETPS Neuropathic Acupuncture ................................................................................................... ............667 Bruce Hocking Chapter 55 Magnetic Biostimulation in Peripheral Neuropathy..................................................................................693 Michael I. Weintraub Chapter 56 Manipulation under Anesthesia: An Anthology of Past, Present, and Future Use ...................................701 Robert C. Gordon, Anthony Rogers, Daniel T. West, Robert S. Matthews, and Mathew R. Miller Chapter 57 Pulsed Signal Therapy: A Practical Guide for Clinicians ........................................................................ 715 Richard Markoll

xii Chapter 58 Infrared Photon Stimulation: A New Form of Chronic Pain Therapy ......................................................729 Jacob Green, Deborah Fralicker, William Clewell, Earl Horowitz, Tim Lucey, Victor John Yannacone, Jr., and Constance Haber Chapter 59 Physical Therapy and Pain Management ..................................................................................................739 C. Kumarlal Fernando Chapter 60 Electromedicine: The Other Side of Physiology.................................................................................. .....749 Daniel L. Kirsch Chapter 61 A Practical Protocol for Electromedical Treatment of Pain.....................................................................7 59 Daniel L. Kirsch

SECTION IX Behavioral, Social, and Spiritual Concerns and Aspects of Pain Management............................................................... 777 Chapter 62 Pain, Disease, and Suicide ..................................................................................................... ...................779 Blake H. Tearnan Chapter 63 Assessing the Veracity of Pain Complaints and Associated Disability ....................................................789 Michael F. Martelli, Nathan D. Zasler, Keith Nicholson, Treven C. Pickett, and V. Robert May Chapter 64 Psychoneuroimmunology ..........................................................................................................................807 Jan M. Burte Chapter 65 Variables in the Sensation and Perception of Pain .............................................................................. .....817 Richard H. Cox and John Essman Chapter 66 Screening for Alcohol and Other Substance Use Disorders.....................................................................825 Nick J. Piazza Chapter 67 Interactive Guided Imagery in Treating Chronic Pain............................................................................ ..833 David E. Bresler and Martin L. Rossman Chapter 68 Behavioral Protocols for Burning and Cramping Phantom Limb Pain....................................................845 Richard A. Sherman Chapter 69 Hypnotherapeutic Advances in Pain Management....................................................................................851 Jan M. Burte Chapter 70 Drug Misuse and Detoxification .................................................................................................. .............861 John Claude Krusz

xiii Chapter 71 A Multi-Systems Approach to Behavioral Health and Pain Management...............................................885 Richard H. Cox

SECTION X Legal Considerations .............................................................. 893 Chapter 72 Promoting Ethics and Objectivity in the Medicolegal Arena: Recommendations for Experts ...............895 Michael F. Martelli and Nathan D. Zasler Chapter 73 Business Side of Pain Management ............................................................................................... ...........909 Devona Slater Chapter 74 Pain Management: Medical and Legal Issues of Undertreatment............................................................915 James S. Lapcevic Chapter 75 Provider Accountability for Inadequate Pain Management......................................................................935 Kathryn L. Tucker Chapter 76 Law Enforcement and Regulatory View about Prescribing Controlled Substances for Pain ..................939 Dale A. Ferranto Chapter 77 Ethics of Care: Pain Management and Spirituality ............................................................................... ...945 Myrna C. Tashner Chapter 78 Documenting Pain ............................................................................................................... ......................955 Barbara L. Kornblau and Lori T. Andersen Chapter 79 Motor Vehicle Accidents ........................................................................................................ ...................963 Christopher R. Brown

SECTION XI Future Trends........................................................................ 979 Chapter 80 Achieving Insurance Independence in the Age of Managed Care ...........................................................981 Christopher R. Brown Chapter 81 A Practical Approach to Outcomes Measurement................................................................................... .995 Michael E. Clark and Ronald J. Gironda Chapter 82 Enhancing Adrenal Function ..................................................................................................... ..............1011 Arnold Sandlow and Afshin Shargani

xiv Chapter 83 Aromatherapy for Pain Relief ................................................................................................... ..............1025 A.R. Hirsch Chapter 84 Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury............................1039 Gabriel E. Sella Chapter 85 From Psychics of the Body to Clinical Outcome via Neurochemistry..................................................1057 Gary W. Jay Chapter 86 Musculoskeletal Ultrasound ..................................................................................................... ...............1061 John Porter and Michael S. Jablon Chapter 87 Minimally Invasive Endoscopic Surgery for the Treatment of Lumbar Discogenic Pain .....................1073 Anthony T. Yeung and John Porter Chapter 88 Phytomedicinal Approaches to Pain Management .................................................................................10 79 James Giordano Chapter 89 The Neurobiology of Pain ....................................................................................................... ................1089 James Giordano

APPENDICES ............................................................................................. 1101 Appendix A Code of Ethics.......................................................................................................................................1103 Appendix B Patient’s Bill of Rights....................................................................................................... ...................1105 Appendix C American Academy of Pain Management Credentialing .....................................................................1107 Appendix D Overview of Academy Services and Products .....................................................................................1 109 Appendix E Definition of Pain Management................................................................................................... .........1111

INDEX........................................................................................................ 1113

Dedication Pain and suffering is an issue that has affected society throughout the ages. Its impact has led healthcare professionals throughout the world to aggressively explore methods to reduce and eliminate the pain that afflicts thousands annually. Numerous attempts have been made to discover effective methods to diagnose and treat the problem time and again, yet the condition continues to exist. Throughout our research and treatments we have learned more about this topic by integrating multiple disciplines and cultures into our quest for answers. By incorporating this broad base of knowledge and experience, we are led to believe that our continuous contribution to this effort gives each of us an opportunity to make a difference in the study of pain management. This book is dedicated to those who can and do make a difference in the lives of others. Special recognition goes to Barbara E. Norwitz, Publisher, CRC Press, Tiffany Lane, Editorial Assistant, Barry E. Cole, M.D., M.P.A., Kathryn A. Weiner, Ph.D., and the Board, Staff, and Members of the American Academy of Pain Management.

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Preface Significant advances in our understanding of pain and suffering, clinical and laboratory reports, and concepts for multidisciplinary team interaction, combined with a renewed desire to understand the whole patient delivery system require updating and further documenting the new information provided in this 6th edition PainofManagement: A Practical Guide for Clinicians . Interest in the field of pain management has grown dramatically since the 1970s. This has been attributable to the outstanding contribution of pioneers, who provided leadership in this field, such as Dr. John Bonica, Dr. Benjamin Crue, Mme. Abel Fessard, Dr. Burtram Wolf, Dr. John Leibskind, Drs. Richard and Kathryn Weiner, and so many others, leading to the current global, exponential, informational avalanche. To bring together this enormous amount of new and refined knowledge and data, the original two volumes have been reorganized and expanded several times. So universal has this interest become, it can be likened to a pebble in the pond starting a propagation wave. Interest has grown exponentially; knowledge and wisdom constantly unfold. Quality pain management originally generated from a relatively small group of specialized experts forming a dynamic epicenter. These early leaders initiated a spread of integrated knowledge, team care, and multidisciplinary responses with many other health professionals, starting from basic neuroscience, which has blossomed to where we now encompass the special interest of many disciplines. Knowledge travels in many directions and today we have many primary care practices able to integrate tools and philosophies refined by pain management over the years. Many pain patients find care with a growing cadre of alternative and integrated disciplines. The primary care physician and clinician are often gate keepers because they are most frequently the first health professionals to see individuals with significant clinical problems and must decide to manage or seek referral from an appropriate specialist. Proper assessment and treatment planning are especially important for complex pain syndromes as they often are present with overlapping preexisting comorbidity. The needs of the patient must be best served when a “cure” is not possible. Chronicity complicates management for the health practitioner and patient. An integrated mind–body–spirit concept provides a fuller understanding for the complaint of pain. This holistic view in turn manifests complex interactive emotional and physical factors. Treatment programs must be individualized. Many pain syndromes are acute, chronic, and/or cancer related; one size does not fit all! New chapters, advances in diagnosis employing new clinical testing methods, increase our scientific perspective and aid in our ability to evaluate the interpretation of many co-existing psychological, physical, functional, pathological, and structural impairments. When they indeed need to be separated or correlated for patient care within managed care agencies and medical–legal communities, we must remember that treatment decisions impact the whole fabric of a person’s life. An appreciation of a “systems” view facilitates change. Clinically applied, this knowledge and experience can better guide treatments that are more cost effective. The clinician must be able to differentiate physiological signs associated with range of motion, reflex, proprioception, and other responses. Activities of daily living, body habits and age-related changes must be evaluated in terms of related impairments and measured for quality of life. How do you evaluate preexisting and comorbid conditions that may overlap in personal injury cases and may be associated with situations where life style matters? How do we factor weight, diabetes, and postoperative failed back syndrome, superimposed on congenital spinal changes and reactive depression? Not a simple matter; only a careful, knowledgeable, and experienced assessment, supported by laboratory data, will be convincing to third party reimbursement programs, and credible for the medical–legal community. When are such tests really necessary? Are there alternatives? A clinical practitioner can choose from more than 8000 laboratory tests. Which are reasonable and necessary to verify injury or disease? There is also the responsibility of the clinician to consider laboratory tests that may have false positive or false negative reports. Relevant, reflective, clinical correlation is required to develop a credible conclusion. Furthermore, the clinician must exercise judgment about when to order a special study. Corroborating or repeating serial tests, whose initial results are felt not to be consistent with clinical findings, may provide valuable information. In certain delivery systems, authorization for a service may be difficult to obtain. Often administrative or clinical denial sets the tone for clinical practice at the new millennium. Test selection is especially important in view of rapidly advancing technology. For example, how do you compare varying magnetic radiation imaging test results between 0.5, 1.0, and 1.5 tesla resolution. When do your order 3-D reconstruction or tomograms? When are vitamins, nutritional,

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xviii or other tests appropriate? It is exceedingly important to consider the fact that abnormal anatomic or structural tests can be misleading. There is no substitute for talking with the patient and often other persons for additional information. Frequently, patients who have injuries that remain unresolved come to involve a medical–legal setting. The inclusion of the judiciary provides an additional interactive issue based on an adversarial approach. The clinician may provide retrospective medical evaluations, declarations of permanent status, and need for future medical and vocational considerations, as well as describe how preexisting or comorbid factors influence rehabilitation. Regional pain syndrome (RPS) that causes functional impairments may be difficult to evaluate. Reimbursement and cost shifting delays often impact care. Today, the astute clinician must understand his or her discipline to be able to work within a multidisciplinary team, document and justify opinions, and handle myriad tasks, that were far less demanding in years gone by. Authors will address these complex issues. Today, there is an unprecedented need to justify treatment. There are barriers facing today’s clinician, namely the highly interpretative rule and documentation to demonstrate necessity and reasonableness of care. Standards have frequently not been defined by statute. Experienced authors will address these issues. Moreover, third party payers are with greater frequency introducing a relatively new type of evolving medical management that could be called “contract medicine.” Access to care is subject to wide interpretations. Disputes arise and this increases the frequency and involvement of the legal community with resultant adversity, which can be protracted and costly. State statutes or rules have long recognized that if there is a dispute, reimbursement may not be paid for extended periods of time, if at all. Practice management must be part of today’s clinician’s repertoire, as the dynamics of health policy and economics change. These issues will be reviewed in this new edition. New and significant pharmacologic advances and treatment with respect to classes of drugs known as analgesics, anti-inflammatories, and receptor-specific forms of intervention are being discovered and re-emphasized. How do we keep up with this enormous growth in the ever expanding annual physician desk reference, compendiums across disciplines, integration of new approaches with traditional methods? New generations of drugs that affect the neuronal network; the ever expanding neural transmitters, presynaptic substance P, and others affecting specific and nonspecific receptors and effectors are updated in these chapters. New information will address complex class drug interactions. We do know that prescribed and frequently modified medication programs must be individualized and monitored. What are the advantages and risks of the Cox I and Cox II medications? New transcutaneous, oral, sublingual, and nasal aerosol delivery systems will be reviewed. Advances in both nonnarcotic and opioid therapy are discussed. How does the patient’s compliance affect the treatment program if some classes of drugs are taken abusively or, conversely, below schedule? What role does psychoneuroimmunology play in etiology and intervention? How can new approaches help trigger informational transmitters that can influence peptides and emotional well-being? What is the role of over-thecounter (OTC) and herbal medications? What may be the effect on polypharmacy, herbaceuticals, and electrotherapy treatments? These questions will be discussed in expanded chapters. Caution must be exercised in prescribing new treatment and new regimes. Is there evidence from clinical trials? Do indications described have regulatory (FDA) approval? The practicing clinician is responsible for keeping current. Advancements in our knowledge and understanding of rehabilitation have occurred in the field of muscular and skeletal disease, and new treatments are reported in this 6th edition. The authors address outcomes of treatment and evidence-based medicine, while retaining an understanding for evaluating meaningful individual responses. Outcome studies are tools that can be used to improve care, but they can be subject to manipulation for restricting access to certain treatment. Thus, it is particularly important to understand today’s political environment and to analyze treatment and the opinions expressed by health professionals concerning policy matters for important decisions, in order to comment upon the milieu of practice. The important role of the health professional is to provide both relevant specialized information and to relate the impact of such information for each patient. Treatment and social decisions depend upon fair and comprehensive assessments. When should disability be reevaluated, especially if improvement occurs or if leisurely recreational personal activities are perceived not to cause significant functional impairment? How do you reevaluate a progressive, worsening condition? Long-term care has at times been called “palliative care.” Where a management treatment program is available to stabilize or improve quality of life, treatment has been ruled reimbursable by some courts despite the fact that a cure is not possible. On the other hand, reimbursement for palliative care programs has also been denied by many thirdparty reimbursement programs. It should be noted that certain classes of diseases are resistant to complete cure, for example, arthritis, cardiovascular disease, certain metabolic diseases, and certain cancer syndromes, in spite of a multidisciplinary approach and may for some be at best only managed. Chronic complex regional pain syndromes associated with ongoing functional impairment such as failed back syndrome and reflex sympathetic dystrophy (RSD) or sympathetically maintained pain (SMP) also fall into this category. Intractable pain can be managed so that the patient can be brought to the highest level of personal activities of daily living and be potentially gainfully employed

xix through rehabilitation. Suffering from “psychological pain impairment,” so well defined as “perceived nociception” by Dr. John Loeser, may be difficult to evaluate, but can often be ameliorated with an individualized, humanistic, behavioral treatment program. These issues and others will be reviewed. When are stress, anxiety, and depression (SAD) misinterpreted as malingering? An exceedingly important question. New therapies are available, based on sound psychological counseling and psychiatric experience. Home care counseling, peer counseling, and cost-effective packaged audio and visual programs are now available for selected patients. These subjects will be addressed by experienced authors. New treatment programs combing electromodulation continue to be developed in a dynamic process as technology changes and evidence is monitored by our continuing use of outcome studies. Integrating new approaches, new routes of delivery, new roles for team members, and even new roles for the patient/client and his or her significant others is addressed in this new edition. These modalities can be adjunctive to other treatments or prescribed alone. There is preliminary evidence that a home care program can significantly reduce costs when supported with good patient education. Electrotherapy treatment modalities that combine both psychological stress, somatic pain management therapy and clarification to help patients search to rediscover meaning in life, are catapulting us to a new frontier in wellness and recovery. Bioengineering principles that benefit and affect pathophysiogical processes, while not harming normal physiology, are the continuing quest for such modality treatment. The technology that results is controlled by regulators and agencies and may be mandated by statutory legislation. A relatively new field that I refer to as “energetics” is emerging in which psychoneuroimmunology is being studied for its ability to modulate response through noninvasive means of therapy. New chapters which review molecular-specific neurophysiological–electrochemical events altered by receptorspecific inducement have been added to this compendium. Concurrently, one notices a move away from ablative surgery in the modulation of intractable, desultory pain syndromes. Some of these chapters critically review newer methods of differentiating algorithmic pathways, clinically quantifying perceptual thresholds of alpha, beta, and C-fibers to wavelength-specific neural pathways of identified subsets of pain sensation. Treatments by electromodulation of spinal and cranial selective stimulation, present significant advances in pain management reported by specialists in neuromodulation of pain. New chapters in alternative medicine borrowed from European and Asian fields of healing have been added and updated. The role of spirituality is better understood in these therapies. Why do some tolerate pain better than others? These subjects will be addressed. Regulatory agencies separate experimental from investigative from approved categories of devices and further sub-classify them into three categories according to the Medical Device Act of 1976. Clinical pain associations network and have liaisons with these institutions. Clinicians are held responsible for using technology that is safe and approved for specific conditions. Scientific associations act as an important liaison between regulatory agencies. Associations help provide for testing of devices and develop guidelines and standards for protocols. The prescribing clinician, however, must be cautious and use only those devices approved for use with human subjects and understand the legal ramifications for using devices and substances for nonapproved indications. Care must be further exercised in not prescribing copied or “me, too” devices with exaggerated claims provided by the marketing department. The clinician must look for devices with established consensus by experienced investigative clinicians incorporating evidence from controlled trials and anecdotal case descriptions. This information will discussed in revised chapters. The all important changes affecting pain management in regard to the medical–legal community are addressed in view of the changing dynamic role of the many important court discussions and new precedents. This area of inquiry assists medical, research, regulatory, legal, judicial, and legislative bodies by updating relevant new information for their respective responsibilities in decision making. As we move forward into the 21st century with improved relations and technologies borrowed from many disciplines, we are closing the gaps in the lack of understanding conferred upon us by scientific ignorance. At the same time we are more cognizant of the need for understanding human relationships, habitats, and social policies. History shows us that the schism of Descartes’ mind–body dualism is being narrowed as we move from Aristotelian understanding of the natural order of things to Bacon’s view of interrelated orders. However, we should recall an observation from Albert Einstein that “All important things cannot be measured and all things that can be measured are not necessarily important.” Clinical judgment based on experience remains, therefore, paramount. As we move into the 21st century, the emerging field of “energetics” will help modify genetics or acquired impaired neural networks that influence perceptual pain, will provide great optimism for improving the future of our ecosystem, and will improve our understanding of simple and complex syndromes. The 21st century will move us out of Descartes’ “cave of ignorance” and beyond physical Newtonian concepts. We still do not understand how an anatomic neural network can also have consciousness, although general systems theory and complex theory aid our understanding. This will provide for treatments not yet imagined. The broad question whether pain perception is peripheral or centrally

xx mediated is still debated. Is it a combination of both? What are the roles of aging, culture, and genetic predisposition? Can we not do more to understand the yin–yang and context of the psychoneural biology of acute, chronic, cancer, and psychogenic pain syndromes, each with its different mechanisms? While learning to view individuals as part of a whole, we continue to learn pattern and structure, environment and heredity, and we improve the credibility of our knowledge. The 6th edition ofPain Managementwill provide the reader with an expanding horizon as we advance, to paraphrase Delaware’s former governor, Russell Peterson, into a better world by applying integrated approaches to pain management as our contribution to a meaningful legacy. According to Hippocrates, “The future is bright but fraught with difficulty.” Some day we may have a dolometer or pain meter. In conclusion, according to Helen Keller, “Alone we can do little, together we do a lot.” This text is dedicated to all those who participate in these initiatives. Pierre L. LeRoy, M.D., F.A.C.S.

Editor’s Note PAIN MANAGEMENT: A NEW APPROACH TO PAIN AND SUFFERING We have entered a new millennium and indications are that we shall continue the odyssey and quest for affordable, quality pain management. We are witness to new emerging historic events. In 2001, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) published new Pain Management Standards. Hospitals, skilled nursing facilities, and other similar programs in the United States desiring JCAHO accreditation must comply with the new Pain Management Standards. The University of Integrated Studies became the first American University to provide distance education and degree granting (M.A. and Ph.D.) in Pain Management, and today more clinicians practice multidisciplinary pain management than ever. As a result of these trends, many people in pain can find improved care and there is renewed hope for further reduction of pain and suffering.

HISTORICAL TREATMENT OF PAIN Throughout the millennia, problems associated with pain and attempts to control pain have historically been one of the principal reasons why individuals have sought health care. Alleviating pain is not a recent concern. Relief of suffering has been the helping profession’s primary objective throughout time. However, the way we view pain and the treatments available have been altered considerably. Individuals in prescientific cultures felt less control over their environment than is common in contemporary society. Consequently, people sought explanations and meaning for their lives in mystical, supernatural, or God-like concepts. The common thread was a feeling of very limited control over events. Attribution theory has been offered by social psychologists to explain coping mechanisms by which people ascribe a cause to an unpleasant event in the hope of establishing a difference between themselves and the “inflicted one.” Such a process could comfort one into a belief of invulnerability. Thus, early men and women attributed pain to evil, at times vengeful, spirits who invaded the body of an unworthy host. However, these spirits were amenable to negotiation. Culturally differentiated rituals were used to exorcize the pain. That ancient communities paid great attention to the treatment of pain is suggested by one of the earliest vocational specialties developed by humanity: the medicine man or witch doctor. Throughout recorded history, the healer or reliever of pain was given a special status in his or her community. Ancient healers or shamans practiced a sacred art and were viewed as catalysts who could negotiate with an angry God or who could, by ritual, restore balance with nature. In this orientation, intervention was possible, but the final outcome was not within the control of mortals. The context of the illness and pain represented more of a wholeness than presently exists in disease of the body, disease of the mind, or disease of the spirit. An illness affected the total person, who consisted of an integration of these components. Philosophically, this concept changed when Descartes conceptually separated the body from the soul and described pain as a signal of mechanical dysfunctioning. As a result, narrow specialties, often fragmented and with little common language, developed. Although such an epistemological approach has resulted in great scientific breakthroughs in many areas of acute health care, it has often created a barrier in our understanding of intractable pain.

THE PROFESSIONAL ENVIRONMENT OF PAIN MANAGEMENT Great strides have been made in our ability to help individuals who suffer from pain. We have gone beyond the historical method of providing treatment in which a sole practitioner works with a chronic pain patient. Interdisciplinary and multidisciplinary pain clinic facilities have demonstrated a new service delivery approach to pain management. There has been a phenomenal growth in the number and variety of inpatient and outpatient clinics. Professionals from several disciplines who work together have reintroduced an awareness that pain patients experience physical, emotional, interpersonal, financial, and spiritual problems. This reintegrated blend of art and science within the team concept helps establish the pain practitioner as a renaissance healer.

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xxii In 1988, the American Academy of Pain Management (AAPM) was incorporated so that clinical pain practitioners from all disciplines could work together for the purpose of developing standards for practice and codes of ethical conduct, and for the purpose of establishing a credentialing process for clinical pain practitioners.

CONTINUING EDUCATION Many current pain management professionals entered the field without the benefit of specific formal graduate training in pain management. Clinicians completed a terminal degree — be that medicine, mental health, pharmacy, or one of the other therapies — and began practice. In recent years, in the United States, a select few physicians, primarily anesthesiologists, could avail themselves of a Fellowship in Pain Management. In 2000, the AAPM developed a graduate curriculum that combined useful and practical information with the distance learning education format. A graduate committee composed of multidisciplinary clinicians and academicians developed a graduate program in Pain Studies. Graduate degrees (M.A. and Ph.D.) became available. As with the new JCAHO Pain Management Standards, the University of Integrated Studies presents evidence that the field of pain management has crossed a watershed.

EMERGING DISCIPLINE The 6th edition ofPain Management: A Practical Guide for Clinicians represents a continuing commitment by the AAPM in assisting pain practitioners to more fully understand the art and science of pain management. The authors whose work is presented in this text are among the leaders in pain management. They write with a vision based on experience. The collection of their wisdom, represented here, is relevant for pain management clinicians and professionals from all disciplines who wish a consultative state-of-the-art resource for their practice. Pain Management: A Practical Guide for Cliniciansis intended to be an updatable resource. Additional chapters will be written, and as new insights are gleaned from the real world of pain management, revisions will allow expansion, both increasing the value of this project and creating a living resource that will not soon become outdated. Each chapter has been written to allow the reader to independently read topics of interest and thus may be viewed as a self-contained study. The collection of chapters allows an authoritative self-study on many of the pressing issues faced by pain practitioners. The writing style of each author has been left intact, further highlighting the unique contribution of each chapter to the total project. The chapters and information presented may not represent any consensus of beliefs. We do not presuppose that all readers will agree with the sentiments that they find here, and some clinicians may disagree with others; however, we hold that by presenting this information, including divergent ideas, we provide a forum for discourse. It remains the clinician’s responsibility to assure that all treatment is consistent with community standards, is lawful, and is approved for the condition being treated. Although we have come a long way in our understanding of the impact of pain and in our ability to help reduce the toll of pain on the lives of our patients/clients, we have not yet eliminated the scourge of pain. It is my hope that this 6th edition will help illuminate our present ability and encourage future analysis.

CONCLUSION Pain is a great leveler. Those in pain and those who suffer recognize that pain perception changes according to intensity, frequency, and duration. The multidisciplinary model remains the best hope for reducing pain and suffering as we integrate information from many disciplines to understand the whole patient. As we look ahead, past and present traveling together, we can envision the spirit of integration leading the world to a better time. The AAPM salutes multidisciplinary pain management professionals as early representatives helping to improve scientific, social, and ethical change affecting health policy in pain management. To that spirit, it is my hope that this edition will help illuminate the road we all travel. Richard S. Weiner, Ph.D. Executive Director American Academy of Pain Management

Editorial Advisory Board • • • • •

Christopher R. Brown, D.D.S., M.P.S. B. Eliot Cole, M.D., M.P.A. Scott Denny, D.C., Ph.D., L.Ac. Arnold Fox, M.D. Paula L. Gilchrist, L.P.T., D.P.M.

• • • • •

Jacob Green, M.D., Ph.D. Barbara Lum, B.S. Carl McNeely, A.P.R.N., P.N.P. Thomas Romano, M.D., Ph.D. Kathryn A. Weiner, Ph.D.

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List of Contributors Christine L. Algren, R.N., M.S.N., Ed.D. Vanderbilt Children’s Hospital Nashville, TN

James P. Boyd, D.D.S. White Memorial Medical Center Los Angeles, CA

John T. Algren, M.D., F.A.A.P. Vanderbilt Children’s Hospital Nashville, TN

David E. Bresler, Ph.D., L.Ac. Academy for Guided Imagery Mill Valley, CA

Alfred V. Anderson, M.D., D.C. Pain Assessment and Rehabilitation Center Edina, MN

Clark Brill, M.D. Maryland Spine and Sports Medicine Columbia, MD

Lori T. Andersen, Ed.D., O.T.R./L. Florida International University Miami, FL

Christopher R. Brown, D.D.S., M.P.S. Dental Diagnostic Services Versailles, IN

Elizabeth Ansel, R.N. Pain Net, Inc. Columbus, OH James H. Ballard, D.Min., C.R.T. The Wellness Center at Hickory Grove Baptist Church Charlotte, NC Robert L. Barkin, M.B.A., Pharm.D., F.A.C., N.H.A., D.A.A.P.M. Rush Pain Center Deerfield, IL

Mary Ann Buchmeier, M.S., R.D. Columbia Medical Plan Pain Management Group Jan M. Burte, Ph.D., D.A.A.P.M. Private Practice Lido Beach, NY C. Stephen Byrum, Ph.D. Memorial Hermann Healthcare System Houston, TX Roger K. Cady, M.D. Primary Care Network Springfield, MO

Stacy Barkin, M.A., M.Ed., Psy.D., D.A.A.F.C. California School of Professional Psychology Alliant University San Diego, CA

Thomas C. Chelimsky, M.D. University Hospitals of Cleveland Cleveland, OH

Samira Kanaan Beckwith, A.C.S.W., L.C.S.W. Hope Hospice Ft. Myers, FL

Michael E. Clark, Ph.D. James A. Haley Veterans Hospital Tampa, FL

Hal S. Blatman, M.D. Private Practice Cincinnati, OH

William Clewell, Ph.D. University of Baltimore Baltimore, MD

Mark V. Boswell, M.D., Ph.D. University Hospitals of Cleveland Cleveland, OH

Misha Cohen, O.M.D., L.Ac. Quan Yin Healing Arts Center San Francisco, CA

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xxvi B. Eliot Cole, M.D., M.P.A., F.A.P.A. University of Integrated Studies Sonora, CA

Robert D. Gerwin, M.D. The Johns Hopkins University School of Medicine Baltimore, MD

Richard H. Cox, M.D., Ph.D., D.Min. Forest Institute of Professional Psychology Springfield, MO

Paula Lizak Gilchrist, L.P.T., D.P.M. Dr. Gilchrist and Associates Pittsburgh, PA

Jeffrey R. Cram, Ph.D. Sierra Health Institute Nevada City, CA

James Giordano, Ph.D. Moody Health Center Pasadena, TX

Jan Dommerholt, P.T., M.P.S. Pain and Rehabilitation Medicine Bethesda, MD

Ronald J. Gironda, Ph.D. James A. Haley Veterans Hospital Tampa, FL

Stuart A. Dorow, M.D., D.C., Ph.D Dorow’s Chiropractic Clinic Oklahoma City, OK

Robert Gordon, B.S.(Ed.), B.S.(Bio.), D.C., D.A.A.P.M. Cornerstone Professional Education, Inc. Salisbury, NC

John Robert Essman, M.A., R.E.E.G./E.P.T., R.P.S.GT. Jacob Green, M.D., Ph.D. Forest Institute of Professional Psychology Southeastern Neuroscience Institute Springfield, MO Jacksonville, FL Jan Fawcett, M.D. Rush Medical College Chicago, IL

Constance Haber, D.C. Alternative Medicine Pain Management Center Monroeville, PA

Thomas Ferguson, Ph.D. Columbia Medical Plan Pain Management Group

Gary M. Heir, D.M.D. University of Medicine and Dentistry of New Jersey Newark, NJ

C. Kumerlal Fernando, M.A., L.P.T. Island Rehabilitation Marco Island, FL Dale A. Ferranto, M.S. California Department of Justice San Clemente, CA Arnold Fox, M.D. Private Practice Los Angeles, CA Barry Fox, Ph.D. University of Integrated Studies Sonora, CA Deborah Fralicker, R.N., D.C. Southeastern Neuroscience Institute Jacksonville, FL R. Michael Gallagher, D.O., F.A.C.O.F.P., F.A.H.S. School of Osteopathic Medicine University of Medicine and Dentistry of New Jersey Moorestown, NJ

Nelson H. Hendler, M.D., M.S. Mensana Clinic Stevenson, MD A. R. Hirsch, M.D. The Smell & Taste Treatment and Research Foundation Chicago, IL Bruce Hocking, D.Ac. Acumed Medical Toronto, Ontario, Canada Linda C. Hole, M.D. Center for Healing Spokane, WA Earl Horowitz, D.P.M. Diabetic Foot Wound Center Jacksonville, FL Michael S. Jablon, M.S.T. Advanced Ultrasound Imaging, LLC Phoenix, AZ

xxvii Gary W. Jay, M.D., F.A.A.P.M., D.A.A.P.M. Headache and Neuro-Rehabilitation Center Lake Mary, FL

Daniel C. Lobash, Ph.D., L.Ac. Chinese Health Institute, KHT Systems Hemet, CA

Julie Jolin, M.D. UCLA Medical Center Los Angeles, CA

Timothy Lucey, B.S. Lake Erie’s College of Osteopathic Medicine, Student Erie, PA

Anne Marie Kelly, B.S.N., R.N.C. Catholic Memorial Home Fall River, MA

Richard Markoll, M.D., Ph.D. Bio-Magnetic Therapy Systems, Inc. Boca Raton, FL

Daniel L. Kirsch, Ph.D., D.A.A.P.M. Electromedical Products International Mineral Wells, TX

Michael F. Martelli, Ph.D. Concussion Care Centre of Virginia Glen Allen, VA

Barbara L. Kornblau, J.D., O.T.R./L., F.A.O.T.A., D.A.A.P.M. Nova Southeastern University Ft. Lauderdale, FL

Richard S. Materson, M.D. Memorial Hermann Continuing Care Corporation Houston, TX

John Claude Krusz, M.D., Ph.D. Private Practice Dallas, TX James S. Lapcevic, D.O., Ph.D., J.D., F.C.L.M. Osteopathic Family Practice and Pain Management Las Vegas, NV Marilyn Lauffer, M.S., R.N. Columbia Medical Plan Pain Management Group Stephen A. Lawson, M.S., C.R.C., C.I.R.S. Lawson Professional Counseling, Inc. Riverbank, CA W. David Leak, M.D., D.A.B.P.M. Pain Net, Inc. Columbus, OH

Robert S. Matthews, M.D. Mathews and Associates Lancaster, PA V. Robert May, Rh.D. May Physical Therapy Services National Association of Disability Evaluating Professionals Richmond, VA Rafael Miguel, M.D. Professor and Chief of Anesthesiology Service H. Lee Moffit Cancer Center and Director of Pain Management Fellowship Program Professor of Anesthesia University of South Florida College of Medicine Tampa, FL

Mathew R. Miller, P.Ac.. Penn Orthopedics of Lancaster Pierre L. LeRoy, M.D., F.A.C.S. Neurological Surgery and Pain Management ConsultantLancaster, PA Newark, DE Keith Nicholson, Ph.D. Toronto Western Hospital Felix S. Linetsky, M.D. Toronto, Ontario, Canada University of South Florida College of Medicine Tampa, FL Gretajo Northrop, M.D., Ph.D. and Southwest Blvd. Family Health Care Assistant Professor Kansas City, KS College of Osteopathic Medicine Nova Southeastern University Linda L. Norton, Pharm.D. Fort Lauderdale, FL University of the Pacific School of Pharmacy and Health and Sciences Private Practice Stockton, CA Palm Harbor, FL

Iva Lim Peck, L.Ac., Dipl.Ac., R.N. Acupuncture and Aesthetics Richardson, TX

Lloyd Saberski, M.D. Yale–New Haven Hospital New Haven, CT

Richard A. Peck, L.Ac., M.B.A. Acupuncture and Aesthetics Richardson, TX

Arnold Sandlow, D.C. Sports Medicine and Rehabiliation Therapy Institute Los Angeles, CA

Nick J. Piazza, Ph.D. University of Toledo Toledo, OH

Gabriel E. Sella, M.D, M.P.H., M.Sc., Ph.D., (Hon.C.), F.A.A.D.E.P., S.D.A.B.D.A., F.A.C.F.E., F.A.C.F.M., D.A.A.P.M. Ohio Valley Disability Institute Martins Ferry, OH

Tr even C. Pickett, A.B.D. Psy.D. Concussion Care Centre of Virginia Glen Allen, VA Diane Polasky, M.A., M.H., D.O.M., Dipl.Ac., D.A.A.P.M. Heights Acupuncture Center Albuquerque, NM John C. Porter, M.D. Spine Health and Rehabilitation Center Phoenix, AZ Juliet Scotti Post, D.C. Columbia Medical Plan Pain Management Group Andrea J. Rapkin, M.D. UCLA Medical Center Los Angeles, CA Anthony Rogers, M.D. Private Practice West Palm Beach, FL Thomas J. Romano, M.D., Ph.D., F.A.C.P., F.A.C.R. Private Practice Wheeling, WV Mary A. Romelfanger, R.N., M.S.N. U.S. Office of Congregational Health Services for the Sisters of Charity Nazareth Louisville, KY

Harry Shabsin, Ph.D. Columbia Medical Plan Pain Management Group Afshin Alan Shargani, D.C. Private Practice Los Angeles, CA C. Norman Shealy, M.D., Ph.D., D.Sc. Holos Institutes of Health, Inc. Springfield, MO Richard A. Sherman, Ph.D. Madigan Army Medical Center Tacoma, WA William D. Skelton, D.Ac. The Center for Pain Management Palmetto Baptist Medical Center Columbia, SC Devona J. Slater, C.M.C.P. Auditing for Compliance and Education Leawood, KS Robert B. Supernaw, Pharm.D. Texas Tech University Health Sciences Center at Amarillo Amarillo, TX

Samuel K. Rosenberg, M.D. University Hospitals of Cleveland Cleveland, OH

Myrna C. Tashner, Ed.D. State of Nevada Bureau of Disability Adjudication Social Security Administration Carson City, NV

Martin Rossman, M.D. Academy for Guided Imagery Mill Valley, CA

Blake H. Tearnan, Ph.D. Reno Spine Center Reno, NV

Ethan B. Russo, M.D. Montana Neurobehavioral Specialists Missoula, MT

Jane Tenberg, M.A. Columbia Medical Plan Pain Management Group

Ole Thienhaus, M.D., M.B.A., F.A.P.A. University of Nevada School of Medicine Reno, NV

Michael I. Weintraub, M.D., F.A.C.P., F.A.A.N. New York Medical College Briarcliff, NY

Robin Thomas, M.S., R.N., R.D. Columbia Medical Plan Pain Management Group

Daniel T. West, D.C. East Earl Chiropractic East Earl, PA

Kathryn L. Tucker, J.D. Perkins COIE LLP Seattle, WA

Kathleen Wooding, M.A. Columbia Medical Plan Pain Management Group

Uday S. Uthaman, M.D., F.A.C.F.P. Private Practice Newark, DE

Victor John Yannacone, J.D. Yannacone and Yannacone Patchogue, NY

Clayton A. Varga, M.D. Pasadena Rehabilitation Institute Pasadena, CA

Anthony T. Yeung, M.D. Arizona Orthopedic Surgeons Phoenix, AZ

Steven D. Waldman, M.D., J.D. Clinical Professor of Anesthesiology Kansas City School of Medicine University of Missouri Leawood, KS

Nathan D. Zasler, M.D., F.A.A.P.M.&R., F.A.A.D.E.P., C.I.M.E., D.A.A.P.M. Concussion Care Centre of Virginia Glen Allen, VA

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Chapter Consultants • • • • • • • • • • • •

A. Elizabeth Ansel, R.N. Peter F. Chase, D.D.S. Arnold Fox, M.D. Bob L. Gant, Ph.D. Karin Hilsdale, Ph.D., L.Ac. Gary W. Jay, M.D. James S. Lapcevic, D.O., Ph.D., J.D. Michael K. Perry, C.R.N.A., Ph.D. Scott Raven Margaret Texidor, Ph.D. C. David Tollison, Ph.D. Tom Watson, M.Ed., P.T.

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Section I Pain in Perspective

1 Pain and Its Magnitude Barry Fox, Ph.D. Trying to estimate the size of the crowd at a large publica greater number of arthritis sufferers, while other groups gathering — such as a protest at the White House — use a narrower, more restrictive definition that produces a can be difficult. People pour through the streets andsmaller tally. One estimate of the number of people sufparks; they do not stand still, they come and go. Youfering from chronic pain will include those with cancer cannot count the number of tickets sold or seats set out pain, while another will not. because there are neither tickets nor seats. The police Despite the many difficulties, several organizations give one estimate of the crowd size, the event’s organizhave developed estimates of the magnitude of the problem ers another. Some people make “guesstimates” of crowd in this country. According to the American Pain Foundasize by tallying up how many t-shirts or bags of popcorntion (APF) (2000), “over 50 million Americans suffer from were sold by vendors, or how much trash remains to be chronic pain …, ” adding that another 25 million develop cleaned up. acute pain following surgery or injuries. The American Determining how many people suffer pain is also aPain Society (APS) presents an expanded set of numbers, difficult proposition. Lacking firm measuring sticks, stating that while 50 million Americans suffer from health statisticians look to several indicators in order tochronic pain, an additional “25 million suffer with modpain, and another 8 million suffer with develop reasonably accurate estimates of the numbers erate-to-severe of people suffering from various types of chronic pain andcancer pain” (Pain Legislation, 2000). These figures, impressive as they are, may understate the problem. In the the associated costs. Unfortunately, even the “best” numbers from the most1998 edition of this volume, Tollison noted that “some 75–80 million people in the United States are estimated prestigious sources are only estimates. It is simply imposto suffer chronic pain,” adding that “this is generally consible to develop precise numbers, for many reasons. To begin with, we do not have a national health registrationsidered a conservative estimate” (Tollison, 1998). system, or a comprehensive national health database to For seniors, pain can be a constant companion. The track the numbers. Instead, the millions of people in thisAmerican Geriatrics Society estimates that “25% to 50% country are treated by a patchwork quilt of HMOs, privateof older persons living in the community have pain problems,” with 20% of older people taking pain medicines physicians, county hospitals, student health centers, etc., several times weekly (National Institutes of Health, 1998). and we do not yet have a system to correlate the statistics from all these disparate entities. But even if we had a Let us set aside the abstract numbers for a moment to national system for tracking all complaints reported tolisten to some of the ways people describe their suffering: physicians, we would not be able to account for thoseAching, agonizing, beating, biting, burning, constant, people who do not report their pain, preferring to ignorecramping, crushing, cutting, darting, depressing, drilling, it, to self-treat, or to seek help from alternative healthdull, excruciating, flickering, grinding, gripping, heavy, providers. To complicate matters more, there are differinghot, intermittent, killing, light, mild, moderate, nagging, nauseating, numbing, piercing, pinching, pounding, pulsways of grouping types of pain. For example, some organizations have a very broad definition of arthritis, yielding ing, racking, radiating, ripping, sharp, shooting, sore, 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

splitting, squeezing, stabbing, stinging, tearing, throbbing, thumping, tight, and tingling. With such an extensive pain vocabulary, it is clear that the problem is signifi cant. No matter whether the total number of people suffering from chronic pain is as high as 80 million or aslow” “ as 50 million, it is clear that the magnitude of the problem is greatand — greatly troubling.

• •

MILLIONS SUFFER FROM THE MAJOR “TYPES” OF PAIN Chronic and intermittent pain comes in a variety of forms, most commonly joint pain, headaches, and back pain, and it may be triggered by a large number of diseases, conditions, and states, including arthritis, bromyalgia, fi injuries, infection, cancer, trigemimal neuralgia, shingles, sickle cell disease, and angina. There is also the aching, burning pain of Central Pain Syndrome, which may develop after one has suffered a stroke or brain or spinal cord injury, developed multiple sclerosis, or had a limb amputated. Here are some estimates of the numbers of people suffering from some of the more common forms of pain:

•

• • Arthritis — According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases (1998), some 40 million Americans are afflicted by arthritis, “and many have chronic pain that limits daily activity. ” The total number of those suffering from arthritis is projected to reach 59 million by the year 2020. The Centers for Disease Control and Prevention (2001) give a slightly higher figure, stating “arthritis and related conditions have affected nearly 43 million Americans in 1998. ” The APF (2000) arrives at an even higher figure, estimating that “1 in 6 Americans suffers from arthritis. ” With a population of slightly over 284 million Americans as of May 2001 (U.S. Census Bureau, 2001), this means that some 47.3 million people have arthritis. Of them, 20.7 million suffer from osteoarthritis, the most common form of the disease, and 2.1 million have rheumatoid arthritis (National Institute of Arthritis, 1999). • Headaches— According to the National Institute of Neurological Disorders and Stroke (NINDS, 2000b),“an estimated 45 million Americans experience chronic headaches. For at least half of these people, the problem is severe and sometimes disabling.” The APF (2000) reports that more than 25 million Americans grapple with migraine headaches. • Back pain— Over 25 million Americans aged 20 to 64 are hit with frequent back pain (APF, 2000). Over 5 million suffer from low back pain

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•

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so severe as to be disabling (Collacott, et al., 2000; American College of Rheumatology).* The Occupational Safety and Health Administration (1993) quotes the Bureau of Labor Statistics to report that “more than one million workers suffer back injuries each year. ” Pelvic pain— One out of every six women suffers from chronic pelvic pain (Adamson, 1998). Cancer pain— In 1999, the American Cancer Society estimated that “approximately 8.2 million Americans alive today have a history of cancer,” and expected another 1.2 million new cases to be diagnosed that year. The Society (1998) further reports that “one out of every three being treated for cancer has related ”pain. Jaw pain — According to a report from The National Institute of Dental and Craniofacial Research, as many as 7.5 million Americans complain of pain in the face, or specifically in the jaw joint (Slavkin, 1996). The APF (2000) weighs in with a much higher number, stating that “20 million Americans experience jaw and lower facial pain (TMD/TMJ) each year. ” Fibromyalgia — Nearly 4 million Americans suffer from the pain of bromyalgia fi (APF, 2000). Most of these are women. Reflex Sympathetic Dystrophy Syndrome — According to the Reflex Sympathetic Dystrophy Syndrome Association of American (2000), the severe burning pain and terrible sensitivity to touch seen with the regional pain syndrome afflict some 1.5 million people in this country. The Association describes the syndrome as being “pain-filled” and “under-treated. ” Whiplash— An editorial appearing in the New England Journal of Medicinenotes that more than 1 million Americans suffer from a whiplash injury every year. Of those, 20 to 40% develop“symptoms that are sometimes debilitating and last for years (Carette, 1994). ” The authors of an article in the Archives of Neurology offer a more conservative estimate of the lasting impact of whiplash, stating that “after 12 months, between 15% and 20% of patients remain symptomatic, and only about 5% are severely affected” (Bogduk & Teasell, 2000). On the job injuries— Reporting on work-related musculoskeletal disorders, the Occupational Safety & Health Administration ([OSHA], 1999) stated that in “ 1996, more than 647,000 American workers experienced serious injuries due to overexertion or repetitive motion on the ”job.

* The American College of Rheumatology puts the number of Americans disabled at 5.4 million.

Pain and Its Magnitude

Just as we have dif ficulty determining the total number of people suffering from pain, we cannot pinpoint the precise number of people suffering from various “types” of pain (arthritis pain, back pain, headache pain, etc.). As you can see from the numbers above, sometimes reporting organizations are fairly close in their estimates, and other times they are far apart. Even reasonably sound numbers put forth by advocacy organizations, such as the American Cancer Society or the Reflex Sympathetic Dystrophy Syndrome Association of American, may be attacked by those who argue that these organizations overstate the magnitude of the problem in order to draw more attention to the problem and/or to raise more money. In the same vein, critics can argue that government organizations such as the National Institute of Neurological Disorders and Stroke exaggerate the scope of a problem because it is the nature of government bureaucracies to view problems as being larger than they really are. Nevertheless, the problem is clearly dramatic, afflicting people from all walks of life.

THE DOLLAR COST OF PAIN

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back pain at $16 billion a year. In an article appearing in theJournal of the American Medical Association, Collacott, et al. (2000) state that “the direct cost of treating low back pain is estimated at $15 billion, with indirect costs as high as $100 billion annually. ” The Bureau of Labor Statistics reports that back injuries are involved in 25% of all claims for workers compensation,“costing industry billions of dollars” (OSHA, 1993). • Headaches— Headaches send people to their doctors for 8 million visits each year, and migraine headaches force people to lose more than 157 million workdays annually (NINDS, 2000). Some $4 billion goes to pay for headache medications every year (Slavkin, 1996). • Work-related musculoskeletal disorders — The repetitive motion injuries, back pain, and other musculoskeletal problems suffered on the job are estimated to cost us between $13 billion and $20 billion annually in the form of compensation claims and lost work days (Steering Committee, 1999).

No one can put a price tag on a person’ s suffering, but we can make some estimates of the dollar cost of pain to the THE PERSONAL COST OF PAIN nation as a whole. As with the numbers of people in pain, We are all familiar with the“watch out!” pain that warns the estimates vary. us, for example, that we’ ve rested a hand on a hot stove • Total Costs— The APF (2000) reports that or pushed the sewing needle just a little too far through “ pain costs an estimated $100 billion each the material and into a finger. We welcome this pain, which year,” and that over 50 million work days per spurs us into taking immediately protective action. We year are lost to pain. The National Institute of have also experienced the “next time you’ll pay more Dental and Craniofacial Research weighs in attention” pain that reminds us, for instance, not to leave with a lower figure, specifically for chronic our fingers between a rapidly closing door and the door pain, stating that “estimated annual costs — jamb. We do not like either of these types of pain, but we including direct medical expenses, lost income, understand their meaning and applaud their purpose. lost productivity, compensation payments and Chronic pain, however, seems to have neither meaning legal fees — are close to $50 billion” (Slavkin, nor purpose. Sometimes the cause of chronic pain is clear: 1996). cancer of the pancreas, for example, which has spread to • Arthritis — According to the Centers for Disthe back. But oftentimes doctors and patients are fled baf ease Control (2001), arthritis costs the nation because the original condition has healed and the pain “nearly $65 billion annually” and is the second should have vanished. And, quite often, no one can deterleading cause of work disability. The Centers mine why the pain developed in the first place. (1999) also report that “persons with arthritis Ultimately, there is no meaning to chronic pain. It is and other rheumatic conditions accounted for not a “watch out!” warning or a“next time you’ll pay 2.4% (approximately 744,000) of all hospital more attention”reminder. It may be telling us that tissue discharges and 2.4% (approximately 4 million) is being damaged, but it keeps telling us, long after we of days of care in 1997. ” have received the message. Sometimes there is no damage • Back pain— “Back pain is the leading cause for the chronic pain to be speaking about. of disability in Americans under 45 years old” Long-lasting and lacking meaning, chronic pain can (APF, 2000). Low back pain is responsible for bring on the “‘terrible triad’of suffering, sleeplessness more than 93 million lost workdays per year and sadness” (NINDS, 2000a). When the “terrible triad” and “costs more than $5 billion in health care sets in, victims find it hard, sometimes impossible, to each year” (Slavkin, 1996). The American Col- work. Certain movements may be ficult, dif even basic lege of Rheumatology puts the costs of low ones such as getting up out of bed or reaching for a glass.

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Sleep may be disturbed, leading to constant fatigue and Moderate to severe chronic pain takes a big bite out weariness. Irritability and depression may soon follow.of quality of life. Eighty-one percent report that their pain The appetite may suffer, or the person may turn to foodhas interfered with their ability to exercise; 79% report in an attempt to assuage distress. Hit by a pain that seems that it interferes with their ability to get a good night’ s to strike without rhyme or reason, unable to find relief,sleep; 67% say it interferes with leisure activities and 65% perhaps told that “it’ s all in your head, ” chronic pain with household chores; 59% report that it hampers walkpatients may lose hope. ing; 54% report pain-related problems with sexual activArnold Fox, M.D. (personal communication, Septem- ity; 49% find that it hampers their ability to concentrate; ber 12, 2000), Past President of the American Academy and 41% say it hinders their ability to do their jobs. Emoof Pain Management, speaks of the “Eight Ds” of chronictional difficulties are triggered by uncontrolled pain. pain, the eight “side effects” he has seen in chronic pain Thirty-five percent report irritability; 27% listlessness; patients. They are 25% depression; 18% feelings of uselessness; 11% feeling unable to cope. 1. Depression— Patients wind up feeling that there Chronic pain patients tend to feel that narcotic mediis no point in trying to get on with their lives. cations do the best job of providing relief, rating them at 2. Distraction — Victims focus on their pain so 7.6 on a scale of 0 to 10 (10 being total relief). Prescription much that they may have ficulty dif handling NSAIDs are rated at 6.2 on the same scale, and over-theother aspects of their lives. counter medicines at 5.2. (Among those in very severe 3. “ Doctor Dancing” — Patients go from one pain, the narcotics, NSAID, and OTC ratings were 7.4, doctor to the next in their desperate search for 5.3, and 4.4, respectively.) relief. Seventy percent of the people report taking their med4. Disability — People in pain may be unable to icines as prescribed by their physicians, but 21% say they work or take care of themselves because of their do not follow their doctor’ s orders. The reasons for this physical or emotional symptoms. Compoundinclude wishing to take their medicine only when they ing the problems, their muscles may weaken need it and wanting to decide how much they will take. because of disuse. 5. Disease— Pain depresses the immune system, rendering us less able to fight off other illnesses. SLEEP AND PAIN 6–7. Drinking and Drugs— Sufferers may go to great lengths in their attempts to block chronic Lack of restful sleep is a common complaint among chronic pain patients. By one estimate, pain costs one third pain. 8. Death — In some cases, suicide may appear to of all American adults 20 hours of sleep per month (APF, 2000). A study conducted at the University of California, be the only way to end the suffering. San Francisco, School of Medicine utilized 24 oncology The Eight Ds may appear singly or in combination.outpatients to examine the relationship between pain, They may attack when pain is new or after it has “settledsleep, and fatigue (Lamberg, 1999b). The researchers found that it took the pain patients four times longer to in.” In any case, they are devastating. fall asleep, on average, than it takes healthy people. The pain patients awakened frequently. And while healthy conPROFILE OF PEOPLE IN PAIN trols had a mean sleepficiency ef (time sleep compared to time in bed) of 90%, the pained subjects had a mean sleep Everyone responds to pain uniquely, but it is possible to efficiency of only 71%. In another measure of the effects sketch pictures of some “typical” pain patients by looking of long-lasting pain on sleep, 141 patients reporting to at the results of a survey of 805 adult pain patients whose Emory University’ s pain clinic were questioned: 127 of pain had lasted at least six months and was rated at “5” them had suffered from problems with sleep (Lamberg, or more on a scale of 1 to 10, and who were not suffering 1999b). A Gallup survey conducted for the National Sleep from pain due to cancer (APS, 2000). Over 50% of pain patients have been in pain for 5Foundation found that one-quarter of American adults had years or more. Some 40% feel their pain is out of control.their sleep disrupted by pain 10 nights or more every Just about all of them have gone to doctors looking formonth — and headaches and back pain were the culprits relief. Almost half have switched physicians at least once,cited most often. Many were able to sleep only 5 hours per night, on average, when pain struck (Lamberg, 1999a). primarily because they still hurt, and also because they ficulty in sleeping. do not feel their doctors know enough about pain and Arthritis patients also report dif When researchers at Texas Women’ s University in Denton do not give the problem as much attention as it deserves. surveyed 90 men and women with osteoarthritis or rheuMore than 20% have changed doctors three or more times for these same reasons. matoid arthritis (Lamberg, 1999b), they found high “

Pain and Its Magnitude

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agreement with the statements, ‘I often have trouble going emotions, psychological makeup, and past experiences to sleep’and ‘Pain often awakens me. ’” affect the way their brains process pain messages. Sleep studies conducted in the laboratory confirm that The sensation of pain, for example, is determined to pain patients have sleep ficulties. dif Donald Bilwise, a surprising degree by a person’ s history of pain experiPh.D., head of Emory University’ s Sleep Disorders Cen- ence. A man who was terrified as a child after being ter, reports that “pain patients have more light sleep and attacked by a dog may find all dog bites extremely painful, less deep slow-wave sleep … as well as more frequent no matter how objectively minor they may seem to a brief arousals and more waking, or alpha brain activity inphysician. Cultural attitudes or genetic makeup also may slow wave sleep than do healthy persons” (Lamberg, affect the way a person experiences pain. Several studies, 1999a). for instance, have found that people of Nordic origin tend The disturbances in sleep patterns may be partiallyto be more stoic about expressing pain than are people of due to the pain itself, as well as accompanying anxietyJewish or Italian stock. Studies also point to differences in the way that northern and southern Italians view and and other emotional upset. Furthermore, many medicines respond to pain. used to treat pain can alter sleep patterns. For example, nonsteroidal anti-inflammatories can delay the onset of Soldiersfighting for a cause they hold dear are often deep sleep, while steroids may decrease REM sleep (Lamable to shrug off pain that might force others who are less berg, 1999a). motivated to give in. But even soldiers fighting for the same cause may react differently to pain. After Allied troops stormed the Italian beach at Anzio in 1944, doctors PAIN IS UNDERTREATED noted that some soldiers with minor injuries reported Most authorities agree that a fair amount of pain is leftsevere pain, while others who were seriously injured regundertreated. The National Institutes of Health reportistered few complaints. Likewise, athletes determined to (1998) that up to “80% of nursing home residents maywin have shown a remarkable tolerance for bearing pain. have substantial pain that is undertreated. ” The pain of A football player with a broken foot may run 90 yards for cancer is “widely undertreated, even though it can bethe touchdown without feeling any pain. Factoring into the pain equation a person’ s attitudes effectively controlled in up to 90 percent of all cancer toward pain, his fears, experiences, religious and cultural patients,” according to Philip Lee, M.D., Assistant Secrebackground, motivation, and other emotional and psychotary for Health, Department of Health and Human Serlogical factors is not yet possible. In the near future we vices, and Director of the Public Health Service (1994). will undoubtedly develop scanners that can count the numPatients at the end of life are also at risk of suffering from ber of sensory neurons in any part of the body, but we inadequate pain management. A 1999 survey released by the American Academy ofdo not even know how to begin to measure the emotional s interpretation Pain Medicine, the American Pain Society (APS) (1999),and psychological influences on the brain’ of pain. And, if we cannot agree on how acute pain should and Janssen Pharmaceutica found that “more than four out be measured, despite knowing exactly what causes the of every 10 people with moderate to severe chronic pain have yet to find adequate relief. ” Alarmingly, 56% of those problem, how can we come to any consensus on measuring chronic pain that appears to have no objective cause, with moderate to severe chronic pain have been hurting let alone set universal standards for treatment? for over 5 years. Patients complain that their doctors are not able to relieve their pain, do not know enough about In the absence of objective means to measure pain, as well as generally accepted treatment guidelines, some pain relief, and do not approach the problem aggressively doctors are worried that pain patients will become or seriously enough. addicted should they be given “too much” of certain medPart of the problem is that we have no objective means of quantifying pain. No one can tell how your pain hurtsications. Other physicians, along with some psychiatrists and psychologists, surmise that people whose pain will you, or to what degree. X-rays may reveal that a bone is not respond to their ministrations are using the pain for broken, and the presence of inflammation indicates that ” to gain sympathy or attention, for examthe body is fighting disease. But only you know if, where,“secondary gain, ple. Or, they conclude, such people are not motivated to and how much you hurt. It would be nice if doctors could recover, are exaggerating their pain to get out of work or say, for example: “Twenty sensory neurons in the patient’ s avoid responsibility, are addicted to pain-killing medicaright little finger are signaling 18 units apiece of pressure tions, or suffer from mental or emotional conditions. pain; 20 times 18 equals a pain rating of ”360. Unfortunately, we cannot do that because we do not know exactly Some patients undoubtedly invent or exaggerate pain symptoms for various reasons. But the overwhelming how many sensory neurons each patient has in his or her body, how much stimulus is required before the nervesmajority of pain patients suffer from real pain. And they will begin firing off pain messages, and how patients’want to be cured.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

National Institute of Arthritis and Musculoskeletal and Skin Diseases. (1998, January). Questions and answers about arthritis pain. http://www.nih.gov/niams/healthinfo/arth Adamson, G.D. (1998). Chronic pelvic pain: Evaluation and pain.htm management, and Chronic pelvic pain: An integrated approach (book review). New England Journal of Med- National Institute of Neurological Disorders and Stroke. (2000a, June 23) Chronic pain — Hope through research. icine, 339(17). http://www.nejm.org/content/1998/0339/ http://www.ninds.nih.gov/health_and_medical/pubs/chronic 0017/1252.asp _pain_htr.htm The American Cancer Society. (2001, August 2). ACS news today: Managing pain, http://www2.cancer.org/zine/ National Institute of Neurological Disorders and Stroke. (2000b, July 27). Headache — Hope through research. http://accesIndex.cfm?fn=004_12101998-0 sible.ninds.nih.gov/health_and_medical/pubs/ headache_ The American Cancer Society. (1999). 1999 facts and figures: htr.htm Cancer: Basic facts. http://www.cancer.org/statistics/ cff99/basicfacts.html, viewed September 9, 2000. National Institutes of Health. (1998, April). Gender and pain: American College of Rheumatology. Fact sheet: Back pain. Future directions. http://www1.od.nih.gov/painrehttp://www.rheumatology.org/patients/factsheet/backsearch/genderandpain/future.htm pain.html Occupational Safety and Health Administration. (1999, FebruAmerican Pain Foundation. (2000). Fast facts about pain. ary). Preventing work-related musculoskeletal disorhttp://www.painfoundation.org/medres/medresfacts.tmpl ders. http://www.osha-slc.gov/SLTC/ergonomics/ergo American Pain Society. (2000, February 17). Chronic pain in factnew.html America: Roadblocks to relief: Survey highlights. Occupational Safety and Health Administration. (1993, http://www.ampainsoc.org/whatsnew/summary030499.htm January 1). OSHA fact sheets: 01/01/1993 – Back injuAmerican Pain Society. (1999, February 17). New survey of ries – Nation’s number one workplace safety problem. people with chronic pain reveals out-of-control symphttp://www.osha-slc.gov/OshDoc/Fact_data/FSNO93toms, impaired daily lives. http://www.ampainsoc.org/ 09.html whatsnew/release030499.htm Pain Legislation S. 941/H.R. 2188 and H.R. 2260/S. 1272. ficeOf Bogduk, N., & Teasell, R. (2000, April). Whiplash: The evidence of Legislative Policy and Analysis. Bethesda, MD. for an organic etiology . Archives of Neurology, 57, 590. Public Health Service (1994, March 2). AHCPR releases cancer Carette, S. (1994, April 14). Whiplash injury and chronic neck pain treatment guidelines. pain [Editorial]. New England Journal of Medicine, Reflex Sympathetic Dystrophy Syndrome Association of America. 330(15), 1083–1084. (2000, March 17). RSDSA Publishers Objective Evidence Centers for Disease Control and Prevention. (1999, May 7). of RSD/CRPS. http://www.rsds.org/objective_evidence.htm Morbidity and mortality weekly report, 48(17). Atlanta, Slavkin, H. (1996). Insights on human health: What we know GA: Centers for Disease Control and Prevention. about pain. National Institute of Dental Research. Centers for Disease Control and Prevention. (2001). Arthritis: http://www.nidr.nih.gov/slavkin/pain.htm The nation’s leading cause of disability. http:// Steering Committee for the Workshop on Work-Related Muscuwww.cdc.gov/nccdphp/arthritis/index.htm loskeletal Injuries: The Research Base, National Collacott, E., et al. (2000). Bipolar permanent magnets for the Research Council. Commission on Behavioral and treatment of chronic low back pain. Journal of the AmerSocial Sciences and Education. (1999). Work-related ican Medical Association, 283 (10), 1322. musculoskeletal disorders: Report, workshop summary, Lamberg, L. (1999a). Chronic pain linked with poor sleep: and workshop papers . Washington, D.C.: National Exploration of causes and treatment. Journal of the Academy Press. American Medical Association, 281 (8), 691–692. Tollison, C.D. (1998). Pain and its magnitude. In R.S. Weiner Lamberg, L. (1999b). Patients in pain need round-the-clock care. (Ed.),Pain management: A practical guide for clinicians Journal of the American Medical Association, (8), 281 (5th ed., pp. 3–6). Boca Raton, FL: St. Lucie Press. 689–690. U.S. Census Bureau. (2001). Population clocks, 15:39 EDT May 23, 2001. http://www.census.gov.

2 Historical Perspective of Pain Management C. Norman Shealy, M.D., Ph.D., D.Sc. and Roger K. Cady, M.D. Most people fear death less than they fear continuing pain. much more significance to the emotional roots of pain. Indeed, many individuals who commit suicide during ter-Looking forward in history, the ancient Greeks introduced minal or potentially fatal illnesses do so to avoid painthe concept that the brain is the organ in which sensation themselves and philosophically to spare their families psy-becomes conscious, although that concept, introduced by chological suffering. Bonica (1990, p. 2) has estimatedAlcmaeon, was vigorously fought by Aristotle, who conthat 15 to 20% of the population has acute pain and 25 to sidered the heart the center of sensation. Hippocrates, the 30% has some form of chronic pain. The Nuprin Pain“father of medicine,” had a concept that was very similar Report (1986) suggests that pain affects a huge majority to the Chinese theory of five elements, except that the of Americans each year. Obviously, any consideration ofChinese included only four humors: blood, phlegm, yelpain has to begin with an understanding that pain is a low bile, and black bile. An excess or deficiency of one natural part of life and has been a major factor in human of the humors was supposed to lead to pain. Eventually, development throughout time. Prehistorical evidencethe reality of the brain as the seat of sensation was recogthrough archeological findings suggests that the most nized, and it was the ancient Greeks who demonstrated primitive of populations suffered from diseases whichthat the brain and the peripheral nerves were intimately would be expected to involve pain, and in the history ofconnected and that there were two types of nerves: those every civilization of the world, there are numerous refer-for muscle control and those for sensation. Ancient Rome ences to the plague of pain. The concept of counter-stimadded relatively little to the concept of pain, but Galen ulation through rubbing, massaging, or pressure on painful demonstrated the central and peripheral nervous system points or around painful areas probably has been used as well as cranial and spinal nerves and sympathetic throughout history. Theory and management have indeed trunks. Even so, Galen continued to follow Aristotle’s evolved together. concept of pain as “a passion of the soul.” At least 4500 years ago, the Chinese already had a The center of civilization moved to Arabia approxiwell-developed system of pain management–acupuncmately 1000 years ago, where Avicenna described 15 difture. Competent pain medicine clinicians today recog-ferent types of pain and treatment, including exercise, nize that acupuncture remains one of the most powerful heat, massage, opium, and other natural herbal remedies. treatments for both acute and chronic pain. Although weParacelsus, who died only 450 years ago, advocated the are not certain of the details involved, it is clear that theuse of opium and natural herbs, but added various elecChinese used herbs and, very early in their history, opi-trical stimulation techniques, massage, and exercise. oids or narcotics. Remarkably, even William Harvey, who described the The Egyptians chronologically stand next in line in circulation of the blood, considered the heart to be the site recorded history. The Egyptians appear to have believed where pain was felt. Descartes, who is often attacked by that pain was inflicted by either a god or a disincarnateholistic philosophers as the individual who tore the body spirit, and, as in India, the Egyptians considered the heart and mind apart, nevertheless made great contributions to to be the center of sensation. The ancient Indians attached the concept of pain. Unfortunately, as was true of much 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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early philosophy, he was rather inaccurate. He considered discrimination. Unfortunately, both the specifi city and that pain was a direct transfer through a tubular structure the pattern theories were incomplete. and that strong impulses were transferred directly from Hardy, Wolff, and Goodell (1952) objected to the patthe periphery to the brain. He is credited with essentiallytern and specificity theories and insisted that there was a creating the first“specialty” therapy for pain transmission. difference between reception of pain and reaction to pain. Although opium and, undoubtedly, alcohol were usedThey, perhaps more than any others of their time, introas analgesics from very early times, exorcism and various duced the concept of major cognitive, psychological, and religious ceremonies were also an integral aspect of pain emotional factors as important in chronic pain managecontrol in many cultures. Nevertheless, many early cul-ment. There are numerous other minor theories related to tures used surgical trephination of the skull for headache, pain, but the next major innovation and the one that and acupuncture, moxibustion, massage, physical exersparked the most intense change in the management of cise, and diet have all been used for pain control in apain in the past 5000 years was gate control. variety of cultures. In ancient Egypt, Greece, and Rome, Melzack and Wall (1965) introduced the theory that electric shock was used for the treatment of gout, headthe information coming in over C-fibers was modulated ache, and neuralgia through the use of the electric fish.through presynaptic inhibition from incoming beta fibers The first major innovation in pain treatment in almost in the substantia gelatinosa. This gating” “ mechanism 2000 years occurred in the late 18th century when Joseph depends upon the relative quantity of information coming Priestley introduced nitrous oxide, and it was later foundin over the larger fibers versus the smaller fibers. Thus, to be a significant analgesic. Throughout the 19th century, there are two major ways in which pain “gets through” great progress was made in neurophysiology in general the gate: either through damage to the beta fibers, which and pain physiology in particular. Johannes Muller intro-allows spontaneous pain or sensory deprivation pain, or duced“The Doctrine of Specific Nerve Energies” in 1840. by activation of the C-fibers by excess stimulation through Other important 19th century innovations were theinflammation or pressure upon the C-fibers (Figure 2.1). isolation of morphine from crude opium; the discovery of Later work by Shealy (1966) physiologically demoncodeine, aspirin, ether, and cocaine (especially as a local strated that approximately 60% of C-fiber activity was anesthetic); needles and syringes; hypnosis; the first neucrossed to the opposite side (Figure 2.1) of the spinal cord rological procedures for ablation of peripheral nerves ofand distributed fairly diffusely in all parts of the spinal the spinal cord in the management of pain; electrotherapy, cord except the dorsal columns. That is, 60% of the total hydrotherapy, and diathermy; and the introduction of thevolume of central distribution of C-fiber activation goes X-ray, for both diagnostic and therapeutic purposes. contralaterally, not into the spinothalamic tracts but During the middle to latter portion of the 19th century, through the entire gray and white matter of the cord other the specificity theory became the dominant concept ofthan the dorsal columns, and 40% is similarly distributed most scientists. Just as Galen, Avicenna, Descartes, and ipsilaterally. Strong stimulation of beta fibers is capable Muller had theorized, specificity seemed to consolidateof inhibiting at this initial gate the activity from the dorsal the idea of specific pathways and specific receptors for columns (Shealy & Tyner, 1966; Shealy & Taslitz, 1967). pain. It is interesting that as early as 1858, Schiff had demonstrated analgesia by sectioning the anterior quadrants of the spinal cord of an animal, and it was over 50 years later that a clinician in Philadelphia introduced the B-fibers concept of spinal cordotomy in the human being. von Frey C-fibers (1894) discovered specific end organ receptors for pain and touch and expanded Muller’ s concept to include warmth and cold. The origin of the pattern theory, another dominant pain theory, was introduced by Goldscheider (1894), who believed that certain patterns of nerve activation The ''gate'' were produced by summation of sensory input from the skin in the dorsal horn. This theory was further formalized when Nafe (1934) introduced the concept that all sensation is the result of spatial and temporal patterns of nerve impulses rather than the result of specifi c receptors or pathways. Building upon this, Sinclair (1955) and Weddell (1955) emphasized that all berfi endings, FIGURE 2.1 The dorsal columns are “pure” projections of beta except those innervating hair follicles, are similar andfibers. The gate is closed by increased input of beta fibers and that it is only the pattern that is important in sensoryopened by excessive C-fiber activity.

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It appears that the major contribution to the spino- Unfortunately, in going from a research project to a thalamic tracts is the input from the gamma-delta fibers,clinical application, the design of the electrodes was which primarily bring in acute or sharp brief pain as well changed from a solid platinum plate to a tinsel wire elecas touch, vibratory sensation, etc. The dominant role oftrode. The solid platinum plate electrodes had proven the dorsal columns seems to be similar to an FM radioremarkably sturdy and ficacious. ef Numerous problems station, modulating input from the other sensory fibers. developed with the tinsel wire electrodes, which seemed Shealy (Shealy, Resnick, & Tyner, 1966; Shealy &to polarize and develop increased impedance or break Taslitz, 1967), after discussing the gate control theory withfairly easily. The thickness of the machine-made elecWall and Melzack, reasoned that stimulation of the dorsaltrodes was also greater than that of the solid platinum columns would conceivably antidromically inhibit the plate, which led to increased technicalficulties. dif As a gate, and he demonstrated this initially in animals andresult, Shealy permanently stopped doing dorsal column later in humans. Both Melzack and Wall, in their original simulation in 1974 because he reasoned that the technoltheory, emphasized that there were descending controls ogy of had not been adequately researched to make the prothe gates coming from the cortex and other central brain cedure widely useful clinically. In his first paper on dorsal locations, as well as the peripheral control through thecolumn stimulation, Shealy had emphasized the possibilbeta fibers. Shealy, Mortimer, and Resnick (1967) hadity of inserting dorsal column stimulators percutaneously, demonstrated adequate safety of long-term stimulation of and it is worth noting that a variety of percutaneous dorsal the dorsal columns, in cats and monkeys, to insert the first column stimulators available today have less risk than the dorsal column stimulator in a human suffering from ter-totally surgically implanted ones that require a laminecminal metastatic cancer. tomy. Nevertheless, the long-term success rate is so poor In 1967, Shealy resurrected an old external electricalthat Shealy still considers dorsal column stimulation to be TM , and began encouraging the a technique that is rarely indicated and then only in stimulator, the Electreat engineers at Medtronic, Inc. to make a modern solid-state extremely desperate situations. electrical stimulator. Shealy, working in collaboration with The same year that Shealy presented his rst paper fi Long, and each working independently, prompted Normanon the experimental results of dorsal column stimulaHagfers (who left Medtronic to form StimTec, Inc.) and tion, Fordyce (1966) introduced the concept of behavDonald Maurer (at that time still with Medtronic) to pro- ioral modification or operant conditioning for manageduce the first two solid-state transcutaneous electricalment of pain. nerve stimulators. Shealy had already demonstrated that In 1970, Shealy recognized that he was selecting only the two most useful types of electric current for pain relief6% of the patients sent to him for dorsal column stimulawere the spike and the square wave. Various transcutanetion and began investigating the possibility of alternative ous electrical nerve stimulation devices were introducedsolutions to pain management in the vast majority of such in the early 1970s, using both square waves and spikes, patients. In 1971, he visited Fordyce’ s program. Fordyce although most devices currently use some form of modi-had treated approximately 100 patients with his 2-month fied square wave. The largest known collection of materialin-patient behavioral modification program, working with related to the use of electrical stimulation for variousup to 25 patients at a time. In 1972, Shealy organized a purposes is at the Bakken Library of Electricity and Lightnational meeting on the management of pain, which some (5337 Zenith Avenue, South Minneapolis, MN 55416); 400 individuals attended. As a result of that meeting, sevEarl Bakken is one of the co-founders and is the chieferal physicians set up similar multidisciplinary compreexecutive of Medtronic, Inc. hensive pain clinics, modeled after the Shealy system. In 1969, following Shealy’ s presentation of the results Over the next few years, increasing numbers of physicians of his first eight cases of dorsal column stimulation, aestablished various types of pain clinics. national Dorsal Column Study Group was formed. Its In 1976,Medical World Newspresented a cover artipurpose was to have a number of neurosurgeons do the cle entitled “Management of Pain, Medicine’ s New procedure and monitor the results over a 5-year period. Growth Industry. ” The article suggested that there were William H. Sweet, former Chairman of the Department ofapproximately 50 pain clinics in the U.S., 20 of which Neurosurgery at Massachusetts General Hospital, Medical World Newsconsidered“ holistic,” with others declined joining the Dorsal Column Study Group, and asbased upon the Bonica model. After the cover article a result, two companies began manufacturing dorsal colappeared, pain clinics indeed did become one of mediumn stimulators, Medtronic and Avery. During the next cine’s growth industries. By 1977, Bonica reported at few years, the Dorsal Column Study Group insertedthe Walter Reed Pain Symposium that there were some approximately 480 dorsal column stimulators. In the fall800 pain clinics in the U.S. of 1972, Avery began advertising dorsal column stimula- Shealy and Shealy’ s (1976) active behavioral moditors as a therapeutic technique for use by all neurosurfication program was transformed in 1974 to place geons, and Medtronic followed suit in the spring of 1973.greater emphasis on biofeedback, autogenic training, and

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

self-regulation techniques as a major modality for changing behavior. Although there have been somenements refi TABLE 2.1 (CONTINUED) in techniques and technology in the last two decades, The History of Pain Treatment there has been no further major innovation in the management of pain. Thus, as we move toward the next Alcohol Herbs millennium, it is worth noting the quantum leaps in the Witch doctors management of pain made in the latter part of the 19th Medicine men century through the introduction of transcutaneous and Prayer percutaneous electrical nerve stimulation, to some extent Exorcism implanted electrical stimulators, and the use of biofeed- Sacrifices back, autogenic training, and related techniques for Religious ceremonies behavioral modification. 18th Century The innovations in pain management sparked by the Mesmerism gate control theory have also led to a number of new Electrotherapy (crude) organizations and pain-related publications. Perhaps one of the most interesting aspects of modern life is that at 19th Century the end of the 20th century, the National Institutes of Nitrous oxide (in medical and dental field in 1863) Health has recognized acupuncture as a useful modalityHypnosis Muller’s specificity theory in the management of pain! Some major American-based organizations related to Morphine Codeine pain are: • American Association for the Study of Headache • International Association for Study of Pain • American Pain Society (regional pain societies, e.g., Eastern, Midwestern) • American Academy of Pain Medicine (originally American Academy of Algology) • American Academy of Pain Management • Some major publications related to pain are • Pain • Headache • Clinical Journal of Pain • Anesthesia & Analgesia — Current Research • Pain Practitioner • The American Journal of Pain Management A summary of the history of development of pain treatment is provided in Table 2.1.

TABLE 2.1 The History of Pain Treatment 2600 + B.C. Acupuncture Massage Exercise Opium

Aspirin (introduced in 1899 by Dreser) Diethyl ether (1846) Needle/syringe Cocaine (1884) Opioid narcotics Opium (1806 by Serturner) Codeine (1832 by Robiguet) Papaverine (1848 by Merck) Local anesthetics (cocaine) Physical therapy Hydrotherapy Thermotherapy (diathermy) Mechanotherapy X-ray for diagnosis and therapy Electrotherapy

20th Century Procaine (introduced in 1905 by Einhorn) Pattern theory Cordotomy Lobotomy Gate control theory Dorsal column stimulation Transcutaneous electrical nerve stimulation Biofeedback Operant conditioning Multidisciplinary pain clinics Neurotomy/neurectomy Modern anesthetics Narcotic agonists/antagonists Nonsteroidal anti-inflammatories Steroids Thalamic stimulation Serotonin-altering drugs Acupuncture approved by NIH

Historical Perspective of Pain Management

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REFERENCES

Behan, R. J. (1922). Pain: Its origin, conduction, perception, and diagnostic significance. New York: Appleton and Co. Bonica, J. J. (1990). The management of pain (2nd ed., Vol. 1). This is a good early treatise. Bonica, J. J. (1967). Management of intractable pain. In E. L. Way Philadelphia: Lea & Febiger. (Ed.),Concepts of pain (pp. 155–167). Philadelphia: Davis. Fordyce, W. (1966).Behavioral models for chronic pain and Bonica has emphasized the necessity for the use of a nerve illness. St. Louis: C.V. Mosby. Goldscheider, A. (1894). Ueber den schmerz im physiologischer block to determine if the surgical procedure would yield the desired results. und klinischer hinsicht . Berlin: Hirschwald. Hardy, J. D., Wolff, H. G., & Goodell, H. (1952). Pain sensations Bonica, J. J. (1976, January). Recent studies on the nature and and reactions . Baltimore: Williams & Wilkins. management of acute pain. Hospital Practice, 6–7. Management of chronic pain, medicine’ s new growth industry. According to John Bonica, the use of narcotics as analgesics (Editorial). (1976, October 18). Medical World News,54. for nonsurgical pain and for surgical anesthesia goes“back 2,000, Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new 3,000 or 4,000 years. ” Morphine was isolated 170 years ago. theory. Science, 150 , 871. Bonica, J. J. (1990). The management of pain (2nd ed., Vol. 1). Nafe, J. P. (1934). The pressure, pain, and temperature senses. Philadelphia: Lea & Febiger. In C. A. Murchison (Ed.),Handbook of general exper“There is only one pain that is easy to bear, ” said the French imental psychology.Worcester, MA: Clark University surgeon Rene Leriche, “and that is the pain of others. ” Press. Nuprin Pain Report (1986). A national study conducted forBraunwald, E., Epstein, S. E., Glick, G., Wechsler, A. S., & Nuprin by Louis Harris & Associates, New York. Braunwald, W. S. (1967). Relief of angina pectoris by Shealy, C. N. (1966). The physiological substrate of pain. Headelectrical stimulation of the carotid-sinus nerves. New ache, 6, 101–108. England Journal of Medicine, 227 , 1278–1283. Shealy, M. C., & Shealy, C. N. (1976). Behavioral techniques Perhaps the first use of implanted stimulators for relief of in the control of pain: A case for health maintenance vs.pain was that of carotid sinus nerve stimulation which relieved disease treatment. In M. Weisenberg & B. Tursky (Eds.),the pain of angina. Pain: New perspectives in therapy and research (pp. Brockbank, W. (1954).Ancient therapeutic arts . London: Heine21–33). New York: Plenum Press. mann. Shealy, C. N., Mortimer, J. T., & Resnick, J. B. (1967). Electrical The Eber’s Papyrus, written about 1500 B.C., has one of the inhibition of pain by dorsal column stimulation: Prelimfirst written records of treatment for pain. For “suffering in the inary clinical report.Anesthesia and Analgesia—Curabdomen, ” they recommended an enema of oil and honey. It is rent Research, 46 , 489–491. interesting to note that at the Massachusetts General Hospital, Shealy, C. N., Taslitz, N., Mortimer, J. T., & Becker, D. P. (1967). when I was a resident, milk and molasses enemas were someElectrical inhibition of pain: Experimental evaluation. times recommended. Anesthesia and Analgesia—Current Research,, 46 Cupping seems to have been practiced in primitive cultures 299–305. for thousands of years, and Hippocrates mentions it as being pracShealy, C. N., Tyner, C. F., & Taslitz, N. (1966). Physiological ticed in 400 B.C. The American Indians used a buffalo horn for evidence of bilateral spinal projections of pain bers fi in cats cupping. Leeching is mentioned at least 200 years B.C. and was and monkeys.Journal of Neurosurgery, 24 , 708–713. an important part of medical and lay healing technique for many Sinclair, D. C. (1955). Cutaneous sensation in the doctrine of centuries. In fact, it is still done in some Third World countries. specific nerve energy. Brain, 78, 584. Blistering also seems to have been used for many years, and written von Frey, M. (1894). Ber. Verhandl. konig. sachs. Ges. Wiss. accounts of the use of blistering appear in the 2nd century. Leipzig. Beitrage zur Physiologie des Schmerzsines, , 46 Hippocrates is quoted as having said, “Those diseases which 185, 188. medicines do not cure, iron cures [meaning the knife]. Those Weddell, G. (1955). Somesthesis in chemical senses. Annual which iron cannot cure, fire cures, and those which fire cannot Review of Psychology,, 6119. cure to be reckoned wholly incurable. ” Fordyce, W. E. (1976). Behavioral methods for chronic pain and illness. St. Louis: C.V. Mosby. ANNOTATED BIBLIOGRAPHY Fordyce created the concept of behavioral responses of operAbbe, R. (1911). Resection of posterior roots of spinal nervesant conditioning as the major underlying causes for pain. The to relieve pain, pain reflex, athetosis, and spastic paral-Fordyce concept is that pain is a learned or conditioned response ysis—Dana’s operation.Medical Records (New York), to a given stimulus or “operant” condition. “Respondents can therefore be said to be controlled by antecedent stimuli. Oper79, 377–381. ants, on the other hand, in contrast, are responsive to the influThe first spinal rhizotomies were done by Abbe. ence of the consequences that systematically follow their Anstie, F. E. (1873). Papers on electrotherapy. 1. On the relations occurrence. Operants can and do occur as a direct and automatic of faradic electricity to pain.The Practitioner: A Jour- response to antecedent stimuli, as is true of respondents. ” In nal, 2351–2360. other words, punishment vs. reward benefits from particular Francis E. Anstie published an article on the relations ofbehaviors determine whether or not they are learned and become faradic electricity to pain in London in 1873. part of the individual.

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Fordyce, W. E. (1988, April). Pain and suffering: A reappraisal.Lytle, L. D., Messing, R. B., Fisher, L., & Phebus, L. (1975). Effects of long-term corn consumption on brain seroAmerican Psychologist, 276–283. tonin and the response to electric shock. Science, 190 , Fordyce emphasizes in particular the difference between 692–694. pain and suffering. Hyperalgesia, which appears with tryptophan ciency defi Francois-Franck, C. A. (1899). Signification physiologique de la (serotonin defi ciency), is well discussed in this article. resection du sympathique dans la maladie de basedow, l’epilepsie, l’idiotie et le glaucome. Bulletin. Academie Mann, F. (1971).Acupuncture: The ancient Chinese art of healing. London: William Heinemann. de Medecine (Paris), 46 , 565–594. The oldest records of acupuncture date to bone etchings Sympathectomy for relief of pain was introduced by Franof 1600 B.C., and the rst fi book on acupuncture was written cois-Franck. about 200 B.C. Garrison, F. H. (1929).History of medicine(4th ed.). PhiladelMedtronic Neuro Division. (1983). A newsletter published by phia: Saunders. Medtronic, Inc., Minneapolis, MN, The pattern theory has been supported by Weddell and SinAn extensive bibliography on transcutaneous electrical clair. A neurologist, Spiller, noted a patient with a tuberculoma of the anterior lateral quadrant of the spinal cord who lackednerve stimulation was published by the Medtronic Neuro Division in March 1983. pain sensation on the opposite side of the body. He encouraged Frazier, a neurosurgeon, to perform a cordotomy in 1899. It was Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new Frazier who also began sectioning roots of the fifth nerve for theory. Science, 150 (3699), 971–979. trigeminal neuraligia in 1901. It was the advent of the gate control theory by Melzack Hammond, B. J. (1965). A history of electric therapy: Part one.and Wall which really revolutionized modern pain therapy. Their theory incorporates both physiological specialization as World Medical Electronics, ,344, well as central summation and input control. Basically, they In 1551, Jerome Cardan differentiated between the electricthat at the level of the substantia gelatinosa in the spinal ity of amber and the magnetism of lodestone and introduced believe a fi C-fibers, is presymmetri“fluid therapy of electricity, ” which is accepted as marking the cord, input over the smallestbers, transition from supernational to physical accounts of the phe-cally inhibited by information coming over the larger beta fibers. Beta ber fi stimulation never creates a painful sensation, nomenon. whereas unopposed C-fi ber sensation is perceived as very agoHorsley, V., Taylor, J., & Colman, W. S. (1891). Remarks on the various surgical procedures device and the relief or curenizing pain. Mitchell, S. W. (1872).Injuries of nerves and their conseof trigeminal neuraltic (“tic douloureux”). British Medquences . Philadelphia: Lippincott. ical Journal, 2, 1139–1143, 1891A; 2, 1191–1193, “Perhaps few persons who are not physicians can realize 1891B; 2, 1249–1252, 1891C. Victory Horsley, the great British neurosurgeon, introducedthe influence which long continued and unendurable pain may have upon both body and mind. ” the concept of gasserian neurectomy in 1891. Jenkner, F. L., & Schuhfried, F. (1981). Transdermal and trans-Mortimer, J. T. (1968).Pain suppression in man by dorsal column electroanalgesia . Unpublished Ph.D. dissertation. cutaneous electric nerve stimulation for pain: The search School of Engineering, Case Western University, Clevefor an optimal wave form.Applied Neurophysiology, land, OH. 44(5–6), 330–337. The subject of pain has been likened by Mortimer to the The question of the optimal waveform for electrical stimufable of the blind men and an elephant. Each saw and interpreted lation has never been adequately settled. Jenkner has emphasized the elephant only as that particular part of the elephant with what he considers to be an optimal waveform. Kellaway, P. (1946). The part played by electric fish in the earlywhich he had come in contact. Thus, pain has been viewed throughout much of history from a noncomprehensive point of history of bioelectricity and electrotherapy. Bulletin of view, each person and each discipline having a rather limited Historic Medicine, 20 , 112–137. This is a marvelous article on the role of the electric fishview of the whole. Reynolds, D. V., & Sjoberg, A. E. (Eds.). (1971). Neuroelectric and was the William Osler Medal Essay. The author comments research: Electroneuroprosthesis, electroanesthesia and that even in the early days in the U.S., electric fish were used nonconvulsive electrotherapy . Springfield, IL: Charles and often kept in tanks on plantations to be used for pain control, C Thomas. and these were “much favored by the Indians and the Negros. ” Kratzenstein, a German physicist, was probably first the Letievant, J. J. E. (1873). Traite des sections nerveuses: Physimodern scientist to report therapy with electrification” “ in ologie pathologique, indications, procedes operatoires . 1744. Interestingly, he reported that it increased his pulse and Paris: Balliere. Apparently the first book on surgery pain was written by allowed a better quality of sleep. He used it to treat partial Letievant in 1873 and was primarily concerned with neurecto-paralysis as well. mies for neuralgias of the face and extremities.

Historical Perspective of Pain Management

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New frontiers in transcutaOf course, we all know the work of Benjamin Franklin, Tapio, D., & Hymes, A. C. (1987). neous electrical stimulation . Minnetonka, MN: LecTec who was very cautious about interpretation. He stated, I never “ Corporation. saw any advantage from electricity in palsies that was permaElectric eels were known by ancient Egyptians and Hipponent.” In the late 1800s, there was a great urryfl of activity in electrotherapy. Rousell reported, It is “ especially in the genital crates as potentially useful for producing an electrical shock to organs that electricity is truly marvelous. Impotence disap-control pain, but it was apparently Scribonius Largus who first used the electric ray torpedic fish for treatment of both headache pears, strength and desire of youth return, and the man, old and gout and recorded it in 46 A.D. William Gilbert was reported before his time, whether by excesses or privations, with the aid to have been the first to classify and generalize the phenomenon of electrical fustigation, can becomefteen fi years younger. ” in Subtil Machines as large as 8 feet in diameter were used to create of anelectricity (1544–1603). In 1756, Richard Lovett,The electrical static discharge. Out of this, of course, grew convul-Medium, proved dozens of cures for many diseases using elecsive electroshock therapy.Some “ treatments and instruments tricity. John Wesley, founder of the Methodist church, was extremely enthusiastic about this treatment and also described have been introduced as original as many as a dozen times many examples of diseases “cured” with electrotherapy, includsince the early 1700s. ” ing sciatica, headache, gout, pleuritic pain, and angina pectoris. Schmidt, J. E. (1959).Medical discoveries . Springfield, IL: Between 1750 and 1780, 26 publications dealing with clinical Charles C Thomas. electricity appeared. John Birch, an English surgeon, used elecSurgeons gradually moved higher and higher in the nervous trical current to control pain in 1772. Beginning in the early system, attempting to relieve pain with destructive procedures. Finally, in 1950 Mandel introduced the frontal lobotomy for the 1900s, various electrical stimulators were sold to the public by door-to-door salesmen as well as in various catalogs. These relief of intractable pain. It had been used, of course, over 10 instruments were very popular and came with all types of claims years earlier for treatment of psychosis (p. 180). and cures, including curing cancer. The FDA banned the sale of Shealy, C. N. (1974). Transcutaneous electrical nerve stimulasuch instruments in the early 1950s. In 1967, Shealy introduced tion for control of pain.Clinical Neurosurgery, 21 , the concept of dorsal column stimulation for control of pain, and 269–277. that led to work with electromodulation. Shealy, C. N., & Mauer, D. (1974). Transcutaneous nerve stim-Thorsteinsson, G., Stonnington, H. H., Stillwell, G. K., & Elveulation for control of pain: A preliminary technical note. back, L. R. (1977). Transcutaneous electrical stimulaSurgical Neurology, (1), 2 45–47. tion: A double-blind trial of its ef ficacy for pain. These are the first two scientific articles on the use of what is Archives of Physical Medicine and Rehabilitation,, 58 known as TENS or transcutaneous electrical nerve stim8–13. ulation. A number of double-blind studies have emphasized that transcutaneous electrical nerve stimulation is not a placebo. Smith, R. H. (1963).Electrical anesthesia . Springfield, IL: Charles C Thomas. U.S. Department of Health, Education and Welfare. National “ Safe anesthesia produced by application of electrical curInstitutes of Health,Pain. (1968, September). rent has been a goal for over eighty years [in 1963!]. ” Russian In 200 A.D., Galen advocated opium and mandragora as electrosleep therapy was described in 1914 by Robinovitch.well as electrotherapy for control of pain. The first public dem“Anesthesia produced by the application of electrical currentonstration of anesthesia on a patient was in 1846. The most has been called electronarcosis. ” In 1902, Leduc published his important contribution to the management of pain was the develearly work with electronarcosis. He tried various frequenciesopment of the syringe and hypodermic needle (1845–1855). of current, but mostly used 100 cycles per second of directCocaine was introduced into medical practice in 1884. Dr. Wilcurrent square wave. Although he produced a rather cataplectic liam Halstead of Johns Hopkins discovered the principle of block state in which patients were unable to move, they were stillanesthesia, which was the injection of cocaine into a nerve trunk. aware of pain. Glen Smith reported successful electronarcosis Spinal anesthesia was introduced in 1898. In 1967, the National in dogs over 200 times, in rhesus monkeys 6 times, and in the Institutes of General Medicine Sciences offered the first center chimpanzee once. grant to the University of Pennsylvania and the second in 1968 Solomon, R. A., Vierstein, M. C., & Long, D. M. (1980, Febru- to Harvard University to develop “anesthesia research and trainary). Reduction of postoperative pain and narcotic useing centers where teams of scientists in many disciplines worked together in studying basic molecular research to anesthesia techby transcutaneous electrical nerve stimulation. Surgery, niques in the operating room. ” 142–146. This is another good article to quote. White, J. C., & Sweet, W. H. (1955). Pain: Its mechanisms and neurosurgical control . Springfield, IL: Charles C Thomas. Spiller, W. G., & Martin, E. (1912). Treatment of persistent pain of organic origin in the lower part of the body by division White, J. C., & Sweet, W. H. (1969). Pain and the neurosurgeon: of the anterolateral column of the spinal cord. Journal A forty year experience . Springfield, IL: Charles C Thomas. of the American Medical Association, 158 , 1489–1490. In more modern times, the classics were written by White According to Sweet and White (1955), in 1905 Spiller of and Sweet. Philadelphia discovered the problem with tuberculoma of pain, and Martin was the one to carry out the rstfisuccessful cordotomy.

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Wolff, H. G. (1963).Headache: And other pain (2nd ed.). New York: Oxford University Press. Headache, one of the most common of major pain complaints, was perhaps most well studied by Harold G. Wolff.

Section II Elements of Multidisciplinary Pain Management

3 Implementing a Pain Management Program Anne Marie Kelly, B.S.N., R.N.C. The purpose of human life is to serve, to show compassion, and to help others. Albert Schweitzer

INTRODUCTION

TABLE 3.1 Key Components of a Successful Program 1. 2. 3. 4.

Institutional commitment Interdisciplinary team Education Continuous quality improvement

Relieving pain and suffering is at the heart of the healthcare profession. Despite attempts at treating pain over the IDENTIFY INSTITUTIONAL LEADERS decades, fear of unrelieved pain remains a major concern of patients in all healthcare settings. In 1992, the Agency for Healthcare Policy and Research (AHCPR) published Well begun is half done. guidelines on acute pain which state that the institutional Aristotle responsibility for pain management begins with the affirmation that patients should have access to the best level The first step in identifying institutional leaders is the of pain relief that may be provided safely. Regarding eth-appointment of a task force to determine a plan of action. ical responsibility, the guidelines stress that the ethicalSeek out the champions” “ in your institution who have a obligation to manage pain and relieve the patient’s suffer-vested interest and knowledge in pain management. It is ing is at the core of a healthcare professional’s commit-important to give those who feel a sense of commitment ment (Acute Pain Management, 1992). Today, healthcare and ownership the opportunity to contribute to the develinstitutions are challenged with the responsibility and eth-opment of the program. Peters (1987) suggests that those ical obligation to develop the necessary means and vested“ look inward, work with colleagues and customers, resources to effectively treat pain in all patients. As thework with everyone, to develop and instill a philosophy and guidelines focus on improving the quality of pain relief, vision that is enabling and empowering” (p. 482). Once the the need for programs that address this is becoming task force has been selected, conduct an institutional assessincreasingly apparent. One of the best means to ensure ment to examine your organization ’s culture, strengths, and optimum pain control is the availability of a pain manage-weaknesses related to current pain management practices. ment program that combines the expertise and commitThis group should address the following issues: ment of a healthcare team whose members are dedicated to the prevention and treatment of pain. Formalized pro- 1. Is pain management an institutional priority? grams are necessary to bring pain control to its rightful 2. Who has a knowledge base about pain place in the healthcare system. This chapter focuses on management? the key components and steps necessary for the successful 3. Do the policies and procedures ensure quality implementation of an effective pain management program pain control? 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

4. Who is accountable for pain management? 5. How is quality measured?

The Joint Commission on Accreditation of Healthcare Organizations (JCAHO, 1999) set new standards for the assessment and management of pain which healthcare Although pain is a common problem, it remains largelyinstitutions must be prepared to meet in 2001 (Dahl, 1999). These standards call upon hospitals, home care an invisible one. The task force can serve as a catalyst involved in promoting increased visibility of the prob- agencies, nursing homes, behavioral healthcare facilities, lem of unrelieved pain. Its focus is to collect and pro-outpatient clinics, and healthcare plans to: vide necessary data to initiate efforts to address the • Recognize the right of patients to receive approexisting problems. The results can provide strong evipriate assessment and management of pain. dence pointing to the need to standardize pain assess• Assess the existence and, if so, the nature and ment policies, make changes in institutional proceintensity of pain in all patients. dures, and develop standards of acceptable practice. • Record the results of the assessment in a way that Making the problem of pain visible in your institution facilitates regular reassessment and follow up. is the initial step in developing a formalized approach to pain management. • Determine and assure staff competency in pain assessment and management. • Address pain assessment and management in DEVELOP A MISSION STATEMENT the orientation of all new staff. FOR THE PROGRAM • Establish policies and procedures which support the appropriate prescription or ordering of It is imperative that the mission statement reflect the valeffective pain medications. ues and purpose of the organization related to pain man• Ensure that pain does not interfere with particagement practices. By articulating its purpose and what it ipation in rehabilitation. stands for, the institution directs the work of the staff. In • Educate patients and their families about effecdescribing the importance of a clearly articulated purpose, tive pain management. Ulschak (1988) states that, “until there is agreement about • Collect data to monitor the appropriateness and purpose, an institution has no direction, no tool to measure effectiveness of pain management. progress, no real reason to be motivated, and no clear • Address patient needs for symptom managefocus for its energy. ” For institutional commitment to be ment in the discharge planning process. achieved, it must start at the top. Administration must provide leadership that can result in institutional change, encourage employee commitment, and ensure improved These standards serve as guidelines in developing policies and procedures for all healthcare facilities. Clearly standards of care. Leaders in the organization will need defined standards will positively affect the quality of to help staff understand why change is necessary and how patient care. The JCAHO standards establish the foundait relates to the mission. Staff members must clearly see that the institution’s priority and goal is to promote high tion for a system-wide initiative in pain management. standards of safe, effective pain relief to all patients within its care. Institutional commitment and administrative supDEVELOP AN INTERDISCIPLINARY port are the foundation on which to build a quality proAPPROACH TO PAIN MANAGEMENT gram and are absolutely essential to success. Because pain is a multidimensional experience, it requires an interdisciplinary approach. Pain profoundly DEFINE STANDARDS OF CARE affects not only the physical, but the psychological, Defining standards is a key step in developing an effec-social, cultural, and spiritual dimensions of life (Ferrell, tive program. Pain management is arguably one of the SuccessDean, Grant, & Coluzzi, 1995; Saunders, 1884). most complex topics in medicine today. From dealingful pain control requires attention to all aspects of care with acute, chronic, and cancer pain, to providing pal-and suffering, and no amount of well-prescribed analgeliative and compassionate end-of-life care, caregivers are sia will relieve the pain unless the elements that are faced with multiple issues that extend far beyond thecompounding the problem are addressed. Care provided question of what medication to administer. Written stan-by a team of specialized healthcare professionals is dards are necessary to defi ne the expectations of the required to treat the diverse aspects of pain. For moderncaregivers and show how the care delivery system is day pain therapy to be effective, institutions need to organized and managed. The mission of the institutiondirect their attention to the importance of interdisciplisets the direction for all written standards. Standardsnary teams. An interdisciplinary team is a valuable make quality a day-to-day goal. resource that serves the organization in many ways:

Implementing a Pain Management Program

• It serves the organization by assisting in the development of policies and procedures, offering consultation, and providing a forum for the resolution of dif ficult pain management issues. • It serves the patients by attending to the multiple dimensions of optimum pain management and integrates all aspects of care. • It serves the families by providing support and guidance as they confront the common challenges associated with caring for a loved one coping with pain. • It serves the community by promoting educational programs for families and the general public that focus on pain assessment, pain treatments, drug addiction, and how to communicate with healthcare professionals about pain. A holistic approach is critical to breaking down the barriers to pain management and is successful because it allows physicians, nurses, and other clinicians to learn more about the “ person” than just the disease (National Institutes, 1987).

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• Assess the physical, psychosocial, spiritual, functional, emotional, and cultural needs of the patient. • Use standard tools to assess the patient. • Discuss summary of findings with attending physician and make appropriate recommendations. • Review treatment plan and pain relief goal with the patient and family and encourage participation in decision making. • Include both pharmacologic and non-pharmacologic therapies. • Attend weekly, interdisciplinary team meetings to review plan of care and problem solve. • Communicate plan of care to appropriate staff members. • Assess for pain relief regularly throughout the course of treatment. • Visit the patient at least once a week to assess progress. • Educate patient and family about pain management. • Measure outcomes to continually improve pain management practices.

A pain management team includes professionals from various disciplines who meet regularly to discuss and develop an individualized plan of care for each patient. ASuccess of the team is measured by its ability to provide pain relief in a safe and effective manner to meet the needs typical team may include one or more physicians, nurses, and expectations of the patient and family. The following pharmacists, physical therapists, occupational therapists, case example, in which the author was part of the interpastoral care counselors, social workers, dieticians, and disciplinary team, illustrates these points. staff educators. Depending on the setting, you may want to include a certified nursing assistant, therapeutic activity therapist, and trained volunteer. A team can address the CASE EXAMPLE great need for accountability in pain management and prevent further fragmentation of care (see Table 3.2). This Mr. F. was a 79-year-old man with terminal rectal is the best approach for responding to pain and a critical cancer who resided in a long-term care facility. He component of an effective pain management program was an alert, oriented, and religious man who under(Gordon, Dahl, & Stevenson, 1996, pp. 10–36). stood his prognosis and elected to receive comfort measures only. His pain had been fairly well controlled and his medications had been titrated up to 400 mg of Oxycontin b.i.d., Actiq 400 mg q 3 h. p.r.n. TABLE 3.2 for breakthrough pain, Celebrex 100 mg b.i.d., and Role of Interdisciplinary Team Nortriptyline 25 mg @ h.s. Mr. F. was able to maintain 1. Identify patient, family, and staff needs in pain management his independence and did not exhibit any major side 2. Assure pain relief goals are met effects from the medications. During this time, he was 3. Collaborate with healthcare providers to facilitate optimum also referred to the pain clinic for consultation regardpain control ing pain control measures. As the rectal tumor 4. Promote practice changes through outcome quality enlarged, his pain escalated and became more ficult dif improvement monitoring to manage. He was once again seen by the anesthesiologist at the pain clinic who recommended the placement of a tunneled, epidural catheter for optimum pain control. Mr. F. consented to the procedure DEFINE ACCOUNTABILITY and his attending physician agreed this was the best Each team member is accountable for carrying out a spe- course to follow. However, this created a challenge cific task and plays a key role in the management of pain. for the long-term care facility for the following reaTeam members: sons:

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

1. The facility had no written policies and procedures for epidural analgesia and the nurses felt ill-prepared having little or no knowledge in this area.

to distract him from any pain; the staff educator provided ongoing education and assessed the competency of the staff; the hospice nurse offered respite care and support to the patient, family, and staff. The interdisciplinary 2. Mr. F. wanted to come back to the facility where he team, composed of dedicated professionals, was a vital felt at “home” and wished to die in a loving environment force in diminishing his physical, psychosocial, and spirwith the staff he considered his “family. ” itual pain. When team members listen and acknowledge all aspects of pain, the patient experiences a feeling of 3. The facility’s mission statement clearly articulated worth, dignity, peace, and wholeness. that the institution’s priority was the relief of pain. Although this was one of the most challenging cases for the long-term care facility, it was also the most Following a discussion with administration and the gratifying. Everyone understoodrsthand fi the meaning interdisciplinary team, all members agreed it was theof institutional commitment and saw how a concerned institution’s responsibility and ethical obligation to pro- and knowledgeable team is vital to successful pain vide the necessary means and resources to care for Mr. management. F. during his final days. With administrative support, the members of the interdisciplinary team developed the necessary policies and procedures and provided education DEVELOP AN EDUCATION PLAN to the clinical staff in every aspect of care. With adequate education and support from the team, the nurses felt There is no knowledge that is not power. confident and prepared for Mr.’sF.return from the hospital. The nurses knew the moment they saw Mr. F. that Ralph Waldo Emerson they had made the right decision. Upon arrival, Mr. F. looking at the nurses with a big smile on his face stated, Traditionally, medical and nursing schools have devoted “ It’ s a miracle. I have no pain. ” His pain was controlled very little, if any, time to the subject of pain management. with 1% Bupivicaine and Fentanyl 5 mcg/cc at 6 to Healthcare providers cannot be expected to practice what 14cc/h and bolus doses of Fentanyl 5 cc q 10 min via they a do not know. Inadequacies in the education of health PCA pump. His pain ratings ranged from 0 to 2 and heprofessionals has contributed to fears and misconceptions remained comfortable until his death, four weeks later.regarding the use of pain medications, addiction, and consequently inadequate pain management (Liebeskind & Although saddened by his death, the staff tempered their grief knowing that they had made a difference in his life.Melzack, 1998). Mr. F. died peacefully, with dignity, and in a loving Education is the key step to improving pain manageenvironment surrounded by dedicated staff who under-ment practices that result in institutional changes. Identistood that life is a gift to be cherished up until its nalfi fying the learning needs of your staff is vital to your moments.His wishes had been fulfilled and the facility’s educational efforts. This can be accomplished in a variety goal had been met. of ways: During those four weeks, the interdisciplinary team • Administer a pretest to assess the knowledge invested all its skill and effort into relieving his pain and level of your staff and to determine who has a suffering. The physician monitored his condition and knowledge base about pain management. ordered medications for pain control; the pharmacist made certain the medications were prepared and deliv- • Involve the interdisciplinary team members in conducting a survey in each of their practice ered in a timely manner; the nurses assessed him reguareas to assess the learning needs of each dislarly for pain relief and potential side effects; the nursing cipline. assistants provided physical care with a compassionate touch; the physical and occupational therapists evaluated • Use the baseline data collected in your institutional assessment about current pain management his ability to maintain optimum independence for as long practices. This is essential to planning education as possible and made recommendations for his comfort; for the improvement of staff performance. the social worker listened to his expressions of fear and other emotions and offered support; the pastoral care • Establish focus groups of about 6 to 10 people from different disciplines and ask their opinions counselor addressed his spiritual needs by praying with about learning needs. Including grass “ roots”input him daily and being present; the dietician monitored his is useful for correcting inadequacies that exist. nutritional needs and paid special attention to his food preferences and his ability to swallow; the recreational therapist provided him with musical tapes he enjoyed Once you have identified the learning needs of the staff, it is important to outline an education plan including and taught him relaxation techniques and guided imagery

Implementing a Pain Management Program

23

curriculum content, staff time, and programming costs. the organization’ s commitment to quality pain For developing a comprehensive pain management promanagement practices. gram, consider including these core content areas: Pain Management Poster Presentations — This is a unique and enjoyable way to involve all • Physiology of pain departments and demonstrate that pain management requires an interdisciplinary • Pain assessment approach. Encourage creativity by inviting • Types of pain employees from all departments to design a • Assessment tools and pain rating scales poster of their choice related to pain manage• Analgesics: non-opioids, opioids, adjuvant ment. Employees can work individually or as medications a group, and are given a deadline to complete • Symptom management the project. Display the posters throughout the • Psychosocial, spiritual, and cultural issues facility. This provides valuable information to • Pain management in the elderly insiders and outsiders. Select different cate• Barriers to effective pain management gories and ask some of your volunteers or • Ethical issues in pain management family members to choose the winning post• Non-pharmacologic interventions ers. Offer prizes that can be donated by your consultants and vendors. Invite the winners to PLAN EDUCATION STRATEGIES THAT give poster presentations and offer participants continuing education credits. Ask your INVOLVE ALL CAREGIVERS public relations department to take pictures of the activities and send an article to the local Organizations learn only through individuals who learn. newspapers. This teaching method generates enthusiasm, teamwork, and publicity and Peter Senge clearly articulates to everyone that successful pain management is the result of interdisciThere are a variety of formal and informal teaching stratplinary involvement. egies that can be used to enhance the learner’ s understanding of pain management. Healthcare educators and pro- Portable Educational Cart — A mobile cart displaying fact sheets and equipment is another viders need to employ creative ways of providing useful way to educate staff. Keep carts in an education to staff, patients, families, and the community area for a specifi ed amount of time allowing that are timely, cost-effective, and informative. Each staff members to use them when time permits. teaching strategy is advantageous for certain outcomes and Quizzes or self-learning packets on the conhas considerations that influence its choice. Some examtent can be given by the staff educator if valples of informal teaching strategies include: idation is required. This is an easy way to impart information that does not require an Pain Management Education Week— Designate explanation or discussion. Depending on a week in your facility that is set aside just for where the cart is located, it is also a good pain management education. This time is a format for providing physicians, patients, and great opportunity to teach everyone that pain families with updated information about pain management is an institutional priority. Invite management. This activity clearly identifi es each interdisciplinary team member to set up that learning about pain control is everyone’ s an exhibit displaying learning materials and responsibility. equipment that can help participants to understand their role in relieving pain. Team memPain Management Bulletin Board — Employ the bers can be available at alternating times for use of an education bulletin board strategically demonstration, skill practice, and answering placed in the facility where it is visible to everyquestions. Communicate this event to everyone one. The board can be used to post brochures throughfliers and newspaper articles. This is an about upcoming workshops, seminars, and proexcellent way for disseminating information to grams on pain management. The facility’ s edustaff, patients, families, other healthcare providcation calendar can be posted, indicating the ers, and the public. It stimulates interest in a times and dates of all pain management inserdynamic way and facilitates education about the vices. Include a spot on the bulletin board to different pain control measures used in the place self-learning packets, updated articles and facility. This strategy serves as a great markethandouts, information on new policies and proing tool by conveying a strong message about cedures, and fliers on special events related to

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

pain management activities. This is a unique way to demonstrate to yourcustomers” “ that pain management education is considered important in the facility.

TABLE 3.3 Why Teamwork in Quality Improvement?

1. 2. These strategies facilitate education that is system- 3. wide and promote public awareness about the institution’ s 4. efforts to provide optimum pain management. They speak 5. loudly about the value of education to those who enter 6.

Instills ownership of the process Involves the people who know best Creates respect, cooperation, and openness Breaks down barriers between departments Spreads quality “None of us is as smart as all of us” More ideas Better ideas

your doors. Formal methods of education can include lectures, case studies, videotapes, audiotapes, teleconferences, CD ROMs, grand rounds, skills labs, closed circuit TV, panel discussions, seminars, and workshops. To keep educa-TABLE 3.4 tional costs at a minimum, ask members of your medical, JCAHO Ten-Step Quality Monitoring Process nursing, and other professional staff who are knowledgeable about pain management to provide inservices to the1. Assign responsibility staff. Videotaping the inservices is a cost-effective means 2. Delineate scope of service of providing education to staff members who are unable 3. Identify important aspects of service 4. Identify indicators related to the important aspects of service to attend the presentations. Education of all healthcare 5. Establish thresholds for evaluation providers involved in the care of the patient is crucial if 6. Collect and organize data you are to have an effective pain management program.7. Evaluate service when indicated by the threshold Institutions need to promote education to students 8. Take action when opportunities for improvement or problems involved in clinical care and continuing education for are identified practicing professionals to keep up with changing trends 9. Assess the effectiveness of actions and maintain their skills and competency. Knowledge 10. Communicate relevant information to the organization-wide about pain management empowers physicians, nurses, and program for continuous quality improvement other clinicians to assume the most basic mission of their From Joint Commission on Accreditation of Healthcare Organizapractice— the relief of pain and suffering. tions, 1991. An Introduction to Joint Commission Nursing Care Standards, Oakbrook Terrace, IL: JCAHO. With permission.

DEVELOP A QUALITY IMPROVEMENT MONITORING PROCESS

three steps refl ect attempts to improve the provision of services rendered. Performance monitoring and improvement are data JCAHO (1994) defi nesquality of careas “the degree to driven. Institutions need to develop a formal plan for evalwhich health services for individuals and populations uating the quality of pain management and collect data increase the likelihood of desired health outcomes and about the needs, expectations, and satisfaction of individare consistent with current professional knowledge. ” uals served. There are a number of ways to obtain input Continuous quality improvement is the key component from these groups, including: that will help to demonstrate the pain program’ s benefit • Periodic satisfaction surveys of patients and to the institution’s mission. CQI is a process that ensures families including questions about pain intenoptimum pain control by building excellence into every sity, pain relief goals, and staff responsiveness. aspect of care and creating an environment that encour• Chart audits to assess documentation of pain ages all disciplines to contribute to its success (see Table assessments, patients’ response to treatment, 3.3). Monitoring pain management outcomes is an ongoand teaching outcomes. ing responsibility shared by members of the interdisci• Chart audits to monitor analgesic drug use and plinary team. Every organization must choose which treatment side effects. processes and outcomes are important to monitor based on its mission and the scope of care and services pro- • Focus groups to elicit feedback regarding pain management practices. vided. JCAHO (1991) has designed a 10-step quality monitoring and evaluation process for healthcare agen- • Regularly scheduled meetings with family members. cies (see Table 3.4). In that 10-step process, rst thefive fi steps establish the mechanism to be used for monitoring and evaluation, the sixth and seventh steps encompass The detail and frequency of data collection is detercollection and evaluation of relevant data, and the lastmined as appropriate for monitoring ongoing performance

Implementing a Pain Management Program

25

by the organization. Whenever possible, data collectionREFERENCES should be incorporated into day-to-day activities. High Acute Pain Management Guideline Panel. (1992). Acute Pain quality pain management is not a static destination to be Management: Operative or Medical Procedures and reached, but a dynamic entity toward which we must conTrauma, Clinical Practice Guideline . AHCPR Pub. No. tinually strive. We must act on the basic belief…the patient 920032, Rockville, MD: Agency for Health Care Policy is the reason we exist.

and Research, Public Health Service, U.S. Department of Health and Human Services. Dahl, J.L. (1999). New JCAHO standards focus on pain manCONCLUSION agement.Oncology Issues, 14 (5), 27–28. Ferrell, B., Dean, G., Grant, M., & Coluzzi, P. (1995). An instiThe reward of a thing well done is to have done it. tutional commitment to pain management. Journal of Clinical Oncology, 13 , 2158–2165. Ralph Waldo Emerson Gordon D.B., Dahl, J.L., & Stevenson, K.K. (1996). Building an institutional commitment to pain management. MadAs we look to the future, we must use our time, skills, ison: University of Wisconsin–Madison Board of and energy to make a defining difference in pain manageRegents. ment. It is time for pain management programs to beJoint Commission on Accreditation of Healthcare Organizations incorporated into all parts of the health- care delivery (JCAHO). (1991).An introduction to Joint Commission nursing standards . Oakbrook Terrace, IL: JCAHO. system, and for physicians, nurses, and other healthcare Joint Commission on Accreditation of Healthcare Organizations providers to make pain control part of their routine prac(JCAHO). (1994). Accreditation manual for hospitals: tice. As professionals involved in a healing ministry, we Vol. 1. Standards . Oakbrook Terrace, IL: JCAHO. must proactively promote optimum pain management by Joint Commission on Accreditation of Healthcare Organizations. interdisciplinary teams that can enhance the quality of life (1999). Joint Commission focuses on pain management . and diminish pain and suffering in patients and families. Oakbrook Terrace, IL: JCAHO. http/www.jeaho.org/news As patient advocates, we must implement quality pro-Liebeskind, J.C., & Melzack, R. (1998, March). The Internagrams that increase our capabilities to serve, show comtional Pain Foundation: Meeting a need for education passion, and help others. in pain management.Journal of Pain and Symptom Management , 131–132. National Institutes of Health Consensus Development Conference. (1987). The integrated approach to the management of pain. Journal of Pain and Symptom Management, ,235–44. Peters, T. (1987). Thriving on chaos . New York: Harper Collins. Saunders, C. (1884). The management of terminal malignant disease(2nd ed.). London: Edward Arnold. Ulschak, F. (1988).Creating the future of health care education . Chicago: American Hospital Publishing.

4 The Classification of Pain Ole Thienhaus, M.D., M.B.A., F.A.P.A. and B. Eliot Cole, M.D., M.P.A., F.A.P.A. INTRODUCTION

centers, mental health facilities, home health services, and health system networks). The International Association for the Study of Pain (IASP) Why do we bother to classify pain? Classifying pain defined pain as “an unpleasant sensory and emotional is necessary for research and clinical purposes. Relating experience associated with actual and potential tissue a clinical database to a categorical reference system facildamage, or described in terms of such damage or both” itates the tasks of clinical assessment, treatment planning, (IASP, 1986). The definition emphasized the subjectiveand formulation of an accurate prognosis. Conventionally, and psychological nature of pain, and appropriatelypain is classified according to location, underlying cause, avoided making the authenticity of pain contingent on anfrequency, intensity, and duration. The clinical data, thus externally verifiable stimulus. Pain was understood tocategorized, serve as an input variable for determining the motivate those afflicted to seek relief from it. correct diagnosis and developing the optimal treatment Price (1999) proposed an updated definition thatplan. Investigators in the field of pain management work described pain as a somatic perception containing a bodily to expand the classification of pain, and to specifically sensation with qualities like those reported during tissue-tailor treatment options for each diagnostic possibility. damaging stimulation, an experienced threat associated Clinicians and researchers must attempt to know the cause with this sensation, and a feeling of unpleasantness or of each pain problem to understand how it is to be treated. other negative emotion based on this experienced threat. Classification improves the flow of communication By modifying the definition, there was no requirement tobetween patient and clinician, ensuring that the clinician objectively demonstrate actual or potential tissue damage obtains a complete picture of the complaint and makes it nor was there a requirement that an association be made possible for both patient and provider to speak the same between sensation and tissue damage. This revised pain language when they try to define the nature of the problem, definition was very helpful because making a linkageresponse to treatment, and the development of secondary between sensation and tissue damage was frequently problems such as side effects of treatment or newly develimpossible to demonstrate. oping symptoms. In setting the stage for the 2001 implementation of There continues to be a need for the expanded classification of pain as long as patients suffer from pains that pain-related standards of care, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) alsowe do not understand and that are inadequately treated. linked pain to both physical and emotional responsesAccording to Wall (1989), pain classified by our ignorance (JCAHO, 2000). As justification for these pain-relatedabout underlying mechanisms and therapy falls into three groups: (1) pains where the cause is apparent but the accreditation standards, the JCAHO linked unrelieved pain to negative physiological and psychological effects, andtreatment is inadequate (deep tissue disorders, peripheral nerve disorders, root and cord disorders); (2) pains where generalized these adverse trends from the traditional acutely hospitalized patient to the majority of patients inthe cause is not known but the treatment is adequate (trigeminal neuralgia, tension headaches); and (3) pains most healthcare settings (hospitals, long-term care, surgical 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

where the cause is not known and the treatment is inade- that she learn to live with the pain, but did not tell her quate (back pain, idiopathic pelvic and abdominal pain, how to do this. Although no specific treatment occurred during the evaluation in a conventional sense, she was migraine headache). fice. of The classification of pain is a source of confusion for relaxed and more comfortable when she left the many clinicians, and as a result of this confusion pain practitioners now commonly use a number of different It is not always certain that pain can be conveniently classification systems. Clear distinctions between painclassified into some system. Some patients will present with more than one pain problem over time, and can have classification systems are not always possible, but the the pains classified simultaneously into different categomore simplistic the classification of pain, the more omisries. The chronic pain patient may experience acute painsions and overlaps occur (Pasero, Paice & McCaffery, ful episodes unrelated to the original pain condition, the 1999). Pain is classified according to the time course, the chronic non-cancer pain patient may develop cancerinvolved anatomy, the intensity, the type of patient, and related pain after years of marginal pain management, and the circumstances of the pathology. To be a successful the acute pain patient may experience a number of differpain practitioner one must be able to work with pain ent aches and pains from the original pathophysiologic classifications encompassing all of these areas, and be process, or as a consequence of the therapies to correct it. capable of switching from one model to another. While the distinctions between one system and another may seem arbitrary, without some framework to categorizeCLASSIFICATION BY LOCATION pain complaints, the unsophisticated clinician easily Pain may be classified by body location. Two overlapping becomes lost in the pain behavior of the patient and the demand for quick solutions. Treatment options are linkedschema relate the pain to the specific anatomy and/or body to the type of pain involved, and accurate pain classifica-system thought to be involved. The anatomical classification addresses sites of pain as viewed from a regional tion is essential for successful pain management. The pain conditions that the clinician cannot recognize and accu-perspective. Typical examples include lower back pain, headache, and pelvic pain. The body system pain classirately diagnose cannot be satisfactorily treated. At a more practical and human level, patients want tofication focuses on classical body systems such as musknow if their pain will ever completely go away. Patients culoskeletal, neurological, and vascular. Both systems of are frightened that their pain is attributable to unrecog-classification address only a single dimension, where or why does the patient hurt, and may ultimately fail to nized pathology and so search for the ultimate cure. Going from practitioner to practitioner serves to worsen theiradequately define the underlying neurophysiology of the pain problem (Turk & Okifuji, 2001). confusion, and patients hope that someone will be able to illuminate their difficulties. By being able to classify the pain into a recognizable and explainable syndrome, the CLASSIFICATION BY TIME COURSE pain practitioner, unlike the other clinicians, is able to offer some hope. Although treatment often does not yieldThe duration of the pain process, the temporal perspective, is the most obvious distinction that is made when classia completely pain-free state for these patients, understandfying most pain complaints. This temporal distinction is ing the basis for their pain and knowing that awful diseases do not exist often provides significant relief from their an important consideration for understanding the neurophysiology of pain (Crue, 1983). Acute pain is limited to suffering. pain of less than 30 days, while chronic pain persists for more than six months. Subacute pain describes the interval Case Example Ms. W. was a 45-year-old woman who had seen a num- from the end of the first month to the beginning of the ber of practitioners during the previous three years since seventh month for continued pain. Recurrent acute pain her car accident. Physical therapy, massage therapy, defines a pain pattern that persists over an extended period acupuncture, and psychotherapy in isolation after thorof time, but recurs as isolated pain episodes. Chronic pain ough evaluation by neurologists, neurosurgeons, and is further divided by the underlying etiology, into nonorthopedic surgeons failed to produce lasting comfort. cancer (often called benign” “ pain) and cancer (often When she was referred to the pain clinic she was tense, called“malignant” pain) related (Crue, 1983; Foley, 1985; angry, and argumentative. She was informed that she Portenoy, 1988). would never be completely pain free as a result of her The primary distinction between acute and chronic well-established myofascial pain, but could eventually pain regardless of the etiology is crucial. Acute pain is resume her life if she entered a pain management prouseful and serves a protective purpose. It warns of danger, gram. She was surprised to learn that her pain condition had a name, was recognized by the physician as a non- limits utilization of injured or diseased body parts, and cancer pain process, and could respond to interdiscipli- signals the departure of pathology when the limiting connary treatment. Previous clinicians had recommended dition resolves. Without acute pain it is doubtful that most

The Classification of Pain

29

of us would be able to survive at all (Cousins, 1989). Weclearly incorrect with the modern recognition that unrewould literally suffer needless burns, cuts, and other inju-lieved pain increases cardiac work, increases metabolic ries. Not being able to experience pain is literally incom-rate, interferes with blood clotting, leads to water retenpatible with life. Chronic pain has little protective signif- tion, lowers oxygen levels, impairs wound healing, alters icance, persists despite normalization after injury orimmune function, interferes with sleep, and creates negdisease, and ultimately interferes with productive activity.ative emotions (Akca, et al., 1999; Dinarello, 1984; Patients with chronic pain live their lives as if they areEgdahl, 1959; Kehlet, 1982; Kehlet, Brandt, & Rem, 1980; having full-time nightmares, where pain relief is con- Liebeskind, 1991; Melzack, 1990). Unrelieved pain may stantly sought yet rarely obtained without professionaldelay the return of normal gastric and bowel function in help, and the pain controls their activities of daily living. the postoperative patient (Wattwil, 1989). Recognition of Chronic non-cancer pain occurs with or without adequatethe widespread inadequacy of pain management prompted patient coping. The patients who cope with the chronicthe U.S. Department of Health and Human Services to pain manage to live productive lives, while the patientspublish the Acute Pain Management Clinical Practice who are not able to cope with their pain are disabled byGuidelinesas the first set of federal practice recommenchronic suffering (Crue, 1983). dations(AHCPR, 1992).

ACUTE PAIN

CHRONIC PAIN

Acute pain is almost always self-limited. When the con-Chronic pain confuses most sufferers because it domidition that produces the pain resolves, or when the nocinates, depresses, and debilitates. If chronic pain is treated ceptive input is blocked by a local anesthetic or alteredby using acute pain models only, it may become more by the use of peripheral or central analgesic medications, intense and the patients may experience increased disabilthe pain leaves. The skin heals, the fractures mend, the ity and suffering. Instead of comfort measures alone, inflammation subsides, and the nociceptive input stops, so chronic pain is managed by the use of rehabilitative techthe pain intensity fades away and disappears (Crue, 1983). niques when it is primarily of a non-cancer origin, or by The use of comfort measures such as applications of heat aggressive and supportive techniques when it is primarily or cold, splinting, casting, or brief, time-limited analgesic due to cancer. medication all help to relieve this discomfort. Sentiments “Tincture of time,” coupled with injury- or illnessof concern and expected recovery from friends and familyspecific therapy, may be appropriate for many acute pain help to aid in the relief of pain for the acute pain sufferer.conditions because most painful conditions are time limited. Acute pain is reasonably managed and usually Case Example resolves with the efforts of a single practitioner; however, Mr. B. was a 22-year-old downhill skier who sustained chronic pain frequently requires the coordinated efforts of a shoulder dislocation in a fall. His shoulder was reloa broadly based treatment team bringing a number of cated in the field and he was placed in a shoulder immophysical, psychological, and spiritual strategies together. bilizer for one week. He was assured that his injury was Chronic pain patients demand more effort and resources not significant by his physician and would not interfere than a single, well-meaning practitioner can usually prowith his participation in an important race later in the vide. In isolation, the solo practitioner is generally unable season. After limited physical therapy to restore his range of motion and strength, he was able to resume to address the variety of complex physical, psychosocial, and spiritual problems that chronic pain causes, and so competitive racing with no detectable ficulties. dif resorts to symptom management usually by overusing a single therapeutic approach. The pain after surgery, postoperative pain, is a specific type of acute pain. No matter how successful or how deftly conducted, operations produce tissue trauma and cause Case Example the release of potent mediators of inflammation and pain. Ms. D. was a 28-year-old woman referred for the manPain is often poorly managed because patients receive agement of chronic, mechanical low back pain secondsignificantly less opioid analgesics than are ordered, the ary to an industrial lifting injury. Her referring neuronursing staff are overly concerned about opioid addiction, surgeon, who had been treating her unsuccessfully for three years, became motivated to refer her to a pain analgesics are irration-ally selected, and many physicians management program when his partners began to comhave inadequate knowledge of the pharmacology of analplain about her drug seeking behavior whenever they gesics (Waldman, 1990). Although postoperative pain is were on call for him. A full review of her medical record experienced by millions of patients throughout the world, revealed that she had received 3900 oxycodone and it is rarely recognized as producing harmful physiological acetaminophen tablets in the six months prior to referor psychological effects (Cousins, 1989). The axiom, “No ral. At the time of referral she was taking 12 to 15 of one ever died from pain, they just wish they could, ” is the oxycodone and acetaminophen combination tablets,

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

60 milligrams of diazepam, and an uncertain number of butalbital, aspirin, and caffeine-containing tablets every day to obtain marginal pain relief. She was admitted to an outpatient chronic pain management program, and over six weeks was successfully detoxified from all of her medications, while simultaneously learning many new strategies to help her deal with her chronic pain. She eventually returned to the work force in a less physically demanding position after completing the chronic pain management program.

their positions for claims of pain and suffering after accidents or injuries, it is necessary to understand whose interests are being served by the evaluations. Patients and lawyers stand to gain more financially from any legal action if patients do not recover from their injuries and illnesses (Chapman & Brena, 1989).

SUBACUTE PAIN

AND

RECURRENT ACUTE PAIN

Subacute pain is possibly the last opportunity for a full restoration and a pain-free existence, much as acute pain A specialized taxonomy was introduced to facilitate must be recognized before the pain becomes chronic. Subthe classification of chronic pain syndromes. This taxonacute pain is quite similar to acute pain in its etiological omy turned out to be of particular utility in the area of and nociceptive mechanisms (Crue, 1983). Unfortunately, pain research (IASP, 1986). The multiaxial approach taken once the pain has been established for more than six in this system was hoped to be of practical use for clinimonths, the likelihood of complete pain relief is small. cians. Using multiaxial categorization by topography, The first 100 days of pain appear to respond fully to organ system, and underlying pathophysiology helped to therapy and return the patients to near normality. Beyond relate the presenting complaint to the domains of tradithe first 100 days, most patients still may recover the tional medical practice, and served to facilitate consultamajority of lost function, but do not feel fully restored or tive communication with patients’primary physicians. comfortable. By the time pain becomes subacute, the rehaDescriptive axes such as axis III (pattern of occurrence) bilitative approach used for chronic pain is usually more and axis IV (intensity) recognized the patients’ experienappropriate than further acute pain management strategies. tial and subjective inputs. These latter two dimensions were subdivided into 10 detailed gradations by severity, Recurrent acute pain is the acute flare-up of peripheral reflected in numerical codes. In clinical investigations (seetissue pathology due to an underlying chronic pathological below), this permitted the application of parametric sta-entity and occurs with headaches, gastrointestinal motility disorders, degenerative disk and joint disease, collagen tistical analysis to database collections. While acute pain usually only briefly disables patientsvascular disease, sickle cell disease, and similar functional during their initial recovery time, chronic pain often pre- processes (Crue, 1983). Unlike chronic or subacute pain, vents patients from ever returning to any meaningful andrecurrent acute pain implies discrete acute episodes, which gainful employment. Some chronic pain patients are notreturn over time. The dividing line between recurrent acute able to return to their former, high-paying work due toand subacute pain is often a judgment decision by the pain practitioner. Daily pain for several weeks is subacute pain, pain-related limitations, and others are unable to return to work due to the unwillingness of their employers to makebut several limited pain episodes over many months or years is typical of recurrent acute pain. The importance reasonable accommodations because they fear losing profof recognizing recurrent acute pain is to apply a more its (Chapman & Brena, 1989). These chronic pain patients are caught in the ridiculous position of having to maintaincomprehensive management approach of patient educatheir disability, rather than risk returning to an entry-leveltion, contingency planning, and family involvement than position with inadequate financial compensation for theira single pain episode would ordinarily require. needs. Legal entanglements further cloud chronic noncancer pain problems and contribute to the inability toCLASSIFICATION BY UNDERLYING resolve the suffering. The desire for the best legal settlePATHOLOGY ment, often the only reward for pain problems, often prevents chronic pain patients from making full recoveries. Regardless of time course of the pain, its intensity, freIt is sadly said that pain problems are chronic in naturequency, and location, every attempt must be made to arrive when the referral letter from one practitioner to anotherat an etiologic formulation. Ideally, treating the underlying begins with an apology for making the referral! Chroniccause will bring about the definitive cure of the pain synpain patients are so often viewed as angry, hostile,drome. At a minimum, etiologic clarification will tell the clinician whether causative or symptomatic treatment is depressed, and manipulative, that they evoke feelings of anxiety, resentment, and desperation in their treating cli-possible or, commonly, whether a combination of both is necessary. Within the classificatory axis of causative facnicians. Pain patients requesting that the results of their initial evaluations must be sent to their attorneys shouldtors, the differentiation between cancer pain and pain due alert pain practitioners to potential involvement in to non-cancer causes assumes particular pertinence whenimpending litigation. As some lawyers actually sendever the evaluator is confronted with pain of more than 6months duration (chronic pain, see above). patients for pain management assessments to strengthen

The Classification of Pain

NON-CANCER

31

used to treat the disease. The need for increasing doses of opioid analgesics is more often related to these situations, Chronic non-cancer pain, the grist for most pain clinics,not to the rapid development of tolerance or medication involves a number of different pathophysiologic problemsabuse, as many practitioners mistakenly believe. Chronic that render the sufferer unable to enjoy life, but do notnon-cancer pain may also worsen over time, resulting in threaten to end life. This type of pain is often describedsignificant behavioral changes (pain behavior) and excesin relationship to an anatomical site and engenders consive use of analgesic medication. siderable anxiety. Myofascial pain, pain arising from mus- It was recommended by Foley (1979, 1985) to classify cle and connective tissue, accounts for a considerable cancer patients with pain into five groups: (1) patients with amount of chronic non-cancer pain, and requires specific acute cancer-related pain, (2) patients with chronic canceractive therapy (stretching, trigger-point injections) andrelated pain due to either progression or therapy, corrective actions for pain relief (Simons, Travell, & (3) patients with preexisting chronic non-cancer pain and Simons, 1999; Travell & Simons, 1983). cancer-related pain, (4) patients with a chemical dependency history and cancer-related pain, and (5) actively CANCER dying patients who must be provided comfort measures (Portenoy, 1988). This system of classifying pain accordChronic cancer pain is generally managed for the patient, ing to the type of patient allowed for a rich psychosocial while non-cancer pain is better managed by the patient approach and prospective planning for the comprehensive through education, empowerment, and rehabilitation. Canneeds of the patient, rather than too narrowly focusing on cer-related pain management, like acute pain managea single dimension of the pain. It also explained some of ment, focuses on the comfort of the patient and involvesthe unusual situations that developed while treating cancer a strategy of palliation. Palliative care involves the liberalpain patients, such as the following. use of medication, often opioid analgesics, with maximum comfort through symptom relief, but with toxicity from Case Example therapy kept acceptable relative to the distress produced Mr. P. was a 50-year-old gentleman with invasive head by the symptoms being addressed. and neck squamous cell cancer. He had previously Cancer pain is divided by the presumed pathophysi- declined surgery but had had radiation therapy 1 year ology into somatic, visceral, and deafferentation (also before entering the hospice program with an ulcerated, called neuropathic). This classification system focuses on foul-smelling neck mass. His pain was initially manthe site of nociception (potential tissue damaging situa- aged by his referring physician with acetaminophen and tions), being peripheral for somatic pain, intra-abdominal codeine elixir, 600 mg/60 mg every 4 h, and oral lidocaine 2% viscous solution every four 4 h as needed. for visceral pain, and involving injury to afferent neural While not appreciated at first, it became readily obvious pathways for deafferentation. The pain that results from that he had a long-standing alcohol abuse disorder. He somatic processes is well localized, constant, aching, or regularly supplemented his gastric tube feedings with gnawing in character. The visceral pain is poorly localized liberal quantities of vodka, beer, and coffee liquor. He by comparison, but is constant and aching in character. It alleged that he only used small amounts of these bevis referred to cutaneous sites. Deafferentation (neuro- erages to cleanse the feeding tube, but was found to be pathic) pain is characterized by tingling, sharp paroxysmal intoxicated on many occasions. When his pain became sensations or burning dysesthesia, and is traditionally more difficult to control with codeine, after 3 months managed with adjuvant medications including antidepres- of hospice involvement, he was given morphine consants and anticonvulsants, not opioid analgesics as are centrate (20 mg/ml) via the gastric tube. He quickly began to abuse the morphine, and occasionally took as visceral and somatic pains (Foley, 1985). much as 100 to 200 mg at a time, when only 20 to Bruera, Walker, and Lawlor (1999) challenged the 30 mg had been prescribed. He ultimately stopped abustraditional view of neuropathic pain management when ing the alcoholic beverages, but enjoyed the large doses they reported that more than two thirds of patients with of morphine at night when he wanted to sleep. neuropathic cancer pain achieved good analgesia with opioids alone in a prospective open study. Because the effec- Few cancer pain patients exist in isolation, and most tiveness of adjuvant medications rarely exceeded 30%, of these patients are cared for to some degree by concerned Bruera, Walker, and Lawlor recommended that opioidsfamily members and friends. The support of the primary remain the first line of treatment for neuropathic paincaregiver, with an emphasis on anticipatory bereavement, patients, with adjuvants added when patients reach opioid is an important element of hospice management. During dose-limiting toxicity. the impending death of the cancer patient, the family memTemporally, chronic cancer pain may worsen overbers frequently become uncertain about their ability to time, due to the disease progression and from the various provide continued care. To be able to keep the dying patient comfortable, unpleasant symptoms (nausea, vomiting, interventions (chemotherapy, radiotherapy, and surgery)

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behavior, are potentially involved with helping the patient seizures, terminal restlessness) are aggressively controlled, to manage the chronic pain. and the caregiver is routinely provided support and respite breaks (Cole & Douglass, 1990).

CLASSIFICATION BY PAIN INTENSITY

MENTAL HEALTH ISSUES IN PAIN CLASSIFICATION

Non-cancer-related pain is often rated along a continuum Co-existing psychiatric disorders are not rare when pain from mild to moderate to severe, but the words incapacis severe (Guggenheim, 2000). Mental health consultants itating, overwhelming , and soul stealingbecome neces- are frequently asked to evaluate patients for suspected sary qualifiers for cancer pain. The intensity of the pain“psychogenic pain. ” This type of pain is included in the is perhaps the least desirable system for classifying pain, Diagnostic and Statistical Manual of Mental Disorders, as intensity varies for most pain patients over time and is Fourth Edition, where it is classified as a Pain Disorder uniquely subjective. One pain patient might describe the(Table 4.1). Pain disorder is characterized by pain in one pain experience due to some pathological condition as or a more anatomical sites that is the predominant focus of 10, while another with the same pathology might feel thatthe patient’s clinical presentation and is of ficient suf severthe intensity of pain is only a 5 (using a 0 to 10 scaleity to warrant clinical attention; the pain causes clinically where 0 signifies no pain at all and 10 represents the worse significant distress or impairment in social, occupational, pain one could ever imagine). This has been noted under or other important areas of functioning; psychological experimental conditions when identically calibrated painfactors are judged to have an important role in the onset, stimuli, such as small electrical impulses, are administered severity, exacerbation, or maintenance of the pain; the to subjects and they rate them at widely divergent intensity symptom or defi cit is not intentionally produced or levels. No clear correlation with any particular descriptorfeigned; and the pain is not better accounted for by a variables of the subjects could be established. Furthermood, anxiety, or psychotic disorder and does not meet more, factors lowering the cancer patient’ s pain threshold criteria for dyspareunia (American Psychiatric Associa(the point at which a given stimulus provokes the reporttion, 1994). This condition further requires coding for the of pain) involve discomfort, insomnia, fatigue, anxiety, subtypes of pain disorder associated with psychological fear, anger, and depression; while restful sleep, relaxation, factors (acute or chronic), pain disorder associated with sympathy and understanding, elevation of mood, andboth psychological factors and a general medical condidiversion from the pain serve to raise the pain threshold tion (acute or chronic), and pain disorder associated with (Twycross, 1980). a general medical condition (acute or chronic). Rather than focus on a specifi c amount of pain, it is There is little doubt that a relationship between pain more useful to look at the disruption that pain causes forand other mental disorders exists, but the exact nature of patients. Pain interfering with appetite, pleasurable activ-the relationship is less than clear (King, 1999). It must be ities, or sleep is more distressing than pain otherwise leavemphasized that all pain is real to the patient, and little is ing an intact life, regardless of the reported intensity. Overto be accomplished by challenging the validity of the pain. time, most patients adapt to the pain and demonstrate either Because pain is experienced in the mind and requires the very little or markedly exaggerated pain behavior. Someinterpretation of bodily sensations, there is a psychologipatients may suffer with modest levels of pain, while otherscal overlay with most pain problems. It is artificial and are able to function despite high levels. Suffering, an emoabsurd to try to partition pain into real or psychological tional response to the pain experience, is not necessarily types, especially when the distinction is too often based linked to only the intensity of the pain as much as it is toupon the treating practitioner’ s lack of ability to identify the co-existence of anxiety, depression, and the failure to objective pathology. To fully understand the relationship integrate the pain into the overall life experience. Sufferingbetween nociception and the psychological effects of becomes an important issue when pain patients have conacute and chronic pain, the practitioner must recognize cerns about the purpose, value, or meaning of their lives emotional distress rather than purely nociception as a and an inability to foresee a future with function. cause of pain, and understand that psychological mechaThere is no way to know how much another personnisms do intensify pain perception (Abram, 1985). An emotional reaction to pain does not mean that pain is is in pain, and it is best to assume that the pain exists caused only by an emotional problem (McCaffery & whenever a patient says it does and is whatever the patient says it is (McCaffery, 1999). Pain behavior is influencedPasero, 1999). and shaped by the environment, so the emphasis on func- Psychosomatic pain is unfortunately synonymous tion over intensity is critical for the rehabilitative approachwith imagined pain, yet this pain may be as severe and to control chronic non-cancer pain. Family members anddistressing as somatogenic pain (Abram, 1985). While the significant others, by altering their response to the painthreshold, the point where pain is first noted, is fairly

The Classification of Pain

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constant from person to person, the tolerance, what pain a person will endure, is highly variable (Bowsher, 1983). TABLE 4.1 Factors such as depression, anxiety, and motivation sigPain Disorder Diagnostic Features nificantly influence the tolerance for pain and may deterA. Pain in one or more anatomical sites is the predominant focus mine the amount of suffering and pain behavior generated. of the clinical presentation and is of ficient suf severity to warrant Secondary gain, the practical advantage resulting from the clinical attention. symptom of pain, is not the same as malingering or facB. The pain causes significant distress or impairment in social, titious disorder and does not signify that pain is purely occupational, or other important areas of functioning. psychological in origin (Dunajcik, 1999). C. Psychological factors are judged to play a significant role in the The use of placebo medication or therapy to determine onset, severity, exacerbation, or maintenance of the pain. the reality of pain is highly deplorable and potentially very D. The pain is not intentionally produced or feigned as in Factitious costly (Frank-Stromborg & Christiansen, 2000). Because Disorder or Malingering. the ability to respond positively to a placebo has to do E. Pain Disorder is not diagnosed if the pain is better accounted for by a Mood, Anxiety, or Psychotic Disorder, or if the pain with the belief system of the patient, nothing about the reality of the pain will be learned from the use of sham presentation meets criteria for Dyspareunia. therapies. The only accurate conclusion about a person Pain Disorder is coded according to the subtype that best characterizeswho responds positively to a placebo is that he wants pain the factors involved in the etiology and maintenance of the pain: relief and that he trusts someone or something to help him (Edmondson, 2000). Curiously, we give placebos to 307.80 Pain Disorder Associated with Psychological Factors: patients who are the least likely to respond to them, the This subtype is used when psychological factors are judged to patients we do not like, and those who do not believe in have the major role in the onset, severity, exacerbation, or our efforts. Rarely do we use placebos with the cooperamaintenance of the pain. In this subtype, general medical conditions play either no role or a minimal role in the onset or tive patients who could respond to them. maintenance of the pain. This subtype is not diagnosed if criteria for Somatization Disorder are also met. RESEARCH CLASSIFICATION Acute: This specifier is used if the duration of the pain is less than 6 months. A complex pain classifi cation system has been published Chronic: This specifier is used if the duration of the pain is by the International Association for the Study of Pain 6 months or longer. (1986), and provides the clinician with descriptive lists 307.89 Pain Disorder Associated with Both Psychological about pain syndromes (Table 4.2). This taxonomynes defi Factors and a General Medical Condition:This subtype is used pain syndromes, allows improved communication between when both psychological factors and a general medical condition clinicians and researchers, and leads to improved treatment are judged to have important roles in the onset, severity, options that are specifi c for each syndrome. Ave fi axes exacerbation, or maintenance of the pain. The anatomical site of coding scheme signifi es the region of the pain (Axis I), the pain or associated general medical condition is also coded. organ system (Axis II), temporal characteristics and pattern Acute: This specifier is used if the duration of the pain is less of occurrence (Axis III), patient’ s statement of intensity than 6 months. Chronic: This specifier is used if the duration of the pain is and duration since onset of pain (Axis IV), and the presumed etiology (Axis V). Using the IASP classifi cation of 6 months or longer. chronic pain the practitioner is able to obtain nition, defi 293.83 Pain Disorder Associated with a General Medical nd- fi Condition: (Note: This subtype of Pain Disorder is not considered site, main features, associated symptoms, laboratory ings, usual course, complications, social and physical disa mental disorder. It is included to facilitate differential diagnosis. ) The pain results from a general medical condition, and abilities, pathology, summary of essential features and psychological factors are judged to play either no role or a minimal diagnostic criteria, and differential diagnosis for most pain role in the onset or maintenance of the pain. The ICD-9-CMcode problems. Specifi c definitions with notes on usage are for this subtype is selected based on the location of the pain or the included, providing consistency in describing pains itself. associated general medical condition if this has been established The IASP pain classifi cation system is not yet proven or on the anatomical location of the pain if the underlying general to be reliable and valid, and has not been widely accepted medical condition is not yet clearly established— for example, low since development in the 1980s. Further research is still back (724.2), sciatic (724.3), pelvic (625.9), headache (784.0), facial (784.0), chest (786.50), joint (719.4), bone (733.90), needed to determine the psychometric properties and to abdominal (789.0), breast (611.71), renal (788.0), ear (388.70), eye facilitate modifications to the system (Turk & Okifuji, 2001). Presently, few clinicians or payment sources in the U.S. use (379.91), throat (784.1), tooth (525.9), and urinary (788.0). From the American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington, D.C. American Psychiatric Press. With permission.

the IASP classifi cation system. It is the most thorough and best effort at codifi cation available at this time. The IASP classification system allows pain syndrome diagnoses to be made with inclusion, not exclusion criteria. Pain syndromes

34

TABLE 4.2 International Association for the Study of Pain Coding for Chronic Pain

Pain Management: A Practical Guide for Clinicians, Sixth Edition

TABLE 4.2 (CONTINUED) International Association for the Study of Pain Coding for Chronic Pain

Axis I: Regions Unknown or other 0.08 Head, face, and mouth 000 Psychological origin 0.09 Cervical region 100 Upper shoulder and upper limbs 200 Examples: Thoracic region 300 Metastatic cancer (0.04) pain involving skull, shoulder, sacrum, Abdominal region 400 hip, femur (900) and surrounding “soft tissue” (30); continuous in Lower back, lumbar spine, sacrum, and coccyx 500 nature with fluctuations related to movement and position (3); Lower limbs 600 severe intensity, more than six months in duration (0.9) is coded Pelvic region 700 as 933.94. Anal, perineal, and genital region 800 More than three major sites 900 Lower back pain (500) due to myofascial dysfunction (30); Axis II: Systems continuous and nonfluctuating (2); mild intensity for more than 6 Nervous system (central, peripheral, and autonomic) and 00 months (0.3); exacerbated by obesity ((0.05) is coded as 532.35. special senses; physical disturbance or dysfunction Nervous system (psychological and social) 10 Abdominal pain (400) due to pancreatitis (50); recurring irregularly Respiratory and cardiovascular systems 20 (4); severe intensity for less than 1 week per episode (0.7) Musculoskeletal system and connective tissue 30 associated with alcohol use (0.05) is coded as 454.75. Cutaneous and subcutaneous and associated glands 40 Note: This system establishes a five-digit code for each chronic pain Gastrointestinal system 50 diagnosis. (From International Association for the Study of Pain (1986), Genitourinary system 60 Classification of chronic pain: Descriptions of chronic pain syndromes Other organs or viscera 70 and definitions of pain terms.Pain, 3 (Suppl.), S1– S225. With More than one system 80 permission.) Unknown 90 Axis III: Temporal characteristics of pain: pattern of occurrence Not recorded, not applicable, or not known 0 are diagnosed by what they are, not what they are not. Single episode, limited duration 1 Patients want to know what they have, not be told to live with what their clinicians cannot diagnose. Continuous or nearly continuous, nonfluctuating 2 Continuous or nearly continuous, fluctuating 3 Recurring irregularly 4 CONCLUSION Recurring regularly 5 Paroxysmal 6 A perceptual phenomenon, like pain, is not accessible to Sustained with superimposed paroxysms 7 objective validation. The subjective experience of pain is Other combinations 8 universal and one of the most common reasons that None of the above 9 patients seek a clinician’ s help. An extensive armamentarAxis IV: Patient’s statement of intensity: time since onset of pain ium of medical, surgical, psychological, social, and rehaNot recorded, not applicable, or not known 0.0 bilitative interventions is available to address pain. In Mild, 1 month or less 0.1 Mild, 1–6 months 0.2 order to intervene effectively, however, the clinician must Mild, more than 6 months 0.3 have a conceptual frame of reference. A biopsychosocial Medium, 1 month or less 0.4 model recognizing the biological/physiological, psychoMedium, 1–6 months 0.5 logical/behavioral, and environmental influences is likely Medium, more than 6 months 0.6 the best conceptualization and the only one able to explain Severe, 1 month or less 0.7 all patients and their pain (Robinson & Riley, 1999). Severe, 1–6 months 0.8 The widespread use of the Internet and the demand Severe, more than 6 months 0.9 by healthcare payers to provide meaningful outcome data Axis V: Etiology has made pain classification more than just an academic Genetic or congenital disorders 0.00 exercise. Pain practitioners from different disciplines and Trauma, operation, burns 0.01 specialties must be able to effectively communicate with Infective, parasitic 0.02 Inflammatory (no known infective agent), immune reaction 0.03 one another. Well-defined pain classification systems are Neoplasm 0.04 necessary and must become part of the clinical record Toxic, metabolic, anoxia, vascular, nutritional, radiation 0.05 (Derasari, 2000). Degenerative, mechanical 0.06 Pain means suffering. It has plagued humanity as long Dysfunctional (including psychophysiologic) 0.07

as humans have existed. To attempt to remedy the suffer-

The Classification of Pain

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Egdahl, G. (1959). Pituitary-adrenal response following trauma ing and relieve the pain, accurate assessment and diagnosis to the isolated leg.Surgery, 46, 9–21. must occur. Although many pain syndromes still do not have specific therapies, by classifying pain into certainFrank-Stromborg, M., & Christiansen, A. (2000). The undertreatment of pain: A liability risk for nurses. Clinical Journal categories it is now possible to design treatment of Oncology Nursing , 4, 41–44. approaches to benefit most of our patients and, over time, Foley, K.M. (1979). Pain syndromes in patients with cancer. In hopefully, we will help the others.

J.J. Bonica & V. Ventafridda (Eds.), Advances in pain research and therapy(Vol. 2, pp. 59–75). New York, NY: Raven Press. REFERENCES Foley, K.M. (1985). The treatment of cancer pain. The New England Journal of Medicine, 313, 84–95. Abram, S.E. (1985). Pain pathways and mechanisms. Seminars Guggenheim, F.G. (2000). Somatoform disorders. In B.J. Sadock in Anesthesia , 4, 267–274. & V.A. Sadock (Eds.),Kaplan & Sadock’s comprehenAgency for Health Care Policy and Research. (1992). Acute Pain sive textbook of psychiatry (7th ed., pp. 1504–1532). Management: Operative or Medical Procedures and Philadelphia, PA: Lippincott Williams & Wilkins. Trauma, Clinical Practice Guideline . (AHCPR Pub. No. International Association for the Study of Pain. (1986). Classi92-0032). Rockville, MD: AHCPR. fication of chronic pain: Descriptions of chronic pain Akca, O., Melischek, M., Scheck, T., Heilwagner, K., Arkilic, syndromes and definitions of pain terms. Pain, 3 C.F., Kurz, A., Kapral S., Heinz, T., Lackner, F.X., & (Suppl.), S1-S225. Sessler, D.L. (1999). Postoperative pain and subcutaneJoint Commission on Accreditation of Healthcare Organizations. ous oxygen tension. Lancet, 354, 41–42. (2000). Pain management today.Pain In assessment and American Psychiatric Association (1994). Diagnostic and stamanagement: An organizational approach , (pp. 1–6). tistical manual of mental disorders(4th ed., pp. Oakbrook Terrace, IL: Joint Commission. 458–462). Washington, D.C.: American Psychiatric Kehlet, H. (1982). The endocrine-metabolic response to postopPress. erative pain.Acta Anaesthesiologica Scandinavica , 74 Bowsher, D. (1983). Pain mechanisms in man. Resident and Staff (Suppl.), 173–175. Physician, 29, 26–34. Kehlet, H., Brandt, M.R., & Rem, J. (1980). Role of neurogenic Bruera, E., Walker, P., & Lawlor, P. (1999). Opioids in cancer stimuli in mediating the endocrine-metabolic response pain. In C. Stein (Ed.),Opioids in pain control: Basic to surgery.Journal of Parenteral & Enteral Nutrition , and clinical aspects , (pp. 309–324). Cambridge, UK: 4, 152–156. Cambridge University Press. King, S.A. (1999). Pain disorders. In R.E. Hales, S.C. Yudofsky Chapman, S.L., & Brena, S.F. (1989). Pain and litigation. In P. D. & J.A. Talbott (Eds.),Textbook of psychiatry(3rd ed., Wall & R. Melzack (Eds.),Textbook of pain(2nd ed., pp. pp. 1003–1021). Washington, D.C.: American Psychiat1032–1041). Edinburgh: Churchill Livingstone. ric Press, Inc. Cole, B.E., & Douglass, M.C. (1990). Hospice, cancer painLiebeskind, J.C. (1991). Pain can kill. Pain, 44, 3–4. management and symptom control. In R.S. WeinerMcCaffery, M. (1999). Pain management: Problems and (Ed.), Innovations in pain management: A practical progress. In M. McCaffery & C. Pasero (Eds.), Pain: guide for clinicians,(pp. 4–30). Orlando, FL: Paul M. Clinical manual (2nd ed., pp. 1–14). St. Louis, MO: Deutsch Press. Mosby. Cousins, M.J. (1989). Acute and postoperative pain. In P.D. WallMcCaffery, M. & Pasero, C. (1999). Assessment: Underlying & R. Melzack (Eds.),Textbook of pain(2nd ed., pp. complexities, misconceptions and practical tools. In 284–305). Edinburgh: Churchill Livingstone. M. McCaffery & C. Pasero (Eds.), Pain: Clinical manCrue, B.L. (1983). The neurophysiology and taxonomy of pain. ual (2nd ed., pp. 35–102). St. Louis, MO: Mosby. In S.F. Brena & S.L. Chapman (Eds.), Management of Melzack, R. (1990). The needless tragedy of pain. Scientific patients with chronic pain,(pp. 21–31). Jamaica, NY: American, 262(2): 27–33. Spectrum Publications. Pasero, C., Paice, J.A. & McCaffery, M. (1999). Basic mechaDerasari, M.D. (2000). Taxonomy of pain syndromes: Classifinisms underlying the causes and effects of pain. In cation of chronic pain syndromes. In P.P. Raj (Ed.), M. McCaffery & C. Pasero (Eds.), Pain: Clinical manPractical Management of Pain (3rd ed., pp. 10–16). St. ual (2nd ed., pp. 15–34). St. Louis, MO: Mosby. Louis, MO: Mosby. Portenoy, R.K. (1988). Practical aspects of pain control in the Dinarello, C. (1984). Interleukin-I.Reviews of Infectious Dispatient with cancer.Ca–A Cancer Journal for Clinieases,6, 51–95. cians, 38, 327–352. Dunajcik, L. (1999). Chronic nonmalignant pain. In Price, D.D. (1999). The phenomenon of pain.Psychological In M. McCaffery & C. Pasero (Eds.), Pain: Clinical manmechanisms of pain and analgesia, Progress in Pain ual (2nd ed., pp. 467–521). St. Louis, MO: Mosby. Research and Management (Vol. 15, pp. 3–14). Seattle, WA: IASP Press. Edmondson, J.C. (2000). Chronic pain and the placebo effect. Robinson, M.E. & Riley, J.L. (1999). Models of pain. In A.R. In B.J. Sadock & V.A. Sadock (Eds.), Kaplan & Block, E.F. Kremer & E. Fernandez (Eds.), Handbook Sadock’s comprehensive textbook of psychiatry (7th ed., of pain syndromes , (pp. 23–40). Mahwah, NJ: Lawrence pp. 1981–2001). Philadelphia, PA: Lippincott Williams Erlbaum Associates, Inc. & Wilkins.

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Waldman, S.D. (1990). Acute and postoperative pain manageSimons, D.G., Travell, J.G., & Simons, L.S. (1999). Travell & ment — An idea ripe for the times. Pain Practitioner, Simons’myofascial pain and dysfunction: The trigger 2, 4, 9–10. point manual(Vol. 1, 2nd ed.). Baltimore, MD: Williams Wall, P.D., (1989). Introduction. In P.D. Wall & R. Melzack & Wilkins. (Eds.),Textbook of pain(2nd ed., pp. 1–18). Edinburgh: Travell, J.G. & Simons, D.G. (1983). Myofascial pain and dysChurchill Livingstone. function: The trigger point manual . Baltimore, MD: Wattwil, M. (1989). Postoperative pain relief and gastrointestinal Williams & Wilkins. motility. Acta Chiurgica Scandinavica, 550 (Suppl.), Twycross, R.G., (1980). The relief of pain in far-advanced can140–145. cer. Regional Anesthesia,, 52–11. Turk, D.C., & Okifuji, A. (2001). Pain terms and taxonomies of pain. In J.D. Loeser (Ed.), Bonica’s management of pain (3rd ed., pp. 17–25). Philadelphia, PA: Lippincott Williams & Wilkins.

5 Starting a Pain Clinic Clayton A. Varga, M.D. DEVELOPMENT CHECKLIST 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Ask: Am I sure I want to do this? Identify a leader: Am I qualified? Select the clinic structure. Assess the need. Develop the business plan. Research financial options. Select the participating professionals. Hire support and administrative personnel. Develop the marketing plan. Select the site. Determine equipment needs. Plan billing and collections procedures. Developing a capitated contract.

IDENTIFY A LEADER Ask yourself: Am I qualified by education and temperament to start and run a pain clinic? Do I possess the specialized clinical background necessary to develop and implement the needed structure for evaluation and treatment of patients in a multidisciplinary setting? Am I able to participate in the development of contracts and marketing plans and oversee administrative decisions? If you are unable to fulfill these requirements, then it is necessary to secure the participation of one or more individuals who can before proceeding to the next step.

SELECTION OF CLINIC STRUCTURE Having made the decision to move forward, the desired clinic structure must be selected. Practice types and accompanying brief descriptions are as follows:

ARE YOU SURE YOU WANT TO DO THIS?

1. Single modality: A single practitioner (e.g., neurologist, acupuncturist, chiropractor) seeing The formation of any business requires a great deal of and treating patients without regular input from forethought and an investment of time, energy, and money other practitioners. to be successful. Starting a pain clinic is no exception. 2. Multimodality: Practitioners of different speIndividuals who wish to engage in the business of pain cialties, treating patients in a similar location should ask themselves the following questions: Am I comwithout regular, structured discussion of the pletely committed to the success of the business? Am I patients by all practitioners. willing to be the effective leader of the business? If not, 3. Multidisciplinary: Practitioners of multiple difdo I have someone to fulfill this function? Do I recognize ferent specialties, including a minimum of one that the financial aspects of the clinic require as much representative from each of the following fields: attention and expertise as the practice aspects? If the physician, physical therapy, and psychology. answer to any of these questions is no, then all further Often present are occupational therapy, efforts will most likely be wasted.

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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acupuncture, nursing, and chiropractic. The members of the clinic have made a commitment to attend regular patient conferences and to provide integrated care of the patient.

be estimated. While no hard and fast rules exist, if the catchment area has a population of less than 100,000, its ability to support a true multidisciplinary clinic or center is questionable. Competing service providers need to be evaluated. If The applicability of each item discussed in this chapterone or several high-quality providers already exist in the will largely depend on the clinic model developed. Theproposed catchment area and if they have excess capacity, less complex the model, the less important certain aspects then concrete reasons for believing that you can capture of the development process become. However, even the a large enough portion of the market share to survive must simplest single-modality model would benefit from fol- be identified before business start-up. In such a situation, lowing most of the steps in the development checklist. contracts with a PPO or IPA to be the sole provider for The more complex the structure, and the greater the pain management services and verbal assurances of appronumber of participants, the more time, energy, andpriate patient referrals from independent physicians money will be required to take the business from conceptshould be obtained prior to entering the marketplace. to a fully operational entity. The remainder of this chapTalk to local HMO, PPO, and IPA administrators. ter is directed toward a multidisciplinary pain clinic that Assess your ability to draw patients from these ranks. has a full-time medical director and provides, as a min-Meet with attorneys, case workers, and insurance carriers imum, physical therapy and psychology services andwho are involved locally in the workers’ compensation may well offer nursing, occupational therapy, and acu-system and assess how many referrals are likely from puncture services. these sources. Having done the above, estimate the total number of monthly referrals you expect from all sources. If enough ASSESSMENT OF NEED patients are forthcoming to support the business, then development of a detailed business plan becomes the next Once a preferred structure for the clinic has been selected, step. If patient referrals appear to be insuf ficient, then it then an assessment of need must take place. The purpose is wise to explore other sources of patient referral before of the assessment of need is to determine the demand for proceeding. If, after further exploration, more patients are the product. It determines if the clinic, in the geographic not forthcoming, it is probably best to rethink your proarea to be served, can reasonably expect to draw enough posed catchment area, moving to one with a more favorpatients to pay all debt and still produce a profit. The able referral pattern. assessment should take into account the following: 1. What is the size of the population served (i.e., what is the catchment area)? 2. What is the willingness of physicians within the catchment area to refer patients for the services you are providing? 3. Who is the competition? Are similar facilities already present? 4. What percentage of the population is served by HMOs, PPOs, or IPAs? What will be your ability to gain access to those patients? 5. Can you develop a relationship with an existing healthcare provider who will guarantee patient referrals prior to beginning operations?

THE BUSINESS PLAN

If, based on the assessment of need, it is likely that the business will be profitable in the selected catchment area, then a detailed business plan is developed. The purpose of the plan is to secure on paper a description of the components of the operation and a schedule of their implementation. This should occur prior to spending the first dollar on the program. The business plan has two major components. The first is a narrative which contains a brief description of the business, in which the purpose and structure of the business are outlined. Included is a description of the personnel involved, the function each fulfills, an outline The first step is to define your likely catchment area.of the marketing plan, and a general description of the facility requirements. The narrative section should briefly This represents the geographic boundaries from which you address each of the following components: can reasonably expect to draw patients. In an urban or suburban environment, this usually represents a distance of 15 to at most 30 miles from the 1. The purpose of the business 2. The market niche served by the business business. Obviously, there will be regional variation in the size of the catchment area, depending on the proximity 3. The personnel involved and the function of each 4. Facility requirements of the clinic to major transportation arteries and fic traf patterns and perceived excellence of the clinic. Once 5. Outline of the marketing plan defined, the population within the catchment area should 6. Plan for dissolution of the business

Starting a Pain Clinic

39

common cause of a new business failure is underThe second portion of the business plan is done as most a spreadsheet. It can be prepared by hand using a large ledger capitalization. It is important to generate at least as much sheet or more easily by using one of a number of commercapital as is required based on the business plan. It is also cially available electronic spreadsheets (e.g., Lotus 1-2-3).wise to have a credit line available for emergencies. Once A sample business plan for a hospital-based multidis-capitalization requirements have been determined, options ciplinary clinic that provides primarily outpatient services for obtaining the capital must be explored. Numerous financing possibilities exist. Those most commonly is shown in Table 5.1. The business plan estimates fixed employed are as follows: and variable costs, revenues, and the amount of start-up capital needed to begin the business and keep it running until the revenue stream produces a profit. Total cost is 1. Joint venture: This almost always consists of a simply the summation of the individual cost estimates. limited partnership. The limited partnership The sample spreadsheet in Table 5.1 lists most of the consists of both limited and general partners. individual cost estimates that are required for a multidisThe general partners oversee the business forciplinary clinic. Each expenditure is estimated on a monthmation and development and have a greater by-month basis for at least one year and entered into the degree of legal responsibility should the enterspreadsheet. This produces a time estimate of how long it prise fail. Limited partners invest money into will take to generate a profit and estimates the revenue the partnership but are passive in the business position of the business at any point along the time line. formation and development. Their losses are limited to their investments. The cost estimate should be as detailed as possible. It is possible to accurately predict almost all of the costs, An example of a joint venture is as follows: especiallyfixed costs, when doing the business plan. This The director of the proposed facility develops is in contrast to revenue estimation, which will be, at best, a detailed business plan. A lawyer is hired to a rough guess. Nailing down the cost projections as accuprepare a joint venture agreement, wherein the rately as possible will, in turn, allow for the greatest posdirector is the general partner and the individsible accuracy in predicting the net revenue estimate. uals supplying the money are limited partners. The director oversees the development and It is best to shift as much of the cost as possible from daily running of the business, for which he or fixed to variable. This minimizes expenses when revenue she receives a portion of the profits generated is low. Several examples of doing this are hiring personnel by the business. The director may also receive on part-time or flexible-time schedules, increasing hours monies generated via professional activities as patient load increases, and having billing and collection carried out at the business. The remaining profdone by an outside service, with cost based on a percentits are disbursed to the limited partners. age of collections. Obtaining the revenue estimate requires developing an 2. Borrowing of money by one or several individuals from conventional lending sources (i.e., a approximate charge per patient. If the clinic is based on practice loan). one or several structured programs, in which each patient participates in a relatively uniform program for a prede3. Utilization of personal capital to begin the termined length of time, then average charges are easy to business. estimate. If the clinic structure is such that revenue generation is spread over a wide range of activities, then SELECTION OF PARTICIPATING generating an average charge per patient is more ficult. dif PROFESSIONALS In this situation, it is necessary to develop multiple average patient charges and estimate what portion of the total The type of clinic or operating structure chosen will deterpredicted patient flow falls into each group. mine the professional components of the clinic. The qualSubtracting total cost from total revenue yields the ity of the professional personnel will be one of, if not the predictedfinancial position of the business at any point most important determinants of success. Careful thought along the time line. It is wise to do estimates using best must be given to this topic. Not only must the professionguess, worst case, and best case revenue projection sceals be well trained in their own disciplines, but they must narios. If you are prepared to survive the worst case sceunderstand the fundamental difference between practicing nario, then the business should succeed. in a unidimensional of fice vs. a multidisciplinary setting. They must be willing to make what are often perceived as personal sacrifices to make the system work and to FINANCING regularly attend patient conference meetings and provide The business plan will project the necessary capitalinput in those meetings in a useful fashion. They must required for business formation and development. Theunderstand the need to promote the clinic as an entity, as

Business formation

Business formation Accounting Attorney corporation fee Business formation fees & licenses Reproduction/printing 9,050

100 7,500 950 500

6,130

Administrative costs

61,900

32,500 23,400 5,000 1,000

1,500 480 150 4,000

25,000 18,000

289,500

90,000 45,500 58,500 50,000 45,500

213,994 631,831

169.165 33,833 10.996

Accounting fees for taxes/audit Payroll, accounting fee Bank fees Quality assurance

Office personnel Administrative costs

Office personnel Office manager Receptionist Recruitment fee Training

a

Program personnel

Program personnela Medical directorb Acupuncturist c Physical therapist b Psychologist consultant d Nurse/social worker 90,000 35,000 45,000 50,000 35,000

20.00% 20.00% 6.5%

Total revenue Deductions from revenue 80% coverage Provision for bad debt Billing expense

Total deductions Net revenue

664,125 181,700

$575 $395

Revenue Full-day nonresidential Half-day nonresidential 845,825

56 33 23

35 20

Patient census Full-day nonresidential Half-day nonresidential

Average length of stay Full-day nonresidential Half-day nonresidential

Total Annual 1

9,050

100 7,500 950 500

511

125 40 13 333

9,742

2,708 1,950 5,000 83

24,125

7,500 3,792 4,875 4,167 3,792

0 0

0 0 0

0

0 0

0 0 0

20,125 7,900

TABLE 5.1 XYZ Office Overhead First Year of Operations

83

511

125 40 13 333

511

125 40 13 333

4,742

83 4,742

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

0 0

0 0 0

0

0 0

0 0 0

20,125 7,900

3

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

0 0

0 0 0

0

0 0

0 0 0

20,125 7,900

2

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

9,089 26,836

7,185 1,437 467

35,925

20,125 15,800

3 1 2

20,125 7,900

4

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

9,089 26,836

7,185 1,437 467

35,925

20,125 15,800

3 1 2

20,125 7,900

5

Month

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

14,181 41,869

11,210 2,242 729

56,050

40,250 15,800

4 2 2

20,125 7,900

6

5 3 2

20,125 7,900

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

19,272 56,903

15,235 3,047 990

76,175

60,375 23,700

7

7 4 3

20,125 7,900

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

26,363 77,837

20,840 4,168 1,355

104,200

80,500 23,700

8

80,500 23,700

7 4 3

20,125 7,900

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

26,363 77,837

20,840 4,168 1,355

104,200

9

5 3

8

20,125 7,900

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

31,454 92,871

24,865 4,973 1,616

124,325

100,625 23,700

10

6 3

9

20,125 7,900

12

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

36,546 107,904

28,890 5,778 1,878

144,450

120,750 23,700

11

Pain Management: A Practical Guide for Clinicians, Sixth Edition

511

125 40 13 333

4,742

83

2,708 1,950

24,125

7,500 3,792 4,875 4,167 3,792

41,637 122,938

32,915 6,583 2,139

164,575

140,875 23,700

01 7 3

20,125 7,900

40

25,000

Marketing costs

f

21,441

1,783

630,048 (139,618)

139,618

60,000 5,000 750 750 See Capital equipment See Business formation 60,750 5,750

109,718

653 42 250 1,379

200 458

63 800 225 1,500 560 12,000 125 258 2,000 703 196 29

1,000

167

833

68,000

53,000 15,000

125 2,000 703 196 29

125 2,000 703 196 29

2,322

5,000

(47,747)

(49,726)

49,726

5,000

47,747

5,000

5,000

6,515

1,843 6,036

653

653

200

225

225

200

63

8,833

833 8,000

63

7,333

6,500

833

(15,661)

42,497

5,000

5,000

7,286

2,459

653

2,000 703 196 29 633 200

125

225

63

833

833

(15,965)

42,801

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

1,000

167

833

(765)

42,635

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

833

833

14,268

42,635

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

833

833

35,203

42,635

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

833

833

35,036

42,801

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

1,000

167

833

50,236

42,635

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

833

833

65,270

125

225

63

833

833

79,503

b

43,435

5,000

5,000

8,224

2,597

653

2,000 703 196 29 633 200

800

42,635

5,000

5,000

7,424

2,597

653

2,000 703 196 29 633 200

125

225

63

833

833

Employee benefits calculated at 28% (e.g., medical/dental/workers’ compensation insurance/FICA/FWH labor costs will vary, depending upon urban location). Medical director and psychologists can be paid on a 1099 basis, assuming IRS criteria are met. c Physical therapist’ s employee benefits 25%. d This individual could function in a marketing capacity in addition to nursing/social work duties. e Federal taxes in first year will be based on the NOI plus capitalized investment not written off in first year. f Capital expenses andfice of rent could be what joint venture partners might provide for an equity interest in the clinic business. Note that both capital investment and business start-up are paid rst back year of in operation. the fi g Net operating income in therst fi year is a function of how quickly the marketing strategy/plan can tap into thesclinic’ catchment referral sources such HMOs, IPAs, personal injury attorneys, and workers’ compensation case workers/attorneys.

a

Net operating income

Property, plant, equipment Office rent (2,000 @ 2.5) Property tax on triple net lease Equipment depreciation Amortized start-up Property, plant, equipment Total expenses

Office operations

800 7,836 500 3,000 28,779

e

63 800 2,700 1,500 560 12,000 1,500 258 24,000 8,430 2,355 350 5,700 2,400 5,500

10,000 8,000 6,500 500

Marketing costs Advertising Brochures Announcements Lectures/slides

750

68,000

Capital & equipment

Office operations Books Business licenses/fees Exchange Insurance/business overhead Insurance casualty Insurance/program liability Laundry/linen Magazines Med supplies Phone/6-line phone Postage/Fed. Express Reproduction/printing Repairs/maintenance Stationary Supplies Taxes/IRS Taxes/state Transcription Miscellaneous expenses Utilities Working capital/line of credit @ 12%

53,000 15,000

Capital & equipment expense Capital expense Small equipment

Starting a Pain Clinic 41

42

Pain Management: A Practical Guide for Clinicians, Sixth Edition

well as themselves as individuals, and be willing to deferdoctors’ offices, ease of access to the likely patient base, cost per square foot, the ability of the site to be tailored at times to other members of the team in the treatment of any particular patient. Many physicians and other profes-to your needs, and the ability to expand into adjacent space sionals are not suited by character to function easily inin the future without having to relocate. such an environment and, despite any academic or other How much and what type of space will be needed will professional qualifications, are best excluded from thebe determined by the clinic structure.fice Of rental cost multidisciplinary setting. When selecting clinical mem- represents one of the largest fixed expenses. The clinic bers for the team, consideration of board certification instructure should be well planned to maximally utilize each pain management should not be overlooked. square foot of space. Initially, some, if not all, of the professional participants will have other practice locations. It is less expensive to time-sharefices of between SUPPORT PERSONNEL practitioners, and it is unusual for all individuals to be Personnel to perform all of the non-patient care activitiesseeing patients at the same time. are obviously necessary for the business to function. These areas include billing and collections, reception, orderingEQUIPMENT of supplies, scheduling, transcription, and paying bills, to name a few. These individuals should already have been Equipment used in a multidisciplinary pain clinic will taken into consideration as part of the business plan. Alldepend on the clinic structure. If the clinic site is within of these people need not be hired at the beginning of the a hospital, often all of the diagnostic, occupational, and business. It is preferable to keep start-up fixed costs as physical therapy, and procedural (nerve block, laboratory lean as possible. Even a multidisciplinary center can easily testing, radiologic, and operating) equipment and facilities start with a single support person if time-consuming tasks, are already available. Supplying a site with the ability to such as billing and transcription, are subcontracted to outsee patients for medical and psychological evaluation, sidefirms. This plan has the advantage of changing a fixed basic physical therapy treatment, minorfice of procedures cost to a variable cost, which will be much cheaper when(such as certain types of nerve blocks), relaxation training, patient volume is low. As patient volume rises, these func-biofeedback, and group as well as individual psychothertions can easily be transferred in-house at such time asapy it will require an expenditure of $50,000 to $75,000. becomesfinancially advantageous to do so. This includes the purchase of furniture, exam and treatfice and medical supplies, biofeedback If one individual is initially hired, then this person ment tables, of equipment, fax, typewriter, photocopy equipment, and a should be told that he or she is expected to be a jack-ofphone system. This may or may not include computer all-trades. This individual should also be someone who can become the of fice manager as other employees are put inequipment for word processing or billing. (As this is expensive, it is another reason to subcontract these serplace. The author believes that it is cheaper to hire one well-paid, highly motivated employee than two poorly vices, at least during the first several years of the business.) paid, poorly motivated employees. As the business matures, additional employees can be added as need dictates.

MARKETING

It is important to have an overall marketing plan that extends for a period of several years. This should take into consideration how much money is to be allocated to marHaving decided upon both the general geographic location and the specific structure of the clinic, it is possible toketing efforts and what types of advertising and other probegin specific site selection. If a joint venture with amotional projects will be undertaken. It is not possible to be all things to all people. The marketing plan needs to hospital has been undertaken, then the hospital may have reflect the market niche and present a consistent message. unused space which can serve as the clinic site. This has several advantages. It serves to bind the interests of the Marketing medical services is a complicated and somehospital and the clinic. It provides the clinic with some times delicate job. Ethical standards regarding medical instant name recognition, if the hospital name is incorpo-marketing vary regionally, and knowledge of local stanrated into the clinic name, and it may help speed referrals dards is crucial prior to beginning the marketing program. to the clinic from members of the hospital medical staff.Being the first to employ a specifi c type of advertising in It also allows easy proximity between inpatient and out-an area (e.g., radio commercials) can have a negative patient care, if both are provided. The hospital may allowimpact with referring physicians. However, certain techthe space to be used in exchange for equity in the business, niques (discussed below) can be used in any environment. thus limiting operational costs. Announcements and brochures should be sent to referIf an off-hospital site is selected, then several factorsring physicians, workers’ compensation caseworkers, and need to be taken into consideration: proximity to otherattorneys. These should be mailed shortly after opening

SITE SELECTION

Starting a Pain Clinic

43

the practice. The announcement should be mailed first, BILLING AND COLLECTIONS with the brochure to follow one to two months later. This Even the best conceived and instituted treatment program reinforces your message and is more effective than sendwill not succeed if ef ficient billing/collections operations ing both at the same time. are not instituted from day one. Billing and collections Taking the time to personally contact and talk to local can be done internally or subcontracted. This decision physicians, workers’compensation caseworkers, and lawshould be made while formulating the business plan. The yers is important in building referral patterns. PPOs, IPAs, billing system should be in place before the first patient and HMOs control a majority of the patient population in is seen. many areas. The clinic director must take the time to educate and negotiate with these groups to secure appro- A number of local and nationwide medical billing services are available and usually charge between 6 and priate patient referral. Lectures and community forums are useful tools for10% of collections. Interview several and consider not educating referring physicians as well as potentialonly the cost, but also the comprehensiveness of the serpatients not only about the problem of pain, but aboutvice rendered. Look for a company that has some expertise in billing for a similar entity or is willing to invest the your business as well. Professionally prepared stationary, the development of a logo, and production of astart-up time to learn the peculiarities of the field. Billing newsletter are all effective means of advertising. Theexternally can significantly reduce capital investment at clinic’s listing in the local phone directory should be the time of business start-up and help to reduce fixed costs easily visible. Radio, television, and print media all offer at a time when cash flow will be slow. opportunities for exposure. These represent expensive If billing is done internally, the appropriate software, and potentially sensitive areas of advertising for whichhardware, and support forms to carry out the task must be purchased. It is important to hire someone with previous local ethos should be considered and professional marbilling experience to make the system work. There are keting help engaged. A presence on the Internet by individual healthcarenumerous companies that sell medical billing systems, providers is becoming progressively more common andwith a large range of capabilities. Billing, collection, in the near future will become ubiquitous. A basic Webscheduling, accounting, and payroll functions are all available. Software and hardware can be purchased separately site can be developed and hosted by a good commercial Web development company relatively inexpensively.or as a complete system. Prices range from $1,000 to This provides an excellent avenue for continuous mar-$50,000 or more, depending on the system. keting exposure and a way for patients, providers, and third party referral sources to access information aboutDEVELOPING A CAPITATED CONTRACT your program at their convenience. A basic site would include information about yourself and any other servicePayment for pain management services is transitioning providers in your practice; your location including from a fee-for-service model to a capitated model. The directions, office hours, and phone numbers; and aextent to which this has already occurred varies dramatidescription of the services provided. More detailed sitescally from region to region. In some large metropolitan can also include information about specifi c procedures areas, the market share of managed care exceeds 80%. In performed by you or your colleagues including photo-other areas, total managed care penetration for 1995 was as low as 7%. Managed care will most likely continue to graphs or even short video segments, hot links to other expand and become de facto market-driven national complementary Web sites, and informational databases. healthcare reform over the next 5 years, irrespective of Your Web address should be included on your business cards and all other promotional materials and activities.any other national or regional political agenda. In this climate, it will be essential for the successful provider of The author recommends dealing with an experienced pain management to understand the differences between Web development and hosting service. Consider starting with a basic Web page that allows for some scalability.fee-for-service and capitated reimbursement models and to be able to negotiate a good capitated contract. This way you can add features or increase the complexity of the site without loosing your investment in the In a capitated contract, the clinic receives a payment initial development. each month based on the number of members covered by Advertising and promotion make physicians andthe contract and the rate per member (the per member per month, or PMPM, rate). If the contract covers 50,000 patients aware of the services the clinic provides. They do members at a rate of $0.20 PMPM, then the payment not replace the need to provide concerned, compassionate, and effective care. If the fice of is disorganized, the recep- would be $10,000 a month. This is independent of the tionist curt, or physicians and therapists chronically late,actual number of patient visits, supplies used, or resources consumed in a particular month. If the cost of service no amount of advertising can overcome the bad will spread delivery for the month was $5,000, then a $5,000 profit by irate patients and referring physicians.

44

Pain Management: A Practical Guide for Clinicians, Sixth Edition

would be realized. Obviously, if the cost to deliver care 1. Input into if not direct control over utilization. under the contract was in excess of $10,000 for the month, If you accept the risk of fixed payments, then then a loss would be incurred. you must be able to control utilization to help In order to be able to develop a price structure that mitigate that risk. makes sense, the following information should be 2. Renegotiation of the contract if actual utilizaobtained and analyzed: tion significantly exceeds projected utilization. 1. The utilization rate for the CPT codes covered under the contract for the most recent 12-month period for the population in question. 2. Your actual reimbursement for each CPT code by insurance type. The most important, of course, is the reimbursement from the entity with which you are negotiating, if you have previous claims experience with that entity. 3. Knowledge of the range of cap rates for similar contracts in your immediate or similar geographic areas.

It is important to have in place a system to monitor utilization prior to beginning the contract. Utilization information, along with expense information, will be needed to determine the profitability of the contract. It is important to monitor this closely and move to renegotiate unprofitable contracts quickly.

BIBLIOGRAPHY

Finkler, S.A. (1992).Finance and accounting for nonfinancial managers . Englewood Cliffs, NJ: Prentice Hall. Gumpert, D.E. (1992).How to create a successful marketing The above information will allow you to develop a plan. Boston: Inc. Publishing. PMPM rate that will maintain profi tability. You should Hammon, J.L. (1993).Fundamentals of medical management . develop a PMPM rate based on your own analysis of prior Tampa, FL: ACPE. utilization. Then check this against other contracts as McKeever, a M. (1988).How to write a business plan . Berkeley, safety check. Obviously, rates can vary extensively dependCA: Nolo Press. ing on which CPT codes are covered by the contract. Porter, M.E. (1985).Competitive advantage . New York: Free It is important to build the following safeguards into Press. Sachs, L. (1987). Marketing for the professional practice . Englethe contract: wood Cliffs, NJ: Prentice-Hall.

6 Multidisciplinary Pain Clinics C. Norman Shealy, M.D., Ph.D., D.Sc. and Roger K. Cady, M.D. INTRODUCTION

to ablation successfully in the long run are cancer pain, trigeminal neuralgia, and facet joint pain. In virtually all The management of chronic pain began to evolve fromother situations, long-term success from neurosurgical the witch doctor approach (exorcism, drugs, and abla-destructive procedures is roughly less than 10%. Thus, tive surgery) to the modern concept as the result ofpatients tend to have nerve blocks and destructive procethree innovations: dures, sometimes have a second set of nerve blocks and destructive procedures, try on a wide variety of drugs, and 1. Dr. John Bonica’s concept of a multidisciat that point are told that “it’ s all in their heads” and sent plinary, interdisciplinary team approach to pain to see a psychiatrist. management Until at least the mid-1970s, many physicians tended 2. The Wall-Melzack theory for gate control of pain to believe that if patients did not respond to surgical abla3. Fordyce’s behavioral modification or operant tive surgery and hard drugs, then they must be “crazy” or conditioning concept seriously psychologically disturbed. On more than one occasion Shealy was told by a psychiatrist, “When you Bonica’s concept of a multidisciplinary, interdiscipli- have taken care of the physical component of the pain, nary clinic began following World War II and evolved over send the patient to me and I will take care of the psychoa period of 10 years or so. As late as 1960, the clinic that logical part.” But Shealy never saw a patient with chronic he founded at the University of Washington was the majorpain helped by a psychiatrist. The major approach of psysuch clinic in the United States, but a few other universitychiatrists has been to make patients feel either guilty, for centers were beginning to follow his model. This modelbeing an imposition on their families or society, or angry is called the nerve block drug-cut psychiatry clinic at someone. This approach simply does not work. because it was originally run entirely by anesthesiologists On the other hand, the basic concept of a true multiand led to an unfortunate sequence of events. Even though disciplinary, interdisciplinary team is currently the most a group of up to 15 to 20 different health specialists werevalid one. The model that Shealy evolved is very different represented in the weekly reviews of patients, the initialfrom that at the University of Washington, where the primajor approach was to look at the patient as having mary a approach has also evolved from just nerve blocks reasonable physical cause of pain and as a potential anaand cutting to what he would call a somewhat more comtomical specimen where one could do a peripheral orprehensive approach. At the present time in Seattle, differential spinal nerve block, relieve the pain, or sendpatients have pain education, physical therapy, occupathe patient to the neurosurgeon for ablation of the approtional therapy, vocational counseling, individual psychopriate pain pathway. therapy, and a modicum of relaxation therapy. The UniThe failure of destructive neurosurgery is what led toversity of Washington program considers itself likely to the development of transcutaneous and dorsal column be successful when the patient is suffering from physicianstimulation, because the only types of pain that respond prescribed inappropriate medications, physical deactiva0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

45

46

Pain Management: A Practical Guide for Clinicians, Sixth Edition

tion, depression, superstitious behaviors and when the sive behavioral modification program, lasted an average patient has beliefs about the body and reasonable outcome of 32 days of inpatient management, with 25 patients in goals. The educational program at the clinic has gradually a special unit where the nurses were trained to ignore pain taken on many of Fordyce’ s concepts, as described later. behavior or pain complaints. The patients were advised in Although Bonica is responsible for the concept of aadvance that this would be the approach. An extremely A .M . following major pain clinic, Wall and Melzack’ s gate control theory active day was planned, beginning at 7:00 breakfast in an ambulatory dining area. During the day, sparked more innovation in the management of pain than any other concept in history. As a direct result of Wall andpatients were scheduled from morning until at least 7:00 Melzack’s theory, Shealy was prompted to develop dorsalP.M . and often until 9:00P.M . They were assigned to walk the hall, given a number of laps which increased each day; column stimulation and transcutaneous electrical nerve stimulation, which by 1971 led him to start the first holistic ride a stationary bicycle for an increasing number of mincomprehensive multimodal, multidisciplinary pain man- utes; and do various other physical exercise activities. Five agement clinic. The details of the gate control theory weredays a week they went to a swimming pool where they had 1 hour of water calisthenics. Five days a week they covered in Chapter 2. Fordyce’s concept of pain as an operant or condi-went to occupational therapy for 1 hour. Each patient had vigorous slapping massage of the area of pain for at least tioned response also has been critically important in the development of today’ s pain clinics. Fordyce (1976) 5 min four times a day, followed by at least a 5-min rubdown of the area of pain. Patients had generalized emphasized that thereinforcing “ consequences” provided by family, friends, and acquaintances when anmechanical vibratory massage for 15 minutes four times individual suffers from pain often reinforce pain behav- day, were in a whirlpool twice a day, and had a hands-on ior. Individuals who have been deprived of social recog-total body massage every other day. Transcutaneous electrical nerve stimulation and acunition and nurturing at a subconscious level often nd fi puncture were intimate parts of pain management in this the tremendous attention that they receive when they clinic from the beginning. For the first year, “group thersuffer from chronic illness provides them a longapy” was handled by a psychiatrist. At the end of that neglected nurturing-type environment. This reinforcetime, having attended one of the group therapy sessions, ment pattern must be brought to the patient’ s attention Shealy believed group therapy had negative reinforcing and often more forcefully to the attention of the spouse qualities and it was discontinued. Instead, he introduced or other family members if the chronic cycle of an invalid autogenic training for 30 min twice a day and began to pain status is to be broken. introduce temperature, EEG, and electromyelogram In 1965, having been sent a copy of the gate control (EMG) feedback. theory of pain prior to its publication, Shealy visited Pat Wall and then theorized that the most effective way to By the end of the first year, Shealy had treated over 400 patients, of whom approximately 6% had had dorsal influence the gate was to stimulate the dorsal column of column stimulators inserted and 1% had had peripheral the spinal cord, because at that anatomical level the beta nerve implanted stimulators. fibers are separated from the C-fibers, the only place in the body where that is a significant anatomical fact. This At the end of 32 days (the average hospital stay), 75% led Shealy to the development of both dorsal columnof the patients were off drugs, were markedly improved stimulation (the first patient being implanted in 1967) andin their pain complaints and behaviors, and had a significant increase in physical activity. Over the next year and the concept that transcutaneous electrical nerve stimulation would be more effective in a wider variety of peoplea half, reliance upon stress reduction and cognitive educational aspects increased, and during this time Shealy than would the implanted device. ® . The Biogenics developed the concept of Biogenics Because of the tremendous number of patients sent to retraining component of Shealy’ s pain management proShealy for dorsal column stimulation who were not cangram (Shealy, 1978) became so prominent that the inpadidates for the procedure due to psychological (operant or tient program was closed in 1974, and Shealy began to behavioral) aspects of their illness, in 1971 Shealy opened run an outpatient-only pain management program. Today, the first nonuniversity pain clinic and the first pain clinic most clinicians consider it inappropriate to hospitalize to offer a truly holistic approach to the concept of pain. From the beginning, the policy was that any safe modalitychronic pain patients for anything other than drug withwould be included, but all the social, environmental, phys-drawal or severe psychiatric problems. ical, emotional, chemical, and spiritual stresses in an individual’s life would also be examined. The treatment proPAIN MANAGEMENT FOR THE 1990S gram evolved from an inpatient treatment program to an outpatient model. The single most important factor in managing chronic Starting in 1971, Shealy’ s program, with an inpatient pain is evaluation of the patient. This must include the following: active behavioral modification program rather than a pas-

Multidisciplinary Pain Clinics

Aspirin, Tylenol, etc. Valium, Ativan, diazepams

Librium

Phenothiazines, Serax, Thorazine, etc.

Tricyclic antidepressants: Elavil (10 mg), Vivactil (5 mg), Tofranil (10 mg), Aventyl

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up to 10 per day up to 20 per day up to 20 mg per day up to 40 mg per day over 40 mg per day up to 20 mg per day up to 40 mg per day over 40 mg per day up to 20 mg per day up to 40 mg per day over 40 mg per day up to 4 per day 4–8 per day 8–12 per day over 12 per day up to 4 per day 4–8 per day over 8 per day

10 25 25 50 75 25 50 75 25 50 75 25 30 40 50 60 75 90

Monoamine oxidizers (antidepressants): Nardil, etc. Mild to moderate addicting, codeine (30–60 mg), Percodan, Talwin tablets, Darvon, Darvocet, Stadol, Nubain, barbiturates (30–60 mg) Demerol, injectable Talwin, up to 4 doses per day 75 morphine, Dilaudid up to 8 doses per day 90 over 8 doses per day 100 Sleeping medicines up to 1 per day 25 2 per day 50

FIGURE 6.1 Drug usage.

1. A comprehensive history of the patient’ s pain problem, including: • Onset

2. 3.

4.

5.

• Predisposing factor • Drug history (see Figure 6.1) • Surgical history • Family history • Social interactions • Symptom index • Pain profile (see Figure 6.2) • Total life stress (see Figure 6.3) A review of all diagnostic tests A comprehensive physical and neuromuscular examination, including particular attention to the sacrum, posture, and spinal mechanics Special tests that might be needed, including: • Myelogram • CAT scan • MRI • EMG and sensory nerve conduction studies • Neuropsychological tests • Psychological tests, including: • California Personality Inventory (CPI) • Minnesota Multiphasic Personality Inventory (MMPI) • Myer-Briggs Type Indicator (MBTI) • Evaluation by a physical therapist • Evaluation by a psychologist The minimum team needed for comprehensive pain management includes: • Physician (M.D. or D.O.) • R.N. • Psychologist, psychotherapist, or someone with a Master’s degree in social work • Physical therapist

On the columns below, grade yourself (circle your choice): Pain intensity (severity) 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Decrease in physical activity 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Percent of time pain felt 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Effect on mood 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Drugs consumed 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Effect on sexual activity 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Overall well-being 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Overall energy 0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 Pain intensity 100 = intolerable, excruciating, horrible Physical activity 100% restricted = bedridden 75% restricted = up and about but very little 50% restricted = can’ t work, up and take care of myself, must rest frequently 25% restricted = must rest every 4–6 hours, light work exhausts me, t do can’ fun activities 0 = normal, I do any physical activity I choose Effect on mood 0 = normal; 100 = totally withdrawn, panicked, overwhelmingly depressed Drugs consumed Doctor will do this; mark all drugs you take on reverse side of this page or separate sheet Sexual function 0 = no activity; 100 = perfectly normal activity Overall feeling of 0 = terrible; 100 = best anybody could feel well-being Overall energy 0 = can’t get up or get going; 100 = mostveI’ ever experienced Name Date

FIGURE 6.2 Pain profile. (©1986 C. Norman Shealy, M.D., Ph.D., Springfield, Missouri.)

95 95 95 95 95 95 95 95

100 100 100 100 100 100 100 100

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

Name:

Date:

Read your stress points on the lines in the right-hand margin and indicate subtotals in the boxes at the end of each section. Then add your subtotals to determine your total score. A. Dietary stress Average daily sugar consumption Sugar added to food or drink 1 point per 5 teaspoons Sweet roll, piece of pie/cake, brownie, other dessert 1 point each Coke®, or can of pop; candy bar 2 points each Banana split, commercial milkshake, sundae, etc. 5 points each White flour (white bread, spaghetti, etc.) 5 points Average daily salt consumption Little or no “added” salt 0 points Few salty foods (pretzels, potato chips, etc.) 0 points Moderate“added” salt and/or salty foods at least once per day 3 points Heavy salt user regularly (use of “table salt” and/or salty foods at least twice per day) 10 points Average daily caffeine consumption Coffee 1/2 point each cup Tea 1/2 point each cup ® Cola drink or Mountain Dew 1 point each cup 2 Anacin® or APC tabs 1/2 point per dose ®, Vivarin®, etc.) Caffeine benzoate tablets (NoDoz 2 points each Average weekly eating out 2–4 times per week 3 points 5–10 times per week 6 points More than 10 times per week 10 points DIETARY SUBTOTAL A B. Environmental Stress Drinking water Chlorinated only 1 point Chlorinated and fluoridated 2 points Soil and air pollution Live within 10 miles of city of 500,000 or more 10 points Live within 10 miles of city of 250,000 or more 5 points Live within 10 miles of city of 50,000 or more 2 points Live in the country but use pesticides, herbicides, and/or chemical fertilizer 10 points Soil and air pollution Exposed to cigarette smoke of someone else more than 1 hour per day 5 points ENVIRONMENTAL SUBTOTAL B C. Chemical stress Drugs (any amount of usage) Antidepressants 1 point Tranquilizers 3 points Sleeping pills 3 points Narcotics 5 points Other pain relievers 3 points Nicotine 3–10 cigarettes per day 5 points 11–20 cigarettes per day 15 points 21–30 cigarettes per day 20 points 31–40 cigarettes per day 35 points Over 40 cigarettes per day 40 points Cigar(s) per day 1 point each Pipeful(s) of tobacco per day 1 point each Chewing tobacco –“chews” per day 1 point each

FIGURE 6.3 Personal stress assessment: total life stress test.

Multidisciplinary Pain Clinics

Average daily alcohol consumption 1 oz. whiskey, gin, vodka, etc. 8 oz. beer 4–6-oz. glass of wine D.

Physical stress Weight Underweight more than 10 lbs. 10–15 lbs. overweight 16–25 lbs. overweight 26–40 lbs. overweight More than 40 lbs. overweight Activity Adequate exercise,* 3 days or more per week Some physical exercise, 1 or 2 days per week No regular exercise Work stress Sit most of the day Industrial/factory worker Overnight travel more than once a week Work more than 50 hours per week Work varying shifts Work night shift

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2 points each 2 points each 2 points each CHEMICAL SUBTOTAL

C

5 points 5 points 10 points 25 points 40 points 0 points 15 points 40 points

3 points 3 points 5 points 2 points per hour over 50 10 points 5 points PHYSICAL SUBTOTAL D * Adequate means doubling heartbeat and/or sweating minimum of 30 minutes per time. E. Holmes-Rahe Social Readjustment Rating* (Circle the mean values that correspond with life events listed below which you have experienced during the past 12 months.) Death of spouse 100 Change in responsibilities at work 29 Divorce 73 Son or daughter leaving home 29 Marital separation 65 Trouble with in-laws 29 Jail term 63 Outstanding personal achievement 28 Death of close family member 63 Spouse begin or stop work 26 Personal injury or illness 53 Begin or end school 25 Marriage 50 Change in living conditions 24 Fired at work 47 Revision of personal habits 23 Marital reconciliation 45 Trouble with boss 20 Retirement 45 Change in work hours or conditions 20 Change in health of family member 44 Change in residence 20 Pregnancy 40 Change in schools 19 Sexual difficulties 39 Change in recreation 19 Gain of new family member 39 Change in church activities 18 Business readjustment 39 Change in social activities 17 Change in financial state 38 Mortgage or loan less than $20,000 16 Death of close friend 37 Change in sleeping habits 15 Change to different line of work 36 Change in eating habits 15 Change in number of arguments with spouse 35 Vacation, especially if away from home 13 Mortgage over $20,000 31 Christmas or other major holiday stress 12 Foreclosure of mortgage or loan 30 Minor violations of the law 11 (Add the mean values to get the Homes-Rahe total. Then refer to the conversion table to determine your number of points.)__ ______ F. Emotional stress Sleep Less than 7 hours per night 3 points Usually 7 or 8 hours per night 0 points More than 8 hours per night 2 points

FIGURE 6.3 (CONTINUED) Personal stress assessment: total life stress test.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

Relaxation Relax only during sleep Relax or meditate at least 20 minutes per day Frustration at work Enjoy work Mildly frustrated by job Moderately frustrated by job Very frustrated by job Marital status Married, happily Married, moderately unhappy Married, very unhappy Unmarried man over 30 Unmarried woman over 30 Usual mood Happy, well adjusted Moderately angry, depressed, or frustrated Very angry, depressed, or frustrated Any other major stress not mentioned above you judge intensity (specify):

10 points 0 points 0 points 1 point 3 points 5 points 0 points 2 points 5 points 5 points 2 points 0 points 10 points 20 points (10–40 points) EMOTIONAL SUBTOTAL

F

Add A _____ + B _____ + C _____ + D _____ + E _____ + F _____ = YOUR PERSONAL STRESS ASSESSMENT SCORE If your score exceeds 25 points, you probably will feel better if you reduce your stress; greater than 50 points, you definitely need to eliminate stress in your life. Circle your stressor with the highest number of points and work first to eliminate it, then circle your next greatest stressor and overcome it, and so on. Copyright ©Norman Shealy, M.D., Ph.D., 1985, Springfield, Missouri.

Conversion Table Your Number of Points 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Holmes-Rahe Less Than 60 110 160 170 180 190 200 210 220 230 240 250 260 265 270 275

Anything Over 351 = 40+

Your Number of Points 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

Holmes-Rahe Less Than 280 285 290 295 300 305 310 315 320 325 330 335 340 345 350

Anything Over 351 = 40+

HOLMES-RAHE SOCIAL READJUSTMENT RATING (CONVERTED)

FIGURE 6.3 (CONTINUED) Personal stress assessment: total life stress test.

E

Multidisciplinary Pain Clinics

6. Once it is ascertained that the patient does not have a problem which needs primary surgery or medical drug management, the following modes of therapy need to be considered: • Educational approaches — Of critical importance to the patient are the following: • Understanding the anatomy and physiology of pain and appropriateness of surgical vs. drug therapy • Thorough understanding of stress: • Physical • Chemical • Emotional • Spiritual • An understanding of the concept of retraining the nervous system (Biogenics) • Understanding the dynamics of interpersonal relationships • Physical approaches • Acupuncture • Nerve blocks of: • Muscle trigger points • Facet joints • Sacroiliac joints • Caudals (rarely) • Intercostal blocks (rarely) • Miscellaneous: • Occipital • Supraorbital • Infraorbital • Mental nerves • Transcutaneous electrical nerve stimulation • Use of different types of devices: • Cranial electrical stimulation • Percutaneous electrical nerve stimulation (medium and intense) • Soft tissue mobilization: • Myofascial massage • Strain/counterstrain • Manipulative techniques • Vibratory massage • Mechanical massage • Heat • Ice • Exercise • Limbering • Aerobic • Muscle strengthening • Work hardening • Pharmacological approaches • Nutritional approaches • Special attention to vitamin C, vitamin B6, and magnesium (all deficient in a majority of patients)

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• Chemical approaches — Possible therapeutic implications include: • Dilantin • Elavil or other antidepressant drugs • Mexitil (especially for sensory deprivation pain) • Psychological and spiritual approaches • Pragmatic • Practical • Spiritually oriented

BIOGENICS The backbone of Shealy’ s self-regulation training program is Biogenics. Biogenics incorporates the work of a number of individuals, including Dr. Elmer Green, Roberto Assagioli, Edmond Jacobson, Emil Coue, Carl Jung, and, of course, J.H. Schultz. Essentially, many of these individuals have touched on aspects that interrelate to one another. As Shealy began synthesizing the techniques of self-regulation, the following steps were most emphasized: • Positive attitude • A belief in self (“I can do it. ”) — Biofeedback proves this • Relaxation • Conscious control of sensation (Balancing Body Feelings) — Individuals are taught the following balancing body feelings techniques: • Talking to the body • Feeling the localizing pulsation of heartbeat • Imaging • Loving the body • Tensing and relaxing • Breathing through the body • Collecting and releasing • Circulating the electrical energy • Expanding the electromagnetic energy eldfi • Mental induction of anesthesia • Balancing emotions • Recognizing that all distress is the result of fear of loss of: • Life • Health • Money • Love • Moral values • Logically and internally recognizing that the only solutions are: • Assertion to correct the problem • Divorcing an unacceptable problem with joy • Accepting and forgiving (going for sainthood)

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

• Programming goals phrases) • Spiritual attunement

(organ-specific

Patients have been incapacitated for 1 to 7 years plus. Medical expenses have ranged from $10,000 to $450,000, with average medical expenses of over $10,000.

Because some 90% of individuals state that they RESULTS FOLLOWING COMPREHENSIVE believe in life after death, God, and living the Golden Rule, this universal belief is incorporated into teaching.TREATMENT Individuals are exposed to philosophical concepts toIn any given year, 5 to 7% of patients who enter the develop the transcendent will or the will of the soul, program fail to complete it. About 1% are sent home starting with the concept that all individuals have basicbecause of open resistance to therapy. The others who needs and desires in addition to those necessary for surdrop out do so because they “don’ t believe in it.” Almost vival. The major part of cognitive understanding relatesall of these dropouts are male smokers and are either to accepting that pain, most psychologically aggravated,workers’ compensation or Medicaid patients. is the result of unfulfi lled desires or failure to accept Of the 94% who complete the program, follow-up data things as they are. Ultimately, individuals must learn thatat 6 months and 2 to 3 years from 800 patients (600 there are a limited number of situations that can be totallyfollowed up at 2 + years and 200 followed up at 6 months) changed and that one should put effort into those that consistently reveal that: can be changed and learn total emotional– psychological detachment from those aspects of life which cannot be • 35% return to work. changed; in other words, to be at peace with the • 90% are off all drugs except aspirin or acetamiunchangeable aspects of life. At the same time, they are nophen. taught to control pain through the Biogenics techniques • 70% are improved 50 to 100% (at 6 months of Balancing Body Feelings. 72% are greatly improved, and over the next 2 Obviously, there are many models of pain clinics. years this decreases to 70%). Some current clinics specialize only in doing nerve blocks, • 30% who do not improve greatly almost invariespecially caudal nerve blocks, whereas others primarily ably did not practice the techniques taught. emphasize transcutaneous electrical nerve stimulation, • 5% had a facet rhizotomy. and still others emphasize more physical therapy • 25% have continued use of transcutaneous elecapproaches. All of these techniques are valuable in mantrical nerve stimulation for at least 6 months. aging chronic pain. The indications for specific physical • Pain intensity is reduced an average of 70%. approaches such as acupuncture and nerve blocks are • Percent of time pain is present is reduced an beyond the province of this chapter. References to some average of 65%. of the technology can be found at the end of this chapter. • Mood is improved in 90% of patients.

COST EFFECTIVENESS OF COMPREHENSIVE PAIN TREATMENT

• A majority have significant stress illness, such as hypertension, diabetes, peptic ulcer, etc. • Less than 5% have additional surgical procedures after treatment. • Drug expenses after therapy are reduced 85%. • Hospitalization after therapy is reduced 90%. • Total medical expenses are reduced after therapy 80 to 85%. • Cost of the treatment ranges from $3,500 to $6,000 and is rarely more, depending upon need for hospitalization, drug withdrawal, etc.

No discussion of pain clinics would be adequate without attention to the catchphrase of today cost — effectiveness. Shealy’ s study in 1984 is one of the few that have been published. At the Shealy Institute, over 7000 patients have been evaluated and/or treated intensely in a 13-day comprehensive program. At the present time, only 10 to 15% of patients evaluated enter the intense program. Most of the others are satisfactorily managed with one or two modal- In 1972, Fordyce reported that his average patient had ities of treatment with occasional follow-up visits. Of prior expenses of $50,000. At the time, his program cost those who enter intense therapy, 60% have had unsuccess$5,000. Most pain clinics today charge from $5,000 to ful back surgery, 10% have back pain without prior sur-$35,000. Fordyce estimated that society would break even gery, 10% have headaches, and the remainder have a wide if only 10% of his patients returned to work. If one takes variety of posttraumatic, postsurgical metabolic or degen-into account the income produced by those who return to erative pain syndromes. Sixty percent are women, and work, even less than a 10% return-to-work success rate 40% are men. They range in age from 8 to 90 years, with would produce a break even for society. most patients between 35 and 67 years old. Approximately Presently, with prior medical expenses often exceed20% have had workers’ compensation injuries. ing $60,000 on average and an average cost of less than

Multidisciplinary Pain Clinics

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$5,000 for the comprehensive treatment program, society CERTIFICATION OF PAIN CLINICS breaks even if only 8% return to work. Because 35% of Shealy’s patients return to work, the cost effectivenessIn 1983, CARF (Commission for Accreditation of Rehabilitation of Facilities) instituted a program of is at least 3.4 to 1. Because total medical expenses are accreditation for both outpatient and inpatient pain clinreduced by well over 75%, the cost of the comprehensive ics. The number of pain clinics in this country is very rehabilitation program is recouped in less than 6 months. difficult to ascertain. Fortunately, in 1996 the American In medical costs alone, in just a 2-year period, the cost effectiveness is 4 to 1. That is, within 2 years, societyAcademy of Pain Management instituted its review process for certification of pain clinics and at that time saves four times as much money as the cost of the treatment program. When the added benefi t of 35% return to certified 70 active pain clinics. These included outpatient facilities, inpatient facilities, and outpatient/inpawork is considered, the cost effectiveness is even greater tient facilities. than 4 to 1. The data reported here apply only to treatment at the Shealy Institute for Comprehensive Health Care and cannot be extrapolated to other pain treatment programs or REFERENCES modalities (Shealy, 1976). The advent of DRGs in 1982 began a process that is Fordyce, W. (1976).Behavioral methods for chronic pain and increasingly cumbersome and detrimental in all aspects illness. St. Louis: C.V. Mosby. of patient care. In no area has this had a greater impact Shealy, C.N. (1976).The pain game . Millbrae, CA: Celestial than in pain management. Although the HMO, PPO, ManArts. aged Care system has continued to cover major intervenShealy, C.N. (1978). Biofeedback training in the physician’ s office: Transfer of pain clinic advances to primary care. tional approaches such as epidurals reasonably well, Wisconsin Medical Journal, 77 , 41–43. almost all other aspects of pain management have been Shealy, C.N. (1984, March). Cost-effectiveness of comprehenseverely curtailed. In our opinion, the least effective treatsive pain treatment. Insurance Adjustor, 46–47. ment for all forms of chronic pain is epidural anesthetics. Shealy, C.N. (1986). Biogenics® health maintenance . Fair Grove, Biofeedback, transcutaneous electrical nerve stimulation, MO: Self-Health Systems. neuromuscular re-education techniques, and acupuncture, Shealy, C.N. (1977). Biogenics: A synthesis of biofeedback and which are the hallmarks for successful pain management, autogenic techniques for control of pain. In L.R. are extremely poorly covered in the current situation. Pomeroy (Ed.),New dynamics of preventative medicine Thus, multidisciplinary pain clinics continue to suffer (Vol. 5, pp. 69–74). from the lack of coverage by third-party payers. Interestingly, at the Shealy Institute patients have been willing to pay out of pocket to obtain the comprehensive care that is often not covered by medical insurance.

7 Columbia Medical Plan Pain Management Group Manual Clark Brill, M.D., Juliet Scotti Post, D.C., Thomas Ferguson, Ph.D., Harry Shabsin, Ph.D., Jane Tenberg, M.A., Kathleen Wooding, M.A., Marilyn Lauffer, M.S., R.N., Robin Thomas, M.S., R.N., R.D., and Mary Ann Buchmeier, M.S., R.D. INTRODUCTION

diabetic patients can minimize the effects of the disease by making the right choices — eating properly, foot All pain practitioners come to realize soon in their careerscare, etc. Conversely, they can jeopardize their health that chronic pain is a volatile mix of pathological stimuli and increase chances for diabetic complications by combined with host factors of pain perception and behav-making poor choices. ioral reaction to the stimuli. Similarly, those with chronic pain can make choices This paradigm forces us to take a more holistic approach to magnify their painful experience or mitigate it. To use to treatment in addressing both the organic stimulus and these a phrase from a family practitioner friend of mine: The host factors when necessary. Obviously, each case lies somepain is there — misery and suffering are optional. where along a spectrum where some patients have a more This then is the mission of treating host factors — we definable pathology and fewer confounding host factors, inmust act as guides to help each patient live a good life which case our efforts are aimed at removing the stimulus despite experiencing chronic pain as opposed to living in via a procedural approach. Others have either less obvious misery with it. pathology or a condition that simply has no effective treat- A group setting is ideal for teaching these skills ment coupled with psychological characteristics of hyper-because it is very cost effective to bring a group of people awareness or magnified response. In these patients the together at one site to present this material vs. repeating resources are better spent working on perception/reaction oneself in an office setting ad nauseum. There is also the behaviors vs. pursuing multiple futile procedures. “group dynamic” effect where patients previously feeling This sounds good on paper but we all know howisolated and hopeless are working together in a positive difficult it can be to treat these “host factors.” We are alsoenvironment and can feed off each other’s strengths. painfully aware that insurance companies seem to be will- What follows is a detailed outline of one such sucing to pay for procedural care more quickly than psycho-cessful group — The Columbia Medical Plan group semlogical techniques targeting these host factors. inar for chronic pain patients — for those interested in Nonetheless, research tells us addressing these charstarting a group of their own. This was an 8-week outpaacteristics such as locus of control, depression, and coping tient group experience that was intensely studied for outstyles is fruitful, as if our own anecdotal testimonials werecomes; these were presented to the American Academy of not sufficient. How then do we address these host factors? Pain Management (AAPM) at the 1994 annual conference. Patients completing the group decreased doctor visits for First, an analogy to other chronic diseases must be drawn. A diabetic has an incurable condition but pain complaints by 50%. 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

The basic philosophy of the group was a simple motto — “no brain, no pain. ” That is, the state of mind one brings to the pain experience affects the pain itself as well as its impact on one’ s life. Each group meeting consisted of a presentation and discussion of areas where patients were encouraged to make good life choices such as exercise, eating habits, III. and thinking patterns. These were areas they still had control over as opposed to focusing on pain levels that they may have had little control over. Of course, the patients had to begin with a belief in this brain–pain model and this foundation was established at the initial meeting by a physician presentation on rudimentary anatomy and physiology of pain mechanisms in the human body, including Gate theory, antipain pathways, IV. serotonin, and other neuromodulation structures. The outline for the Columbia Medical Plan Group treatment for chronic pain follows.

PURPOSE OF MANUAL This manual is designed to assist healthcare providers in running groups for chronic pain patients. The outlines of material to be presented are general. Providers are encouraged to add their own individual creativity and to adapt the manual to their own particular needs.

OVERALL PAIN CLINIC PROGRAM A pain management group is an effective and cost-effective modality, and an important part of an overall pain treatment program that may include pharmaceutical management, physical therapy, injection therapy, exercise, biofeedback, and psychotherapy. An ongoing support group for chronic pain patients helps them maintain the benefits gained from the pain management group.

PAIN MANAGEMENT GROUP

3. An exercise therapist 4. A nutritionist D. Each week, the session involves 1. Presentation on pain management 2. Discussion time 3. A relaxation exercise Participants A. Most pain patients in pain clinic recommended for the Pain Management Group B. Preferable that clients complete biofeedback before entering group C. Patients who cannot interact well in a group setting and those who have a high rate of cancellation not recommended for the group Outline of the Pain Management Group A. Weekly presentations made on some aspect of pain management by a member of the treatment team covering: 1. Anatomy and physiology of pain — physiatrist 2. Exercise and pain management — exercise therapist 3. Treatment of pain — physiatrist 4. Imagery techniques in pain management — exercise therapist 5. Cognitive treatment of pain — psychologist 6. Behavioral treatment of pain — psychologist 7. Nutrition and pain management — nutritionist B. Presentations followed by group discussion C. Relaxation training included in each session D. Homework reviewed weekly 1. A pain management chartlled fi out weekly 2. Exercise and relaxation practice charted weekly 3. Thoughts and emotions in response to pain examined E. Patients referred to Chronic Pain Support Group after completing Pain Management Group

I. Objectives of Pain Management Group A. Educating patients in causes and treatment of pain THE PROGRAM B. Helping patients develop cognitive and behavioral skills for pain management WEEK ONE C. Creating a support group for pain patients and those involved with them to manage pain Summary behavior II. Structure of group sessions I. Welcome and introductions A. A closed 8-week group for 12 to 15 patients II. Presentation by physiatrist B. Group that runs for 1 h, once a week A. Anatomy and physiology of pain C. Group that is staffed by B. Discussion of presentation 1. A psychotherapist who is present every III. Homework — weekly pain management chart week A. Explaining chart 2. A physiatrist B. Emphasizing daily relaxation

Columbia Medical Plan Pain Management Group Manual

IV. Relaxation— progressive V. Closing

WEEK ONE I. Welcome and introductions A. Group leader introducing self and welcoming group B. Other professionals introducing themselves C. Group members introducing themselves D. Guidelines for group 1. Attendance 2. Fees 3. Outline of program 4. Announcement of Chronic Pain Support Group (biweekly) II. Presentation by physiatrist on anatomy and physiology of pain A. Definition — “Pain is a stimulus that is perceived as uncomfortable” 1. Stimulus a. Torn tissue b. Loud noise c. Discomforting sight d. Stressful situation 2. Perceptions a. Perception depends on mind set b. Distraction decreases perception c. Focusing on perception makes it stronger 3. Being uncomfortable a. Not able to measure discomfort or suffering b. Relativity — difference among people’s sensitivities and tolerances c. Existence of cultural differences d. Dependence on past history of experiences B. Pain pathways 1. Stimulus site a. Nerve endings firing even after stimulus removed b. Chemicals released that enhance strength of stimulus c. Additive effects of stimuli 2. Spinal cord a. Nerves entering at “gate” that can be open or closed b. Competing stimuli at this level c. Example of gate: rubbing skin when bump leg 3. Brain a. No pain until conscious appreciation

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b. No brain — no pain! c. Making a conscious decision — “this is uncomfortable” d. Degree of discomfort depending on mind set — stress, depression e. If no other stimuli present, pain getting in — night pain C. Antipain pathways 1. Descending pathways a. Nerves coming down from brain to close gates b. Nerves coming down from brain to release endorphins 2. Endorphin system a. Body’s natural pain-fighting system b. Responsible for placebo response c. Can be elevated by many means i. Drugs ii. Relaxation iii. Exercise d. Causes natural “high” D. Summary— pain not “all in your head” or “all in your body” E. Discussion of presentation III. Homework A. Introducing weekly pain management chart — see Appendix 7.1 B. Any questions/discussions arising from review of chart IV. Relaxation A. Progressive relaxation — see Appendix 7.2 B. Sharing relaxation experience C. Stressing importance of daily relaxation V. Closing A. Thanking presenter B. Checking that everyone will attend next week C. Positive comments about today’ s group

WEEK TWO Summary I. Welcome and check-in II. Presentation by exercise therapist A. Role of exercise in pain managementpart — I B. Discussion of presentation III. Homework A. Recording exercise and relaxation on chart B. Discussing pain management section of chart IV. Relaxation— flowing light V. Closing

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

WEEK TWO I. Welcome and check-in A. Group leader and staff members reintroducing themselves B. Patients giving brief comments on how the week has been — especially new and good examples C. Group leader checking who has done relaxation and exercise D. Giving out Exercise Handout* I II. Presentation by exercise therapist on role of exercise in pain management — part I A. Attitudes toward exercise 1. Eliciting words from the group members that describe what comes to their minds when they think of “exercise” (writing these words on blank flip chart — both positive and negative — and discuss) 2. Emphasizing importance of developing “positive” attitudes toward exercise 3. “No pain, no gain” a. Philosophy obsolete b. New focus: “Train, don’ t strain” B. Benefits of exercise 1. Physical a. Increases stamina, strength, flexibility, coordination b. Improves cardiovascularficiency ef c. Affects medical problems i. Hypertension ii. High cholesterol levels iii. Diabetes d. Increases lung capacity e. Burns calories — weight control f. Increases pain tolerance g. Is associated with longevity 2. Psychological a. Improves self-image/self-esteem b. Helps alleviate depression c. Enhances ability to handle stress d. Fosters sense of “being in control” C. Disadvantages of exercise 1. Overexercise possibly causing injuries 2. May increase pain short term 3. Takes time D. Proper way to exercise — choose proper sport for your body 1. Type a. Aerobic vs. anaerobic b. Using large muscle groups *

Handouts are not provided as part of this manual. It is suggested that program leaders provide material for the specific needs of their groups from materials collected and available to them.

c. Low impact d. Examples i. Biking ii. Walking iii. Swimming iv. Aerobic dance 2. Frequency a. 3 to 5 days per week 3. Duration a. Ideal 15 to 60 min b. Minimum: 15 to 20 min, plus warmup and cool-down 4. Intensity— based on target heart rate a. Review of heart rate chart b. Level of perceived exertion c. Medication possibly affecting heart rate 5. Measuring heart rate a. Where? i. Neck ii. Wrist b. How? i. Counting for 1 min or 15 s four times c. When? i. At rest ii. During exercise iii. After exercise 6. Importance of practice a. Walking program with warm-up and cool-down E. Exercise precautions—be careful if the following occur: 1. Dizziness 2. Light headedness 3. Chest pain or pressure 4. Excessive fatigue 5. Excessive shortness of breath F. Exercise clothing 1. Hot weather a. Loose, light layered b. Avoiding heavy sweaters, plastic or rubberized clothing 2. Cold weather a. Layered, porous clothing b. Avoiding overdressing c. Covering head, ankles, and hands G. Exercise shoes 1. Choosing correct shoes for your sport 2. Awareness of stability, cushioning 3. Wearing absorbent socks 4. Preventing blisters H. Strategies to get going 1. Making walking a pleasure a. Scenery b. Cassettes, radio

Columbia Medical Plan Pain Management Group Manual

c. Pleasant company 2. Linking walking with a pleasurable activity as a “reward” 3. “Foot out the door” approach I. Discussion of presentation III. Homework A. Commenting on weekly pain management charts by patients B. Stressing importance of relation — checking who did it C. Collecting charts and giving out new ones D. Giving out “Tapes and Books for Health Management”— see Appendix 7.3 IV. Relaxation A. Flowing light relaxation — see Appendix 7.4 B. Sharing relaxation experience C. Asking how relaxation was helpful to patients this week V. Closing A. Thanking presenter B. Checking next week’ s attendance C. Positive comments about today’ s group

WEEK THREE Summary I. Welcome and check-in II. Presentation by physiatrist A. Treatment of chronic pain B. Discussion of presentation III. Homework — reviewing exercise and relaxation A. Reviewing weekly pain management charts IV. Relaxation— breathing and beach imagery V. Closing

WEEK THREE I. Welcome and check-in A. Welcoming everyone back 1. Positive comments on attendance 2. Positive comments on adherence B. Checking on who has done exercise, relaxation charts C. Brief review of week 1. Positive orientation encouraged D. Announcing Chronic Pain Support Group again II. Presentation by physiatrist on treatment of pain A. Must fight pain at all levels — cannot separate body/brain B. Pharmaceutical management 1. Decreasing narcotics — interfering with natural pain-fighting systems

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2. Serotonin possibly useful — pumps up body’s pain-killing system 3. Other useful medications a. Anti-inflammatories b. Antihistamines c. Antivascular d. Antianxiety e. Antidepressants C. Physical management 1. Exercise a. Increases endorphins b. Increases pain threshold c. Helps mood d. Reconditions body 2. Activity gates a. Heat b. Cold c. Nerve stimulation d. Acupuncture 3. Inactivity increasing pain by decreasing competitive stimuli D. Psychological management 1. Decreasing perception using power of the mind a. Biofeedback b. Relaxation c. Hypnosis d. Imagery 2. Addressing other cortical issues that increase pain a. Depression b. Anxiety c. Stress 3. Support systems a. Family b. Pain support groups c. Outside activities E. Role of pain 1. At first, pain may be useful — acute for protection a. Causes withdrawal, e.g., broken limb — not using it 2. Later, pain can be a useless habitual signal 3. Pain can even cause benefits at times a. Financial b. Attention 4. Internal vs. external focus of control a. Making changes — flexibility b. Avoiding joylessness 5. Victor vs. victim 6. Process takes courage F. Discussion of presentation III. Homework A. Commenting on how patients did on charts

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B. Collecting old charts and giving out new ones IV. Relaxation A. Breathing induction and beach imagery B. Sharing relaxation experience C. Exploring images that help patients reduce pain V. Closing A. Thanking presenters B. Checking next week’ s attendance C. Reminding patients about charts

e. Considering nutrients that fight pain and depression — amino acids and B vitamins 2. Long-term effects are preventative maintenance for the body a. Proper diet can help ward off i. Osteoporosis ii. Heart disease iii. Certain cancer types iv. Diabetes v. Gallbladder disease, etc. b. Need to avoid or deal with obesity to lessen certain muscle, bone, or joint pain * B. Dietary Guidelines for Americans C. NRC’s dietary recommendations 1. Eating five or more half-cup servings of vegetables and fruits every day 2. Moderating protein intake — Recommended Daily Allowances (RDA) to twice RDA 3. Maintaining adequate RDA calcium intake 4. Avoiding use of dietary supplements in excess of RDA 5. Maintaining optimal intake of fluoride D. Relating guidelines to balanced diet (food groups) E. Examining own diet (class exercise) 1. Writing 24-hour dietary recall 2. Comparing to dietary guidelines and food groups 3. Determining strong and weak points of diet and prioritize any desirable changes 4. Working on making dietary changes F. Diet and drug interactions 1. Obtain a list of medications used by class participants prior to this presentation 2. Adverse side effects with nutritional implications a. Drugs that may cause these side effects b. Dietary suggestions to alleviate or prevent side effects G. Arthritis (if time and relevant to class participants) 1. No nutritional cures, though many myths abound a. No proof that selenium, turnips, fish oils, or vitamins help b. Possible that saturated fats, dairy products, chocolate, tomatoes, and citrus fruits may aggravate rheumatoid arthritic symptoms in some people

WEEK FOUR Summary I. II. III. IV.

Welcome and announcements Homework — daily pain management charts Relaxation — self-guided — classical music Presentation by nutritionist A. Nutrition and pain management B. Discussion of presentation V. Closing

WEEK FOUR I. Welcome and announcements A. Checking on week B. Checking on relaxation practice and exercise II. Homework A. Introducing new daily management charts 1. To be done for 2 weeks — see Appendix 7.4 B. Collecting old charts and giving out new C. Reinforcing adherence to charts, exercise, relaxation III. Relaxation A. Relaxation induction using breathing B. Self-guided imagery using classical music C. Bringing patients back to group and discussing experiences IV. Presentation by nutritionist on nutrition and pain management A. Short-term/long-term effects of diet on wellbeing 1. Short-term effects less obvious — therefore often neglected a. Affecting energy level for work, play b. Needed for steady supply of fuel — sugar for effective pain management c. Constant supply of blood sugar necessary for optimal functioning of brain, muscles, and organs d. Avoiding destabilizers in sugar supply (e.g., caffeine, alcohol)

*

Giving out nutritional handouts.

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a. Not applicable to everyone, therefore 2. Achieving healthy body weight test own reactions a. Being overweight — stress aggravatb. Most common offenders ing to arthritic joints c. Reading food labels b. Following diet low in fat, sugar, and salt and high in complex carbohy4. Dietary suggestions to alleviate anorexia drates and nausea c. Increasing physical activity to burn J. Discussion of presentation more calories V. Closing d. Rheumatoid arthritis — food conA. Thanking presenter sumption— underweight B. Emphasizing to patients importance of looke. Increasing calories to offset being ing at their thinking patterns this week underweight f. Adjusting meal planning and food WEEK FIVE preparations to offset stiffness, pain, Summary and fatigue 3. Reasons to eat well I. Welcome and announcements a. Boosts energy II. Presentation by behavioral psychologist b. Makes you feel healthier A. Cognitive treatment of pain c. Reducesflare-ups B. Discussion of presentation d. Helps you cope better with arthritis III. Discussing thought substitution chart H. Vitamin and other supplements IV. Relaxation — progressive/imagery 1. Reasons for taking supplements V. Homework — daily pain management chart a. Meeting unusually high demand for VI. Closing nutrients i. Pregnancy WEEK FIVE b. Poor nutritional status i. Iron deficiency ii. Anemia I. Welcome and announcements c. Diet that does not meet body’ s nutrient A. Welcoming groups and positive comments needs regarding progress of group 2. RDA vs. megadoses B. Checking on who has done exercise, relaxation, charts a. RDA encompassing nutrient needs of general population C. Brief check-in by patients b. Megadoses usually of no benefit and D. Announcing Chronic Pain Support Group often harmful to health II. Presentation by behavioral psychologist on c. Vitamin C only proven effective in cognitive treatment of chronic pain reducing cold symptoms, yet chronic A. Henry Beecher — soldier vs. civilian story megadoses possibly cause diarrhea — see Appendix 7.6 and kidney stones 1. Meaning of story d. Megadoses of fat-soluble vitamins and 2. Group’s reaction iron are toxic B. Pain vs. bodily sensation e. Other examples 1. How we label something that will affect f. Obtaining nutrients through foods safe our experience of it and natural a. Snake story — see Appendix 7.7 3. Health claims on nutritional supplements b. Childbirth — the stronger the contraca. How to determine legitimacy tions, the closer the birth b. Always checking with physician c. Difference in labeling pain as a “senbefore taking megadoses sation” instead of “suffering” c. Asking pharmacist about potential 2. Control of sensory input dangers a. Focusing on pain that may increase I. Migraine headaches tension and therefore intensify pain 1. Well-balanced diet and evenly spaced meals b. Distractions such as entertainment, 2. Relatively safe foods relaxation, and meditation decrease 3. Foods to avoid list tension and pain

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c. Some examples of controlling sensory A. Family interactions and pain management input through altered states are dental B. Becoming an exceptional patient hypnosis and fire walking C. Discussion of presentation III. Small group discussion C. Meaning of patient symptoms IV. Homework — patient management chart 1. Attributing meaning to our symptoms A. Discussing thought substitution chart with whether we are aware of it or not family a. e.g., religious meaning — ”offer it up” V. Closing — story of Job b. Personal identity — pain and illness possibly beginning to define who the WEEK SIX person is c. Symptoms that determine the roles we I. Welcome and introductions play in relationships such as A. Welcoming and explaining why families i. Victim were invited ii. Martyr B. Having patients introduce family members iii. Hero and tell why they are important d. Spinal cord experience — paraplegics C. Any additional comments from family choose opposite responses story — see members Appendix 7.8 D. Checking on who did relaxation and exercise D. Developing internal locus of control II. Presentation by behaviorist on family interac1. Internal vs. external locus of control tions in management of chronic pain a. Patients with internal locus of control A. Stranger, supportive spouse, unsupportive b. Relaxation and meditation ways to spouse story — see Appendix 7.11 help develop internal locus of control 1. Meaning of story 2. Man’s search for meaning story — see 2. How others can affect pain perception Appendix 7.9 3. How others are affected by pain E. Discussion of presentation 4. Group’s reaction to story III. Discussing thought substitution chart B. What others can do to help pain patients 1. Not overreacting (not just doing someA. Reviewing thought substitution chart — see thing; sitting there) Appendix 7.10 a. Letting patient care for self B. Having one patient describe event b. Not discussing/asking about sympC. Having other patients complete columns on toms chart c. Treating person in a normal fashion D. Repeating exercise for second event 2. Attention for nonpain behavior E. Discussing how patients are working on their a. Inappropriate attention only remindthinking/feeling patterns ing person of symptoms IV. Relaxation b. Persons in pain needing to be left A. Progressive relaxation — Appendix 7.2 alone, not attended B. Imagery of place in nature i. Go to their rooms V. Homework ii. Praise for nonpain behavior A. Asking patients to discuss thought substitu3. Acute vs. chronic pain tion chart with their families 4. Other means of expressing love and conB. Collecting daily pain management charts cern besides attending to pain and giving out new ones C. Conclusion — persons with chronic pain VI. Closing helped best by A. Reminding patients that family members are 1. Increasing self-reliance invited next week 2. Increasing levels of activity B. Thanking presenter 3. Treated as well, instead of ill D. Becoming an exceptional patient — Bernie WEEK SIX Siegel, M.D. Summary 1. Defining the exceptional patient a. 15 to 20% of patients are I. Welcome and introductions i. Dif ficult II. Presentation by behavioral psychologist ii. Uncooperative

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v. Repeated discussion of symptoms iii. Assertive with others iv. Demanding 5. At peace with life and death v. Optimistic a. Getting well not the only goal vi. Rule breakers b. Importance of learning to live without b. Exceptional patients are the ones most fear and to be at peace with life and likely to get well death c. Exceptional patients are willing to 6. How to become an exceptional patient accept all the risks and challenges of a. Assertiveness life b. Having information/knowledge 2. Taking responsibility for your own health c. Having hope a. Refusing to be a victim d. Taking good care of yourself b. Recognizing that happiness is an e. Letting go of fear “inside job” f. Finding inner peace c. Asking to be educated by your doctor 7. Discussion of presentation and becoming your own doctor III. Small group discussion d. Refusal to hope is nothing more than A. Inviting group to divide up into small groups a decision to die: “In the face of uncerof two or three patients tainty, there is nothing wrong with B. Discussing what response from family memhope” — Bernie Siegel bers really helps client and what they learned e. Becoming a survivor! Ignoring the stafrom thought substitution chart tistics C. If appropriate, therapist intervening to conf. We missed that one story — see front patterns that maintain pain behavAppendix 7.12 ior/thinking 3. Letting go of fear IV. Homework a. Exceptional patients knowing that A. Collecting daily pain management charts health depends on inner peace and letand giving out new weekly charts ting go of fear B. Giving out another copy of thought substib. Finding ways to make peace with tution chart to work on with family member yourself V. Closure c. Finding ways to make peace with A. Thanking family members for coming others B. Asking if they would like to come again in d. Taking good care of yourself through week 8 relaxation (having fun), exercise, and C. Thanking presenter good food 4. Helping yourself decrease or eliminate WEEK SEVEN symptoms a. Decreasing need to attend to symp- Summary toms b. Understanding possible payoff of I. Welcome and announcements symptoms, e.g., avoidance of something II. Discussing what patients want to do in last sesc. Developing positive attribution style sion — I am hopeful III. Relaxation — healing visualization for pain d. Learning distraction techniques management e. Reevaluating what you can learn from IV. Presentation by exercise therapist your symptoms A. Exercise and pain management — part II i. Appreciating good health B. Discussion of presentation ii. Having empathy with people V. Homework — weekly pain management chart f. Recognizing situations that are related VI. Closing to the onset of symptoms g. Avoiding onset situations such as WEEK SEVEN i. Stress ii. Specific physical activities I. Welcome and announcements iii. Anticipatory anxiety A. Discussing reactions to family coming to iv. Overreacting group

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c. Muscles burn more calories B. Reviewing charts, relaxation, exercise practice d. Muscles contour the body II. Discussing what patients want to do in last sese. Firm muscles reinforce joints, reducsion — possible options: ing sprains and strains A. Discussing their ideas f. Using dumbbells, circuit weights B. Sharing and feedback C. Home exercise equipment 1. Patients sharing what they have learned 1. Exercise bikes in the group and what changes still have a. Not weather dependent to be made in their lives b. Transferring skills outside 2. Family members sharing what changes c. Addition of fans, book stands, digital they have seen in patient while they have readouts been in treatment 2. Rowing machines 3. Group members giving each other feeda. Use of upper and lower body back on changes they have seen in each b. May not be good for back problems other and offering any suggestions for the 3. Cross-country skiing equipment future a. Uses upper and lower body C. Small group discussion b. Can be expensive 1. Patients divide into small groups based 4. Treadmills on common symptoms for discussion D. Health clubs a. Headaches 1. Aspects to consider in a health club b. Back pain a. Equipment c. Fibromyalgia, etc. b. Costs— especially extras III. Healing visualization c. Location— close by? A. Explaination of designing your own imagery d. Hours— work for you? — healing visualization —see Appendix 7.13 e. Membership contracts B. Patientsfilling out imagery sheets E. Handouts— Exercise Handout II C. Guiding patients through imagery 1. Reviewing exercise comparison D. Patients sharing imagery in pairs 2. Reviewing cost/benefit ratios E. Discussing imagery with group F. Conclusion:“Adding years to your life and IV. Presentation by exercise therapist on role of adding life to your years through exercise” exercise in chronic pain management — part II G. Discussion of presentation A. Review V. Homework 1. Targeting heart rates — discussing any A. Give out weekly pain management charts problems patients may have B. Reinforce ongoing exercise and relaxation 2. Exercise records — checking everyone is programs as lifestyle changes exercising regularly VI. Closing B. Three parts of exercise A. Thanking presenter 1. Endurance B. Reminding patients to bring family mema. Heart— increased size, decreased rate ber/friend next time, but if you can’ t, to b. Arteries— dilated come anyway c. Muscles— increased oxygen absorpC. Inviting group members to bring snacks for tion final session d. Lungs— increased capacity 2. Flexibility WEEK EIGHT a. Increasing agility and mobility Summary b. Decreasing chances of injury c. Improving posture I. Welcome and announcements d. Relieving tension and stiffness II. Group discussion 3. Strength III. Ongoing group treatment a. Cannot grow new muscles — must IV. Closing tone what we have V. Evaluation of program b. Muscle cells take less space than fat cells VI. Refreshments

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WEEK EIGHT

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HANDOUTS

Exercise Handout I I. Welcoming and announcements A. Welcome patients and families 1. Reasons to exercise 1. Positive comments on progress of the group 2. Heart rate chart B. Patients reintroducing family members/ 3. Sample walking program friends 4. Information on exercise shoes II. Group discussion 5. General stretching exercises A. Discuss whatever patients may have 6. Comparisons of different forms of exercise requested during last session 7. Log of exercise practice B. Alternatives 8. Cost/benefit ratios of different forms of exercise 1. Patients share what they have changed in their lives as a result of being in the group 2. Family members share positive changes Exercise Handout II they have seen 1. Guidelines for working out 3. Patients give each other feedback on 2. Lower-body warm-up exercises growth they have seen in each other over 3. Middle-body warm-up exercises the weeks 4. Upper-body warm-up exercises C. Small group discussions, divided by symptoms 1. Headaches Nutritional Handout 2. Back pain 3. Fibromyalgia, etc. 1. Nutritional guidelines III. Ongoing group treatment 2. Foods that may increase pain — headaches A. Introducing therapist from Chronic Pain 3. Nutrients that fight pain — amino acids Support Group 4. Dietary supplements/vitamins in a healthy diet B. Patients committing to ongoing treatment in 5. Caffeine content of beverages group 6. Drug-nutrient information sheet IV. Closing V. Pain group evaluations — see Appendix 7.14 VI. Refreshments

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Appendices Week One Appendix 7.1 — Weekly Pain Management Chart Appendix 7.2 — Progressive Relaxation Week Two Appendix 7.3 — Tapes and Books for Health Management Appendix 7.4 — Flowing Light Relaxation — with Relaxation Music Week Four Appendix 7.5 — Daily Pain Management Chart Week Five Appendix 7.6 — Henry Beecher —Soldier vs. Civilian Story — Can How We Think Affect How We Feel?

Appendix 7.7 — Snake Story — Thinking Precedes Feeling Appendix 7.8 — Paraplegics Choose Opposite Responses Appenxix 7.9 — Man’s Search for Meaning Appendix 7.10 — Thought Substitution Chart Week Six Appendix 7.11 — Supportive Spouse Story — A Sight for Sore Eyes Appendix 7.12 — We Missed That One! Week Seven Appendix 7.13 — Healing Visualization Week Eight Appendix 7.14 — Pain Group Evaluation

WEEK ONE APPENDIX 7.1

WEEKLY PAIN MANAGEMENT CHART

Name: Week number: Day (Example)

Date: Monday

Tuesday

Wednesday

Thursday

Friday

Saturday

Sunday

Daily relaxation: 30 min Practice: Legs Time: Heavy Experience: Relieved Headache Exercise time: 40 min Type: Walking Self-talk re: Pain: This pain is terrible. When will it end? Daily medications: Aspirin

APPENDIX 7.2

PROGRESSIVE RELAXATION

A. Using relaxation music, asking group to tense and release their muscles in the following sequence: 1. Clenching hands and relaxing 2. Bending hands back at wrist and relaxing 3. Tensing biceps and relaxing 4. Tensing forehead (raise brows) and relaxing 5. Tensing face (squinting) and relaxing 6. Tensing mouth and jaw and relaxing 7. Tensing neck and upper shoulders (neck and chest) and relaxing 8. Tensing shoulders, back, and chest (taking a large breath and pull shoulders back) and relaxing

B.

C. D. E.

9. Tensing stomach and relaxing 10.Tensing thighs (raising legs up slightly) and relaxing 11.Tensing calves (heels off floor) and relaxing 12.Tensing feet (curl up toes) and relaxing Asking patients to bring themselves back by being aware of the room around them and of other group members Asking patients to open their eyes as you count from one through five Asking group members to share their relaxation experience and whether anyone had any ficulties dif Encouraging daily relaxation practice at home

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WEEK TWO APPENDIX 7.3 Tapes

TAPES

AND

BOOKS

FOR

HEALTH MANAGEMENT Harp and Soul — Georgia Kelly, Heru Records Path of Joy — Daniel Kobialka, Li-Sem Enterprises Silk Road — Kitaro, Sound Design Silver Road — Kitaro, Sound Design Silver Cloud — Kitaro, Sound Design Toward the West — Kitaro, Sound Design Silver Wings— Mike Rowland, Music Design, Inc. Fairy Ring — Mike Rowland, Music Design, Inc. Lovely Day — William Aura, Higher Octave

Letting Go of Stress — Emmett Miller Images for Optimal Health — Emmett Miller Change the Channel on Pain — Emmett Miller Headache Relief — Emmett Miller Healing Journey — Emmett Miller Positive Imagery for People with Cancer — Emmett Miller All available from: Source, P.O. Box W, Stanford, CA 94309, (415) 328–7171 or (800) 52-TAPES Music Seasons for Healing — Stress and Pain Management — Jule Scotti Post (Vol. 1 — Winter-Spring; Miracles— Rob Whitesides-Woo, Search for Serenity Vol. II — Summer–Fall) Mountain Light — Rob Whitesides-Woo, Search for Available from: Healing Imagery, 4520 Kingscup Serenity Court, Ellicott City, MD 21042 Classical Music for Relaxation Health Journeys — Belleruth Naparstek Classic Fantasy — Anugama, Higher Octave Music Relax with the Classics, Vol. I–IV — Lind Institute Cancer Chemotherapy Depression Great Lakes Suite — Dan Gibson Grief General wellness The Classics — Dan Gibson Available from: Image Paths, Inc., P.O. Box 5714, Cleveland, OH 44101 Books Cancer — Discovering Your Healing Power — Louis Hay Burn, David. (1981).Feeling Good — The New Available from: Hay House, Inc., Santa Monica, Mood Therapy . New York: Signet Penguin CA, (213) 394–7445 Books. Rapid Pain Control — Carol Erickson and Thomas Catalona, Ellen Mohr. (1987). The Chronic Pain Condon Control Work Book . Oakland, CA: New HarSelf-Hypnosis for Reducing Your Stress — Carol binger Publications. Erickson Chopra, Deepak. (1989). Quantum Healing: ExplorAvailable from: Changeworks, P.O. Box 4000-D, ing the Frontiers of Mind/Body Medicine . New Berkeley, CA 94706 York: Bantum. Dachman, Ken and Lyons, John. (1990). You Can Relieve Pain . New York: Harper & Row. Relaxation Music Frankl, Viktor. (1984).Man’s Search for Meaning . Zen Waterfall — Eliotoshu and Paul L. Warner, New York: Simon & Schuster. Global Pacific Distributions Linchitz, Richard. (1987).Life without Pain. New Caverna Magica —Andreas Vollenweider, CBS York: Addison-Wesley. Records Moen, Larry. (1992).Guided Imagery,(Vol. I–III). White Winds — Andreas Vollenweider, CBS Naples, FL: United States Publishing. Records Moyers, Bill. (1993).Healing and the Mind . New The Sky of the Mind — Andreas Vollenweider, CBS York: Doubleday. Records Pitzele, Sefra Kobrin. (1988). One More Day — Comfort Zone — Steve Halpern, Halpern Sounds Daily Meditations for the Chronically Ill . CenSpectrum Suite — Steve Halpern, Halpern Sounds ter City, MN: Hazelden. Winter Solstice — David Lanz and Michael Jones, Siegel, Bernie S. (1986). Love, Medicine & MiraNarada Productions cles. New York: Harper & Row. Pianoscapes — Michael Jones Sternbach, Richard. (1987). Mastering Pain. New York: Putnam. Petals— Marcus Allen et al., Dreamwater Music

Columbia Medical Plan Pain Management Group Manual

APPENDIX 7.4

FLOWERING LIGHT RELAXATION —

WITH

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RELAXATION MUSIC

A. Breathing induction — give patients the following instructions 1. Begin by taking a few deep breaths 2. Let go of any tension throughout your body as you breathe 3. Notice that as you become more relaxed, your breathing becomes softer and gentler 4. Be aware of the rising and falling of your chest while breathing in and out B. Flowing light imagery 1. Continue with the following instructions: a. In your mind’s eye, picture a small ball of radiant light resting gently on top of your head; either see the light or have a sense of it being present b. Imagine that light is now flowing down over your head around the back of your head and around your face c. Let any tension in the muscles in your head and face dissolve in that flowing light; let those muscles become deeply relaxed 2. Continue relaxation instructions, asking patients to picture a warm lightowing fl around the following areas: a. Back and front of neck b. Shoulders and back

c. Arms and hands d. Chest and stomach e. Thighs and calves f. Feet and toes 3. After mentioning each area, ask patients to let any tension in the muscles in that area dissolve in that warm flowing light, and let those muscles become deeply relaxed 4. When patients have relaxed all parts of their bodies, ask them to see that warm light flowing all around them and to feel themselves floating in that light C. Coming back 1. Ask patients to begin bringing themselves back by having an awareness of their bodies sitting in chairs with their feet on the floor 2. Suggest patients be aware of the sounds around them in the room and how they are currently feeling 3. Ask patients to open their eyes as you count back from five to one D. Sharing 1. Ask patients to share what this relaxation was like for them 2. Call on individuals who haven’ t shared much with group

WEEK FOUR APPENDIX 7.5

DAILY PAIN MANAGEMENT CHART

Name: Week Number: Time of Symptoms

Daily Change in Intensity Example 8:15 a.m. I can’t stand this pain.

Activity

Consequences of Choices Comments Made (Including Meds, Relaxation, etc.)

Exerciese

Daily When Pain Level Changed Headache Walking

Medication

Relaxation

Getting ready to go to work Asprin

I stayed at home

Took Demerol (amount)

1/2 hour

WEEK FIVE APPENDIX 7.6

HENRY BEECHER — SOLDIER VS. CIVILIAN STORY — CAN HOW WE THINK AFFECT HOW WE FEEL?

Some years ago, Henry Beecher, a physician interested the in amount of pain experienced. Dr. Beecher hypothesized human pain mechanism, designed a study to investigate that the amount of pain a person felt was directly related the amount of tissue damage sustained in an injury and to the extent of an injury or the amount of damage to bone,

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muscle, or other tissue. To prove this theory, he studied After further investigation, Dr. Beecher concluded that a person’ s reaction to injuries could affect the soldiers wounded in battle. Dr. Beecher was able to ascertain the amount of injury by examining the medical recordamount of pain experienced. When he asked the soldiers of soldiers wounded in battle. He then compared thiswhat their injuries meant to them, they told him they information with the amount of morphine, a narcotic anal-were primarily relieved that their wounds had not resulted in death and that they felt confi dent about recovgesic, each of the soldiers took to control pain. As he had expected, the greater the amount of bodily injury, theering and returning home. In other words, they reacted in a positive fashion to their injuries. Civilians, on the greater the amount of morphine used by the wounded soldiers to obtain relief from pain. From these studies, Dr.other hand, saw their injuries from a much more negative Beecher concluded that pain was solely the result of injuryperspective, describing their injuries and accidents as awful events resulting in their lives being disrupted. For to tissue and did not have a higher cognitive component related to thinking or to emotional reactions to an injury.the most part, soldiers understated their pain and felt it To apply these findings to civilians, Dr. Beecher didwas minor and it was tolerable. Civilians, however, additional research with patients who were not soldierstended to describe their pain as more intense and unbearable. Since these studies, many other reports have also and who received injuries from various accidents such as falls or automobile collisions. To help make his point, Dr.described how emotional or cognitive reactions to injury can affect perceptions of pain. Beecher even matched up the wound between soldiers and the civilians. As before, he found that the greater the injury Based on the research of Henry Beecher and others, to the civilians, the more morphine they took to controlthe response to the question, “Can how we think affect how we feel?” appears to be yes. For those of you expepain. However, there was one difference between the soldiers and the civilians that Dr. Beecher had troubleriencing chronic pain, this implies that by learning to react differently to your pain symptoms or by adopting different accounting for. For the same amount of tissue damage, coping strategies, you can affect the amount of pain you civilians took almost three times as much morphine as did experience. In other words, if you are willing to think the soldiers to control pain. It began to appear that something else besides tissue damage wasuencing infl the more positively about your life and your symptoms, you can learn to do something to help yourself feel better. amount of pain patients were experiencing.

APPENDIX 7.7

SNAKE STORY — THINKING PRECEDES FEELING

One of the contributing authors to this manual, Dr. Tho-would translate into a physiological response and then an mas Ferguson, described an experience he had in the emotion. The adrenaline would start pumping. You would following way: then be in a “fight or flight” mode, and you would either attack the snake to kill it, if you perceived it as dangerous, I attended graduate school at Arizona State University, or you would flee, if you were fearful. However, if you and since this university is in the desert, there was an knew this friend had a great sense of humor and loved to example given by one of my major professors of how play practical jokes, you might look at the snake a little thinking precedes feeling. This was a novel thought to me more closely to make a determination whether it was real at that time, and I was skeptical until he gave an example or not. If you decided it was not real, then you would react that convinced me of the accuracy of this hypothesis. with calm or laughter, rather than with the adrenalineengendered“fight or flight” syndrome. The professor stated that if you went to a friend’ s Therefore, if you examine your emotions, you will see house or apartment to water his plants while he was away that how you perceive a situation makes a difference in on vacation and, as you opened the door, you saw what how you respond emotionally. looked like a snake, you would have a thought! He said if you believed that it was a real snake, then this thought

APPENDIX 7.8

PARAPLEGICS CHOOSE OPPOSITE RESPONSES

In 1967, a patient at Stanford Hospital was there to have stantly miserable and complaining. He was obviously bitback surgery. He was struck by how differently two otherter and angry. patients in the ward responded to their physical conditions. It was amazing to see that two people in such ficult dif Both patients had similar spinal cord injuries, leavingcircumstances could respond in such opposite ways. Both them paraplegic. were paraplegic, but while one suffered constantly, the One patient really enjoyed listening to music, espe-other was determined to live life as fully as he could. cially Aaron Copeland’ s “Appalachian Spring. ” He was We also have a choice about how we respond to our pain very upbeat and entertaining. The other patient was con— to suffer constantly or make the most of the life we have.

Columbia Medical Plan Pain Management Group Manual

APPENDIX 7.9

MAN’S SEARCH

FOR

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MEANING

The concept of internal vs. external locus of control isHe felt that they had complete control over him, with best examined by a readingMan’s of Search for Meaning the exception of one aspect of his life they — could not by Victor Frankl, M.D. Dr. Frankl was a Jewish psychi- control how he decided to respond to this abomination. atrist living in Germany during the Nazi regime. At some He decided that he would tell the world what happened point, he was arrested and taken to a concentration camp. and that he would write a book about his experiences. During the first few nights in the concentration camp, a His heroic struggle to survive for 5 years in Nazi connumber of prisoners would hang themselves from thecentration camps is an inspirational one to read. It underrafters out of despair. Dr. Frankl wrote that he also con-lines the importance of recognizing that no one can considered suicide as he examined his losses. The Nazis had trol how you respond to your external world, no matter taken his home, his profession, and his money. They had how traumatic that may be. killed his family. They had even taken his bodily hair.

APPENDIX 7.10

THOUGHT SUBSTITUTION CHART

Give at least five examples of your own automatic negative positive thoughts you could substitute for your automatic thoughts in response to pain and stress, and the feelings thoughts, and what new feelings and consequences these and consequences that follow them. Think about whatwould bring you. See the following example. Feeling/Consequences Substitute Thoughts Event Automatic Thoughts Responses Responses New Feeling e.g., Pain begins. This is going to be I feel angry, scared, I become more tense. It is time to relax terrible. I can’t bear it. anxious. I hate the pain. through the pain. I The pain increases. I take can deal with it. my pain killer.

Consequences I feel calm. I am used to it. I become relaxed focused. The pain is bearable. I avoid taking pain medication.

WEEK SIX APPENDIX 7.11 SUPPORTIVE SPOUSE STORY — A SIGHT

FOR

SORE EYES

although sympathy may be appropriate for short or acute We have all heard the phrase “a sight for sore ”eyes, but periods of pain, the researchers concluded that for patients what about a sight for sore backs, or heads, or arms, or with chronic pain, a person providing sympathy over a stomachs, or any other part of the body? Is it possible that prolonged period of time may begin to be viewed as just the sight of another person can make us feel better or rewarding. Because rewards tend to increase the behavior worse? The answer appears to be yes. We have all at one time or another thought about others as being a “pain in that obtained them, the sight of a rewarding person can the neck. ” However, for most of us, this is just a way to increase pain if that pain was the reason for obtaining the indicate that we are experiencing stress related to another reward of sympathy in the past. The opposite also appears person. We usually do not mean we actually have the to be true. If a person ignores a family member’ s pain, that person’ s pain tends to decrease because there are no physical sensation of pain in our necks. However, a group of researchers reported in the journal Pain that just the positive benefits for having it. If this seems far-fetched, think of the example of working for a salary. If you were sight of another person might actually increase or decrease paid $50,000 or $100,000 a year for going to work, the the experience of painful sensations. In this study, patients in the hospital for chronic pain were observed for signschances are good that you would continue to go to work of painful discomfort under three conditions: in the pres-the next day. On the other hand, if you were paid only $5,000 a year, you might soon start missing days or leave ence of a supportive spouse, in the presence of a nonsupyour job altogether because your salary (reward) for workportive spouse, and in the presence of a neutral observer. The results from this study showed that patients withing was not worth the effort. chronic pain appeared to be in more pain in the presence These examples illustrate how powerful the effect of rewards (or lack of rewards) can be on our behavior. of a supportive spouse compared with a neutral person, Although many times we are aware of how rewards affect but seemed to experience less pain when in the company of a nonsupportive spouse compared with a neutralour behavior, we do not necessarily have to be aware of this reward–behavior relationship to be affected by it. This observer. These results may seem surprising. However,

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seems to be the case for patients with chronic pain. Even and friends interact with an individual with chronic pain though we may not be aware of it, the way family memberscan affect how that person feels.

APPENDIX 7.12

WE MISSED THAT ONE!

Contributing author Dr. Ferguson described another extraordinary experience in the following words: Dr. Bernie Siegel’ s quote, “In the face of uncertainty, there is nothing wrong with hope, ” was demonstrated to me in a courageous fashion by a 19-year-old patient that I treated during an internship at the University of Minnesota Hospital. He had been in a motorcycle accident and as a result was paraplegic. After surgery, he was sent to the rehabilitation medicine unit where I was serving as a psych intern. During our staff conferences on this patient, it was my assignment to convince him that he would never walk again, as he was in denial about the severity of his condition. He was insisting that

he would overcome it. I spent the next three months working with him and after a relatively brief period of time gave up trying to convince him that he wasn’ t going to walk again. Instead, I supported his efforts to work hard in rehabilitation. llI’ never forget the moment when he started to recover some movement in his lower extremities. By the time I finished my internship, he was walking with the aid of crutches. When I questioned the physiatrist about what had happened with the diagnosis, he shrugged his shoulders and said, “We missed that one. ” It taught me an important lesson: to never give up in the face of what appears to be a hopeless condition.

WEEK SEVEN APPENDIX 7.13

HEALING VISUALIZATION: PAIN MANAGEMENT

Name: _________________ History No: ____________

Date: ___________

1. Begining relaxation by breathing deeply 2. Imagining a warm light flowing all through your body, relaxing every muscle 3. Picturing your pain symbolically 4. Picturing the healing process symbolically

5. Seeing the healing process winning over the pain 6. Seeing your own body feeling good and relaxed and comfortable 7. Seeing yourself doing something you love to do 8. Having awareness of your body, and the room around you; when ready, opening your eyes

WEEK EIGHT APPENDIX 7.14

PAIN GROUP EVALUATION

I. Please rate the following presentations in terms of their effectiveness for your pain management:

II. Please use the following rating scale to answer the following questions: 1. Very much 2. Some

Very helpful

Somewhat helpful

Not helpful

Causes and treatment of chronic pain Exercise and pain management Changing your thinking/working with family members Nutrition and pain management Relaxation and imagery

3. Not at all

1. How relevant were the presentations to the type of pain you experience? 2. Did you learn new information from the presentations? 3. Did the presentations change the way you think and/or feel about pain? 4. Did you feel able to speak freely in the group? 5. Overall, how much did the group experience help you?

Columbia Medical Plan Pain Management Group Manual

III. Please rate the following aspects concerning pain and its effect on your life since taking this course. Improved greatly

Somewhat improved

Not improved

1. Actual pain level experienced 2. Feelings of control over your pain 3. Feeling depressed or moody because of pain

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4. Feeling good about yourself because of new skills or attitudes IV. Please answer in your own words: 1. What did you like most about the group? 2. What would you like to see changed about the group? 3. What other comments do you have about the group? 4. Will you attend the bimonthly follow-up group?

Section III Treatment of Commonly Occurring Pain Syndromes

8 Clinical Diagnosis of Heel Pain Paula Lizak Gilchrist, L.P.T., D.P.M. Heel pain (calcaneal pain) is one of the most common foot Practitioners from many arenas of traditional medicine problems presenting to the clinical practitioner. In 1999,and complementary care medicine treat heel pain. We all over 2 million doctor visits were involved with the treat- have our niche. Medical physicians tend to give medicament of heel pain. Age is not a discriminating factor. Heeltion for pain and inflammation. Podiatrists offer use of pain can occur with any age group, but is most commonlymedication, orthotics for foot balancing, strapping, splintfound from the age of 8 to 80 years of age. Heel pain ising, casting injections, and surgery. Osteopaths offer mednoted in women, men, and children. It is responsible forication and bony adjustment (such as for a short leg). Chiropractors offer spinal alignment. Acupuncturists and loss of work days, loss of school days, and loss of income. Disability from heel pain can be short term and mild acupressurists offer pain blocking care. Therapists, physto long term and fully debilitating. Problems with the heelical, massage, and others, offer deep tissue relief, myofascial care, scar reduction and body awareness. All have the can be associated with activity change, increase in weight, same goal: reduction of pain, reduction of inflammation, and change in shoe gear. Foot type (pronated or supinated foot) as well as atrophy of fat pads in the heel can con-and increase in function. There is no simple single line of treatment and no single rate of cure for those patients with tribute to heel pain. In 1999 alone, a MedLine Search showed 11,849heel pain. “hits” with questions on heel pain. These questions ranged Infectious processes as well as systemic diseases can cause heel pain. Diseases such as gout, rheumatoid arthrifrom the definition of heel pain, to causes, to treatments, tis, psoriatic arthritis, Reiter’s syndrome, and ankylosing to support groups. spondylitis can cause heel pain. However, for purposes of Care for heel pain can range from the most conservathis discussion, the following pathologies are discussed: tive to the most radical. A myriad of treatment exists. Treatment such as rest, ice, compression, elevation, med1. Plantar fasciitis ication (oral anti-inflammatories, oral steroids, vitamin therapy), steroid injections, orthotics, physical therapy 2. Heel spur syndrome modalities, exercise for strength and flexibility, massage 3. Haglund deformity therapy, acupuncture, acupressure, splinting, strapping, 4. Retrocalcaneal exostosis/Achilles tendon calcification and casts are a few of the conservative care measures. Steroid creams and anti-inflammatory creams have also 5. Achilles tendonitis 6. Tarsal tunnel syndrome been used. Radical care, generally reserved for the most resistant 7. Flexor hallucis longus tendonitis cases, does include surgical measures. Plantar fasciotomy, plantar fasciectomy, exostectomy, bursectomy, calcaneal For an anatomical review of the foot, the reader is osteotomy, neurolysis and lysis of adhesions, and tendon advised to consult a standard anatomy text for illustrations lengthening are all within the surgical realm of possibility. of the foot. 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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There are 26 bones in the human foot. This amounts to one fourth of the bones found in the entire human body. The foot itself is divided into three bony sections. 1. Rearfoot: consisting of talus and calcaneus 2. Midfoot: consisting of navicular, cuboid, and cuneiform bones 1, 2, 3 3. Forefoot: consisting of metatarsals 1, 2, 3, 4, 5 Five proximal phalanges Four middle phalanges Five distal phalanges Note that the hallux (great toe) has only a proximal and a distal phalanx. In terms of foot musculature, there are four distinctFIGURE 8.1 Different types of orthotics. layers of plantar muscles. The layers ranging from superficial (plantar) to deep (dorsal) are These four canal areas are prevented from bowstringing during standing and walking by the laciniate ligament First layer: abductor digiti quinti, flexor digitorum (flexor retinaculum). The medial calcaneal nerve, a branch brevis, abductor hallucis from the posterior tibial nerve, is noted to pierce through Second layer: tendon of flexor hallucis longus, tenthe laciniate ligament and give sensory innervation to the don flexor digitorum longus, four lumbricales, medial side of the heel. and quadratus plantae Third layer: adductor hallucis, flexor hallucis brevis, flexor digiti minimi brevis PLANTAR FASCIITIS Fourth layer: three plantar and four dorsal interossei Plantar fasciitis may perhaps be the most common heel problem presenting to the clinician. It is often associated Note that the tendon of the peroneus longus and tendon of the posterior tibialis muscles in the posterior halfwith repetitive stress injuries and is not usually the result of direct trauma. It is a soft tissue problem that can be of the foot are close to this layer. present for years (to some degree) before the patient seeks The plantar fascia, often discussed as an inflamed area in heel pain, consists of three separate compartments. any type of treatment. Heel spurs can be present on radiograph without symptoms of plantar fasciitis. Poststatic dyskinesia is often noted. Pain occurs with Medial fascia: encompasses abductor hallucis muscle great intensity when the patient arises from a resting posCentral fascia: encompasses flexor digitorum brevis ture or from sleep. Pain is noted to diminish with activity; Lateral fascia: encompasses abductor digiti minimi however, as the course of the day progresses, pain can be The tarsal tunnel, located on the medial side of theseen to increase. The greatest pain is noted after rest. ankle, is often implicated in impingement syndromes that Inflammation can be detected at any area of the plantar fascial areas, but it is most commonly noted at the medial can cause heel pain. The tarsal tunnel has four distinct canals that have the laciniate ligament (flexor retinaculum)calcaneal tubercle attachments of the fascia onto the heel. This bony prominence serves as the point of origin of the as the roof and 2 septa that form the borders of the canals. anatomic central band of the plantar fascia, and the abducCanal 1: contains tibialis posterior muscle (primary tor hallucis, flexor digitorum brevis, and abductor digiti function is to assist in plantar flexion and inver- minimi muscles. Pain is generally elicited with deep palpation directly in front of the medial tubercle. Pain is also sion of the foot) Canal 2: contains flexor digitorum longus (assists in greatest at the push-off phase of gait when the already inflamed fascia is stressed and stretched as the forefoot bending of the toes) Canal 3: contains posterior tibial nerve (L4, L5, S1, begins to accept more body weight. S2, S3 nerve root) posterior tibial artery and It is important to remember that the plantar fascia vein assists in maintaining the arch height of the foot; it conCanal 4: contains exor fl hallucis longus muscle nects the heel to the forefoot. With pathology present, the (responsible for great toe flexion and assists in medial longitudinal arch of the foot can flatten. Passive push-off phase of gait; also assists in decelera- toe extension with the ankle in full dorsiflexion and the tion of forward motion of the tibia) knee in extension can elicit pain at the heel.

Clinical Diagnosis of Heel Pain

FIGURE 8.2 Cavus foot (high arch).

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of the muscle is apt to occur. This shortening may cause a secondary Achilles tendonitis. Plantar fasciitis can occur in either a supinated (cavus, high-arch type of foot) or in a pronated (low-arch) type of foot. In pronation, the talus plantarflexes and adducts while the calcaneus everts. A cavus-type of foot is noted to be inherently more rigid. This foot type may require extra cushioning for relief of heel pain. A planus-type of foot is generally quite flexible. Patients with this foot type may only require a heel lift for care. Note that a hint for balance is to assess the foot with the subtalar joint in neutral position and the midtarsal joint maximally pronated. Either foot type can respond nicely with the use of a mechanically balanced custom-made orthotic to control subtalar joint motion. In the early stages of treatment, a foot strapping to lock the first ray and transfer pressure away from the fascia and onto the tendons and toes may help relieve pain. It is not uncommon to find scar tissue formation on the medial side of the heel due to repetitive stress in an unbalanced foot. Lateral shift of the infracalcaneal fat pad and atrophy of the infracalcaneal fat pad can occur. A heel cup may eliminate lateral shift and a heel lift may assist in cushioning the foot. Scar tissue may be eradicated with deep soft tissue massage and fascial release therapy.

HEEL SPUR SYNDROME Infracalcaneal pain (heel spur syndrome) can occur if plantar fasciitis progresses and microtears of the proximal fascia occur at the calcaneal attachments. Low-grade periostitis occurs along with thickening in the area of trauma. Pain from plantar fasciitis can be noted to increase when there is a decrease in theexibility fl of the gastro-soleus Edema and fibroblastic inflammatory cell infiltration can also occur. Periosteal calcification occurs near fascial and (triceps surae) complex at the calf area. The triceps surae tendonous attachments. The infracalcaneal heel spur sends a slip of attachment to the plantar fascia. However, forms in this manner. A “traction” type of spur from excesremember that when the plantar fascia is stretched, inversive pulling of the tissue is noted. sion of the heel occurs to a slight degree. Peroneal musculature (evertors) can be involved. Evaluation cannot always Lateral, oblique, and calcaneal axial X-rays of the foot are helpful to assess heel pain. However, for infracalcaneal be contained to the heel itself. Musculature attachments to the heel and around the heel must be assessed. One method to assess for calf tightness is to apply a heel lift that does not compress to less than 1/2 to 1 in. If the plantar heel pain eases, then calf tightness must be addressed in the process of eliminating heel pain. If calf tightness is noted, it is best to stretch the Achilles tendon bilaterally. The stretch should be done with the subtalar joint of the foot in neutral position. This helps maximize the stretch of the Achilles tendon. All stretches should be done as static holds, no bouncing. If heel lifts are needed, then the lifts should be worn in both shoes to reduce the risk of back pain until the flexibility of the gastro-soleus complex is restored. Comment:When bouncing instead of static stretches is done during exercise, shortening rather than lengthening FIGURE 8.4 Infracalcaneal heel spur.

FIGURE 8.3 Pronated foot (low arch).

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spurs, the lateral X-ray view often yields the most inforPain symptoms are generally reported as dull aching mation as to the type and extent of spurring. Direct bonyat the posterior aspect of the heel, lateral to the attachalignment of the foot can also be a contributing factor toment of the tendon Achilles. The pain is greatest when heel spur formation. the foot is dorsiflexed. A possible etiology for this pain Pain presentation is very similar to that of plantaris the pinching of the retrocalcaneal bursal sac between fasciitis. Etiology can be overuse, excess weight in athe Achilles tendon and the heel. An adventitious (not pronated or supinated foot type. Conservative treatment an anatomically correct) bursal sac can form at the is the same as in plantar fasciitis. The physical therapy superficial surface of the Achilles tendon, which can modalities of iontophoresis and phonophoresis andfurther enhance pain. electrical stimulation may be of great help to reduce Conservative treatment for this problem includes inflammation. rest, soft heel lifts, and nonsteroidal anti-in flammatory Note that not all infracalcaneal spurs are symptom-medication or drug, NSAID, occasional removal of the atic. Occasionally if the foot is well compensated, anposterior aspect of the heel counter, or open back shoes. infracalcaneal spur can be an incidental nding fi on XHeel lifts of 1/2 to 3/8 in. are used to raise the point ray examination. of heel irritation just superior to the counter of the Special attention to the thickness of the infracalcanealshoes. Ice massage may also help. If conservative care fat pad is needed to assist in pain relief. Soft shoes with fails, then removal of the infl amed bursal sac and partial a long medial counter for cushioning and shock absorption calcaneal exostectomy or calcaneal osteotomy may be may be helpful. Medial longitudinal arch support may alsorequired. assist in easing inflammation. Some clinicians may advocate steroid injection into the bursal sac only; however, this must be done with great caution and skill. If steroid is inadvertently placed into HAGLUND DEFORMITY the Achilles tendon, spontaneous rupture of the tendon Synonyms for Haglund deformity include pump bump can occur. (from female high heel shoes) and retrocalcaneal bursitis. This bony problem is often confused with Achilles tenRETROCALCANEAL donitis or bursitis. This condition can occur in patients with a prominentEXOSTOSIS/ACHILLES TENDON posterosuperior aspect of the calcaneus who wear tight CALCIFICATION rigid counter shoes. It refers to the part of the shoe that In this malady, heel spur or calcification is noted at the “cups the heel” and gives the heel stability in the shoes. The lateral X-ray view of the foot helps to assess thisinsertion of the Achilles tendon onto the posterior aspect problem. In this entity, the counter of the shoe rubs theof the heel or within the tendon itself. This problem can be isolated or can be found in combination with retrocalheel and causes pain and further enlargement of the poscaneal bursitis of Achilles tendonitis. The Achilles tendon terosuperior aspect of the calcaneus. Clinically, the examitself can become thick and wide; lateral radiographs iner should view the posterior aspect of the heels with the reveal calcification in the Achilles tendon. patient standing. The bulge is quite evident and is seen Pain symptoms include dull aching, especially near lateral to the Achilles tendon. the insertion of the Achilles tendon onto the heel. Pain

FIGURE 8.5 Haglund deformity. Note enlargement of the posFIGURE 8.6 Retrocalcaneal and infracalcaneal spur. terosuperior area of the calcaneus.

Clinical Diagnosis of Heel Pain

FIGURE 8.6A Note calcification in the Achilles tendon.

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FIGURE 8.7 Achilles tendonitis.

frequently occurs in the patient who is involved in athletics athletes, dancers, and jumpers. Tendonitis crepitans can or dancing activities due to the active or passive range of ammation of the area. motion of the ankle as well as with direct palpation of thebe noted due to chronic infl area. Slightly less dorsiflexion of the involved ankle can Tendons, in general, receive blood supply from four areas: muscles, bone, paratenon, and mesotenon. The be noted due to bony block and crepitation of the tendon. Crepitation can occur due to chronic inflammation andAchilles tendon has little supply from bone or muscle; much of its blood supply comes from the paratenon. fibrous deposition throughout the tendon. Conservative care consists of rest and modality care Achilles tendonitis is generally noted to be posterior on the heel with great tenderness noted approximately 3 with great emphasis placed on stretches of the triceps cm proximal to the insertion of the Achilles tendon onto surae. Ice can also decrease edema and decrease poststatic dyskinesia. Surgical exostectomy can require split-the heel. Pain is noted with dorsiflexion of the ankle due ting of the Achilles tendon or detaching the Achilles to tension on the heel cord itself. Tenderness can be associated with swelling, redness, and thickening of the tendon tendon from the heel to gain exposure of the retrocalcaitself. In dancers, pain can be noted during landing just neal spur. The muscle does tend to lose strength with after a jump because the triceps surae is a decelerator of this type of radical approach. foot motion. Treatment consists of longer warm-ups, use of heel ACHILLES TENDONITIS lifts and flexibility training, cross-fiber massage, modaliTendon disabilities can be caused by irritation around aties, and nonsteroidal anti-inflammatories. Stretching is tendon sheath (paratenosynovitis), pathology of thethe key and can be done in several positions. sheath itself (tenosynovitis), lesions between the sheath and the tendon (such as lipoma), and lesions within the TARSAL TUNNEL SYNDROME tendon itself (tenosynovitis). Peritendonitis is a term used to describe infl ammation of a tendon with or with- The tarsal tunnel is located on the medial side of the ankle. out a sheath. The Achilles tendon is the largest and The roof of the tunnel is made up of the laciniate ligament. strongest tendon in the body. There are four distinct canals in the tarsal tunnel, which Tendonitis is an infl ammation of the tendon itself are formed by two individual septa. The contents of the canal are generally caused from repetitive stress experienced by

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the source of pain, but may only describe general areas of pain located at the inferior region of the medial malleolus. Pain with this syndrome is generally of gradual onset and is described as aching, burning, and unremitting. The triad of pain, paresthesia, and numbness are not uncommon with nerve injury. Pain is noted with weight bearing and with nonweight bearing. Pain can begin in the posterior aspect of the heel and can continue forward to just below the medial malleolus and into the toes themselves. FIGURE 8.8 Radiograph of planus foot type. Note sagging of A positive Tinel (pain radiation to toes) or Vallieux sign midfoot. (pain radiation to calf) can be noted with percussion and compression of the posterior tibial nerve as it courses Canal 1: posterior tibial muscle around the medial malleolus. An electromyogram may Canal 2: flexor digitorum longus muscle Canal 3: posterior tibial nerve (L4 L5 S1 S2 S3) help to clinch the diagnosis. Causes for tarsal tunnel syndrome include pronated artery and vein (flat foot) that is decompensated, hypertrophy of the Canal 4: flexor hallucis longus muscle abductor hallucis longus muscle (causing nerve pressure), Tarsal tunnel syndrome is generally the compressioncysts of the nerve itself, or a poorly applied cast that or entrapment of the posterior tibial nerve as it coursesincorporates the foot. under the laciniate ligament. The posterior tibial nerve Differential diagnoses are many, including plantar divides into the medial and lateral plantar nerves and isfasciitis, medial calcaneal neuroma, digital plantar nerve entrapment, vascular disease, and lumbosacral radiculresponsible for great areas of sensory innervation in the foot. As a result, patients may not be able to pinpointopathy.

FIGURE 8.9 Low-arch foot prior to orthotic care.

FIGURE 8.9A Low-arch foot with orthotic care. Note straighter position of Achilles tendon.

Clinical Diagnosis of Heel Pain

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Conservative care of this lesion can include a medialportion of the tendon. Tenderness is detected more superlongitudinal arch support, strapping, and control of theficial and distal to the area where heel spur tenderness subtalar joint with a custom-made control orthotic. Theis expected. The medial calcaneal tubercle is generally goal is to control pronation. Medication and steroidnot tender. injection can help in some cases when pathology is diag- Treatment for this lesion consists of soft sole shoes, nosed early. modalities, and massage. A transverse archband may also help. Tendon injection with steroid medication is questionable and may cause tendon rupture. FLEXOR HALLUCIS LONGUS It is hopeful that with therapeutic discussion of the TENDONITIS prior pathologies, the practitioner may gain additional The flexor hallucis longus muscle assists in plantar flexioninformation for use in treatment of patients, or clients, of the great toe. During the push-off phase of gait, thewith clinical heel pain. muscle locks the proximal phalanx of the great toe and assists in ease of weight distribution. This muscle helps MISCELLANEOUS decelerate the forward motion of the tibia onto a fixed foot. When tendonitis occurs here, it is generally the resultDid someone mention “heel pain?” of a mechanical disturbance. Overuse, other than direct trauma, is a common etiology. The patient complains of discomfort in the sole of the foot. Tendon pain is not generally noted with passive stretch or dorsifl exion of the great toe. Pain is noted with local pressure at the point of pathology. On examination, the flexor hallucis longus tendon stands out when the toe is passively dorsifl exed. Pain can occur the length of the tendon, but is more commonly noted at the proximal

FIGURE 8.11 Did somebody mention heel pain?

REFERENCES

FIGURE 8.10 Flexor hallucis longus tendonitis.

Anderson, J.E. (1978). Grant's atlas of anatomy (7th ed., pp. 488–4-122). A. M.r. Agur (Ed.). Baltimore: Williams & Wilkins. Barrett, S., & O'Malley, R. (1999). Plantar fasciitis and other causes of heel pain. American Family Physician, 59 (8), 2200-2206. Barry, N.N., & McGuire, J.L. (1996). Overuse syndrome in adult athletes.Musculoskeletal Medicine, 22 (3), 515-530. Bateman, J.E. (1982). The adult heel. In M.H. Jahss (Ed.), Disorders of the foot(pp. 764–775). Philadelphia, PA: W.B. Saunders. Baxter, D.E. (1994). The heel in sport. Clinical Sports Medicine, 13, 683–693. Cimino, W.R. (1990). Tarsal tunnel syndrome. Review of the Literature. Foot and Ankle, 11 , 47–52. Cornwall, M.W., & McPoil, T.G. (1999). Plantar fasciitis: Etiology and treatment. Journal of Orthopedic and Sports Physical Therapy, 29 (12), 756–760.

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(pp. 497–504). Gudeman, S.D., Eisele, S.A., Heidt, R.S., Colosimo, A.J., &Netter, F.H. (1989).Atlas of human anatomy CIBA-Geigy Corporation. Stroupe, A.L. (1997). Treatment of plantar fasciitis by iontophoresis of 0.4% dexamethasone. American JourPfeffer, G.P. (1995). Plantar heel pain. In D. E. Baxter (Ed.), The nal of Sports Medicine, 25 , 12–16. foot and ankle in sport (pp. 195–205). St. Louis: MosbyYearbook. Hoppenfeld, S. Physical examination of the foot by complaints. In M.H. Jahss (Ed.),Disorders of the foot(Vol. I, pp. Root, M.L., Orien, W.P., Weed, J.H., et al. (1977). Normal and 103–107). Philadelphia, W.B. Saunders Co. abnormal function of the foot. In Clinical biomechanics (Vol. 2). Los Angeles: Clinical Biomechanics CorporaLuther, L. (1991). Soft tissue trauma of the hindfoot. In G.J. tion. Sammarco (Eds.), Foot and ankle manual (pp. 116–125). Malvern: Lea and Febiger. Scioli, M. (1994). Achilles tendonitis.Orthopedic Clinics of North America, 25 , 177. Malay, D.S., & Duggar, G.E. (1992). Heel surgery. In E.D. Van Wyngarden, T.M. (1997). The painful foot. Part II: Common McGlamry, A.S. Banks, & M.S. Downey (Eds.), Comrearfoot deformities.American Family Physician, 55 (6), prehensive textbook of foot surgery (Vol. 1, 2nd ed., pp. 2207–2212. 431–455). Philadelphia: Williams & Wilkins.

9 Cervicogenic Processes: The Results of Injury Alfred V. Anderson, M.D., D.C. Injuries to the cervical spine present unique problems forCERVICAL SYNDROMES the health care practitioner. This fragile stem between the There are numerous cervical syndromes varying from body and the head is extremely vulnerable. As a result of developmental and congenital disorders to degenerative injury, the spine develops processes to accommodate the processes. Also included are conditions such as strain, mechanical and physiological changes that inherently take sprains, subluxation, and chronic conditions such as place due to such injury. This chapter is based on the author/practitioner’sfibromylagia. experience over 30 years, applying a multidisciplinary approach to chronic, intractable pain. One of the firstCERVICAL ACCELERATION/DECELERATION: components was an exercise regimen. AN EXAMPLE Pain is currently defined as an unpleasant senCervical acceleration/deceleration (CAD) is an ideal consory/emotional experience related to tissue damage or dition to illustrate cervicogenic processes, because this described by the patient in such terms. Chronic noncancer type of injury and its sequelae involve almost all of the pain (CNCP) is generally defined as pain lasting at least syndromes of the cervical spine. 6 months, more time than expected for tissue-to-tissue healing or the resolution of the underlying disease process. The CAD pain patient is sometimes misled by myths It may be due to a condition where there is ongoingthat cause as much damage to the psyche as the physical nociception. Chronic noncancer pain is different thaninjury. Myth: “ The injury is simple strain and sprain, it will ” Fact: The sudden acceleration/decelacute pain in both its presentation and pathophysiology.heal in 6 to 12 weeks. eration injuries are six to ten times more likely to develop Progress in basic science research is gradually discovering the biochemical and structural mechanism of periph-spondylosis or degenerative changes within the joints and disks leading to prolonged recovery time (Norris and Watts, eral and central sensitization that maintains chronic pain. 1983). Over the past several decades, the author has utilized this Myth: “Permanent injuries from sudden acceleration schematic of pain. Pain becomes the center of the patient’ s ” Fact: Approximately life producing inactivity, fatigue, anger, depression, anddeceleration trauma are very rare. frustration (Figure 9.1). However, the most important40% have some persistent recurring pain; approximately aspect of this patient’ s life is function. Function is regained 20% have pain that alters the quality of life (Taylor and with the use of appropriate modalities, exercise, and, ifFinch, 1993). necessary, medication to help the patient deal with the Myth: “ The client had preexisting spinal degenerpain associated with increased activity. ation; the pain is due to this rather than the accident. ” There is a wide range of pain sensitivity, even with theFact: It is the experience of the author that patients can same“ objective” findings. Variations may be dependent onhave degenerative changes occurring down through several factors including the patient’ s early experiences with their life without any symptoms whatsoever. However, pain. Even genetics may play a role in pain perception. when subjected to trauma such as a sudden accelera0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Inactivity Frustration

Fatigue PAIN Anger

Drugs Depression FIGURE 9.1 The results of pain.

tion/deceleration injury, these patients are predisposed to chronic pain.

ANATOMIC INJURIES

FIGURE 9.2 A, normal axis of movements of C5 on C6; B, change of axis and sudden acceleration/deceleration (SAD).

Anatomic injuries are addressed according to the intensity When the cervical spine incurs acceleration/decelof the associated pain. Facet joints are now considered eration injury, there is a substantial alteration of the primary pain generators; they are subject to degeneration mechanics of the spine. Studies by Ono, Daneoka, Witas well as capsular injury. The facets may undergo hypertrophy. They develop loss of articular cartilage, sclerosis,tek, and Kajzer (1997) and Croft (2000) have shown that there is an instantaneous change in the axis of irregularity, and osteophytes; and these alterations take extension of C5 on C6. The pivot point of extension place over a number of years following trauma. normally is in the upper vertebral body of C6 (Figure 9.2). During a sudden acceleration/deceleration SYMPTOMS injury, the pivot point moves up to the lower portion of The facet joints are supplied with proprioceptive fibers;the vertebral body of C5, causing a crushing type of impact to occur with the facets of C5 onto the superior when these are traumatized, they tend to deliver signals to the brain that can confuse the brain’ s perception of articulating surface of C6. This research shows that in visual and vestibular input. This condition is referred toa low impact accident of 6 mi/h, the spine obtains an as cervicogenic vertigoand is related to symptoms of “ S” configuration with hyperflexion of the upper cerviunsteadiness that patients may describe as “standing incal a spine and hyperextension of the lower cervical spine, particularly C5. The studies done by Ono and associates rocky boat.” Fractures of the facets can also lead to subshow that in low impact accidentsthe neck rarely stantial changes in the mechanical function of the joint. exceeds the normal limits of range of motion; however, Case of facet injury —A 32-year-old male, wearing the substantial change in the force factors applied to the a seat belt, was hit from the left at approximately 30 mi/h facets results in signifi cant injury. by a car running a stoplight. He suffered immediate pain in the cervical spine with painful range of motion. He was Bogduk and Marsland (1988) have estimated that about 60% of acceleration/deceleration injuries have taken to an emergency room on a backboard; evaluations were done, including X-ray studies in which a fracturetheir origins in the facet joints. Autopsies of persons subjected to acceleration/deceleration trauma who subwas suspected. Approximately 2 weeks later, a magnetic sequently died of unrelated causes showed that signifi resonance imaging (MRI) scan was done, which did reveal a facet fracture. The patient was immobilized with a Phil-cant trauma had occurred around the facet joints, which adelphia collar for approximately 6 weeks. A good unionmay not have been detectable by MRI scans. New diagnostic and treatment procedures such as facet nerve was obtained. However, the pain persisted in the cervical spine with radiating pain into the base of the skull as wellinjections and radiofrequency rhizotomies have been as localized pain at the lower part of the neck. A facetshown to be effective in reducing the pain complex originating from facet joint injuries. Unfortunately, the nerve injection was done that substantially reduced the hypertrophy occurring after trauma to the facet joints symptoms. As a result of this procedure, the patient elected to have a radiofrequency rhizotomy performed. This sub-also adds to the possibility of stenosis in which the stantially reduced the pain complex. He was followed forintervertebral foramina become narrowed, compressing 6 months with good results. the nerve root.

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In chronic cases where bleeding or trauma occurstenderness at T1 through T3. A MRI scan of the cervical around the nerve root, fibrosis can develop following thisspine showed interspinous tearing at C7 to T1 and T1 to hemorrhage, producing adhesions between the nerve and T2. A later study of the 24-year-old female showed a the spinal ligaments. MRI scans can detect this as perineuherniated disk at the C5 to C6 and C6 to C7 level. ronal fibrosis (Seletz, 1958). When disk injury occurs in the upper three to four segments of the spine, it is not unusual for headaches to arise from these areas. However, many patients who have Invertebral Disk had successful disk surgery at the C4-5 and C5-6 levels Just opposite the nerve root is the intervertebral disk. report significant relief from cervicogenic headaches. In a sudden acceleration/deceleration injury the inter- Headaches are common to persons suffering from vertebral disk at C5 to C6 is subjected to a signifi cant sudden acceleration/deceleration injuries. The headshear force, causing disruption and tearing of the annuaches can result from injury to the facet structures as lar fibers. Thesefibers support one vertebra to the next well as the other pain generators of the cervical spine and also retain the normal confi guration of the nucleus disks. Some authorities have suggested that musclepulposus. contracture headache diagnoses be replaced with cerviThere are, however, many cases in which the findings cogenic headache diagnoses in the posttrauma victims. of the examination do not specifically correlate with theA cervicogenic headache diagnosis seems feasible conMRI studies. Schellhas, Smith, Gundry, and Pollei (1996)sidering the pain associations relating to facets and published a study relative to prospective correlation ofdisks. Persons with prior headaches are going to be MRI and discography in asymptomatic subjects as wellpredisposed to exacerbated pain following a sudden as pain sufferers. Their conclusion showed that significant acceleration/deceleration injury. cervical disk annular tears often escape MRI detection and that MRI cannot reliably identify the sources of cervical Muscles discogenic pain. Clinical indications for cervical discography includes cases of chronic neck pain, head pain, or Variousmuscleshave been implicated in headaches. Hack, radicular pain. Discography should also be considered Koritzer, Robinson, Hallgren, and Greenman (1995) where normal, equivocal, or contradictory lateralizing described the rectus capitis posterior minor muscle, in pain complaints exist. which there is a connective bridge between this muscle and the dorsal spinal dura at the atlano-occipital junction. Freeman (1997) showed that damage to intervertebral disk results in infiltration of pain fibers into the inner third This was observed in every muscle specimen examined. Other muscles involved in cervicogenic headaches include of the anulus fibrosus and into the nucleus pulposus. These all the suboccipital muscles as well as the upper trapezius findings tend to further validate the disk as a pain generand levator scapulae. After signifi cant trauma, trigger ator in chronic spine pain. points found in these muscle structures typically refer pain Although Freeman’ s (1997) studies were done primato the head. Patients respond well to trigger point injecrily on low back pain patients, it certainly would seem tions, massage therapy, and stretching exercises. Acupuncfeasible that this information could be extrapolated to the ture, manipulation, and other modalities have also been cervical spine as well. His findings of isolated nerve fibers useful in controlling the pain of cervicogenic headaches. that express substance P (an excitatory amino acid) deep within deceased intervertebral disks and their association A common sequel to the process of tissue repair is the its , with pain suggests that nerve growth into the intervertebraldevelopment of inflammation of the muscle andfascia disk may play a role in the pathogenesis of low back pain.commonly referred to as myofaciitis. Characteristic of myofaciitis is the presence of small sensitive nodes (trigger points), which are in the fascial sheath. Trigger points Ligaments are painful hypersensitive areas within the muscle or its Ligamentous injuryis another result of sudden accelera-associative supportive tissue (fascia). Normal muscles do tion/deceleration. In a 15-mi/h collision, the head wouldnot contain trigger points, they do not have taut bands of accelerate with a force of 10 g (Macnab, 1964). musclefibers, they are not tender to firm palpation, they A 24-year-old female was seatbelted when hit fromdo not exhibit local twitch responses, and they do not refer behind at approximately 15 mi/h. She was looking up andpain in response to applied pressure (Travell and Simons, 1992). to the right. Following the accident she had severe neck pain with headaches. She was taken to the emergency If the head and neck were subjected to impacts exceedroom; X-rays were taken and she was released. Two weeks ing 10 to 15 mi/h, it would seem logical that muscle and later an examination showed a normal neurological func-ligaments would be injured, thereby generating the contion with the exception of dizziness on range of motionditions described by Travell and Simons (1992). She testing. She had substantial loss of flexion with pointdescribes the brous fi bands, containing trigger points,

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which again are considered pain generators. Pain manageas an individual looking in the rearview mirror at the time ment specialists have treated these conditions for years of impact (Havsy, 1994). with good results. How a person sits in the car is also a decisive factor in the amount of damage resulting from a collision. If a Spinal Cord person slouches with the head tilted somewhat forward, increasing the distance between the head and the headrest, Other research currently underway shows that physiologa greater stress on the cervical vertebral would occur with ical changes within the spinal cord, particularly the dorsal a rear-end collision. horn of the spine are associated with pain. Excitatory Shoulder harnesses, although proven to be life-saving amino acids such as substance P, glutamate, gamma amidevices, have contributed to increased numbers of neck nobutyric acid (GABA), N-methyl-D-asparte (NMDA), injuries. The shoulder belt holds the torso in place, allowand other factors that sensitize the dorsal horn, are impliing the head and neck to move forward in a much smaller cated in pain. Much of current research emphasizes medarc than is allowed without the shoulder belt. A shorter ication that modifies the activities of these substances. An radius and the chin colliding with the chest produce more ongoing study at the University of Minnesota has demondamage to the structures of the neck and temporomandibstrated that labeled substance P normally affects the tip of ular joint. the dorsal horn. However, in the study of rats subjected to lengthy periods of pain, substance P was found to migrate deeper into the dorsal horn. At the time of thisTREATMENTS publication, it is postulated that if this phenomenon conTreatmentsfor the various conditions that are described tinues over a period of time that a permanent alteration in the physiology of the dorsal horn may occur. Many moreearlier were derived from the basic premise of exercise. Exercise, however, is sometimes intolerable to patients studies are being done concerning the hypersensitivity of with moderate to severe pain. Therefore, the judicious use the dorsal horn. of adjunctive medication is recommended to help the patient through the initial phases of an exercise program. FACTORS INFLUENCING PROGNOSIS Medication gives the patient confidence to proceed with OF INJURIES exercise as well as control of the increased pain brought on by stressing the various anatomic structures. Factors influencing the prognosis of an individual include symptoms that have lasted over 6 months. As pointed out BIOFEEDBACK by Loeser (2000), chronic pain is different from acute pain in that measures that provide only transient pain relief doBiofeedbackhas been helpful in controlling stress factors not lead to resolution of the underlying pathological pro-involved with pain. This technique also offers the patient cess. Loeser goes on to point out that injuries to the nera method of relaxing neck muscles when they are tending vous system, either because of direct trauma or because toward stages of spasm. Biofeedback is especially useful of alterations related to massive input, may lead to chronic in the treatment of headaches resulting from the sequelae pain. Noxious stimuli can lead to changes within theof cervical spine injuries. Patients learn to focus on the peripheral and central nervous system that alter the spinal subocciptal muscles, the muscles of the temporomandibcord, particularly the dorsal horn. ular joints, and as has been recently discovered, the rectus If disk injury, nerve trauma, or specific joint injury capitis posterior minor muscles. are involved, the chances of total resolution of the pain complex are significantly reduced. In this respect, olderCHIROPRACTIC MANIPULATION individuals, who have progressive degeneration, typically have a more dif ficult time in recovery due to changes Chiropractic manipulationhas long been effective in treatwithin the structure of the spine, which predisposes them ing neck injuries. Manipulation of traumatized joint structo additional injury when they are subjected to furthertures increases range of motion for damaged facet structrauma (Ameis, 1986). tures. Kirkaldy-Willis, et al. (1985) studied the phenomenon Some elements of the trauma incident contribute toof manipulation and found that therapeutic effects of manipthe type and severity of injury. If an individual is in a ulation involved breaking interarticular adhesions, freeing small car, hit by a large car, the impact and the forces the fixated joint, and stretching the supporting muscles. It involved probably cause more damage to the individualsis his opinion that manipulation also tends to widen and occupying the smaller car. improve the opening of the foramina, thereby reducing irritation to a potentially entrapped nerve. He is also of the Other risk factorsinvolved that increase a person’ s opinion that stimulating the joint mechanoreceptors relieves chances of substantial damage would include having the pain. The stimulation of joint mechanoreceptors tends to head turned to one side or the chin elevated slightly such

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override the pain impulses at the dorsal horn. For example, must sign an informed consent narcotic agreement. if one hits a thumb with a hammer, the rstfiimpulse is to Examples of these narcotic agreements are available in shake the hand andngers. fi It is postulated that this tends other chapters of this text. to stimulate the joint mechanoreceptors, thereby overriding Prior to starting advanced medication, priorities must the pain impulses at the dorsal horn. This is, of course, also be placed on increasing the patient’ s overall capacity for the concept in mobilizing the joints with exercise. Vernon,exercise, emphasizing increased function as the primary et al. (1986) also postulated that there is an increase goal. in Medication cannot be justified on a long-term basis endorphins released after spinal manipulation. if the patient is not showing some indication of increasing function. In severe cases, this may only mean regaining and maintaining the ability to perform the activities of TRIGGER POINT INJECTIONS daily living or sustaining the will to live it. Trigger point injections as advocated by Travell, have been Many authors have defined pain down through the used for years by this author; the techniques and results years. It is this author’ s opinion that Dr. Janet Travell are well documented in other chapters of this text. defines pain in the most accurate terms. Pain“ is what the patient says it is .”

OTHERS Currently, other treatments, modalities, and systems that REFERENCES are implemented, include facet nerve injections, facet nerve rhizotomies, occipital nerve rhizotomies, and inter-Ameis, A. (1986). Cervical whiplash: Considerations in the rehadiscal electrothermy (IDET). Many of these treatments are bilitation of cervical myofascial injury,Canadian Family Physician, 32, 1871–1876. reviewed in other chapters. Future pain management will probably include newBogduk, N., & Marsland, A. (1988). Cervical zygapophysial joints as a source of neck pain. Spine, 13, 610–617. medications affecting the physiology of dorsal horn, medFreeman, A. (1997). Nerve ingrowth into disease intervertebral ications such as COX 2 inhibitors to assist in reducing discs and chronic pack pain. Lancet, 350, 178–181. inflammatory processes, and other pharmaceuticals to Hack, G.D., Koritzer, R.T., Robinson, W L., Hallgren, R.C., & modify the transmission of pain. The use of light and Greenman, P.E. (1995). Anatomic relation between the sound brain entrainment formerly known as evoked potenrectus capitis posterior minor muscle and the dura mater. tials may also prove helpful. Spine, 20 (23), 2484–2486. The author advocates the use of any treatment helpful Havsy, A.F. (1994, January). Whiplash injuries of the cervical in the care of an individual patient. After 30 years of spine and their clinical sequelae. American Journal of Pain Management , 803–821. practice it has become obvious that treatment plans must be individualized. Treatment must be geared towardKirkaldy-Willis, W.H., et al. (1985). Spinal manipulation in the treatment of low back pain. Canadian Family Physician , increased function as well as decreased pain. When uti31, 535–540. lizing medication, the World Health Organization Clinical Journal of Pain, (WHO) criteria are appropriate and should be followedLoeser, J.D. (2000). Pain and suffering. 16 Supplement , S2–S6. as closely as possible. This protocol starts the patients Macnab, I. (1964). Acceleration extension injuries of the cervical on adjunctive medication that might include antidepresspine. Journal of Bone, Joint Surgery,46A(8), sants, anti-inflammatories, as well as dietary modifi ca1797–1799. tions and vitamin therapy. Cessation of tobacco useNorris, S.H., & Watts, I. (1983). The prognoses of neck injuries should be encouraged. resulting from rear-end vehicle collisons. Journal of The next step is the prescribing of a narcotic, as well Bone, Joint Surgery, 65B(5), 608–611. as exercise instruction to enhance overall function of theOno, K., Daneoka, D., Wittek, A., & Kajzer, J. (1997). Cervical injury mechanism based on the analysis of human cerpatient. The practitioner should not be fearful of includvical vertebral motion and head-neck-torso kinematics ing the more potent narcotics when necessary. Responses during low speed velocity rear end impacts. 41st Stapp vary from patient to patient and each patient may respond Car Crash Conference Proceeding. SAE paper 975540, differently to variations in dosages and/or types of drugs. 556–559). Although one patient may respond very well to one type Schellhas, K.P., Smith, M.D., Gundry, C.R., & Pollei, S.R. of narcotic, another patient may not. There is no formu(1996). Cervical discogenic pain. Spine, 21 (3), 300–312. lary or predictive element involved in the selection of aSeletz, E. (1958). Whiplash injuries: Neurophysiological basis specific narcotic for a particular patient. Judicious use for pain and methods used for rehabilitation, Journal of of narcotics should be maintained; but the practitioner the American Medical Association, 168 (13) 1750–1755. must keep in mind the variations in tolerance from oneTaylor, J.R., & Finch, P. (1993). Acute injury of the neck: Anapatient to the next. When chronic opioid analgesic thertomical and pathological basis of pain. Annals Academy apy (COAT) is employed, both the patient and the doctor of Medicine, 22 (2), 187–192.

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Hohl, M. (1974). Soft tissue injuries of the neck in automobile accidents: Factors influencing prognosis. Journal of Travell, J.G., & Simons, D.G. (1992). Myofascial pain and dysBone and Joint Surgery, 56A (8), 1675–1682. function. In J.P. Butler (Ed.) , The trigger point manual: The lower extremities (Vol. 2). Baltimore, MD: Williams Jackson, R. (1977). The cervical syndrome (4th ed.). Springfield, & Wilkins. IL: Charles C Thomas. Vernon, H.T., et al. (1986). Spinal manipulation and beta endor-Kenna, C.J. (1984). The whiplash syndrome: A general practiphin: A controlled study of the spinal maniupulation on tioner’s viewpoint,Australian Family Physician, 13 (4), plasma beta endorphin level in normal males. Journal 256–58. of Manipulation and Physiological Therapeutics . Macnab, I. (1971). The “whiplash syndrome. ” Orthopedic Clinics of North America, (2), 2 389–403. Murphy, D.J. (1995, April). Whiplash distortions, cervical zygapophysial joint injury and chronic posttraumatic neck pain. Journal of Clinical Chiropractic, 31 . ADDITIONAL READING Nordhoff, L. (1994).Motor vehicle collision injury for the 1990’ s doctor/attorney . Automotive Injury Research Institute. Allen, B.J., Li, J., Menning, P.M., Rogers, S.D., Guilardi, J., Mantyh, P.W., & Simone, D.A. (1999). Primary afferent Olney, D.B., & Marsden A.K. (1986). The effect of head restraints and seat belts on the incidence of neck injury fibers that contribute to increased supstance P receptor in car accidents.Injury, 17, 365–367. internalization in the spinal cord after injury. Journal of Porter, K.M. (1989, April). Neck sprains after car accidents. Neurophysiology , 81(3), 1379–1390. British Medical Journal, 298, 6679, 973–974. Cailliet, R. (1991).Neck and arm pain(3rd ed.). Philadelphia: Quebec Task Force on Whiplash-Associated Disorders (1995). F.A. Davis. White paper.Spine, 20 (8S). Croft, A.C. (2000, July). Whiplash.Journal of the American Quintner, J.L. (1989). A study of upper limb pain and parastheChiropractic Association , 32–42. siae following neck injury in motor vehicle accidents. Croft, A.C. (1995). Biomechanics. In S.M. Foreman & A.C. British Journal of Rheumatology, ,28 528–533. Croft (Eds.),Whiplash injuries: The cervical acceleration/deceleration syndrome (2nd ed., pp. 66–71). Balti- Robinson, D.D., & Cassar-Pullicino, V.N. (1993). Acute neck sprain after road traf fic accident: A long term clinical more: Williams & Wilkins. and radiological review.Injury, 24(2), 79–82. David, A.G. (1945). Injuries of the cervical spine. Journal of the Salmi, R.L. (1989). The effect of the 1979 French seat-belt law American Medical Association, 127 (3), 149-156. on the nature and severity of injuries to front-seat occuForeman, S.M., & Croft, A.C. (1988). Whiplash injuries: The pants:Accident Analysis and Prevention,, 21 589. cervical acceleration/deceleration syndrome . Baltimore: Williams & Wilkins.

10 Thyroid and Parathyroid Diseases and Pain Stuart A. Dorow, M.D., D.C., Ph.D. and Gretajo Northrop, M.D., Ph.D. INTRODUCTION

THYROID AND PARATHYROIDS IN HEALTH In the current medical arena, pain is often the most important indicator of the nature and seat of disease. It frequently sigThe thyroid located just below the larynx is composed of nals an interruption of the harmony of the bodily organs; and left and right lateral lobes that lie on either side of the many physicians insist most strenuously that the distinctive trachea. Both lobes are connected in the midline by a mass characteristics of the various kinds of pain be described as of tissue known as an isthmus and the entire structure is accurately as possible by the patient. Pain presenting asina front of the trachea just inferior to cricoid cartilage. throbbing sensation synchronous with the heart’s action is When present, there is an additional projection, which called pulsating pain. Pain described as a feeling of tightness extends cephalad from its attachment at the isthmus and is referred to as tensive and when combined with heat, it is is known as the pyramidal lobe. This endocrine gland called burning. On the other hand, nervous pain may be weighs approximately 25 g and is profused by approxirecognized by its disposition to follow a certain course, with-mately 80 to 120 ml of blood per minute. The thyroid out being rigidly limited to one particular part; by its subjec-gland has a unique configuration histologically. It is comtion to perfect intermissions; and by the suddenness with posed of spherical sacks known as thyroid follicles with which it comes and goes. Spasmodic pain is mitigated by the walls of each sack consisting of cells that project into pressure, by frictions, and by applications of heat; it presents the lumen of the follicle and another layer of cells that suddenly with greater or lesser severity, terminating abruptly. does not. Cells in contact with the lumen area are called Pain that is deemed inflammatory is constant, is attended by follicular cells whereas those not in contact are called C heat and quickened pulse, is increased by movement of the cells or parafollicular cells. When actively secreting horaffected part, by touch, or pressure, and is usually relieved mones, the cells take on a columnar appearance and when by rest. Frequently, pain occurs not in the diseased part but not in an active state, they appear cuboidal in shape. in a distant one and this manifestation is well known as Follicular cells synthesize and liberate the substance referred pain. This is all very tidy and lends itself well by known as thyroxine, or T4, by a process known as iodiextrapolation to the Fox equation, which holds that “Germ nation, and the coupling of two tyrosine molecules while X = disease X, germ Y = disease Y” (Fox & Fox, 1992). attached to a complex protein called thyroglobulin. T4 However, as that educator and countless others have discovsignifies that thyroxine contains four atoms of iodine. ered, this model fails in regard to that all-too-frequently illuTriiodothyronine, or T3, is synthesized as well in the sive pain. A pain that defies labeling by any of the preceding colloid and contains three iodine atoms. Collectively, these definitions is, in every way, equally as debilitating. Is it two hormones comprise the thyroid hormones. Thyroxine merely psycogenic or some supratentorial phenomenon? is present in greater quantity, whereas T3 is several times Thus, some rethinking of the concepts involving pain may more potent and is formed in peripheral tissues such as be required, particularly the pain resulting from thyroid and the liver and kidneys as well as in most other cells by the parathyroid diseases. deiodination of T4. Reverse T3 is biologically inactive and 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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is the metabolized form of T4. It is, however, the activeIt is a well-known fact that thyroid hormones increase form of T3 that binds to receptor sites and thus triggersthe rate of absorption of carbohydrate from the gasend-organ effects. Functionally, both T3 and T4 are similartrointestinal tract, albeit most likely independently of any because they regulate metabolism, growth, and developcalorigenic action. In hyperthyroid patients, the blood ment, as well as the activity of the nervous system.glucose level can be seen to rapidly rise after a carbohyParafollicular C cells are not without their own manufac-drate meal, often exceeding the renal threshold and subturing plant where they synthesize and secrete calcitonin, sequently fall just as rapidly. A topic that takes a proma compound that serves to lower the blood levels of cal-inent place in conversations today is cholesterol levels. cium by its action on bones to increase absorption. The thyroid hormones are not without their effect on Clearly, thyroid cells can be seen to have three actions: cholesterol levels because they have been shown to lower the collection and transport of iodine, the synthesis ofcirculating cholesterol. The level of plasma cholesterol thyroglobulin for its secretion into the colloid, and the decreases prior to the metabolic rate rising and this action removal of the thyroid hormones from thyroglobulin for indicates that it may be independent of stimulation of secretion into circulation (Ganong, 1989). oxygen consumption as well. Normal growth, developThe parathyroid glands, four in number, are embedded ment, and skeletal maturation are, in large measure, in the four poles of the thyroid gland. There are twodependent on the thyroid hormones. Nowhere is this more superior and two inferior glands located on the thyroidevident than in a child who is hypothyroid and in whom gland. These measure about the size of the tip of a small bone growth is retarded and epiphyseal closure is child’s little finger. From the perspective of histology, two delayed. The list of effects of the thyroid hormones on types of cells are represented, and are epithelial in nature. bodily tissues appears to be endless and those discussed The chief cells, or principal cells, synthesize parathyroidhere represent only a few of them. hormone (PTH) and are the most numerous. PTH is The regulation of secretion of thyroid hormones can released in response to a fall in extracellular ionized cal-be seen in the hypothalamic–pituitary–thyroid axis where cium. PTH is carried by the blood to the kidney where itthe tripeptide thyroid-releasing hormone (TRH) is causes calcium reabsorption and conversion of 25-secreted by the hypothalamus and triggers synthesis of a hydroxy-vitamin D3 to 1,25-dihydroxy vitamin D glycoprotein hormone, thyroid-stimulating hormone 3. This metabolite increases intestinal absorption of calcium and (TSH), from the anterior pituitary. TSH secretion sets in with PTH causes bone reabsorption of calcium. These are motion the synthesis of thyroid hormones T3 and T4. In only a few of the actions of PTH. At different concentra- turn, TSH production is regulated by feedback from cirtions of PTH, action on target tissues may differ. Lowculating, unbound thyroid hormones (free T3 and T4). In levels of PTH result in skeletal anabolic action, whereasthe investigation of patients with thyroid disease, an high levels of PTH may result in bone lysis. The remainingunderstanding of these basics is essential for accurate cells are called oxyphils and are believed to manufacture interpretation of test results. a reserve supply of PTH.

HORMONAL REGULATION

THYROID AND PARATHYROIDS IN DISEASE

The thyroid and parathyroid glands never sleep because Hyperthyroidism and hypothyroidism are fairly welltheir role in active metabolism prohibits it. Thyroid hor- known disease entities, with the former being exposure of mones are essential for the normal maturation and metabthe tissues to exorbitant amounts of thyroid hormones, and olism of all bodily tissues. The effects of thyroid hor- the latter a paucity of those hormones. In the purest sense, mones on metabolism are, needless to say, diverse. for one to be hyperthyroid, there must be an overactivity Thyroid hormonal effects can be seen in their calorigenicof the thyroid gland itself, but thyrotoxicosis can manifest action where T3 and T4 increase the oxygen consumption itself with ingestion of excess T4. In some cases, overof almost all metabolically active tissues with the excep-stimulation of the thyroid by pituitary TSH can occur, tion of the adult brain, testis, uterus, lymph nodes, spleen, although this is considered rare. Many factors enter into and anterior pituitary. Nervous system effects can be seen the differential diagnosis of hyperthyroidism, including centrally as well as in the peripheral nervous system. The overingestion of T4 as previously mentioned. Drugs freeffects on skeletal muscle become apparent in the patient quently can be ingested and classified as goitrogens (goiwith hyperthyroidism (thyrotoxic myopathy). Most of ter-producing agents), such as the antithyroid agents prothese patients demonstrate marked muscle weakness. pylthiouracil (PTU), carbimazole, and methimazol (Adler, Beta-adrenergic receptors on the heart are increased et in al., 1988). Amiodarone drops have been shown to prenumber and af finity due to thyroid hormones. The cipitate hyperthyroidism (Gaw, et al., 1995, p. 84). In increase in the number of receptors and finity af on the addition, p-aminosalicylic acid (PAS), sulfonamides, heart resembles the action of beta-adrenergic stimulation. amphenone, phenylbutazone, iodides, lithium carbonate,

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and cobalt have been indicated in diffuse goiter formationtoms referable to stretching of the thyroid capsule, prin(Murphy, 1988, p. 107). An often-overlooked common cipally pain over the thyroid or pain referred to the lower source of iodine ingestion, which may be seasonal, but jaw, ear, or occiput. Local or referred pain can predominevertheless can be taken in excess is expectorants (Hope, nate. Less commonly, the onset is acute, with severe pain et al., 1996, p. 542). Among the more innocuous appearing over the thyroid accompanied by fever and occasionally agents in goiter formation are soy milk/flour, turnips, cab-by symptoms of thyrotoxicosis. Cardinal physical findings bage, brussels sprouts, and rutabagas, to mention a few. include exquisite tenderness and pain on palpation of the Causative agents identified here should not, by any means, nodular thyroid. be construed as all-inclusive. Multinodular goiters can be Other types of thyroiditis include chronic lymphoof the nodular hyperplastic type or adenomas, which are cytic thyroiditis (typically referred to as Hashimoto’ s multiple. Benign adenomas, colloid nodules, thyroglossalthyroiditis). This disease has also been referred to as duct cyst, granulomatous disease, lobulations of the thystruma lymphomatosa and wasrstfi described by the roid, and hematomas comprise a miscellaneous group of Japanese surgeon H. Hashimoto who wrote his M.D. solitary nodules. Malignancies such as lymphoma, anathesis on struma lymphomatosa (Firkin & Whitworth, plastic carcinoma, follicular carcinoma, medullary carci- 1990, p. 444). In the United States, it is the most common noma (or a combination of follicular/papillary, papillary cause of goiter production, as well as the most common carcinoma, and metastatic disease) may also fall under the inflammatory thyroid gland condition (Hay, 1985; Hamsolitary classification (Burrow, 1987, p. 474). burger, 1986). Dayan and Daniels (1996) indicate that According to Ingbar and Braverman (1986, p. 809),lymphoma of the thyroid can be a complication of this thyrotoxicosis or hyperthyroidism may manifest with disease but fortunately does not occur with great freeither elevated or normal blood levels of T3 or T4. Euthy-quency. Several Type III autoimmune hypersensitivity s syndrome, rheumatoid arthriroid Graves’disease is diagnosed when blood levels ofreactions such as Sjogren’ tis, and systemic lupus erythematosus (SLE) have been T4 and T3 are normal yet the patient has the thickened extraocular muscles associated with Graves’ disease. associated with chronic lymphocytic thyroiditis. DiabeGraves’disease is an autoimmune disease in which anti-tes mellitus and pernicious anemia have also been assobodies stimulate thyroid release from the gland. In addi-ciated with chronic lymphocytic thyroiditis (Dayan & tion, human chorionic gonadotropin (HCG) secretingDaniels, 1996). tumors such as choriocarcinoma, hydatidiform moles, Acute supportive thyroiditis is an inflammatory conand testicular embryonal cell carcinomas can stimulatedition resulting from invasion of the thyroid gland by the thyroid gland abnormally. In cases of thyrotoxicosisStaphylococcus aureus or other Gram-positive organisms. without hyperthyroidism, as evidenced by a suppressed It is reported thatS. aureusis the most common invader TSH in the TRH test, extrathyroidal sources of hormone(Dayan & Daniels, 1996). Patients may present with neck such as iatrogenic or factitious ingestion may be suspect. pain and/or tenderness, which appears localized to the Jod–Basedow disease is an iodine-induced source of thythyroid gland. Pain associated with supportive thyroiditis rotoxicosis demonstrating reduced radioactive iodinedoes not appear in the posterior cervical region, assisting uptake (RAIU). in differentiating it from that of musculoskeletal pain. The Thyroiditis is considered a group of inflammatory thy- gland may also manifest rubor and calor, and cause dysroid disorders that may present as thyrotoxicosis withoutphagia, which can be seen in association with pharyngitis hyperthyroidism. This group is composed of subacute thy-and not surprisingly, tachycardia (Levine, 1983). Forturoiditis in either its “silent” (nonpainful) form, known as nately, the disease process is usually self-limiting and can subacute lymphocytic thyroiditis, or its alternative “pain- be treated conservatively with microbial-sensitive antibiful” form, known as giant cell thyroiditis (collectively otics, corticosteroids, aspirin, localized heat, and restricted referred to as simply subacute thyroiditis). However, theactivity. Should an abscess develop, incision and drainage are indicated; if resolution is not obtained, surgical draingranulomatous form appears to be the most common cause of thyroid gland pain. Postpartum thyroiditis may evolveage may become a necessity. as hyper-, hypo-, or euthyroidism. Present thoughts are Riedel’s thyroiditis/struma (invasivebrous fi thyroidithat pregnancy decreases immunologic responses whereas tis) has the distinction of being the least common of the during the postpartum there is a “rebound effect” usuallygroup of inflammatory thyroid diseases. It is a chronic resulting in hyperthyroidism. Granulomatous thyroiditis thyroiditis of unknown etiology marked by localized has been known to follow upper respiratory infections ofareas of stony hardbromas fi (Firkin & Whitworth, 1990). adenovirus, Epstein-Barr virus, echovirus, mumps virus,Riedel’s thyroiditis is characterized by intense brosis fi and coxsackie virus (Farwell & Brauerman, 1996).of the thyroid gland and of the surrounding structures According to Bonica (1990, pp. 864–865), symptoms usu-that lead to induration of the tissues of the neck, assoally follow those of a respiratory infection as stated andciated with some pain in the region of the neck. The include pronounced malaise and asthenia, as well as sympcondition can also be associated with mediastinal and

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retroperitonealfibrosis. It is unfortunate that this slowly enlarging, or in some cases suddenly expanding, hardTABLE 10.1 mass in the anterior neck is often mistaken for thyroidSigns and Symptoms of Hyperthyroidism cancer. Hypothyroidism occurs when the insidious Symptom fibrous infiltration finally invades the entire thyroid gland Sign (Ferri, 1998, pp. 352– 353). Multifocal fibrosclerosis can Restlessness Increased bowel elimination/frequency be expected, as well as involvement of various sitesNervousness Weight loss despite increased appetite distant to the neck. The location of the involved struc- Overactivity Onycholysis separation at distal tuft Menstrual dysfunction, oligo/amenorrhea tures determines the manifest symptoms, which canTremor Diffuse goiter with/without detectable bruit include dysphagia, stridor, and dyspnea (Malotte, et al.,Heat intolerance Velvet skin with moist warm hands 1991). This disease is frequently self-limited but on Sweating Pulse pressure increases occasion, may require surgical resection (Levine, 1983;Hyperreflexia Increased lacrimation Malotte, et al., 1991). Uncommonly, the diseases classi-Insomnia a a Exophthalmos Pretibial myxedema fied as thyrotoxicosis may be caused by pituitary adeTachycardia Panic attacks nomas, struma ovarii, metastatic thyroid cancer, embry-Lid lag Fixed gaze stare onal carcinoma of the testes, chorio-carcinoma,Photophobia Emotional lability hyperemesis gravidarum, and isolated pituitary resis-Diplopia Atrial fibrillation tance to thyroid hormone (Ferri, 1994, p. 47). Systolic flow murmur Blurring of vision a

GRAVES’ DISEASE (TOXIC DIFFUSE GOITER)

Restricted to Graves’ disease.

disease when present; however, it may not be present at Thyrotoxicosis is one of the most common endocrine dis-all or may be very minor in its presentation, and it may orders. Its incidence is highest in women 20 to 40 years present at virtually any stage of the disease process. The of age. Thyrotoxicosis, when associated with ocular signs protrusion of the globe from its orbital rim is believed (ophthalmopathy) and related disturbances as well as to a be the result of mucopolysaccharide deposition and diffuse goiter, is given the name of Graves’ disease and fat accumulation behind the globe accompanied by is the most common cause of hyperthyroidism (Graber, et edema of the extraocular muscles. Of interest is the fact al., 1994, p. 214). In European and Latin American coun-that the cause of Graves’ disease has not been elucidated. tries, this disease may be referred to as Basedow’ s disease Familial predisposition to the disease has led researchers and is reported as such in their literature. This disease to is strongly suspect genetic etiology. The classic maniinteresting and often a clinical puzzle because instead of festations of the disease such as goiter, ophthalmopathy, a diffuse goiter being present, a nodular toxic goiterand dermopathy may well be based on thyrotoxicosis (Hashitoxicosis) may demonstrate all the metabolic fea-and are often present independent of each other, possibly tures of thyrotoxicosis and may occasionally be present exhibiting cyclic periods of exacerbation and remission without any visible or palpable enlargement of the thyroidthroughout the course of the disease. The manifestations gland. Hyperthyroidism is a condition caused by the over-with which the patient presents, increased serum T3 secretion of hormones by the thyroid gland that ultimatelyand/or T4, and suppression of TSH levels found by radioinfluences the metabolism of cells throughout the body.immunoassay, can confi rm the increased activity of the Graves’disease is an autoimmune disease associated with thyroid gland. Elevated levels of antithyroid immunogloa TSH-like immunoglobulin that binds to the TSH receptorbulins evidenced on blood tests may lend credence to a sites of the thyroid gland, and in so doing stimulates thediagnosis of Graves’disease. Graves’disease and its thyroid gland to increase production and release of thyroidprognosis vary on a case-by-case basis. Should symptom hormone. The signs and symptoms of hyperthyroidismremission and eradication of disease-associated immuapply and are listed in Table 10.1. noglobulins result from appropriate treatment, recovery Two signs that appear to be restricted to thyroidremains while immunoglobulins are reduced. With a disease are pretibial nonpitting edema ltrative (infi der- resurgence of thyroid-stimulating immunoglobulins mophathy) of myxedema and exophthalmos (proptosis).(TSI), the patient again becomes hyperthyroid. A potenIn a small number of patients with Graves’ disease (less tially fatal Graves’disease complication known as thy“ than 5%), pretibial myxedema presents as a violaceous roid storm,” presents as a severe episode of thyrotoxicononpitting thickening of the skin in the pretibial region, sis with rapid onset of delirium, tachycardia, sweating, ankles, and/or feet and is the result of mucopolysacchafever, pulmonary edema, and congestive heart failure ride infiltration of the dermal tissue (DeBello, 1992, p. requiring immediate emergency medical intervention 219). Exophthalmos is considered diagnostic of Graves’(Bulens, 1981, pp. 669– 670).

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as sort out nonspecific physical exam findings coupled with misinterpreted and often misleading laboratory findHypothyroidism refers to a condition in which a paucity ings. In all cases of suspected hypothyroidism in children, of thyroid hormones is manufactured in, or secreted by,therapy is essential to preserve mental function in the the thyroid gland. In adults, severe thyroid ciency defi neonate and to preserve normal growth patterns in the is referred to as myxedema. In utero and in the newborn, child. Anhalt, et al. (1956, p. 153) warn, “Despite the fact undiagnosed and untreated hypothyroidism leads tothat screening for congenital hypothyroidism is now cretinism (Fisher, 1981). Cretinism can usually be diag-almost universal in the United States, there are certain nosed clinically without dif ficulty, but at times it must methodologicflaws with the testing; thus, when encounbe distinguished from mongolism and other genetictering a child with suspicious signs and/or symptoms, the disturbances. Immunochemisty is important in makingphysician must always keep this diagnosis in mind. ” the diagnosis. Fortunately, cretinism is appearing with less frequency today than in the past, in part, due to more aggressive detection efforts (Fisher, 1987). Con-HYPOTHYROIDISM (MYXEDEMA) genital hypothyroidism in the neonate is usually The thyroid gland is a uniquely regulated metabolic detected early by statewide screening programs. Since powerhouse and maintains its uniqueness among other their inception in the 1970s, the incidence and compli-glands of the body in that it can synthesize and store cations of untreated cases of primary congenitalimmense quantities of hormones and then slowly and hypothyroidism have dramatically decreased. In lightdeliberately release these hormones in response to bodily of the severity of long-term effects of hypothyroidism demands (Tilkian, 1993). The causes of hypothyroidism on brain tissue maturation (mental retardation), thein the adult can be of primary, secondary, or tertiary origin. mandated newborn TSH, free T3, T4 testing has brought Primary hypothyroidism refers to thyroid hormone defisome welcome relief. ciency as a result of thyroid gland disease or dysfunction Congenital hypothyroidism results from glandular and constitutes greater than 90% of the cases of hypothyabsence (athyreosis), ectopic thyroid, lingual thyroidroidism. Among the etiologies comprising the primary gland, or dyshormonogenesis (Burg, 1990, pp. 134–135). category is Hashimoto’ s thyroiditis (chronic lymphocytic Most often, infants with congenital hypothyroidism thyroiditis). According to Nagataki (1993, pp. 539–545), appear normal at birth but can appear placid and freHashimoto’s thyroiditis may well be the most common quently require arousal to feed. Typically, the infant pre-producer of hypothyroidism in America with some 5% of sents 6 to 12 weeks after birth with a common finding ofeuthyroid, Hashimoto thyroiditis-af flicted persons advancprolonged jaundice and prolonged indirect hyperbiliru-ing to the hypothyroid state with each passing year. Idiobinemia. The cry of the infant sounds harsh or hoarse and pathic myxedema, which may be a nongoiterous form of the infant may also be constipated. Additionally, macro-Hashimoto’s thyroiditis, is also included in the primary glossia similar to that seen in Down’ s syndrome may be category. The category is further expanded by the incluapparent along with an umbilical hernia, muscle hypo-sion of those persons who have been treated for hyperthytonia, and bradycardia. Infants with hypothyroidism mayroidism with iodine 131 therapy or have had subtotal have a history of full-term or even post-term birth. thyroidectomy or radiation therapy of the neck for maligA second category of acquired hypothyroidism maynant disease. Subacute thyroiditis and iodine deficiency appear and in this category, an autoimmune phenomenon or excess along with drugs such as lithium, p-aminosaliwith lymphocytic infiltration of the thyroid gland is most cylic acid (PAS), sulfonamides, phenylbutazone, amiocommon. Hypothyroidism is often insidious in onset. darone, and thiourea or prolonged treatment with iodides Complaints of a neck mass or dysphagia along with weight add to the list. Congenital cases constituting approxigain, dry skin, constipation, and intolerance to cold maymately 1:4000 live births are also included. Secondary be reported by a parent. A goiter is characteristic of thecauses result from TSH deficiency in the pituitary gland acquired form of hypothyroidism and is usually small andand can be due to any pituitary dysfunction such as postfirm, having a “bosselated” texture typical of that seenpartum necrosis, neoplasm, and TSH deficiency secondary with thyroiditis (Mahoney, 1987). If the disease appearsto infiltrative disease. Hypothalamic disease due to neoduring the growing years, there may be obvious failure onplasms, granulomas, or irradiation contributes to the terthe part of the child to grow normally with delayed pubertytiary category of hypothyroidism and results in a defimanifested as well. Of interest is the often-reported obserciency of TRH from the hypothalamus. As expected, the vation of excellent school performance owing to the rel-prevalence (number of cases of a disorder that exist) varies ative indistractibility of the child with hypothyroidism. with location and by study. Graber, et al. (1994) indicate Accurate diagnosis of hypothyroidism in children fre- that hypothyroidism is present in 1 to 6% of the populaquently requires the physician to painstakingly collect andtion. Signs and symptoms related to hypothyroidism are listed in Table 10.2. synthesize a host of vague complaints on history as well

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TABLE 10.2 Signs and Symptoms of Hypothyroidism Sign

Symptom

Fatigue Lethargy Constipation Arthralgias Bradycardia Retarded cerebration Paresthesias Blunted effect Muscular stiffness Pericardial effusion Hearing impairment Dry, cool, doughy skin Brittle, coarse hair & loss Vitiligo Ascites

Muscle weakness Weight gain Slowed speech & deepened voice Vocal hoarseness Reduced memory Loss of memory Intolerance to cold Cerebellar ataxia Carpal tunnel syndrom Distant heart sounds DTR delayed relaxation Slow moving lips Thickened tongue

level of consciousness. With prolonged, severe myxedema, overt psychosis may develop. Attempted suicide has also been reported with some patients never regaining sanity; “myxedema madness” has been applied to these conditions (Christy, 1975). With substitution therapy, the psychosis usually clears but on occasion, patients may develop overt psychosis with the advent of the therapy regimen.

HYPERPARATHYROIDISM, PRIMARY, SECONDARY, TERTIARY

Primary hyperparathyroidism refers to the condition in which the parathyroid glands liberate an excess of PTH (parathyroid hormone). The excess may result from one or more of the glands in spite of the fact that plasma ionizeded calcium is elevated. The normal adaptive response for the release of PTH involves parathyroid Nonpitting edema eyelids and hands hyperplasia in reaction to lowered serum calcium levels. Loss of temporal one third of eyebrows When prolonged for extended periods, these glands can and will hypertrophy, becoming a cause for secondary hyperparathyroidism. The majority of patients suffering with hyperparathyroidism appear to be women. The conHYPOTHYROIDISM (MYXEDEMA COMA) dition appears to be much less common in children. In Myxedema crisis or coma fortunately is rare, developingprimary hyperparathyroidism the pathogenesis appears to in only 1% of hypothyroid patients, but nevertheless itbe unrestrained liberation of PTH but the etiology is is a life-threatening complication of hypothyroidism unknown. In about 80% of patients a solitary benign para(Myers, 1991). Bodily stresses such as cold, trauma,thyroid adenoma is responsible. A low percentage of surgery, infection, and medications including iodides,hyperparathyroidism cases are due to parathyroid cancer. narcotics, and sedatives have been identified as precipiThe small size of the gland can create a dilemma for the tating factors. Hypothyroid decompensation in the formsurgeon. Fortunately, the hormone secreted by this gland of severe respiratory failure (CO (parathyroid hormone) can be stained in paraf fin sections 2 narcosis), hypothermia, or sluggish cerebral perfusion all contribute to theand be used for the identification of normal parathyroid development of coma. The diagnosis is based upon the tissue or that ravaged by an invading carcinoma, particuclinical presentation and therapy must be institutedlarly when the carcinoma occurs as a metastasis. This before the clinical suspicions are substantiated by laboprocedure takes about 30 minutes (Sherrod, 1986). An ratory tests, because delay may lead to a fatal outcome equally small percentage of hyperpathyroidism appears to in this medical emergency (Cecil, 1993). Clinical aware-be familial, with a portion of this category being associness of the wide spectrum of presentation and a high ated with the syndromes of multiple endocrine neoplasia index of suspicion of hypothyroidism will generally (MEN I, MEN IIa, IIb). The condition becomes suspect serve to identify most cases. However, a number of clin-when routine blood chemistry reveals high calcium levels ical conditions such as nephritic syndrome and cirrhosis,(total serum calcium > 10.5 mg/100 ml). Other conditions including an associated reduction in serum TBG (thyroidincluded in the differential may be hypercalcemia due binding globulin) and consequent low serum total T4primarily to increased bone resorption as a consequence values can mimic hypothyroidism. of prolonged immobilization, hyperthyroidism, or maligPatients with hypothyroidism may live for years but nancy involving bone such as metastic carcinoma to bone, with some dysfunction of many organs are less able to leukemia, lymphoma, or multiple myeloma. Addison’ s tolerate the stress of additional illness, i.e, infection,disease, sarcoidosis, hypervitaminosa A or D can result in surgery, seizures, congestive failure, stroke, drug toxic-hypercalcemia. Renal calcium reabsorption increases secity, or exposure to extremes in heat or cold. T4 replace-ondary to thiazide diuretic use. Addison’ s disease or familment is indicated. Expert modern medical management ial hypocalciuric hypercalcemia can also raise serum calis essential. The mortality rate is still 50% and survivalcium levels as can ectopic hyperparathyroidism. depends on early recognition and treatment of theBronchogenic carcinoma has been known to cause hyperhypothyroidism and any other factors contributing to thecalcemia by enhanced absorption of calcium from the GI extremely serious medical condition including an alteredtract, kidney reabsorption, and resorption of calcium from

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bone. The ingestion of large quantities of calcium carbon-revealing stones may serve as a clue to the hyperparathyate and milk (milk-alkali syndrome) also elevate serumroid condition. When there is hypocalcemia, the parathycalcium levels. The signs and symptoms of hypercalcemia roid glands sense the calcium reduction and begin the are listed in Table 10.3. Symptoms are usually due to bone process of hyperplasia and initiate the secretion of PTH pain/fracture, renal stones, nonspecific abdominal pain, in an adaptive effort to restore the body’ s mineral balconstipation, duodenal ulcer, pancreatitis, or depression. ance. If or when the patient suffers from renal failure, Ask a medical student for the symptoms of hyperparathy-malabsorption syndrome, vitamin D defi ciency, or renal roidism associated with hypercalcemia and after a short tubular defects which lead to excess loss of calcium, moment, his or her head will begin to nod and swayhypocalcemia ensues and secondary hyperparathyroidrhythmically as they mentally recite the poetic mnemonic:ism prevails. Drugs such as phenobarbital and phenytoin “Bones stones, abdominal groans and psychic moans. ” actively interfere wtih metabolism of vitamin D and in Unfortunately, no rhythmic mnemonc exists for the addi-so doing diminish the ability of the gastrointestinal tract tional presentations of joint stiffness, gait disturbances,to absorb calcium. Renal tubular acidosis also contribhypertension, myopathy, dehydration, confusion, thirst,utes to calcium loss. nocturia, and anorexia due to increased calcium levels. For osteomalacia in adults and rickets in children to Approximately 25% of patients with hyperparathyroidism occur defective mineralization of bone must precede it. have prominent psychitric symptoms that may resembleMultiple types of osteomalacia exist depending upon the mania, schizophrenia, or acute confusional states while an pathophysiology of the disease or malfunctioning diseased additional 50% may display symptoms suggesting depresorgan. Chronic renal failure results in phosphate retention sion (Cogan, 1987). with a reciprocal decrease in calcium leading to secondary In hypercalcemic cases ectopic hyperparathyroidismhyperparathyroidism. Because of the effects of markedly as well as malignancy of lung, kidney, or pancreas mayelevated PTH levels upon metabolism, osteosclerosis, well come to mind. Granulomatous conditions, for exam-osteoporosis, and von “ Recklinghausens’ s disease of ple, sarcodiosis, tubercolisis, and others that may convert bone” (osteitis fibrosa cystica) may manifest as renal 25-(OH)2D3 to 1,25-(OH)2D3 in an unregulated fashion osteodystrophy (Price, 1986). Another form of oseodysmay lead to increased calcium adsorption from the gut as trophy may develop because of the severity of the renal well as increased bone resorption. Routine radiographic disease. The kidneys may no longer be capable of comfindings may reveal osteoporosis wtih vertebral compres-pleting the conversion of 25-(OH) 2,D3 into the active form 1,25-dihydroxycholecalciferol (1,25-(OH) sion fractures on even more telltale subperiosteal resorp2,D3 vitamin D) tion of the phlanges. Cyst-like lesions may be found inresulting in the most common bone disorder, osteomalacia any part of the skeleton, even the skull (osteitis fibrosa(adult rickets). The disease can be identified radiologically by translucent bands (Loeser’ s lines) that are pseudofraccystica ostodystrophy). tures involving part of the cortex perpendicular to the These bone cysts are frequently seen and are accompanied by pain, especially when there is involvement ofperiostal margin of the bone. These lesion (infarctions) in surrounding periosteum. Calcifi cation of soft tissue such the bone represent infarctions in the bone caused by compressive stresses that produce small cracks in the cortex as lungs, tendon attachments, pancreas, or kidneys

TABLE 10.3 Signs and Symptoms of Hypercalcemia (Hyperparathyroidism) Neuromuscular

Gastrointestinal

Kidney

Myopathy Vomiting Renal stones Hypotonia Constipation Skin Muscular weakness Ileus Pruritus CNS Pancreatitis Cardiovascular Emotional labiality Nausea Hypertension Mental confusion Anorexia QT interval shortened Lethargy Bradycardia Stupor Digitalis toxicity, increased potential Coma Delirium Headache Azotemia (caused by effects of calcium precipitation in the renal parenchyma) Polyuria (ADH prohibited by calcium from binding to receptor sites in the distal convoluted tubule)

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and are pathognomonic of osteomalacia (Albright, 1946).ensues with all its ramifi cations. This condition is relaPseudofractures are frequently bilateral and symmetrical tively rare and most commonly occurs following inadand are commonly seen in the axillary border of the scapvertent removal of all four parathyroid glands during ula, the ribs, pubic and ischial rami, medial aspect of thethyroid cancer surgery. Fortunately, congenital, genetic, neck of the femur, iliac bones, radii, and ulna (Aronoff, idiopathic, and autoimmune causes are extremely rare 1985). They werefirst described by Milkman (1930, 1934) but do exist (Damjanov, 1996, p. 423). Irradiation to the and later became known as “Milkman’ s syndrome. ” For neck rarely may result in hypoparathyroidism, as can many years, it has been known that vitamin D (as above) massive radioactive iodine administration for cancer of is necessary for proper assimilation of calcium throughthe thyroid gland. Candidiasis endocrinopathy synthe gastrointestinal tract (Hannon, 1934). Previously there drome is an inherited disease of functionally defective was a siege of childhood rickets due to decreased vitamin T cells. It is characterized by susceptibility to candidal D in the diet or from lack of exposure to ultraviolet rays.infection with a strong predilection for parathyroid and This siege was eventually eradicated with the fortificationadrenal glands. Autoimmune destruction of these glands of many foods and food additives with vitamin D. Casesmay be due to an autoimmune disorder called multiple of vitamin D-resistant or persitent rickets, an X-linked endrocrine defi ciency, autoimmune candidiasis autosomal dominant disease, have also occurred (Nora, (MEDAC) syndrome (Camargo, 1987, p. 708). Glandu1994). Most cases of vitamin-D resistant or persistentlar destruction regardless of the cause results in hyporickets (rachitis tarda) probably represent osteomalacia parathyroidism and/or Addison’ s disease (Rubin & Farcaused by renal tubular insuf ficiency (Fanconi syndrome), ber, 1995, p. 84). a primary defect in renal tubular phosphate resorption. A severe form of defi cient T-cell immunity is With the decreased active form of vitamin D, absorptionDiGeorge syndrome. This syndrome is caused by defecof calcium from the gut is grossly impaired. Osteomalaciative embryological development of the third and fourth is seen in nearly 60% of all pateints with chronic renalpharyngeal pouches that become the thymus and parathyfailure. Defective dimineralization of the bone occurs roid glands. In the absence of a thymus, T-cell maturation when there is a low serum calcium level and ineffectiveis interrupted at the pre-T-cell stage, and in the absence vitamin D leading to the replacement of normal bone withof parathyroid glands, hypoparathyroidism is inevitable osteoid tissue. Bone with wide osteoid seams is structur(Sadler, 1990, p. 310). In the alcoholic patient, hypoally inferior to normal bone and easily deforms undermagnesemia is a common concern; and when not replaced, stress and is prone to fractures. it can lead to hypoparathyroidism and ultimately hypoOsteodystrophy may be detected using plain lm fi calcemia by either impairing the secretion of PTH or radiographs that show bone with decreased density, most interfering with end-organ responsiveness to the hormone. commonly in the fingers, skull, spine, and ribs. OsteitisWith an insidious onset of hypocalcemia, signs and sympfibrosa cystica occurs in more than 30% of patients withtoms may be negligible or absent altogether. Patients can hyperparathyroidism and is characterized by osteolyticbe asymptomatic and have total serum calcium as low as resorption of bone and its replacement by fibrous tissue. 5 to 6 mg/100ml. The signs and symptoms of hypoparThe lesions of demineralization may appear to be local-athyroidism are those of hypocalcemia (Dambro & Grifized and cystic, hence its name, osteitis fibroa cystica. fith, 1997) and are listed in Table 10.4. Radiographically, the lesions may show a generalized When there is significant hypocalcemia, tetany may decrease in bone density. Classically, the lesion associated well be most striking in clinical presentations. Facial with this disease is the subperiosteal resorption of bone spasms can be so debilitating that the patient is unable to at the phalanges with or without scattered areas of demspeak. Spasms affecting the hands and feet are frequently ineralization in the skull that resemble a moth-eatenseen. When spasms become of such a magnitude that appearance. Osteosclerosis is the least common bone disprevents the patient from talking, the clinician as well as order and on radiographs demonstrates a characteristic family members must be diligent in looking for signs of “Rugger jersy spine” appearance which gives vertebralaryngeal spasm requiring breathing assistance should resalternating dark and light bands respresenting bone denpiration become significantly compromised. Trousseau’ s sity variations. These lesions may appear solo or in any sign (carpal spasm in the hand) can be demonstrated by combination with other radiographic signs. producing ischemia with a blood pressure cuff placed on the arm and inflated above the systolic blood pressure and held for 3 min. The hand will draw toward the ear and the HYPOPARATHYROIDISM fingersflex. The resultant carpal spasm is seen in the hand. Hypoparathyroidism is defi ned as a decrease in the pro- Chvostek’s sign is a facial twitch that may be induced by duction of parathormone or parathyroid hormone by thegently tapping the skin of the face over the area of the parathyroid glands. As a consequence, concentrations facial nerve slightly in front of the tragus of the ear. of circulating calcium are reduced and hypocalcemiaNumbness or tingling sensations of the face, hands, lips,

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loss from blood to the tissues. In addition, increased lactic acid itself increases the respiratory effort. Thus, hypoxTABLE 10.4 emia and hyperthermia plus respiratory alkalosis that lead Signs and Symptoms of Hypocalcemia to increased binding of ionized calcium to albumin lower (Hypoparathyroidism) the blood calcium in these patients. If tenany develops due to low calcium, additional lactate accumulates. ImpairDiarrhea Neuromuscular irritability Fatigue ment in liver function makes lactate metabolism more Weakness Abdominal cramping Alkalosis difficult so a continuous cycle is established. Weight loss, dry skin Bone pain Tetany According to Herman and Sullivan (1959), biopsies Paresthesias Carpal pedal spasm Myalgia taken from the livers of gold miners after suffering heat Headache Depression Dementia Seizures Chvostek’ s sign Trousseau’ s sign stroke revealed histological evidence of liver damage in the form of centrolobular necrosis and extensive cholestasis. It has been stated that the signs and symptoms of and tongue are common findings in hypocalcemia, as are hypoparathyroidism are those of hypocalcemia. In light dryness of the skin, coarse dry hair with some hair loss, of the previous discussion and with continued research, and fingernails with ridges that run longitudinally to the heat stroke might in future literature be a viable candidate nail. Should extrapyramidal signs that resemble parkin-for addition to the list of etiologies in hypocalcemia. sonism be exhibited, calcification of the basal ganglia may Pseudohypoparathyroidism is an autosomal recesbe the culprit and the plain skull film showing basal gan-sive disorder in which PTH target cells fail to respond glia calcification can be confi rmatory. Psychic distur- to appropriate hormonal stimulation. Characteristically, bances (see Table 10.4) can be seen when hypocalcemia the patient may be obese with short stature and round becomes chronic and the patients may exhibit signs of face, may be mentally retarded, and may demonstrate increased intracranial pressure with resultant papilledema. shortened metacarpals and metatarsals on radiographic Hypotension, malabsorption syndrome, cataracts, and proexamination (Ferri, 1998, p. 364). Resistance to multiple longation of the Q wave to T wave (QT) interval are all hormones in addition to PTH may also occur in patients consequences of hypocalcemia. In cases of acidosis, cirwith Albright’s hereditary osteodystrophy. This is culating calcium is liberated from albumin and ionized reported as pseudohypoparathyroidism Type I (Hope, et calcium levels rise sharply. Conversely, alkalosis causes al., 1996, p. 542). ionized calcium to bind to albumin binding sites that would be otherwise occupied by hydrogen ions; therefore, SUMMARY the manifestations of hypocalcemia become exaggerated in either respiratory alkalosis or metabolic alkalosis. In this chapter an attempt was made to discuss the major An interesting biochemical phenomenon occurs in thefeatures of the thyroid and parathyroid glands, in health normocalcemic patient whereby hyperventilation canand disease and their relationship to pain. The authors now blow off CO2, creating a respiratory alkalosis; this, in turn, have a greater appreciation of, and renewed empathy for, reduces the amount of circulating ionized calcium, andthe individual who sets out to go fishing with a large results in low calcium tetany if prolonged. An excellent bucket filled with water and a cooler full of ice to safely study was conducted that reviewed the metabolic and resstore the catch of the day, only to look into the bucket and piratory changes in 21 patients who had suffered heat cooler at the end of the expedition and find a lot of water stroke reported that the predominant change was that of and a lot of ice. However, if you ask the fisherman how metabolic acidosis secondary to an increased lactate conthe day went, the reply might be something like, “I did tent, and/or a respiratory alkalosis. The study furthernot catch much, but I had a wonderful time and I learned reported that many of the patients also had hypo-calcemia. a lot about fishing. ” The authors of this chapter would like The researchers postulated that the lactic acidosis was to echo the sentiment by saying we didn’ t catch much, most likely due to increased metabolic requirementsbut we had a wonderful time and we learned a lot about resulting from hyperthermia compounded by hypotensionthyroid and parathyroid glands during this fishing expeand hypoxemia and an impairment in liver function thatdition. Other than the specific relationships mentioned decreased the capacity to dispose of the lactate once about it these glands and pain, there is paucity in the vast formed. They reported that the cause of the hypocalcemia sea of literature concerning this relationship. Quite possiwas unclear (Appenzeller, 1986, p. 70). The authors ofbly (and more likely, probably) other researchers have this chapter suggest that the reason for hypocalcemia in embarked on this same fishing expedition and in utter these and heat stroke patients is hypoxemia and hyperexasperation simply poured out the water and the ice at thermia shifting the oxygen disassociation curve to thethe end of the day and put away the boat only to fish in right, which resulted in additional oxygen given off to the more fertile waters on the next expedition. A wealth of knowledge that far exceeds the scope and intentions of tissues as well as increased respiratory effort to meet the

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Dambro, M.E., & Griffith, J.A. (1997).Griffith’s 5 minute clinthis chapter is available on the endocrine scene concerning ical consult. Baltimore: Williams & Wilkins. the thyroid and parathyroid glands; therefore, it is left for Damjanov, I. (1996).Pathology for the health-related professome future expedition. Our commitment was to seek out sions. Philadelphia: W.B. Saunders. research that addresses a relationship between these two Dayan, D.M., & Daniels, G.H. (1996). Chronic autoimmune glands and pain and to report them. To this degree our thyroiditis. New England Journal of Medicine, 335, expedition was a success. 99–107. Furthermore, when one reads in every book dealing DeBello, P. (1992).Pocket clinical & drug guide(3rd ed.). Hendwith pain that it is a subjective finding encompassing a erson, NV: Tortoise Books. lifetime of emotions and feelings, there is small wonderFarwell, A.P., & Braverman, L.E. (1996). Inflammatory thyroid why so little is written pertaining to the subject. We condisorders.Otolaryngologic Clinics of North America, clude that there may be much more to the subject of 29, 541–556. thyroid and parathyroid diseases and pain, but the fi- dif Ferri, F.F. (1994).The internal medicine companion . St. Louis, culty may not be so much the manifestation of the pain MO: Mosby-Year Book. (4th ed.). St. but instead the verbal expression of it. Additionally, theFerri, F.F. (1998).The care of the medical patient Louis, MO: Mosby-Year Book. pain associated with diseases of the thyroid and parathyroid glands may, in actuality, not be attributable to directFirkin, B.G., & Whitworth, J.A. (1990).Dictionary of medical eponyms . Park Ridge, NJ: The Parthenon Publishing pain. Instead, pain associated with these glands may be Group. due to the diverse effects on the body, and its cells and Fisher, D.A., et al. (1981). Thyroid development and disorders systems. Duress of disease influences sman’ ability not of thyroid function in the newborn. New England Jouronly to deal with the pain but also to express it.

nal of Medicine, 304,702–712. Fisher, D.A. (1987). Effectiveness of newborn screening programs for congenital hypothyroidism. Pediatric Clinics REFERENCES of North America, 34,879–888. Adler, S.N., et al, (1988). A pocket manual of differential diag- Fox, A., & Fox, B. (1992). Sleep and weight problems associated nosis (2nd ed, pp. 87–113). Boston: Little, Brown. with pain.Innovations in Pain Management: A Practical Guide for Clinicians, 35,1–24. Albright, F., et al. (1946). Osteomalacia and late rickets: The various etiologies met in the United States, with empha-Ganong, W.F. (1989). The thyroid gland. Review of Medical sis on that resulting from a specific form of renal aciPhysiology, 18,267–279. dosis, the therapeutic indications for each etiologicalGaw, A., et al. (1995).Clinical biochemistry . New York: subgroup, and the relationship between osteomalacia Churchill Livingstone. and Milkman’s syndrome.Medicine, 25,399. Graber, M.A., et al. (1994). The family practice handbook. St. Anhalt, H., et al. (1996). Outpatient endocrinology and disorders Louis, MO: Mosby-Year Book. of growth. In D. Bernstein & S. P. Shelov (Eds.), PediHamburger, J. L. (1986). The various presentations of thyroiditis. atrics (p. 133). Baltimore: Williams & Wilkins. Diagnostic considerations. Annals of Internal Medicine, Aronoff, G.M. (1986).Evaluation and treatment of chronic pain . 104, 219–224. Baltimore: Urban & Schwarzenberg. 371. Hannon, R.R., et al. (1934). Calcium and phosphorus metaboAppenzeller, O. (1986). Clinical autonomic failure . Amsterdam: lism in osteomalacia, the effect of vitamin D and its Elsevier Science. apparent duration. Chinese Medical Journal, 48, 623. Bonica, J.J. (1990). Management of pain (Vol. 1, 2nd ed.). Phil- Hay, I.D. (1985). Thyroiditis: A clinical update. Mayo Clinic adelphia: Lea & Febiger. Proceedings, 60,836–843. Bulens, C. (1981). Neurologic complications of hyperthyroid- Herman, R.H., & Sullivan, B.H. (1959). Heat stroke and jaunism. Archives of Neurology, 38 , 669–670. dice. American Journal of Medicine, 27, 154–166. Oxford handbook of clinical medicine Burg, F.D., et al. (1990). Treatment of infants, children andHope, R.A., et al. (1996). (3rd ed.). New York: Oxford University Press. adolescents. Philadelphia: W.B. Saunders. Burrow, G.N. (1987). The thyroid: Nodules and neoplasms. InIngbar, S.H., & Braverman, L.E. (Eds.). (1986). Classification of the causes of thyrotoxicosis. In S.C. Werner (Ed.), P. Felig, et al. (Eds.),Endocrinology and metabolism Werner’s the thyroid: A fundamental and clinical text (2nd ed., pp. 473–507). New York: McGraw-Hill. (pp. 809–810). Philadelphia: Lippincott. Camargo, C.A. (1987). Endocrine disorders. In M.A. Krupp, et Levine, S.N. (1983). Current concepts of thyroiditis. Archives of al. (Eds.),Current medical diagnosis and treatment (p. Internal Medicine, 143,1952–1956. 708). Old Tappan, NJ: Appleton & Lange. Mahoney, C.P. (1987). Differential diagnosis of goiter. Pediatric Christy, N.P. (1975). Diseases of the endocrine system: HypothyClinics of North America, 34,889–904. roidism and myxedema. In P.B. Beeson & W. McDermott (Eds.),Textbook of medicine (Vol., II, 14th ed., p. Malotte, M.S., et al. (1991). Riedel’ s thyroiditis. Archives of 1722). Philadelphia: W.B. Saunders. Otolaryngology Head and Neck Surgery, 117, 214–217. Milkman, L.A. (1934). Multiple spontaneous idiopathic symCogan, M.G. (1987). Central nervous system manifestations of metrical fractures.American Journal of Roentgenology, hyperparathyroidism.American Journal of Medicine, 32, 622–634. 65, 563–630.

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Essential pathology. New York: Murphy, T.A. (1988). Endocrine/metabolic system: Goiter. In Rubin, E., & Farber, J.L. (1995). J.B. Lippincott. S.N. Adler, et al. (Eds.), A pocket manual of differential Sadler, T.W. (1990). Head and neck. In J. Langman (Ed.), Meddiagnosis(2nd ed., p. 107). Boston: Little, Brown. ical embryology(6th ed., p. 310). Baltimore: Williams Myers, L., et al. (1991). Myxedema coma. Critical Care Clinics, & Wilkins. 7, 43–56. Nagataki, S., et al. (1993). Eighty years of Hashimoto disease. Sherrod, A.E., & Taylor, C.R. (1986). Nonlymphocyte tumor markets in tissues. In N.R. Rose, et al. (Eds.), Manual Amsterdam: Elsevier Science. of clinical laboratory immunology (3rd ed., pp. Nora, J.J. (1994).Medical genetics principles and practice (4th 938–947). Washington, D.C.: American Society for ed., p. 211). Philadelphia: Lea & Fabiger. Microbiology. Price, S.A., & Wilson, L.M. (1986).Pathophysiology clinical Clinical implications of laboratory tests concepts of disease processes (3rd ed). New York: Tilkian, S., et al. (1993). (3rd ed). St. Louis, MO: C.V. Mosby. McGraw-Hill.

11 Posttraumatic Headache: Pathophysiology, Diagnosis, and Treatment Gary W. Jay, M.D., F.A.A.P.M., D.A.A.P.M. INTRODUCTION

Organization, 1997). This criterion states that the headache onset must occur within 2 weeks of the traumatic Posttraumatic headache (PTHA), as the name indicates, event or the patient’s return to consciousness. However, is a general, descriptive term for headache that occurs posttraumatic cluster headache, for example, typically posttrauma. The types of trauma do not necessarily need does not fit this time course. Furthermore, their criteria to include an actual blow to the head, or even loss of for acute or chronic PTHA require one of the following: consciousness. The majority of patients who experience loss of consciousness, a period of antrograde amnesia of PTHA do not have an associated minor traumatic brain at least 10 min, or abnormal neurological examinainjury (MTBI); however, PTHA is one of the most comtion/neurodiagnostic testing. The ICD-10 criteria find that mon sequelae of MTBI, but not moderate or severe trauacute PTHA resolves in 8 weeks, whereas chronic PTHA matic brain injury. lasts longer than 8 weeks. This is in counterdistinction to Some have argued that PTHA is no different than the IHS criteria (Headache Classification Committee nontraumatic headache in etiology or treatment. In many [HCC], 1988). cases this may be true, although the assessment and diagnosis can be complex. Still, some researchers and clini- These criteria are contrary to the most commonly accepted criteria, those of the brain injury special interest cians are adamant about their feelings: PTHA is a sham; PTHA almost always has its etiology in the neck; thegroup of the American Congress of Rehabilitation Medipathophysiology of PTHA is very different from other, cine (Kay & Harrington, 1993), which states that MTBI primary forms of headache; and so on. This authoris a “traumatically induced physiological disruption of brain function” associated with at least one of the followbelieves that there is a spectrum of primary headache disorders, with PTHA a form of a primary headache dis-ing: any period of loss of consciousness; any memory loss order with possibly enhanced pathophysiological difficul-for events just before or after the accident; any alteration ties. Ockham’s razor may be useful, but the clinical realityin mental state at the time of the accident, such as feeling disoriented, or confused; and focal neurological appears to necessitate a greater breadth of knowledge dazed, by deficits that may or may not be transient. Most importhe clinician. On the other hand, there are pitfalls in the currenttantly, there is no necessity of direct head trauma to meet classification systems, which seem to ensure difficultiesthe diagnosis. in diagnosis, and not just nosologically. The ICD-10 clas- Another nosological problem is the synonymous use sification system is based on criteria that primarily areof various terminology: concussion, MTBI, postconcussion syndrome/disorder, and posttrauma syndrome. For concerned with the temporal relationship as well as pathogenicity between the relationship of PTHA to trauma, anda number of specific reasons, this author believes the ignore the clinical features of the PTHA (World Health postconcussion syndrome, which affects multiple organ 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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systems, should be differentiated from MTBI (Jay, 2000).“rear-end” automobile accident or slip and fall. Why, it is Patients with PTHA do not, by definition and clinical asked, do professional football players, for instance, not have a high incidence of PTHA and/or MTBI. The answer analysis, have to have an MTBI. Very briefly, the basic elements found in an MTBI is simple and is based on two circumstances: physical conditioning and the fact that when they play, these people may include axonal shearing; marked increases in the excitotoxic neurotransmitters including acetylcholine andare always very prepared and always anticipate the possibility of physical contact or trauma. This differentiates glutamate; a lack of the cohesiveness of the blood–brain barrier, which become “porous” for 8 to 24 h or more; them from the vast majority of people who are not even close to being in optimal physical condition, who are and possible changes in the hemodynamics of the brain. injured unexpectedly, before they are even aware of the (Please see textbook for details [Jay, 2000].) The most important aspect to keep in mind is that the “type” ofimpending trauma and are therefore unable to physically prepare themselves for a trauma, for example, by bracing PTHA must be accurately diagnosed so that appropriate themselves against the headrest before their car is struck treatment can be prescribed. Typically, PTHA is noted after acceleration/decelera-from behind. tion injuries (whiplash) in up to 90% of patients who A great deal of research has shown that when the head experience MTBI (Keidel & Diener, 1997). These head-is free instead of confined, it is more susceptible to the aches can be determined to be posttraumatic tension-type, effects of an acceleration/deceleration injury. Six decades migraine, cluster, or possibly cervicogenic headache.ago, it was shown in cats that less force was required to PTHAs may be secondary to work-related injuries, slipproduce concussion when the head was free to move, as and fall injuries, and violent altercations, aside from motorcompared with when it was fixed or confined in place vehicle injuries. These headaches are frequently part of (Denny-Brown & Russell, 1941). The concept of whipthe postconcussive syndrome, which refers to a large numlash, essentially a legal term, medically known as accelber of signs and symptoms that may follow a blow to theeration/deceleration, is very important because it involves head or an acceleration/deceleration injury, which may ora multitude of medical aspects. When an acceleramay not induce an MTBI. tion/deceleration injury occurs (most frequently from a Acute posttraumatic tension type of headache, therear-end automobile accident), the physical or gravitational forces of a massive object such as a car striking most frequently diagnosed PTHA, (defined as 15 headanother automobile are passed onto the most fragile and ache days or less a month) may last up to 3 to 6 months; after that it becomes, nosologically, chronic. The IHS hasmovable object not firmly secured in the automobile that was struck: the passenger. Even when the passenger is determined that 15 headache days or more a month defines wearing a seat belt, the head — the ball at the end of a chronic headache (HCC). General pain management principles place pain as chronic after 3 to 6 months, aftertether (the neck) — is first thrown forward, and then physiological healing has occurred. Up to 80% of PTHAbackward, when the tether can reach no farther and snaps patients have their pain remit within 6 months, leaving anback. If the head is turned at the moment of impact, the estimated 20% of patients with chronic PTHA, which mayrotational forces are also very important, particularly when an MTBI is found. last years in many cases. A simple concussion may also be associated with Posttraumatic headache encompasses a number of difPTHA, as well as, in the extremes, vegetative and even ferent diagnostic entities. Specific diagnosis is needed for psychotic difficulties (Kojadinovic, Momcilovic, Popovic, appropriate treatment. These diagnoses include et al., 1998; Muller, 1974). PTHA may also be associated with dizziness, irritability, and decreased concentration, • Posttraumatic tension-type headache even without the additional finding of an MTBI. (Again, • Posttraumatic migraine headache for the differentiation between the postconcussive syn• Posttraumatic cluster headache drome and MTBI, please see the MTBI chapter in this • Cervicogenic headache textbook.) • Temporomandibular joint (TMJ)-related headThe chronic PTHA patient frequently engenders sigache nificant difficulties for the typical general practitioner, as • Neuropathic pain syndromes well as the neurological specialist. This may be especially true if there is evidence of de novomigraine or cluster headache. POSTTRAUMATIC TENSION-TYPE Medico-legally, PTHA is a common problem, becauseHEADACHE the patient does not “look” ill and may have few if any abnormalities on examination. In depositions, or in court,PTTHA (with or without secondary analgesic rebound a physician is frequently asked to explain why such aheadache) is probably the most common primary headache significant problem was found after a relatively minor disorder found after trauma. Diagnostically, and clinically,

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this entity appears to be similar to acute and chronic ten- Nosologically, PTHA is incident to trauma. Some of sion-type headache without a traumatic etiology. the problems in making this diagnosis: the patient may The diagnostic criteria of tension-type headache,not experience direct trauma to the head, but have an according to the IHS (HCC, 1998), states that episodicacceleration/deceleration injury (whiplash); there may not be significant physical findings on examination (contension-type headache is a recurrent headache occurring fewer than 15 days a month, lasting from 30 min to 7versely, there may be physical findings that are missed days. The pain characteristics include two of four of theunless a good musculoskeletal examination is done); secfi the following: pain that has a pressing/tightening (nonpulsat-ondary to the lack of profound physicalndings, ing) quality; pain that is mild to moderate in intensity andpatient may be labeled with a psychogenic diagnosis, or may inhibit, but not prohibit activities; pain that is always worse, with the term malingering. bilateral; and pain that is not aggravated by walking stairs When one understands the pathophysiology of the or doing other routine physical activity. These criteria alsoproblem, specifically PTTHA, it should be understood that state that both the following are true: no nausea or vomthe history and physical examination must be done quite iting, but anorexia may occur, and photophobia andspecifically, not “one size fits all diagnoses. ” Knowing phonophobia are absent, or one but not the other is present. what questions to ask and what, on occasion, can be fairly All other organic diagnoses must be ruled out first, as wellsubtle physical findings to look for on examination is as other primary headache diagnoses, including migraine obviously important. and cluster headache. In PTTHA, like non-posttraumatic tension-type headPATHOPHYSIOLOGY OF ache, the pain is typically described as aching or pressureTENSION TYPE like. The pain has also been described as feeling like POSTTRAUMATIC a tight band, or a vice around the head. The pain is typicallyOF HEADACHE bilateral, although it may be unilateral. It may include various areas, some or all the occipito-nuchal, bifrontal,The typical PTTHA begins postacceleration/deceleration bitemporal, and suboccipital regions at the vertex (crown)injury, which most frequently occurs during a motor vehicle accident. A slip and fall accident as well as a sportsof the head, as well as extend into the neck and shoulders. The pain intensity may wax and wane depending onrelated injury or more obviously, a postviolent altercation a number of factors including movement, activity level, can be the initiating event. stress, and others. Even in PTTHA, emotional/psycho- As described previously, the head and the neck, likened to a ball on a chain, is flung forward and backward logical aspects may increase pain. There is a female from acceleration/deceleration forces, frequently without preponderance. Unlike migraine headache patients, PTTHA patientsdirect trauma to the head, or following direct trauma to may carry on with their activities. Most take some formthe head. However it occurs, the physical forces involved of analgesic, frequently on a daily basis. Without question,cause the cervical and shoulder musculature, at a miniPTTHA patients may also have migraine, posttraumaticmum, to be suddenly stretched and sustain both microtears and strain/trauma as well as endure a reflex muscle conor otherwise. The chronic PTTHA patient has headache 15 or moretraction after the sudden stretching. All this being said, it is obviously important to understand the myofascial pain days a month. This is also a diagnostic exercise, because most frequently, nosologically, PTTHA may be one of syndrome (MPS). several headache diagnoses. All these are part of a chronic Pathological changes in the musculoskeletal system daily headache differential, which would include analge-may initiate, modulate, or perpetuate PTTHA. Episodic and chronic PTTHA are, at least at first, secondary to a sic rebound headache, at a minimum. PTTHA patients frequently have a headache daily ormuscle-induced pain syndrome that is typically associated with the previously mentioned MPS. every other day. The headache is typically there when they awaken, and remains until they go to sleep. The intensity The central nervous system (CNS) controls muscle of the pain varies, decreasing for several hours after analtone via systems that infl uence the gamma efferent neugesics are taken. The majority of PTTHA patients, if seenrons in the anterior horn cells of the spinal cord, which early on, have associated pericranial muscle spasm or act on the alpha motor neurons supplying muscle spinpain, whereas others do not, yet still complain of pain. dles. The Renshaw cells, apparently via the inhibitory Patients with PTTHA also endure elements of depres-neurotransmitter gamma aminobutyric acid (GABA) influence this synaptic system. There is also supraspinal sion and anxiety. There is a “chicken and egg” aspect to control from cortical, subcortical, and limbic afferent and this, in terms of which problem comes first. In many cases, efferent systems. Physiological and emotional inputs central neurochemical changes begin concurrent to the interact in the maintenance oruxfl of muscle tone. injury and manifest as both pain and affective disturbances Adverse influences from both localized or regional (see later).

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myofascial nociception, with or without limbic (affec- & Olesen, 1987). Another study (Langmark, Jensen, tive) stimulation, may produce signifi cant muscle spasm; Jensen, & Olesen, 1989) found that pressure pain threshif prolonged, this spasm becomes tonic with the addi-olds in patients with CTTHA were highly dependent on myofascial factors. This study indicated that the generally tional aspects of increased anxiety or a maintained muscle contraction– pain cycle (Diamond & Dalessio, 1980; lower pain thresholds in the chronic tension-type headache patients suggested a dysmodulation of central nociception. Speed, 1983). This helps to differentiate acute vs. chronic A lower pain threshold in chronic tension-type headache PTTHA, to a degree. Tonic or continued posttraumatic muscle contractionpatients, when compared with normal volunteers, was also may induce hypoxia via compression of small blood ves-noted (Borgeat, Hade, Elie, & Larouche, 1984). sels. Ischemia, the accumulation of pain-producing metab- Scalp muscle tenderness and sensitivity to pain in both olites (bradykinin, lactic acid, serotonin, prostoglandins,migraine and tension-type headache patients was meaetc.) may increase and potentiate muscle pain and reactive sured in another study, and the author indicated that the spasm. These nociception-enhancing or algetic chemicals pathophysiology of tension-type headache may involve a may stimulate central mechanisms that, through continued diffuse disruption of central pain-modulating mechanism stimulation, may induce continued reactive muscle(Drummond, 1987). Lower pain thresholds were also spasm/contraction and maintenance of the myogenic nocifound in patients diagnosed with MPSs, including lower ceptive cycle (Dorpat & Holmes, 1955; Hong, Kniffki, & back pain (Yang, Richlin, Brand, Wagner, & Clark, 1985; Schmidt, 1978; Perl, Markle, & Katz, 1934). Malow, Grimm, & Olsen, 1980). It should be noted that the diagnoses in the majority of research papers include As discussed later, the myofascial aspects of tensiontype headache are clinically identical to those of PTTHA;tension-type headache (TTHA), but whether they were the significant difference in diagnoses is the etiology, post-associated with trauma is not indicated. traumatic or otherwise. Both PTTHA and TTHA patients frequently have a The MPS was, for a long while, ignored in the patho-stereotypic posture, with their shoulders raised and their headsflexed forward. This tightly held posture, or musphysiology of headache of any type. Some researchers cular splinting, is effective in preventing unconscious head found a causal relationship between muscle spasm and headache (Martin & Mathews, 1978; Rodbard, 1970;movement that may induce pain. The continued splinting, by maintaining tonic muscle contraction, also works to Sakuta, 1990) whereas others have felt that muscle spasm increase myogenic nociception and perpetuate this cycle. associated with headache is an epiphenomenon, not the etiology of headache (Haynes, Cuevas, & Gannon, 1982; The pericranial muscles are innervated by sensory Philips, 1978; Philips & Hunter, 1982; Riley, 1983; Rob- fibers in nerves from the second or third cervical roots inson, 1980; Simons, Day, Goodell, & Wolff, 1943), but and in the trigeminal nerve (Langemark & Jensen, 1988). a reflexive response. Other authors have indicated that The functions of these muscles contribute to the mainmuscle activity/spasm or increased tone may be more tenance of posture and the stabilization of the head, as pronounced in migraine than in tension-type headaches well as withdrawal and protection of the head. These (Bakal & Kaganov, 1977; Cohen, 1978). factors contribute to the myofascial aspects of both Unfortunately, this research, which was obtained viaTTHA and PTTHA. electromyographic (EMG) studies, appears to be problem- Muscle fatigue occurs, both metabolic and neuroatic, because the various authors evaluated different chemical in nature, and typically follows prolonged or groups of muscles in different types of patients, many oftonic muscle spasm. It may be secondarysympathetto “ whom had poorly defined diagnoses (Anderson & Franks,icopenia”or the depletion of epinephrine and norepineph1981; Bakal & Kaganov, 1977; Martin & Matthews, 1978; rine (NEP), the peripheral sympathetic transmitters Pozniak-Patewicz, 1976). Other authors defined chronic (Cailliet, 1993). The muscle spindle is directly affected tension-type headache (CTTHA) as an entity with or with-by the sympathetic nervous system via these neurotransout associated pericranial muscle disorder. The concept of mitters, particularly NEP. Prolonged and sustained muscle fatigue was not taken into consideration; metabolperipheral sympathetic activity may lead to depletion of ically spent muscles that may become relatively flaccid,NEP at the synaptic receptors. Continued afferent symlose aspects of increased tonus or spasm. pathetic input from myogenic nociception, at least in part Also of interest is the fact that the vast majority of from buildup though ischemia of nociceptive metabolites, may result in sympatheticopenia (Cailliet, 1993; Jay, research deals with tension-type headache, not PTTHA, cant sympathetic aspects of in spite of identical physical/clinical findings as well as 1996). There are also signifi historical findings, all are essentially the same, except formyofascial pain, which are not dealt with in this chapter (Jay, 1995). the presence of initiating trauma. One study found a positive correlation between peri- Tenderness of the cervical, thoracic, and lumbar cranial muscle tenderness and headache intensity, with the paravertebral muscles is also positively correlated with former felt to be a source of nociception (Langemarkpericranial muscle tenderness (Langemark, Olesen,

Posttraumatic Headache: Pathophysiology, Diagnosis, and Treatment

Poulsen, & Bech, 1988). It has also been noted that the contraction of shoulder and cervical muscles as well as emotional arousal contribute to TTHA (Murphy & Lehrer, 1990). These issues also are significant factors in PTTHA. Three mechanisms of muscle pain are thought to be relevant to acute, but more often CTTHA, which has the same physiological stigmata of PTTHA, in that myogenic nociception may be induced by (1) low-grade inflammation associated with the release of algetic, or pain-inducing substances, instead of signs of acute inflammation; (2) short- or long-lasting relative ischemia; and (3) tearing of ligaments and tendons secondary to abnormal sustained muscle tension (Langemark & Jensen, 1988). These factors do not take into consideration the possibly more significant initial trauma from acceleration/deceleration injuries, slip and fall accidents, and other reasons for direct or indirect head trauma that induces muscle trauma, primarily or secondarily.

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A

TP1

B

TP2

C

TP3

D

TP4

MYOFASCIAL PAIN SYNDROME Travell and Rinzler identified the contribution of musculoskeletal factors in the etiology of acute and CTTHA (Travell & Rinzler, 1952). They demonstrated that thereFIGURE 11.1 Referred pain patterns from trigger points ×) in ( the left temporalis muscle. Dark areas show essential zones; spillare consistent patterns of referred pain from trigger points spokes” “ of pain arising form within specific muscle and defined perpetuating factorsover zones are stippled. (A) Anterior that convert acute myofascial pain into a chronic painthe anterior fibers — trigger point 1 region. (B) and (C) Middle spokes— trigger point 2 and 3 regions. (D) Posterior suprasyndrome (Travell & Simons, 1983). auricular spoke —trigger point 4 region. (From Jay, G.W., in The MPS is a localized or regional pain problem asso-Treating the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) ciated with small zones of hypersensitivity within skeletalMarcel Dekker, New York, 1995, pp. 211– 233. With permission.) muscle called trigger points. With palpation of these points, pain is referred to adjacent or even distant sites. Other authors (Fricton, Kroening, Haley, & Siegart, Trigger points in the head, neck, and upper back may elicit 1985) found that a large percentage of patients suffering headache, as well as tinnitus, vertigo, and lacrimation, allfrom an MPS of the head and neck were found to have features noted in patients with PTTHA as well as CTTHAsignificant postural problems, with forward head tilt and (Jay, 1995). (Figures 11.1 to 11.8). rounded shoulders, as well as poor standing and sitting Trigger points may be active, with consistently repro-posture, all findings frequently seen in both CTTHA ducible pain on palpation, or latent, with no clinically patients as well as those with PTTHA. associated complaints of pain but with associated muscle An MPS of the head and neck, via myofascial trigger dysfunction. Trigger points may shift between active andpoint referred pain, may mimic other conditions, including latent states. Clinically, continuous myogenic nociceptionmigraine headache, TMJ dysfunction, sinusitis, and cerfrom active trigger points appears to be a prime instigatorvical neuralgias, as well as various otological problems of the central neurochemical nociceptive dysmodulationincluding tinnitus, ear pain, and dizziness (Fricton, 1990). found in patients with chronic tension-type headache as The onset of an acute, single muscle MPS may be well as PTTHA. associated with trauma, such as an acceleration/deceleration injury, a slip and fall, or even a direct blow. It may Increased stiffness, weakness, and fatigue as well as also come on insidiously, for example, in patients who a decreased range of motion are typically found in muscles in which trigger points are identified. These muscles maywork multiple hours at a typewriter or at the computer. be shortened, with increased pain perceived on stretching. The MPS may show a spontaneous regression to a Patients may protect these muscles by adapting poor poslatent status, with continued muscular dysfunction, but ture with sustained contraction, as noted previously (Fric-with significant diminution of the initial pain complaints. ton, 1990; Langemark & Jensen, 1988). The resultingIn other patients, the MPS may “metastasize” and involve muscular restrictions may perpetuate existing triggerassociated musculature, becoming regional, or even points and aid in the development of others. involving multiple muscular regions.

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A

B

A

B

FIGURE 11.4 Referred pain patterns with location of corresponding trigger points×)( in the right sternocleidomastoid muscle. Dark areas show essential zones; spillover zones are stippled. (A) The sternal (superficial) division. (B) The clavicular (deep) dividion. (From Jay, G.W., inTreating the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) Marcel Dekker, New York, 1995, pp. 211–233. With permission.)

headache. This is frequently seen in the patients with the postconcussive syndrome. Patients with MTBI have other significant emotional stigmata that contribute to FIGURE 11.2 Each × indicates a trigger point in various parts this headache diathesis. of the masseter muscle. Dark areas show essential zones; spill- A major difficulty in the literature is the fact that over zones are stippled. (A) Superficial layer, upper portion. (B)determinations of depression, anxiety, and other affective Superficial layer, mid-belly. (C) Superficial layer, lower portion. components to the PTTHA are found to occur in patients (D) Deep layer, upper part — just below the temporomandibularwith CPTTHA. Without premorbid psychological analyjoint. (From Jay, G.W., inTreating the Headache Patient , Cady, ses, it is very dif ficult to state with any certainty whether R.K. and Fox, A.W. (Eds.) Marcel Dekker, New York, 1995, pp. these patients were depressed or anxious prior to the onset 211–233. With permission.) of their headache problems. It is therefore possible that the neurochemical changes associated with CPTTHA, such as probable central serotonergic dysfunction, initiate depression as a response to these pain-induced neurochemical changes (see later). Some authors have noted that the conversion “ V” found in the hypochondriasis, depression, and hysteria scales of the Minnesota Multiphasic Personality Inventory (MMPI) is a marker for CTTHA as well as PTTHA, however, similar responses are found in chronic nonheadache pain patients (Jay, Grove, & Grove, 1987; Kudrow, 1986; Martin & Rome, 1967). C

D

A

B

FIGURE 11.3 Referred pain pattern (A) of trigger points ×) (in ASSOCIATED SLEEP DISORDERS the left lateral pterygoid muscle (B). Note the similarity to temporomandibular disorder. (From Jay, G.W.,Treating in the Head- There appears to be an important relationship between ache Patient , Cady, R.K. and Fox, A.W. (Eds.) Marcel Dekker, sleep, headache, and muscle– pain syndromes. Central bioNew York, 1995, pp. 211–233. With permission.) genic amines, particularly serotonin and norepinephrine,

are important to sleep physiology as well as to the central pain-modulating systems. Both human and animal research OTHER CLINICAL ASPECTS indicates that central serotonin metabolism plays a role in After the onset of chronic posttraumatic tension type ofpain modulation, affective states, and regulation of nonheadache (CPTTHA), emotional/psychological factorsrapid eye movement REM sleep (Goldenberg, 1990). including stress, anxiety, and depression may become A high incidence of sleep dif ficulties has been found important in the maintenance or perpetuation of thein CTTHA (Matthew, Glaze, & Frost, 1958). Different

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A

TP1

B

FIGURE 11.6 Pain patterns (shaded areas) referred from trigger points (×) in the occipitofrontalis muscle, commonly associated with unilateral, supraorbital, or ocular headache. 9a) right frontalis belly. (B) Left occipitalis belly. (From Jay, G.W.,Treating in the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) Marcel FIGURE 11.5 Referred pain pattern and location of trigger Dekker, New York, 1995, pp. 211–233. With permission.) point (×) in the upper trapezius muscle. Dark areas show essential zones; spillover zones are stippled. (From Jay, G.W., in Treating the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) including rheumatoid arthritis (Goldenberg, 1989). The Marcel Dekker, New York, 1995, pp. 211–233. With permission.)alpha-non-REM disturbance has also been seen in asymp-

tomatic people as well as in those who experience severe emotional stress, such as combat veterans (Goldenberg, sleep disorders appear to be associated with different headache entities. CTTHA and CPTTHA appear to be1990). In the latter group, the veterans with this sleep similar if not identical. Migraine has been found to occurdisorder also complained of chronic headaches, diffuse pain, and emotional distress. in association with REM sleep, and to have an association with excessive stages 3 and 4 and REM sleep (Shahota & Sleep disturbance is also associated with increased pain severity. As noted earlier, chronic headache patients Dexter, 1990). Chronic TTHA has been found to be assoseem to have a higher incidence of sleep abnormalities ciated with frequent awakenings and decreased slow wave than do normal, pain-free subjects. Etiologic aspects of sleep, as well as an alpha-wave intrusion into stage 4 sleep chronic headache may be linked to sleep abnormalities as (Drake, Pakalnis, Andrews, & Bogner, 1990). Moldofsky et al. (1975) noted a disturbance in stagean initiating event or as the result of the underlying pathologically dysmodulated neurochemical factors inducing a 4 sleep to be the first laboratory-based abnormality found in fibromyalgia. They induced a similar alpha-non-REM sleep disorder. pattern of alpha-wave intrusion in delta (stage 4) sleep in normal subjects by stage 4 sleep deprivation. These subOTHER POSSIBLE ASSOCIATED FACTORS jects developed musculoskeletal pain and affective changes comparable with those seen bromyalgia in fi There are several possible mechanical etiologies of patients. Small doses of serotonergic tricyclic antidepreschronic PTTHA. First is cervical spondylosis, which is sant medications, which reduced the alpha intrusions into defined as a degenerative disease affecting intervertebral stage 4 sleep, were utilized to ameliorate the symptoms.disks and apophyseal joints of the cervical spine. Although Alpha-wave intrusions into deep sleep have also been several authors indicate a possible correlation between found in patients with other chronic pain syndromes,cervical spondylosis and TTHA and PTTHA (Diamond

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& Dalessio, 1980; Simons, Day, Goodell, & Wolff, 1943; Finally, the dental literature has been most active in Speed, 1983), others conclude the contrary (Iansek, Heyreporting a possible correlation between TMJ dysfunction wood, Karnaghan, & Nalla, 1987), suggesting that theand TTHA, including PTTHA (Forsell, 1985; Mikail & basis of existing headache is secondary to muscle contracRosen, 1980). The relationship appears to be dependent tion and/or central neurochemical dysmodulation. Cervi-mainly on tenderness of the masticatory muscles, which cogenic headache, which is discussed in detail later, is may a have other etiologies and induce TMJ dysfunction, second suggestive diagnosis. when it exists, on a secondary basis (Langemark, Olesen, Poulsen, & Bech, 1988; Magnusson & Carlsson, 1978a, 1978b). Clinically, in the presence of direct trauma to the TMJ, the incidence of anatomic dysfunction is increased. Splenius capitis

NEUROPHYSIOLOGICAL CHANGES

Fewer than 50% of PTTHA patients complain of mild associated autonomic symptoms such as lack of appetite, hyperirritability, dizziness, and increased light sensitivity (photophobia) (Olesen, 1988). Notably, some of these symptoms may be secondary to autonomic changes assoA ciated with active myofascial trigger points located in the head and neck. Although muscle contraction and tenderness may be interpreted as primary symptoms of PTTHA, EMG activSplenius Splenius cervicis cervicis ity and muscle tenderness increase, in some studies more upper TP lower TP often during migraine than in TTHA (Cohen, 1978; Olesen, 1978; Tfelt-Hansen, Lous, & Olesen, 1981). In research comparing TTHA with common migraine patients exposed to auditory stimulation, TTHA patients showed a lower heart rate reactivity than migraine patients experience (Ellertsen, Norby, & Sjaastad, 1987). It was B shown that TTHA patients exhibited the greatest cardioFIGURE 11.7 Trigger points ×( ) and referred pain patterns vascular arousal during headache (Haynes, 1981). In another study (Bakal & Kaganov, 1977), both migraine (shaded areas) for the right splenius capitis and splenius cervicis muscles. (A) the splenius capitis trigger point, which overlies theand TTHA patients decreased pulse velocity. In a psychooccipital traiangle. (B) (Left) The upper splenius cervicis triggerphysiological comparison of migraine and tension-type point (TP) refers pain to the orbit. The dashed arrow represents headache, it was found that migraine patients are vasodithe pain shooting from the inside of the head to the back of the lated and TTHA patients are vasoconstricted both during eye. (Right) Another site of pain referral. (From Jay, G.W., inand between headache episodes (Cohen, 1978). During Treating the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) another study, administration of ergotamine tartrate, a vasMarcel Dekker, New York, 1995, pp. 211– 233. With permission.) oconstrictor, increased the pain of TTHA, whereas amyl nitrate, a vasodilator, yielded only transient pain relief (Tunis & Wolff, 1954). Greater sympathetic arousal was found in TTHA patients as compared with controls (Murphy & Lehrer, 1990). Another study reported both TTHA and migraine patients demonstrated cardiovascular sympathetic hypofunction, indicated by low basal levels of norepinephrine (NEP), as well as orthostatic hypotension (Mikamo, Takeshima, & Takahashi, 1989). It has been suggested that TTHA patients have phasic hypersympathetic activA B ity, whereas migraineurs do not differ from controls during psychogalvanic response testing (Covelli & FerranFIGURE 11.8 (A) Referred pain pattern (shaded area) of triggernini, 1987). points (×) in the right suboccipital muscles (B). (From Jay, G.W., Evidence of pupillary sympathetic hypofunction and in Treating the Headache Patient , Cady, R.K. and Fox, A.W. (Eds.) subtle anisocoria has been found in both TTHA and Marcel Dekker, New York, 1995, pp. 211– 233. With permission.) migraine patients (Takeshima, Takao, & Takahashi, 1987).

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It was suggested that this may have reflected a central changes, pain perception, and hypothalamic regulation of bioaminergic system dysfunction. Another study sug-hormone release (Raskin, 1988a). gested a pupillary sympathetic system imbalance in The endogenous opiate system (EOS) within the CTTHA patients, who showed asymmetrical mydriasiscentral nervous system may act as a nociceptive “ rheoafter tyramine instillation and in the physiological pupil- stat” or “algostat,” setting pain modulation to a speci fic lary tests (Shimomura & Takahashi, 1986). Oculomotorlevel. As this level changes, an individual ’s pain tolerdysfunction in the amplitude and number of correctiveance may also change. Fluctuations in pain intensity saccades during testing of TTHA patients has also been may be interpreted as being secondary fluctuations to in found (Rosenhall, Johansson, & Orndahl, 1987). the function of antinociceptive pathways (Fields, 1988; Drummond (1986) has reported increased photophoWall, 1988). Headache, along with other “ nonorganic” bia in TTHA patients as compared with controls. Hecentral pain problems are thought to be the most comhypothesized that changes in central neurotransmitter mon expression of impairment of the antinociceptive modulation may induce increased sensitivity or hyperex-systems (Sicuteri, 1982). citability-induced photophobia. The EOS modulates the neurovegetative triad of pain, Episodic platelet abnormalities with associated sero-depression, and autonomic disturbances that are found in tonergic dysfunction has been well documented inonly two conditions — CTTH (posttraumatic or othermigraine (D’Andrea, Toldedo, Cortelazzo, & Milone, wise) and acute morphine abstinence (Sicuteri, 1982). The 1982; Hanington, Jones, Amess, & Wachowicz, 1981).EOS is also implicated as primary protagonists in idioNonepisodic decreased platelet serotonin in CTTHApathic headache (Sicuteri, 1982; Sicuteri, Spillantini, & patients has also been documented (Rolf, Wiele, &Fanciullacci, 1985). Reduced plasma concentrations of Brune, 1981). beta-endorphin have been found in idiopathic headache Again, it must be reiterated that the single differenti-patients, including those with chronic (and posttraumatic) ating aspect between CTTHA and CPTTHA patients istension-type headache (Facchinetti & Genazzani, 1988; the historical factor of some form of trauma. Findings onGenazzani et al., 1984; Mosnaim et al., 1989; Nappi et al., examination, treatment techniques, and methodology are 1982). the same, with the same outcomes in both entities, if done A primary relationship also exists between the EOS appropriately. The research noted earlier does not differand the biogenic amine systems that are intrinsic to both entiate the TTHA patients from those with PTTHA. Clin- the pathophysiology of pain modulation and its treatment. ically and diagnostically there are few, if any, differences.Clinical and neuropharmacological information indicates that dysmodulated serotonergic neurotransmission probably generates chronic headache and head pain. It has also NEUROANATOMY AND been noted that the ordinary, acute or periodic headache NEUROCHEMISTRY may be the noise” “ of serotonergic neurotransmission (Raskin, 1988b). The central modulation of pain appears to originate in the brain stem and involves at least two systems. The Decreased levels of serotonin (Giacovazzo, Bernoni, Di Sabato, & Martelletti, 1990; Rolf, Wiele, & Brune, “descending” inhibitory analgesia system appears to regulate the “gating” mechanisms of the spinal cord. This1981; Shimomura & Takahashi, 1990) (with good indications of an impairment of serotonergic metabolism in system includes the midbrain periaquaductal gray region, patients with CTTHA), substance P, an excitatory neuthe medial medullary raphe nuclei, and the adjacent reticropeptide (Almay et al., 1988; Pernow, 1983) and plasma ular formation, as well as dorsal horn neurons in the spinal cord (Basbaum & Fields, 1984). The “ascending” painnorepinephrine (Takeshima et al., 1989) are found in modulation system originates in the midbrain and is pro-CTTHA patients. The latter is also indicative of peripheral jected to the thalamus (Andersen & Dafny, 1983). Bothsympathetic hypofunction, which may also participate in the etiology or maintenance of central opiod dysfunction systems utilize biogenic amines, opiod peptides and nonopiod peptides (Anderson & Dafny, 1983; Basbaum &(Nappi et al., 1982). Platelet GABA levels are significantly increased in CTTHA patients. This may also act as a Fields, 1984; Raskin, 1988b). balance mechanism to deal with neuronal hyperexcitabilThe ascending system appears to show more relevance ity and may also be associated with depression (Kowa, to headache disorders. This system has projections from Shimomura, & Takahashi, 1992). the brain stem to the medial thalamus, which include large numbers of serotonergic and opiate receptors. The mid- The opiod receptor mechanisms appear to be very susceptible to desensitization, or the development of tolbrain dorsal raphe nucleus, a serotonergic nucleus, erance. In CTTHA patients, opiod receptor hypersensitivprojects to the medial thalamus and is associated with pain perception. Serotonergic projections to the forebrain are ity is marked, secondary to the chronically diminished implicated in the regulation of the sleep cycle, moodsecretion of neurotransmitters. Thisempty “ neuron

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syndrome” may involve both autonomic and nociceptive afferent systems, as well as latent, subpathological or Affective Myofascial Disorders Nociception pathological characteristics with spontaneous manifestations (Sicuteri, Nicolodi, & Fusco, 1988). Limbic The EOS modulates the activity of monoaminergic Spinal System Mechanisms neurons. A chronic EOS deficiency can provoke transmitter leakage, of both opiod and bioaminergic neurotransCentral Nervous System mitters, and lead to neuronal exhaustion and “emptying, ” as well as compensatory effector cell hypersensitivity. The Central Dysmodulation of Nociception poor release of neurotransmitter along with cell/receptor (Serotonin, Norepinephrine, Endogenous Opiates, etc.) hypersensitivity appears to be the most important phenomWith MTBI--> DAI, enon of the hypoendorphin syndromes. It has also been Excitotoxic cell death, concluded that CTTHA (and, clinically, PTTHA) may BBB abnormalities, neurochemical result from dysmodulation of nociceptive impulses, with additional Sleep Disorder dysmodulation associated sensitized receptors (Langemark, Jensen, Jensen, & Olesen, 1989). Tension-Type Headaches CTTHA, including the CPTTHA may be, along with other chronic idiopathic headaches, pain a “ disease” Posttraumatic Headache directly linked to central dysmodulation of the nociceptive and antinociceptive systems, either latent or pathological in nature. Research indicates that at least two arms of the May include Posttraumatic main endogenous antinociceptive systems, the EOS and Cervicogenic Vascular Headache Headache the serotonergic systems, are involved in the pathogenesis of CTTHA. Clinical diagnosis and treatment of PTTHA Chronic Daily Headache demonstrates identical findings. This problem appears to be progressive, and the dysfunctions may result from Analgesic Rebound Vascular Rebound neuronal exhaustion secondary to continuous activation of Headache Headache these systems (Facchinetti & Genazzani, 1988; Sicuteri, Nicolodi, & Fusco, 1988). Migraine Headache

PATHOPHYSIOLOGY

FIGURE 11.9 Headache diatheses found in posttraumatic headache patients.

By looking at the upper portion of Figure 11.9, most of the basics have been mentioned: Continuous peripheral stimulation from myofascial nociceptive input from a feedback mechanisms may react until central neurochemMPS, with or without trigger points, may effectively ical mechanisms dominate, secondary to neurotransmitter trigger a change in the central pain rheostat” “ associated exhaustion, and receptor hypersensitivity and abnormal with nociceptive input, secondary to the continuous needbiogenic amine metabolism/exhaustion occurs. These neufor pain-modulating antinociceptive neurotransmitters.rochemical changes may induce and/or exacerbate a sleep The affective aspects of pain — including depression, disorder (serotonergic in nature, from the nucleus raphe anxiety, and fear —are secondary to changes in neu-magnus); by itself this disorder can perpetuate the central rotransmitters such as serotonin and NEP, directlyu-infl neurochemical dysmodulation, which is primarily responence myofascial nociception, and further reinforce cen-sible for CTTHA. CPTTHA, whether or not it is associated with a MTBI, tral neurochemical changes. has After 4 to 6 and 12 weeks or so, changes in the CNS the same pathophysiological mechanisms. In the prescentral modulation of nociception can occur. Secondaryence of an MTBI, other significant pathophysiological to continuous peripheral nociceptive stimulation, in asso-changes occur that can potentiate or exacerbate the mechciation with affective changes, the central modulatinganisms described earlier. mechanisms assume a primary instead of a secondary or In the face of dysmodulated neurochemical systems reactive role in pain perception, as well as antinociception,found in CTTHA, add direct myofascial trauma as an shifting the initiating aspects of pain perception from theinitiating event. The effects of diffuse axonal injury from MTBI, which also affects the neurochemistry of peripheral regions to the CNS. This intrinsic shift may make innocuous stimuli more the brain as neuronal degeneration and death occurs, aggravating to the pain-modulating systems, the “irritablecan exacerbate the neurotransmitter pathophysiology. everything syndrome. ” The already dysmodulated internal This may also explain the initiation ofde novo

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migraine, because brain stem trigeminovascular mechEVALUATION AND TREATMENT OF POSTTRAUMATIC anisms may obviously be affected. Finally, excitotoxic TENSION-TYPE HEADACHE injury that leads to cell death from the overexuberant production of acetylcholine and glutamate also mayThe neurological examination of migraine patients is, in the absence of complicated aura, negative. The examinainduce significant neuropathologicalholes” “ in the prition of the cluster headache patient may yield signs of a mary neurotransmitter systems and exacerbate the partial Horner’s syndrome. The examination of the patient headache pathophysiology. Affective changes follow, with the additional problem with PTTHA may yield a great deal of information. Typically, the neurological examination is negative. of possible cognitive changes resulting from MTBI. The The musculoskeletal evaluation gives you the facts. Begin latter may make treatment of PTTHA moreficult. dif by observing the patient’ s shoulders. In the vast majority PTTHA is the most common sequelae of an MTBI. It of cases, there is an asymmetry of the acromioclavicular may also be associated with iatrogenic analgesic abuse. joints, with one being higher than the other secondary to Before treatment or even diagnosis of cognitive deficits is greater ipsilateral muscle spasm. The large muscles should attempted, inappropriate medications must be stopped and be carefully palpated both for general tenderness and the the headache ameliorated. Most commonly, for this to be presence of trigger points. These include the trapezius done, the patient must be treated using an interdisciplinary muscles, the deltoids, the scalenes, the rhomboids, the headache treatment protocol. Please The see Headache levaeter scapulae, and all associated muscles (including Handbook: Diagnosis and Treatment for the details of this the pericranial musculature). Pay careful attention to the protocol (Jay, 1999). sternocleidomastoid muscles, particularly in patients comThe neurochemical factors leading to the perpetuation plaining of dizziness and tinnitus. Palpate the bioccipital of PTTHAs appear to be further and more complexly and bitemporal insertions. Look for true pericranial musinvolved than in CTTHA without associated MTBI. Treat- cle tenderness, as well as masseter pain or tenderness. ment is most appropriately and cost-effectively performedObserve the patient open their mouth: look for the amount in an interdisciplinary headache rehabilitation program.of space between the teeth and see if the jaw deviates. Tricyclic medications, GABAnergic medications, and Perform the passive as well as the active cervical range nonsteriodal anti-infl ammatory drugs (NSAIDs) are of motion. Observe the patient’ s head: is it flexed forward? appropriate, whereas narcotics, Dilantin, barbiturates, and Is it tilted to one side? What about the shoulders: are they early generation benzodiazepines are not. rounded or rolled forward? Evaluate the presence and It is worth noting that patients with MTBI who degree of muscle spasm found in the paravertebral muscomplain of headache do not appear to perceive their cles over the entire length of the spine. If the patient is a headache pain the same way a headache patient without CTTHA sufferer, posttraumatic or otherwise, or if there an MTBI does. These patients know that they haveis a complaint of upper extremity or hand numbness, perheadaches. On a scale of 0 (no pain) to 10 (worst pain form an axillary stretch maneuver as well as the Adson’ s imaginable— you could not tolerate it for a moment maneuver to evaluate for a myogenic thoracic outlet synor two), individual patients, whenrst fi seen, give you drome. These are just the basics. high numbers (e.g., 7 to 10). These numbers are corre- Until you know what you are dealing with physiologlated to pathophysiological myofascialndings, fi includ- ically, it is impossible to determine an appropriate treating decreased cervical range of motion, muscle spasm, ment plan. Once you know, and are positive about your active trigger points, and more. As they go throughdiagnosis reached by the history and physical/neurological treatment, you see the patients regain appropriate physexamination, you can begin to formulate a treatment plan. ical functioning: normal cervical range of motion, amelioration of spasm and trigger points, etc., with a TREATMENT OF ACUTE POSTTRAUMATIC marked associated improvement of function. The TENSION- TYPE HEADACHE patients’appear brighter; they smile, have fewer if any pain behaviors, and resume doing the physical things The medical management of acute, or episodic PTTHA is they enjoy. relatively simple. Remember that the older nomenclature Yet, when asked, they continue to state that their headtitled these headaches as “acute muscle contraction headache pain is at the same level of 7 to 10 as when they ache” or “tension headache. ” This form of headache is the were first seen. Whether they are perseverating or are just most common, as previously indicated, accounting for up unable to give an accurate subjective pain level (frontalto 80% of all nonorganic types of headache. It has been lobe involvement?), their stated pain levels may notestimated that over 90% of Americans experience an acute change very much at all. Therefore, you must evaluate TTHA, with or without predisposing trauma, at some time. them on improvements in function, not by self-reportedThe majority of these headaches are self-treated with overthe-counter medications and therefore never come to the subjective decrements in headache pain levels.

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attention of a physician. This indicates that the statisticscombination drugs (Anacin), and aspirin, acetaminophen, are probably low, in that a fairly large number go unno-and caffeine combinations (Excedrin extra-strength, ticed by physicians. Excedrin migraine, and Vanquish). The recommended The greatest problem in the treatment of acutedosage is two tablets every 6 h as needed. PTTHA is the avoidance of the development of analgesic The biggest problem is that taking aspirin, acetamirebound headache, which can easily occur if a patient is nophen, or combination tablets daily or even every other overmedicated. This is one step into the development of day for a week or more (possibly less) can induce the CPTTHA or daily PTTHA. Physicians should be partic- problem of analgesic rebound headache (which is disularly familiar with the various types of medications that cussed later). can be utilized for patients complaining of acute PTTHA. As with birth control pills, when you ask patients what The old adage, that less is better, certainly appliesmedications they are taking, they may forget that the birth here. Many patients deal with the pain and discomfortcontrol pill, aspirin, or acetaminophen are medications; by taking two aspirin and relaxing. Exercise is useful,they may forget to tell you, or even be too embarrassed as is a simple glass of wine, on an occasional basis. Any to tell you, because they are taking a large number of pills type of relaxation that distracts patients from their head-each day, so you must be certain to ask specifically. ache is useful. There are a number of NSAIDs that are prescribed. In dealing with the medication management, physi-Because of the variability in their ficacy, ef pharmacokicians have a more than ample supply to chose from. It may netics, and side effects, patients may need to be tried on be therefore tempting to overtreat a minor headache with more than one, sequentially, not in combination, to determedications that have a signifi cant risk of dependency. mine the best one for them. The simple analgesics are easily chosen by the The NSAIDs work, as noted before, by interfering patient, if not the physician. They are inexpensive andwith the action of cyclooxygenase in the synthesis of easy to get. They include aspirin and acetaminophen. Like prostaglandins. GI side effects are common, in up to 15 the NSAIDs, aspirin appears to work by inhibiting the to 20% of patients; and may include epigastric pain, nausynthesis of prostaglandin by blocking the action ofsea, heartburn, and abdominal discomfort. A history of GI cyclooxygenase, an enzyme that enables the conversion bleeding or ulcerations should indicate that great caution of arachidonic acid to prostaglandin to occur. Remembermust be used, if these medications are used at all. that prostoglandins are synthesized from cellular membrane phospholipids after activation or injury, and sensi-Most Frequently Prescribed Medications tize pain receptors. Aspirin, the prototypical NSAID, has anti-inflamma- Naproxen sodium (Anaprox) reaches peak plasma levels tory and antipyretic properties, along with its pain-reliev-in 1 to 2 h, and has a mean half-life of 13 h. It can be taken at 275 or 550 mg every 6 to 8 h, with a top dosage ing properties. The recommended adult dose for treatment of acute PTTHA is 650 mg every 6 h. Taking the aspirinof 1375 mg/day. Remember that this NSAID is useful in with milk or food may decrease gastric irritation. Aspirin treating hormonally related migraine. can also double bleeding time for 4 to 7 days after taking Ibuprofen (Motrin) is prescribed in dosages of 600 0.65 g. Peak blood levels are found after 45 min. Theand 800 mg per tablet. The suggested dosage for mild to moderate pain is 400 mg every 4 to 6 h as needed. plasma half-life is 2 to 3 h. Acetaminophen usage is common. It provides about Ketoprofen (Orudis) is a cyclooxygenase inhibitor, but also stabilizes lysosomal membranes and possibly antagthe same amount of analgesia as aspirin, but does not have onizes the actions of bradykinin. Its peak plasma level is the gastrointestinal (GI) side effects. It has been suggested that acetaminophen may work by inhibiting prostaglandinreached in 1 to 2 h and has a 2-h plasma half-life. It is now over the counter (12.5-mg tablets), but is best used synthesis in the CNS has been suggested. It has much weaker anti-inflammatory activity than that of aspirin. as 50 to 75 mg capsules. The recommended daily dosage is 150 to 300 mg a day in three or four divided doses. GI Peak plasma levels occur between 30 and 60 min. The side effects are generally mild. Care should be taken when plasma half-life of acetaminophen is 2 to 4 h. Ibuprofen, an NSAID, is also available over the given to a patient with impaired renal function. counter in doses of 200 mg per tablet. It can cause signif- Keterolac tromethamine (Toradol) can be given orally icant GI distress. It has a half-life of 2 to 4 h, with peakor parentally for moderate to severe acute headache pain. plasma levels attained in 1 to 2 h. The adult dosage is 200 Peak plasma levels occur after intramuscular (IM) injecto 400 mg every 4 to 6 h, with a maximum of 1200 mg/day.tion in about 50 min. Its analgesic effect is considered to These medications are frequently sold in combinationbe roughly equivalent to a 10 mg dose of IM morphine. with other drugs such as caffeine, which exerts no specific The typical injectable dose is 60 mg. Because of its potenanalgesic effects, but may potentiate the analgesic effects tially significant hepatic/renal side effects, the Food and of aspirin and acetaminophen. There are aspirin–caffeine Drug Administration (FDA) has stated that Toradol should

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be given orally, after an IM injection of 60 mg, at 10 mg, is 4 to 6 h. The recommended dose is 2400 to 3200 mg a day in divided doses (tablets are 400 mg each). It should every 8 h, for a maximum of 5 days. The cyclooxygenase-2 (COX-2) inhibitors (celecoxib be used carefully in patients with impaired liver function, and rofecoxib) are nonsteroidal anti-inflammatory agentsand should not be used at all in patients with significant that also have analgesic properties without, for mostrenal or liver disease as well as a history of drug-induced patients, the typical GI problems associated withanemias. Side effects include nausea, vomiting, GI upset, NSAIDS. They appear to work by inhibiting prostaglandin drowsiness, dizziness, headache, nervousness, and irritasynthesis, via inhibition of COX-2, which corresponds tobility as well as rash or pruritis. Jaundice and hemolytic its improved GI side effect profile, while not affecting the anemia are rare. COX-1 isozyme, responsible for its anti-infl ammatory Methocarbamol (Robaxin) is a centrally acting skelefunctions. Celecoxib may be taken twice a day, 100 to 200 tal muscle relaxant. It may inhibit nerve transmission in mg twice a day, whereas rofecoxib is taken once a day, at the internuncial neurons of the spinal cord. It has a 30dosages ranging from 12.5 to 50 mg. min onset of action. Peak levels are found in about 2 h, Muscle relaxants are given for acute TTHA by someand its duration of action is 4 to 6 h. It comes as 500 and clinicians. They are probably best utilized during the first750 mg tablets. Tablets containing methocarbamol and aspirin (Robaxisal) are also available. The recommended 3 weeks of post-injury-related headache. They are useful in patients with significant muscle spasm and pain, whichdose of Robaxin is 750 mg three times a day. As with all these medications, it should be taken for 7 to 10 days. It may be seen in acute PTTHA, but are not usually seen with an episodic TTHA. They are used appropriately afteris well tolerated, with initial side effects that resolve over including lightheadedness, dizziness, vertigo, headthe development of muscle spasm after injury such as time, a slip and fall, motor vehicle accident, work and athleticache, rash, GI upset, nasal congestion, fever, blurred vision, urticaria, and mild muscular incoordination. In injuries, or overstretching. These medications work via the development of asituations of severe, seemingly intractable muscle spasm, Robaxin may be given intravenously in doses of about a therapeutic plasma level. Their exact mechanism of action is unknown, but they do not directly affect striated muscle,gram every 8 to 12 h. the myoneural junction, or motor nerves. They produce Orphenedrine citrate (Norflex, Norgesic) is a centrally acting skeletal muscle relaxant with anticholinergic proprelaxation by depressing the central nerve pathways, possibly through their effects on higher CNS centers, whicherties thought to work by blocking neuronal circuits, the modifies the central perception of pain without effectinghyperactivity of which may be implicated in hypertonia and spasm. It is available in injectable and oral formulathe peripheral pain reflexes or motor activity. tions. The IM dose of Norflex is 2 mg, whereas the intraCarisoprodol (Soma) is a CNS depressant that metabolizes into a barbiturate, which makes it both addictive andvenous dosage is 60 mg in aqueous solution. The oral particularly inappropriate to use for patients with pain fromformulation (Norflex) is given in 100 mg tablets — one muscle spasm in addition to MTBI. It acts as a sedativetablet every 12 h. Norgesic is a combination form, includand it is thought to depress polysynaptic transmission ining caffeine and aspirin and should be given 1 or 2 tablets interneuronal pools at the supraspinal level in the brainevery 6 to 8 h. Norgesic Forte, a stronger combination, is stem reticular formation. It is short lived, with peak plasmagiven one half to one tablet every 6 to 8 h. Because of its levels in 1 to 2 h and a 4 to 6 h half-life. Dosage is 350anticholinergic effects, it should be contraindicated in mg every 6 to 8 h. It should not be mixed with other CNSpatients with glaucoma, prostatic enlargement, or bladder outlet obstruction. Its major side effects are also secondary depressants. It is also marketed in two other combined forms (with aspirin as Soma Compound and with codeine)to its anticholinergic properties, and include tachycardia, palpitations, urinary retention, nausea, vomiting, dizzifor additional analgesic effects. Chlorzoxazone (Parafon Forte DSC) is a centrally act-ness, constipation, and drowsiness. It may also cause coning muscle relaxant with fewer sedative properties. Itfusion, excitation, hallucinations, and syncope. Many of these medications are given in combination inhibits the reflex arcs involved in producing and mainwith other drugs, including barbiturates (butalbatal and taining muscle spasm at the level of the spinal cord and meprobamate) and narcotics (codeine, oxycodone, prosubcortical areas of the brain. It reaches peak plasma level in 3 to 4 h, and duration of action is 3 to 4 h. It is well poxyphene, etc.) This is probably not a good idea, because tolerated, and side effects are uncommon. Dosage the is barbiturates and narcotics can easily help develop patient dependence. 500 mg three times a day. Metaxalone (Skelaxin) is a centrally acting skeletal A good combination utilized by the author is methmuscle relaxant that is chemically related to mephenaxaocarbamol 750 mg three times a day for 10 days in lone, a mild tranquilizer. It is thought to induce musclepatients with significant spasm, accompanied by ketoprorelaxation via CNS depression. Onset of action is about fen, 75 mg every 6 to 8 h as needed, with food as needed. 1 h, with peak blood levels in 2 h; and duration of actionFor the acute PTTHA, one tablet of each taken together

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every 6 to 8 h for two to three doses works very well. Another excellent medication is Clonazepam, a fifth Again, narcotic medications should not be used for thegeneration form of benzodiazepine. It is GABAnergic in patient with acute PTTHA, because the risk of depen-effect. It works at the level of the internuncial neurons of the spinal cord to enhance muscle relaxation. It helps, a dence is too great. Remember, too, that simple acute PTTHA is a prob-bit, with anxiolysis. It has a side effect of sedation. In doses of 4 to 12 mg a day, it works as an anticonvulsant. lem that the headache specialists are rarely called to see. The patient’s family physician or chiropractor most fre- At smaller doses, 0.5 to 1 mg given at night, it is very useful in the treatment of patients with CTTHA. The sedaquently sees this problem. tion lasts for a shorter time than the sedation from tricyclics, and this itself is useful. MEDICATION MANAGEMENT OF CHRONIC If the acute use of muscle relaxant medications is not POSTTRAUMATIC TENSION-TYPE HEADACHE enough to end the problem, Tizanidine is a good choice The medication treatment of choice is the tricyclic anti-of medication after the first 3 weeks or so has gone by depressants (TCAs), or the specific serotonergic reuptake and the patient is still exhibiting painful neuromuscular inhibitors (SSRIs). spasm. Tizanidine is an alpha-2-noradrenergic agonist The TCA medication of choice is amitriptyline, a (Coward, Davies, Herrling, & Rudeberg, 1984; Sayers, sedating tricyclic antidepressant. Like all the tricyclics, it Burki, & Eichenberger, 1980). It has supraspinal effects works in the synapse to decrease reuptake of serotonin by inhibiting the facilitation of spinal reflex transmission and (depending on the individual medication) NEP. Ami-by the descending noradrenergic pathways, as it decreases triptyline, unlike the other TCAs, also works to repair thefiring of the noradrenergic locus ceruleus (Palmeri & Wiedamage in stage 4 sleep architecture. It is the most sedatsendanger, 1990). It acts presynaptically in the spinal cord ing tricyclic. The typical dosage is between 10 and 50 mginducing a polysynaptic reduction in released excitatory at night. The author has found it rare to need more than transmitters (Davies, Johnson, & Lovering, 1983). It also 20 or 30 mg at night. decreases hyperexcitability of the muscle without acting Doxepin is also a very good tricyclic. Anticholinergic on the neuromuscular junctions or muscle fibers (Wagstaff side effects such as sedation are reduced (but not by much) & Bryson, 1997). Short acting, its maximum plasma conwhen compared with amitriptyline. It does not work on centrations are reached within 1 to 2 h (Wagstaff & Brythe sleep architecture. It is used at the same dosage levels son, 1997). It has a large first pass metabolism, with a of amitriptyline. half-life of 2.1 to 4.2 h (Koch, Hirst, & von Wartburg, Notice that the tricyclics are not used in their antide-1989). Dosages should be slowly increased, starting at 1 pressant dosages, anywhere from 100 to 350 mg a day. to 2 mg at night and slowly increasing to 20 to 24 mg. Even though the doses are low, their effectiveness in the Maximum dosage is 36 mg in divided dosages, typically treatment of chronic PTTHA is there. found in patients who need an antimyotonic. Interestingly, The SSRIs include Prozac, Paxil, and Zoloft. Thesethis medication appears to decrease muscle pain while medications are not typically sedating (although for someproviding its antimyotonic effects. patients they may be) and with the exclusion of those Finally, treating patients with CPTTHA with tricypatients, they are energizing. They should be given in the clics, physical therapy, psychotherapy, etc., Will Not Work morning. Prozac and Paxil should start at 10 to 20 mg ifa the patient is taking daily or four times a week analgesic day, and they can be increased to 60 to 80 mg. Zoloft medications of any type! In the presence of analgesic should be given at 25 to 50 mg in the morning, up torebound headache, nothing shows long-lasting effective150 mg in divided doses. You should divide the doses,ness until the chronic analgesics are stopped. giving one when the patient gets up in the morning (around 7:00 A .M .) and one at noon. Explain to the patients thatCOST-EFFECTIVE TREATMENT OF CHRONIC taking these medications later than noon can, in many POSTTRAUMATIC TENSION-TYPE HEADACHE cases, give them problems sleeping. You can also safely combine 10 to 40 mg of ProzacTreatment of CPTTHA is best accomplished via an interor Paxil, or 50 mg of Zoloft with a small dose of amitrip- disciplinary rehabilitation approach, the main purpose of tyline or doxepin (10 to 30 mg) at night. Inappropriatewhich is not to “teach the patient to live with the headache,” but to properly diagnose and effectively ameliorate dosages of these two forms of medications can, rarely, or stop it. induce the serotonin syndrome. There are other excellent antidepressants such as Drug detoxification is the necessaryrstfi step, whether Wellbuterin, Serzone, and Effexor. These should be conthe patient is overutilizing simple, over-the-counter analsidered as needed. Do not combine these medications gesics, narcotics, or barbiturates. Chronic daily analgesics with the monoamine oxidase (MAO) inhibitors. It is just appear to prevent appropriate functioning of the EOS not a great idea. (via negative neurochemical feedback loops) and other

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associated antinociceptive systems, inducing analgesic The trigeminovascular system is of great importance rebound headaches, which are secondary problems from in migraine (Jay, 1999). In some children who develop the medications that induce headache secondary to purely posttraumatic neurological deterioration without focal neurochemical/neurophysiological changes. Vascularlesions after minor head trauma, there may be an associrebound headaches from overutilization of vasoconstric-ation with an “unstable trigeminovascular reflex, ” which tors may also occur and must be stopped before other induces the release of perivascular vasodilatory peptides treatment is applied. Clinically, an effective way to detox-that can contribute to cerebral hyperemia (Sakas, Whitify CTTHA patients is with the repetitive DHE-45 pro- taker, Whitwall, & Singounas, 1997). tocol described by Raskin (Raskin, 1988a). Concurrently, TGA was initially attributed to bilateral temporal lobe prophylactic medications should be started. The use of seizure phenomena, but more recently attributed to prophylactic medications, as well as physical therapy and migraine by some (Jay, 1999), and thought to be a totally other treatments given while a patient is enduring anal-separate disorder by others, possibly due to a different gesic rebound headaches, is an ineffectual waste of time form of paroxysmal disorder in the brain stem (Schmidtke and money. & Ehmsen, 1998). TGA in the pediatric population is still After detoxification, an outpatient interdisciplinary felt to be secondary to ischemia of the temporo-basal headache rehabilitation program utilizing neuropharma-structures induced by an MTBI and associated with a cological therapy (to restore neurochemical homeostasis), migrainous diathesis (Vohanka & Zouhar, 1988). physical therapy (Jay, Brunson, & Brunson, 1989), psy- Migraine equivalents, transient neurological sympchotherapy, and stress management (including biofeedtomatology not associated with headache, are not uncomback-enhanced neuromuscular reeducation and muscle mon: proper diagnosis is more ficult dif to the generalist, relaxation) is the most time and cost-effective treatment.as well as the neurologist. In some, possibly more suscepOptimal psychotherapy or physical therapy regimes bytible individuals, minor, even trivial, head trauma can themselves do not resolve myofascial ficulties dif or induce a migraine equivalent known as footballer’ “ s depression if the affective sleep and CNS neurochemical migraine” as well as posttraumatic “ cortical blindness. ” dysmodulation affecting them are not concurrently andThis particular migraine equivalent is certainly rare, but appropriately treated. The interdisciplinary treatment par-transient, total blindness may certainly be cause to call out adigm also enables fine-tuning of diagnosis and possible a total, “full court press”workup (Harrison & Walls, 1990). determination of a secondary or “hidden” etiology for a Another more common form of transient neurological patient’s headaches. disturbances associated with migraine are brain stem Failure to treat the CPTTHA patient with an interdis- symptoms including vestibular dif ficulties such as dizziciplinary, whole-person approach (see Figure 11.9) isness, disequilibrium, vertigo, and motion intolerance. responsible for multiple treatment failures as well as mon-These symptoms may also present as a migraine equivaetary waste, because long-term responseheadache — lent, between migraine headache episodes or instead of remediation— is most often not achieved. the cephalic pain. Vertigo as a migraine equivalent may occur in about 25% of migraine patients, with the diagnosis made typically by history of familial migraine, POSTTRAUMATIC MIGRAINE because all testing is typically negative. Migraine can also mimic Meniere’s disease, with vestibular Meniere’ s disPosttraumatic migraine, which may begin de novo— without a previous personal or family history of migraine — ease being more frequently but still not commonly assomay have neurochemical similarities with MTBI, although ciated with migraine (Baloh, 1997; Harker & Rassekh, 1988). Also, one should not forget the cervical causes of they are not always found together. These may include vertigo and dizziness, secondary to posttraumatic cervical increased extracellular potassium and intracellular sodium, myofascial pathophysiology. calcium, and chloride; serotonergic changes; decreases and/or in magnesium; excessive release of excitatory amino acids; There is also a question of the possible relationship between posttraumatic migraine and posttraumatic benign changes in catecholamine and endogenous opiod tonus; encephalopathy. The latter, in children, may be associated decreased glucose utilization; changes in neuropeptides and abnormalities in nitric oxide formation and function with cortical blindness, brain stem disturbances, and seizure, lasting from 5 min to 48 h (Vohanka & Zouhar, 1990). (Jay, 1999, pp. 17– 32; Packard & Ham, 1997). A significant question then arises. Posttraumatic verMigraine, including posttraumatic migraine, may be associated with a number of neurological symptoms ortigo or dizziness is a very frequent accompaniment to MTBI. It may be secondary to peripheral, labyrinthine phenomena. This may include transient global amnesia (TGA), vestibular dysfunction, visual and auditory disturbance, or brain stem disturbance secondary to trauma; or it may be a migraine equivalent. The imporchanges, and possibly increased incidence of seizures (Buchholz & Reich, 1996; Jay, 1999; Leisman, 1990). tance of this differential is most significant, possibly, when

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treatment is attempted. Clinically, this would be an impor-Arnold, this pain is known as occipital neuralgia. It is tant avenue of treatment to explore. always in the C2 distribution at the back of the head. As noted, trauma may induce the first migraine attackIndomethacin may be an effective treatment for this problem. Steroidal injections may also be utilized. in a possibly susceptible patient or increase the frequency and possibly the severity of preexisting migraine. TheNeuroablative procedures should be performed only when all other treatment has failed. etiology of these changes may be secondary to neuronal Preexisting arthritis or discogenic disease may also be and/or axonal abnormalities secondary to trauma. exacerbated by the initial trauma. An appropriate neuroProphylactic treatment is typically with valproic acid, logical evaluation helps with these entities. an anticonvulsant medication. The use of beta-blockers The dysautonomic cephalalgia of Vijayan (1977) is such as propranolol may also be useful, but it may have associated with injury to the anterior aspect of the carotid significant side effects. The same is true for verapamil. sheath. The headache is severe and unilateral, in the fronThe use of a triptan for abortive care is well tolerated, if totemporal area and associated with ipsilateral hyperused appropriately. hidrosis and dilatation of the ipsilateral pupil. The role of Cluster headache has also been seen secondary to head sympathetic nervous system dysfunction, although it may trauma, again possibly secondary to neuronal and/or remain controversial, is shown in many studies, as noted axonal injury. The incidence ranges from 6 to 10% earlier. Also, the signs and symptoms are, of course, sim(Duckro, et al., 1992; Packard & Ham, 1997). Many times, ilar to cluster headache. this is seen as a primary chronic, instead of episodic form of cluster, or clusterlike headache. Clinically, this is one of the rarest forms of PTHA seen. Treatment, abortive orCERVICOGENIC HEADACHE prophylactic, has been dealt with elsewhere (Jay, 1999). Just as the community of headache specialty physicians were rather hesitant to accept the fact that the musculature OTHER ASPECTS OF POSTTRAUMATIC had any role in TTHA, posttraumatic or otherwise, the idea that headache can arise from the structures of the HEADACHE neck still has many detractors. An initial trauma may involve soft tissue injury to the Dwyer, Aprill, and Bogduk (1990) utilized fluoroscalp or face, which may be followed by an entrapmentscopic control to stimulate joints at segments C2–C3 to of a sensory nerve, or the sensory nerve may have been C6–C7 by distending the joint capsule with injections of cut during the trauma via laceration. The entrapment may contrast medium. They were able to show that each joint also occur during suturing of a laceration. Such entrap-produced a clinically distinguishable, characteristic patments may induce nerve, or neuropathic pain. This istern of referred pain that enabled the construction of pain easily differentiated from other primary headache types.charts to be used in determining the segmental location The pain is constant, burning, and relegated to the sensory of symptomatic joints in patients presenting with cervical distribution of the affected nerve. Anticonvulsant medica-zygapophyseal pain. tions such as carbamazepine are best for the first-line The diagnostic criteria for cervicogenic headache treatment. Neuronton has been used, but it has different, (CGHA) have been noted by several authors to differ a possibly more significant side effects in some patients,bit. Bogduk, et al. (1985) defined CGHA as referred pain particularly in those with a concurrent MTBI. In some perceived in any region of the head that was referred by cases, neurolytic procedures such as radiofrequency coaga primary nociceptive source in the musculoskeletal tisulation or cryoablation may be necessary. Both are good sues innervated by cervical nerves. Clinical features procedures, but have varying durations of benefit, most included pain that was not lancinating, and was dull or typically between 6 and 12 months. aching but could be throbbing — located in the occipital, Without question, injuries to the cervical spine, theparietal, temporal, frontal, or orbital regions, unilaterally superficial and deep structures of the neck (muscles,or bilaterally. There was some indication of cervical spine ligaments, bone, disks, or nerve roots) may occur. Cerabnormality such as neck pain, tenderness, impaired cervical pain from trigger points in spasmed musculaturevical motion, aggravation of the headache by neck moveas well as from cervical joint dysfunction may be ments, or history of cervical trauma. referred to the head. Bogduk’s diagnostic criteria included (Bogduk, et al., If the posttraumatic pain is suboccipital with lanci- 1985) identification by clinical examination or by imaging nating, electrical-like shooting pain attributes, secondaryof a cervical source of the pain that is found by valid to involvement of the occipital neurovascular bundle (theantecedent studies to be reliably associated with the head occipital nerve, artery, and vein), or secondary to pro-pain, or complete relief of the head pain that is seen after longed muscle spasm/contraction or excessive vascular controlled local anesthetic blockade of one or more cerdilatation impinging on the greater occipital nerve of vical nerves or structures innervated by cervical nerves.

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Sjaastad, Fredriksen, and Pfaffenrath (1990) also c. Dizziness weighed in with specifi c criteria. They noted that d. Blurred vision ipsilateral to the pain cervicogenic headaches were one sided, but could also be e. Difficulty with swallowing bilateral “unilaterally on two sides. ” The duration of a f. Fluid around the eye on the same side as headache or exacerbation ranged from several hours to the pain several weeks. Initially the headache may be episodic, but can later chronically fluctuate. Symptoms and signs were The anatomic basis of CGHA is thought to be secreferable to the neck, and included decreased range ondary of to convergence in the trigeminocervical nucleus cervical motion and mechanical precipitation of attacks,between nociceptive afferents from the field of the trigemwith autonomic symptoms such as nausea and photophoinal nerve and the receptive fields of the first three cervical bia not marked, if at all present. A positive response tonerves. Headache appears to be secondary to structural appropriate anesthetic blockade is considered essential.problems in regions innervated by C1 to C3. These regions Sjaastad, Fredriksen, and Pfaffenrath (1990) noted include the muscles, joints, and ligaments of the upper several major criteria: three cervical segments, as well as the dura mater of the 1. Symptoms and signs of cervical involvement a. Provocation of an irradiating head pain similar to the spontaneously occurring one i. By neck movement and/or sustained awkward head positioning ii. By external pressure over the upper neck or head on the side ipsilateral to the pain b. Restriction of cervical range of motion c. Ipsilateral neck, shoulder, or arm pain of a vague, nonradicular nature, or, on occasion, sharp arm pain in a radicular region (Symptoms and signs 1a to 1c are listed in “order of importance. ” One or more of these must be present for the term cervicogenic headache to be used. Point 1a is itselffi-suf cient criteria, but 1b and 1c are not. Point 2 is a necessary additional point.) 2. Confirmation by diagnostic anesthetic blocks — necessary point 3. Unilateral pain not shifting from side to side 4. Pain characteristics a. Nonthrobbing pain, usually beginning in the neck b. Episodes of varying duration c. Fluctuating, continuous pain 5. Other characteristics of some importance a. Marginal or no effect from treatment with indomethacin b. Marginal or no effect from treatment with triptans or ergots c. Female preponderance d. History of head or neck trauma (None of the single points under 4 or 5 are essential.) 6. Other descriptions of less importance (various headache-related phenomena that are rarely present, and of only mild to moderate severity when present) a. Nausea b. Photo- and phonophobia

spinal cord and the posterior cranial fossa and the vertebral artery (Bogduk, 1992). Other anatomic causation has been identifi ed and includes (Blume, 1997): 1. Disrupted and/or ruptured cervical disks with irritation of the sympathetic sinu-vertebral nerves (in the disk) and nerve roots by mechanical and chemical means at single or multiple levels 2. Irritation of the articular branches to the cervical zygapophyseal joints derived from the medial branches of the cervical dorsal rami 3. Irritation of the peripheral branches and unmyelinated nerve structures to the muscle attachments at the spinous process of C2 supplied by the C2 and C3 nerve roots, including the rectus capitis posterior, major obliquus capitis inferior major, semispinalis cervicis multifidus, semispinalis capitis major and rectus capitis posterior minor and interspinal, muscles at C1 to C2 and C2 to C3 4. Pain from the end fibers of the greater tertiary occipital and sympathetic nerve structures with its C fibers including the periosteum and suboccipital musculature (semispinalis capitis, rectus capitis posterior minor and major, trapezius, and occipitalis) The treatment of CGHA begins with diagnostic anesthetic blocks that are typically mixed with long-acting steroids such as hydrocortisone. This should temporarily relieve the CGHA for hours to days. If pain relief lasts for weeks to months, blocks should be repeated. Once a specific targeted joint or disk is identified, the latter with discography if needed, a number of procedures have been utilized for treatment of CGHA. These include 1. Neurolysis of the C2 nerve root via decompressive surgery (Poletti, 1983) as well as partial

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2.

3.

denervation of the suboccipital and paraspinal musculature (Pikus & Phillips, 1995) Radiofrequency lesions to the muscle attachments of the spinous process at C2 (Blume, Kakolewski, Richardson, & Rojas, 1982; Rogel, 1995) Radiofrequency neurotomy of the sinuvertebral nerves to the upper cervical disk, as well as to the outer layer of the C3 or C4 nerve root (Sluijter, 1990) Radiofrequency denaturation of the occipital nerve (Blume, 1976; Blume, Kakolewski, Richardson, & Rojas, 1981; Blume & Ungar-Sargon, 1986) Radiofrequency denaturation of the C2 medial rami (Rogal, 1986) Cervical discectomy and fusion C2 ganglionectomy (Jansen & Spoerri, 1985)

known. In the presence of an MTBI they become more difficult to tease out and deal with, because the patients may be dealing with pain as well as changes in cognition and behavior, including frontal lobe ficulties dif such as increased irritability and labile emotionality.

CONCLUSION

Other major problems facing patients and their treating physician(s) are the questions of medico-legal disabil4. ity secondary to the PTHA syndrome, with or without the question of MTBI. Patients whose injuries involved a skull fracture, subdural hematoma, or severe lacerations and whose gray matter is leaking out of their ears may not 5. have a problem in regard to disability. Unfortunately for patients and their physicians, insurance problems do exist, 6. beginning with getting approval to treat a PTHA syndrome. 7. Some insurance companies deny that there is such a thing as an MTBI, or PTHAs. They have a number of paid The latter procedure is not often performed, although there remain proponents of radiofrequency lesioning vs. theconsultants to assure the legal system that this is so. They try to prevent clinicians from even getting involved with “old” cervical discectomy and fusion. It is imperative to differentiate CGHA from both treating these patients by refusing to pay them for treatment.It does not matterhow devastating a patient’ s sympmigraine headache and PTTHA, because the treatments dif and totally unjusare completely different. Unfortunately, the literature in toms are; the patient still faces aficult tified legal battle just to get treatment approved, never general argues the question of cervicogenic headache, minding the question of disability compensation. although not the idea that headache may be associated with cervical pathology. It should be noted that the Inter- It is interesting that the vast majority of patients with national Association for the Study of Pain (IASP) hasPTHAs, particularly those with headaches as part of a postconcussion syndrome, present the same way. Maybe recognized cervicogenic headache as a pain syndrome (Zwart, 1997). This criteria uses neck mobility as thethey all spoke together on the Internet and planned it out. major indicator of this diagnosis, but both TTHA and They are for real and are expressing the same symptommigraine have associated decrements in cervical mobility.atology from the same causation (head trauma or accelThe different criteria for the diagnosis of CGHA make eration/deceleration injuries). This is just like patients with chicken pox who initially present, clinically, in the other previously recognized primary headache sufferers same way. fall into a diagnostic hole. There appears to be too much overlap in the varying diagnoses. Likewise, patients with Then there is the M word — malingering. This is the diagnosis of CGHA may also fall into other diagnosticassociated with the idea that settlement of litigation is all that is needed to put a stop to the PTHA syndrome. This categories, or even multiple diagnostic categories (Leone, 1998; Pfaffenrath & Kaube, 1990; Treleaven, Jull, & is also a favorite theme of the insurance companies. True malingering is almost as rare as hens’ teeth. There are Atkinson, 1994). published studies that demonstrate that legal settlement Not to be forgotten is the fact that the diagnosis spehas nothing to do with the patients’ symptoms ending or cifically may follow an acceleration/deceleration injury or encouraging them to return to work (Cicerone, 1992; other cervical trauma (Obelieniene, et al., 1998; TreElkind, 1989; Evans, 1992; Merskey & Woodford, 1972). leaven, Jull, & Atkinson, 1994). This makes it imperative CPTTHAs, with or without the other aspects of the to consider the diagnosis of CGHA in patients with PTHA who do not show improvement following appropriate post-concussion syndrome, are extremely common after head trauma and acceleration/deceleration injury. These treatment for other diagnosed headache diatheses. On the other hand, clinically, CGHA appears to be found in lesspatients are very consistent in their presentations in their than 3 to 5% of the PTTHA population. If a PTHA patient descriptions of their symptoms and sequelae. This consisalso has an MTBI, the level of dif ficulty in making the tency is strong evidence that their problems are organic diagnosis and treating that patient increases dramatically.in nature and produced by the trauma. Psychological factors are there — the neurochemical Most patients with PTHAs have their headaches aspects of depression and anxiety, for instance, are well resolve if they are given appropriate medical treatment.

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About 15 to 20% have prolongedficulties. dif Correct diag- Cicerone, K.D. (1992). Psychological management of post-concussive disorders.Physical Medicine and Rehabilitanosis and treatment in the majority of cases should tion: State of the Art Review,, 129–141. 6 decrease this percentage. Cohen, M.J. (1978). Psychological studies of headache: Is there a similarity between migraine and muscle contraction headaches? Headache, 18 , 189. REFERENCES Covelli, V., & Ferrannini, E. (1987). Neurophysiologic findings in headache patients. Psychogalvanic reflex investigaAlmay, B.G.L., Johansson, F., von Knorring, L., et al. (1988). tion in migraineurs and tension headache patients. Acta Substance P in CSF of patients with chronic pain synNeurologica, 9 , 354. dromes.Pain, 33, 3. Andersen, E., & Dafny, N. (1983). An ascending serotonergicCoward, D.M., Davies, J., Herrling, P., & Rudeberg, C. (1984). Pharmacological properties of tizanidine (DS 103-282) pain modulation pathway from the dorsal raphe nucleus (pp. 61–71). New York: Springer-Verlag. to the parafascicularis nucleus of the thalamus. Brain D'Andrea, G., Toledo, M., Cortelazzo, S., & Milone, F. F. (1982). Research, 269 , 57. Platelet activity in migraine.Headache, 22 , 207. Anderson, C.D., & Franks, R.D. (1981). Migraine and tension Davies, J., Johnson, S.E., & Lovering, R. (1983). Inhibition by headache: Is there a physiological difference? Head3H)aspartate release from spinal cord DS 103-282 of D-( ache, 21, 63. slices. British Journal of Pharmacology, 78 , 2P. Bakal, D.A., & Kaganov, J.A. (1977). Muscle contraction and Denny-Brown, D., & Russell, W. R. (1941). Experimental ceremigraine headache: Psychophysiologic comparison. bral concussion. Brain, 64 , 93. Headache, 17 , 208. Diamond, S., & Dalessio, D.J. (1980). The practicing physician’s Baloh, R.W. (1997). Neurotology of migraine. Headache, 37 , approach to headache (3rd ed.). Baltimore: Williams & 615–621. Wilkins. Basbaum, A.I., & Fields, H.L. (1984). Endogenous pain control systems: Brainstem spinal pathways and endorphin cir-Dorpat, T.L., & Holmes, T.H. (1955). Mechanisms of skeletal muscle pain and fatigue. Archives of Neurologic Psychicuitry. Annual Review of Neuroscience, , 309. 7 atry, 74 , 628. Blume, H.G. (1976). Radiofrequency denaturation in occipital pain: A new approach in 114 cases. Advanced Brain Drake, M.E., Pakalnis, A., Andrews, J.M., & Bogner, J.F. (1990). Nocturnal sleep recording with cassette EEG in chronic Research Therapy,, 1691–698. headaches.Headache, 30 , 600. Blume, H.G. (1997). Diagnosis and treatment modalities of cerDrummond, P.D. (1986). A quantitative assessment of photophovicogenic headaches. Head and Neck Pain, Newsletter bia in migraine and tension headache. Headache, 26, of the Cervicogenic Headache International Study 465. Group, 4, 1–2. Blume, H.G., Kakolewski, J.W., Richardson, R.R., & Rojas, Drummond, P.D. (1987). Scalp tenderness and sensitivity to pain in migraine and tension headache. Headache, 27 , 45. C.H. (1981). Selective percutaneous radiofrequency thermodenervation of pain fibers in the treatment ofDuckro, P.N., Greenberg, M., Schultz, K.T., et al. (1992). Clinical features of chronic post-traumatic headache. Headoccipital neuralgia: Results in 450 cases. Journal of ache Quarterly, ,3 295–308. Neurologic Orthopedic Surgery,, 2261–268. Blume, H.G., Kakolewski, J.W., Richardson, R.R., & Rojas, Dwyer, A., Aprill, C., & Bogduk, N. (1990). Cervical zygapophyseal joint pain patterns. I: A study in normal volunC.H. (1982). Radiofrequency denaturation in occipital teers.Spine, 15, 453–457. pain: results in 450 cases. Applied Neurophysiology, 45 , 543–548. Elkind, A.H. (1989). Headache and facial pain associated with head injury.Otolaryngology Clinics of North America , Blume, H.G., & Ungar-Sargon, J. (1986). Neurosurgical treat22, 1251–1271. ment of persistent occipital myalgia-neuralgia syndrome. Journal of Craniomandibular Practice, , 4 Ellertsen, B., Norby, H., & Sjaastad, O. (1987). Psychophysio65–73. logical response patterns in tension headache: Effects of tricyclic antidepressants. Cephalalgia, 7, 55. Bogduk, N., Corrigan, B., Kelly, R., et al. (1985). Cervical headache.Medical Journal of Australia, 143 , 202–207. Evans, R.W. (1992). The postconcussion syndrome and the sequelae of mild head injury. Neurology Clinic, 10 , Bogduk, N. (1992). The anatomical basis for cervicogenic head815–847. ache.Journal of Manipulative Physiology and Therapy, 15, 67–70. Facchinetti, F., & Genazzani, A.R. (1988). Opiods in cerebrospinalfluid and blood of headache sufferers. In J. Olesen Borgeat, F., Hade, B., Elie, R., & Larouche, L.M. (1984). Effects & L. Edvinsson (Eds.),Basic mechanisms of headache. of voluntary muscle tension increases in tension head(p. 261). Amsterdam: Elsevier Science. ache.Headache, 24 , 199. Buchholz, D.W., & Reich, S.G. (1996). The menagerie of Fields, H.L. (1988). Sources of variability in the sensation of pain. Pain, 33, 195. migraine.Seminars in Neurology, 16 , 83–93. Forsell, H. (1985). Mandibular dysfunction and headache. ProCailliet, R. (1993).Pain: Mechanisms and management (p. 83). Philadelphia: F. A. Davis. ceedings of the Finnish Dental Sociey,(Suppl. 81 2), 591.

122

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Fricton, J.R., Kroening, R., Haley, D., & Siegart, R. (1985). Jay, G.W. (1995). Chronic daily headache and myofascial pain syndromes: Pathophysiology and treatment. In R.K. Myofascial pain syndrome of the head and neck: A Cady & A.W. Fox (Eds.),Treating the headache patient review of clinical characteristics of 164 patients. Oral (pp. 211–233). New York, Marcel Dekker. Surgery, 60 , 615. Pain Fricton, J.R. (1990). Myofascial pain syndrome. In J. R. FrictonJay, G.W. (1995). Sympathetic aspects of myofascial pain. Digest, 5, 192–194. & E. Awad (Eds.),Advances in pain research and therapy (Vol. 17, p. 107). New York: Raven Press. Jay, G.W. (1999).The headache handbook: Diagnosis and treatment. Boca Raton, FL: CRC Press. Genazzani, A.R., Nappi, G., Gacchinetti, F., et al. (1984). Progressive impairment of CSF B-EP levels in migraine Jay, G.W. (2000).Minor traumatic brain injury handbook: Diagsufferers.Pain, 18, 127. nosis and treatment . Boca Raton, FL: CRC Press. Giacovazzo, M., Bernoni, R.M., Di Sabato, F., & Martelletti, P. Kay, T., Harrington, D.E., et al. (1993). Definition of mild trau(1990). Impairment of 5HT binding to lymphocytes and matic brain injury.Journal of Head Trauma Rehabilitamonocytes from tension-type headache patients. Headtion, 8(3), 86. ache, 30, 20. Keidel, M., & Diener, H.C. (1997). Post-traumatic headache. Goldenberg, D.L. (1989). Diagnostic and therapeutic challenges Nervenarzt, 68 , 769–777. of fibromyalgia.Hospital Practice, 9 , 39. Koch, P., Hirst, D.R., & von Wartburg, B.R. (1989). Biological Goldenberg, D.L. (1990). Fibromyalgia and chronic fatigue synfate of sirdalud in animals and man. Xenobiotica, 19 , drome: Are they the same? Journal of Musculoskeletal 1255–1265. Medicine, 7, 19. Kojadinovic, Z., Momcilovic, A., Popovic, L., et al. (1998). Hanington, E., Jones, R.J., Amess, J.A.L., & Wachowicz, B. Brain concussion—A minor craniocerebral injury. Med. (1981). Migraine: A platelet disorder. Lancet, ii, 720. Pregl., 51, 165–168. Harker, L.A., & Rassekh, C. (1988). Migraine equivalent as aKowa, H., Shimomura, T., & Takahashi, K. (1992). Platelet cause of episodic vertigo. Laryngoscope, 98 , 160–164. gamma-amino butyric acid levels in migraine and tension-type headache. Headache, 32 , 229. Harrison, D.W., & Walls, R.M. (1990). Blindness following minor head trauma in children: A report of two casesKudrow, L. (1986). Muscle contraction headaches. In F.C. Rose (Ed.), Handbook of clinical neurology (Vol. 48, pp. 343). with a review of the literature.Journal of Emergency Amsterdam: Elsevier Science. Medicine, 8, 21–24. Langemark, M., & Jensen, K. (1988). Myofascial mechanisms Haynes, S.N., Cuevas, J., & Gannon, L.R. (1982). The psychoof pain. In J. Olesen & L. Edvinsson (Eds.), Basic mechphysiological etiology of muscle-contraction headache. anisms of headache (p. 321). Amsterdam: Elsevier SciHeadache, 22 , 122. ence. Haynes, S.N. (1981). Muscle contraction headache — Psychophysiological perspective. In S.N. Haynes & L.R. Gan- Langemark. M., Jensen, K., Jensen, T.S., & Olesen, J. (1989). Pressure pain thresholds and thermal nociceptive threshnon (Eds.), Psychosomatic disorders: A psychoolds in chronic tension-type headache. Pain, 38, 203 physiologyical approach to etiology and treatment . New York, Praeger Press. Langemark, M., & Olesen, J. (1987). Pericranial tenderness in tension headache. A blind controlled study. Cephalalgia, Headache Classification Committee of the International Head7, 249. ache Society. (1988). Classification and diagnostic criteria for headache disorders, cranial neuralgias andLangemark, M., Olesen, J., Poulsen, D.P., & Bech, P. (1988). facial pain.Cephalalgia, 8(7). Clinical characterization of patients with chronic tension headache.Headache, 28 , 590. Hong, S., Kniffki, K., & Schmidt, R. (1978). Pain abstracts. Second World Congress on Pain, , 58. 1 Leisman, G. (1990). Lateralized effects of migraine and ANS seizures after closed head injury. International Journal Iansek, R., Heywood, J., Karnaghan, J., & Nalla, J.I. (1987). of Neuroscience, 54 , 63–82. Cervical spondylosis and headaches. Clinical Experimental Neurology, 23e , 175. Leone, M., D’Amico, D., Grazzi, L., et al. (1998). Cervicogenic headache: A critical review of the current diagnostic Jansen, J., & Spoerri, O. (1985). Atypical retro-orbital pain and criteria. Pain, 78, 1–5. headache due to compression of upper cervical roots. In V. Pfaffenrath, P.O. Lundberg, & O. Sjaastad (Eds.),Magnusson, T., & Carlsson, G.E. (1978a). Comparison between Updating in headache(pp. 14–16). Berlin: Springertwo groups of patients in respect to headache and manVerlag, 1985. dibular dysfunction.Swedish Dental Journal,, 285. Jay, G.W., Brunson, J., & Branson, S. J. (1989). The effectiveness Magnusson, T., & Carlsson, G.E. (1978b). Recurrent headaches of physical therapy in the treatment of chronic daily in relation to temporomandibular joint pain-dysfunction. headaches.Headache, 29 , 156. Acta Odontologia Scandinavia, ,36 333. Jay, G.W., Grove, R.N., & Grove, K.S. (1987). Differentiation Malow, R.M., Grimm, L., & Olsen, R.E. (1980). Differences in pain perception between myofascial pain dysfunction of chronic headache from non-headache pain patients and normal subjects: A signal detection analysis. Jourusing the Millon Clinical Multiaxial Inventory (MCMI). nal of Psychosomatic Research,, 24 303. Headache, 27 , 124. Martin, M.J., & Rome, H.P. (1967). Muscle contraction headJay, G.W. (1996). The autonomic nervous system: Anatomy and ache: Therapeutic aspects. Research in Clinical Studies pharmacology. In P. Raj (Ed.), Pain medicine — A comof Headache , 1, 205. prehensive review(pp. 461–465). St. Louis: Mosby.

Posttraumatic Headache: Pathophysiology, Diagnosis, and Treatment

123

Martin, P.R., & Mathews, A.M. (1978). Tension headaches: Psy-Pikus, H., & Phillips, J. (1995). Characteristics of patients successfully treated for cervicogenic headache by surgical chophysiological investigation and treatment. Journal of decompression of the second cervical nerve root. HeadPsychosomatic Research, 22, 389. ache, 35,621–629. Mathew, N.T., Glaze, D., & Frost, J. (1985). Sleep apnea and other sleep abnormalities in primary headache disorders. Poletti, C.E. (1983). Proposed operation for occipital neuralgia: In C. Rose (Ed.),Migraine. Proceedings of the 5th InterC2 and C3 root decompression. Neurosurgery, 12, national Migraine Symposium, 1984 (p. 40). London: 221–224. Basel, Karger. Pozniak-Patewicz, E. (1976). Cephalgic spasm of head and neck Merskey, H., & Woodford, J.M. (1972). Psychiatric sequelae muscles.Headache, 15,261. after minor head injury.Brain, 95, 521–528. Raskin, N.H. (1988a). Headache(2nd ed.). New York: Churchill Mikail, M., & Rosen, H. (1980). History and etiology of myoLivingstone. fascial pain-dysfunction syndrome. Journal of ProsRaskin, N.H. (1988b). On the origin of head pain. Headache, thetic Dentistry, 44,438. 28, 254. Mikamo, K., Takeshima, T., & Takahashi, K. (1989). CardiovasRiley, T.L. (1983). Muscle-contraction headache. Neurology cular sympathetic hypofunction in muscle contraction Clinic, 1, 489. headache and migraine. Headache, 29,86. Moldofsky, H., Scariabrick, P., England, R., et. al. (1975). Mus-Robinson, C.A. (1980). Cervical spondylosis and muscle contraction headaches. In D.J. Dalessio (Ed.), Wolff’s headculoskeletal symptoms and non-REM sleep disturbances ache and other head pain (4th ed., p. 362). New York: in patients with fibrositis syndrome and healthy subjects. Oxford University Press. Psychosomatic Medicine, 37, 341. Mosnaim, A.D., Diamond, S., Wolf, M.E., et al. (1989). Endog- Rodbard, S. (1970). Pain associated with muscle contraction. Headache, 10,105. enous opiod-like peptides in headache: An overview. Rogal, O.J. (1986). Successful treatment for head, facial and Headache, 29,368. neck pain.The TMJ Dental Trauma Center, 3–10. 1, Muller, G.E. (1974). Atypical early posttraumatic syndromes. Rogal, O.J. (1995, September). Rhizotomy procedures about the Acta Neurologica Belgica, 74, 163–181. face and neck for headaches . Paper presented at the Murphy, A.I., & Lehrer, P.M. (1990). Headache versus nonheadNorth American Cervicogenic Headache Conference, ache state: A study of electrophysiological and affective Toronto. changes during muscle contraction headache. Behavioral Medicine, 16,23. Rolf, L.H., Wiele, G., & Brune, G.G. (1981). 5-HydroxyNappi, G., Gacchinetti, G., Legnante, G., et al. (1982). Impairtryptamine in platelets of patients with muscle contracment of the central and peripheral opiod system in headtion headache.Headache, 21,10. ache. Paper presented at the Fourth InternationalRosenhall, U., Johansson, G., & Orndahl, G. (1987). Eye motility Migraine Trust Symposium, London. dysfunction in patients with chronic muscular pain and Obelieniene, D., Bovim, G., Schrader, H., et al. (1998). Headdysesthesia.Scandanavian Journal of Rehabilitative ache after whiplash: A historical cohort study outside Medicine, 19,139. the medico-legal context. Cephalalgia, 18,559–564. Sakas, D.E., Whittaker, K.W., Whitwell, H.L., & Singounas, Olesen, J. (1978). Some clinical features of the acute migraine E.G. (1997). Syndromes of posttraumatic neurological attack. An analysis of 750 patients. Headache, 18,268. deterioration in children with no focal lesions revealed Olesen, J. (1988). Clinical characterization of tension headache. by cerebral imaging: evidence of a trigeminovascular In J. Olesen & L. Edvinsson (Eds.), Basic mechanisms pathophysiology.Neurosurgery, 41,661–667. of headache(p. 9). Amsterdam: Elsevier Science. Sakuta, M. (1990). Significance of flexed posture and neck instaPackard, R.C., & Ham, L.P. (1997). Pathogenesis of posttraubility as a cause of chronic muscle contraction headache. matic headaches and migraine: A common headache Rinsho Shinkeigato, 30, 254. pathway?Headache, 37,142–152. Sayers, A.C., Burki, H.R., & Eichenberger, E. (1980). The pharPalmeri, A., & Wiesendanger, M. (1990). Concomitant depresmacology of 5-chloro-4-(2-imidazolin-2-gamma-1sion of locus coeruleus neurons and of flexor reflexes amino)-2,1,3-benzothiadiazole (DS 103 282), a novel by an alpha 2-adrenergic agonist in rats: A possible mechmyotonic agent.Arzneimittelforschung, 30, 793–803. anism for an alpha Neuro2-mediated muscle relaxation. Schmidtke, K., & Ehmsen, L. (1998). Transient global amnesia science, 34,177–187. and migraine. A case control study. European NeurolPerl, S., Markle, P., & Katz, L. N. (1934). Factors involved in ogy, 40, 9 –14. the production of skeletal muscle pain. Archives of Shahota, P.K., & Dexter, J.D.S. (1990). Sleep and headache Internal Medicine, 53,814. syndromes: A clinical review. Headache, 30,80. Pernow, B. (1983). SubstancePharmacology P. Review, 35, 85. Pfaffenrath, V., & Kaube, H. (1990). Diagnostics of cervicogenicShimomura, T., & Takahashi, K. (1986). Pupillary functional asymmetry in patients with muscle contraction headheadache.Functional Neurology, 5,159–164. ache.Cephalalgia, 6,141. Philips, C. (1978). Tension headache: Theoretical problems. Shimomura, T., & Takahashi, K. (1990). Alteration of platelet Behavior Research Therapy, 16, 249. serotonin in patients with chronic tension-type headache Philips, C., & Hunter, M.S. (1982). A psychophysiological invesduring cold pressor test. Headache, 30,581. tigation of tension headache. Headache, 22,173.

124

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Tfelt-Hansen, P., Lous, I., & Olesen, J. (1981). Prevalence and Shoenen, J., Pasqua, V.D., & Sianard-Gainko, J. (1991). Multiple significance of muscle tenderness during common clinical and paraclinical analyses of chronic tensionmigraine attack.Headache, 21,49. type headache associated or unassociated with disorder Travell, J., & Rinzler, S.H. (1952). The myofascial genesis of of the pericranial muscles. Cephalalgia, 11,135. pain. Postgraduate Medicine, 11, 425–434. Sicuteri, F. (1982). Natural opiods in migraine. In M. Critchley, Myofascial pain and dysA.P. Friedman, & S. Gorini, et al. (Eds.), Advances in Travell, J.G., & Simons, D.G. (1983). function: The trigger point manual . Baltimore: Williams neurology(Vol. 33, p. 65). New York: Raven Press. & Wilkins. Sicuteri, F., Nicolodi, M., & Fusco, B.M. (1988). Abnormal sensitivity to neurotransmitter agonists, antagonists andTreleaven, J., Jull, G., & Atkinson, L. (1994). Cervical musculoskeletal dysfunction in post-concussional headache. neurotransmitter releasers. In J. Olesen & L. Edvinsson Cephalalgia, 14,273–279. (Eds.),Basic mechanisms of headache (p. 275). AmsterTunis, M.M., & Wolff, H.G. (1954). Studies on headache: Cradam: Elsevier Science. nial artery vasoconstriction and muscle contraction Sicuteri, F., Spillantini, M.G., & Fanciullacci, M. (1985). headache.Archives of Neurologic Psychiatry, 71, 425. “Enkephalinase” in migraine and opiate addiction. In C. Rose (Ed.),Migraine: Proceedings of the Fifth Interna- Vijayan, N. (1977). A new post-traumatic headache syndrome. Headache, 17,19–22. tional Migraine Symposium(p. 86). London: Basel, Vohanka, S., & Zouhar, A. (1988). Transient global amnesia after Karger. mild head injury in childhood.Act. Nerv. Super. Simons, D.J., Day, E., Goodell, H., & Wolff, H.G. (1943). Exper(Praha.), 30,68–74. imental studies on headache: Muscles of the scalp and neck as sources of pain. Associated Research on Ner- Vohanka, S., & Zouhar, A. (1990). Benign posttraumatic encephalopathy.Act. Nerv. Super. (Praha.), 32, 179–183. vous and Mental Disorders Proceedings , 23, 228. Sjaastad, O., Bovim, G., & Stovner, L.J. (1992). Laterality of Wagstaff, A.J., & Bryson, H. (1997). Tizanidine: A review of its pharmacology, clinical ef ficacy and tolerability in the pain and other migraine criteria in common migraine. management of spasticity associated with cerebral and A comparison with cervicogenic headache. Functional spinal disorders.Drugs, 53, 435–452. Neurology, 7,289–294. Sjaastad, O., Fredriksen, T.A., & Pfaffenrath, V. (1990). Cervi-Wall, P.D. (1988). Stability and instability of central pain mechanisms. In R. Dubner & M. R. Bond (Eds.), Proceedings cogenic headache diagnostic criterion. Headache, 30, of the Fifth World Conference on Pain (p. 13). Amster725–26. dam: Elsevier Science. Sluijter, M.E. (1990).Radiofrequency lesions in the treatment of cervical pain syndromes . Procedure Technique Series World Health Organization (1997). ICD-10 Guide for Headaches.Cephalalgia, 17 (S19). (pp. 2–19). Holland: Radionics. Yang, J.C., Richlin, D., Brand, L., Wagner, J., & Clark, W.C. Speed, W.G. (1983). Muscle contraction headaches. In J. R. (1985). Thermal sensory decision theory indices and Saper (Ed.),Headache disorders (p. 115). Boston: John pain threshold in chronic pain patients and healthy volWright. unteers.Psychologic Medicine, 47, 461. Takeshima, T., Takao, Y., & Takahashi, K. (1987). Pupillary sympathetic hypofunction and asymmetry in muscleZwart, J.A. (1997). Neck mobility in different headache disorders.Headache, 37,6–11. contraction headache. Cephalalgia, 7,257. Takeshima, T., Takao, Y.U., Urakami, K., et al. (1989). Muscle contraction headache and migraine. Platelet activation and plasma norepinephrine during the cold pressor test. Cephalalgia, 9,7.

12 Posttraumatic Headache: Practical Interdisciplinary Approaches to Diagnosis and Treatment Nathan D. Zasler, M.D., F.A.A.P.M.&R., F..A.A.D.E.P., C.I.M.E., D.A.A.P.M. and Michael F. Martelli, Ph.D., D.A.A.P.M. INTRODUCTION

PTHA. We hope that this chapter provides some edification on the need to assess these patients in a more global The literature on posttraumatic headache (PTHA) appears manner instead of using what seems to be the traditional to be replete with much confusion concerning nomencla-Ockham’s razor approach. Significant deficiencies in our ture. Oftentimes, clinicians incorrectly assume thatunderstanding of PTHA clearly remain which can be seen because someone has complaints of PTHA, they have in the lack of good epidemiological, treatment, and outsustained some type of insult to their brain. Individualscomes research. These limitations must be acknowledged may develop PTHA and related disability due to a varietyin the context of clinical care (Zasler, 1999). of causes including brain injury, cranial or cranial adnexal injury, and/or cervical acceleration/deceleration injury CLASSIFICATION OF POSTTRAUMATIC (Zasler, 1999). Some individuals consider the diagnosis of PTHA toHEADACHE be a so-called “garbage can” diagnosis. The phrase cation systems for PTHA have much to be PTHA does not tell patients, family, or other health careCurrent classifi practitioners what they did not already know, that is, thatdesired given their general nature, as well as the empirical basis for the defi nitional criteria. If one examines the Headthey were involved in a trauma and subsequently have cation Committee of the International Headsuffered from a headache condition. More importantly,ache Classifi s (IHS) (1988) classifi cation for PTHA or the many practitioners believe that it is important to specif-ache Society’ cation of Diseases and Related Health ically identify the pain generators in the context of pro-International Classifi viding diagnostic labels that may better guide clinicalProblems, 10th edition (ICD-10) (World Health Organization, 1997) system, it is readily apparent that there are at treatment (Zasler, 1996). Appenzeller (1993) has been noted to have said, “Noleast some problems with the current taxonomy for PTHA. Refer to Table 12.1 for a conversion chart between ICDwhere is scientific medicine less evident than in the treat10 and IHS classifi cation systems for PTHA. ment and management of post-traumatic headaches.” As The ICD-10 classification system uses criteria that are practitioners in the field of brain injury care, we could not primarily concerned with the temporal onset and pathoagree more. There is much confusion in the field across genetic relationship of the headache to the trauma and not both medical and nonmedical disciplines as to the exact nature of the beast with regard to the diagnostic entity ofwith the clinical features of the headache condition. ICD0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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TABLE 12.1 Conversion Table: IHS and ICD-10 Classification Codes ICD-10 Code IHS Code 5. 5.1

5.2

Headache associated with head trauma Acute posttraumatic headache 5.1.1 With significant head trauma and/or confirmatory signs 5.1.2 With minor head trauma and no confirmatory signs Chronic post-traumatic headache 5.2.1 With significant head trauma and/or confirmatory signs 5.2.2 With minor head trauma and no confirmatory signs

Etiologic Code

Headache Code

S06 S09.9

G44.88 G44.880 G44.880 G44.880 G44.3 G44.30

S06 S09.9

10 criteria for PTHA require that headache onset occurthe system have been incorporated into the ICD-10. The within 2 weeks of the traumatic event or regaining con-IHS criteria use both clinical features and laboratory sciousness. This temporal onset criterion appears to have testing to provide inclusion criteria. As with ICD-10, been determined only on the basis of empiricism. Clearly,headache associated with head “ trauma”is divided into although it tends to be the exception instead of the rule, acute and chronic PTHA. A second edition of the IHS there are patients who develop headache that is fully Classification was published in 1999. There is fairly good apportionable to their original injury beyond the 2-weekcorrespondence between the ICD-10 and IHS headache rule. Another problem with the time designation of 2 classification systems. weeks is that often patients may have significant multitrauma with other more painful conditions (e.g., neckEPIDEMIOLOGY AND OUTCOME injury) than their headache, causing them to focus their attention on the more painful body part. Additionally, PTHA is clearly the most common symptom following some may also argue that in more severe brain injury, mild brain injury and/or concussion, as well as cervical patients’cognitive status may limit their ability to identify whiplash (acceleration/deceleration type injuries). and/or appreciate head pain. Because of the lack of accurate registries and the fact that Also of concern is the fact that the ICD-10 criteria for many persons with these types of injuries are never seen either acute or chronic PTHA require one of the following:in acute care settings, the true incidence of this disorder a loss of consciousness, a period of antegrade amnesiainofour society at large is unknown. at least 10 min, or abnormal neurodiagnostic/neurological Surveys examining the number of individuals who exam. Certainly, such inclusion criteria exclude patientsdevelop PTHA as a result of minor head injury range with various forms of PTHA including referred pain from anywhere from 30 to 50% (Evans, 1992; Alves et al., cervical injury, as well as direct cranial and/or cranial1986). Additionally, there seems to be a clear, albeit to adnexal injury, among other “posttraumatic” etiologies.some extent controversial, correlation between severity of Although there are classifications for other types of head-brain injury and incidence of PTHA. The majority of ache that may be applicable to these patients, they would studies, as well as extensive clinical experience by pronot by definition fall under the rubric of PTHA by ICD- fessionals who have seen thousands of persons with cere10 criteria. Of some import is the fact that a separatebral, cranial, and cervical injuries, support the conclusion codification identifies patients with “minor head traumathat persons with milder injury seem to have a higher and no confirmatory signs” under this classification. Acutefrequency of headache complaints. To most, this would PTHA by ICD-10 definition resolves within 8 weeks with seem paradoxical based on the anticipated pathoetiology chronic PTHA being defined temporally as any PTHA of PTHA. One of the classic studies examining this phelasting longer than 8 weeks (HCCIHS, 1988); this defini-nomenon was performed by Yamaguchi (1972) and pubtion is not consistent with common parlance of howlished in 1992. He found that 72% of persons with mild chronic pain is typically defined (Zasler, 1999). injury vs. 33% of those with severe injury developed headThe IHS criteria were published (HCCIHS, 1988) to ache. He noted that abnormal findings on cervical radioaddress the lack of operational rules and nonuniformitygraphs including degenerative changes positively correlated with complaints of more severe headache. Just as of nomenclature in the headache eld. fi The classifi cation system defi nes 13 major categories of headache with twointerestingly, he noted that abnormalities on mental status testing and static brain imaging were negatively correlated broad categories (primary vs. secondary headaches). The IHS classification system has been endorsed by thewith headache complaints and incidence (Yamaguchi, World Health Organization (WHO) and the principles of 1992). In a rather extensive review conducted by Appen-

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zeller (1993), he concluded that PTHA incidence wasPTHA and have a greater risk for chronic PTHA much higher in patients with less severe brain injury. (CPTHA). However, a study by Jensen and Nielsen The whole issue of correlating brain injury severity (1990) found that patients suffering from headache prewere no more likely to suffer PTHA than patients with extent of subsequent headache complaints seems, injury in without a preinjury headache history. our view, to be “missing the boat, ” given that there is a There is excellent literature with regard to cervical significant absence of literature exploring the incidence spine acceleration/deceleration injury and chronic pain, and severity of associated injury to the cranium and/or although not necessarily involving headache, that must be cervical spine in PTHA. Both the neck and head may be appreciated by any clinician involved with PTHA manthe source of pain generators in PTHA, either directly or agement (Freeman & Croft, 1997; Radanov et al., 1993). indirectly as a result of referred pain. At the same time, If one agrees with the experiential data and some research however, one would expect worse cranial and cervical data indicating that cervicogenic referred pain is the priinjuries in patients with more severe brain injury, given mary etiology of PTHA, then it is not surprising to note the magnitude of forces applied to the neural axis and therefore the skull and cervical spine. Thus, one wouldthat the observed higher incidence of PTHA in women of men (Jensen & Nielsen, 1990) may in fact have expect more, not less, headache in patients subjected instead to a pathoanatomic basis. Research has shown greater accelmore significant forces across the neural and musculoerative forces in whiplash injuries in women than in men, skeletal axes. deemed to be due to differences in cervical muscle bulk Theoretically, the previously mentioned paradox may and/or neck length (Siegmund, King, Lawrence, Wheeler, be explainable by speculating that patients with severe Brault, & Smith, 1997). brain injury and/or multitrauma are commonly treated with paralytic agents, as well as prolonged bed rest, as part of their acute neurosurgical care. If one accepts that PATHOETIOLOGY cervicogenic headache is the most frequent etiologic explanation for PTHA, although this remains controver-The exact pathoetiology of nontraumatic headache consial, one might also conclude that typically rendered treat-tinues to be debated. The pain generators and pathoetiolment via muscle paralysis or prolonged immobilizationogy of PTHA are even less well understood. When one may coincidentally be therapeutic for concomitant cervi-considers the anatomic correlates of recurring benign head cal musculoligamentous injury sustained by patients withpain, one can make some general statements that are likely more severe brain injury. In fact, this explanation, to ajust as applicable for nontraumatic headache as they are great extent, supports the position that majority the of for traumatic headache (Packard, 1992). PTHA may have nothing to do with brain injury per se. There are multiple pain-sensitive structures in the Most studies have been unable to delineate the specific head, both intra- and extracranially, that may be pain gendemographic factors related to the incidence of PTHA.erators. There are also pain generators more caudally in The preponderance of data indicate that most individuals the neck that may refer pain into the head, either by direct who sustain this type of posttraumatic impairment areor by indirect means. Pain, in general, is transmitted from injured in the context of motor vehicle accidents and mostthe periphery by small myelinated fibers and unmyelinated of these individuals are male. In order of frequency, otherC fibers that terminate in the dorsal horn of the spinal types of injuries that are associated with head trauma and cord. Thesefibers also have end terminals in the trigeminal brain injury include falls, assaults, and sports-related inju-nucleus caudalis. Secondary neurons from the dorsal horn ries. A rather high incidence of concurrent use of alcoholreach the thalamus by the spinothalamic pathways. The has been noted in a number of studies examining comorupper cervical spine contains pain fiber systems for the bidities of these types of injuries (Packard, 1999). entire head/neck region. The trigeminal cervical nucleus There has been very little methodologically soundis the anatomic structure critical to the concept of cervical research looking at preexisting and/or injury-related fac-headache, as well as head/neck referred pain. Sensory tors that may predispose to perpetuation of headache afferents from the trigeminal nerve, as well as the upper symptomatology following concussion. Aside from somethree cervical spinal nerves, have been theorized to relay literature examining the role of ongoing litigation as asensory information through the trigeminal cervical factor in subjective headache complaints, there is nonucleus (May & Goadsby, 1999). Bogduk (1982) has prosignificant body of literature looking at musculoskeletal posed that there are overlapping and convergent second(including posture), neurological, and/or individual/fam- order neurons that serve as the pathoetiologic basis, as ily history issues plus their potential role in postconcus-well as pathoanatomic basis, for referred pain. Cervical sive headache symptom maintenance. A prime example pain can, therefore, be perceived in the territory of the of a prognostic factor associated with PTHA that istrigeminal nerve, particularly in the ophthalmic division accepted asgospel” “ by many physicians is that persons due to epaptic transmission through the proximal portion with preinjury headache are more prone to developof the C-2 root. This second-order neuron phenomenon is

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also the basis for frequent observation of referred orbitalhe or she could not develop a different type of headache and frontal pain emanating from cervical pain generators.or a worsening of the preinjury condition following The exact role that central modulation of trigemi- trauma. The major questions relative to the headache pronovascular pain plays in headache, in general, and postfile that need to be asked are expressed in the pneumonic traumatic headache, specifically, is yet to be determined, COLDER: character, onset, location, duration, exacerbaas is the role of so-called central sensitization. This lattertion, and relief. Additional questions concerning the frephenomenon, which is a well-described event in the ani-quency and severity of headache, time of day of headache, mal literature, remains somewhat controversial in the con-and associated symptomatology (including aura, pain text of various neurological and psychiatric disorders inreferral patterns, and familial headache history) should be the human population. It is manifested by increased sponinquired about, among multiple other possibilities. Less taneous impulse discharges, increased responsivenesscommon to causes of PTHA should always be considered noxious and nonnoxious peripheral stimuli, and expanded when the obvious ones do not pan out based on the history receptive fi elds of nociceptive neurons. So-called provided by the examinee. Some of the less commonly “windup” is a short-lasting phenomenon and thereforeseen variants of PTHA include posttraumatic sinus probcannot explain central sensitization that is of longer dura-lems, posttraumatic epilepsy, tension pneumocephalus, tion and may involve changes in neuronal plasticity.extraaxial collections such as subdurals and epidurals, Windup may, however, be the trigger to longer lastingcluster headache, paroxysmal hemicrania, dysautonomic neuronal sensitization and therefore potentially to chronicor sympathetic headache (anterior and posterior forms), headache pain, posttraumatic or otherwise (Sessle, 1999). and basilar artery migraine (BAM). Drug use history, In the context of assessment of a patient with PTHA,whether prescription or recreational, should also be one must assess pain generators from the face, cranium assessed including the potential for drug-induced and/or (including cranial adnexal structures), cerebrum, andrebound headache, the latter which is commonly iatroneck. There are multiple structures in the neck that have genic. With the appropriate history and descriptive clues, been hypothesized to produce head pain, including zygathe clinician is then armed to conduct a clinical examinapophyseal joints of the second and third vertebra, mustion to allow a more specific conclusion as to the origin culoligamentous attachments of the atlantoaxial joints,of the headache condition (Zafonte & Horn, 1999). and upper paravertebral muscles, as well as the muscles The physical examination of the patient who presents innervated by the eleventh cranial nerve (e.g., trapezius with PTHA should be comprehensive but focused based and sternocleidomastoid), the spinal dura mater (see on a good clinical history. At a minimum, the exam should later), the vertebral artery, and the C2– C3 intervertebral include a screening neurological and musculoskeletal disks (Horn, 1992). There has been some manual mediassessment. The basics of physical examination should be cine literature suggesting that attachments of the liga-conducted with a focus to the suspected pain generators. mentum nuchae exist to the posterior cervical spinal dura The exam should include inspection, palpation, and, as and the lateral part of the occipital bone (Mitchell, Hum-appropriate, percussion and auscultation. Inspection phreys, & O’Sullivan, 1998). This anatomic discovery should focus on posture and body asymmetries, among may be of significance in terms of understanding the other areas assessed. Musculoskeletal assessment should biomechanics and symptomatic sequela of cervicalinclude an adequate examination of the cranium, cranial acceleration/deceleration (whiplash) injury, particularly adnexal structures, and cervicothoracic spine as deemed in relation to rotational movements of the head in therelevant to the patient’ s headache complaints. Palpatory sagittal and transverse planes, as related to cervicogenic exam might include checking for neuromatous or neuritic headache following trauma. pain generators, myofascial trigger points, vertebral somatic dysfunction, sinus tenderness, and/or temporomandibular joint (TMJ) dysfunction (Horn, 1992; Zafonte CLINICAL ASSESSMENT & Horn, 1999). It is important for the examining clinician to keep the different mechanisms of PTHA in mind. Additionally, the MANAGEMENT mechanism of injury responsible for the initial insult should also be investigated; specifically, inquiry concern-MYOFASCIAL PAIN ing history pertaining to three main phenomena: cerebral, cranial/cranial adnexal, and/or cervical injury. Myofascial pain is one of the more common etiologies One of the major clues for the examiner relative toof PTHA, although to some extent the diagnosis of the origin of the headache should come from establishing myofascial pain remains somewhat controversial across the symptom profile for that particular headache, as wellmedical specialties. Myofascial pain typically presents as the patient’ s preinjury history of headache. Just becauseas a regional pain disorder characterized by localized an individual had headache preinjury does not mean that muscle tenderness in association with discomfort/pain.

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It is quite common following cervical accelera- importantly, body asymmetries and postural issues. tion/deceleration injuries, whether of exion/extension a fl Additionally, ergonomic issues should be examined in nature or lateral impulse type of force. Research has the workplace, as well as at home; included in the latter shown that referred pain, as well as so-called localshould be assessment of sleep habits such as use and twitch response, which are both characteristics of myo-type of head supports and bed (Travell & Simons, fascial trigger points, is related to spinal cord mecha-1983). Therapeutic exercise is a critical component of nisms (Bisbee & Hartsell, 1993). It has been theorizedmaintaining pain relief and should include both exifl that the taut band of skeletal muscle bers fi that contain bility and strengthening components. Education conthe myofascial trigger point is produced by an excessivecerning the need for compliance with any treatment amount of acetylcholine in the abnormal end plateintervention should be part and parcel of any treatment (Hong & Simons, 1998). regimen. A trigger point is defined as a localized deep tenderness in the taut band of skeletal muscles that is responsible NEURALGIC AND NEURITIC PAIN for the pain in the zone of reference. Clinicians must differentiate between latent and active trigger points. TheIt is not uncommon after cervical whiplash to find patients with signs of occipital neuralgia, involving either the zone of reference is defined as the area of perceived pain referred by the irritable trigger point and is usually locatedlesser or greater occipital nerves. This type of problem over the trigger point or spreads out from the trigger pointgenerally responds well to local anesthetic blockade (sometimes in conjunction with steroids) (Waldman, to a distant site (Travell & Simons, 1983). Treatment for myofascial pain should be holistic. 1991). Unless associated myofascial dysfunction is also addressed in the context of the overall treatment, occipital Muscle exercises should include stretching and strengthening, as well as postural. Trigger point therapy is clearlynerve irritation may return fairly quickly. an important part of the overall armamentarium and may Surgical decompression of the occipital nerve should be considered when entrapment is felt to be the pathoetinclude such techniques as ultrasound, ischemic presiologic mechanism responsible for continued pain, sure, accupressure, and massage, among others. Counterstimulation techniques involving Fluori-Methane, although the procedure may not produce complete pain relief. In more intractable cases, consideration can be diathermy, and heat and/or ice can also be used. Direct given for injection of neurolytic agents and/or more current stimulation via such techniques as electroacupuncture, transcutaneous electrical nerve stimulation,aggressive techniques such as destruction of the involved nerve via such procedures as cryoablation and/or open and direct current stimulation can also be considered. surgical neurectomy (Horowitz & Yonas, 1993). Surgical Acupuncture may serve as an adjutant therapy; however, its role in myofascial pain has not been well studied.excision may result in deafferentation pain and/or neuTrigger point injections with local anesthetic and/or ste-roma formation. Of note, however, is that some experienced clinicians do not recommend the treatment due to roid and dry needling are the most common techniques ef remains poorly studied used to treat this problem. Trigger point injections notthe fact that the proceduralficacy (Bogduk & Marsland, 1986). only reduce pain and increase range of motion in a musFollowing more significant cranial injuries, it is not cle that is typically shortened but also improve circulation to the muscle. It is not critical to inject anything uncommon to develop neuromas in the scalp particuinto the trigger point for the needling to have a thera-larly after craniotomies. For more diffuse neuritic scalp topical capsaicin can be considered. When peutic effect, because the latter appears to be due irritation, to mechanical disruption of the trigger point by the needle,there is a question of a more focal neuromatous lesion, local anesthetic blockade can be helpful. Enteral medinstead of the substance injected per se. Trigger point injections with local anesthetic are generally more effec-ications traditionally used in the treatment of neurotive and comfortable than dry needling or injecting otherpathic pain can also be used for neuritic and neuromatous pain. These medications include nonsteroidal antisubstances. Some clinicians have reported success modulating myofascial pain symptoms with botulinum toxin inflammatories, tricyclic antidepressants, and anticoninjections (Chesire, Abashian, & Mann, 1994). Spray andvulsants (such as gabapentin, carbamazepine, and phenytoin), among others. stretch techniques, as well as other manual strategies including strain–counterstrain, soft tissue mobilization, Less commonly, neuralgic problems can be encounand myofascial release techniques, have also been found tered secondary to facial trauma. The nerves that are most to be quite effective in ameliorating myofascial pain commonly involved are the supraorbital and infraorbital (Travell & Simons, 1983). nerves. These nerves can be injected locally with good resolution of facial pain and/or dysesthetic symptoms Perpetuating factors must be addressed in the treatment of myofascial pain including psychoemotional (Waldman, 1991). Sometimes, as with other injections, status, metabolic and hormonal factors, and, mostserial procedures are required.

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If and when it is suspected clinically and/or proven by diagnostic testing, such as magnetic resonance imaging Posttraumatic migraine accounts for up to 20% of(MRI), that there is significant intra-articular pathology, CPTHA. It is generally treated similarly to nontraumatic arthroscopic intervention is generally indicated. Rarely, migraine. There are some atypical variants of posttrau-one finds the necessity to proceed to open arthrotomy for matic migraine, such as BAM, that are known to occurdisk repositioning and/or arthroplasty. Generally, experimore frequently in young females, particularly follow- ence has shown that surgical outcome from the latter type ing whiplash injury (Jacome, 1986). The exact reasonof procedure tends to be guarded. In extreme cases of for this is unknown. BAM is generally treated with intracapsular damage, caused by the initial injury, or by atypical migraine medications such as carbamazepine failed surgery, condylectomy and costochondral reconor valproic acid. struction of the articulation may be required. When there Migraine treatment should include looking at all asso-is significant meniscal injury, an artificial meniscus can ciated factors that may influence this headache picture be considered. including reduction of so-called trigger factors (this may include certain food groups as well as external and internal CERVICAL ZYGAPOPHYSEAL JOINT PAIN stressors). Treatment should be directed at minimizing the functional disability associated with the headache throughCervical zygapophyseal joint pain can cause both neck C2–joint other interventions including appropriate medication pre-pain and referred head pain. Pain from the C3 scription that may be abortive, symptomatic, and/or pro-is perceived posteriorly in the upper neck extending into C4 joint phylactic. A small percentage of women who take birththe occipital region, whereas pain from the C3– control pills may be exacerbating their migraines and thisand any cervical joint caudal to that does not refer into should be considered in the overall holistic treatment ofthe head. Treatment considerations can include intrapatients with posttraumatic migraine. Other interventionsarticular injections of local anesthetic at the joint level for blocks of the medial branches of the dorsal rami that such as relaxation training and biofeedback may also be supply the joint. Joint blocks should be ideally performed used (Bell, Kraus, & Zasler, 1999). under fluoroscopic control through either a posterior or a lateral approach. Cervical medial branch blocks are a TEMPOROMANDIBULAR JOINT DISORDERS more expedient way to block a cervical zygapophyseal Although true intra-articular pathology is not fre- joint in that they are not only easier but also less painful quently seen following whiplash-induced temporoman-to the patient and provide the same diagnostic informadibular joint disorders (TMJD), myofascial dysfunction tion (Lord, Barnsley, & Bogduk, 1993). Other more in the muscles of mastication is frequently noted.aggressive modalities for treatment of this type of pain Appropriate workup is necessary, however, to rule outinclude percutaneous radiofrequency neurotomy via intra-articular pathology and, if present, to address itmedial branches, although this remains a controversial accordingly. In most cases, a referral to an oromaxil-treatment strategy on several levels (Lord, Barnsley, & lofacial surgeon would be warranted. Local treatment,Bogduk, 1995). as per the discussion of myofascial pain for trigger points involving the muscles of mastication (tempora-SOMATIC DYSFUNCTION lis, masseter, medial pterygoid, lateral pterygoid) Manual medicine techniques for the treatment of cershould be aggressively pursued. As indicated, interventions for bruxing should be suggested, for example,vical pain remains somewhat controversial. We are intraoral appliances such as occlusal splints (Fricton,quite convinced that craniocervical and cervicothoracic 1995). Appropriate education concerning minimizing somatic dysfunction following traumatic neck injuries foods that require signifi cant chewing is generally ben- has the potential to generate head pain. There have been numerous studies involving the benefi ts of mobilization eficial during the more acute and subacute treatment phase for myofascial pain involving the muscles ofof the cervical spine in chronic headaches, posttraumatic and otherwise, which have shown that cervical mastication. The patient should be instructed in the use cial in these of simple jaw exercises including passive jaw openingmobilization/manipulation can be benefi with the thumb and forefi nger and a gentle scissorlike types of clinical conditions (Jensen, Nielsen, & Vosaction to a position just short of pain onset. Nonsurgicalman, 1990). These procedures are utilized by not only chiropractors but also physical therapists, as well as treatment continues to be considered the most effective way of managing over 80% of all patients who presentappropriately trained physicians (both M.D.s and with symptoms of TMJD in the absence of intra-artic- D.O.s). Mobilization with impulse (also referred to as ular pathology (Dimitroulis, Gremillion, Dolwick, & high-velocity, low-amplitude thrust) is based on the principle of overcoming the resistive barrier in the Walter, 1995).

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direction of loss of range of motion. Reduction of normal restoration of function and perpetuate painful hypertonicity in segmentally related paraspinal musclesexperience; and in a cyclic fashion, it reinforces avoidresults through a hypothesized effect on mechanorecepance, inactivity, and increased pain. Finally, the longer tors and stimulation of the afferent loop of the appli- pain persists, the more recalcitrant it becomes and the cable reflex arc. There are many other techniques in themore treatment goals move toward management of pain manual medicine armamentarium. Some of the directand coping vs. cure (Penzien, Jeanetta, & Holroyd, 1993). (resistive barrier is engaged) interventions include soft According to Miller (1993) chronic pain often repretissue and articulatory muscle energy and myofascialsents the “weak link” in the cycle of “postconcussion release, as well as craniosacral manipulation. Some of invalidism.” Given that PTHA is the most common postthe indirect (resistive barrier is not engaged) interven-concussive symptom (Packard, 1994; Goldstein, 1991) tions include balance and hold, as well as strain –counand hence the most frequent type of posttraumatic pain terstrain (Greenman, 1989). Treatment contraindica-associated with mild traumatic brain injury (MTBI), it tions, both relative and absolute, must be appreciated follows that resolution of the postconcussion syndrome, by any clinician using these techniques as complica-and successful posttraumatic adaptation, may frequently tions have been reported (Dvorak & Orelli, 1985). rely on success in coping with PTHA symptomatology. The introduction of biopsychosocial models represents alternative theoretical approaches to dualistic and reducDYSAUTONOMIC HEADACHE tionistic biomedical conceptualizations that explain disCertain nerve fibers in the neck, anteriorly as well asease and health primarily in terms of measurable biologposteriorly, may be damaged from excessive flexion orical variables. A derived stress and coping formulation of extension of the neck associated with cervical accelerapostinjury recovery conceptualizes adaptation to injury as tion/deceleration insult. These types of injuries may pro-a series of stressful demands that require coping. Coping duce an uncommon PTHA variant known as dysauto-represents an interaction between existing coping nomic cephalalgia. There may be partial or total insult toresources and injury-related demands. Bolstering of copthese nerves that impacts on how the condition is treated ing resources presumably allows for improved adaptation relative to medication choices (Vihayan, 1977). Involve-to stressful life events. PTHA does not occur in a vacuum. ment of posterior cervical sympathetic dysfunction (alsoInstead, it occurs in a biological system within specific known as Barre-Lieou syndrome) may produce symptoms psychological and social contexts. It reflects an interaction of pain in the back of the head, tinnitus (buzzing in theof organic and emotional factors. ears), blurry vision, and vertigo (Barre, 1926). Although similar to natural headaches in clinical presentation of subtypes and biochemical mechanisms, RARE CAUSES OF POSTTRAUMATIC HEADACHE PTHA is oftentimes resistant to traditional headache treatment. Medication management alone may lead to There are multiple rare causes of headache that should unwanted side effects (e.g., adverse effects on sleep, menalso be considered in the posttrauma population. Approtal alertness, sexual functioning, work performance) and priate neurodiagnostic tests such as computerized tomography (CT) or magnetic resonance imaging (MRI)certainly does not address adaptation to chronic pain scanning of the brain, plain X-rays, electrodiagnostic andthrough development of new coping skills (Martelli, Zasler, & MacMillan, 1998). Conversely, PTHA patients vascular studies, and laboratory tests should be conhave been reported to exhibit minimal response to nondrug ducted as deemed appropriate by the treating clinician (Zafonte & Horn, 1999). These tests should not be(i.e., psychological) treatments alone (Jensen, Nielsen, & ordered unless it is felt that the results will alter clinical Vosmar, 1990). Treatments that are holistic in nature, targeting not only the pain directly but also the patient’ s treatment planning. reaction to pain within his or her daily life, typically fare better than treatments with a more narrow focus (e.g., PSYCHOLOGICAL FACTORS medication management or nondrug therapies alone). Understanding vulnerability issues as predictors of poor Chronic pain or pain that persists 6 months or longer after injury: (1) reflects ambiguous pathways between injurychronic pain adaptation is also critical in this context (Bennett, 1988) (Table 21.2). Currently, multicomponent treatsites and the central nervous system, (2) communicates ment packages are the preferred treatment choice for useless information that perpetuates physiological protective responses long after removal of possibility of injury PTHA (Packard & Ham, 1997). extension and/or despite lack of underlying tissue dam- The assessment phase is the starting point of any age, and (3) poses a liability to postinjury adaptation.psychological treatment protocol. Detailed individual Importantly, chronic pain is typically associated with assessment is necessary to consider specifi c treatment response patterns involving decreases in, and avoidance issues (e.g., personality variables, social support) and of, activity. Decreased activity, in response, can preventfacilitate the patient– therapist relationship. A thorough

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TABLE 12.2 Vulnerability to Disability Rating Scale Increased Complaint Duration 0 = < 6 Months 1 = < 12 Months 2 = > 12 Months Especially with expectation of chronicity, poor understanding of symptoms

Severity of Current Psychosocial Stress 0 = Nonsignificant 1 = Mild/moderate 2 = Significant

Complaint Inconsistency/ Vagueness

Previous Treatment Failure

Collateral Injury/Impairment

0 = Little 0 = Insignificant 0 = Insignificant 1 = Mixed 1 = Mixed 1 = Mild/moderate 2 = Mostly inconsistent 2 = Mostly or all 2 = Significant failures Multiple, vague, variable Especially with Especially if silent and sites; anatomically complaint of involving adaptation inconsistent; sudden onset treatments worsening reducing without accident or cause; pain or causing impairments not affected by weather; injury, and performing no work or expectation that chores, or avoiding easy future treatments will tasks but performing most fail hobbies, enjoyments; pain only occasional Psychological Coping Victimization Liabilities Perception Social Vulnerability 0 = Few 0 = Little 0 = Little 1 = Mild/moderate 1 = Mild/moderate 1 = Mild/moderate 2 = Significant 2 = Significant 2 = Significant

Sum of peronal, social, Premorbid, comorbid: financial, emotional, depression; identity, activity posttraumatic anxiety; stresses, life somatization (and disruption, repressive) defenses; premorbid coping emotional immaturity/ style disruption, etc. inadequacy with poor and including injury/ coping skills; impairment X coping hypochondriacal traits style incongruence; (e.g., postinjury MMPI-3 persistent premorbid > 85; preinjury > 70); psychosocial stress passive coping style; levels childhood trauma (esp. death of parent; child or sex abuse); anger/resentment; posttraumatic adjustment problems (see“Vulnerability to Disability” tables — psychological impediments); alcohol, substance use/abuse; limited premorbid intellect, education, skills; preinjury psychiatic treatment; poor premorbid work history

Externalized“blame” for accident, disability, etc.; perceived mistreatment; anger, fear, resentment, distrust concerning accident, treatment, understanding (family, employer, doctors, etc. — esp. given characterologic tendencies concerning victimization, resentment, suspiciousness, distrust, etc.)

Lack of family support, resources, romantic support (esp. if recent conflict, divorce); lack of community support/resources/ involvement; lack of employer, co-worker, insurance manager support; etc.

Vulnerability to Disability Rating Scale (VDRS) — General Version: M.F. Martelli, Ph.D. © 1996.

Pre/Comorbid Medical History 0 = Insignificant 1 = Mild/moderate 2 = Significant

Medication Reliance 0 = Little 1 = Moderate 2 = Significant

Seizure disorder; > 4X/week narcotic, diabetes; hypnotic or benzohypertension; brain diazepine injury, stroke or other tranqulizer; neurological insult or perceived inability to vulnerability (esp. if cope without undiagnosed); medication preinjury medication reliance Illness Reinforcement Vulnerability Score 0 = Little 1 = Mild/moderate 2 = Significant _____ Total points (Max: 22) Secondary gain: Preliminary attention, support in a interpretive guidlines dependency-prone person; avoidance of Scores of 13 or above stressful or suggest high displeasing life or job vulnerability to responsibilities or chronic disability demands (esp. with recent or imminent job/job duty changes or reorganization); financial compensation (esp. if litigation; or current income = preinjury/ preimpairment)

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and validating their pain may help to gain client trust behavioral assessment may include a detailed clinical and commitment. interview and other assessment instruments such as pain diaries and various standard pain and headache questionBiofeedback naires. Psychophysiological assessment is an additional option, if feasible, and typically involves examination of muscle tension or electromyogram (EMG) for different Although an abundance of research reports the success of biofeedback for the treatment of tension-type migraine, muscle groups in the head (forehead, masseter, temporal, mixed migraine, and tension-type headaches, many studoccipital) and neck (trapezius, cervical paraspinal) areas. The assessment phase concludes when the results ies of listed PTHA among the exclusionary criteria. As a result, few studies have examined the ficacy ef of biofeedevaluation have produced a specifi c case conceptualizaback for PTHA specifically. A number of studies used tion that identifies a specifi cally tailored treatment plan. EMG biofeedback (forehead and neck sites) in combinaFeedback to the patient using assessment results provides tion with other treatment modalities (e.g., cognia framework for the treatment intervention, defi nes goals tive–behavioral treatment, medication) and reported sigand patient/therapist expectations and sequences, and nificant improvement in PTHA (Duckro, Tait, Margolis, provides the forum for presenting general information concerning PTHA and rationale for treatment and enlist-& Silversintz, 1985; Medina, 1992). Ham and Packard (1996) reported that combined EMG and thermal biofeeding participation. back resulted in at least moderate improvement for 53% Although there is an abundance of headache treatment of 40 chronic PTHA patients, most of whom had previoutcome studies available, there are relatively few studies ously received medication, physical therapy, chiropractic specifically examining the psychological treatment of treatment, and/or trigger point injections without signifiPTHA as a distinct subgroup of headaches in general. The cant success. However, it is ficult dif to make firm concluliterature suggests that PTHA and natural headaches may sions concerning the ficacy ef of biofeedback alone for share common pathways, and clinical presentations are PTHA given the small sample size and the use of other generally very similar if not identical (Haas, 1993). Consimultaneous treatments in these studies. Although empirsequently, standard psychological treatments for headache ical research examining the utility of biofeedback specifare presumed to share common mechanisms of action. ically for PTHA is sparse, many clinical researchers feel Although PTHA treatment outcome studies suggest that that biofeedback, when combined with medical treatment combined psychological treatments are generally ficaef and/or psychotherapy, augments the treatment response cious, evidence suggests that PTHA is often more recalfor many persons with PTHA. citrant to standard psychological treatment compared with natural headaches. However, the severity and frequency Relaxation Training of pain attacks and chronic pain-related sequelae such as coping abilities, depression, and anxiety may be signifi-Various forms of relaxation training have been used for cantly improved by combined psychological treatmentthe treatment of chronic headache (e.g., autogenics, medprotocols (Miller, 1993; Packard & Ham, 1997; Parker,itation); however, progressive muscle relaxation (PMR) 1995). Supportive counseling that begins early afterhas been most widely studied (Blanchard, 1994). PMR trauma and is continuous results in better patient response involves the systematic tensing and relaxing of various (Ham & Packard, 1996). muscle groups to elicit a relaxation response. Diaphragmatic breathing is generally taught in combination with relaxation exercises. Meta-analytic reviews generally Patient Education conclude that relaxation training and biofeedback trainPackard directly asked,What “ does the headache patient ing are equally effective for headache reduction, producwant?” and detailed the stated treatment priorities ofing improvement rates between 44.6 and 59.2% for tenheadache patients (Packard, 1979). Education concernsion-type headaches and migraines (Martin, 1993). ing the causes of headaches was listed as a top priority. Information can be individualized for the patient and Operant Treatment ideally presented while providing feedback after the behavioral assessment phase. It is especially important Fordyce (1976) pioneered the behavioral approach to psyas pain professionals to emphasize to patients that their chological assessment and treatment of chronic pain. pain is real. Some patients, when told by physicians that Although not specifically developed for use with PTHA, medical tests are inconclusive or that their headache the concept follows the operant model to reduce general pain is due to stress, may interpret this information aschronic pain behaviors. That is, the operant model hypoth“ it’ s all in my head. ” Anecdotally, many patients are esizes that pain-related behaviors may be positively reinconfused or angry when referred to a psychologist forforced by desirable consequences (e.g., sympathy, nurpain treatment. Explaining the cycle of stress and painturance), while simultaneously negatively reinforced by

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avoidance of aversive consequences (e.g., undesirable mented the application of imagery for PTHA, in particular work or social obligations). Treatment based on the oper(Daly & Wulff, 1987). ant model requires altering environmental contingencies to eliminate pain behaviors (e.g., verbal complaints, inac-Biofeedback-Assisted tivity) and reward “well” behaviors (e.g., exercise, Cognitive–Behavioral Therapy increased activity level). The effi cacy of EMG biofeedback and cognitive –behavCognitive–Behavioral Treatments ioral therapy (CBT), singularly and in combination in multicomponent treatment packages, has been demonCognitive approaches for headache treatment are derived strated for the treatment of various pain disorders (e.g., from several cognitive theorists and typically train theheadache, facial pain). The majority of multicomponent headache patient to identify and refute maladaptive beliefs treatment packages in the literature to date utilize distinct concerning pain. Specific cognitive strategies and skillstechniques for biofeedback and CBT. Grayson (1997) are taught to replace inappropriate negative expectations presented a promising single-case research design outlinand beliefs. Holroyd and Andrasik (1978) have generallying a multicomponent treatment protocol (biofeedbackled the field in cognitive therapy for chronic headache.assisted CBT; B-CBT) that synthesizes the two in the Cognitive stress-coping therapy has been successfully treatment of chronic posttraumatic pain. The B-CBT proapplied to tension-type headache patients in group, minitocol combines cognitive, emotional, and physiological mal-therapist-contact, and home-based formats (Tobin, (e.g., muscle tension) elements to heighten awareness of Holroyd, Baker, Reynolds, & Holm, 1988). Cognitive self-control. It provides immediate physiological feedstress-coping therapy proposes that maladaptive cognitive back during the cognitive behavior therapy process to responses are present that contribute to keeping the headheighten awareness of psychophysiological reactions and ache patient stressed/tense by keeping the sympathetic to facilitate change. Through the process of shaping, nervous system activated. Pain protocols based on this patients learn to monitor and control their physiological approach alter the maladaptive beliefs that mediate the reactions in conjunction with reviewing and modifying stress reaction to presumably alter the stress reaction cognitive and emotional aspects of activating stressful (muscle tension) leading to increased pain. In essence, the events. In addition, a cognitive exposure method can be patient with PTHA is trained to shift attention from one utilized by having the patient repeatedly relate the actiaspect of the environment (e.g., internal pain) to another vating event, while attempting to maintain physiological (internal or external). responding below a gradually reducing threshold level. Relaxation techniques such as deep breathing and proSocial and Assertiveness Skills Training gressive relaxation training may be also used. Initial findMiller (1993) recommended social skills training in a ings for this procedure have been very encouraging and further research is warranted. group format as an adjunct to standard psychotherapeutic interventions for chronic pain. Assertiveness training, in Habit Reversal particular, may help some patients to communicate needs more effectively. This, in turn, increases the likelihood of need fulfillment and more desirable situational outcomes.In a promising new approach to managing facial pain and tension headaches, Gramling, Neblett, Grayson, and Subsequent reduction of stressful events, anger, and other Townsend (1996) used a habit reversal treatment distressful emotional states associated with need frustraapproach. They taught patients with facial pain to detect, tion can reduce associated physiological arousal that coninterrupt, and reverse maladaptive habits (e.g., suboptimal tributes to headache pain. head/jaw posture, jaw tension, and negative cognitions). The main premise of this program is that participants can Imagery and Hypnosis learn specific skills to reverse habits as well as reverse stressful thoughts and feelings that precipitate these habSeveral studies have reported success with imagery-based its. The treatment program begins by teaching exercises treatments for headache in general (Martin, 1993). Procedures vary by study, but training generally includes auto-that increase awareness of the habit. Awareness training is facilitated by relaxation training exercises that are hypnosis and suggestions of relaxation and visual imagery. Generally, the patient is instructed to visualize the paintaught in conjunction with deep breathing exercises. As (i.e., give it form) and focus on altering the image topain patients become more aware of maladaptive habits and the situations in which they occur, they are taught to reduce the pain. Imagery-based treatment is recommended c exercises (e.g., facial exercises) and deep following establishment of a good therapeutic alliance touse specifi facilitate patient compliance. At least one study docu-breathing as competing responses. A similar process is

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used to help pain patients become more aware of habitual nosis than PTHA) and/or treated should not be labeled, stress-inducing thoughts and beliefs. as a rule, as MMI. Packard and Ham (1993) proposed a reasonable alternative to the AMA impairment rating system using the IMPAIRMENT AND DISABILITY acronym IMPAIRMENT and a 0 to 2 rating scale. The IN POSTTRAUMATIC HEADACHE acronym stands for intensity, medication use, physical Currently, we have poor tools for gauging impairmentsigns/symptoms, adjustment, incapacitation, recreation, miscellaneous activity of daily living, employment, numassociated with headache. For example, the American Medical Association (AMA) (1993) does not provide a ber (frequency), and time (duration of attacks). Additionspecific methodology for calculation of impairment ally, there are three physician modifiers scored from 0 to –4 points for motivation for treatment, overexaggeration related to any type of headache but instead allows the rater to “estimate” the impairment. Pain is therefore rated inor overconcern, and degree of legal interest. Although this qualitative terms relative to frequency and intensity. Oneparadigm for ascertaining an impairment level in PTHA is more cumbersome than the AMA Guides, the Packard must understand, however, that the rating is based purely on patient report and therefore is totally subjective, asand Ham methodology is one viable option that provides opposed to most of the AMA ’s guidelines for impairment a more multidimensional and logical approach to rating determination that are based on objective clinical examimpairment in PTHA. findings. It is also important for readers to understand that the AMA guides were established through an empirical CONCLUSIONS AND consensus process and would not stand up to current methRECOMMENDATIONS odologies used in the development of evidence-based standards or guidelines. There is much to be learned about PTHA conditions. The AMA guidelines state,An “ individual who comThere must be a greater effort at bringing together the plains of constant pain but who has no objectively valimultiple disciplines involved with PTHA assessment and dated limitations in daily activities has no impairment” treatment to address many of the issues discussed in this (AMA, 1993, p. 309). This statement confuses issues gerchapter, as well as others not discussed because of space mane to differentiation of impairment from functional dislimitations. Education concerning PTHA for “frontline” ability. That is, impairment should not be gauged by funcclinicians in the disciplines of emergency medicine, neutional ability or disability but by objective examination findings on physical and/or psychiatric examination. It isrology, and family practice is essential if these individuals of utmost importance for clinicians, as well as lawyers, toare to receive appropriate treatment. There must be develkeep the distinction between impairment (what one findsopment of multidisciplinary consensus opinion concernon examination) and disability (how the impairment ing issues dealing with nomenclature, screening examinaimpacts on functional abilities) clear and not intermingletion, classification, and accepted algorithms for treatment. PTHA classification must be more in depth and specific and/or analogize these terms. The AMA guidelines also state,The “ vast majority than that currently provided by ICD-10 or IHS. Better and of patients with headache will not have permanentmore objective impairment and disability assessment techimpairments” (AMA, p. 312). First, this statement dis- niques need to be developed for PTHA, preferably ones that have face validity and good inter-rater reliability with cusses headache in only a very general sense, and there internal “checks” for symptom magnification, as well as are clearly differences in headache conditions that affect prognosis, as well as anticipated impairment and disabil-response bias. Research efforts should be directed at ity that are lost when making such a generalization. Thisexamining PTHA subtypes in primary not tertiary PTHA patient populations that have been identified relative to statement also has the potential to bias less experienced evaluators and lead to their dismissal of chronic PTHAhistorical factors and specific subpopulations (e.g., cerecomplaints as nonorganic, “ ” litigious, or attention-seek- bral, cranial, cranial adnexal, cervical, posttraumatic psychological, or mixed impairments). ing behaviors. Ultimately, there is still much that is not understood Finally, impairment ratings are considered appropriate only after an individual has reached maximumabout PTHA. Misinformation, lack of information, and medical improvement (MMI); specifi cally, this implies incomplete understanding of pathoetiology, as well as natural history of the condition, continue to be problematic that there is no more than a 3% change in whole body impairment rating expected over the ensuing yearissues. We must commit to addressing these deficits in (AMA, 1993). An individual who has not been ade- knowledge through multicenter, multidisciplinary, proquately assessed (e.g., there is no more specifi c a diag- spective research.

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REFERENCES

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Fricton, J.R. (1995). Management of masticatory myofascial pain. Seminars in Orthodontics , 1(4), 229–243. Alves, W.M., Colohan A., O’Leary T.J., et al. (1986). Under- Goldstein, J. (1991). Post-traumatic headache and the post-concussion syndrome. Medical Clinics of North American . standing post-traumatic symptoms after minor head 75, 641–651. injury. Journal of Head Trauma Rehabilitation , 1,1–12. American Medical Association. (1993). Guides to the Evaluation Gramling, S.E., Neblett, J., Grayson, R.L., & Townsend, D. (1996). Temporomandibular disorder:ficacy Ef of an oral of Permanent Impairment (4th ed.) Chicago: AMA. habit reversal treatment program. Journal of Behavioral Appenzeller, O. (1993). Post-traumatic headache. In D.J. DaleTherapy and Experimental Psychiatry , 27, 212–218. sio & S.D. Silberstein (Eds.), Wolff's headache and other head pain(6th ed., pp. 365–383). New York: Oxford Grayson, R.L. (1997, November). EMG biofeedback as a therapeutic tool in the process of cognitive behavioral therUniversity Press). apy: Preliminary single case results. Poster presented at Barre, J.A. (1926). The posterior cervical sympathetic syndrome the Association for Advancement of Behavior Therapy and its frequent cause: Cervical arthritis. Review of (AABT), 31st annual convention, Miami, Florida. Neurology, 53, 12-46. Principles of manual medicine . BaltiBell, K.R., Kraus, E.E., & Zasler, N.D. (1999). Medical man- Greenman, P.E. (1989). more: Williams & Wilkins. agement of post-traumatic headaches: Pharmacological and physical treatment. Journal of Head Trauma Reha- Haas, D.C. (1993). Chronic post-traumatic headache. In J. Olesen, P. Tfelt-Hanson, & K.M.A. Welch (Eds.), The headbilitation, 14(1), 34–38. aches (pp. 629–637). New York: Raven Press. Bennett, T. (1988). Post-traumatic headaches: Subtypes and Ham, L.P., & Packard, R.C. (1996). A retrospective, follow-up behavioral treatments. Cognitive Rehabilitation . 6(2), study of biofeedback-assisted relaxation therapy in 34-39. patients with post-traumatic headache. Biofeedback Self Bisbee L.A., & Hartsell, H.D. (1993). Physiotherapy manageRegul a tion, 21(2), 93–104. ment of whiplash injuries. In R.W. Teasell & A.P. Shapiro (Eds.),Cervical flexion-extension/whiplash injuries Headache Classification Committee of the International Headache Society. (1988). Classification and diagnostic cri(pp. 501–516). Phildelphia: Hanley & Belfus. teria for headache disorders, cranial neuralgias and Blanchard, E.B. (1994). Behavioral medicine and health psyfacial pain. Cephalalgia. 8(7). chology. In A.E. Bergin & Z.H. Garfield (Eds.), HandHolroyd, K.A., & Andrasik, F. (1978). Coping and the selfbook of psychotherapy and behavior change . New York: control of chronic tension headache . Journal of ConsultJohn Wiley & Sons. ing and Clinical Psychology . 5,1036–1045. Bogduk, N., & Marsland, A. (1986). On the concept of the third Hong, C.Z., & Simons, D.G. (1998). Pathophysiologic and elecoccipital headache . Journal of Neurology, Neurosurtrophysiologic mechanisms of myofascial trigger points. gery, and Psychology . 49, 775–780. Archives of Physical Medicine and Rehabilitation , 79, Bogduk, N. (1982). The clinical anatomy of the cervical dorsal 863–872. rami. Spine, 7, 319–330. Horn, L.J. (1992). Post-concussive headache. In I.J. Horn & Cheshire, W.P., Abashian, S.W., & Mann, J.D. (1994). Botulinum N.D. Zasler, N.D. (Eds.), Rehabilitation of post-concustoxin in the treatment of myofascial pain syndrome. sive disorders(pp. 69–88). Philadelphia: Hanley & BelPain, 59(1), 65–69. fus. Daly, E., &Wulff, J. (1987). Treatment of a post-traumatic head-Horowitz, M.B., & Yonas, H. (1993). Occipital neuralgia treated ache. British Journal of Medical Psychology , 60(Pt 1), by intra-dural dorsal nerve root sectioning. Cephalal85–88. gia. 13, 354–360. Dimitroulis, G., Gremillion, H.A., Dolwick, M.F., & Walter, J.H. Jacome, D. (1986). Basilar artery migraine after uncomplicated (1995). Temporomandibular disorder. 2. Non-surgical whiplash injuries. Headache , 26, 515–516. treatment. Australian Dental Journal40(6), 372–376. Jensen, O.K., Nielsen, F.F., & Vosmar, L. (1990). An open study Duckro, P.N., Tait, R., Margolis, R.B., & Silversintz, S. (1985). comparing manual therapy with the use of cold packs Behavioral treatment of headache following occupain the treatment of post-traumatic headache. Cephalational trauma.Headache , 25, 180–183. lgia, 10, 241–250. Dvorak, J., & Orelli, F.V. (1985). How dangerous is manipulation Jensen, O.K., & Nielsen, F.F. (1990). The influence of sex and to the cervical spine? Case report and results of a survey. pre-traumatic headache on the incidence and severity of Man and Medicine,1, 1–14. headache after head injury. Cephalalgia, 10(6), Evans, R.W. (1992). The post-concussion syndrome and the 285–293. sequelae of mild head injury.Neurologic Clinics, 10, Lord, S.M., Barnsley, L., & Bogduk, N. (1993). Cervical zygapo815–847. phseal joint pain in whiplash. In R.W. Teasell & A.P. Fordyce, W.E. (1976). Behavioral methods for chronic pain and Shapiro (Eds.),Cervical flexion-extension/whiplash injuillness. St. Louis: Mosby. ries (pp. 355–372). Philadelphia: Hanley & Belfus. Freeman, M.D., & Croft, A.C. (1997). The controversy over lateLord, S.M., Barnsley, L., & Bogduk, N. (1995). Percutaneous whiplash: Are chronic symptoms after whiplash real? radiofrequency neurotomy in the treatment of cervical In M. Szpalsk & R. Gunzburg (Eds.) Whiplash injuries. zygapophyseal joint pain: Aa caution. Neurosurgery . 36(4), 732–739. New York: Lippincott-Raven.

Posttraumatic Headache: Practical Interdisciplinary Approaches to Diagnosis and Treatment

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Martelli, M.F,, Zasler, N.D., & MacMillan, P. (1998). Mediating Penzien, D.B., Jeanetta, C.R., & Holroyd, K.A. (1993). Psychological assessment of the recurrent headache sufferer. In the relationship between injury, impairment and disabilC.D. Tollison & R.S. Kunkel (Eds.), Headache: Diagity: A vulnerability, stress and coping model of adaptanosis and treatment . Baltimore: Williams and Wilkins. tion following brain injury. NeuroRehabilitation: An interdisciplinary journal, 11(1), 51–68. Radanov, B.P., Di Stefano, G., Schnidrig, A., et al. (1993). Factors influencing recovery from headache after common Martin, P.R. (1993).Psychological management of chronic headwhiplash. British Journal of Medicine,307,652–655. aches. New York: The Guilford Press. May, A., & Goadsby, P.J. (1999). The trigeminovascular systemSessle, B.J. (1999) Neural mechanisms and pathways in craniofacial pain. Canadian Journal of Neurological Science , in humans: Pathophysiologic implications for primary 3:S7–11. headache syndromes of the neural influences on the cerebral circulation. Journal of Cerebral Blood Flow Siegmund, G.P., King, D.J., Lawrence, J.M., Wheeler, J.P., and Metabolism,19(2), 115–127. Brault, J.R., & Smith, T.A. (1997). Head/neck kinematic response of human subjects in low-speed rear-end colMedina, J.L. (1992). Ef ficacy of an individualized outpatient lisions (pp. 357–385). SAE paper 973341. program in the treatment of chronic post-traumatic headache. Headache . 32(4):180–183. Tobin, D.L., Holroyd, K.A., Baker, A., Reynolds, R.V.C., & Holm, J.E. (1988). Development in clinical trial of a Miller, L. (1993). Psychotherapy of the brain injured patient . minimal contact, cognitive-behavioral treatment for tenNew York: W.W. Norton. sion headache.Cognitive Therapy and Research , 12, Mitchell, B.S., Humphreys, B.K., & O'Sullivan, E. (1998). 325–339. Attachments of the ligamentum nuchae to cervical posMyofascial pain and dysterior spinal dura and the lateral part of the occipital Travell, J.G., & Simons, D.G. (1983). function: The trigger point manual . Baltimore: Willbone. Journal of Manipulative Physiology and Therapy, iams & Wilkins. 21(3), 145–148, . Vihayan, N. (1977). A new post-traumatic headache syndrome; Packard, R. (1979). What does the headache patient Headwant? clinical and therapeutic observations. Headache , 17, ache,19, 370–374. 19–22. Packard, R.C., & Ham, L.P. (1993). Impairment rating for postWaldman, S.D. (1991). The role of neural blockade in the evaltraumatic headache.Headache , 33, 359–364. uation and treatment of common headache and facial Packard, R.C., & Ham, L.P. (1997). Pathogenesis of post-traupain syndromes. Headache Quarterly Current Treatmatic headache and migraine: a common headache pathment Research,(4), 2 286–291. way? Headache , 37(3), 142–152. World Health Organization. (1997). ICD-10 guide for headaches. Packard, R.C. (1999). Epidemiology and pathogenesis of postCephalalgia. 17(S19). traumatic headache.Journal of Head Trauma RehabilYamaguchi, M. (1992). Incidence of headache and severity of itation. 14(1):9–21. head injury. Headache , 32(9), 427–431. Packard, R.C. (1994). Post-traumatic headache. Seminars in Zafonte, R.D., & Horn, L.J. (1999). Clinical assessment of postNeurology, 14, 40–45. traumatic headache. Journal of Head Trauma RehabiliPackard, R.C. (1992). Post-traumatic headache: permanency and tation, 14(1), 22–33. relationship to legal settlement. Headache , (10), Zasler, N.D. (1996). Post-traumatic headache: A pain in the 496–500. brain? i.e. Magazine . 3(3), 8–23. Parker, R.S. (1995). The distracting effects of pain, headaches, and hyper-arousal upon employment after minor headZasler, N.D. (1999). Post-traumatic headache: Caveats and controversies. Journal of Head Trauma Rehabilitation . injury. Journal of Cognitive Rehabilitation . 13(3), 14(1):1–8. 14–23.

13 Orofacial Pain and Temporomandibular Disorders Gary M. Heir, D.M.D. HISTORICAL PERSPECTIVE

the physician’s approach to managing headache and facial pain was almost exclusively pharmacological, and mediHead and facial pain has plagued mankind throughout cations were selected based on their ficacy ef with little recorded history. In ancient times it was believed that theunderstanding of their pharmacodynamics. In modern victim’s suffering was due to evil spirits and humors thattimes it was the work of Wolff (1948) and his contempoinvaded the cranium. Prayers of exorcism and the appliraries who continued this pursuit. cation of magic potions were often performed to drive While the debate as to the etiology and treatment of away these demons and end the victim’s misery. migraine headache continued, little effort was made to The search for valid etiologies over those more mysunderstand other forms of head and facial pain. Facial tical may have begun with Hippocrates who suggested pain was thought to be mostly due to dental causes or, that noxious vapors from the liver and other poorly in some cases, thought to be of psychogenic origin. understood maladies were the cause of head pain. The Attention was first drawn to facial pain of nonheadache release of these vapors was accomplished by the use of and nonodontogenic origin in 1934 when Costen publeeches, bleeding, and in extreme cases trephination; lished his treatise on a syndrome of ear and sinus symphowever, at least according to Hippocrates, these were toms dependent on disturbed function of the temporothe remedies of choice. The term hemicraniais attributed mandibular joint (TMJ). to the ancient Roman physician Galen, and the origins Now we are in a new era. Science is beginning to of the term migraine may also be traced back to this understand the mechanisms of pain transduction, transperiod (Kiester, 1989). mission, modulation, and perception. With a more clear During the ensuing centuries there was slow but steady understanding of pain mechanisms, the healthcare sciprogress in the understanding of head and facial pain. The ences have been able to identify more specific etiologic use of analgesics began in the 13th century and evolved factors and conditions for our patient’ s complaints. to the use of cocaine and the discovery of other analgesic For the purpose of this discussion, orofacial pain is preparations, but these efforts to relieve pain did not categorized by the systems from which it may seem to explain its mechanism. arise (Merrill, 1997). This discussion reviews head and Thomas Willis offered a “vascular hypothesis” in the facial pain of odontogenic, vascular, musculoskeletal, neu17th century (Frank, 1990). He suggested that head pain rogenous, and psychogenic origin. By evaluating sympwas due to swelling of blood vessels in the cranium, a s suffering theory that was generally accepted within the medicaltoms on this basis, the source of the patient’ may be identified and appropriate therapeutic measure community and became the basis for much of the 20th may be instituted. century pharmacotherapies. In fact, by the 19th century

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OROFACIAL PAIN

wrong in his or her life. Chronic pain has biological ramifications as well as sociocultural and psychological Orofacial pain can be acute and related to trauma, dental effects (Grzesiak, 1991). injuries, dental pathologies, and acute dysfunction of the Chronic pain is both a cognitive and emotional expemasticatory system. Acute orofacial pain may include denrience and can be destructive. Management may be diftal pathology, dysfunction of the masticatory musculature, ficult. Patients develop chronic pain syndromes that rule and temporomandibular disorders (TMD). Acute pain is their lives. Chronic pain patients regularly abuse the more readily diagnosed and treated, and often there is an healthcare system, overuse medications, and have fi- dif identifiable precipitating event associated with the onset culty with interpersonal relationships. Chronic pain is of acute symptoms that leads the clinician to the source inevitably depressing, but may be synchronous with of the problem. depression and not caused by it. The longer pain continChronic orofacial pain is more dif ficult to diagnose, ues, the deeper the depression may be. Chronic pain and the source of the patient’ s complaint is frequently monopolizes the patient’ s attention, compromising elusive. The clinician must have the knowledge and clinbehavior and thinking. Expectations for recovery are poor ical expertise to accurately pursue the assessment, diag(Wall, 1999). nosis, and treatment of complex chronic orofacial pain and dysfunction disorders, including oromotor and jaw In practice, the chronic pain patient with psychological affect may be identified by a variety of factors. The behavior disorders, chronic head, neck, and facial pain, and have knowledge of the underlying pathophysiologyduration of their pain is longer than would be expected and, if associated with illness or injury, extends beyond and mechanisms of these disorders (American Academy the time required for normal healing or recovery. Chronic of Orofacial Pain [AAOP], 1998). Chronic, complex orofacial pain may be of muscu-pain patients tend to dramatize their complaints. They may exaggerate symptoms verbally or demonstrate comproloskeletal, vascular, neurogenous, and infrequently psychological origin. There is a clear distinction betweenmised functional ability beyond what would be expected. Chronic pain patients provide a history of a variety of complex chronic orofacial pain and acute pain. diagnostic failures and present as a diagnostic dilemma. There may be a history of excessive use of medications ACUTE PAIN both by prescription or over-the-counter preparations. Chronic pain patients demonstrate dependence on family Acute pain is biologically useful. It occurs as a result of and friends, become withdrawn, and avoid painful or a noxious mechanical, thermal, or chemical stimulus. The potentially painful activities. Depression is evident; decisymptoms and history of the onset of pain help in assesssion making, antisocial behavior, and rejection by friends ing the problem. A diagnosis for the cause of acute pain and family may also become evident with a carefully is facilitated by an assessment of the location, the duration, elicited history (Rosch, 2000). and the intensity of the patient’ s pain. Treatment efforts vary depending on the diagnosis; however, the diagnostic Although a psychological diagnosis may be inappropriate if made by a healthcare practitioner not trained in process is usually not dif ficult. The acute pain of an infected tooth or an acute dislo-psychology, recognition of the emotional components of chronic pain should prompt an appropriate referral for cation of the TMJ does not present as a significant diagadditional assessment. nostic problem. The onset of pain symptoms presents in such a way that the diagnostic process is fairly clear. The emotional reaction to acute pain is also somewhat ODONTOGENIC PAIN predictable. The reaction to the sudden onset of acute pain is anxiety. There is fear that the sudden onset of spontaIt is not the purpose of this chapter to discuss odontogenic neous pain represents a life-threatening illness or that pain pain. However, inasmuch as dental pain is the primary after trauma is due to a serious injury. However, once the etiologic factor in the production of facial pain, a brief patient understands the source of pain and the clinician discussion is required. acts to alleviate the cause and symptoms, the patient’ s Consider the tooth as a specialized primary afferent anxiety dissipates. nociceptor. A tooth is a hard container composed of enamel, dentin, and cementum. It is firmly attached to the supporting bone by the periodontal ligament. This “hard CHRONIC PAIN case” contains the dental pulp. The dental pulp is the Unlike acute pain, chronic pain has no biological utility. principal source of pain within the mouth. This pink, Chronic pain may not be due to nociception or centralcoherent, soft tissue is dependent on the hard tissues of neural input. The location of pain does not aid in thethe tooth for its for protection. Once exposed, it is diagnosis. The patient may feel as though something is extremely sensitive to all stimuli (Ogilvie, 1969).

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Although the dental pulp is often referred to as theodontal inflammation or infection within the periodontal nerve, it is not just a mass of raw nociceptive neural tissue. space produces or increases pain. The pulpal tissue of the tooth resembles other loose con- The mechanisms of periodontal injuries are either nective tissues of the body more than it differs from them.mechanical or chemical (infection). One of the most comThere are connective tissue cells of various types, as well mon sources of periodontal irritation is trauma from occluas intercellular components made up of ground substance sion often caused by premature dental contacts or bruxism. and fibers. Among this lies a complex network of blood Bruxism may produce pain in the masticatory system, vessels, lymphatics, and nerve tissue (Seltzer, 1988). Stimas has been documented experimentally (Christensen, ulation of the dental pulp elicits a painful response. 1971). The pain may arise from muscles, periodontium, Not all dental pain is a consequence of direct stimu-and TMJ. Pain produces unbalanced, sustained, abnormal lation of the pulpal tissue. Inasmuch as this complex strucmuscle activity, increasing the risk of injury (Arima, ture has great similarities to other tissues in the body, itSvensson, & Arendt-Nielsen, 1999). responds in a like fashion to injury or trauma. The As stated, pain from the periodontal ligament space response is inflammation and/or necrosis. is musculoskeletal in character. Chronic pain arising The classic signs of inflammation — heat, swelling, from the periodontal ligament has the ability to refer pain and, of course, pain — may all be manifest as a result of to other structures. The pattern of tooth reference pain pulpal pathology or injury (Byers & Narhi, 1999). The is well documented in the literature (Simons, Travell, & endodontist may also bear witness to the fourth sign ofSimons, 1998). inflammation, redness. Erythema is a classic characteristic From the preceding discussion of dental pain, it may of an inflamed pulp, which may be observed upon itsbe noted that an attempt is made to categorize the various removal during endodontic therapy. Unlike an injury to symptoms as arising from vascular, neurogenous, or musany other part of the body, once inflammation of the dentalculoskeletal origin. This technique is also suggested when pulp begins, the swelling tissue is trapped in the hardconsidering head and facial pain of nondental causes. container and, in effect, has no place to go. An injured or diseased dental pulp may go through several stages, all of which produce pain. These stages HEADACHE of pulpal involvement respond differently to diagnostic testing. The clinically normal pulp is vital to testing proce- “ Headache has been called the most common medical dures, responsive to a variety of excitations, but free ofcomplaint of civilized man”(Dalessio, 1987). If dental spontaneous symptoms. Histologically, it is free of anystructures are not the primary source of facial pain, vascular head, and facial pain, which includes such entities inflammatory changes. Mild irritation of the pulpal tissue, such as causedas migraine and cluster headaches, must be considered by thermal, mechanical, or chemical irritants, maynext. Familiarity with these entities is important because their region of onset often overlaps dental and masticacause a dental pulp to become hyperreactive to stimutory structures. lation. Of these, dental caries or tooth decay is the most The evaluation and management of headache disorfamiliar. In the case of stronger irritants or more ders are adequately discussed in another section of this advanced decay, a transitory hyperemia or reversible text. However, a basic review of various headache disorinflammation may occur (Scimone, 1976). An acute ders that may present as orofacial pain is provided. reversible pulpitis may become chronic and lead to The mechanism of headache of vascular origin is pulpal necrosis and pain. currently best explained as a sterile ammation infl of the Orofacial pain of dentigerous origin may be referred trigeminovascular system (Buzzi & Moskowitz, 1993; throughout the face by such inflamed or diseased teeth. Moskowitz, 1993). Pharmacological management of Various stages of dental caries may provide adequate etithese patients is often possible. Although, it is incumology for these pulpalgias. Therefore, the patient who presents to the physician or dentalfice of with facial pain bent on the dental practitioner to have the ability to recognize migraine, as well as other head or facial pains must have a complete examination of the dentition. fi diagnosis The periodontal membrane, otherwise known as theof vascular origin, the responsibility fornal and treatment of these disorders should be with our periodontal ligament, responds to stimulation in the same medical colleagues. manner as any other ligament. In fact the teeth are attached to the supporting bone by the periodontal ligament, form- It should also be remembered that there are a number ing a synarthrodial joint. Irritation of this generously of painful vascular conditions of the face that either produce pain referred to the teeth or may on occasion affect innervated tissue results in the classic musculoskeletal symptoms of dull, aching pain. This pain is localizable tooral vasculature, thus producing a perception of toothaches or TMD. These include facial migraine, cluster a general area and may be provoked by percussing the headache, angina pectoris, and temporal arteritis. These suspected teeth. Increased pressure on a tooth with a peri-

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conditions must be recognized and treated (Buxbaum, similar ratio. Differential diagnosis of cluster headache Myslinski, & Myers, 1989). includes dental infection and acute pain of the masticatory musculature.

MIGRAINE CHRONIC PAROXYSMAL HEMICRANIA

Included in the classifi cation of vascular disorders that are often confused with masticatory pain are migraineAnother benign headache disorder known as chronic parheadaches. Migraine is an idiopathic, recurring headache oxysmal hemicrania has characteristics similar to cluster. disorder that occurs in attacks that may typically lastWhereas cluster headache occurs more commonly in men, from 4 hours to as many as 3 days. This headache chronic is paroxysmal hemicrania is more common in usually unilateral, moderately severe, and pulsating inwomen. The attacks are more frequent and of shorter duraquality. Migraine is generally aggravated by routine tion but distributed in similar areas as symptoms associated physical activity and may be associated with nausea, with cluster headache. Between attacks, there may be a photophobia, and phonophobia. It is not uncommon forcontinuous, sore feeling in the usually painful areas: the the migraineur to seek a dental consultation for reliefocular–periocular regions, the forehead and temporal area, from what is perceived to be dental or masticatory mus-neck, and shoulders (Sjaastad, 1987). One diagnostic criculature pain. terion of this form of headache is that it is invariably Migraine with aura has similar characteristics, as doesrelieved by indomethacin. Differential diagnosis of chronic migraine without aura. The difference in this case is thatparoxysmal hemicrania is the same as for cluster headache. the headache is normally preceded by a preheadache neurosensorial disturbance. This may be a series of idiopathic, LOWER-HALF MIGRAINE recurring neurological symptoms, which usually develops Other forms of facial pain of vascular origin may include over a 5- to 20-min period and may last less than 1 hour. “Nausea is the complaint of the vast majority of patients;migraine of the midfacial region sometimes called lowervomiting, in addition to nausea, occurs in just over onehalf migraine. Patients with this form of vascular pain report pain in the jaw and neck periorbitally and in the maxilla. half of the patients. These gastrointestinal disturbances usually start sometime after the onset of the pain butThere may be tenderness of the carotid artery (Raskin, 1988, Chapter 11); therefore, this disorder is known as carotidynia occasionally precede the headache” (Raskin, 1988, p. 44). A typical aura may consist of visual disturbances,(Fay, 1932). As with migraine, this condition predominately affects women. The symptoms are of a dull pain with superhemisensory symptoms, hemiparesis, dysphasia, or comimposed throbbing that may occur once or several times binations of these phenomena. Gradual development, duration of less than 1 h, and complete reversibility char-weekly. Exacerbations may last minutes to hours. Differenacterized the aura, which is associated with this form oftial diagnosis includes TMD, pain of the myofascial pain, and masticatory musculature and dental pain. headache. Differential diagnosis of migraine headache includes myalgia, myositis or myofascial pain of the masTENSION-TYPE HEADACHE ticatory musculature, TMDs, and tooth pain. Tension-type headache is described as recurrent episodes of headache lasting minutes to days. The pain is typically pressing or tightening in quality. Discomfort extends into The presentation of cluster headache is classic. Cluster the face and masticatory musculature. Many individuals headache consists of attacks of severe, strictly unilateral describe this sensation as similar to wearing a tight hat. It pain in and around the eye and/or temporal region. This temporal, periorbital pain is frequently confused with ais of mild or moderate intensity, is bilateral in location, and masticatory or dental pain. The attacks may last from adoes not usually worsen with routine physical activity. Nausea is absent, but photophobia and phonophobia may few minutes to as much as 3 h. The attacks occur from be present. once every other day up to eight times per day. They are associated with one or more of the following: conjuncThe patient with tension-type headache may seek the tival injection, lacrimation, nasal congestion, rhinorrhea,advice of a dentist on the referral of a physician. Chronic, forehead and facial sweating, miosis, ptosis, and eyelid muscle tensionlike headaches such as these may have the edema. Attacks occur in series lasting for weeks orcapacity to refer pain to the masticatory structures months. These are the so-called cluster periods. These (Simons, Travell, & Simons, 1998). Again, care should be periods are separated by periods of remission, which may taken to ensure that the patient’ s complaint is truly a result last months or years. Cluster headache predominately of masticatory function and not simply referred to the face affects men in a ratio of 5:1 to women. This is in contrastand jaw from other areas. Differential diagnosis includes to migraine, which predominately affects women in amyofascial pain and dental pain.

CLUSTER HEADACHE

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GIANT CELL (TEMPORAL) ARTERITIS

Myogenous pain disorders affecting the masticatory musculature are no different from those that affect other A discussion of cephalgic and facial pain is not completemusculoskeletal structures. They include, myofascial pain, without some mention of temporal, or giant cell, arteritis.fibromyalgia, myositis, myospasm, and local myalgia. This condition is usually attended by the onset of a new The quality of musculoskeletal pain is deep, constant, headache in an individual of at least 50 years of age. One dull, and occasionally sharp. The most important features or both of the temporal regions are involved. Moderate toof musculoskeletal orofacial pain are that it is made worse severe headache, polymyalgia, and claudication of the maswith movement of the jaws and that the pain is provocable. ticatory muscles may be present. The occurrence of this Movement of the affected joint or muscle can reproduce symptom is signifi cant, because claudication of the masti-musculoskeletal pain. The intensity of pain is true to the catory musculature may be diagnosed as a TMD. There degree of provocation. may be a swollen and tender scalp artery, usually the superIn addition to the increase of pain with physical activficial temporal artery, which unless carefully palpated may ity, chronic pain of the masticatory musculature can refer mimic tenderness of the temporalis muscle. The patient to other areas. Referred pain is the phenomenon of perwith giant cell arteritis may have an elevated red blood cell ception of pain at a site that is not the source of pain. count (RBC) sedimentation rate. A temporal artery biopsy Referred pain is diffuse and poorly localized. Referred is more definitive for giant cell arteritis (Headache Classipain is characteristic of myofascial pain. fication Committee of International Headache Society, 1998). This form of headache must not be overlooked MYOFASCIAL PAIN because it has a potential for dire consequences. Untreated, temporal arteritis may cause blindness, stroke, or death.Myofascial pain is a regional muscle disorder that is the If a patient of 50 years or older presents with a com-most common cause of persistent pain in the head, face, plaint of dull temporal pain, fatigue of the masticatory and neck. It is characterized by one or more hyperirritable muscles, and joint pain and reports headache of recent sites within the muscle called myofascial trigger points. onset, which is chronic, and possibly worsening, temporal A myofascial trigger point is a tender point of localized arteritis must be ruled out. Differential diagnosis includesdeep tenderness located in a taut band of skeletal muscle, myofascial pain and dental pain. tendon, or ligament. Myofascial trigger points are approximately 2 to 5 mm in diameter and when provoked can refer pain to another region known as a zone of reference. The zone of reference is distant from the involved muscle As stated, the dentition and supporting structures of the and may not be in the same dermatome. The pattern of teeth are the primary source of facial pain. If a thoroughpain referral is reproducible and consistent, and serves as dental evaluation eliminates the possibility of odontogenica guide to locate the source of the myofascial pain. pain, and facial pain of vascular origin has been eliminated Myofascial pain is also characterized by increased as a possibility, pain of musculoskeletal origin should bemuscle fatigue and stiffness. The patient may exhibit a considered next. Acute muscle pain is easily diagnosed mildly restricted range of motion. Pain may be elicited and managed; however, the management of chronic muswhen the muscle is stretched. The patient may also report cle pain can be dif ficult. Masticatory pain of musculo- a sense of subjective weakness in the affected muscle or skeletal origin can arise from the TMJs, the masticatorymuscles. Myofascial pain can be localized involving one musculature, or both (Delcanho, 1995). or two myofascial trigger points or generalized due to muscle injury. It may coexist with other conditions such TEMPOROMANDIBULAR DISORDERS as cervical or facet joint injuries. TMD is defined as clinical problems that involve the mas- There are two types of myofascial trigger points. A latent myofascial trigger point is painful at the site of ticatory musculature, the TMJs and associated structures, palpation but is not associated with referred pain. An or both. TMDs are considered the most common musculoskeletal disorder causing orofacial pain. Pain may be ofactive myofascial trigger point is painful at the site of muscular origin arising from the muscles of masticationpalpation and also causes spontaneous referred pain duror referred to the masticatory musculature from cervicaling palpation and muscle use. Myofascial trigger points cycle between an active and a latent state. and/or shoulder structures. Myogenous pain occurs more

MUSCULOSKELETAL PAIN

frequently than articular disorders. Articular disorders of the TMJs often coexist with TEMPOROMANDIBULAR JOINT masticatory muscle pain. Articular disorders of the TMJs Intracapsular disorders of the TMJs result from abnormal include disk displacement disorders, arthritic and degenbiomechanics. To appreciate the complexity of intracapsular erative changes, and neoplasm (AAOP, 1996).

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disorders of the TMJ, a fundamental understanding of nor- Interposed between the condyle and fossa is a fibromal anatomy and biomechanics is required. cartilagenous interarticular disk. This disk is attached to The TMJ is a synovial joint. That is, it is encapsulatedthe mandibular condyle by medial and lateral collateral and stress bearing. It is possibly the most complex jointligaments. This allows the disk to move anteriorly and in the body. The articulating surfaces are covered withposteriorly on the condylar head, but does not allow the fibrocartilage. It is a compound joint with four separatedisk to move away from an intimate contact with the articular surface of the condyle. Attached anteriorly to the articulating surfaces; the superior aspect of the mandibular condyle functions on the inferior surface of the interartic-superior lateral pterygoid muscle and posteriorly to the ular disk. The superior surface of the disk functions onfossa, the disk separates the synovial space of the joint the posterior slope of the articular eminence of the tem-into superior and inferior compartments. poral bone. The disk is unique to this joint. It separates During normal function, the mandibular condyle starts its movement from a closed mouth position with the articthe intracapsular space into an inferior and a superior joint ular disk seated on the posterior slope of the mandibular compartment. These are separate and isolated from one condyle. Movement begins with a rotation of the condyle another by the disk and anterior and posterior attachment against the inferior articular surface of the disk. Translatissue. The retrodiscal tissue, a mass of loosely packed, disk highly innervated and vascularized connective tissue,tion combined with rotation allows the condyle– assembly to slide down the articular eminence to a more occupies the posterior aspect of the joint space. The upperforward and downward position. Translation and rotation most layer of this posterior discal tissue is composed of elastic fibers. This elastic layer composes what is calledallow for full maximum opening. the superior retrodiscal lamina. The interarticular disk is held tightly to the mandibular ABNORMAL BIOMECHANICS condyle by a medial and lateral colateral ligament. These ligaments are intimately incorporated within the capsularTMDs consist of three basic components: limitation of function, joint pain, and joints sounds. Limited function ligament. An injury to the capsule is painful. The position of the disk should be between themay result from muscle guarding or contraction following condyle and the articular eminence during all mandibularoveruse or injury. Contracture, splinting, or spasm of the movements. A displacement of the disk, typically anteriormandibular elevator muscles result in limited mandibular range of motion. Pain is not always present. Limitation of to the condyle, is the cause of most of joint sounds permandibular range of motion due to disk displacement may ceived during joint function. also occur in the absence of pain.

ARTICULAR DISK DISORDERS Intracapsular disorders of the TMJs involve partial or totalNEUROGENOUS PAIN displacement of the articular disk, inflammation of theThe face is the most richly innervated structure of the body retrodiscal tissues, and degenerative changes of the articand represents the majority of input to the somatosensory ular surfaces. cortex of the brain. Facial pain is mediated by the trigeminal nerve. Specifically, nociception is transmitted to the central nervous system via two types of nerves or primary NORMAL BIOMECHANICS afferent nociceptors. These are the thinly myelinated AThe TMJ is a ginglymoid arthrodial joint. It has a rota- delta fibers and the unmyelinated C fibers (Sessle, 1999). tional as well as translatory movement. The mandibular Under normal conditions, primary afferent nocicepcondyle is ovoid in shape, although the shape of thetors are not responsive to nonnoxious stimuli. To stimulate condyle varies from patient to patient and there may be or transduce an action potential, the primary afferent nociasymmetrical condyles in the same patient. ceptive receptor must be activated to threshold by a tissue The ovoid- or football-shaped condyle functions with damaging, or potentially tissue-damaging, stimulus. Such can be via mechanical deformation of tissue, noxthe glenoid fossa of the temporal bone. The fossa is stimuli a ious temperature, or chemical injury. depressed area at the base of the skull that is delineated by the TMJ capsular ligaments. The anterior aspect of When an adequate noxious stimulus is encountered, the fossa includes the articular eminence, a raised rama cascade of events occurs that sensitizes the nociceptive plike structure anterior to the depressed area of the fossa. nerve ending, thereby making it receptive to further stimThe posterior wall of the glenoid fossa is bounded byulation and allowing transmission information to the centhin bone that separates the fossa from the external auditral nervous system. This information is modulated in tory meatus. The lateral aspect of the joints is enclosed the dorsal horn of the spinal chord where it is then within the capsular ligament and the medial aspect oftransmitted to a second-order neuron. The peripheral the joint is osseous. sensitization is the result of the release of a variety of

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excitatory mediators, neuropeptides associated withcondition and provide a more descriptive and diagnostic inflammation, and the endogenous release of additional nomenclature. It is postulated that AO is a neuropathic pain inflammatory mediators such as substance P. The presdisorder (Graff-Radford & Solberg, 1992). Pain, often ence of these neuropeptides in the area of the injury described as burning and spreading, may occur at the site results in the perception of pain for the injured area untilof tooth extraction. Other concomitant factors may include healing occurs. Once the tissue damage has resolved traumatic or injury, various routine dental procedures, endothe noxious stimulus has abated, peripheral sensitization dontic therapy, endodontic surgery on teeth (apicoectomy), ends and pain abates. periodontal surgery, and dental implants (Vickers, Cousins, Walker, & Chisholm, 1998). AO can also follow seemingly innocuous dental proNEUROPATHIC PAIN cedures such as crown preparation, cavity preparation, and The mechanisms underlying neuropathic pain differ fromperiodontal scaling. It is more likely to develop in a tooth those involved in “normal” pain. Neuropathic pain resultsthat was painful prior to dental intervention. from a dysfunction of the transmission system that carries Most patients are 40- to 50-year-old females. AO is nociception from the periphery. Neuropathic pain does notrare in younger age groups. These patients are usually require a noxious stimulus, but may be self-propagating.examined and treated by a number of clinicians before It is maintained by injury or functional abnormalities of being properly diagnosed. They often have a history of many failed dental treatments that serves to perpetuate the the pain transmission system (Pertes & Heir, 1991). Pain pain instead of relieving it. It is not uncommon for a may be severe, have a delayed onset after injury, and patient with AO to have received multiple endodontic therpersist for years or even decades after noxious stimulation apies and surgery, as well as multiple extractions. has ceased and the damaged tissue has healed (Benoliel Clinical characteristics of AO are continuous or almost & Sharav, 1998). Severity and chronicity of neuropathic pain are notcontinuous pain in a tooth or tooth site, with constant, clearly related to a specifi c etiology and may result from a dull, aching pain of moderate to severe intensity. There may be an associated hyperesthesia (tooth is tender to variety of causes. Possible mechanisms for neuropathic pain include continued sensitization of peripheral nociceptivefinger pressure). The clinical findings, chief complaints, and fact that pain has been present for more than 4 months receptors and central neuroplasticity (Sessle, 2000). This suggests the development or activation of aberrant inputs with to no obvious local dental cause lead to this diagnosis. The patient must have a negative clinical examination, central, second-order pain transmission neurons. There can be a loss of afferent inhibition known as deafferentationnormal radiograph, and no history or evidence of significant psychopathology. Somatic nerve block or local anessyndrome. In deafferentation syndrome, nociceptive inputs thesia does not entirely relieve the discomfort. produce an exaggerated response such as seen in postherpetic neuralgia. Neuropathic pain may also include activa- There are several theories for the etiology of this condition that include neurovascular, psychological, and neution of the sympathetic nervous system. In the case of sympathetically maintained pain, dysfunctional pain ropathic diagnoses. It is unlikely that AO is related to migraine, because AO is a continuous pain and migraine transmission cells are sensitized to the activity of the symis episodic. pathetic system and respond with nociception (Sessle, 2000). Neuropathic pain may be characterized by sensory Scientific support for a psychological basis for AO is deficit in the affected region or by pain, which may be lacking. There is no increase in Minnesota Mulitphasic bright, burning, and stimulating. Neuropathic pain mayPersonality Inventory (MMPI) scales when compared with other chronic pain patients. also present as dysesthesia or a mild, uncomfortable but nonpainful sensation, paresthesia, and numbness. Care Deafferentation is the most likely mechanism. Deafmust be taken in evaluating the patient with possibleferentation is the partial or total loss of an afferent nerve supply from a particular area. Trauma to a nerve comneuropathic pain, because differential diagnosis requires the elimination of myofascial and dental pain as themonly follows dental procedures involving the dentin, pulp, or periodontal tissues. Although this type of injury source of the patient’ s symptoms. may be reversible within a short time, in a small percentage of patients (less than 3%) who have undergone a dental ATYPICAL ODONTALGIA procedure, pain persists even after healing has apparently Atypical odontalgia (AO) is a poorly understood chronic occurred. Pain may not appear for weeks, months, or even a year after the procedure. pain disorder that presents as a persistent pain in apparently normal teeth and adjacent oral tissues. It is generally agreed There may also be involvement of the sympathetic that the termatypical odontalgia does not adequately nervous system. Sympathetically maintained pain (SMP) describe this entity. At the time of the writing of this chapter,involves a neuropathology process where the activity of a taxonomy committee is hard at work to better fine dethis the sympathetic system activates injured primary afferent

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nociceptors. Blockade of the sympathetic symptom mayour patients. Where our skills and knowledge fail us is provide relief. Diagnosis of AO requires the elimination where our humanity must begin. any odontogenic causes. If a dental source of the pain is “I think that the lives of all people are linked to each not found, no dental treatment should be initiated. Differ-other. We are always helping and have been helped by ential diagnosis includes trigeminal neuralgia, facial orothers. We can always do something to help. It is not midface migraine, myofascial referred tooth pain, maxil-difficult. Many times it is enough just to say something lary sinusitis, and TMDs. good, give a little attention, listen a little or just smile” (C. Nasri, personal communication, June 1999).

BURNING MOUTH SYNDROME (BMS) REFERENCES A review of the medical and dental literature suggests that over 40% of postmenopausal women suffer from symptoms of burning tongue or mouth. On examination, theseAmerican Academy of Orofacial Pain. (1998). J.P. Okeson (Ed.), Orofacial pain, guidelines for assessment, diagnosis, and patients have negative clinical findings for abnormalities management . Carol Stream, IL: Quintessence Books. or pathology of the oral cavity or mucogingival structures. Arima, T., Svensson, P., & Arendt-Nielsen, L. (1999). ExperiThe only common feature is the history of the onset of mental grinding in healthy subjects: A model for posttheir symptoms after menopause. exercise jaw muscle soreness. Journal of Orofacial Pain, It has been postulated that the etiology for BMS is a 13(2), 104–114. result of changes in estradiol levels that may have a detBell, W. (1980). Lecture notes on Differential diagnosis of facial pain. rimental effect on the function of the special sensory component of CN VII (chorda tympani) (Grushka, Epstein, & Benoliel, R., & Sharav, Y. (1998, November). Neuropathic orofacial pain. Compendium of Continuing Education in Kawale, 2000). Dentistry, 19(11), 1099–1104. Symptoms of intraoral burning are considered idioBuxbaum, J., Myslinski, D., & Myers, D.E. (1989). Dental manpathic. However, a growing body of evidence indicates agement of orofacial pain. In C.D. Tollison (Ed.), Handthat BMS it is a neuropathic disorder resulting from disbook of chronic pain management (pp. 297–319). inhibition of nociception regulated by interactions Baltimore: Williams & Wilkins. between taste centers in the brain and CN-VII, V, and IX.Buzzi, M.G. & Moskowitz, M.A. (1993). The trigemino-vascular BMS has also been associated with hormonal imbalance, system and migraine.Cerebrovascular and Brain trauma, nutritional disorders, and positive psychological Metabolism Reviews,(3), 5 159–177. findings. Conditions that may mimic BMS include dentureByers, M.R., & Narhi, M.V. (1999). Dental injury models: Experirritation, infection, oral lesions, xerostomia, and mouth imental tools for understanding neuroinfl ammatory interbreathing, as well as gastric, rheumatologic, and other actions and polymodal nociceptor functions, Critical Reviews in Oral Biology and Medicine,(1), 10 4–39. disorders. Treatment strategies depend on an accurate Christensen, V. (1971). Facial pain and internal pressure of the diagnosis (Nasri et al., 2000). masseter muscle in experimental bruxism in man. Archives of Oral Biology, 16,102. SUMMARY Costen, J.B. (1934). A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomanComplex chronic orofacial pain syndromes have multiple dibular joint. Annals of Otology, Rhinology, and Larynetiologies and treatment possibilities. When examining gology, 43,1–15. and managing orofacial pain patients, it is important toDalessio, D.J. (Ed.). (1987). Wolff's headache and other head set goals to achieve an acceptable degree of success. The pain (5th ed.). New York: Oxford University Press. first goal is to establish a specifi c diagnosis. This goal Delcanho, R.E. (1995). Masticatory muscle pain: A review of clinical features, research findings and possible mechacan only be achieved if the clinician has a basic undernisms.Australian Prosthodontic Journal, 9, 49–59. standing of, and familiarity with, those conditions that can lead to orofacial pain. Without knowledge of mus-Fay, T. (1932). Atypical facial neuralgia, A syndrome of vascular pain. Annals of Otolaryngology, Rhinology, and Larynculoskeletal and other systemic disorders that may cause gology, 41,1030–1062. orofacial pain, a differential diagnosis cannot be made. Frank, R.G., Jr. (1990). Thomas Willis and his circle: Brain and Having missed the rst fi goal, diagnosis, the treating docmind in seventeenth-century medicine. In G.S. Rousseau tor cannot logically establish the second goal, manage(Ed.), The languages of Psyche: Mind and body in ment of the disorder. When an accurate diagnosis is enlightenment thought . Berkeley: University of Califormade, the correct treatment often becomes apparent nia Press. (Bell, 1980). Graff-Radford, S.B., & Solberg, W.K. (1992). Atypical odontalIn some cases, despite all our best efforts and scientific gia. Journal of Craniomandibular Disorders, (4), 6 knowledge, there are times when we are at a loss to help 260–265.

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Headache(2nd ed.). New York: Grushka, M., Epstein, J., & Kawalc, J. (2001). Burning mouthRaskin, N.H. (1988). Facial pain, Churchill & Livingstone. syndrome. In S. Silverman, Jr., L.R. Eversole, & E. Rosch, P. (2000, September). The eights D’ of chronic pain. Truelove (Eds.), Essentials of oral medicine(pp. Presented at the American Pain Management Society, 354–358). Hamilton, Ontario: B.C. Decker. Las Vegas. Grzesiak, R.C. (1991). Psychologic considerations in temporomandibular dysfunction. A biopsychosocial view of Scimone, F.S. (1976). Bruxism, pulpal pain and restorative material. Dental Survey, 52,62–63. symptom formation.Dental Clinics of North America, Seltzer, S. (1988).Endodontology: Biologic considerations in 35(1), 209–226. endodontic procedures(2nd ed.). Philadelphia: Lea & Headache Classification Committee of the International HeadFebiger. ache Society (1998). Classification and diagnostic criteria for headache disorders, cranial neuralgias andSessle, B.J. (1999). Neural mechanisms and pathways in craniofacial pain. Canadian Journal ofNeurological Scifacial pain.Cephalalgia, 8(Suppl. 7). ences, 26(Suppl. 3), S7–11. Kiester, E., Jr. (1987, December). Doctors close in on the mechSessle, B.J. (2000). Acute and chronic craniofacial pain: Brainanisms behind headache. The Smithsonian Magazine , stem mechanisms of nociceptive transmission and neu175–190. roplasticity, and their clinical correlates.Critical Merrill, R.L. (1997). Orofacial pain mechanisms and their clinReviews in Oral Biology and Medicine,(1), 11 57–91. ical application.Dental Clinics of North America, 41 (2), Simons, D.G., Travell, J.G., & Simons, L. (1998). Myofascial 167–188. pain and dysfunction: The trigger point manual (2nd Moskowitz, M.A. (1993). Neurogenic inflammation in the pathoed., Vol. 1). Baltimore: Lippincott, Williams & Wilkins. physiology and treatment of migraine. Neurology, 43 (6, Sjaastad, O. (1987). Chronic paroxysmal hemicrania and similar Suppl. 3), S16-20. headaches. In D.J. Dalessio (Ed.), Wolff's headache and Nasri, C., Okada, M., Oliveira, M.F., Formigoni, G., Teixeira, other head pain , (5th ed., pp. 131–135). New York: M.J., Siqueira, J.T.T., & Heir, G.M. (2000, May). BurnOxford University Press. ing mouth: A multi-disciplinary assessment . Orofacial Pain Team, Division of Dentistry, Hospital das Clínicas, Vickers, E.R., Cousins, M.J., Walker, S., & Chisholm, K. (1998). Analysis of 50 patients with atypical odontalgia. A preMedical School of the University of São Paulo, Brazil. liminary report on pharmacological procedures for diagPaper presented at the International Congress on Orofanosis and treatment. Oral Surgery, Oral Medicine, Oral cial Pain, Seoul, Korea. Pathology, Oral Radiology and Endodontics, (1), 85 Ogilvie, A.L. (1969). Histology of the dental pulp. In J.L. Ingle 24–32. (Ed.), Endodontics . Philadelphia: Lea & Febiger. . London: Pertes, R.A., & Heir, G.M. (1991). Chronic orofacial pain. A Wall, P.D. (1999). Pain: The science of suffering Weidenfelf & Nicolson. practical approach to differential diagnosis. Dental ClinWolff, H.G. (1948).Wolff’s headache and other head pain . New ics of North America, 35 (1), 123–140. York: Oxford University Press.

14 Chinese Medicine and Acupuncture for Pain Management in HIV/AIDS Misha R. Cohen, O.M.D., L.Ac. CHINESE TRADITIONAL MEDICINE IN PAIN MANAGEMENT

ISSUES IN HIV/AIDS PAIN MANAGEMENT

In my experience, for the last 17 years of working with Acupuncture and other forms of Chinese traditional med-people with AIDS, the assembly of a comprehensive care team is central to the treatment of people with HIV/AIDS icine have been used for centuries to treat acute pain due to trauma, chronic pain due to injuries, and pain fromwho are dealing with various pain syndromes. The person in charge is the person with HIV/AIDS, who is the captain organic illnesses. In Chinese traditional medicine, pain is often associ-of the healing team. ated with imbalances within the body that lead to a slow- In conjunction with the captain, there is the need to ing down or blockage of the body’s energy (Qi). This isdevelop a whole and unified team, which may include a known as Stagnant or Stuck Qi or with the blockage ofnumber of practitioners as well as caregivers. In pain management in HIV/AIDS, it is important that there be Blood (Xue) due to an acute trauma or a worsening of the an integrated approach because pain syndromes are often Stagnant Qi. difficult to manage successfully and there is a relationship Pain can also be related to Damp accumulating in the Channels, to deficient Qi and Xue, to Stagnation of Cold,to the overall treatment plan for HIV/AIDS. If a person with AIDS is in pain, it is difficult to manage other aspects or to association with Heat or Damp Heat. of care, and vice versa. For example, peripheral neuropathy can be associated in the early stages with Damp in the Channels (associated Therefore, the pain management team would with numbness), later with Heat or Cold, and — as it getsinclude the person with HIV/AIDS as the captain; at least one Western physician; and then other members worse — Qi and Xue Deficiency-type numbness. The most commonly used treatment in Chinese tradi-would be included such as a licensed acupuncturist and tional medicine and acupuncture is to unblock the Qi orherbalist, a massage therapist, a physical therapist, an Xue to relieve the pain. However, removing Dampness,occupational therapist, a chiropractor, an osteopathic clearing Heat, and resolving Damp Heat may also bephysician, and a psychologist. treatment principles for pain management. In HIV/AIDS, it is important to always have a Western baseline for ongoing care and treatment. Some pain may Western science has documented some ways in which be resolved through changes in medications (sometimes acupuncture relieves pain — there are several mechanisms. The most notable is through stimulation of endor-added, sometimes subtracted). Often the pain can be assophins. Another mechanism is through stimulation of sero-ciated with opportunistic infections that need to be treated tonin levels within the brain, which leads to a sense ofwith pharmaceuticals or herbal medicine. Neurological pain, for example, may be mitigated through medication, well-being as well as pain relief. 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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herbs, acupuncture, other modalities, or a combination of several modalities.

CHINESE TRADITIONAL MEDICINE (CTM) EVALUATION AND TREATMENTS When using Chinese traditional medicine as a main form of treatment in HIV/AIDS related pain syndromes, some or all of the following comprehensive protocols could be adopted:

• Abdominal pain (which may be associated with diarrhea or opportunistic infections) • Sinus pain/headaches (which may occur as part of chronic sinusitis) • Peripheral neuropathy (which can include pain and numbness) • Joint pain (which may be associated both with various viral coinfections or are a result of drug side effects)

HIV ASSOCIATED PERIPHERAL NEUROPATHY

• • • • • • • •

Evaluation/diagnosis Acupuncture Moxibustion Chinese herbal medicine Qi Gong/other exercises Professional massage Meditation Food therapy

Acupuncture is used in the clinic in conjunction with other therapies for treatment of peripheral neuropathy in people with HIV/AIDS. There have been varying studies on its use. Unfortunately, none have been well designed and undertaken long enough to show conclusive results. However, our clinical observations give us the direction for further study. The following studies are examples of some research Chinese medicine is a complete medical system with to date. its own forms of diagnosis, treatment, prognosis, and therapies. Chinese medicine treatments address disharmonies using acupuncture, moxibustion, food therapy/diet, herbalRESEARCH remedies, Chinese exercise, and meditation along with A PILOT STUDY OF ACUPUNCTURE FOR THE Western therapies. Acupunctureis the art of inserting fine sterile metal SYMPTOMATIC TREATMENT OF HIV ASSOCIATED needles into certain body or ear points to control thePERIPHERAL NEUROPATHY* body’s energy flow. Acupuncture is relatively painless, often accompanied with a sensation of heaviness, warmth, • The objective is to study the outcome of patients or movement of energy at the point of insertion or along receiving acupuncture treatment for the sympthe energy channels. Acupuncture helps to relieve pain as tomatic treatment of HIV-related peripheral well as rebalance energy and heal symptoms. Electrostimneuropathy, not due to drug toxicity. We evalulation may also be used with acupuncture for pain. uated objective and subjective nerve function and quality of life measurements. Moxibustionis the burning of the common herb mugwort over areas of the body for stimulation or warmth. • Methods include 39 patients receiving acupuncHeat packs may also be used during treatment. ture twice weekly for 6 months in a nonranChinese herbal medicine can be used for all types of domized observational study. No particular disease. There are thousands of Chinese herbs. Usually prescription was used, with the treatment they are put together into formulas to have the most effect. choice left to the practitioner’ s discretion. Neurological and QOL assessments were comExerciseincludes martial arts as well as more subtle pleted at entry, months 2 and 6. movement such as Tai Ji, Qi Gong, and Yoga. Gym workouts or aerobic exercise are also suggested. • In summary, 26 patients returned for the first follow-up at 2 months. The 13 lost to followMeditation may include traditional Asian forms as up had more severe neuropathy and lower QOL well as relaxation exercises, hypnotherapy, and biofeedscores than those who completed the treatment. back.Massageincludes meridian pressure such as Shiatsu, Qi Gong, or Thai massage or muscle massage. Food ther• Significant improvement was found for QST of apy focuses on improving digestion, increasing energy, the toe (p = 0.05). No trends were found in a and balancing body energy. Food therapy often increases subjective symptom list. Five of seven QOL the effect of other treatments. scales showed improved (none were signi ficant). • In discussion, this study suggests that there may be a role for acupuncture as a treatment ACUPUNCTURE IN HIV PAIN MANAGEMENT Acupuncture is often used in HIV/AIDS for various kinds * Jonathan Ammen, AMFAR study 1991–1992, and Chinese Medicine Conference 1994. of pain management.

reported at HIV/AIDS

Chinese Medicine and Acupuncture for Pain Management in HIV/AIDS

for peripheral neuropathy… future controlled studies may help further defi ne the efficacy of this method. This 1994 pilot study shows potential to study peripheral neuropathy using traditional Chinese medicine diagnosis and treatment. However, the pilot was too short and uncontrolled to lead to any real conclusion. It is likely that in neuropathy, 8 weeks is too short a time to really see statistically signifi cant differences. However, the conclusion appears to be consistent with this observation.

CHINESE MEDICINE IN THE TREATMENT PERIPHERAL NEUROPATHY*

OF

• The issue is that peripheral neuropathy in the HIV/AIDS population is a serious and debilitating problem that requires an effective treatment protocol. • The project at Quan Yin Healing Arts Center — a nonprofit community-based complementary medicine clinic that has delivered Chinese medicine for over 16 years in San Francisco — involved 533 HIV/AIDS clients treated in 1996, which included 66% of its client base. Over 75% of the people with HIV/AIDS at Quan Yin Healing Arts Center presented with peripheral neuropathy, from mild to severely debilitating. All women and men with neuropathy received a combination of treatments including one or more of the following interventions: acupuncture, electroacupuncture, massage therapy, moxibustion (an herbal heat therapy), and herbal medicine. Clients received treatment in time intervals from twice a month to three times a week. • Results were chart reviews and surveys conducted by the executive director, revealing that over 75% of HIV + clients who were reviewed had reduced symptoms including decreased pain, reduced numbness, and increased mobility (including walking/running when unable to do so previously). Variations in response were related to total number of treatments, number of weeks of treatment, compliance with selfcare (such as self-moxibustion), and combination of medications that caused neuropathy. Some patients were able to discontinue treatments for neuropathy after several sessions because they no longer had neuropathy-related complaints. Others needed ongoing care for *

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neuropathy, especially those who continued on drug combinations that are highly likely to cause neuropathy. • Lessons learned include a combination of Chinese medicine therapies that appears to have a high effect rate in decreasing symptoms in HIV+ people with the serious debilitating problem of peripheral neuropathy. With the apparent rate of clinical success in a large number of clients, a controlled pilot study is recommended as a follow-up to this chart review and collection of surveys.

BODY ACUPUNCTURE IN HIV-RELATED PAIN SYNDROMES BY CONDITION • General pain: Liver 3, Large Intestine 4 (Four Gates) • Abdominal pain: Ren 12, Stomach 25, Liver 5, Zigong, Ren 4, Ren 6 • Epigastric pain: Ren 14, Ren 12, Stomach 34, Spleen 4, Spleen 6 • Sinus pain: Bitong, Yintang, Large Intestine 4, Large Intestine 20, Gallbladder 20, Du 23, Urinary Bladder 2, Stomach 3 • Hand neuropathy: Large Intestine 4, Zhongwan, Bafeng, San Jiao 5 • Foot neuropathy: Liver 3, Stomach 41, Spleen 6, Baxie • Muscle pain whole body: Spleen 21 • Liver/costal pain: Liver 14, Gallbladder 24, Liver 13, Japanese Mu Points • Herpes Zoster /Shingles: Liver 2, Liver 5, Surround the Dragon in the local area

BODY ACUPUNCTURE IN HIV-RELATED PERIPHERAL NEUROPATHY BY CTM SYNDROMES • Four Gates for Pain: Liver 3, Large Intestine 4 • Damp in the Channels: Spleen 6, Spleen 9 • Deficient Qi and Xue: Stomach 36, Spleen 6, Kidney 3, Spleen 4 • Stagnant Xue: Spleen 10, Large Intestine 11, Spleen 6 • Stagnant Cold: Ren 6, Kidney 7 • Heat and Damp Heat: Liver 2, Liver 5, Large Intestine 11

BODY ACUPUNCTURE PAIN SYNDROMES

Carla Wilson, Executive Director, Quan Yin Healing Arts Center, Poster Session, 12th International AIDS Conference, Geneva, 1998.

IN

HIV-RELATED

• Four Gates for Pain: Liver 3, Large Intestine 4 • Damp in the Channels: Spleen 6, Spleen 9

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Heel

Finger

Toe

Liver Yang

Ankle Knee

External Genital

Shenmen Hip Sa cr Sympathetic al Buttock

Ischium

C

Sm

C e r vica l Ve r teb

al l in te st ar in da Qu c oder e um

Ur e Ki ter dn ey

s d ry ea ad ina r cr llbl Ur dde n a Blae Pa G rg La tine ix Liver es nd Chest int pe p A us ag h Spleen op Es Trachea Heart

Lung

Nose

rae

Burn

Elbow Thoracic Vertebrae

Shoulder

Clavicle

Occiput Temple Forehead

U Superior Ear Root

Heart

Lower Back

Jaw

loo

rB

e pp

Spiral Cord Tongue

re

su

es

r dP

er

Brain

Triple

Lumbo-sacral Vertebrae br ae

te

rtebrae

Pharynx and Larynx

Ve r er

Stomach

Lower Portion of Rectum

Wrist

Thoracic Ve

Urethra

Internal Nose

Internal Tubercle

Middle

Blood

ure

Press

Face Anterior Ear Lobe

Eye

Middle Back

Cheek Inner Ear

Spleen

Lower Blood Pressure Liver

Lung Upper Back Tonsils

Ear Acupuncture Points

Kidney Lower Root of the Ear

Back of Ear

FIGURE 14.1 Ear acupuncture points. (From Cohen, M. (1996). The Chinese Way to Healing: Many Paths to Wholeness . New York: Perigree. With permission.)

• Deficient Qi and Xue: Stomach 36, Spleen 6, Moxibustion (Figure 14.2) can be used in the following ways: Kidney 3, Spleen 4 • Stagnant Xue: Spleen 10, Large Intestine 11, • We can use it over areas of pain. Spleen 6 • We can use moxa on the same points as in • Stagnant Cold: Ren 6, Kidney 7 acupuncture. • Heat and Damp Heat: Liver 2, Liver 5, • For abdominal pain, we often use cones of moxa Large Intestine 11 on salt and the herb aconite or ginger over the navel on the point Ren 8. For details, see The EAR ACUPUNCTURE IN HIV/AIDS-RELATED Chinese Way to Healing (Perigee, 1996) or The PAIN SYNDROMES HIV Wellness Sourcebook (Henry Holt, 1998) • Moxibustion is generally contraindicated with • Overall pain: Ear-Shen-Men, Ear-Sympathetic, heat or damp heat syndromes, although there Ear-Brain are exceptions such as abdominal cramping • Choice of other points according to the area in related to damp heat type of chronic diarrhea the ear associated with the organ or body part because there is always an underlying spleen (Figure 14.1) deficiency (Figure 14.3)

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HERBS FOR PAIN SYNDROMES IN HIV/AIDS ABDOMINAL PAIN • Channel flow— Qi and Xue Stagnation with Cold • Source Qi — for diarrhea accompanied by bloating and abdominal pain; used for the Chinese diagnosis of Spleen Qi and Yang Deficiency diarrhea with Cold

HERPES ZOSTER/SHINGLES In this case we treat the underlying condition of Damp Heat or Liver Heat of Heat in the Xue (Blood) with formulas such as: • Long Dan Xie Gan Tang • Coptis Purge Fire • Clear Heat

FIGURE 14.2 Moxibustion in HIV-related pain syndromes. (From Cohen, M. (1996).The Chinese Way to Healing : Many Paths to Wholeness . New York: Perigree. With permission.)

Peripheral Neuropathy Cold: Mobility 3 with Channel Flow Heat: Mobility 2 with Channel Flow Damp in Channels: Shu Gan Wan Damp Heat: Long Dan Xie Gan Tan or Coptis Purge Fire Qi and Xue Stagnation with Cold: Channel Flow Qi and Xue Deficiency: Eight Precious Pills FIGURE 14.3 Abdominal treatment with navel. (From Cohen, M. (1996).The Chinese Way to Healing : Many Paths to Whole ness. New York: Perigree . With permission.)

CHINESE HERBAL MEDICINE FOR HIV/AIDS

MASSAGE/ACUPRESSURE FOR HIV/AIDS PAIN EAR ACUPRESSURE

The following formulas are examples that we use in the Chinese traditional medicine clinic on a regular basis for regulating the immune system and for differential diagnosis.

• Stimulates the specific points that correspond to the areas of the body where there is pain • Also uses Ear-Sympathetic and Ear-ShenMen

(See Figure 14.1)

IMMUNE MODULATION BODY ACUPRESSURE • Enhancement — tonifies Qi, Xue, Jing; strengthens Marrow and Spleen/Stomach/Kidney; clears Heat and toxins • Tremella American Ginseng — tones Yin, Qi, X u e , J i n g ; s t r e n g t h e n s M a r r ow a n d Spleen/Stomach; clears Heat and toxins • Cordyseng— strengthens Qi, tones Yin and Yang, and strengthens the Spleen, Stomach, Kidney, and Lung

• For upper back and shoulder problems — Pericardium 6, Small Intestine 11 • For tendons, muscle pain, and tightness — Gallbladder 34 • For pain in the head and abdomen — Large Intestine 4 • To relieve Liver Qi stagnation — Liver 3 • Chest and abdomen pain — Pericardium 6

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PATIENT SELF-CARE TREATMENT FOR ACHES, PAINS, AND FIBROMYALGIA

Acupressure points follow: • For upper back and shoulder problems — Pericardium 6; Small Intestine 11 • For tendons, muscle pain, and tightness — Gallbladder 34 • For pain in the head and abdomen — Large Intestine 4 • To relieve Liver Qi Stagnation — Liver 3

STEP ONE: STRETCHING OUT • With chronic pain, aerobic or weight-bearing exercise can be overstimulating or aggravating to sore joints and muscles. However, gentle Qi Gong exercises can dispel tension and help you relax. • It may also help to do mild stretching exercises, head rolls, hamstring stretches, or perhaps the Yoga routine called Bow to the Sun that gently massages each part of the body. • A mild full-body massage is also a terrific way to relax and extend tense muscles and joints, but be careful not to overstimulate or irritate the nerves and muscles. Avoid intense Shiatsu-style massage. • If your diagnosis indicates Dampness, Cold, and Deficiency, massage with warming and stimulating oils infused with cinnamon essential oil. • Meditation and the practice of mindfulness — being in the moment and quieting the mind — keeps the mind from amplifying or fixating on pain.

For ear acupuncture, stimulate the specific points that correspond to the areas of the body where there is pain. Also use Ear-Sympathetic and Ear-ShenMen. (See Figure 14.1.) Moxibustion can be applied on any area where there is pain without inflammation or redness.

ACUPUNCTURE GUIDE FOR PRACTITIONERS

For all pain, especially Stagnant Qi — Four Gates: Liver 3, Large Intestine 4 For pain related to Damp in the Channels — Spleen 6, Spleen 9 For pain related to deficient Qi and Xue — Stomach 36, Spleen 6, Kidney 3, Spleen 4 For pain related to stagnant Xue — Spleen 10, Large Intestine 11, Spleen 6 For pain related to stagnant Cold — Ren 6, Kidney 7 STEP TWO: FEEL THE WARMTH For pain related to Heat or Damp Heat — Liver 2, If you have not been diagnosed with a Heat disorder, and Liver 5, Large Intestine 11 do not have a skin rash or fever, you may find hot herbal compresses are very soothing. They come premade at MOXIBUSTION IN THE CLINIC health supply stores and herbal outlets, but you can make AND FOR SELF-CARE them at home. • Combine one cup fresh rosemary, thyme, and mint. • Wrap in a double ply piece of cheesecloth. Secure the ends. • Immerse the cheesecloth package in a pot of boiling water. • Remove from water and wrap in thick towel. • Place on your sore joints or muscles until the towel cools.

STEP THREE: GETTING

TO THE

POINT

Moxibustion is especially good over areas of pain as well as appropriate points. Moxa on the same points as listed in the preceding acupuncture guide — unless diagnosis is Heat or Damp Heat. Then moxa is not recommended.

REFERENCES Cohen, M. (1996).The Chinese way to healing: Many paths to wellness. New York: Perigee. Cohen, M. (1998).The HIV wellness sourcebook . New York: Henry Holt.

Acupressure and moxibustion to ease pain can be done by your practitioner or at home. If you cannot reach these points yourself, use a partner to lend a hand.

15 Mild Traumatic Brain Injury and Pain Gary W. Jay, M.D., F.A.A.P.M., D.A.A.P.M. There are a number of factors that must be considered The most common cognitive, emotional, and behavwhen one clinically evaluates and treats a patient with a ioral deficits include mild or minor traumatic brain injury (MTBI) and pain. The literature is rife with overbroad terminology that • Memory impairment when dissected makes little sense. Words are used syn- • Lack of initiative onymously when they most probably should not be. Most • Depression specifically, in many papers, MTBI is felt to be the same • Problemsfinding work as the postconcussive syndrome. When looking at the • Irritability etiology of specific problems encountered by these • Decreased ability to concentrate patients, it appears to this author that “lumping,” instead • Anxiety of looking more specifically at both nomenclature and • Poor impulse control what each term entails, and why is extremely important. • Loss of self-esteem Therefore, prior to looking at MTBI, specifi cally its • Slowed behavioral processing pathophysiology and how that affects pain, “ ” we look at • Job loss/disruption the postconcussion syndrome (PCS). • Behavioral/personality changes • Denial • Perseveration POSTCONCUSSION SYNDROME • Difficulties with social interactions and family The PCS appears to include multiple signs and symprelationships toms consisting of neuropathological, neurophysiological, and neuropsychological as well as physical and The PCS can be both chronic and disabling, or short psychological or emotional aspects secondary to MTBIlived and benign. A possible explanation for this may be (Binder, 1986). the interaction between organic and psychological factors The most common medical problems found in the(Bohnen & Jolles, 1992). It is very dif ficult to differentiate patient with PCS (and MTBI) include between the effects of primary neurological, neurophysi• • • • • •

ological, and neuropathological injury and secondary psyPosttraumatic headache chosocial factors. It is thought by some that the typical Posttraumatic musculoskeletal pain syndromes PCS symptoms, including headache, dizziness, and irritaVestibular disturbance bility, result from emotional stress associated with diminVisual disturbance ished cognitive performance secondary to minor acquired Fatigue traumatic brain injury (MATBI) (Bohnen, Twijnstra, & Posttraumatic seizure disorder Jolles, 1992).

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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to the patient’ s interpretation of the effect of the trauma than The influence of accident mechanisms associated with to objective “indicators of brain injury severity. ” more severe symptoms was studied and it was found that patients with more severe deficits at the time of a motor Landy (1998) looked at the more objective symptoms of headache and cervical pain and found that 70% of vehicle accident had been an unprepared occupant, had been in a rear-end collision, with or without subsequentpatients “ get better” within a few weeks post-MVA, frontal impact; and had a rotated or inclined head positionwhereas about 30% continued to complain of headaches at the moment of impact (Sturzenegger, DiStefano,and/or cervical pain. He felt that prolonged management and slow court settlement lead to extensive introspection Radanov, & Schnidrig, 1994). The postconcussional disorder (PCD) has beenby the patient and thus prolongation of symptoms. His accepted into and is found in an appendix of the DSM-results also repeat the long-held knowledge that patients IV. A major criterion is loss of consciousness (Anderson,with more severe head or neck injury have a lessor incidence of chronic posttraumatic headaches or cervical 1996), and it is believed that it would be better to use the Brain Injury Special Interest Group (BISIG) definition symptoms. Barrett, Ward, Boughey, et al. (1994) compared two from the American Congress of Rehabilitation Medicine groups of PCS patients, one of which was hospitalized for (Kay, et al., 1993). This definition states: A patient with observation following a brief loss of consciousness, while mild traumatic brain injury is a person who has had a the others went to the emergency department, and then traumatically induced physiological disruption of brain home. It was found during follow-up at 2 and 12 weeks function, as manifested by at least one of the following that the type and frequency of complaints were similar in (Kay, et al., 1993): both groups. However, at 12 weeks, the number of complaints/symptoms was significantly less in the group of 1. Any period of loss of consciousness hospitalized patients. 2. Any loss of memory of events immediately Several groups noted that the PCS was more frebefore or after the accident quently found after blunt head trauma and other trauma, 3. Any alteration in mental state at the time of the than would have been predicted (Chambers, Cohen, Hemaccident (e.g., feeling dazed, disoriented, or minger, et al., 1996; Szymanski & Linn, 1992). confused) By using a questionnaire, Bohnen, Van Zutphen, 4. Focal neurological deficit(s) that may or may Twijnstra, et al. (1994) evaluated the longevity of longnot be transient term PCS complaints. Their results indicated that MTBI might not, in a percentage of patients, ever resolve. The severity of the injury does not exceed: In an attempt to evaluate the importance of psychological factors in the outcome of whiplash injuries, Mayou 1. Loss of consciousness of approximately 30 min and Bryant (1997) utilized interviews at 3 and 12 months or less postinjury. The majority of the patients in their study 2. After 30 min, an initial Glasgow Coma Scale continued to complain of persistent cervical symptoms, of 13 to 15 was found whereas a “sizable minority” reported specific posttrau3. Posttraumatic amnesia of not greater than 24 h matic psychological symptoms, such as intrusive memories and phobic travel anxiety; and this was belived to be “similar to those described by patients suffering multiple Note that the definition includes patients who experi-injuries.” They concluded that travel, social, and psychoence direct head trauma as well asthose who suffer an logical morbidity were more prevalent than previously acceleration/deceleration injury (whiplash) without spe-recognized. They did not deal with the issue of the reccific direct head trauma. Loss of consciousness notisa ognized posttraumatic stress disorder (PTSD). clinical requisite for a classification of MTBI. It is also Cicerone and Kalmar (1997) urged clinicians to use a noted that the symptoms of MTBI (or MATBI) may last great deal of caution before attributing PCS symptoms or varying lengths of time and can consist of persistent physneuropsychological deficits to a preexisting affective disical, emotional, cognitive, and behavioral symptoms thatorder. Leininger, Gramling, Farrell, et al. (1990) looked may produce a behavioral disability (Kay, et al., 1993).into the idea that MTBI patients do not develop persistent This is our operational definition of MTBI. neuropsychological deficits. They found that patients with Many researchers have looked for a primary psycho-the PCS/MTBI had measurable neuropsychological defilogical/emotional etiology for the PCS (Karzmark, Hall, & cits and the severity of these deficits was independent of gross neurological status immediately postinjury. Englander, 1995). Gasquoine (1997) felt that symptom persistence was associated with increased emotional distress. Looking at symptomatic patients 2 years post-whipHe does note that this fact is also true in patients with severe lash injury, DiStefano and Radanov (1995) evaluated head injury as well as back injury, and that it relates morecomplaints of memory and attentional ficulties dif with

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neuropsychological testing. They found that memorysional activity, memory defi cits, headache, dizziness and problems were minimal, whereas problems in selectivevertigo, behavioral and emotional disturbances, and aspects of attentional functioning after whiplash wereother neurological symptoms. Initially, all three evoked present, and these could explain the patients ’ cognitive potentials were abnormal, showing prolonged latencies, complaints and induce adaptational problems in daily life.indicative of disseminated axonal damage. Only the An interesting study was performed by Parker andMLEAPs correlated to outcome at 3 months, particularly in its psychocognitive aspects, suggesting that organic Rosenblum (1996) who looked at intelligence and personp araventricular primary damage may ality difficulties after whiplash or MTBI in adults, an diencephalic– account for the presence of the PCS. average of 20 months post-motor vehicle accident (MVA). Positron emission tomography (PET), single photon They found a mean loss of 14 points of full-scale IQ from emission computed tomography (SPECT), and magnetic the estimated preinjury baseline (using WAIS-R) with no resonance imaging (MRI) studies have been done to evidence of recovery. They also found a number of perattempt to correlate cerebral dysfunction to PCS sympsonality dysfunctions including organic or cerebral pertoms. PET looks at glucose metabolism (in these studies), sonality disorder. Of 33 patients, 30 had psychiatric diagwhile SPECT looks at cerebral perfusion. noses including PTSD, psychodynamic reactions to impairment, and persistent altered consciousness. They Six patients with PCS and 12 normal controls were concluded that cognitive loss was induced by the interactested. The patient group had significant hypometabolism tion of brain injury with “distractions” including pain and and hypoperfusion in the bilateral parietooccipital regions, emotional distress. This report also repeated the fact that as compared with the controls. In some patients there was the presence of MTBI after MVAs was probably consis-also hypometabolism found in other regions. It was tently underestimated. hypothesized that parietooccipital hypometabolism can be caused by activation of nociceptive afferent nerves from Although the PCS has been thought of as a reflection of the psychological response to injury, there is consider-the upper cervical spine (Otte, Ettlin, Nitzsche, et al., 1997). able evidence suggesting that the PCS is primarily a physAnother study examined 13 patients with late whipiological disturbance (Szymanski & Linn, 1992). Reaction syndrome, using PET and SPECT. The authors did time testing, for example, has been used to support lash a not find hypometabolism in the parietotemporooccipital structural, organic etiology for the PCS (Jacobson, Gaadsregions. They didfind hypometabolism in the frontopolar gaard, Thomsen, & Henriksen, 1987). It has been found that cervical injury likely contributes and lateral temporal cortex and in the putamen. They did to the symptomatology post-PCS/MTBI and vice versanot recommend that PET or SPECT be used as a diagnos(Barrett, Buxton, Redmond, et al., 1995). Testing hastic tool for routine examination of patients with late whipshown that cervical injuries secondary to whiplash canlash syndrome (Bicik, Radonov, Schafer, et al., 1998). induce a distortion of the posture control system as a result SPECT was compared with MRI/computerized axial of disorganized cervical proprioceptive activity (Gimse, tomography (CAT) scans in 43 patients. The SPECT was Tjell, Bjorgen, & Saunte, 1996). Others note that restrictedfound to be abnormal in 53% of patients, MRI was abnorcervical movements and changes in the quality of propri-mal in 9%, and CAT scan was abnormal in 4.6% of oceptive information from the cervical spine region affectpatients post-MTBI/PCS. The SPECT scan appeared to voluntary eye movements. Acceleration/decelerationbe more sensitive to post-MTBI changes, especially in (flexion/extension) injury to the neck secondary to whip-patients with the persistent PCS (see later) than MRI or lash may result in a dysfunction of the proprioceptiveCAT scan. No statistical relationships were found between system. Oculomotor dysfunction after cervical traumathe SPECT scan results and age, previous psychiatric history, history of substance abuse, history of multiple MTBI, may therefore be related to disturbances in cervical afferent input (Heikkila & Wenngren, 1998). Patients who haveor concurrent neuropsychological symptoms (Kant, Smith-Seemiller, Isaac, & Duffy, 1997). sustained head or cervical trauma appear to exhibit an increased reliance on accurate visual input and are unable “ The truth is out there, ” but we do not seem to have to utilize vestibular orienting information to resolve con- determined the best method of identifying it. The tests flicting information from the visual and somatosensorynoted earlier were given to patients with the PCS, by author systems (Rubin, Woolley, Dailey, & Goebel, 1995). statement. The relationship between the PCS and MTBI is Soustiel, Hafner, Chistyakov, et al. (1995) evaluateddiscussed later, and the situation may not be that simple. 40 patients post-mild head trauma using brain stem Nosologically, it is difficult to determine exactly what trigeminal and brain stem auditory evoked potentialsconstitutes the PCS. Evans (1992) states that the PCS (BTEP, BAEP) and middle-latency auditory evoked refers to the large number of signs and symptoms found potentials (MLAEP) within 48 h of injury and again at alone or in combination following MATBI, including 3 months. They defi ned PCS as the presence of at leastheadache, memory problems, dizziness, fatigue, irritabilfour of the following: failure to resume previous profes- ity, anxiety, insomnia, and sensitivity to light and sound.

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He further indicates that studies have substantiated the ander believes, are secondary to neuronal injury, whereas existence of the PCS and that it is common, with resolu-the headache may be secondary to cervical injury, neution in 3 to 6 months, but with persistent symptoms andronal injury, or a combination; cervical pain secondary cognitive deficits persisting for months or years. to soft tissue problems; dizziness secondary to peripheral Headache, dizziness, and memory cits defi are the vestibular dysfunction or cervical injury; and anxiety, most common combination of PCS symptoms (Young,moodiness, and irritability secondary to neurological 1985). There is no specifi c symptom complex found in injury, pain, and/or psychological factors. the majority of patients with acute or chronic PCS (Alves The term PCS, in the author’s opinion, should not & Jane, 1990). The multiplicity of signs and symptomsinclude central nervous system (CNS) deficits. Vestibular dysfunction secondary to brain stem injury should be of the PCS have been well documented (Bohnen & Jolles, 1992; Brenner, Friedman, Merritt, & Denny-Brown, included in the MTBI, whereas peripheral dysfunction 1944; Brenner & Gillingham, 1974; Hoganson, Sachs,would be a part of the PCS. These differences are most Desai, & Whitman, 1984; Jones, 1974; Oddy, Humphrey,important when planning and executing an appropriate & Uttley, 1978; Rimel & Jane, 1985; Ritchie, 1974; Ruth- treatment plan/paradigm. This appears to be more impordif obtaining insurerford, Merrett, & McDonald, 1977; Symonds, 1965; tant when one encounters theficulties ance approval to treat an ailment (MATBI) that some Young, 1985). insurers do not even believe exists. One group has suggested that the PCS should include all the consequences of head injury, regardless of its sever- To the extent plasticity allows, neuronal recovery is ity and the nature of the injury (Rutherford, Merrett, & certainly taking place at 1 month after injury (Dikmen, McLean, Temkin, et al., 1986; Elson & Ward, 1994; GenMcDonald, 1978–1979). Berrol (1992) states that the term mild traumatic brain tilini, Michelli, & Shoenhuber, 1985; McLean, Dikmen, injury (MTBI) is preferable, because it identifies the eti- Temkin, et al., 1984; Stuss, Stethem, Hugenholtz, et al., ology of the injury, its degree, and the pathological sub-1989). Neurological recovery is thought to be “substanstrate much better than other past terms: minor head tial,” by some, at 3 months (Levin, Mattis, Ruff, et al., injury, traumatic head syndrome , postconcussive syn- 1987). At this point postinjury, 30 to 50% of patients have drome, posttraumatic syndrome , postbrain-injury syn- continued complaints (Dikemen, Temkin, & Armsden, 1989). Over the next 6 to 12 months (longer than a year drome, and traumatic cephalgia . The term postconcussive syndrome (PCS) continues postinjury) most patients show continued improvement to be frequently used in the literature. The important noso-and “recovery” (McFlynn, Montgomery, Feuton, & Rutherford, 1984). logical question is whether the PCS is secondary to the It has been found that even “well-recovered” patients MTBI, or the cognitive/neurological deficits found after are still susceptible to periodic impairments secondary to MTBI are a separate entity. physiological or psychological stress (Ewing, McCarthy, The termPCS would then encompass the nonneuroGronwall, et al., 1980; Gronwall & Wrightson, 1974), logical, neurocognitive, and neurophysiological deficits, which indicates that recovery is most likely the wrong leaving PCS to be used specifically for the other organ term. That these patients have “compensated” for their (noncerebral) systems that display posttraumatic signs and injury may be more nearly correct. To say that patients symptoms. may have a permanent sense of decreased mental or cogTeleologically, it appears to make more sense to sepnitive efficiency (Stuss, Ely, Hugenholtz, et al., 1985) arate the etiologies of the problems encountered postwould also be a function of incorrect terminology (i.e., MATBI. A patient with physical findings such as posttraurecovered vs. compensated). matic headache may indeed, posttrauma, have a PCS. Patients with neurocognitive deficits and other neurological difficulties have direct evidence of an MTBI. The PERSISTENCE OF SYMPTOMS author believes it is more appropriate to differentiate between the two disorders. This would mean that a patient At 1 year, 85 to 90% of patients are felt to be “recovered” may indeed have an MTBI as well as a PCS. Both entities but are still symptomatic (Rutherford et al., 1978–1979; must be treated, and, as discussed later, the PCS should McLean, Temkin, Dikmen, et al., 1983), leaving 10 to be treated first. 15% of patients who are not only “not recovered, ” but also Soon after injury, patients have complaints referable“not compensated” and still very symptomatic. The literature is replete with studies showing persistence of sympto several different organ systems. Alexander (1995) identoms after the magic, if not mythical, 3-month period. This tifi es this as the PCS. He notes that the MTBI, which can lead to brain injury, can also cause injury to the head,literature indicates the symptoms and deficits following MTBI and PCS may last for 6 to 12 months and even neck (whiplash and soft tissue damage), vestibular system, and psychological functioning. The initial com- longer (Berrol, 1992; Boll & Barth, 1983; Jones, Viola, plaints of deficits in cognition and sleep disorder, Alex- LaBan, et al., 1992; Katz & DeLuca, 1992; Leininger et

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al., 1990; McSherry, 1989; Stuss, et al., 1985; Wrightsonand paid for, do a great disservice to MTBI patients. & Gronwall, 1989). Constant repetition by even well-meaning physicians of Much of the literature equates MTBI and PCS, essen-the mantra, “There is nothing wrong with you. You look tially using the terminology interchangeably. The majority fine. There’s no problem here, ” demonstrably disrupt of the literature includes cognitive and other neurologicalpatients’ sense of self, their life, and their feelings that deficits in the PCS. This statement is cautionary, as one there are indeed people (specifically doctors and insurance must read the literature with great care to see what exactly companies)“out to get them. ” This induces iatrogenic is being done to exactly what problem or problems. exacerbation of their symptoms, as the patients strive, A survey of rehabilitation specialists who followed consciously or unconsciously, to prove someone to that patients with MTBI for 6 to 18 months found that 21% they do have a problem. Then, to add insult to injury, this of the patients experienced symptoms of the PCS 2 to iatrogenically 6 induced problem is used against them both months after their initial injury, and that 20% of theseby other physicians and the legalwarriors” “ who are patients had the post-MTBI “ syndrome” (Harrington, bound and determined, in the court case after a motor Malec, Cicerone, & Katz, 1993). In another survey of 51vehicle accident, to prove that there is nothing wrong with patients, where 23 responded, 25% of the respondents them, thus saving their insurance company clients money. reported continued sequelae from their injury. The patients with sequelae after 1 year were found to have reported more symptoms 1 week after injury (Middelboe, Ander-PERSISTENT POSTCONCUSSIVE SYNDROME son, Birket-Smith, & Friss, 1992). Cicerone (1992) indicated that there was considerable Alexander (1992, 1995) has written extensively about the evidence to show that PCS symptoms persisted in a sig(PPCS). These nificant proportion of patients after MTBI, and such symp-“ persistent postconcussive syndrome” patients, after 1 year, continue to have symptoms comtoms were particularly prevalent in patients who indicated monly seen in acute PCS, such as headache, sleep disorthat they needed clinical attention. der, balance problems, dizziness, sensory hyperesthesias, Symptoms with organic etiologies, it has been noted, can mimic functional disorders (Russell, 1974). Alvesand cognitive symptoms including deficits in attention, memory, and executive functioning. They are also fre(1992) indicated that as recovery occurred, persistent quently noted to have prominent emotional symptoms symptoms could be secondary to an interaction between including irritability, depression, nervousness, discourageorganic and psychosocial factors. These persistent symptoms are more than would be expected from the initialment, and anger. Alexander (1995) identifies some “predictors” of the organic damage alone. Alves further stated that a signifi development of PPCS, including the female sex, litigation, cant percentage of patients would exhibit persistent problems with symptoms 12 months postinjury. He felt thatlow socioeconomic status, prior MTBI, headache, and recovery from MTBI should also be considered in theserious associated systemic injury. Although these factors social context in which it occurred. By recognizing the may be implicated, he states that none accounts for more than a small percentage of cases of PPCS. complexity of the recovery process, we should extend the Other authors identify pain severity postinjury as a concept of morbidity to include the specifi c socioeconomic and emotional sequelae that the patient experienced. predictor of the development of the PPCS post-MTBI Mateer (1992) found that patients post-MTBI were (Ettlin, Kischka, Reichmann, et al., 1993; Radanov, Di Stefano, Schnidrig, et al., 1991). Additional data suggests more acutely aware of their cognitive deficits andficuldif ties with functional abilities. These patients would go toa greater frequency of anxiety and depression months after initial injury (Schoenhuber & Gentilini, 1988). a physician and be found to have a negative neurological examination. They would be told that there was no organic Dizziness is a frequent symptom of the PCS. It is reason for their problems. They also would be told thatnoted that peripheral vestibular injury with dizziness also they should wait longer for recovery, learn to live with has a close relationship with psychiatric disorders, particularly with affective disease and anxiety. Unfortunately, their problems, or seek psychiatric help. These iatrogenically induced problems (cause andthe significant aspects of dizziness secondary to myofaseffect) most likely lengthen the patients’ symptomaticcial problems are often ignored. Zasler (1992) discusses period, as they begin to feel an ever increasing loss ofcervicogenic dizziness. Dizziness secondary to myofascial control, fear of the unknown, and concern that they musttrigger points in the sternocleidomastoid muscles is also frequently overlooked. In contradistinction, Alexander be “going crazy.” It doesn’t matter what the medical problem is, partic- (1995) does not appear to anticipate the psychological ularly when, like most patients with MTBI, they look aspects secondary to this problem, making it seem to be “normal.” Physicians with little or no background in the more of a primary psychological problem than one secdiagnosis of MTBI or PCS, or consultants who are boughtondary to a true organic problem.

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Chronic pain and headache are fairly universal accomaffected by the cognitive problems brought on by an paniments of the PPCS. It is also known that patients who MTBI. The affective/emotional problems found in MTBI experience chronic headache not associated with a PCS would also affect the patient with physical problems have many of the same complaints, including fatigue,from a PCS. However, acute and chronic pain engenders sleep disorder, depression, and occasionally dizziness, affective as changes by their presence, on a neurochemical well as difficulties with concentration and memory. Psy- basis as well as secondary to sleep disorders (also a chological factors may aggravate these headaches. neurochemical problem) and learned behaviors from each patient’ s past. It is recognized that anxiety may decrease concentration and complex mental processes (Binder, 1986; Krap- This means that there is a lot to dissect or tease out nick & Horowitz, 1981). Depression can cause decreased in a patient with the PCS as well as an MTBI. Only by cognitive functioning, particularly in concentration, mem- determining and differentiating between the physiory and executive functions (Cicerone, 1992; Leininger &cal/peripheral problems and those from the CNS resulting Kreutzer, 1992; Weingartner, Cohen, Murphy, et al.,from an MTBI can a proper treatment plan be created and 1981). The latter problem has also been called “depressive performed. For example, the author has found that it is pseudodementia” (Wells, 1979). best to treat depression and posttraumatic headache first, Therefore, one cannot assume that if everyone with before a endeavoring to treat the MTBI. The patient outPCS/MTBI has impaired concentration, then everyonecomes, over two decades, appear far superior to those seen with impaired concentration after PCS/MTBI has a neu-when one tries to treat everything at once. Knowing a bit rological etiology. The problem is that patients with about what happens in the CNS to patients with a MTBI PCS/MTBI associated with pain and affectiveficulties dif is also important, particularly when attempting to treat may have impaired concentration for multiple reasons,these patients. including post-MTBI neuropathological changes. Alexander (1995) asks the question: When does the MINOR TRAUMATIC BRAIN INJURY physiogenesis of a clinical problem become psychogenesis? This may be dif ficult to determine and may have an Because we are dealing in this chapter with MTBI — the iatrogenic component. Alexander does indicate that the effects of direct trauma-induced focal lesions — contumajor issue is physiogenesis transforming to psychogensions, hematomas, edema, hydrocephalus, and so on — esis, but he notes that physiogenesis can be very underesare not covered. For those who are interested, they have timated. He also indicates that there is no single psychobeen well described by Jay (2000). logical, physiological, or demographic factor leading to Diffuse injury to the brain is seen with MTBI and is the PPCS. dealt with here, along with the neurochemical pathophysFenton (1996) attempted to reappraise the PCS. He iology, which is of equal or possibly more importance in reviewed data from two U.K. prospective studies of thethe entity called MTBI. initial aspects and course of postconcussive symptomaThe two categories of diffuse injury important to this tology using parallel psychosocial, neuropsychiatric, discussion are mild concussion and “classical” cerebral quantitative electroencephalogram (EEG or QEEG), and concussions (Jay, 2000). brain stem evoked potentials. Abnormal, prolonged brain stem evoked potentials were seen in between 27 and 46% Mild Concussion of patients. Prolonged symptomatology was noted in 13% of patients and was associated with a high percent• There is no loss of consciousness, but transient age of brain stem dysfunction. The degree of QEEG neurological disturbance may be seen. recovery is related to the intensity of early symptom • The patient may be confused, disoriented, and reaction to trauma. Fenton believed that levels of permay or may not have amnesia. ceived stress at the time of the injury or afterward were • Posttraumatic headache is frequently seen. not related to symptom formation; however, chronic social diffi culties were seen in 21% of patients who initially showed improvement but later, between 6 weeks “Classical” Cerebral Concussion and 6 months posttrauma, experienced an exacerbation • The patient may show temporary, reversible of symptomatology. neurological deficits secondary to trauma, assoThus, are the PCS and MTBI absolutely two separate ciated with a brief loss of consciousness (less entities? I believe that the answer to this question is yes, than 1 h) with some degree of posttraumatic with an important corollary. Because both problems amnesia. begin together, after a motor vehicle accident, for instance, the presence of both problems affects each • A mild or moderate degree of microscopic neuronal abnormalities can be found. other. The physical problems found in the PCS are

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• There may be an associated focal brain injury (contusion). • Posttraumatic headache, tinnitus, and subtle changes in memory or psychological functioning may be seen.

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a closed head injury. The most common locations of DAI include cerebral hemispheric gray–white matter interfaces and subcortical white matter, the body and the splenium of the corpus collosum, the basal ganglia, dorsolateral aspects of the brain stem, and the cerebellum. MRI technology is continually evolving. Nonhemorrhagic lesions can be seen via MRI usinguid fl attenuated inversion Caveats— Very Important recovery (FLAIR) techniques, proton-density, and T2 • Physiological and (neuro) psychological dys- weighted images. Old hemorrhagic lesions are best seen function may occur in the absence of anatomic with the use of gradient echo sequences (Parizel, Ozsarla, Van Goethem, et al., 1998). (macroscopic) lesions. A good tool utilized in the investigation of DAI is • Functional disruption, which precedes anabeta-amyloid precursor protein (beta-APP). In one tomic disruption, is always the greater. series, DAI was seen in 65 to 100% of all cases of closed • Clinically, patients with mild concussion synhead injury, fatal cerebral ischemia/hypoxia, and brain dromes and classical” “ cerebral concussion may have physiological dysfunction as well as death with a survival time of greater than 3 h. Cases with microscopic anatomic disruptions that may be a posttraumatic interval of less than 180 min did not in contradistinction to the apparent severity of express beta-APP (Oehmichen, Meissner, Schmidt, et al., 1998). The extent and severity of DAI cannot be prethe injury. dicted from biomechanical data alone, such as the height • Traumatic brain injury (TBI) defi cits are of a fall; total axonal injury in a given patient is a variable additive. mixture of DAI and focal axonal injury from secondary The neuropathology of TBI is, as with most aspectsmechanisms. Beta-APP immuno-staining is not able to of the disorder, replete with knowns, unknowns, and vari-distinguish between primary and secondary axonal injury (Abou-Hamden, Blumbergs, Scott, et al., 1997). Still ables. Research has established many of the basic facts, another study found beta-APP immunostaining demonbut the exact how, when, why, and where are still subject strations of positive axonal swelling 1.75 h postinjury in to debate. Clinical practice indicates that a CAT scan should beboth mild and severe TBI groups, and demonstrated a spectrum of axonal injury in TBI. The study found that performed on patients post-TBI. However, as noted earlier, the timing of the test is important. It is important to repeataxons were more vulnerable than blood vessels and those axons in the corpus callosum and fornices were the most a CAT scan on a patient who begins to decompensate vulnerable of all (Blumbergs, Scott, Manavis, et al., neurologically. An acute subdural hematoma or subarachnoid hemorrhage may occur in patients with normal Glas-1995). gow Coma Scale (GCS) scores (GCS = 15) typically Findings from another study express that neurofilawithin 24 h. Other authors believe that when the first CATmentous disruption is a pivotal event in axonal injury. The scan is performed within 3 h of injury, another should beauthors studied the progression of TBI-induced axonal done within 12 h (Servadei, Nanni, Nasi, et al., 1995). change at the ultrastructural level using two antibodies Quantitative MRI analyses have shown significant dif-(NR4, to target light neurofilament subunits, and SMI32, ferences in TBI patients with unimodal gray matter–whiteto target the heavy neurofilament subunit). Changes noted at 6 h postinjury entailed focally enlarged immunoreactive matter histograms, as compared with normals, who demonstrate bimodal gray matter– white matter histograms axons with axolemmal infolding or disordered neurofila(Thatcher, Camacho, Salazar, et al., 1997). The MRI isments. By 12 h, some axons showed continued neurofilamentous misalignment, pronounced immunoreactivity, also better than the CAT scan at determining other postinjury pathology including diffuse axonal injury (DAI) and vacuolization, and —on occasion —disconnection. glial scarring. The MRI scan is also useful in morphomet-Between 30 and 60 h, further accumulations of neurofilric analysis of the brain, showing diffuse neuronal degen-aments and organelles induced further expansion of the eration after TBI with more severe injury. This may axis cylinder and disconnected reactive swellings were include larger ventricle to brain ratios and temporal hornrecognized. During later times, focally enlarged disconvolumes, which may relate to neuropsychological out-nected axons were observed in relation to axons showing less advanced reactive changes (Christman, Grady, come (Gale, Johnson, Bigler, & Blatter, 1995). DAI is one of the most prevalent and well-acknowl- Walker, et al., 1994). edged primary and secondary postinjury pathophysiolog- Axonal injury including DAI was noted by several ical phenomenon. The brain tissue, or parenchyma, can authors in the brains of patients who were victims of blunt be severely injured secondary to axonal shearing forces head trauma/assault (Crooks, Scholtz, Vowles, et al., 1992; during acceleration/deceleration and rotational injuries inImajo, 1996; Ramsay & Shkrum, 1995).

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Other studies reinforce the fact that neuronal loss after Increased neurotransmitter release is recruited to increase head injury is secondary to both primary and secondary depolarization as injury severity increases. The release of mechanisms. One study also found that microglial activa-these excitatory amino acids (EAAs) significantly contribtion was a delayed result of TBI (Engel, Wehner, & Mey-utes to the high levels of K+ release following TBI. ermann, 1996). Another study that evaluated Purkinje cell After moderate and most probably mild TBI, tissue vulnerability in mild TBI, found that there was a close deformation may open ion channels resulting in anuxinfl anatomic association between activated microglial cellsof K+ large enough to induce abnormal levels of exciand Purkinje cells, which suggests that Purkinje cell injurytatory neurotransmitter release and therefore further is the cause of microglial cell activation (Fukuda, Aihara,depolarization. Sagar, et al., 1996). Mild–moderate TBI induces increases in glutamate Povlishock’s (1992) and Povlishock and Jenkins’ and ACH. Increased ACH release and increased cholinergic (1995) work comes to some of the same conclusions, neuronal activity in some regions of the brain (such as the but by a different road. They believe that the TBI itself hippocampus) may persist for hours or longer after injury. does not cause axonal disruption. Instead, focal, subtle Posttraumatic changes in the blood– brain barrier axonal changes that occur over time lead to impaired(BBB) may also contribute to posttraumatic receptor dysaxoplasmic transport, continued axonal swelling, andfunction by allowing the abnormal passage of blood-borne finally disconnection. Povlishock attributes the traumaexcitatory exogenous neurotransmitters and neuromoduto altering the axolemmal permeability, direct cytoskel-lators into the brain. These additional excitatory neuroetal damage or disruption, or more overt metabolic andchemicals may act synergistically with endogenously functional disturbances. Trauma may induce axonalincreased excitatory neurotransmitters (ENTs). Moderate change, Wallerian degeneration, and nally fi deafferen- experimental TBI without contusion in the rat leads to tation. Povlishock also thinks that traumatically inducedacute BBB dysfunction in the hippocampus and the cortex DIA leads to diffuse deafferentation and notes that post-that may last more than 12 h. Other research suggests that traumatically, the cerebral parenchyma is involved withdysfunction of the BBB secondary to TBI may allow blood increased neuronal sensitivity to secondary ischemia. plasma constituents such as ACH (at levels 7 times greater Furthermore, he believes that this increased sensitivitythan in the cerebral spinal fluid [CSF]) to gain access to is secondary to the neurotransmitter storm that follows the brain and influence injury processes. a TBI, which can induce sublethal neuroexcitation. Most Moderate TBI can induce significant reductions in importantly, Povlishock (1992) and Povlishock and Jenmuscarinic cholinergic receptor binding. Decreased bindkins (1995) indicate that the damage noted does not take ing by glutaminergic receptors, specifically the NMDA place immediately posttrauma, but takes place over days receptors, also occurs following moderate TBI. or even weeks. The predominant changes seen only in the NMDA receptors suggest that the ENT agonist–receptor interaction secondary to moderate TBI occurs predominately at NEUROCHEMICAL ASPECTS OF this receptor subtype. This is supported by the protection TRAUMATIC BRAIN INJURY given by administration of NMDA antagonists. Abnormal agonist–receptor interactions related to excito- Reduced motor and memory deficits can be seen with toxic processes may contribute to the pathophysiology ofpharmacological antagonism of NMDA receptors using TBI. Activation of the muscarinic cholinergic or Nphencyclidine, MK-801, dextrorphan, and others. This methyl-D-aspartate (NMDA) glutamate receptors appearappears to be secondary to their ability to restore2+MG to contribute to TBI pathophysiology. (magnesium) levels postinjury. TBI-induced membrane depolarization causes a mas- Receptor activation by ENTs may contribute to cellusive release of excitatory neurotransmitters, particularlylar metabolic alterations after TBI. Further results indicate acetylcholine (ACH) and glutamate. The posttraumaticthat EAA neurotransmitters may be involved in injuryinduced disruption of ionic homeostasis and ion-induced overproduction/release of these chemicals may induce cytotoxic cerebral edema. abnormal activation of receptors that can produce changes in intracellular signal transduction pathways and thereby TBI produces widespread neuronal excitation causing induce short-term, long-lasting, or irreversible changes inprolonged, usually sublethal, pathological changes in neucell function. Such deficits can occur with sublethal cellronal activity that disrupt many functions, including memdisruption or cell death. ory. Inhibitory neurotransmitters such as gamma-amiExperimental TBI is known to produce widespreadnobutyric acid (GABA) and the opiods may also be neuronal depolarization, which is demonstrated by largereleased with TBI to try to decrease the excitatory state. increases in extracellular potassium (K+) resulting from Oxygen free radicals (OFRs) may also be important mediators of TBI and cerebral edema. Sources for oxygen neuronal discharges and not neurotransmitter release.

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free radicals include catecholamines, amine oxidases, and mild to severe. Interestingly, the patients with mild TBI peroxidases among others. Pharmacological agents being had significantly higher levels of BE than those patients considered to decrease OFR damage include vitamin E, with severe head trauma. The BE levels did not correlate dimethyl sulfoxide (DMSO), and lipid peroxidation inhib- with early prognosis (Pasaoglu, Inci Karakucuk, Kurtsoy, itors (lazaroids). & Pasaoglu, 1996). Another group of patients had lumbar punctures done Some conclusions that can be drawn follow. on days 1, 4, and 7, head following injury; and the levels • Excitotoxic phenomena may render neurons of leucine or leu-enkephalin (LENK) and methianine or met-enkephalin (MENK) were determined in the CSF. It dysfunctional but not necessarily kill them was found that MENK levels were constantly elevated, (although that also occurs). • TBI results in widespread depolarization and whereas LENK levels decreased in patients with GCS scores of 8 or less, and might provide a poor prognostic nonspecific release of many excitatory and factor. It was indicated that LENK and MENK appeared inhibitory neurotransmitters. • Significant changes in the BBB are found that to be linked to different pathophysiological functions (Stachura, Kowalski, Obuchowicz, et al., 1997). may last for hours or more. Although endogenous opiates are found in the • The resultant sublethal toxicity appears to be mediated via increases in intracellular cal- human gut, BE is produced in the hypothalamus. It is broken down to the smaller forms of endogenous opicium levels. • These processes, including DAI, may begin at ates, LENK and MENK. It would therefore be more the time of an accident, but take days or even likely to be found in the CSF, along with enkephalins and dynorphins, which together help mediate the central weeks until they end. • There are three subtypes of glutamate receptors: perception of pain. Primary metabolites of norepinephrine (methoxyhyNMDA, quisqualate, and kainate. droxyphenylglycol [MHPG]), serotonin (5-hydroxyin• The NMDA receptors may protect against TBI dole-acetic acid [5HIAA]) and dopamine (homovanillic secondary to trauma and cerebral ischemia. acid [HVA]) were assayed in CSF taken from comatose • Cholinergic systems have roles in mediation of patients after severe head injury. Samples were taken TBI and neuronal recovery, including behavwithin days of the injury and again after clinical improveioral suppression. Long-term motor defi cits ment (13/20 patients) or deterioration (7/20 patients) was may be decreased by the ACH medications seen. Clinical improvement was associated with signifiblocking release of excitotoxins. cant decreases in HVA and 5HIAA. The levels of all three • Catecholamines (especially norepinephrine) metabolites remained high in patients who deteriorated. appear to help in TBI recovery. These results appeared to indicate that increased turnover • Alpha-noradrenergic agonists and probably of CNS neurotransmitters in severe head injury normaldopaminergic agonists accelerated motor recovized during recovery (Markianos, Seretis, Kotsou, & ery after experimental injury to the sensorimotor Christopoulous, 1996). cortex. Their antagonists retarded recovery. In another study, CSF levels of serotonin (5-HT), sub• Early postinjury use of benzodiazipines may stance P (SP), and lipid peroxidation (LPx) products were slow neural recovery and possible restoration measured in patients with TBI and compared with conof neural recovery. trols. The levels of SP and 5-HT in patients with head • Most likely, “therapeutic cocktails” of more trauma were lower than those found in controls. The CSF than one agent are necessary for appropriate LPx products were signifi cantly increased in the TBI treatment of TBI. patients. There was no correlation between the CSF levels and the GCS at admission (Karakucuk, Pasaoglu, Pasaoglu, & Oktem, 1997). BIOGENIC AMINES AND THE The loss or decrement of cholinergic neurotransmisENDOGENOUS OPIATE SYSTEM sion has been implicated in both cognitive dysfunction Acute traumatic injury of any type engenders the produc-and memory impairment after TBI. One group looked at tion of beta-endorphin (BE) as well as other endogenous presynaptic markers related to cholinergic neurotransmisopiates. One group looked at BE levels in the blood aftersion via choline acetyltransferase activity as well as hightrauma and found, to little surprise, that there was noaffinity nicotinic receptor binding sites in the inferior temcorrelation between serum BE and pain severity (Bern-poral gyrus, cingulate gyrus, and superior parietal cortex stein, Garzone, Rudy, et al., 1995). When looking at CSF in postmortem brains. They found that the correlation of BE levels, it was found that significant changes in CSFcholine acetyltransferase activity with synaptophysin BE levels are found in patients with the full range of TBI, immunoreactivity revealed a deficit of cholinergic presyn-

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• There are significant neurochemical and neuroaptic terminals in postmortem human brain after TBI physiological abnormalities that occur in MTBI (Murdoch, Perry, Court, et al., 1998). and affect some of the same neurotransmitter An inverse relationship between plasma norepinephsystems needed by the nociceptive and antirine and thyroid hormones is found in patients with hypernociceptive systems; these abnormalities can or hypothyroidism or severe stress. Head injured patients lead to perturbations in the experience, percepwere found to have low thyroxine (T4), low triiodothytion, and appropriate recognition of pain and/or ronine (T3), and high reverse T3. When phenytoin was pain relief. used for seizure control, T3 and T4 were lowered, but • The affective/emotional changes that accomthyroid-stimulating hormone was increased. In these pany both chronic pain and MTBI are subserved patients there was no correlation between NE and T3 by the same neurochemical systems, many of (Ziegler, Morrissey, & Marshall, 1990). which are affected by pain as well as, pathoA great deal of evidence indicates that dopamine neuphysiologically, trauma (from both primary and rotransmission dysfunction after mild to moderate TBI is secondary effects). involved in the induction of posttraumatic memory defi• The MTBI patient with pain must therefore be cits. By using anesthetized animals that were given dealt with on multiple levels: the soft tisMTBIs, it was found that mice were impaired in task sue/musculoskeletal pain problems from the performance. They had prolonged latencies for finding and injury; the neuropathological changes, seconddrinking in a retention test and retest. If these animals ary to DAI, excitotoxic cell injury, BBB were injected with haloperidol 15 min posttrauma, they changes, and the effects of possible neurotranshad a shortened latency in both of the tests, which mitter system damage secondary to these facappeared to show that the use of dopamine receptor antagtors; and the neurotransmitter system changes onists was beneficial for recovery of posttraumatic memthat are known to accompany chronic pain, ory dysfunction. For looking closer at the receptor sites, which may be exacerbated or changed secondresearchers used a D1 receptor antagonist, SCH-23390, ary to the CNS effects of the MTBI. These facand sulpiride, a D2 receptor antagonist, in the same expertors make treatment more challenging, because imental protocol. The use of sulpiride, but not SCH-23390, medication management, for example, may be improved the deficits in task performance, indicating that more diffi cult as well as different when looking the D2 receptors were the major site of action. A positive at a patient with only chronic benign pain. interaction was noted when both D1 and D2 receptor antagonists were given together at individually subtherapeutic levels, indicating that interaction between the two The pathophysiological changes that occur after an MTBI may last for days or weeks. The resultant deficits receptors was involved. The dopaminergic mechanisms do appear to contribute to memory dysfunction after TBImay therefore not become manifested for more weeks or months. This leads to an important consideration. What if (Tang, Node, & Nabeshima, 1997). the patient complains of cognitive or emotional problems within days or several weeks of the initial insult? First, is MINOR TRAUMATIC BRAIN INJURY AND the patient experiencing all the problems that are going to arise from the injury, or only those that have been detected PAIN: SOME CONCLUSIONS at that time? Second, can you see a good reason for conThe various pathophysiological aspects of MTBI andsidering serial neurological examinations? pain therefore appear to encompass several important Somehow it has become an “urban medical legend” etiologies: that all patients with an MTBI will miraculously be healed within 3 months. This may be true for a simple majority • At the time of trauma, there may typically be of patients who are not experiencing a significant MTBI. soft tissue injuries, at a minimum. Those However, as documented earlier, anywhere from 5 to 20% patients who experience significant TBI may of these patients do not get “all better” in 3, 6, or even 12 need to be sedated, and even paralyzed; and months. therefore may have their perception of pain As clinicians take the patient’ s history of cognitive dealt with on a secondary basis. problems, they may also find frequent complaints of post• Moderate to severe TBI may make the patient traumatic myofascial or soft tissue pain problems, includunable to cognitively deal with pain. ing posttraumatic headache, cervical pain, and low back pain, as well as sleep disorder. • Patients with MTBI may be so overcome with pain immediately postinjury that cognitive If the patient who complains of pain is seen soon after changes and problems may not be either relevant the injury, physical therapy may be all that is needed to stop these problems before the onset of chronicity, with or even looked for at that time.

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its attendant affective and neurochemical alterations. The REFERENCES use of narcotic analgesics should be strongly discouraged, Abou-Hamden, A., Blumbergs, P. C., Scott, G., et al. (1997). Axonal because they may further enhance cognitive ficulties. dif injury in falls. Journal of Neurotrauma, 14, 699–713. If after 6 to 12 weeks there is no significant diminution Alexander, M.P. (1992). Neuropsychiatric correlates of persisof the pain and/or headache, along with depression, content postconcussive syndrome. Journal of Head Trauma sideration of a specialty pain program should be given, as Rehabilitation, 7(2), 60–69. long as the pain practitioner understands the effects of TBI Alexander, M.P. (1995). Mild traumatic brain injury. Pathophyson pain. iology, natural history and clinical management. NeuThere is an interesting dichotomy in the majority of rology, 45, 1253–1260. patients with pain and MTBI. Patients in an interdisci- Alves, W.M. (1992). Natural history of post-concussive signs plinary pain program are typically taught to rate their and symptoms.Physical Medicine and Rehabilitation: pain, on a momentary basis on a 0 (no pain) to 10 or State of the Art Reviews,(1), 6 21–32. 100 scale. When they begin treatment, the numbers are Alves, W.M., & Jane, J.A. (1990). Post-traumatic syndrome. In typically high and correspond with physicalndings fi of J.R. Youmans (Ed.), Neurological Surgery(3rd ed., pp. 2230–2240). Philadelphia: W. B. Saunders. muscle spasm, trigger points, and loss of specifi c funcAnderson, S.D. (1996). Postconcussional disorder and loss of tion such as decreased range of motion or weakness. As consciousness. Bulletin of American Academy of Psytreatment progresses, typically during 4 to 6 weeks, the chiatric Law, 24,493–504. patients’pain complaints may not change. That is, their identification of their pain level (such as 7 over 10) mayBarrett, K., Buxton, N., Redmond, A.D., et al. (1995). A comparison of symptoms experienced following minor head not change or change only minimally, whereas funcinjury and acute neck strain (whiplash injury). Journal tional evaluation reveals a return to a normal range of of Accident and Emergency Medicine, 12, 173–176. motion, for example, or absent palpable muscle spasm Barrett, K., Ward, A.B., Boughey, A., et al. (1994). Sequelae of or trigger points. minor head injury: The natural history of post-concusIt is extremely important to realize that this dichotomy sive symptoms and their relationship to loss of conis not a manifestation of malingering, but appears to be sciousness and follow-up.Journal of Accident and more of a learned or even perseverative response. On Emergency Medicine, 11, 79–84, 1994. observation, pain behaviors are diminished and theBernstein, L., Garzone, P.D., & Rudy, T., et al. (1995). Pain patients’ affect is improved, but they may still claim to perception and serum beta-endorphin in trauma patients. Psychosomatics, 36, 276–284. endure what appears to be an artificially high pain level. Berrol, S. (1992). Terminology of post-concussive syndrome. Evaluationmust be functional in nature, not subjective. Physical Medicine and Rehabilitation: State of the Art Even more importantly, in the presence of severe pain, Reviews, ( 6 1), 1–8. a neuropsychological evaluation or cognitive evaluation is Bicik, I., Radanov, B.P., Schafer, N., et al. (1998). PET with not accurate and should not be performed. This means, 18fluorodeoxyglucose and hexamethylpropylene amine MTBI patients with pain should have their pain ameliooxime SPECT in late whiplash syndrome. Neurology, rated and their depression lifted as much as possible prior 51, 345–50. to any formal cognitive evaluation and/or treatment . Binder, L.M. (1986). Persisting symptoms after mild head injury: The PCSs as well as the PPCSs are not symptoms or A review of the postconcussive syndrome. Journal of syndromes looking for patients. As indicated earlier, the Clinical Experiment, (84), 323–346. author believes that the PCS is different from an MTBI.Blumbergs, P.C., Scott, G., Manavis, J., et al. (1995). Topography Still, patients from around the country, around the globe, of axonal injury as defined by amyloid precursor protein complain of the same symptoms after an acceleraand the sector scoring method in mild and severe closed head injury.Journal of Neurotrauma, 12, 55–72. tion/deceleration injury. There are tests and many studies Bohnen, N., & Jolles, J. (1992). Neurobehavioral aspects of that show the presence of abnormalities. Again, we do not postconcussive symptoms after mild head injury. Jouryet seem to know the best tests, the best window to pernal of Nervous and Mental Disease, 180 (11), 683–692. form them, or the best way to interpret them. As clinicians, we also know that we have to listen toBohnen, N., Twijnstra, A., & Jolles, J. (1992) Post-traumatic and emotional symptoms in different subgroups of patients our patients. If something they say does not make sense, with mild head injury.Brain Injury, 6(6), 481–487. it is the clinician’s medical responsibility to actively invesBohnen, N., Van Zutphen, W., Twijnstra, A., et al. (1994). Late tigate what the patient is trying to say. outcome of mild head injury: Results from a controlled To be antagonistic to a diagnosis, to not accept the postal survey.Brain Injury, 8, 701–708. presence of a diagnosis because of preconceived notions Boll, T.J., & Barth, J. (1983). Mild head injury. Psychiatric or initial thoughts of patient malingering or because your Development, 28 (5), 509–513. opinion depends on who pays you, puts us back into the Brenner, C., Friedman, A.P., Merritt, H.H., & Denny-Brown, era of the Inquisition. That is not our job; “to do no harm” D.E. (1944). Post-traumatic headache. Journal of Neuis our responsibility. rosurgery, 1,379–391.

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Brenner, D.N., & Gillingham, J.F. (1974). Patterns of convales-Gentilini, M., Michelli, P., Shoenhuber, R., et al. (1985). Neuropsychological evaluation ofr mild head injury. Journal cence after minor head injury. Journal Royal College of Neurology, Neurosurgery, and Psychiatry, 48, Surgery, Edinburgh, 19, 94–97. 137–140. Chambers, J., Cohen, S.S., Hemminger, L., et al. (1996). Mild Gimse, R., Tjell, C., Bjorgen, I.A., & Saunte, C. (1996). Distraumatic brain injuries in low-risk patients. Journal of turbed eye movements after whiplash due to injuries to Trauma, 41,976–980. the posture control system. Journal of Clinical and Christman, C.W., Grady, M.S., Walker, S.A., et al. (1994). UltraExperimental Neuropsychology, 18, 178–186. structural studies of diffuse axonal injury in humans. Gronwall, D., & Wrightson, P. (1974). Cumulative effects of Journal of Neurotrauma, 11, 173–186. concussion. Lancet, 1, 995. Cicerone, K.D. (1992). Psychological management of post-concussive disorders.Physical Medicine and Rehabilita- Harrington, D.E., Malec, J., Cicerone, K., & Katz, H. . (1993). Current perceptions of rehabilitation professionals tion: State of the Art Reviews,(1), 6 129–141. toward mild traumatic brain injury. Archives of Physical Cicerone, K.D., & Kalmar, K. (1997). Does premorbid depresMedicine and Rehabilitation, 74 (6), 579–586. sion influence post-concussive symptoms and neuropHeikkila, H.V., & Wenngren, B.I. (1998). Cervicocephalic kinessychological functioning?Brain Injury, 11, 643–648. thetic sensibility, active range of cervical motion, and Crooks, D.A., Scholtz, C.L., Vowles, G., et al. (1992). Axonal oculomotor function in patients with whiplash injury. injury in closed head injury by assault: A quantitative Archives of Physical Medicine and Rehabilitation, 79, study. Medical Science Law, 32 (2), 109–117. 1089–1094. Dikmen, S.S., McLean, A., Temkin, N., et al. (1986). NeuropHoganson, R.C., Sachs, N., Desai, B.T., & Whitman, S. (1984). sychological outcome at one month post injury. Archives Sequelae associated with head injuries in patients who of Physical and Medical Rehabilitation, 67, 507–513,. were not hospitalized: A follow-up survey. NeurosurDikmen, S.S., Temkin, N., & Armsden, G. (1989). Neuropsygery, 14,315–317. chological recovery: Relationship to psychosocial funcImajo, T. (1996). Diffuse axonal injury: Its mechanism in an tioning and postconcussional complaints. In H.S. Levin, assault case.American Journal of Forensic Medical H.M. Eisenberg, & A.L. Benton (Eds.), Mild head injury Pathology, 17,324–326. (pp. 2241–2290). New York: Oxford University Press. Jacobson, J., Gaadsgaard, S. E., Thomsen, S., & Henriksen, P. DiStefano, G., & Radanov, B.P. (1995). Course of attention and B. (1987). Prediction of post-concussional sequelae by memory after common whiplash: A two year prospective reaction time test.Acta Neurologica Scandanavica, study with age, education and gender pair-matched 75(5), 341–345. patients.Acta Neurologica Scandanavica, 91, 346–352. Jay, G.W. (2000).Mild traumatic brain injury handbook: DiagElson, L.M., & Ward, C.C. (1994). Mechanisms and pathophysnosis and treatment . Boca Raton, FL: CRC Press. iology of mild head injury.Seminars in Neurology, 14, Jones, J.H., Viola, S.L., LaBan, M.M., et al. (1992). The inci8–18. dence of post minor traumatic brain injury syndrome: Engel, S., Wehner, H.D., & Meyermann, R. (1996). Expression A retrospective survey of treating physicians. Archives of microglial markers in the human CNS after closed of Physical and Medical Rehabilitation, (2), 73 145–146. head injury. Acta Neurochirugica Suppl. (Wien), 66, Jones, R.K. (1974). Assessment of minimal head injuries: Indi89–95. cations for in-hospital care.Surgical Neurology, 2, Ettlin, T.M., Kischka, U., Reichmann, S., et al. (1993). Cerebral 101–104. symptoms after whiplash injury of the neck: A prospec- Kant, R., Smith-Seemiller, L., Isaac, G., & Duffy, J. (1997). Tctive clinical and neuropsychological study of whiplash HMPAO SPECT in persistent post-concussion syninjury. Journal of Neurology, Neurosurgery, and Psychidrome after mild head injury: Comparison with atry, 55, 943–948. MRI/CT. Brain Injury, 11, 115–124. Evans, R.W. (1992). The postconcussion syndrome and the Karakucuk, E., Pasaoglu, H., Pasaoglu, A., & Oktem, S. (1997). sequelae of mild head injury. Neurology Clinical, 10 (4), Endogenous neuropeptides in patients with acute trau815–847. matic head injury. II: Changes in the levels of cerebral Ewing, R., McCarthy, D., Gronwall, D., et al. (1980). Persisting spinalfluid substance P, serotonin and lipid peroxidation effects of minor head injury observable during hypoxic products in patients with head trauma. Neuropeptides, stress.Journal of Clinical Neuropsychology,, 147–155. 2 31, 259–263. Fenton, G.W. (1996). The postconcussional syndrome reapKarzmark, P., Hall, K., & Englander, J. (1995). Late-onset postpraised.Clinical Electroencephalography, 27, 174–82. concussional symptoms after mild brain injury: The role Fukuda, K., Aihara, N., Sagar, S.M., et al. (1996). Purkinje cell of premorbid, injury-related, environmental, and personvulnerability too mild traumatic brain injury. Journal of ality factors.Brain Injury, 9, 21–26. Neurotrauma, 13,255–266. Katz, R.T., & DeLuca, J. (1992). Sequelae of minor traumatic Gale, S.D., Johnson, S.C., Bigler, E.D., & Blatter, D.D. (1995). brain injury. American Family Physician, 46 (5), Nonspecific white matter degeneration following trau1491–1498. matic brain injury.Journal of International Neuropsy- Kay, T., et. al. (1993). Definition of mild traumatic brain injury. chology Society, 1,17–28. Journal of Head Trauma Rehabilitation,(3), 8 86–87. Krapnick, J.L, & Horowitz, M.J. (1981). Stress response synGasquoine, P.G. (1997). Postconcussion symptoms. Neuropsydromes.Archives of General Psychiatry, 38, 428–435. chology Review, 7,77–85.

Mild Traumatic Brain Injury and Pain

167

Pasaoglu, H., Inci Karakucuk, E., Kurtsoy, A., & Pasaoglu, A. Landy, P.J. (1998). Neurological sequelae of minor head and (1996). Endogenous neuropeptides in patients with neck injuries.Injury, 29, 199–206. acute traumatic head injury, I: Cerebrospinal fluid betaLeininger, B.E., Gramling, S.E, Farrell, A.D., et al. (1990). Neuendorphin levels are increased within 24 hours following ropsychological deficits in symptomatic minor head the trauma.Neuropeptides, 30, 47–51. injury patients after concussion and mild concussion. Journal of Neurology, Neurosurgery, and Psychiatry, 53, Povlishock, J.T. (1992). Traumatically induced axonal injury: 293–296. Pathogenesis and pathobiological implications. Brain Leininger, B.E., & Kreutzer, J.S. (1992). Neuropsychological Pathology, 2,1–12. outcome of adults with mild traumatic brain injury: Povlishock, J.T., & Jenkins, L.W. (1995). Are the pathobiological Implications for clinical practice and research. Physical changes evoked by traumatic brain injury immediate and Medicine and Rehabilitation: State of the Art Reviews irreversible?Brain Pathology, 5,415–426. 6(1), 169–182. Radanov, B.P., DiStefano, G., Schnidrig, A., et al. (1991). Role Levin, H., Mattis, S., Ruff, R., et al. (1987). Neurobehavioral of psychosocial stress in recovery from common whipoutcome following minor head injury: A three center lash. Lancet, 338,712–715. study. Journal of Neurosurgery, 66, 234–243. Ramsay, D.A., & Shkrum, M.J. (1995). Homicidal blunt head Markianos, M., Seretis, A., Kotsou, A., & Christopoulos, M. trauma, diffuse axonal injury, alcoholic intoxication and (1996). CSF neurotransmitter metabolites in their clincardiorespiratory arrest: A case report of a forensic synical state.Acta Neurochirugica (Wien), 138, 57–59. drome of acute brainstem dysfunction. American JourMateer, C.A. (1992). Systems of care for post-concussive synnal of Forensic Medicine and Pathology, 16, 107–114. drome. Physical Medicine and Rehabilitation: State of Rimel, R.W., & Jane, J.A. (1985). Minor head injury: Managethe Art Reviews (1), 6 143–160. ment and outcome. In R.H. Williams & S.S. Rengachary Mayou, R., & Bryant, B. (1997). Outcome of “whiplash” neck (Eds.), Neurosurgery (pp. 1608–1611). New York: injury. Injury, 27, 617–623. McGraw-Hill. McFlynn, G., Montgomery, F., Fenton, G.W., & Rutherford, W. Ritchie, W.R. (1974). Recovery after minor head injury [Letter (1984). Measurement of reaction time following minor to the Editor].Lancet, 2,1315. head injury.Journal of Neurology, Neurosurgery, and Rubin, A.M., Woolley, S.M., Dailey, V.M., & Goebel, J.A. Psychiatry, 48,137–140. (1995). Postural stability following mild head or whipMcLean, A., Dikmen, S.S., Temkin, N., et al. (1984). Psychosolash injuries.American Journal of Otology, 16, 216–221. cial functioning at one month after head injury. NeuroRussell, W.R. (1974). Recovery after minor head injury [Letter surgery 14,393–399. to the Editor].Lancet, ii, 1315. McLean, A., Temkin, N.R., Dikmen, S.S., et al. (1983).The Rutherford, W.H., Merrett, J.D., & McDonald, J.R. (1977). behavioral sequelae of head injury. Journal of Clinical Sequelae of concussion caused by minor head injuries. Neuropsychology, 5, 361–376. Lancet, 1,1–4. McSherry, J.A. (1989). Cognitive impairment after head injury. Rutherford, W.H., Merrett, J.D., & McDonald, J.R. (1978–1979). American Family Physician 40 (4), 186–190. Symptoms at one year following concussion from minor Middelboe, T., Anderson, H.S., Birket-Smith, M., & Friss, M.L. head injuries. Injury, 10, 225–230. (1992). Minor head injury: Impact on general health Schoenhuber, R., & Gentilini, M. (1988). Anxiety and depresafter one year. A prospective follow-up study. Acta Neusion after mild head injury: A case control study. Jourrologica Scandanavica 85 (1), 5–9. nal of Neurology, Neurosurgery, and Psychiatry, 51, Murdoch, I., Perry, E.K., Court, J.A., et al. (1998). Cortical 722– 724. cholinergic dysfunction after human head injury. JourServadei, F., Nanni, A., Nasi, M.T., et al. (1995). Evolving nal of Neurotrauma, 15,295–305. brain lesions in the rst fi 12 hours after head injury: Oddy, M., Humphrey, M., & Uttley, D. (1978). Subjective Analysis of 37 comatose patients. Neurosurgery, 37, impairment and social recovery after closed head injury. 899– 906. Journal of Neurology, Neurosurgery, and Psychiatry, 41, Soustiel, J.F., Hafner,H., Chistyakov, A.V., et al. (1995). Trigem611–616. inal and auditory evoked responses in minor head injuOehmichen, M., Meissner, C., Schmidt, V., et al. (1998). Axonal ries and post-concussion syndrome. Brain Injury, 9, injury—A diagnostic tool in forensic neuropathology? 805–813. A review. Forensic Science International, 95, 67–83. Otte, A., Ettlin, T.M., Nitzsche, E.U., et al. (1997). PET and Stachura, Z., Kowalski, J., Obuchowicz, E., et al. (1997). Concentration of enkephalins in cerebrospinal fluid of SPECT in whiplash syndrome: A new approach to a patients after severe head injury. Neuropeptides, 31, forgotten brain?Journal of Neurology, Neurosurgery, 78–81. and Psychiatry, 63,368–372. Parizel, P.M., Ozsarla, K., Van Goethem, J.W., et al. (1998).Sturzenegger, M., DiStefano, G., Radanov, B.P., & Schnidrig, A. (1994). Presenting symptoms and signs after whipImaging findings in diffuse axonal injury after closed lash injury: The influence of accident mechanisms. Neuhead trauma.European Radiology, 8, 960–965. rology, 44, 688–693. Parker, R.S., & Rosenblum, A. (1996). IQ loss and emotional dysfunctions after mild head injury incurred in a motor Stuss, D.T., Ely, P., Hugenholtz, H., et al. (1985). Subtle neuropsychological deficits in patients with good recovery vehicle accident.Journal of Clinical Psychology, 52, after closed head injury. Neurosurgery, 17,41–47. 32–43.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

Stuss, D.T., Stethem, L.L., Hugenholtz, H., et al. (1989). Reac-Weingartner, H., Cohen, R.M., Murphy, D.L., et al. (1981). Cognitive processes in depression. Archives of General Psytion time after traumatic brain injury. Fatigue, divided chiatry, 38, 42–44. and focused attention and consistency of performance. American Journal of PsyJournal of Neurology, Neurosurgery, and Psychiatry, 52, Wells, C.E. (1979). Pseudodementia. chiatry, 136,895–900. 742–48. Wrightson, P., & Gronwall, D. (1989). Time off work and sympSymonds, D. (1965). Concussion and its sequelae. Lancet, 1, toms after minor head injury. Injury, 12(6), 445–454. 1–5. Szymanski, H.V., & Linn, R. (1992). A review of the postcon- Young, B. (1985). Sequelae of head injury. In R. H. Williams & S. S. Rengachary (Eds.), Neurosurgery(pp. 1691–1693). cussion syndrome. International Journal of Psychiatry New York: McGraw-Hill. in Medicine, 22,357–375. Tang, Y.P., Noda, Y., & Nabeshima, T. (1997). Involvement ofZasler, N.D. (1992). Neuromedical diagnosis and management of post-concussive disorders. Physical Medicine and activation of dopaminergic neuronal system in learning Rehabilitation: State of the Art Reviews, (1),6 33–67. and memory deficits associated with experimental mild traumatic brain injury.European Journal of Neuro- Ziegler, M.G., Morrissey, E.C., & Marshall, L.F. (1990). Catecholamine and thyroid hormones in traumatic injury. science, 9,1720–1727. Critical Care Medicine, 18,253–258. Thatcher, R.W., Camacho, M., Salazar, A., et al. (1997). Quantitative MRI of the gray-white matter distribution in traumatic brain injury.Journal of Neurotrauma, 14, 1–14.

16 Trauma and Soft Tissue Injuries: Clinic and Courtroom Thomas J. Romano, M.D., Ph.D., F.A.C.P., F.A.C.R. Astute clinicians have long known that physical trauma,do some patients develop chronic posttraumatic headaches sometimes seemingly trivial, can result in medical condi-whereas others involved in similar traumas do not? Why tions characterized by persistent pain (Ashburn & Fine,do some patients develop fibromyalgia after traumatic 1989; Romano, 1990), fatigue (Romano, 1990), frustra-events and others do not? The list goes on and on. tion, and psychological distress (Aaron, et al., 1997). It is Although the answers to these questions will probably certainly true that most patients who have sustained injunever be totally forthcoming, it is useful to think of the ries from motor vehicle accidents, physical assaults, and problem in the following way. We human beings are falls recover fully. At the other end of the spectrum, somehighly complex biological systems. We are certainly no individuals die of their traumatically induced injuries. less complex than bacteria, goldfish, or zebras. Thus, prinTypically, the clinicians who specialize in pain manage-ciples of biodiversity certainly should apply to how each ment do not have the opportunity to treat patients who fallof our individual complex biological systems (i.e., our into any of the preceding two categories. It is our respon-own bodies) reacts to certain physical stressors such as sibility to treat those patients who have neither died as physical a trauma. result of their injuries nor fully recovered. Our patient I often visit the American Museum of Natural History populations tend not to be composed of cross sections of in New York City. Several years ago a new exhibit hall, society but by their very nature are skewed. We treat the the “Hall of Biodiversity,” was dedicated. It celebrates the patients who have not recovered and probably will notamazing and wondrous variety of plant and animal life on fully recover. Most have already been treated by emer-this planet. Not only interspecies variability but also gency room physicians, primary care doctors, physicalintraspecies diversity is described and catalogued. Certherapists, and other healthcare providers with less than tainly all zebras are not exactly the same; neither are all satisfactory results. Our patients complain of chronic pain,salamanders nor all butterflies. Each individual within a headaches, fatigue, and neurological problems, and are species has its own unique physical and behavioral charoften frustrated and angry. This is understandable because acteristics, but, of course, there are many characteristics many have been injured in either an accident or a physical it shares with the remainder of the members of its species. assault and are often involved in litigation at some level. Dr. Stephen Jay Gould — a frequent contributor to Although it has been known for many years that numerous Natural History Magazine(a publication of the American individuals suffer persistent pain following trauma (Ash- Museum of Natural History) and a famed geologist and burn & Fine, 1989; Romano, 1990), it is the purpose ofbiologist as well as a prolific author — celebrates biodithis chapter to explain why. versity in his workFull House (Gould, 1996). He makes Why do some patients involved in whiplash motor a claim with which I heartily agree. He maintains that if vehicle accident recover fully, while others do not? Whyone wishes to describe a complex biological system using

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measures of central tendency such as averages or means, damage. This actually does make sense if one remembers he or she will be wrong. It is interesting to me that hethere is a large degree of biological variability among uses the wordwill as opposed to might. accident victims (Radanov & Sturzenegger, 1996). This We are all distinct individuals. A mere average cannotcould help explain why some high-speed impacts may describe our experiences or predict our future behavior. leave some drivers relatively unscathed, whereas some However, is that not exactly what insurance companies, low-impact collisions can be devastating to others. managed care organizations, and even some members of What about the cervical spine X-ray? The cervical the legal profession wish for us to do? How often have aspine X-ray typically taken in the emergency room to rule patient’s medical benefits following an injury been termi- out a fracture/dislocation of the cervical vertebral bodies nated because the insurance adjustor or the physician probably is not a good predictor of how much chronic working for the insurance company has determined that pain the patient will have months, and even years, after a the patient should have recovered? particular trauma. One must remember that the emergency Although it may be true that most patients with soft room physician is worried about acute spinal cord transectissue injuries totally recover within 4 to 6 weeks, it is tion, acute cervical fractures, etc. Having worked in many unscientific and, dare I say, dishonest to maintain that all emergency rooms including Bellevue Hospital in New soft tissue injury patients do so. Is it then fair to expectYork City and St. Louis City Hospital, I can assure you that every patient must recover in 4 to 6 weeks or in some that the emergency room doctor’ s duty is not to concern other arbitrary length of time and that benefits will be cuthimself or herself with chronic conditions. The duty is to off at the end of that predetermined time period regardless keep the patient alive, diagnose any acute injuries, and of whether the patient and the treating physician maintainrefer to the appropriate follow-up physician. otherwise? How frustrating it must be for the clinician and An Australian study (Taylor & Taylor, 1996) revealed the patient to be told that the injury in question shouldthat even though cervical spine X-rays had been read as have healed within a certain period of time, yet knowingnormal, there was a great deal of damage done to cervical that there is still much more to be done to get the patient spine structures. Of the 109 cases, 102 or 94% had injuries back on his or her feet. Is the doctor incompetent? Is the more often to the intervertebral joints than to the vertebrae. patient malingering? Why has the patient not recovered Spinal cord injuries were seen in 25% of cases, and nerve within the specified interval of time? This chapter seeksroot injuries in 14 to 33% of cases. This is consistent with to answer such questions and perhaps to outline a strategy the fi ndings of an earlier study (Jonssan, Bring, for the clinician to practice to the best of his or her abilityRauschning, & Sahlstedt, 1991). Is it any wonder that a without interference and for the patient to receive what-patient with an occult cervical spine fracture without disever damages he or she is entitled to as a result of someone location would be in intense pain and perhaps not be given else’s negligence. sufficient medication … or suf ficient respect? After all, the cervical spine X-ray was normal. Would such a sequence of events not make the ground fertile for the CERVICAL SPRAIN: AND BEYOND development of such chrohnic problems as dizziness (Mallison, Longridge, & Peacok, 1996), headache (Lord & The scenario of a patient complaining of intense neck pain Bogduk, 1996), widespread musculoskeletal pain, or even after a trauma, such as a motor vehicle accident, despite a normal cervical spine X-ray is a common occurrence infibromyalgia (Buskila, 1997a)? our society. What is causing the pain? There is no fracture; Persistent symptoms after whiplash injuries have been the speed of the respective motor vehicles was not great; the subject of several review articles (Curtis, Spanos, & the physical damage to the vehicles was negligible. WhyReid, 1995; Havsy, 1994a; Havsy, 1994b) and books is the patient still in pain? The answers to these questions (Foreman & Croft, 1988; Swerdlow, 1998; Tollison & probably lie in the ability to more fully appreciate the Satterthwaite, 1992). Various factors have been demonmechanisms of cervical injuries and the potential for suchstrated to influence long-term outcome. A statistically siginjuries to evolve into a chronic pain state that for far toonificant positive correlation has been shown to exist long may have been underestimated. between poor prognosis (i.e., chronic pain and impairFor example, it might seem logical that the greater thement) and the following findings shortly after the trauma: impact of two vehicles in a collision and/or the greaternumbness and/or pain in either arm, sharp reversal of the the property damage sustained by these vehicles, the more cervical lordosis as demonstrated on cervical spine X-ray, serious and intense is the chronic pain suffered by those need for a cervical collar for more than 12 weeks, need injured. However, the conventional wisdom identified byfor home traction, or need to resume physical therapy the previous statement seems to be incorrect. A study by more than once because of a recurrence of symptoms Croft (1996) showed that there was no scientifically or(Hohl, 1974). This early study also showed that recovery empirically sound basis for judging injury potential from occurred in only 57% of patients after 5 to 6 years. Degenthe speed of the involved vehicles or from vehicle propertyerative changes developed after the injury in 39%.

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A later study (Gargon & Bannister, 1990) with a headaches) is available. Brain Single Photon Emission longer follow-up period (mean 10.8 years) revealed thatComputerized Tomography (SPECT) scanning is a useful, only 12% of patients who had sustained soft tissue injuries relatively noninvasive (i.e., one intranvenous injection of of the neck recovered completely. The authors reported a radioactive isotope), fairly safe, and sensitive test (Holthat residual symptoms wereintrusive” “ in 28% and man & Devous, 1992; Nedd, et al., 1993; Newton, et al., “severe” in 12%. They further noted that after 2 years1992; Wyper, 1993). Although the SPECT scan does not from the date of the trauma, symptoms did not tend tomake the diagnosis (the clinician needs to correlate the alter with the further passage of time. Persistent symptoms results with all other aspects of the patient’ s problem), it posttrauma are not limited to neck pain, stiffness, headcan be a very useful tool in making an accurate diagnosis aches, etc. Cognitive deficits have been noted in patients and in directing therapy. If a patient has an imbalance in with cervical spine injuries (Radanov, Dvorak, & Valach, brain circulation as measured by a brain SPECT scan, the 1992). These included dizziness, poor concentration, irri-rationale for the use of such prophylactic agents mentability, sleep disturbances, forgetfulness, loss of control,tioned earlier is obvious and compelling. On the other and many others — including, most commonly, head-hand, if the posttraumatic headaches have their origin in aches. muscle tension or intervertebral joint pathology with little, if any, contribution from abnormalities in cerebral circulation, then the treatment plan would weigh more heavily POSTTRAUMATIC HEADACHES in favor of trigger point therapy, anti-inflammatory/antiarthritic medication, or physical modalities such as manipMany patients complain of rather severe headaches after ulation/adjustment, etc. being involved in traumatic events such as a motor vehicle accident or a fall. The cause of posttraumatic headaches Patients with cervical spine injuries who complain of headaches may also have a MTBI that should be evaluated has been known for many years. Often it is a mixed headthoroughly. One must not assume that the chronic headache disorder developing because of muscle tension and ache is cervicogenic, although there may be a cervicogenic vascular type of headache phenomena. In fact, many patients with cervical spine trauma also have mild trau-component. Brain SPECT scanning is a relatively noninmatic brain injuries (MTBIs) that can result in the patientvasive and potentially very helpful test and is much more suffering from chronic headaches resembling migrainessensitive than magnetic resonance imaging (MRI) or comin their intensity, characteristics, and frequency. Someputed tomography (CT) (Tikofsky, 1994) and twice as neurologists have called such headaches posttraumatic sensitive as computerized electroencepholography (Romano, 1995) for detecting chronic traumatic brain migraines. I prefer the termposttraumatic headaches or posttraumatic vascular headaches because these terms injury. I must stress that in the initial evaluation of patients suspected of having an acute brain injury, MRI and/or CT tend not to be confused with common migraine headaches, typically idiopathic in nature. Often patients who com- can be invaluable. Such problems as subdural hematomas and intracerebral hemorrhage can be promptly identified plain of headaches after an injury are treated symptomatically but little is done to look into the mechanism of the with the preceding techniques and emergency measures headaches or to validate the patient’ s complaints with can be taken. Brain SPECT scanning in the context of posttraumatic headaches should be utilized if the patient objective testing. Perhaps it is because such patients are has persistent headaches and/or cognitive dysfunction not believed or are thought to be exaggerating their pain. Many such patients are involved in litigation, making theirmonths, or even years, after the trauma. At that point motives suspect to the inadequately trained clinician. Itintracerebral pathology either had been ruled out or was no longer a realistic consideration. must be stressed that there is no medical evidence that Many patients who have suffered whiplash injuries faking such symptoms is common. A study (Packard, 1992) written to put this questionalso complain of a veritable litany of symptoms including light-headedness, dizziness, vertigo, double vision, to rest consisted of a large series of patients diagnosed blurred vision, ringing of the ears, being hard of hearing, with posttraumatic headaches. These patients continued memory problems, trouble concentrating, being easily disto seek treatment and had persistent symptoms, often severe, despite the resolution of their litigation. That beingtracted, fatigue, anxiety, excessive sweating, sadness, trouble sleeping, moodiness, irritability, changes in menstrual the case and knowing that certain medications such as calcium channel blockers, beta-blockers, and tricyclicperiods, impaired vaginal lubrication, impotence, and lack of interest in sex. Do these patients haveficient suf injuries agents can be used prophylactically to prevent vascular headache symptoms vis( a vismigraine), then the need to to their brains to be considered as suffering postconcussional problems? indentify those patients whose posttraumatic headaches have a vascular component becomes obvious. Such conditions can arise even if there is only a A method to detect vascular instability in the cerebralmomentary change in the level of consciousness — and circulation (often a harbinger of intense vascular-typeeven if no change in consciousness — at the time of the

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trauma. Closed head injuries have been associated with level.” Once the nervous system exhibits “posttraumatic depression, anxiety, personality changes, cognitive defihyperirritability” or other perpetuating factors exist and cits, and other such symptoms (Kant, 1996). This neu-are left untreated, “an acute myofascial pain syndrome robehavioral morbidity is more common than oncecharacteristically becomes chronic. ” believed (Brown, Fann, & Grant, 1994) and, if not treated, When I first read the preceding description, I immedican cause severe impairment, resulting in a marked deteately knew that Dr. Simons and I had something in common. rioration in the quality of life. This often manifests itself We both saw numerous chronic pain patients and we both as the loss of one’ s job, marital difficulties, and the loss took the time to analyze their situations. He could have of friendships. Economic hardship often accompanieseasily been describing patients I see and treat every day. He these other problems. and I know these patients are suffering and in trouble. They did not choose to be injured; they need our help. The concept of perpetuating factors has been known MYOFASCIAL PAIN SYNDROME for many years (Travell & Simons, 1983), yet many The definition and characteristics of myofascial pain syn-patients who have severe, chronic MPS (often posttrauma) drome (MPS) have been amply covered in this textbookare met with skepticism and even disbelief. Bayer (1999, (Margoles, 1998; Gerwin & Dommerholt, 1998) and otherp. 171) wrote, “It is amazing if not amusing that insurers texts (Travell & Simons, 1983; Rachlin, 1994). The diag-and their attorneys cannot believe that a patient who has suffered an injury can continue to experience symptoms nosis of MPS is based on the detection of objective abnor” malities on careful physical examination. These includeof pain months or years after the injury. However, the reality of the situation can be summed the findings of trigger points, taut myofascial bands, local up as follows: (1) some patients develop severe, chronic twitch responses of the taut bands (Simons, 1987), and MPS and even FS as the result of an injury; (2) some of even characteristic electrical activity of trigger points these patients are treated unfairly and are not evaluated measured by the electromyogram (Hubbard & Berkoff, thoroughly because they may not be believed, especially 1993; Romano & Stiller, 1997). The role of trauma in the generation and perpetuationwhen personal injury litigation is pending; and (3) the pain of trigger points, long known to be the hallmark physicalmanagement specialist must rely on medical knowledge and scientific validity in formulating diagnoses and progfindings of MPS, was perhaps most succinctly stated by Rachlin (1994): “Injuries and surgical procedures maynoses— not on bias or innuendo. lead to the formation of trigger points causing repeated Stress plays a role in the severity of illness — any illness, not just musculoskeletal or neurological. What episodes of pain. ” The worst cases of MPS seem to be the result ofsane physician would encourage a patient with high blood pressure, heart disease, or ulcers to continue a stressful traumatic events such as an automobile accident or fall. and unhealthy lifestyle? Thus, in treating the patient with Simons (1987) noted that such patients “suffer greatly and are difficult to help.” He went on to write, “They exhibit chronic MPS, the clinician needs to help minimize stress a posttraumatic hyperirritability of their nervous system— not contribute to it. The evaluation and treatment must and of their trigger points. ” The trauma in question, be done honestly and professionally, realizing that the vast majority of patients diagnosed with posttraumatic MPS according to Simons, is “severe enough to damage the (PTMPS) are in a great deal of pain; they also are probably sensory pathways of the central nervous system. ” In a study of Israeli trauma victims (Buskila, Neumann, Vais-anxious, depressed, and frustrated due to the severity and berg, Alkalay, & Wolfe, 1997a), the authors suggested thatlongevity of their pain as well as probably having previthe reason fibromyalgia syndrome (FS) followed neckously been given “short shrift” by a system that is supinjury 13 times more often than lower extremity injury posed to help them. If patients with PTMPS are not treated promptly or if their pain cannot be controlled, they may was because of this very mechanism. The involvement of the nervous system probably is very important in the per-even develop FS. petuation and prolongation of the pain, thus preventing full recovery. Simons (1987) opined that damage to thePOSTTRAUMATIC FIBROMYALGIA nervous system “… apparently acts as an endogenousSYNDROME perpetuating factor susceptible to augmentation by severe pain, additional trauma, vibration, loud noises, prolongedFS is a soft tissue rheumatic disorder characterized by pain associated with a defiphysical activity, and emotional stress. ” In describing the widespread musculoskeletal ciency of deep (i.e., stage 4, non-rapid eye movement, patients who developed such severe MPS, Simons noted, “From the date of the trauma, coping with pain typically delta wave) sleep, headaches, fatigue, decreased stamina, and other symptoms (Romano, 1990). A committee becomes the focus of life for these patients who previously paid little attention to pain. They are unable to increaseappointed by the American College of Rheumatology their activity substantially without increasing their pain (ACR) published FS criteria (Wolfe, et al., 1990) that are

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still in use todaynot only in the United States but also 1997). These authors correctly state that the Vancouver throughout the world. Consensus Report is likely to be used in the legal setting The concept of posttraumaticbromyalgia fi syndrome and further aptly remark that in such a setting “…causality entails only 51% certainty, usually stated in terms of rea(PTFS) has been discussed in another chapter in this book ” They go on to state that “…it (Romano, 1998a). However, additional remarks concern-sonable medical probability. seems more than 51% likely that trauma does play a causing the validity of a PTFS diagnosis need to be stressed. ative role in some FMS (fibromyalgia) patients…”. They There have been numerous reports and book chapters in cite articles on clinical patterns (Bennett, 1993; Moldofwhich the authors link trauma and FS (Bennett, 1989; sky, et al., 1993; Pellegrino, 1996; Romano, 1990; Wolfe, Greenfield, Fitzcharles, & Esdaile, 1992; Moldofsky, 1994), other case studies (Bengtssom, et al., 1986; BusWong, & Lue, 1993; Rice, 1987; Saskin, Moldofsky, & kila, et al., 1997a; Greenfield, et al., 1992; Yunus & Alday, Lue, 1986; Smythe, 1989). Despite this wealth of infor1993), and biological plausability concerning central nermation, most doctors at a conference in Vancouver, Britvous system plasticity (Coderre, Katz, Vaccarino, & ish Columbia, in 1994 could not link trauma to FS in a Melzack, 1993; Dubner & Ruda, 1992; Yunus, 1992) as cause–effect relationship. They concluded that at the time “…data from the literature are insuf ficient to indicate the basis of that statement. whether a causal relationship exists between trauma and FS does not develop after all, or even most, traumatic FM (fibromyalgia)” (Wolfe, 1996). Many of the confer- events but it can evolve after such traumas as physical ence attendees opined that based on only four studies assaults, motor vehicle accidents, and/or falls. FS takes at published up to that time (Greenfi eld, Fitzcharles, & least 3 months to evolve according to ACR criteria (Wolfe, Esdaile, 1992; Moldofsky, Wong, & Lue, 1994; Romano,1990). Thus, FS does not occur at the exact time of the 1990; Saskin, et al., 1986) they did not have enoughtrauma, but instead can develop weeks to months later as evidence to conclude that trauma could cause FM. The a direct consequence of the trauma. The real question committee chairman, Dr. Wolfe, was quick to add thatconfronting the clinician and about which he or she may the absence of evidence “…however, does not mean that need to offer legal testimony is whether a specific trauma causality does not exist, rather that appropriate studies caused a specific FS in a specific patient at a specific time. have not been performed. ” Since the Vancouver confer- To determine that, a careful record review, a thorough ence, subsequent articles have been published (Aaron, medical et history, and a physical examination must be al., 1997; Alexander et al., 1998; Waylonis & Perkins,obtained so that a conclusion can be reached based on the 1994) linking trauma and FM including a case reportfacts as opposed to prejudice or bias. (Wolfe, 1994) and a controlled study of 161 cases of Infections can also trigger or precipitate the developtraumatic injury (Buskila, et al., 1997a) — both authored ment of FS. An association between infections and FS has by Wolfe. In the latter study, Wolfe and the other authorsbeen known for a long time (Beetham, 1979). There have conclude that FM was 13 times more frequent followingbeen numerous case reports of patients developing FS as neck injury than following lower extremity injury. Fur- a result of certain infections. For example, FS has been thermore, the article ends with the following two sen-reported to have been caused by hepatitis virus (Buskila, tences:“ Thus, trauma may cause FMSbromyalgia (fi syn- et al., 1997b), human immunodefi ciency virus (HIV) drome), but it does not necessarily cause work disability.(Simms, et al., 1992), Borrelia burgdorferi(Lyme disease) These findings have important implications for many (Dinerman & Steere, 1992), and coxsackie virus and parindustrialized countries. ” vovirus (Leventhal, Naides, & Freundlich, 1991). GolDespite these new data, the Vancouver conference prodenberg (1993) attempted to explain how infections trigceedings continue to be quoted out of context and sections ger FS by theorizing that such infections may “promote a of the text have been unfairly used to discredit patientsmaladaptive behavior pattern which secondarily leads to who have developed PTFS. As an attendee of the Vancoufibromyalgia.” Other explanations, including a disruption ver FS Conference and a participant in the discussions,ofI normal sleep pattern and/or endocrine abnormalities, did not initially appreciate that this academic endeavormay be equally valid. would be used for purposes unintended by most, if not Regardless of how infections trigger FS, they can and all, participants. When I returned from the conference, Ido cause FS in some patients. Considering that the preswitnessedfirsthand how attorneys and even medical eval-ence of FS diminishes the quality of life (Burckhardt, uators have incorrectly stated the findings of the Vancou-Clark, & Bennett, 1993; Martinez, Ferraz, Sato, & Atra, ver conference to gain an advanatge in such medico-legal 1995; Turk, Okifuji, Sinclair, & Starz, 1996), the develproceedings as depositions and even trials. opment of FS as a result of an infection is an important Such misrepresentations, often blatant, of what hap-component of the patient’ s medical history. If the infection pened at that meeting motivated some attendees to publish comes about as the result of negligence or even malice, a report to correct any misconceptions about the Vancouthe clinician may be called on to render an expert opinion ver conference (Yunus, Bennett, Romano, Russell, et al., concerning causation, severity, and prognosis.

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If asked to testify in court concerning soft tissue inju- author notes that there is no substitute for clinical acumen ries, the healthcare professional must remember that the and that these formulas must not be used as a substitute for court needs to know (1) what the patient is suffering from,sound clinical judgment. (2) whether the medical problem (e.g., FS or MPS) could have been precipitated or caused by trauma, (3) whether DISABILITY the problem was indeed precipitated or caused by the accident/incident in question (i.e., if the trauma had notThe assessment of impairment and disability can be a occurred, would the patient have this problem), (4)difficult task, especially when the patient in question whether the problem is temporary or permanent, and (5) has chronic pain (Teasell & Merskey, 1997) with little what the cost of future care will be for the patient for theor no skeletal deformity as is the case with soft tissue injuries sustained in the accident/incident. The court needs rheumatic syndromes such as FS and MPS (Bennett, to know these facts to a reasonable degree of medical 1996; Crook, Moldofsky, & Shannon, 1998; Monsein, probability or certainty. The physician’ s education, train- 1994; Reilly, 1998). Because the issues are varied and ing, and experience, as well as his or her knowledge of complex, only clinicians with suf ficient knowledge and the particular patient in question, should be the basis for experience in the evaluation and treatment of such giving such opinions. patients should render opinions concerning disability There is no cure for FS and it does not decrease (Bennett, 1996). longevity. Therefore, the use of standard actuarial/mortal- The majority of patients who suffer from painful soft ity tables such as those provided by government agencies tissue problems remain in the workforce. However, some (Vital Statistics of the United States, 1992) is a reasonable are so impaired that they need to seek disability benefits. way to determine the number of additional years a givenFor example, patients with FS caused by trauma or illness patient is expected to live. are more disabled than other FS patients (Greenfield, et With that information and the knowledge of what the al., 1992). FS is as disabling as rheumatoid arthritis (Bomindividual PTFS patient would need for his or her futurebardier, et al., 1986; Cathey, Wolfe, & Kleinheksel, 1988; care, the practitioner would be in a good position to render Russell, Fletcher, Tsui, & Michalek, 1989). The FS patient an opinion as to the cost of future medical care for thecan be disabled because of not only pain but also inability treatment of the injuries in question. Typically this treat-to perform repetitive muscular tasks (Bennett, 1993); the ment would include of fice visits, oral medications (e.g., disability is probably because of fatigue, abnormal hormuscle relaxants, analgesics), topical preparations (lini-mone production, and other factors including lesions in ments), local injections, physical modalities (e.g., massage muscle that result in low levels of high-energy phosphates therapy, manipulation, or adjustment), and blood tests to and altered microcirculation. Some FS patients can remain determine whether the oral medications were causing side employed only if there are significant workplace modifieffects, etc. cations. These include reverting to part-time status, The treatment of FS can result in diminution of symp-freelancing if possible, and alteration of the patient’ s toms with resultant clinical improvement, albeit tempo- workstation itself including the provision of special ergorary. A cure, thus far, has not been forthcoming (Kennedynomically suitable aids. When these fail or are impractical, & Felson, 1996; Wolfe, et al., 1997a; Wolfe, et al., 1997b).FS patients often enlist the aid of their doctors in obtaining It has been reported that cost of treatment of FS patients disability benefits. is substantial (White, Speechley, Harth, & Ostbye, 1999; What is meant by the term disability? The Social Wolfe, 1995), in part due to the chronicity of this syn- Security Administration (1998) defi nesdisability as,“An drome. Often the cost of future treatment for the remainder inability to perform any substantial gainful activity of a patient’s life is in six figures, especially if the patient because of a medically determinable physical or mental is under the age of 40, and therefore is likely to liveimpairment which can be expected to last for a continuous another 30 to 40 years (Vital Statistics, 1992), or if theperiod of not less than 12 months. ” Of course, there are patient in question requires a large number of medications numerous other sources of potential disability benefi ts or procedures. Of course, these projections must be tailorranging from private insurance disability policies to benmade for each individual patient. efits offered by companies and state agencies. The fi- de An even greater challenge to the pain practitioner is the nition of disability by these other entities must be ascertask of estimating the relative contribution of each of severaltained by reading the individual policies. Consequently, traumas to the patients’ chronic pain state. Although the a discussion of this topic must of necessity be limited to clinician must call on his or her years of education, training,the Social Security system’ s definitions and procedures. and experience to perform such an apportionment, a method To that agency,“ substantial gainful activity”means work to help do this using mathematical formulas has been pubthat “ (a) involves doing signifi cant and productive physlished (Romano, 1998b). This method can be applied to ical or mental duties; and (b) is done (or intended) for patients with either PTFS, PTMPS, or both. However, thepay or profit.”

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There are several reasons why a person would not be addresses itself to the patient’ s pain and the credibility of eligible for Social Security disability benefits. If a person the patient. Where applicable the physician should also is working (except in a “sheltered” setting) even if chron-indicate that he or she has expertise in FS and has treated ically ill or if he or she has recovered within 12 monthsmany such patients. Because of the nature of FS and of the onset of a potentially disabling illness, benefits areunfounded bias against this diagnosis, it is worthwhile for not granted. Furthermore, benefits are denied if the claimthe doctor to state emphatically that the patient is not ant is judged not to have a medically determinable impair-exhibiting secondary gain or is not a malingerer. It is ment. That is where the patient’ s treating physician essential to state that the patient’ s symptoms are consistent becomes a part of the disability process. with the findings and diagnosis of FS. The role of the physician in the disability process is The Social Security system tends to be slow and somea crucial but often frustrating one. Often the patient doeswhat reluctant in granting disability benefits in general. not understand that the determination of partial or totalTherefore, if the initial application is rejected, the truly disability does not rest in the hands of the doctor. In truth,disabled FS patient needs to follow an orderly and logical the physician may be able to rate impairment but disabilityprocess to obtain disability benefits. There are several is usually determined by a board that not only takes intosteps ranging from a request for reconsideration to a hearaccount the patient’ s impairment but also considers other ing before an administrative law judge to an appeal factors such as the individual’ s age and education, job through the U.S. District Court. An attorney, of course, is opportunities, and local economy. Although the doctornecessary for these latter two steps in the disability promay be convinced that the patient is disabled, he or she cess. Paradoxically, even the denials can be helpful to the often is put in the unenviable position of having to explainapplicant, because they usually contain suggestions for the vagaries and intricacies of this system to the patient alternative work possibilities (practical or not) and may who has just been denied disability benefits. suggest changes in strategy. This turn of events is especially likely for the patient For example, because there is no specific listing for with FS. The reasons for this are numerous. Despite the FS (as is also the case with newly described diseases and establishment of FS criteria by the ACR in 1990 and insyndromes) and if the patient is denied disability benefits subsequent studies showing that FS patients have numeron the basis of FS, the physician may be able to find ous objectively measurable abnormalities (e.g., low mag-“acceptable” disease entities (i.e., those that are listed) nesium levels (Romano and Stiller, 1994); decreased that could explain the patient’ s symptoms. Many FS growth hormone levels (Bennett, Clark, Campbell, & patients exhibit, in addition to musculoskeletal pain and Burkhardt, 1992)), the very existence of FS is doubted byfatigue, many psychiatric symptoms such as anxiety, those who have not kept up with the medical literature.and/or depression (listing 12) or may be considered to Furthermore, the physician may have aficult dif time in have a somatoform disorder (listing 12.07). This is not to rating impairment and justifying that rating to disability suggest that FS is a psychiatric disease but the ravages of boards because the American Medial Association Guide FS with its concomitant chronic pain, sense of loss, and to the Evaluation of Permanent Impairment does notecnomic hardship certainly can predispose one to psychoaddress FS. In fact, this publication needs revision for a logical problems. Another tactic is to attempt to get disnumber of different reasons (Cocchiarella, Turk, & Ander-ability benefits based on organic brain dysfunction (i.e., son, 2000; Speiler, Barth, Burton, Himmelstein, & diffuse impairment of cerebral tissue function), which is Rudolph, 2000). Finally, the FS patient typically does notlisted as 12.02. Many FS patients have significant cognilook ill. tive problems that have been correlated with brain abnormalities detected by cranial SPECT imaging (Romano & However, despite all these apparent disadvantages, the FS patient who cannot work should apply for disability Govindan, 1996), an objective neurodiagnostic test. Although this may not be the most ideal way to obtain benefits with the expectation that fairness and reason will prevail. For this to happen, a collaborative effort betweenbenefits, it may be the only recourse for some FS patients, patient, physician, and — in most instances — attorneyespecially under the present circumstances. is necesary (Potter, 1992). The FS patients who are denied disability benefi ts freThe treating physician’ s medical report is essential for quently ask me to explain why they were not granted what the awarding of disability benefits, but the doctor mustthey felt they deserved. I cannot answer this question fully take care to provide detailed and clear (and, of course, because I am not privy to the machinations and workings of honest) statements concerning the patients’ impairments. the disability boards. However, I have a good idea why FS Terse opinions that the patient cannot work or is disabled patients frequently run into problems. It stems from how the are insufficent. The narrative report should follow a famil- FS patient is perceived. There are many different ways the iar forensic format with a detailed history, a thoroughFS patient may be viewed depending on the nature and/or physical examination, an enumeration and explanation of bias of the observers. For example, managed care and health relevant test results, and a discussion that directlymaintenance organizations claim that healthcare costs must

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be curbed. That translates into the very real possibility that broad knowledge base necessary for understanding the doctors are to be limited in what they can do for their patients biopsychosocial concept of disease. ” I heartily agree with — FS and MPS sufferers included. If chronic soft tissuehis opinion that it is “preferable that both (those) groups problems such as FS and MPS are perceived to be less exempt themselves, from the disability evaluation proimportant than other disorders, these patients may go undicess.” One can but hope … and dream. agnosed, untreated, or undertreated. It certainly seems that it is in the best interest of the health insurance industry to THE CLINICIAN IN THE COURTROOM withhold or delay issuing funds for care. Anyone who doubts this statement has only to read articles that appeared The in pain management clinician should take an active role American Medical News(Jacob, 1998; Mitka, 1996) in the legal process. First, as a member of the community describing the high salaries of managed care executives. he or she should get involved in community matters, espeGovernmental agencies, moreover, experience budgetary cially those that affect his or her patients. Obviously this constraints. This has been especially true as the national debt may include the medical/legal arena. If the clinician has has risen. Thus, patients whose problems are not immediknowledge concerning a patient’ s medical condition that ately life-threatening make handy scapegoats for the healthwould benefit the court, the practitioner has a duty to care providers who treat them. present that knowledge at the proper time whether it be What is the answer? How is the FS patient to proceed? in the form of a deposition or as an expert witness giving If the FS patient is truly unable to work, he or she musttestimony in a courtroom. I am not alone in this opinion. become thoroughly familiar with the disability determi- As a member of the American Medical Association nation process and proceed accordingly. The treating phy(AMA) and as a Fellow of the American College of Physician’s report is a very important part of this process. Thesicians, I have reviewed the ethics manuals for each group FS patient, however, must not be unduly discouraged by (American College of Physicians, 1998; American Media system that is less that ideal. It is only through dogged cal Association Council on Ethical and Judicial Affairs, determination and persistance that justice is truly served 1996–1997). Both publications clearly state that if the not only for the individual FS patient presently seekingphysician has knowledge that can be useful to the court, disability benefits but also for all FS patients who ulti- it is his or her duty to present such knowledge when asked. mately need respect and understanding from our society I have participated in hundreds of trials and deposiin addition to medical treatment. tions mostly as a witness giving expert medical testimony Even more frustrating and challenging is the task ofconcerning patients that I am actively treating. Some attorrendering an opinion as to the extent of partial disabilityneys have wrongly intimated that because of this, I cannot or impairment. How does one give such an opinion for FSbe objective, that I have an interest in the outcome of the patients, for example, whose symptoms wax and wane case, and/or that I am being less than truthful in my depending on such variables as weather changes, stress, responses because the plaintiff in question is my patient. and severity of concomitant illnesses? One way to perform These are common tactics used to undermine the credisuch an analysis is to do so by having the patient fill outbility of expert witnesses. However, despite the innuendo pain and activity questionnaires (Callahan, Smith, & Pin-I willingly testify at trials because I believe it is the right cus, 1989; Meenan & Pincus, 1987; Pincus, Summey, thing to do, especially considering my unique perspective Soraci, Hummon, & Wallston, 1983; Wolfe, 1995) on as a pain management specialist. This is even more so if multiple occasions or keep a daily diary of symptoms andthe patient in question is being treated by me and I have activities. If, for example, half the time a particular patientexamined him or her on numerous occasions. When I is totally incapacitated (even bed-bound) due to severe FS perform a medical evaluation for the purpose of rendering pain, fatigue, or excrutiating headaches, but the remainder an opinion only, I strive to be objective, relying on estabof the time, normal activities can be pursued, then it islished criteria for FS and MPS as well as testing with a reasonable to assign that particular patient a 50% impairdolorimeter and a tissue compliance meter (Smiley, Cram, ment of the “whole person. ” There is no easy formula to Margoles, Romano, & Stiller, 1992). estimate impairment and/or disability for the patient with The court is not interested in “may be” or “could” be. FS or other forms of painful soft tissue rheumatic prob-The court wants to know whether a patient has a particular lems. That is where the skill and experience of the clini-condition as a result of a particular trauma “to a reasonable cian truly comes into play. degree of medical probability. ” That means is it more Bennett (1996) noted that for FS patients a biopsy-likely than not that the trauma in question caused the patient to develop a medical problem for which he or she chosocial model of disease must be used in their disability evaluations and that opinions need to be expressed is in being treated. For example, did the motor vehicle acciterms of reasonable probability. He further states thatdent of 3 years ago cause the patient to develop FM? One does not need to know with 100% certainty that a given some physicians feel “uncomfortable” in the assessment s medical problem in question; of chronic pain and “others will not have acquired thetrauma caused a patient’

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however, based on the clinician’ s education, training, and formed, or lacking in scientific/medical validity. Doing so experience he or she often can given an opinion “to adoes not make the clinician an advocate in court, but reasonable degree of medical probability” whether theinstead it helps the court make a decision based on sound trauma in question caused a patient’ s injuries. This is an medical principles as opposed to ignorance and/or misimportant concept and one that is often lost on academirepresentations. cians and scientists who are used to expressing their It should be remembered that medicine is an art that thoughts to a degree of certainty approaching 95 to 100%.uses scientific principles, but an art, nonetheless. Some The court is especially interested in the objective find-medical experts are more skilled than others. The clinician ings that help form the bases for the opinions rendered. who specializes in pain and has particular expertise in After performing a range of motion and/or a trigger pointevaluating individuals claiming chronic painful problems examinations, the clinician in the role of expert witnessposttrauma deserves to have his or her opinions regarded must stress that such findings on physical examination are carefully and with respect. So, too, do our patients deserve objective. Other objective findings include muscle spasm,our respect and that of the courts. jump signs, swelling, discoloration, especially reticular skin changes, taut myofascial bands, muscle atrophy, asymmetry of muscle size or strength, and deep tendon REFERENCES reflex abnormalities. The greater the skill of the examiner, the more likely such abnormalities will be observed andAaron, L.A., Bradley, L.A., Alarcon, G.D., Triana-Alexander, M., Alexander, R.W., Martin, M.Y., & Alberts, K.R. recorded. Most neurologists and orthopedists do not have (1997). Perceived physical and emotional trauma as prethe required expertise to perform an FS tender point count cipitating events in fibromyalgia. Arthritis and Rheumaor an MPS trigger point exam. According to Simons tism, 40,453–460. (1987), the diagnosis of FS and/or MPS “…would probAlexander, R.W., Bradley, L.A., & Alarcon, G.S., Trina-Alexably be missed on routine conventional examination. The ander, M., Aaron, L.A., Alberts, K.R., Martin, M.Y., & examiner must know precisely what to look for, how to Stewart, K.E. (1998). Sexual and physical abuse in look for it, and then must actually be looking for” Is it. it women with fibromyalgia: Association with out-patient any wonder that patients who have been diagnosed with health care utilization and pain medication usage. either FS and/or MPS are sent by insurance companies to Arthritis Care and Research, 11, 102–115. doctors with little or no experience in the diagnosis ofAmerican College of Physicians. (1998). Ethics manual (4th ed.). these disorders? Is it not in the best economic interest of Annals of Internal Medicine, 128, 576–592. American Medical Association. (1993). Guide to the evaluation such corporations to muddy the waters, so that the true of permanent impairment. Chicago: American Medical extent of the patients’ injuries are not appreciated? Association. However, absence of proof is not proof of absence. It is beyond the control of the pain practitioner to alter theAmerican Medical Association Council on Ethical and Judicial Affairs (1996–1997 edition). Code of medical ethics. view of the insurance industry that invididuals who claim Current opinions with annotations. Section 9.07 (pp. not to have recovered from an injury and therefore suffer 148–149). Chicago: American Medical Association. resultant chronic painful conditions are exaggerating their Ashburn, M. A., & Fine, P. G. (1989). Persistent pain following pain, malingering, or suffering from mental problems. trauma.Military Medicine, 154,86–89. However, it is within the expertise of the knowledge- Bayer, J.D. (1999). Defense of a trigger point patient: Trigger able clinician to be diligent in taking a medical history, points are myogenic, not psychogenic. In M. Margoles circumspect in reviewing pertinent medical records, and & R. Weiner (Eds.),Chronic pain assessments, diagnothorough in performing a physical examination so that he sis and management (pp. 171–178) . Boca Raton, FL: or she can make an accurate diagnosis in the ficeofand CRC Press. explain the salient findings in legal proceedings. What isBeetham, W.P. (1979). Diagnosis and management of fibrositis syndrome and psychogenic rheumatism. Medical Clinwrong with the best trained and most skilled examiners ics of North America, 63, 433–439. testifying in court? It appears to be in the best interest of Bengtsson, A., Henrikson, K.C., Jorfeldt, L. Kagedal, B., Lennthe insurance companies to place blame on the patient and marker, C., & Lindstron, F. (1986). Primary fibromyalto ignore important facts about MPS and/or FS as well as gia. A clinical and laboratory study of 55 patients. Scanother important details about those individuals suffering dinavian Journal of Rheumatology, 15, 340–347. from disorders stemming from a traumatic event. Bennett, R.M. (1989). Fibrositis. In W.N. Kelley, E.D. Harris, The clinician as an expert witness must not take sides S. Ruddy, & C.B. Sledge (Eds.), Textbook of rheumain a personal injury lawsuit. He or she must be honest, tology (3rd ed., pp. 541–553). Philadelphia: W. B. Sauntruthful, and professional at all times. However, having ders. sworn to tell the whole truth, he or she must point out toBennett, R.M. (1993). Disabling fibromyalgia: Appearance verthe court if and how insurance company adverse medical sus reality [Editorial]. Journal of Rheumatology, ,11 evaluations were either inadequate, inappropriately per1821–1824.

178

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Bennett, R.M. (1996). Fibromyalgia and the disability dilemma.Gerwin, R.D., & Dommerholt, J. (1998). Treatment of myofascial pain syndromes. In R. S. Weiner (Ed.), Pain manArthritis and Rheumatism, 39, 1627–1634. agement: A practical guide for clinicians (5th ed., pp. Bennett, R.M., Clark, S.R., Campbell, S.M., & Burkhardt, C.S. 217–230). Boca Raton, FL: St. Lucie Press. (1992). Somatomedin C levels in patients with the fibromyalgia syndrome: A possible link between sleep andGoldenberg, D.L. (1993). Do infections trigger fibromyalgia? Arthritis and Rheumatism, 36, 1489–1492. muscle pain.Arthritis and Rheumatism, 35, 1113–1116. Bombardier, C., Ware, J., Russell, I.J., Larson, M., Chalmers, A.,Gould, S.J. (1996).Full house. New York: Harmony Books. & Read, J.L. (1986). Auranofi n therapy and quality of life Greenfield, S., Fitzcharles M.A., & Esdaile, J.M. (1992) Reactive fibromyalgia syndrome.Arthritis and Rheumatism, 35, in patients with rheumatoid arthritis — results of a multi678–681. center trial.American Journal of Medicine, 81 , 565. Brown, S.J., Fann, J.R., & Grant, I. (1994). Post concussionalHavsy, S.L. (1994a). Whiplash injuries of the cervical spine and their clinical sequellae. PartAmerican I. Journal of Pain disorder. Time to acknowledge a common source of Management , 4, 23–31. neurobehavioral morbidity. Journal of Neuropsychiatry, 6, 15–22. Havsy, S.L. (1994b). Whiplash injuries of the cervical spine and their clinical sequellae. Part II. American Journal of Pain Burckhardt, C.S., Clark, S.R., & Bennett, R.M. (1993). FibroManagement,4, 73–82. myalgia and quality of life. A comparative analysis. Journal of Rheumatology, 20, 475–479. Hohl, M. (1974). Soft-tissue injuries of the neck in automobile accidents. Factors influencing prognosis. Journal of Buskila, D., Neumann, L., Vaisberg, G., Alkalay, D., & Wolfe, Bone and Joint Surgery, 56-A, 1675–1682. F. (1997a). Increased rates of fibromyalgia following cervical spine injury. Arthritis and Rheumatism, 40, Holman, B.L., & Devous, M.D., Sr. (1992). Functional brain SPECT: The emergence of a powerful clinical method. 446–452. Journal of Nuclear Medicine, 33, 1888–1904. Buskila, D., Shnaider, A., Neumann, L. Zilberman, D., HilBuskila, D., Shnaider, A., Neumann, L. Zilberman, D., Hubbard, D.R., & Berkoff, G.M. (1993). Myofascial trigger points studied by needle EMG. Spine, 18 , 1803–1807. Hilzenrat, N., & Sikuler, E. (1997b). Fibromyalgia in hepatitis C infection.Archives of Internal Medicine, 157, Jacob, J. (1998, October 5). HMO top salaries average $2 million 2497–2500. in 1997.American Medical News, 28. Callahan, L.F., Smith, W.J., & Pincus, T. (1989). Self-report Jonssan, H., Jr., Bring, G., Rauschning, W., & Sahlstedt, B. questionnaires in five rheumatic diseases. Arthritis Care (1991). Hidden cervical spine injuries in traf fic accident Research, 2,122–131. victims. Journal of Spinal Disorders, 4, 251–263. Cathey, M.A., Wolfe, F., & Kleinheksel, S.M. Arthritis Care Kant, R. (1996). Post concussion syndrome A— neuropsychiatric Research, ,185. perspective.St. Francis Journal of Medicine, 111– 2, 114. Cocchiarella, L., Turk, M.A., & Anderson, G. (2000). Improving Kennedy, M., & Felson, D.T. (1996). A prospective study of the evaluation of permanent impairment. Journal of the fibromyalgia syndrome.Arthritis and Rheumatism, 39, American Medical Association, 283, 532–533. 682–682. Coderre, T.J., Katz, J., Vaccarino, A.L., & Melzack, R. (1993) Leventhal, L J., Naides, S.J., & Freundlich, B. (1991). Fibromyalgia and parvovirus infection. Arthritis and RheumaContribution of central neuroplasticity to pathological tism, 34,1319–1324. pain. Review of clinical and experimental evidence. Pain, 52, 259–285. Lord, S.M., & Bogduk, N. (1996). The cervical synovial joints, as sources of post traumatic headache. Journal of MusCroft, A.C. (1996). Low speed rear impact collision: In search culoskeletal Pain, 4,81–94. of an injury threshold.Journal of Musculoskeletal Pain, 4, 39–46. Mallison, A.J., Longridge, N.S., & Peacok, C. (1996). Dizziness, imbalance and whiplash. Journal of Musculoskeletal Crook, J., Moldofsky, H., & Shannon, H. (1998). Determinants Pain, 4, 105–112. of disability after a work related musculoskeletal injury. Journal of Rheumatology, 25, 1570–1577. Margoles, M.S. (1998). Myofascial pain syndrome: Clinical examinaton and management of patients. In R. S. Weiner Curtis, P., Spanos, A., & Reid A. (1995). Persistent symptoms (Ed.),Pain management: A practical guide for clinicians after whiplash injuries. Implications for prognosis and (5th ed, pp. 191–216). Boca Raton, FL: St. Lucie Press. management.Journal of Clinical Rheumatology, 1, 149–157. Martinez, J.E., Ferraz, M.B., Sato, E.I., & Atra, E. (1995). Fibromyalgia versus rheumatoid arthritis: A longitudinal Dinerman, H., & Steere, A. (1992). Lyme disease associated with comparison of the quality of life. Journal of Rheumafibromyalgia. Annals of Internal Medicine, 117, tology, 22,270–274. 281–285. Dubner, R., & Ruda, M.A. (1992) Activity-dependent neuronal Meenan, R.F., & Pincus, T. (1987). The status of patient status measures. (Editorial).Journal of Rheumatology, 14, plasticity following tissue injury and inflammation. 411–414. Trends in Neurosciences, 15, 96–103. Foreman, S.M., & Croft, A.C. (1988). Whiplash injuries. The Mitka, M. (1996, February 5). HMO executives claim fat paychecks.American Medical News, 3. cervical acceleration/deceleration syndrome. BaltiMoldofsky, H., Wong, M.T.H., & Lue, F.A. (1993). Litigation more: Williams & Wilkins. sleep symptoms and disabilities in post accident pain Gargon, M.F., & Bannister, G.C. (1990). Long-term prognosis (fibromyalgia). Journal of Rheumatology, 20, of soft-tissue injuries of the neck. Journal of Bone and 1935–1940. Joint Surgery, 72-B,904–906.

Trauma and Soft Tissue Injuries: Clinic and Courtroom

179

Monsein, M. (1994). Disability evaluation and management ofRomano, T.J., & Govindan, S. (1996). Abnormal cranial SPECT scanning in fibromyalgia patients with headaches. Amermyofascial pain. In E.S. Rachlin (Ed.), Myofascial pain ican Journal of Pain Management, 118–122. 6, and fibromyalgia(pp. 91–119). St. Lous: Mosby. Nedd, K., Sfakianakis, G., Ganz, W., Uricchio, B., Vernberg, D.,Romano, T.J., & Stiller, J.W. (1994). Magnesium deficiency in fibromyalgia syndrome.Journal of Nutrition and MedVillanveva, P., Jabir, A.M., Bartlett, J., & Kena, J. icine, 40, 165–167. (1993). 99mTc-HMPAO SPECT of the brain in mild to moderate traumatic brain injury patients: ComparedRomano, T.J., & Stiller, J.W. (1997). Needle EMG in myofascial with CI — A prospective study.Brain Injury, 7, pain patients, correlation with physical findings in gen469–479. eral rheumatology practice. American Journal of Pain Management, 7,19–21. Newton, M.R., Greenwood, R.J., Britton, K.E., Charlesworth, M., Nimmon, C.C., Carroll, M.J., & Dolke, G. (1992). Russell, I.S., Fletcher, E.M., Tsui, J., & Michalek, J.E. (1989). A study comparing SPECT with CT and MRI after Comparisons of rheumatoid arthritis and fibrositis/fibroclosed head injury. Journal of Neurology and Psychiatry, myalgia syndrome using functional and psychological 55, 92–94. outcome measures. Arthritis and Rheumatology,32, 570, B121. Packard, R.C., (1992). Posttraumatic headache: Permanency and Saskin, P., Modolfsky, H., & Lue, F.A. (1986). Sleep and postrelationship to legal settlement. Headache, 32,496–500. traumatic rheumatic pain disorder (fibrositis syndrome). Pellegrino, M.J. (1996).Understanding post-traumatic fibromyPsychosomatic Medicine, 48, 319–323. algia. Columbus, OH: Anadem Publishing. Pincus, T., Summey, J.A., Soraci, S.A., Jr., Hummon, N.P., &Simms, R.W., Zerbini, C.A.F., Ferrante, N., Anthomy, J., Felson, D.T., Crager, D.E., & the Boston City Hospital AIDS Wallston, K.A. (1983). Assessment of patient satisfacTeam (1992). Fibromyalgia syndrome in patients tion in activities of daily living using a modified Staninfected with human immuno deficiency virus. Annals ford health assessment questionnaire. Arthtritis and of Internal Medicine, 92,368–374. Rheumatism, 26, 1346–1353. Potter, J.W. (1992). Helping fibromyalgia patients obtain SocialSimons, D.C. (1987). Myofascial pain syndromes due to triger points. In M. Osterweis, A. Kleinman, & D. Mechanic Security benefits.Journal of Musculoskeletal Medicine, (Eds.), Pain and disability(pp. 285–292). Washington, 9, 65–74. D.C.: National Academy Press. Rachlin, E.S. (1994). Trigger points. In E.S. Rachlin (Ed.), Myofascial pain and fibromyalgia(pp. 146–147). St. Louis: Smiley, W.M., Cram, J.R., Margoles, M.S., Romano, T.J., & Stiller, J. (1992). Innovations in soft tissue jurispruMosby. dence.Trial Diplomacy Journal, 15,199–208. Radanov, B.P., Dvorak, J., & Valach, L. (1992). Cognitive ficits de in patients after soft tissue injury of the cervical spine. Smythe, H. A. (1989). Nonarticular rheumatism and psychogenic musculoskeletal syndromes in arthritis and allied condiSpine, 17,127–131. tions. D.J. McCarthy (Ed.), A textbook of rheumatology Radanov, B.P., & Sturzenegger, M. (1996). The effect of accident (11th ed., pp. 1241– 1254). Philadelphia: Lea & Febiger. mechanism and initial findings on the long-term outcome of whiplash injury.Journal of Musculoskeletal Social Security Administration (1998, January). Disability evaluation under Social Security, fice Of of Disability. Pain, 4, 47–59. Reilly, P.A. (1998). Work disability and soft tissue rheumatism. Spieler, E.A., Barth, P.S., Burton, J.F., Jr., Himmelstein, J., & Rudolph, L. (2000). Recommendations to guide revision Journal of Rheumatology, 25, 1454–1456. of the guides to the evaluation of permanent impairment. Rice, J.R. (1987). Fibromyalgia. A disorder for all clinicians. In Journal of the American Medical Association, 283, J.I. Walker, J.T. Brown, & R.A. Gallis (Eds.), The com519–523. plicated medical patient (pp. 58–70). New York: Human Swerdlow, B. (1998).Whiplash and related headache . Boca Sciences Press, Inc. Raton, FL: CRC Press. Romano, T J. (1990). Clinical experiences with post-traumatic fibromyalgia syndrome. West Virginia Medical Journal, Taylor, J.R., & Taylor, M.M. (1996). Cervical spine injuries: An autopsy study of 109 blunt injuries. Journal of Muscu86, 198–202. loskeletal Pain, 4,61–79. Romano, T.J. (1995). Abnormal central nervous system neurodiagnostic testing in post traumatic fibromyalgia Teasell, R.W., & Merskey, H. (1997). Chronic pain disability in the workplace.Pain Research Management,197–225. 2, (Abstr). Journal of Musculoskeletal Pain, (Suppl. 3 1), Tikofsky, R.S. (1994). Evaluating traumatic brain injury: Corre106. lating perfusion patterns and function. Journal of Romano, T.J. (1998a). A rheumatologist's perspective on pain Nuclear Medicine, 35,227. management. In R.S. Weiner (Ed.), Pain management: Painful cerA practical guide for clinicians(5th ed., pp. 355–371). Tollison, C.D., & Satterthwaite, J.R. (Eds.). (1992). vical trauma.Baltimore: Williams & Wilkins. Boca Raton, FL: St. Lucie Press. Myofascial pain and dysRomano, T.J. (1998b). Proposed formula for the estimation ofTravell, J.G., & Simons, D.G. (1983). function: The trigger point manual . Baltimore: Williams pain caused by each of several traumas involving soft & Wilkins. tissue. American Journal of Pain Management, 8, Turk, D.C., Okifuji, A., Sinclair, J.D., & Starz, T.W. (1996). Pain, 118–123. disability, and physical findings in subgroups of patients Romano, T.J. (1999). Fibromyalgia. In M. S. Margoles & R. with fibromyalgia. Journal of Rheumatology, 23, Weiner (Eds.),Chronic pain, assessment, diagnosis, and 1255–1262. management(pp. 95–103). Boca Raton, FL: CRC Press.

180

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Vital Statistics of the United States (1992). Life tables, VolumeWolfe, F., Smythe, H.A., Yunus, M.B., Bennett, R.B., Bombardier, C., Goldenberg, D.L., Tugwell, P., Campbell, S.M., II, Section 6 (p. 12). U.S. Dept. Health and Human Abeles, M., Clark, P., Fam, A.G., Farber, S J., Fiechtner, Services. Public Health Service. J J., Franklin, C.M., Gatter, R.A., Hamaty, D., Lessard, Waylonis, G.W., & Perkins, R.H. (1994). Post-traumatic fibroJ., Lichtbroun, A.S., Masi, A.T., McCain, G.A., Reymyalgia, a long-term follow-up.American Journal of nolds, W.J., Romano, T.J., Russell, I J., & Sheon, R.P. Physical Medicine and Rehabilitation, 73, 403–412. (1990). The American College of Rheumatology criteria White, K.P., Speechley, M., Harth, M., & Ostbye, T. (1999). The for the classification of fibromyalgia.Arthritis and Londonfibromyalgia epidemiology study: Direct health Rheumatism, 33, 160–172. care costs of fibromyalgia syndrome in London. Canadian Journal of Rheumatology, 26, 885–889. Wyper, D.J. (1993). Functional neuroimaging with single photon Wolfe, F. (1994). Post-traumatic fibromyalgia: A case report emission computerized tomography (SPECT). Cerenarrated by the patient. Arthritis Care and Research, 7, brovascular and Brain Metabolism Reviews, 5, 161–165. 199–217. Wolfe, F. (1995). Health status questionnaire. Rheumatism Clin- Yunus, M.B. (1992). Towards a model of pathophysiology of ics of North America, 21,445–464. fibromyalgia: Aberrant central pain mechanisms with Wolfe, F. (1996). The fibromyalgia syndrome: A consensus peripheral modulation.Journal of Rheumatology, 19, report on fibromyalgia and disability. Journal of Rheu846–850. matology, 23,534–539. Yunus, M.B., & Alday, J.C. (1993). Clinical and psychological Wolfe, F., Anderson, J., Harness, D., Bennett, R.M., Caro, X.J., features of regional fibromyalgia: Comparison with Goldenberg, D.L., Russell, I.J., & Yunus, M.B. (1997a). fibromyalgia syndrome.Arthritis and Rheumatism, 36, Health status and disease severity in fibromyalgia. S221. Results of a six-center longitudinal study. Arthritis and Yunus, M.B., Bennett, R.M., Romano, T.J., Russell, I.J., & other Rheumatism, 40, 1571–1579. members of the Fibromyalgia Consensus Report AddiWolfe, F., Anderson, J., Harkness, D., Bennett, R.M., Caro, X. tional Comments Group (1997). Fibromyalgia consenJ., Goldenberg, D.L., Russell, I.J., & Yunus, M.B. sus report, additional comments. Journal of Clinical (1997b). Work and disability status of persons with Rheumatology, 3,324–327. fibromyalgia.Journal of Rheumatism, 24, 1171–1178.

17 Neuropathic Pain: Mechanisms and Management Mark V. Boswell, M.D., Ph.D., Samuel K. Rosenberg, M.D., and Thomas C. Chelimsky, M.D. INTRODUCTION

to the pain ascribed to common injuries not considered neuropathic in nature, such as burns and sprains. This Neuropathic pain is a common cause of chronic pain.ambiguity in character may simply reflect the relatively Neuropathic pain is a challenge to clinicians because it is limited number of ways that pain can be encoded by the difficult to diagnose and often is resistant to analgesics, nervous system. such as opioids (Arner & Meyerson, 1988; Dellemijn, A peculiar property of the nervous system is its plas1999; Portenoy, Foley, & Inturrisi, 1990). Classic exam-ticity. Damage to nerves often results in alteration or ples of neuropathic pain include trigeminal neuralgia, pos-amplification of the signal encoded by the nerve. For therpetic neuralgia, diabetic neuropathy, phantom limbexample, peripheral nerve ablation, performed with good pain, and pain associated with plexopathy and radiculoptherapeutic intentions, may result in a pain syndrome that athy (see Table 17.1). Neuropathic pain often complicates is worse than the one originally being treated. When dealthe treatment of cancer pain. For example, brachial plexing with the nervous system, “shooting the messenger” opathy occurs in approximately 15% of patients with can-(the nerve) often intensifies and distorts the message. The cer and pain is the most common complaint associated new pain syndrome may be more severe, and associated with brachial plexopathy (Foley, 1987). Thus, successfulwith allodynia, hyperalgesia, and spontaneous and paroxmanagement of cancer pain frequently requires manageysmal pain, all in the presence of mild to moderate cutament of neuropathic pain. neous numbness. This complex of signs and symptoms is From a theoretical standpoint, neuropathic pain is rel-paradoxical to the patient and confusing to the clinician, atively simple to define. It is an abnormal pain state thatbut quite typical of neuropathic pain. arises from a damaged peripheral nervous system (PNS) The ambiguity notwithstanding, it is important to conor central nervous system (CNS) (Merskey & Bogduk,sider neuropathic pain in the differential diagnosis of chronic pain, because neuropathic pain may be treated 1994). Indeed, peripheral neuropathies, particularly those with some success using adjuvant analgesics, medications associated with diabetes, are a frequent cause of neuropathic pain (Galer, 1995). However, from a clinical per-not traditionally considered to be pain relievers (Hegarty spective, neuropathic pain may be difficult to diagnose& Portenoy, 1994). Adjuvant analgesics, such as tricyclic antidepressants and anticonvulsants, do not have strong with certainty, because its clinical characteristics are rather nonspecific. Neuropathic pain may be hard for someantinociceptive analgesic properties in experimental or clinical studies, but have been shown to be helpful in patients to describe, but frequently is characterized as burning or stabbing, descriptors that are not unique toneuropathic pain states (McQuay, et al., 1996; Swerdlow, 1984). Indeed, the mainstay of treatment of neuropathic, neuropathic pain. Indeed, neuropathic pain may be similar 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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In contrast, neuropathic pain may be thought of as pathophysiological, because it arises from a damaged PNS or TABLE 17.1 CNS and provides no obvious protective benefit (Bennett, Common Causes of Neuropathic Pain 1994; Tanelian, & Victory, 1995). However, from a clinPolyneuropathy ical perspective, this distinction is seldom straightforDiabetes (insulin-dependent and non-insulin-dependent) ward, because physiological pain often is associated with Alcoholism early clinical findings generally considered neuropathic Human immunodeficiency virus in nature, such as allodynia and paresthesias (tingling Hypothyroidism sensations). Moreover, chronic neuropathic-like pain Renal failure occasionally may follow an injury that did not appear to Chemotherapy (vincristine, cisplatinum, paclitaxel, involve nerve damage, such as a simple soft tissue injury. metronidazole) Anti-HIV drugs On the other hand, pain associated with peripheral neurB-12 and folate deficiencies opathy may be maintained by sustained peripheral nociMononeuropathy ceptive input (Gracely, Lynch, & Bennett, 1992). Strong Entrapment syndromes nociceptive input often produces central sensitization, an Traumatic injury abnormal pain amplification process in the CNS. ThereDiabetes fore, the definitional borders of neuropathic pain are Vasculitis becoming more diffuse, not more distinct, as we gain a Plexopathy better understanding of the remarkable plasticity of the Diabetes nervous system and its close association with the various Avulsion tissues that it innervates. Tumor Root Syndromes and Radiculopathy Neuropathic pain may be classified as stimulusCompressive lesions evoked or stimulus-independent pain. Stimulus-evoked Inflammatory pain can result from stimulation of nervi nervorum Diabetes present in connective tissue surrounding otherwise intact Postherpetic neuralgia nerves. Painful stimuli that activate nociceptors around Trigeminal neuralgia nerves include inflammation and tissue injury from tumor Phantom limb pain or trauma (Woolf & Mannion, 1999). Stimulus-indepenRSD/Causalgia/CRPS dent neuropathic pain may result from damage to afferent sensory fibers in the PNS or CNS. In this case, ongoing Modified from B.S. Galer, 1995. Neurology, 45(Suppl. 9), S17–S25. inflammation is usually absent. Days to months after pain is pharmacologic, and effective regimens oftenperipheral nerve injury, persistent abnormal primary require multiple medications. In addition, the possibleafferent activity from the periphery may arise from effectiveness of opioids for neuropathic pain should nothypersensitive nerve terminals or nerves (Price, Mao, be overlooked, although doses may be considerably higher Mayer, 1994). than typical antinociceptive doses. The clinician should There is substantial pharmacological evidence that also keep in mind that successful management of chronic abnormal nerve activity is an important mechanism underpain often requires treating neuropathic pain as well as lying the spontaneous pain typical of neuropathic pain pain associated with tissue injury, because both conditions states (Devor, 1994, 1995; Tanelian & Victory, 1995). It may coexist and interact to maintain the painful condition.is hypothesized that sites of ectopic foci develop on injured or regenerating nerves in the periphery, at the level of the nociceptor, neuromas, or segments of injured MECHANISMS OF NEUROPATHIC PAIN nerves; at the dorsal root ganglion; and in the dorsal horn Neuropathic pain may result from a pathological processof the spinal cord. Indeed, after nerve transection, occurring at any level of the nervous system, from theincreased sensitivity occurs, followed in a few days by nociceptor, the distal nerve, the plexus level, the dorsal spontaneous activity. These abnormal ectopic foci may be root ganglion, the root entry zone, the dorsal horn of thethought of as spontaneous pain generators, resulting in spinal cord, and higher levels in the CNS, particularly theparoxysmal and spontaneous pain. Precise pathophysiolmedulla and thalamus. It has become popular to contrast ogy is unclear, but pharmacological evidence suggests that neuropathic pain with typical postinjury, nociceptive ectopic activity is due to an increased number of sodium pain. Nociceptive pain, typically thought to indicate a channels, or more likely an abnormal subtype of sodium properly functioning nervous system, is considered phys-channel, resulting in unstable sodium channel activity iological because it results from activation of nociceptors,(Chaplan, 2000). Pharmacological evidence supporting specialized nerve endings that respond to high threshold this hypothesis is the effectiveness of local anesthetics and noxious stimuli and generally serve a protective function.some anticonvulsants (sodium channel-blocking drugs) in

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neuropathic pain. These drugs presumably produce frewhether segmental, supraspinal, or both, may also cause quency and voltage-dependent blockade of sodium channeuropathic pain (Woolf & Mannion, 1999). After deafnels on damaged neurons (Devor, 1995). The abnormal ferentation injury, particularly following loss of C fibers, sodium channel involved in neuropathic pain states may arborization of Aβ fibers into the substantia gelatinosa of be a tetrodotoxin-insensitive subtype, found only in neuralthe dorsal horn may result in central sensitization and tissue (Novakovic, et al., 1998). Accumulation of atypicalallodynia(Woolf, Shortland, & Coggeshall, 1992). Availas well as tetrodotoxin-sensitive sodium channels (responable evidence supports the contention that tactile allodynia sible for normal nerve conduction) may explain the oftenis mediated by large myelinatedβ Aafferents with input inadequate therapeutic benefit of current sodium channelthat is modulated at supraspinal sites in the dorsal columns blocking drugs. (Ossipov, Lai, Malan, & Porreca, 2000). This may explain Work in animal models demonstrates that voltage-why transcutaneous electrical nerve stimulation (TENS) and spinal cord stimulation, which produce a low threshdependent calcium channels may also be important in modulating neuropathic transmission. Unfortunately, theold, tingling sensation, characteristic of large fiber afferent currently available calcium channel blockers are cardio-activation, may be effective in chronic pain states, particselective, and are not particularly effective in neuropathicularly neuropathic pain. Tactile allodynia should be differentiated from thermal allodynia, which appears to be pain. There appear to be at least six calcium channel subtypes, and studies with novel N-type calcium channelmediated by nonmyelinated C fibers and amplified by blockers are promising in animals (Chaplan, 2000). Pre-pathological spinal dynorphin (discussed later). liminary studies with conotoxin (SNX-111) are positive, Various studies suggest that stimulus-evoked neuroalthough the drug must be administered spinally. pathic pain is more sensitive to opioids than stimulusindependent pain (Dellemijn, 1999). Opioid responsiveGabapentin, a novel anticonvulsant, appears to bind to the α2δ subunit of a voltage-dependent calcium chan-ness may be maintained in some forms of stimulus-evoked nel. Work by Chaplan (2000) and colleagues demon-pain, because opioid receptors in the substantia gelatinosa are preserved. On the other hand, segmental loss of prestrates that messenger RNA and protein forαthe 2δ subsynaptic central opioid receptors occurs following injury unit are increased more than 10-fold in dorsal root ganglia following nerve injury, but are not changed after tissueor loss of C fibers, typically seen after deafferentation injury. Blockade of a retrograde signal from the injury injury. However, the magnitude of receptor loss is minimal site (which may involve nerve growth factor) preventsand largely segmental, and only partly explains the diminupregulation of theα2δ subunit. Chaplan points out that ished opioid-responsiveness characteristic of neuropathic the α2δ subunit does not seem to play a role in normalpain (Ossipov, et al., 2000). channel kinetics but may effect calcium channel assembly Supraspinal facilitative mechanisms may also be and insertion into the neuronal membrane. Thus, the subinvolved in maintenance of neuropathic pain and opioid unit may act as a drug-binding site and secondarily modresistance. Evidence suggests that sustained afferent drive ify channel kinetics. induces facilitation of spinal cord pain transmission Following peripheral nerve injury, concomitant alter- involving a descending pathway from the rostroventral nations may be evident in dorsal root ganglia, includingmedial medulla (RVM) (Ossipov, et al., 2000). Tonic facilitation may involve supraspinal cholecystokinin (CCK), transmitter changes and increased density of sympathetic nerve terminals (McLachlan, Janig, Devor, & Michaelis, traditionally thought of as a visceral hormone that regu1993). Tyrosine hydroxylase positive cell terminals thatlates emptying of the gallbladder. CCK antagonists produce norepinephrine, migrate from vessels supplyinginjected into the RVM in animals reverse tactile and therthe dorsal root ganglion to nerve ganglion cells followingmal allodynia produced by spinal nerve ligation (Kovelowski, Ossipov, Sun, Malan, & Proecca, 2000). Mechasciatic nerve injury. The dorsal root ganglia then expresses α-adrenergic receptors. This may be a putative linknistically, these antiopioid and pronociceptive actions may between peripheral tissue injury, nerve injury, and sym-occur at spinal and supraspinal sites. Spinal CCK may antagonize opioid effects at the level of the primary afferpathetically maintained pain states, such as reflex sympathetic dystrophy and causalgia (complex regional painent terminal in the spinal cord. Both CCK and opioids colocalize on primary nociceptive afferent neurons in the syndromes Type 1 and 2, respectively). In the periphery, sprouting nerve terminals may exhibit sensitivity to pros-dorsal horn. In addition, CCK may act on supraspinal These kinds of opioid-dependent pathways in the RVM to reduce opioid taglandins, cytokines, and catecholamines. responsiveness, and thus impair descending inhibition, an changes further increase the complexity of the neuropathic pain picture and blur the distinctions between nociceptiveimportant mechanism involved in opioid pain relief. Ultimately, CCK antagonists may prove useful for treating and neuropathic pain. It should be noted that not all stimulus-independentneuropathic pain states. pain is mediated by spontaneous activity in primary sen- The phenomenon of reduced opioid responsiveness sory neurons. Loss of normal inhibitory mechanisms,in neuropathic pain has prompted extensive studies in

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animals, particularly the effects of intrathecal opioids onas well as formulation of a rational approach to medicapain associated with thermal and tactile stimulation. Thetions, interventions such as nerve blocks, and psychologsimilarities between opioid tolerance and neuropathicical and physical therapies. pain are also an area of active study (Vanderah, et al., The nature, duration, and severity of pain should be 2000). It is well known thatN-methyl-D-aspartate evaluated in detail, including appropriate physical and (NMDA) antagonists appear to minimize the develop-neurological examinations. For example, performing a ment of opioid tolerance. Spinal dynorphin may be aneurological examination looking specifi cally for evicommon link between NMDA, central sensitization, anddence of nerve injury, such as the presence of hypoesthereduced opioid responsiveness. Following spinal nervesias or reflex changes, may suggest neuropathy or radicligation, dynorphin levels in the spinal cord increase,ulopathy, and help guide treatment. It is crucial that suggesting that dynorphin may act as a pronociception psychosocial and emotional factors be explored, because mediator (Ossipov, et al., 2000). Although, under certainthere is a high comorbidity of depression and anxiety circumstances, dynorphin appears to have analgesic propdisorders in patients with chronic pain. Moreover, given erties, it is becoming increasingly clear that dynorphinthe similarities between the pharmacology of mood and also has nonopioid, antianalgesic properties. Antiserum depression and pain transmission (e.g., serotonin and to dynorphin blocks thermal hyperalgesia after nervenorepinephrine), patients with concomitant systemic illinjury in rats. Moreover, antiserum to dynorphin or ness and stress may be at risk for depression and develMK801, an NMDA antagonist, restores normal spinalopment of an abnormal chronic pain state. Pharmacologmorphine analgesia following spinal nerve ligation. Fur-ical management of depression may improve neuropathic thermore, both agents restore morphine synergy between pain by addressing overlapping, but distinct mechanisms. the brain and spinal cord (Ossipov, et al., 2000), which After multiple medication trials in which there has is required for the full clinical analgesic effects of mor- been minimal therapeutic benefit and perhaps significant phine. Therefore, current evidence suggests that the paindrug-related side effects, patients may believe that they promoting effect of dynorphin is mediated by the NMDA have little recourse but to undergo invasive, ablative proreceptor. Although the full clinical ramifi cations of dynor- cedures in attempts to relieve their pain. Specific treatment phin are far from understood, it is clear that sustainedmodalities aimed at the underlying pathophysiology are nociceptive drive from the periphery maintains elevatedusually not possible in most neuropathies, particularly levels of spinal dynorphin, which in turn, may have toxic with chronic sensory polyneuropathies. In general, ablaeffects on the spinal cord. Thus, reducing sustained tive procedures are not warranted, because of the high peripheral nociceptive input into the spinal (i.e., painprobability of long-term worsening of pain. Except for relief) may be an important way to reduce the incidencepatients with advanced cancer-related pain, nerve ablation of neuropathic pain (Caudle & Mannes, 2000). is likely to provide only temporary benefit, leaving the Currently, NMDA antagonists, such as ketamine, havepatient with sensory and perhaps motor deficits. Exceponly limited indications because of significant side effects.tions to this phenomenon appear to be ablation of sympaUltimately, however, medications such as NMDA antag-thetic fibers, visceral plexi, and medial branch nerve onists may become available that can reduce the effects blocks, which denervate painful facet joints in the spine. of pathological spinal dynorphin. In cases of nerve entrapment, where ongoing nerve compression is likely to be responsible for pain, neurolysis or transposition of the nerve may provide benefit, as long as MANAGEMENT OF NEUROPATHIC PAIN: pain is not due to irreversible underlying nerve damage. GENERAL CONSIDERATIONS In all cases of neuropathic pain, even when neuropathy is Management of neuropathic pain is a complicatedevident, it is appropriate from time to time to reevaluate the presumed etiology of the neurological problem. endeavor and often is frustrating to patient and physician alike. This stems from our relatively poor understanding When a medication trial proves to be ineffective, a of mechanisms and the limitedficacy ef of currently avail- multidimensional or interdisciplinary approach should be able analgesics. Therapeutic approaches vary greatly considered. Again, this includes an attempt to treat the among physicians, which reflects the paucity of random-underlying disease, as well as specifi c pharmacological, ized clinical trials, particularly those comparing different psychological, and physical therapy interventions. The drug regimens. Given our current level of understandingoutcome measure for successful treatment should include of neuropathic pain mechanisms and the limitations ofincreased activity as well as decreased subjective pain available drugs, nonpharmacological methods may be as ratings and improved patient satisfaction. The treatment effective as pharmacological approaches. Recalcitrant goal in chronic neuropathic pain is different from that in chronic pain syndromes warrant an interdisciplinaryacute pain. In the usual acute pain setting, the goal is approach, which may include attempts to treat the undernearly complete relief of pain, to allow recovery of norlying disease (e.g., causes of the peripheral neuropathy) mal function during the healing process. With chronic

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neuropathic pain, limitations of current analgesics usuallystabilizing agents and medications that enhance inhibitory make complete pain relief a very unrealistic goal. There-mechanisms in the dorsal horn. This classification system fore, attention to increasing function and comfort andmay provide a simple framework with which to approach treating associated problems, such as depression, become therapy; however, it should be kept in mind that most of paramount. Reducing dependence on opioid medications these drugs have multiple mechanisms of action, and their may or may not be an important goal. The objectives toeffects often may overlap. Given the limitations of our consider with chronic opioid therapy include determiningcurrent drugs, pain management often becomes an exerwhether nonopioid approaches have been tried, whether cise in polypharmacy, where the clinician uses multiple the pain syndrome is opioid responsive, and whether the medications to target different symptoms. This strategy patient demonstrates appropriate improvement in func-may optimize the chances for success, but complicates tion, without undo side effects or evidence of abuse ofmanagement issues when side effects develop. medications. Membrane stabilizing agents include local anesthetics Nonpharmacological approaches to treating neuro-such as lidocaine and some anticonvulsant drugs, includpathic pain include the use of a TENS unit, although reliefing carbamazepine, phenytoin, and valproic acid (Tanelian may be poor when burning pain is a prominent complaint.& Victory, 1995). Their molecular mechanism of action This may be explained by the fact that burning pain is ainvolves blockade of frequency and voltage-dependent C-fiber-mediated sensation, whereas TENS units probably sodium channels on damaged or regenerating neuronal modulate large fiber input into the dorsal horn. membranes (Devor, 1994, 1995). It appears that minimal Spinal cord stimulation may beficacious ef for chronic doses of suppressive drugs may inhibit ectopic discharges pain, including neuropathic pain (North, Kidd, Zahurak, without interfering with normal neuronal function. It is James, & Long, 1993) and reflex sympathetic dystrophyalso possible that the sodium channel targets are atypical (Kemle,r et al., 2000). Mechanisms involved are poorlyand not involved in normal neuronal conduction. Although understood, which reflects current understanding of neuthe evidence is less substantial, corticosteroids also appear ropathic pain states in general. However, central effects to have effects on membrane conductance (Castillo, et al., may include alteration in dorsal horn processing and trans1996; Devor, Govrin-Lippmann, & Raber, 1985). In addimission in the tract of Lissauer (Iacono, Guthkelch, &tion, tricyclic antidepressants, such as amitriptyline, have Boswell, 1992) and suppression of sympathetic outfloweffects on sodium channels (Pancrazio, Kamatchi, Roscoe, from the intermediolateral gray column of the spinal cord.& Lynch, 1998), an action that is distinct from their effects The latter effect may explain improved peripheral bloodon the reuptake of serotonin and norepinephrine. The latter flow in patients with chronic peripheral vascular insuf fiare traditionally thought to be responsible for their effects ciency. The CraigPENS technique, a novel application ofon depression and pain. electroacupuncture (percutaneous neural stimulation Conventional wisdom maintains that the adjuvant anal[PNS]) has been shown effective in herpes zoster, diabetic gesics, particularly the tricyclic antidepressants, and clonperipheral neuropathy, and sciatica (Ahmed, et al., 1998; azepam and baclofen, modulate inhibitory mechanisms in Ghoname, et al., 1999; Hamza, et al., 2000). the spinal cord and brain. Inhibitory pathways descend from Available evidence indicates that nonpharmacologicalthe periaqueductal gray, reticular formation, and nucleus approaches such as TENS and CraigPENS can provide an raphe magnus in the dorsolateral funiculus to the dorsal initial rational therapeutic strategy, and may obviate thehorn. These pathways mediate antinociception by adrenerneed for potentially toxic medications, improve the effec-gic, serotonergic, GABAergicγ-amino ( butyric acid), and tiveness of current analgesic regimens, or reduce the opioid mechanisms (Yaksh, 1979). Although the putative amount of medications required. Spinal cord stimulationmechanisms are complex and poorly understood, serotonstill tends to be a treatment of last resort, although judi-ergic effects are mediated in part by action on GABAergic cious use earlier in the course of treatment is probably interneurons (Alhaider, Lei, & Wilcox, 1991). For example, warranted in carefully selected patients. Considering the facilitory effects of large myelinated afferent fibers may be current high cost of medication, alternative approaches, if suppressed by tonic GABAergic activity, removal of which efficacious, may prove to be cost effective. results in allodynia (Yaksh & Malmberg, 1994). As noted earlier, tricyclic antidepressants alter monoamine transmitter activity at neuronal synapses by PHARMACOLOGY OF blocking presynaptic reuptake of norepinephrine and seroNEUROPATHIC PAIN tonin, thereby modulating descending inhibitory spinal From a practical standpoint, medications remain the pillarpathways. However, additional mechanisms include effects on membranes, interaction with NMDA activity of pain management strategies, despite their limitations. (Eisenach & Gebhart, 1995), and sodium channel blockFrom a conceptual standpoint, adjuvant analgesic drugs ade (Pancrazio, et al., 1998). may be categorized into two broad classes, membrane

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Carbamazepine has a long history of use for neuropathic pain, particularly trigeminal neuralgia. Trigeminal TABLE 17.2 neuralgia is an FDA-approved indication for the drug. Adjuvant Analgesics for Neuropathic Pain Carbamazepine is chemically related to the tricyclic antiDrug Class Mechanism of Drug Action depressant imipramine, has a slow and erratic absorption, and may produce numerous side effects, including sedaAnticonvulsants tion, nausea, vomiting, and hepatic enzyme induction. In Carbamazepine Sodium channel blockade 10% of patients, transient leukopenia and thrombocytopePhenytoin Sodium channel blockade Valproic acid Sodium channel blockade nia may occur, and in 2% of patients hematologic changes Gabapentin Calcium channel binding can be persistent, requiring stopping the drug (Hart & Clonazepam GABAegic mechanism Easton, 1982; Sobotka, Alexander, & Cook, 1990; Tohen, Antidepressants Castillo, Baldessarini, Zarate, & Kando, 1995). Aplastic Amitriptyline As a group Norepinephrine and serotonin anemia is the most severe complication associated with Nortriptyline reuptake effects, possible NMDA effects, carbamazepine, which may occur in 1:200,000 patients. Imipramine and sodium channel blockade Although requirements for hematologic monitoring Desipramine remain debatable, a complete blood cell count, hepatic Fluoxetine Serotonin selective effects enzymes, blood urea nitrogen (BUN), and creatinine are Paroxetine Serotonin selective effects recommended at baseline; and these are checked again at Venlafaxine Adrenergic and opioid receptor binding 2, 4, and 6 weeks, and every 6 months thereafter. Carbameffects Antiarrhythmics azepine levels should be drawn every 6 months and after Lidocaine As a group sodium channel-blocking effects changing the dose to monitor for toxic levels and verify Mexiletine that the drug is within the therapeutic range (4 to 12 EMLA cream µg/cc). Patients with low pretreatment white blood cell Miscellaneous counts are at increased risk of developing leukopenia Corticosteroids Antiinflammatory and membrane stabilizing (WBC < 3000/mm3). Because toxicity is entirely unpreeffects dictable, it is important to instruct patients to recognize Baclofen GABA-B agonist clinical signs and symptoms of hematologic toxicity, such Capsaicin Vanilloid agonist and C-fiber neurotoxin as infections, fatigue, ecchymosis, and abnormal bleeding, and to notify the physician if they develop. To improve From a practical standpoint, it helpful to consider thecompliance, carbamazepine should be started at a low various medications useful for neuropathic pain in termsdose (e.g., 50 mg twice daily) and increased over several of their traditional pharmacological indications (eg, anti- weeks to a therapeutic level (200 to 300 mg four times a day). convulsants and antidepressants). However, it is necessary to keep in mind that all these drugs have incompletely Phenytoin also has well-known sodium channelunderstood mechanisms of action, and the drug categories blocking effects and is useful for neuropathic pain (Swerdare more conventional than mechanistic (Table 17.2). low, 1984). However, carbamazepine is more effective than phenytoin for trigeminal neuralgia (Blom, 1962). Phenytoin has a slow and variable oral absorption. ToxicANTICONVULSANTS ity includes CNS effects and cardiac conduction abnorAnticonvulsants are useful for trigeminal neuralgia, post-malities. Side effects are common and include hirsuitism, gastrointestinal and hematologic effects, and gingival herpetic neuralgia, diabetic neuropathy, and central pain (Hegarty & Porteny, 1994; Swerdlow, 1984). Although hyperplasia (Brodie & Dichter, 1996). Allergies to phenytoin are common, and may involve skin, liver, and bone anticonvulsants have traditionally been thought of as most useful for lancinating pain, they may also relieve burningmarrow. Phenytoin doses in the range of 100 mg twice or three times a day may be helpful for neuropathic pain; dysesthesias. Chemically, anticonvulsants are a diverse µg/ml. 20 group of drugs, are typically highly protein bound, andtherapeutic blood levels are in the range of 10 to undergo extensive hepatic metabolism. At present it isThere are numerous potential drug interactions, including induction of cytochrome P450 enzymes, which may acceluncertain whether anticonvulsants or antidepressants are erate the metabolism of other drugs. Because of side better for neuropathic pain, because similar results have been obtained with both types of drugs (McQuay, et al.,effects and toxicity, phenytoin is not a first-line drug for 1996). Indeed, the choice of a particular drug, whetherneuropathic pain. anticonvulsant or antidepressant, may be based more on Valproic acid appears to interact with sodium channels a clinician’s experience with the drug, the expected timebut may also alter GABA metabolism. The principle use to therapeutic benefit, or a drug side effect profile, instead of valproic acid for neuropathic pain is for the prophylaxis of theoretical mechanisms of action. of migraine headache (Matthew, et al., 1995). Potential

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toxicity includes hepatic injury and thrombocytopenia, Although gabapentin is not an NMDA antagonist, there is particularly in children on multiple antiepileptic medica- evidence that gabapentin interacts with the glycine site on tions, although valproic acid is generally considered safethe NMDA receptor (Jun & Yaksh, 1998). for adults. Ligation of rat spinal nerves L5 and L6 (the Chung model) produces characteristic pain behaviors, including Divalproex sodium is better tolerated than valproic allodynia, which are typical of neuropathic pain. Chapacid. The recommended starting dose is 250 mg twice man, Suzuki, Chamarette, Rygh, and Dickenson (1998) daily, although some patients may benefit from doses up demonstrated that gabapentin reduces pain in the Chung to 1000 mg/day. As a prophylactic drug, valproic acid can model. Gabapentin appears to act primarily in the CNS, reduce the frequency of migraine attacks by about 50% in contrast to amitriptyline, which seems to act centrally (Matthew, et al., 1995). Although there is little published and peripherally (Abdi, Lee, & Chung, 1998). Gabapentin information on the ef ficacy of valproic acid for other neualso is effective in reducing pain behavior in phase 2 of ropathic pain syndromes, based on its mechanism of the formalin test, a model of central sensitization and action it may be useful alone or in combination with other neuropathic pain (Shimoyama, Shimoyama, Davis, Inturadjuvant drugs. risi, & Elliott, 1997). Gabapentin reduces spinally mediClonazepam may be useful for radiculopathic pain and ated hyperalgesia seen after sustained nociceptive afferent neuropathic pain of a lancinating character. Clonazepam input caused by peripheral tissue injury. Gabapentin also enhances dorsal horn inhibition by a GABAergic mechaenhances spinal morphine analgesia in the rat tail-flick nism. The drug has a long half-life (18 to 50 h), which test, a laboratory model of nociceptive pain (Shimoyama, reduces the risk of inducing an abstinence syndrome on abrupt withdrawal. The major side effects of clonazepamShimoyama, Inturrisi, & Elliott, 1997). include sedation and cognitive dysfunction, especially in Gabapentin is effective in reducing painful dysesthethe elderly. Although the risk of organ toxicity is minimal, sias and improving quality of life scores in patients with some clinicians recommend periodic complete bloodpainful diabetic peripheral neuropathy (Backonja, et al., count (CBC) and liver function tests for monitoring. Start- 1998). Of patients randomized to receive gabapentin, 56% achieved a daily dosage of 3600 mg divided into three ing doses of 0.5 to 1.0 mg at bedtime are appropriate to doses per day. The average magnitude of the analgesic reduce the incidence of daytime sedation. Gabapentin is a popular anticonvulsant for neuro-response was modest, with a 24% reduction in intensity at the completion of the study compared with controls. pathic pain. Gabapentin was released for use in the United States in 1994, for the treatment of adults with partialSide effects were common. Dizziness and somnolence epilepsy. Almost immediately after its release, physiciansoccurred in about 25% of patients, and confusion occurred in 8% of patients. began to use gabapentin for various neuropathic pain disorders, such as diabetic peripheral neuropathy and post- Morello, Leckband, Stoner, Moorhouse, and herpetic neuralgia. The structural similarity of gabapentinSahagian (1999) compared gabapentin with amitriptyline to GABA suggested that the drug might be useful forfor diabetic neuropathy and found both equally effective. neuropathic pain. Although tricyclic antidepressants haveAlthough gabapentin probably has fewer contraindicabeen proven clinically effective for neuropathic pain for tions than tricyclic antidepressants, it is considerably years, they often fail to provide adequate pain relief ormore expensive. cause unacceptable side effects. Therefore, when gaba- Postherpetic neuralgia (PHN) is anotherficult dif neupentin became available, its benign side effect le profi ropathic syndrome. PHN affects approximately 10 to 15% quickly made it very popular among physicians. Althoughof patients who develop herpes zoster, and is a particularly initial enthusiasm for the drug was based largely on wordpainful syndrome associated with lancinating pain and of mouth, anecdotal published reports, and discussions burning at dysesthesias. The incidence of PHN is ageclinical meetings, animal studies have substantiated the related, with up to 50% of patients older than 60 years of efficacy of gabapentin in various types of neuropathicage developing persistent pain after a bout of herpes pain. Over time, a growing consensus concerning the usezoster. Pain relief usually requires pharmacological therfulness of gabapentin has emerged. apy. Unfortunately, most medications are not very effecIt is clear that gabapentin is not a direct GABA ago-tive. For example, only about one half of patients obtain nist, although indirect effects on GABA metabolism or adequate relief with antidepressants. action may occur. A leading hypothesis suggests that gaba- Rowbotham, Harden, Stacey, Bernstein, and Magpentin interacts with a novel receptor on a voltage-acti-nus-Miller (1998) evaluated the ficacy ef of gabapentin vated calcium channel (Chaplan, 2000; Taylor, et al.,for the treatment of PHN. Of patients taking gabapentin, 1998). Inhibition of voltage-gated sodium channel activity65% achieved a daily dosage of 3600 mg. Although the (such as occurs with classical anticonvulsants, e.g., phenyaverage magnitude of pain reduction with gabapentin toin and carbamazepine) and amino acid transport, which was modest, with approximately a 30% reduction in pain alters neurotransmitter synthesis, may also occur.compared with controls, statistically pain reduction was

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highly significant. In addition, gabapentin improved a given drug. For example, when a patient is having difsleep parameters and quality of life scores. Adverseficulty sleeping because of pain, a more sedating drug, effects that occurred more commonly in the gabapentinsuch as amitriptyline, may be indicated. On the other hand, group included somnolence (27%), dizziness (24%),desipramine, which is less sedating, may be better tolerataxia, peripheral edema, and infection (7 to 10%). Based ated in elderly patients. on the data of Rowbotham and colleagues, it is reason- The tricyclic antidepressants are generally highly proable to consider gabapentin as rst-line fi therapy for post- tein bound with large volumes of distribution and long herpetic neuralgia. Gabapentin probably is at least as elimination half-lives. They undergo extensive hepatic effective as antidepressants, with fewer contraindica-first-pass metabolism and typically have active metabotions. Gabapentin may be used as monotherapy or addlites. Although effective doses may be lower than typically on treatment. used for depression, this is often not the case. Patients must be warned of potential side effects including sedaAlthough gabapentin can be started at 300 mg three tion, cognitive changes, and orthostatic hypotension from times a day with most patients, giving the drug three times α-adrenergic blockade. Anticholinergic side effects are a day with meals and again at bedtime may be more common and include constipation, urinary retention, and effective. Use of a bedtime dose may assist with sleep and prevent pain from developing at night. With some patients,exacerbation of glaucoma. Antihistaminic effects may a more gradual titration may be better tolerated. In addi-cause sedation. Because of their long half-lives, these tion, this reduces the risk of patients stopping the drugdrugs may be given as a single bedtime dose. To minimize because of side effects, before a therapeutic dose side is effects, small doses (e.g., 10 to 25 mg) are used achieved (David Longmire, personal communication,initially and increased over several weeks to a therapeutic dose, generally in the range of 50 to 150 mg/day. An 2000). For example, start with a bedtime dose of 100 mg electrocardiogram (ECG) is recommended if there is a and then increase the daily dose to 100 mg twice a day history of cardiac disease. ECG changes such as QRS with meals and at bedtime, for 2 days. Thereafter, the dose PR and QT prolongation, and T wave flattening can be increased to three times a day with meals and widening, at bedtime. Further titration every 3 to 7 days can be con-can be induced by these agents. Tricyclic antidepressants tinued until pain relief, side effects, or a maximum daily may have quinidine-like actions, consistent with their sodium channel-blocking effects, particularly in patients dose in the range of 2400 to 3600 mg/day is reached. An instruction sheet for the patients is helpful in clarifying with underlying ischemic cardiac disease or arrhythmias (Glassman, Roose, & Bigger, 1993). Because abrupt disthe dosage schedule and explaining possible side effects. Gabapentin is generally well tolerated, even in thecontinuation of antidepressants may precipitate withdrawal symptoms, such as insomnia, restlessness, and geriatric population, and has a safer side effect profile than tricyclic antidepressants. In the PNH study, the majorityvivid dreams, a gradual taper over 5 to 10 days is recommended. Occasional blood levels are recommended, as of patients were titrated to 3600 mg/day, and the median well as CBC and hepatic studies to monitor for organ patient age was 73 years. The kidneys excrete gabapentin, toxicity. and the dosage must be reduced for patients with renal Amitriptyline is a tertiary amine that inhibits norepiinsufficiency (Beydoun, Uthman, & Sackellares, 1995). nephrine and serotonin reuptake equally American ( Medical Association Drug Evaluations Annual , 1993). AmiANTIDEPRESSANTS triptyline is probably the most commonly used tricyclic Tricyclic antidepressants have been used for years for agent for neuropathic pain. Amitriptyline also is the most the management of neuropathic pain syndromes, includsedating of the tricyclic antidepressants and has the most ing diabetic neuropathy, postherpetic neuralgia, andpotent anticholinergic effects. A starting dose of 25 mg at migraine headache (Max, 1994; McQuay, et al., 1996;bedtime is recommended. Onghena & van Houdenhove, 1992). However, pain Amitriptyline is metabolized into nortriptyline, a secrelief is often modest and accompanied by side effects. ondary amine with twice as much inhibition of norepiControlled studies indicate that approximately one thirdnephrine reuptake, compared with serotonin. Nortriptyline of patients will obtain more than 50% pain relief, oneis less sedating than amitriptyline with less anticholinergic third will have minor adverse reactions, and 4% will side effects. A starting dose of 10 mg at bedtime is gendiscontinue the antidepressant because of major side erally well tolerated. effects (McQuay, et al., 1996). Fortunately, some patients Imipramine is a tertiary amine with equal inhibition of obtain excellent pain relief. norepinephrine and serotonin uptake. This drug is moderBecause comparisons between tricyclic antidepres-ately sedating and has average anticholinergic effects. The sants have not shown great differences ficacy in ef (Max, suggested starting dose is 25 mg at bedtime. Because of 1994; McQuay, et al., 1996), the choice of which antide-unpredictable metabolism, occasional blood levels are sugpressant to use often depends on the side effect profile gested. of Imipramine is metabolized to a secondary amine,

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desipramine, which is a much more selective inhibitor ofinfusion of lidocaine is effective, a trial of oral mexiletine is worth considering. norepinephrine uptake. Desipramine is less sedating and has fewer anticholinergic effects than imipramine or ami- Prior to starting mexiletine, a baseline ECG is recomtriptyline, is at least as effective for pain control, and ismended if the patient has underlying ischemic heart disbetter tolerated by elderly patients. ease. Dosages may be increased from 150 to 250 mg three Compared with tricyclic agents, serotonin selectivetimes a day over several days. Taking the medication with food may minimize gastric side effects, which are comreuptake inhibitors (SSRIs) for neuropathic pain have been relatively disappointing. In addition, they are more expen-mon and a major reason for discontinuing the drug. Other side effects of mexiletine are nervous system effects such sive than the older generic agents. Nonetheless, at relatively high doses, (e.g., 60 mg) paroxetine is effective foras tremor and diplopia. Once on a stable dose, a serum diabetic neuropathy (Sindrup, Gram, Brosen, Eshj, &level should be obtained (the therapeutic range is between Morgensen, 1990). Fluoxetine may also be useful in the0.5 and 2.0µg/ml). Topical preparations of local anesthetics may be effectreatment of rheumatic pain conditions, many of which tive for neuropathic pain when there is localized allodynia have neuropathic components (Rani, Naidu, Prasad, Rao, & Shobhar, 1996). SSRIs are better tolerated than tricyclicor hypersensitivity. Topical blockade of small- and largefiber nerve endings should reduce mechanical and thermal antidepressants and should be considered rst-line as fi drugs in patients with concomitant depression. In thisallodynia. A topical lidocaine patch (Lidoderm 5% lidocaine) has become available, which can be applied to group they may serve double duty. Venlafaxine is a novel phentylethylamine antide- painful areas in shingles (herpes zoster). Up to three pressant that is chemically distinct from the older tricy-patches may be applied at one time to the painful area. The patches can be worn for up to 12 h a day. A topical clic antidepressants and the serotonin selective uptake inhibitors. Although venlafaxine blocks serotonin and cream, eutectic mixture of local anesthetic (EMLA cream), a mixture of lidocaine and prilocaine, may also norepinephrine reuptake, its analgesic actions may be be useful for cutaneous pain. The cream may be applied mediated by both an opioid mechanism and adrenergic effects (Shreiber, Backer, & Pick, 1999). The drug maythree or four times a day to the painful area. be at least as well tolerated as tricyclic agents and more CORTICOSTEROIDS effective for pain than standard doses of serotonin-selective drugs. Indeed, an initial report suggests that venCorticosteroids are clearly useful for neuropathic pain, lafaxine is effective for neuropathic pain (Galer, 1995). particularly in stimulus-evoked pain such as lumbar radicVenlafaxine should be started at one half of a 37.5 mgulopathy. The anti-inflammatory effects of corticosteroids tablet twice daily and titrated weekly to a maximum of are well known, which may partly explain theirficacy ef 75 mg, taken twice a day. Nausea appears to be the most for pain. When administered epidurally for treatment of common side effect. discogenic radiculopathy, corticosteroids inhibit phospholipase A2 activity and suppress the perineural inflammatory response caused by leakage of disk material around the painful nerve root (Saal, et al., 1990). However, corAntiarrhythmics block ectopic neuronal activity at central ticosteroids also act as membrane stabilizers by suppressand peripheral sites (Chabal, Jacobson, Mariano, Chaney, ing ectopic neural discharges (Castillo, et al., 1996; Devor, & Britell, 1992). Lidocaine, mexiletine, and phenytoin Govrin-Lippmann, & Raber, 1985). Therefore, some of — type I antiarrhythmics — stabilize neural membranesthe pain-relieving action of corticosteroids may be due to by sodium channel blockade. Lidocaine suppresses spona lidocaine-like effect. taneous impulse generation on injured nerve segments, Depot forms of corticosteroids injected around injured dorsal root ganglia, and dorsal horn wide dynamic range nerves provide pain relief and reduce pain associated with neurons (Abram & Yaksh, 1994; Sotgiu, Lacerenza, &entrapment syndromes. Corticosteroids are also effective Marchettini, 1992). Lidocaine infusions have been usedif given orally or systemically. In cancer pain syndromes, to predict the response of a given neuropathic pain disorsteroids such as dexamethasone may be first-line therapy der to antiarrhythmic therapy (Burchiel & Chabal, 1995).for neuropathic pain. The potential side effects of cortiLidocaine may be effective at subanesthetic doses, and costeroids are well known and may be seen whether given following nerve blocks analgesia may outlast conductionorally, systemically, or epidurally. block for days or weeks (Burchiel & Chabal, 1995; Chaplan, Flemming, Shafer, & Yaksh, 1995; Jaffe & Rowe, BACLOFEN 1995). It has been reported that patients with PNS injury experience better pain relief than those with central painBaclofen is useful for trigeminal neuralgia and other types syndromes (Galer, Miller, & Rowbotham, 1993). If a trial of neuropathic pain (Fromm, Terrence, & Chattha, 1984),

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particularly as an add-on drug. Baclofen is a GABA-B membranes. Medications that enhance dorsal horn inhibiagonist and is presumed to hyperpolarize inhibitory neu-tion appear to act by augmenting spinal biogenic amine rons in the spinal cord (Yaksh & Malmberg, 1994), and GABAergic mechanisms. From a clinical standpoint, thereby reducing pain. This GABA effect appears to begiven the paucity of our understanding of neuropathic pain similar to benzodiazepines, such as clonazepam. Side mechanisms and how the medications actually work, it is effects of baclofen can be significant and include sedation, probably more useful to classify adjuvant drugs according confusion, nausea, vomiting, and weakness, especially in to their traditional therapeutic indications (e.g., antidethe elderly. A typical starting dose is 5 mg three times apressants and anticonvulsants). This point of view is day. Thereafter, the drug can be increased slowly to 20 strengthened by the fact that most drugs appear to have mg four times a day. Abrupt cessation may precipitatemultiple mechanisms and sites of action, making further withdrawal with hallucinations, anxiety, and tachycardia.subclassification arbitrary and probably inaccurate. The drug is excreted by the kidneys and the dosage must Anticonvulsants, particularly carbamazepine (and be reduced in renal insuf ficiency. more recently gabapentin), are useful for neuropathic pain. Although conventional wisdom suggests that anticonvulsants may be most effective for lancinating pain, anticonCAPSAICIN vulsants also are useful for burning dysesthesias. The Capsaicin is a C-fiber-specific neurotoxin and is one ofmechanism of action of gabapentin is poorly understood, the components of hot peppers that produces a burning but the drug has been demonstrated to bind to a novel sensation on contact with mucous membranes. Topical voltage-dependent calcium channel receptor. Gabapentin preparations are available over the counter and are widely reduces the pain due to diabetic peripheral neuropathy and used for chronic pain syndromes. Capsaicin is a vanilloidpostherpetic neuralgia; and the overall safety record with receptor agonist and activates ion channels on C fibers gabapentin is good, making it an attractive alternative to that are thermotransducers of noxious heat (>C)43° carbamazepine and tricyclic antidepressants, particularly (Caternia, et al., 1997). With repeated application in suf-for elderly patients. ficient quantities, capsaicin can inactivate primary afferent Clonazepam is another option and also poses mininociceptors. For patients with pain due to sensitized nocimal risk from the standpoint of organ toxicity. Clonceptors, capsaicin may be effective, if they can tolerateazepam may be useful for radicular pain and pain assothe pain induced by the medication. The drug causes ciated with tumors, such as plexopathy. In addition, intense burning, which may abate with repeated applicaclonazepam may be used to supplement other adjuvant tions and gradual inactivation of the nociceptors. However,drugs. When given at bedtime, the mild sedating effect in patients with tactile allodynia, which is probably medi- of clonazepam can be helpful for patients who have ated by large fibers, capsaicin may not be as effective. difficulty sleeping because of pain. Capsaicin extracts are available commercially as topical Antidepressants have been used effectively for years preparations, containing 0.025 and 0.075% and should be in the management of multiple pain syndromes, includapplied to the painful area three to five times a day. The ing diabetic neuropathy, postherpetic neuralgia, rheupreparation may be better tolerated if it is used after appli-matoid arthritis, osteoarthritis, migraine headache, low cation of a topical local anesthetic cream. back pain, and bromyalgia. fi However, pain relief is often modest and accompanied by side effects. Studies indicate that only one third of patients obtain more than SUMMARY AND RECOMMENDATIONS 50% pain reduction. However, some patients obtain draNeuropathic pain is a common cause of chronic pain and matic pain relief. tends to be resistant to usual doses of traditional analgesic The choice of which antidepressant to use for neumedications. Classic examples of neuropathic pain include ropathic pain often depends on the particular side effect trigeminal neuralgia, postherpetic neuralgia, and diabeticprofile of a given drug, because comparisons of individneuropathy. Neuropathic pain is often described as lanciual tricyclic antidepressants have not shown great differnating or burning in nature. Both types of pain may beences in ef ficacy. When a patient is having ficulty dif present at the same time, often accompanied by allodynia. sleeping because of pain, a more sedating drug, such as Neuropathic pain may be manageable with one oramitriptyline is appropriate. On the other hand, which is considerably less sedating and has more adjuvant analgesic drugs, often prescribed as part desipramine, of fewer anticholinergic effects, may be much better tolera comprehensive treatment plan. From a theoretical point of view, it may be helpful to categorize adjuvant analgesicsated in elderly patients. into two broad classes of drugs, agents that act as mem- Serotonin-selective reuptake inhibitors for neurobrane-stabilizing agents and drugs that enhance dorsal pathic pain have been disappointing, although paroxetine horn inhibition. Membrane-stabilizing drugs may act by at relatively high doses is useful for diabetic neuropathy. blocking sodium and calcium channels on damaged neural Fluoxetine may be useful in the treatment of rheumatic

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pain conditions, many of which have neuropathic compo-more attractive. In our clinic, gabapentin often is our first nents. As with the tricyclic agents, the SSRIs are probably choice, followed by a tricyclic antidepressant, such as interchangeable. However, SSRIs are better tolerated than nortriptyline. Both drugs must be started slowly and tricyclics and may be extremely effective in treating titrated to effect, perhaps to rather high levels, for full patients with chronic pain and concomitant depression. benefit. However, tricyclics have many potential side It remains unclear whether anticonvulsants or antide-effects that must be considered, particularly anticholinpressants should be first-line therapy for neuropathic pain. ergic and cardiac interactions and organ toxicity. Clearly, Similar results have been obtained with both, and current gabapentin is a safer drug, but may cause sedation or evidence concerning drug ficacy ef does not support the dysphoria in some patients. Occasionally, patients comuse of one drug over another. In many cases, selection plain of of weight gain and nonpitting edema. Other disada particular drug may depend more on expected side vantages of gabapentin include its cost (approximately ten effects (e.g., sedation) or the clinician’ s experience with times the cost of a generic tricyclic antidepressant at usual the drug, than theoretical considerations about mechastarting doses) and the need to take the drug three or four nisms of drug action. It must be remembered that treattimes a day. Keep in mind that the dosage of gabapentin ment of neuropathic pain remains largely empirical. Inmust be reduced appropriately for patients with renal addition, for maximum analgesic benefit, more than oneinsufficiency. A comparison of gabapentin with tricyclic drug may be necessary. Until more effective medicationsantidepressants is provided in Table 17.3. When an appropriate medication trial has been inefbecome available, polypharmacy will remain the rule fective, an interdisciplinary approach should be considinstead of the exception. This is probably understandable, given the multiple mechanisms involved in the pathophys-ered. With chronic neuropathic pain, limitations of current iology of neuropathic pain. analgesics usually make complete pain relief a very unreIn general, for neuropathic pain either gabapentin oralistic goal. Therefore, improving function and comfort amitriptyline (or a similar tricyclic antidepressant) should and treating associated problems, such as depression, become important goals. Reducing dependence on opioid be first-line therapy. When considering issues such as time to effective analgesic action and toxicity, gabapentin ismedications may or may not be a primary goal, depending

TABLE 17.3 Comparison of Gabapentin and Generic Tricyclic Antidepressants: Dosages, Side Effects, and Cost Drug Gabapentin (Neurontin)

Amitriptyline

Nortriptyline

Desipramine

Dosage

Side effects

Starting dose: 300 mg b.i.d. to t.i.d. (patient Somnolence, dizziness, ataxia, and may start with bedtime dose) peripheral edema. Elderly patients: 100 mg twice a day Reduce dosage in renal insuf ficiency Effective dose: 1800 to 2400 mg/day (25 mg/kg/day); e.g., 600 mg with meals and at bedtime) Note: studies used doses as high as 3600 mg/day Titrate by increasing daily dose every 3 to 7 days, patient instruction sheet helpful Starting dose: 25 mg at bedtime; elderly Sedation, cognitive problems, patients: 10 mg at HS anticholinergic side effects, weight Effective dose: 25 to 150 mg/day gain, orthostatic hypotension, Titrate by increasing daily dose every 7 days; arrhythmias; rare hepatic injury patient instruction sheet helpful Starting dose: 10 mg at HS; effective dose:Less sedation, fewer anticholinergic 10 to 100 mg/day effects than amitriptyline; otherwise Titrate by increasing daily dose every 7 days; same effects as amitriptyline patient instruction sheet helpful

Approximate Cost to Patient 300 mg capsules t.i.d.: $106/month ($118/100 capsules) No laboratory studies needed to monitor therapy.

25 mg tablets at bedtime: $7.80/month ($26/100 tablets) Laboratory studies needed to monitor therapy; consider baseline ECG 10 mg tablets at bedtime: $12/month ($40/100 tablets) 25 mg tablets at bedtime: $24/month ($80/100 tablets) Lab studies, ECG Starting dose: 25 mg at bedtime; elderly Less sedation, less anticholinergic 25 mg tablets at bedtime: $9/month patients: 10 mg HS effects, otherwise same effects as ($30/100 tablets) Effective dose: 25 to 150 mg/day amitriptyline Lab studies, ECG Titrate by increasing daily dose every 7 days, patient instruction sheet helpful

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Bennett, G.J. (1994). Neuropathic pain. In P.D. Wall & R. on whether the pain syndrome is opioid responsive, the Melzack (Eds.),Textbook of pain(3rd ed., pp. 201–224). patient is demonstrating appropriate improvements in Edinburgh: Churchill Livingstone. function, and there are not undo side effects or evidence Beydoun, A., Uthman, B.M., & Sackellares, J.C. (1995). Gabaof drug abuse. pentin: Pharmacokinetics,ficacy, ef and safety.Clinical Current evidence indicates that nonpharmacological Neuropharmacology, 18, 469–481. approaches may be reasonable, obviate or reduce the need Blom, S. (1962). Trigeminal neuralgia: Its treatment with a new for potentially toxic medications, and improve the effecanticonvulsant drug (G-32883). Lancet, 1,839–840. tiveness of analgesic regimens. Spinal cord stimulation Brodie, M.J., & Dichter, MA. (1996). Antiepileptic drugs. New may reduce pain in selected patients. Less invasive techEngland Journal of Medicine, 334, 168–175. niques, including TENS units and percutaneous nerve Burchiel K.J., & Chabal C. (1995). A role for systemic lidocaine stimulation, are also beneficial. challenge in the classification of neuropathic pains. Pain Effective management of neuropathic pain requires Forum, 4, 81–82. patience on the part of the clinician and the patient, and Castillo, J., Curley, J., Hotz, J., Uezono, M., Tigner, J., Chasin, the willingness to evaluate different treatment approaches, M., Wilder, R., et al. (1996). Glucocorticoids prolong rat sciatic nerve blockade in vivo from bupivacaine including trials of various medications. This may be a microspheres.Anesthesiology, 85, 1157–1166. time-consuming process. Insofar as possible, it is helpful to target specific symptoms, for example, burning painCaternia, M.J., Schumacher, M.A., Tominga, M., et al. (1997). The capsaicin receptor: A heat-activated ion channel in with tricyclic antidepressants and lancinating pain with the pain pathway.Nature, 389,816–824. anticonvulsants. However, from a practical standpoint, Caudle, R.M., & Mannes, A J. (2000). Dynorphin, friend or foe? pharmacological choices are often based on physician Pain, 87, 235–239. comfort with a given drug and expected side effects. MoreChabal, C., Jacobson, L., Mariano, A., Chaney, E., & Britell, C. over, the high cost of newer drugs may make the older W. (1992). The use of oral mexiletine for the treatment tricyclic antidepressants, such as amitriptyline, the only of pain after peripheral nerve injury. Anesthesiology, 76, cost-effective alternative for some patients. Until more 513–517. effective drugs become available, the pharmacologicalChaplan, S.R. (2000). Neuropathic pain: Role of voltage-depenapproach remains largely one of trial and error. In the dent calcium channels. Regional Anesthesia and Pain meantime, nonpharmacological strategies may assume a Medicine, 25,283–285. larger role in clinical practice. Chaplan, S.R., Flemming, B.W., Shafer, S.L., & Yaksh, T.L. (1995). Prolonged alleviation of tactile allodynia by intravenouslidocaine in neuropathic rats. AnesthesiolREFERENCES ogy, 83,775–785. Chapman, V., Suzuki, R., Chamarette, H.L.C., Rygh, L.J., & Abdi, S., Lee, D.H., & Chung, J.M. (1998). The anti-allodynic Dickenson, A.H. (1998). Effects of systemic carbameffects of amitriptyline, gabapentin, and lidocaine in a azepine and gabapentin on spinal neuronal responses in rat model of neuropathic pain. Anesthesia and Analgespinal nerve ligated rats. Pain, 75, 261–272. sia, 87, 1360–1366. Dellemijn, P. (1999). Are opioids effective in relieving neuroAbram, S.E., & Yaksh, T.L. (1994). Systemic lidocaine blocks nerve pathic pain? Pain, 80, 453–462. injury-induced hyperalgesia and nociceptor-driven spinal Devor, M. (1994). The pathophysiology of damaged peripheral sensitization in the rat. Anesthesiology, 80, 383–391. nerves. In P.D. Wall & R. Melzack (Eds.), Textbook of Ahmed, H.E., Craig, W.F., White, P.F., et al. (1998). Percutanepain (3rd ed., pp. 79–100). Edinburgh: Churchill Livous electrical nerve stimulation: an alternative to antiviingstone. ral drugs for acute herpes zoster. Anesthesia and Devor, M. (1995). Neurobiological basis for selectivity of Analgesia, 87,1–4. sodium channel blockers in neuropathic pain. Pain Alhaider, A.A., Lei, S.Z., & Wilcox, G.L. (1991). Spinal 5-HT3 Forum, 4, 83–86. receptor-mediated antinociception: Possible release of Devor, M., Govrin-Lippmann, R., & Raber, P. (1985). CorticosGABA. Journal of Neuroscience, 11, 1881–1888. teroids suppress ectopic neural discharge originating in Arner, S., & Meyerson, B.A. (1988). Lack of analgesic effect of experimental neuromas. Pain, 22,127–137. opioids on neuropathic and idiopathic forms of pain. Eisenach, J.C., & Gebhart, G.F. (1995). Intrathecal amitriptyline Pain, 33, 11–23. acts as anN-methyl-D-aspartate receptor antagonist in American Medical Association (1993). Drugs used in mood disthe presence of inflammatory hyperalgesia in rats. Anesorders.AMA Drug Evaluations Annual(pp. 277–306). thesiology, 83,1046–1054. Chicago: American Medical Association. Backonja, M., Beydoun, A., Edwards, K.R., Schwartz, S.J., Fon-Foley, K.M. (1987). Pain syndromes in patients with cancer. Medical Clinics of North America, 71, 169–184. seca, V., Hes, M., LaMoreaux, L., & Garafalo, E. (1998). Gabapentin for the symptomatic treatment of painful Fromm, G.H., Terrence, C.F., & Chattha, A.S. (1984). Baclofen in the treatment of trigeminal neuralgia: Double-blind neuropathy in patients with diabetes mellitus. A randomstudy and long-term follow-up. Annals of Neurology, 15, ized controlled trial.Journal of the American Medical 240–244. Association, 280,1831–1836.

Neuropathic Pain: Mechanisms and Management

193

Classification of Galer, B.S. (1995). Neuropathic pain of peripheral origin: Merskey, H., & Bogduk, N. (Eds.). (1994). chronic pain. Descriptions of chronic pain syndromes Advances in pharmacologic treatment. Neurology, 45 and definitions of pain terms (2nd ed.). Seattle: IASP (Suppl. 9), S17–S25. Press. Galer, B.S., Miller, K.V., & Rowbotham, M.C. (1993). Response to intravenous lidocaine infusion differs based on clin- Morello, C.M., Leckband, S.G., Stoner, C.P., Moorhouse, D.F., & Sahagian, G.A. (1999). Randomized double-blind ical diagnosis and site of nervous system injury. Neustudy comparing the ficacy ef of gabapentin with amirology, 43, 1233–1235. triptyline on diabetic peripheral neuropathy. Archives of Ghoname, E.A., White, P.F., Ahmed, H.E., Hamza, A., Craig, W.F., Internal Medicine, 159,1931–1937. & Noe, C.E. (1999). Percutaneous electrical nerve stimulation: An alternative to TENS in the management of North, R.B., Kidd, D.H., Zahurak, M., James, C.S., & Long, D.M. (1993). Spinal cord stimulation for chronic, intracsciatica.Pain, 83,193–199. table pain: Experience over two decades. Neurosurgery, Glassman, A., Roose, S., & Bigger, J. (1993). The safety of 32, 383–394. tricyclic antidepressants in cardiac patients. Risk-benefit reconsidered.Journal of the American Medical Associ- Novakovic, S.D., Tzoumaka, E., McGivern, J.G., et al. (1998). Distribution of the tetrodotoxin-resistant sodium chanation, 269,2673–2677. nel PN3 in rat sensory neurons in normal and neuroGracely, R.H., Lynch, S.A., & Bennett, G.J. (1992). Painful pathic conditions. Journal of Neuroscience, 18, neuropathy: Altered central processing, maintained 2174–2187. dynamically by peripheral input. Pain, 51, 175–194. Hamza, M.A., White, P.F., Craig, W.F., Ghoname, E.S., et al.Onghena, P., & van Houdenhove, B. (1992). Antidepressantinduced analgesia in chronic non-malignant pain: A (2000). Percutaneous electrical nerve stimulation: A novel meta-analysis of 39 placebo controlled studies. Pain, 49, analgesic therapy for diabetic neuropathic pain. Diabetes 205–220. Care, 23,365–370. Ossipov, M. H., Lai, J., Malan, T. P., & Porreca, F. (2000). Spinal Hart, R.G., & Easton, J.D. (1982). Carbamazepine and hematoand supraspinal mechanisms of neuropathic pain. logical monitoring.Annals of Neurology, 11, 309–312. Annals. New York Academy of Sciences, 909, 12–24. Hegarty, A., & Portenoy, R.K. (1994). Pharmacotherapy of neuPancrazio, J J., Kamatchi, G.L., Roscoe, A.K., & Lynch, C., III. ropathic pain.Seminars in Neurology, 14, 213–224. + channels by antide(1998). Inhibition of neuronal Na Iacono, R.P., Guthkelch, A.N., & Boswell, M.V. (1992). Dorsal pressant drugs. Journal of Pharmacology and Experiroot entry zone stimulation for deafferentation pain. Stemental Therapeutics, 284, 208–214. reotactic and Functional Neurosurgery, 59, 56–61. Jaffe, R.A., & Rowe, M.A. (1995). Subanesthetic concentrationsPortenoy, R.K., Foley, K.M., & Inturrisi, C.E. (1990). The nature of opioid responsiveness and its implications for neuroof lidocaine selectively inhibit a nociceptive response in pathic pain: New hypotheses derived from studies of the isolated rat spinal cord. Pain, 60, 167–174. opioid infusions.Pain, 43, 272–286. Jun, J.H., & Yaksh, T.L.(1998). The effect of intrathecal gabapentin and 3-isobutyl gamma-aminobutyric acid on thePrice, D.D., Mao, J., & Mayer, D.J. (1994). Central neural mechhyperalgesia observed after thermal injury in the rat. anisms of normal and abnormal pain states. In H.L. Anesthesia and Analgesia, 86, 348–354. Fields & J.C. Liebskind (Eds.),Pharmacological approaches to the treatment of chronic pain: New conKemler, M.A., Barendse, G.A.M, van Kleef, M., de Vet, H.C.W., cepts and critical issues. Progress in pain research and Rijks, C.P.M., Furnee, C.A., & van den Wildernber, management(Vol. 1, pp. 61–84). Seattle: IASP Press. F.A.J.M. (2000). Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. New England Rani, P.U., Naidu, M.U.R., Prasad, V.B.N., Rao, T.R.K., & Journal of Medicine, 343,618–624. Shobha, J.C. (1996). An evaluation of antidepressants in rheumatic pain conditions. Anesthesia and Analgesia, Kovelowski, C.J., Ossipov, M.H., Sun, H., Malan, T.P., & 83, 371–375. Porecca, F. (2000). Supraspinal cholecystokinin may drive tonic descending facilitation mechanisms to main-Rowbotham, M., Harden, N., Stacey, B., Bernstein, P., & Magtain neuropathic pain in the rat. Pain, 87, 265–273. nus-Miller, L. (1998). Gabapentin for the treatment of postherpetic neuralgia. A randomized controlled trial. Matthew, N.T., Saper, J.R., Silberstein, S.D., Rankin, L., MarkJournal of the American Medical Association, 280, ley, H G., Solomon, S., et al. (1995). Migraine prophy1837–1842. laxis with divalproex. Archives of Neurology, 52, 281–286. Saal, J.S., Franson, R.C., Dobrow, R., Saal, J.A., White, A.H., & Goldthwaite, N. (1990). High levels of inflammatory Max, M. (1994). Antidepressants as analgesics. In H.L. Fields phospholipase A2 activity in lumbar disc herniations. & J.C. Liebskind (Eds.),Pharmacological approaches Spine, 15,674–678. to the treatment of chronic pain: New concepts and critical issues. Progress in pain research and manage-Schreiber, S., Backer, M.M., & Pick, C.G. (1999). The antinociment (Vol. 1, pp. 229–246). Seattle: IASP Press. ceptive effect of venlafaxine in mice is mediated through McLachlan, E.M., Janig, W., Devor, M., & Michaelis, M. (1993). opioid and adrenergic mechanisms. Neuroscience LetPeripheral nerve injury triggers noradrenergic sprouting ters, 273,85–88. within dorsal root ganglia.Nature, 363,543–546. Shimoyama, N., Shimoyama, M., Davis, A.M., Inturrisi, C.E., McQuay, H.J., Tramer, M., Nye, B.A., Carroll, D., Wiffen, P.J., & Elliott, K.J. (1997). Spinal gabapentin is antinocicep& Moore, R.A. (1996). A systematic review of antidetive in the rat formalin test. Neuroscience Letters, 222, pressants in neuropathic pain. Pain, 68, 217–227. 65–67.

194

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Shimoyama, M., Shimoyama, N., Inturrisi, C.E., & Elliott, K.J. Tohen, M., Castillo, J., Baldessarin, R.J., Zarate, C., & Kando, J.C. (1995). Blood dyscrasias with carbamazepine and (1997a). Gabapentin enhances the antinociceptive valproate: A pharmacoepidemiological study of 2,228 effects of spinal morphine in the rat tail-flick test. Pain, patients at risk.American Journal of Psychiatry, 152, 72, 375–382. 413–418. Sindrup, S.H., Gram, L.F., Brosen, K., Eshj, O., & Morgensen, E.F. (1990). The selective serotonin reuptake inhibitorVanderah, T.W., Gardell, L.R., Burgess, S.H., et al. (2000). Dynorphin promotes abnormal pain and spinal opioid paroxetine is effective in the treatment of diabetic neuantinociceptive tolerance. Journal of Neuroscience, 20, ropathy symptoms.Pain, 42, 135–144. 7074–7079. Sobotka, J.L., Alexander, B., & Cook, B.L. (1990). A review of carbamazepine’ s hematologic reactions and monitoring Woolf, C.J., & Mannion, R.J. (1999). Neuropathic pain: Aetiology, symptoms, mechanisms, and management. Lancet, recommendations.DICP, Annals of Pharmacotherapy, 353, 1959–1964. 24, 1214–1219. Sotgiu, M.L., Lacerenza, M., & Marchettini, P. (1992). Effect of Woolf, C.J., Shortland P., & Coggeshall, R.E. (1992). Peripheral nerve injury triggers central sprouting of myelinated systemic lidocaine on dorsal horn neuron hyperactivity afferents.Nature, 355,75–77. following chronic peripheral nerve injury in rats. SomaYaksh, T.L. (1979). Direct evidence that spinal serotonin and tosensory and Motor Research,227–233. 9, noradrenaline terminals mediate the spinal antinocicepSwerdlow, M. (1984). Anticonvulsant drugs and chronic pain. tive effects of morphine in the periaqueductal gray. Clinical Neuropharmacology, 7, 51–82. Brain Research, 160, 180–185. Tanelian, D.L., & Victory, R.A. (1995). Sodium channel-blocking agents. Their use in neuropathic pain conditions.Yaksh, T.L, & Malmberg, A.B. (1994). Central pharmacology of nociceptive transmission. In P.D. Wall & R. Melzack Pain Forum, 4,75–80. (Eds.), Textbook of pain(3rd ed., pp. 165–200). EdinTaylor, C.P., Gee, N.S., Su, T.Z., Kocsis, J.D., Welty, D.F., burgh: Churchill Livingstone. Brown, J.P., Dooley, D.J., Boden, P., & Singh,(1998). L. A summary of mechanistic hypotheses of gabapentin pharmacology.Epilepsy Research, 29, 233–249.

18 Primary Headache Disorders R. Michael Gallagher, D.O., F.A.C.O.F.P., F.A.H.S. MANAGEMENT OF PRIMARY HEADACHE DISORDERS

a classification system for headache disorders. Although they were designed to help diagnose patients for clinical trials, the IHS criteria reflect international expert consensus INTRODUCTION and, unlike earlier headache diagnostic criteria (Friedman, Finley, & Graham, 1962), they outline the specific characHeadache disorders are an exceedingly common patient teristics necessary to confirm and to exclude a broad range complaint that have been described throughout recorded of headache disorders. According to the IHS, most chronic medical history. Symptoms of head pain were noted as early or recurring head pain can be classified as one of the “prias 7000B.C. (Lyons & Petrucelli, 1978), and Neolithic mary headache disorders”: tension type, migraine, or cluster. trepanned skulls suggest the extreme measures once taken Each of these headache types, as the descriptor suggests, can to relieve head pain that was attributed to evil spirits (Venoccur without the presence of an underlying disorder. The zmer, 1972, p. 19). Currently, the National Headache FounIHS system classifies all other types of headache as “secdation (2000) reports that more than 45 million Americans ondary headache disorders,” because they can always be have chronic, recurring headaches. Each year, U.S. busiattributed to one of hundreds of indirect causes of head pain nesses lose approximately $50 billion to absenteeism and (e.g., fever, trauma, subarachnoid hemorrhage, medication). medical expenses caused by headache, and headache sufThis chapter reviews the diagnosis and treatment of the three ferers spend in excess of $4 billion on nonprescription analprimary headache disorders. gesics (NHF, 2000). Headache is responsible for approximately 10 million physician consultations per year (Linet OVERALL APPROACH & Stewart, 1987), and it is the fourth most common reason for emergency room visits in the United States. The vast majority of headache patients can be successfully Although the last two decades of the 20th centurytreated. When therapy is successful, the management of produced significant advances in our understanding ofheadache can be extremely rewarding for the patient and headache, the precise pathophysiology of the primary for the physician. Therapy can be time consuming and headache disorders remains unknown. For many years, difficult in some cases, however. When it does not succeed, primary headaches were classified symptomatically, as or it succeeds only partially, the challenge can quickly eithervascular headaches (migraine and cluster) or nonvabecome frustrating. Help for headache sufferers rests with scular headaches (tension type). Technological advances the empathetic, knowledgeable medical professional who in the 1980s allowed researchers to see for the first time is willing to establish an honest partnership that aims at that changes in cerebral blood flow during headache epirelieving symptoms, restoring function, and reducing dissodes, particularly in migraine, did not occur exclusivelyability, not toward “curing” their “problem.” In many in areas defined by vascular boundaries. cases, a clinician’ s ability to educate patients is key; all The Headache Classification Committee of the Interna-headache patients should clearly understand the goals of tional Headache Society (IHS) ([ACCIHS], 1988) publishedtheir treatment plan. Unfortunately, many headache

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patients seek medical attention during severe attacks, TTH is the most common type of headache and is which demand immediate attention and prevent the evalconsidered to have episodic (ETTH) and chronic uation necessary to making an accurate diagnosis. The (CTTH) variants. One-year period prevalence estimates most productive time for assessment is when the patient using the IHS criteria indicate that as many as 93% of is headache free or not so debilitated as to interfere with the general population have at least one tension-type a complete history taking and examination. After the diag-headache per year (Rasmussen, Jensen, Schroll, & Olenosis is made, the clinician and patient can develop sen, a 1991), although some investigators have found realistic, achievable treatment plan. ETTH rates as low as 14.3% (Lavados & Tenhanun, There are two main elements of headache treatment. 1997). CTTH sufferers (more than 180 headache attacks Abortive treatmentaims at relief once a headache attackper year) are far less common than ETTH sufferers; the has begun, and prophylactic treatmentis used to prevent highest 1-year period prevalence ever recorded for or reduce the likelihood of headache episodes before they CTTH was 8.1% (Tekle Haimanot, Seraw, Forsgren, occur. Abortive treatment is used for patients whose headEkborn, & Ekstedt, 1995). aches are infrequent and for those headaches that break Both ETTH and CTTH are characterized by intermitthrough in spite of prophylactic therapy. When headaches tent or persisting bilateral pain, often described as a are frequent or unresponsive to abortive medication, prosqueezing pressure or a tight band around the head. Some phylactic measures should be taken. Many clinicians begin patients experience pain in the temporal or occipital prophylaxis when a patient has more than three severe regions, the forehead, or the vertex. The location of sympheadache attacks per month. toms can vary from attack to attack, and associated tightWhether preventive or abortive therapy is indicated,ness of the neck and shoulders is common. Unlike management should follow a definite plan incorporatingmigraine, TTH is not preceded by prodromal symptoms, the physician and the patient into a team that worksand TTH are not episodes typically associated with nausea actively to reduce the frequency and/or severity of head-or vomiting. The intensity of pain in TTH varies widely, aches. The physician’ s impressions and physical findings but it is not usually incapacitating. TTH can last from should be completely explained to the patient no matterhours to days and, in some cases, persist for months. The what level and pace are required to ensure complete underIHS diagnostic criteria for ETTH and CTTH are listed in standing. The headache condition should also be Table 18.1 (HCCIHS, 1988). explained, emphasizing the fact that the disorder is real, not imagined, and that it is controllable, not curable. OncePRECIPITATING FACTORS a plan is developed, follow-up and continuing care are TTH frequently occurs during periods of stress or emoimportant elements in a successful outcome. tional upset. Some CTTH patients may display evidence of anxiousness, as well as poor coping and adaptation TENSION-TYPE HEADACHE skills. If headaches are frequent or near daily, depression may be involved and should be considered, even in the In the 1988, IHS classifi cation of headache, a headache absence of obvious signs, such as mood changes, crying type once known asmuscle “ contraction headache” was spells, or loss of appetite. Organic processes may also be renamed “ tension-type headache”(TTH) (HCCIHS, involved in the precipitation of TTH. When the cause is 1988). Traditionally, it was believed that TTH was organic instead of psychogenic, the pain may also be caused by sustained muscle contraction of the neck, jaw, resistant to usual treatment modalities. Organic causes can scalp, and facial muscles. It has since been learned, be numerous, but the more commonly encountered in however, that the sustained contraction of pericranial clinical practice include degenerative joint disease of the muscles associated with TTH may occur as an epiphecervical spine, head or neck trauma, temporomandibular nomenon to possible central disturbances, not as a prijoint dysfunction, or ankylosing spondylitis. mary process. Alterations in the levels of serotonin (5HT), substance P (SP), and neuropeptide Y in the serum TREATMENT or platelets have been shown in patients affected by ETTH can be resolved with nonpharmacological meaTTH, leading to speculation that these neurotransmitters are involved in the genesis and modulation of pain insures, analgesic medications, or some combination of the condition (Ferrari, 1993; Gallai, et al., 1994; these modalities. Nonpharmacological options for TTH Nakano, Shimomura, Takahashi, & Ikawa, 1993; Rolf,include manipulation, massage, exercise, cold or warm Wiele, & Brune, 1981; Schoenen, 1990; Shukla,compresses, stress avoidance, and relaxation techniques Shanker, Nag, Verma, & Bhargava, 1987; Takeshima,(Table 18.2) (Stevens, 1993). When these approaches do Shimomura, & Takahashi, 1987). Without concrete evi-not provide adequate relief, simple analgesics, such as dence of central activity, however, the cause of TTHacetaminophen (APAP), aspirin (ASA), or ibuprofen (IB), often relieve the symptoms of ETTH. If simple analgesics remains unknown.

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TABLE 18.1 IHS Diagnostic Criteria for Episodic Tension-Type Headache

TABLE 18.2 Nonpharmacological Management of Headache

A. At least 10 previous headache episodes fulfilling criteria B to D listed next; number of days with such headache < 180/year (< 15/month) B. Headache lasting from 30 min to 7 days C. At least two of the following pain characteristics: Pressing/tightening (nonpulsating) quality Mild or moderate intensity (may inhibit, but does not prohibit activities) Bilateral location No aggravation by walking stairs or similar routine physical activity D. Both of the following: No nausea or vomiting (anorexia possibly occurring) Photophobia and phonophobia are absent, or one but not the other is present E. At least one of the following: History, physical, and neurological examinations not suggesting one of the disorders listed in groups 5 to 11 History and/or physical and/or neurological examinations suggesting such disorder, but ruled out by appropriate investigations Such disorder present, but tension-type headache not occuring for the first time in close temporal relation to the disorder

Topical heat or cold packs Topical analgesic balms Respite from stressors (rest, sleep) Stress-reduction techniques (e.g., exercise, sexual activity, relaxation modalities) Regular exercise Physical therapy Relaxation techniques (including biofeedback, hypnotherapy, vacation) Manipulative therapy From Stevens, M.B. (1993).American Family Physician, 47, 799–805. With permission.

from the combination of isometheptene, acetaminophen, and dichloralphenazone. Other options include the alphaagonist tizanidine, ASA combined with the muscle relaxants orphenadrine or carisoprodol, or APAP added to chlorzoxazone. In some patients, the symptoms of TTH can be extremely severe and require potentially addictive analgesic combination drugs containing butalbital, meprobromate, or an opioid. These drugs provide analgesia and reduce the anxiety often associated with pain (Table 18.3). As with any potentially addicting drug, however, limit the amounts prescribed and make sure that patients underFrom HCCIHS (1988).Cephalalgia, 8(Suppl. 7), 1–96. With perstand that they should contact you about a change in mission. prescription instead of beginning daily or near-daily use fail, caffeinated combination analgesics often provideof a medication with a high risk of addiction. effective relief. In TTH studies, it has been shown that it Patients with CTTH require a different approach. Pretakes about 40% more of a simple analgesic to equal the scribing the stronger medications in this patient subset analgesic potency of the simple analgesic plus caffeine greatly enhances the risk of abuse. Prophylactic treatment (Laska, et al., 1984; Migliardi, Armellino, Friedman, Gill- may be needed for CTTH patients or for those whose ings, & Beaver, 1994). If a prescription is required toattacks are caused by organic abnormalities. Pharmacoprovide adequate relief, some patients with ETTH benefitlogical treatment of CTTH can include the judicious use

TABLE 18.3 Selected Prescription Medications for Tension-Type Headache Drug

Brand Name

Aspirin Bayer Acetaminophen Tylenol Aspirin/acetaminophen/caffeine Excedrin Ibuprofen Advil/Motrin Naproxen Aleve Orphenadrine/aspirin/caffeine Norgesic Isometheptene/dichloralphenazone/acetaminophen Midrin Carisoprodol/aspirin Chlorzoxazone Butalbital/aspirin/caffeine Butalbital/acetaminophen/caffeine Tizanidine

Soma compound Parafon Forte Fiorinal Fioricet/Esgic Zanaflex

Dose — Prn 650 mg every 4–6 h 500–1000 mg every 4–6 h 2 tablets every 4–6 h 400 mg every 4–6 h 275–550 mg every 6–8 h 2 tablets every 4 h 2 tablets at onset followed by 1 tablet hourly (up to 5 tablets) 2 tablets every 4 h 1 tablet every 4–6 h 1 tablet every 4 h 1 tablet every 4 h 2–4 mg every 4 h

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of sedatives or muscle relaxants, but most patients who intensity, aggravation by routine physical activity, and respond do so only temporarily, and the risk of habituationassociation with nausea, photo-, and phonophobia” is significant. (HCCIHS, 1988). Migraine does not occur on a daily T h e n o n s t e r o i d a l a n t i - i naflm m a t o r y d r u g s basis; typical frequency is one to four per month. In some (NSAIDs) and antidepressants appear to be the most patients, the migraine may occur once yearly or as often useful in preventing TTH (Gallagher & Freitag, 1987b). as 15 to 20 times per month. Most CTTH patients who improve with NSAID treatMigraine pain typically affects one side of the head, ment do so in 2 to 3 weeks. Side effects of the NSAIDsand may switch sides. The headache can become generalinclude fluid retention, nausea, diarrhea, dizziness, andized. Many patients report that their pain localizes around gastric and duodenal irritation. Renal function monitor-or behind the eye, or in the frontotemporal area. The pain ing must be done periodically to avoid renal injury in may radiate toward the occiput or upper neck during an patients who take NSAIDs regularly. Antidepressants,attack. The shoulder and lower portion of the neck may also in a single bedtime dose, may also be effective in reducbe involved. In some cases, the pain radiates to the face. ing the frequency of CTTH pain. Therapeutic response A number of associated symptoms can accompany the can take as long as 4 weeks. The regimen should begin pain of an acute attack. Nausea or vomiting, in addition with a low dose and gradually be titrated to the individ-to either photophobia or phonophobia, are required for the ual patient’s needs. Side effects vary depending on thediagnosis of migraine (HCCIHS, 1988). However, dizziagent and the patient, but they most frequently includeness, lightheadedness, blurred or double vision, anorexia, drowsiness, postural hypotension, weight gain, consti-constipation, diarrhea, chills, tremors, cold extremities, pation, and dry mouth. ataxia, and dysarthria may also be present. Some patients Nonpharmacological options for CTTH include may experience lethargy and fatigue for several days folmanipulation and soft tissue massage techniques to the lowing an attack. scalp, cervical, or thoracic areas, reduction of stress and A prodrome or aura often precedes migraine attacks. muscle tension, and biofeedback. Consider psychotheraAura symptoms are usually visual, typically start just peutic interventions for patients whose headaches are before the acute headache, and continue for less than 1 h. related to significant emotional confl ict or are treatment Prodromal symptoms include scotomata, teichopsia, forrefractory. Choices can range from supportive to longtification spectra, photopsia, paresthesias, visual and auditerm and may involve the family physician, psychiatrist,tory hallucinations, hemianopsia, and metamorphopsia or psychologist. (Diamond, 1997). Despite the absence of visual and other prodromal characteristics, migraine without aura sufferers have also described premonitions of impending migraine MIGRAINE attacks. These symptoms are usually vague and can occur An estimated 28 million Americans, about 18% of womenfrom 2 to 72 h before an attack. The list of painless and 6% of men, suffer from migraine (Stewart, Lipton, warnings includes hunger, anorexia, drowsiness, depresCelentano, & Reed, 2000). This chronic, neurologic dis-sion, irritability, tension, restlessness, talkativeness, order is characterized by periodically recurring attacks ofexcess energy, and euphoria. Table 18.4 lists the complete IHS criteria for migraine with aura and migraine without head pain that are accompanied by gastrointestinal, visual, and auditory disturbances (HCCIHS, 1988). Although theaura (HCCIHS, 1988). intensity and severity of attacks tend to vary throughout the migraine population, as well as within the samePRECIPITATING FACTORS migraineur over a series of episodes, estimates suggest Certain factors, known as “triggers, ” can play a precipithat pain and disability are mild in approximately 5 to tating role in the onset of migraine attacks. Migraine trig15% of attacks, moderate to severe in 60 to 70% of attacks, gers can be categorized as physiological, psychological, and incapacitating in 25 to 35% of attacks (Stewart,or external stimuli. Although they are highly individualSchecter, & Lipton, 1994). The disorder occurs most fre-ized, some of the most common migraine triggers appear quently among persons aged 25 to 55 (Stewart, Lipton, in Table 18.5. Celentano, & Reed, 1992), concentrating its burden on those who are typically in their most productive years.Physiological Migraine patients consistently report lower mental, physical, and social well-being than do unaffected controlsMigraine sufferers can be particularly sensitive to changes in eating and sleeping patterns. Fasting or miss(Terwindt, et al., 2000; Lipton, et al., 2000). According to the IHS, migraine isan “ idiopathic, ing a meal is a known headache trigger. All migraine patients should be encouraged to maintain a regular meal recurring headache disorder manifesting in attacks lasting 4–72 hours. Typical characteristics of headache areschedule. Over- or undersleeping can also precipitate a unilateral location, pulsating quality, moderate to severemigraine. Migraine attacks that occur on weekends, on

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TABLE 18.4 IHS Diagnostic Criteria for Migraine without Aura and Migraine with Aura

TABLE 18.5 Recognized Migraine Triggers

Migraine without Aura A. At least five attacks fulfilling B–D B. Attack lasts 4–72 h (untreated or unsuccessfully treated) C. Attack with at least two of the following characteristics: Unilateral location Pulsating quality Moderate or severe intensity (inhibits or prohibits daily activities) Aggravation by walking stairs or similar routine physical activity D. During attack at least one of the following: Nausea and/or vomiting Photophobia and phonophobia E. At least one of the following: History, physical, and neurological examinations not suggesting a secondary disorder History, physical, and/or neurological examinations suggesting such disorder, but ruled out by appropriate investigations Such disorder present, but migraine attacks not occurring for the first time in close temporal relation to the disorder

Fasting, missing a meal, Stress (external or Bright or flickering or other changes in unconsciously lights eating patterns created by patient) Over- or undersleeping Repressed hostility Loud noises Oral contraceptives in Depression Strong odors migraine patients Cyclical hormonal Fear Rapid changes in changes; hormone barometric replacement therapy in pressure; travel to postmenopausal areas with different women altitudes Food triggers including: Anger Airline flights Alcoholic drinks Coffee, tea, and cola Aged cheese Chocolate Cured meats Chinese food Smokedfish, nuts, and pickled or marinated foods Drugs Anxiety Allergens Atenolol Caffeine (and caffeine withdrawal) Danazol Diclofenac H2 receptor blockers Hydralazine Indomethacin Nifedipine Nitrofurantoin Nitroglycerin Oral contraceptives Reserpine

Migraine with Aura A. At least two attacks fulfilling B B. At least three of the following four characteristics: One or more fully reversible aura symptoms indicating focal cerebral cortical and/or brain stem dysfunction At least one aura symptom developing gradually over more than 4 min or, 2 or more symptoms occuring in succession No aura symptom lasting more than 60 min, if more than one aura symptom present, accepted duration is proportionally increased Headache following aura with a free interval of less than 60 min (may also begin before or simultaneously with the aura) C. At least one of the following: History, physical, and neurological examinations not suggesting a secondary disorder History, physical, and/or neurological examinations suggesting such disorder, but ruled out by appropriate investigations Such disorder present, but migraine attacks not occurring for the first time in close temporal relation to the disorder

Physiological

Psychological

External

mond, 1997). Many report a remission of migraine after the first trimester of pregnancy. Many female patients see a reduction in frequency or complete remission of their headaches after menopause (Honkasalo, Kaprio, Heikkilä, holidays, or during vacations have been linked to over-Sillanpää, & Koskenvuo, 1993). Oral contraceptives sleeping (Wilkinson, 1986). To avoidweekend” “ head- should be used judiciously in migraine patients, because these drugs have long been known to increase the freaches, patients should be instructed to go to bed only quency, severity, duration, and complications of migraine when they are tired and to arise at the same time each (Whitty, Hockaday, & Whitty, 1966). Also, hormone day. Lack of sleep and fatigue may also provoke an acute replacement therapy (HRT) should be avoided in postmigraine attack. A relationship between the menstrual cycle andmenopausal migraineurs, because these hormones can migraine attacks is well documented and partiallyexacerbate or restart migraine attacks. However, side accounts for the higher prevalence of migraine in women.effects have been reduced with the patch delivery system Among female migraineurs, 60 to 70% note a menstrualand lower doses of estrogen, as well as with progesterones. link to their migraine attacks, with severe attacks occur- The link between diet and migraine depends on the ring immediately before, during, or after their period (Dia- individual patient. The amines, including tyramine and

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phenylethylamine, nitrates, monosodium glutamateand nonpharmaceutical pain management approaches (MSG), and alcohol, have all been implicated as triggers.(prophylactic or abortive medications, manipulation and Tyramine is found in aged cheese, pickled foods, fresh-massage, cold compresses, or warm baths). Determining baked yeast breads, and marinated foods. Another amine, the relative value of these strategies for each patient phenylethylamine, is contained in chocolate. The nitrates, shapes the course of both acute and long-term therapy. which promote vasodilation, are found in cured meats. Behavioral changes and nonmedicinal treatments can Many food additives and Chinese foods contain MSG,be valuable, particularly in patients with frequent or severe which has been associated with headache. Alcohol has migraine attacks. Most treatment plans incorporate behavboth central and direct vasodilating properties, and, inioral modification in the form of avoiding foods, beversome patients, migraine attacks can be precipitated, espeages, or situations that trigger attacks; each patient is cially with wine. Other possible triggers for migraine unique in this regard. Similarly, the use of cold cominclude caffeine, nicotine, ergotamine, hypoglycemia,presses, warm baths, or massage for migraine should be allergy, ingestion of ice cream, and monoamine oxidase governed by the nature of the individual’ s disorder. inhibitors (MAOIs). Migraineurs who are sensitive to If medication is a part of the treatment plan, the selecdietary triggers should be instructed to avoid the sub-tion can be tailored to the migraine patient’ s needs. Before stances to which they are susceptible whenever possible. recommending or prescribing any medication for migraine, however, it is crucial to determine all remedies Psychological the patient may have already tried before consulting, because detailed information in this area may reveal Stress is probably the most readily identifi ed psychologimportant therapeutic limitations and opportunities. ical trigger of an acute migraine attack. However, many Familiarity with the wide range of options for migraine migraine patients remain headache free during a stressful pharmacotherapy can increase the likelihood of meeting period only to experience a severe headache when the an individual patient’ s needs. stress has resolved. Depression, fear, anger, anxiety, and repressed hostility may also be associated with migraine. Although avoiding stress is dif ficult, reducing stress is Standard Migraine Medications not, and instruction on coping methods may be benefi cial Pharmacological therapy is often the main component in for “ overloaded”patients. Other psychological triggers migraine therapy. There are three broad categories of pharmay require additional counseling, concomitant treat-macological treatment of migraine: prophylactic, abortive, ment, or both. and symptomatic. If migraine attacks occur four or more times per month, or if attacks are incapacitating, many clinicians consider prophylactic therapy. If a patient has three or fewer migraine attacks per month, abortive treatSome migraine patients describe a relationship between ment may be indicated. When acute pain does not respond their headaches and weather. Rapid changes in barometric to abortive measures, symptomatic therapy can be pressure as well as extreme variations in weather have been shown to provoke a migraine attack in certainemployed as a backup. External Stimuli

patients (Diamond, Nursal, Freitag, & Gallagher, 1989).Prophylactic Treatment During or subsequent to travel to an area with an altitude Prophylactic medications are used to prevent the onset of substantially different from the patient’ s norm (i.e., the migraine attacks and to reduce their frequency and severmountains for those who live at sea level and vice versa), ity. The decision about which class to use generally a patient may report an increase in headache frequency. depends on comorbidities and interactions with concomA diuretic, such as acetazolamide, used on the day of a itant medications. Beta-blockers, for example, could be flight may help to prevent these headaches. Other external migraine triggers include bright or flashing lights, loud used in patients with hypertension but are contraindicated noises, and strong odors (such as smoke, perfume, in or those with asthma (Rapoport & Adelman, 1998); a depressed patient taking a selective serotonin reuptake cleaningfluids). inhibitor (SSRI) should not take an MAOI for migraine because of dangerous interactions. Drugs currently TREATMENT approved for long-term use in migraine prophylaxis With a confirmed diagnosis of migraine, the clinician include propanolol, timolol, divalproex sodium, and methysergide (Diamond, 1997). and patient should begin to devise a treatment plan that Propanolol, an adrenergic blocker, one of the most accounts for the practical realities of the patient’ s lifestyle. Migraine treatment plans usually involve somefrequently used drugs in the prophylactic therapy of combination of behavioral change (avoiding triggers,migraine, must be given carefully in patients with coroincreasing exercise, and relaxation) and pharmaceutical nary heart disease and thyrotoxicosis. It may exacerbate

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coronary ischemia and can produce unstable angina or & Scott, 1999). Among migraine prevention medications, myocardial infarction (Diamond, 1997). Propanolol is a unique side effect of topiramate is that it may cause contraindicated in patients with asthma, chronic obstruc-some patients to lose weight during a course of therapy. tive lung disease, congestive heart failure, or arteriovenWith a positive efficacy and safety profile, topiramate tricular conduction disturbances. In some patients, adminappears to be a promising treatment option for patients istration may cause depression, nightmares, lethargy, with refractory migraine. fatigue, sexual dysfunction, and weight gain (Rapoport & Adelman, 1998). Patients being treated with insulin, oralAbortive Treatment hypoglycemia drugs, or MAOIs should not be treated withAbortive medications used in the treatment of migraine propanolol. Propanolol is administered from 60 to 240include the nonprescription agents, IB and APAP/ mg/day in a simple, long-acting dosage or in dividedASA/CAF, as well as a range of prescription-only medidoses. If propanolol is not tolerated, timolol, another beta-cation (including isometheptene mucate, ergotamine preparations, prescription-strength NSAIDs, dihydroergotablocker, can be used in doses of 5 to 30 mg/day. Other mine mesylate (DHE) and DHE nasal spray), and the 5beta-blockers, such as nadolol, atenolol, and metoprolol, HT1D receptor agonists (including sumatriptan, naratriphave been used with varying degrees of success. The alpha agonist, clonidine, may be useful fortan, rizatriptan, and zolmitriptan). Selected abortive agents are reviewed next. migraineurs who are sensitive to cheeses and other foods containing tyramine (Diamond, 1997). Side effects are APAP/ASA/CAF — Lipton, Stewart, Ryan, Saper, Silusually mild and include drowsiness, dry mouth, consti-berstein, and Sheftell (1998) published the results of three pation, and occasional disturbance of ejaculation. Mildstudies comparing the nonprescription combination of orthostatic hypertension and depression may also occur.APAP 250 mg, ASA 250 mg, and CAF 65 mg with placebo. Divalproex sodium is FDA approved for migraine A single two-tablet dose of this nonprescription compound prevention and is particularly indicated for migraineurswas highly effective in relieving both migraine pain and with epileptic seizures, bipolar disorder, and possiblyassociated symptoms. There were no serious side effects. head trauma (Rapoport & Adelman, 1998). An extended- Ergotamine preparations — The utility of these release formulation of divalproex, which produces lessmedications in arresting migraine attacks is due to their ability to counteract the dilation of some arteries and fluctuation in plasma concentrations than the standard arterioles, primarily the branches of the external carotid therapy, is also available. The recommended starting dose for the extended-release formulation is 500 mgartery. Nausea is a common side effect of ergotaminedaily and can be increased to 1000 mg daily. Divalproextreated patients. Once used, ergotamine should not be sodium should be avoided in any patient with a historyrepeated for 4 days to avoid the possibility of ergotamine of hepatitis or abnormal liver function; it is contraindi- rebound headache, a relatively prevalent side effect characterized by a self-sustaining cycle of daily or almost daily cated in pregnancy, because it is associated with neural tube defects. Divalproex sodium can be effectively com-migraine headaches coupled with the irresistible use of bined with tricyclic antidepressants in patients with ergotamine tartrate to alleviate them (Gallagher, 1983). Ergotamine and its derivatives should be avoided in eldchronic recurrent migraine. Closely related (and similar in some long-term effects)erly and, because of their ability to induce labor, in pregnant patients. Dihydroergotamine, which was developed to ergotamine and its derivatives, methysergide promotes serotonin inhibition and mild vasoconstriction. This agentas an improvement over ergotamine tartrate, has a better safety profile. It is available in parenteral and nasal foris usually prescribed in doses of 2 mg three times a day mulations. A 2-mg dose of the nasal spray formulation of (t.i.d.) and should not be used for more than 4 consecutive months, after which a minimum 1-month hiatus is requiredthis agent has a rapid onset of action, a low recurrence before resuming therapy. Approved by the FDA for rate, and completely resolves a migraine attack in up to migraine prophylaxis, the drug’ s sustained use is contrain- 70% of patients within 4 h (Gallagher, 1996). dicated because of the potential for cardiopulmonary and NSAIDs — In prescription doses, NSAIDs have been retroperitonealfibrosis (Diamond, 1997). During the treat- shown to be superior to placebo and equivalent to other reference drugs in the abortive treatment of migraine (Pradment period, the patient should be examined at regular intervals to detect the development of fibrotic conditions,alier, Clapin, & Dry, 1988). Two nonprescription formulations of IB have also been approved for the treatment of murmurs, or pulse deficits. Topiramate, a polysaccharide anticonvulsant with sev-acute migraine. Although fewer side effects are reported eral mechanisms of action, has also been assessed in with an NSAIDs than with ergotamine preparations, the gasopen label study of migraine. With an average daily dosetrointestinal, renal, and hepatic risks linked with NSAID of 325 mg/day in two divided doses, investigators noteduse are well documented (Rapoport & Adelman, 1998). an average decrease in attack frequency of 72% and an Isometheptene— This sympathomimetic with vasoaverage decrease in the severity of attacks of 55% (Kruzs constrictive effects is found in combination with acetami-

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nophen 325 mg, and dichloralphenazone 100 mg. The class (Buchan, 1998). This characteristic may be responcombination can be effective in migraine without aura. Itsible for the low rate of headache recurrence seen in frois taken orally, two capsules at onset and one each hour vatriptan-treated patients (Goldstein, Keywood, & Hutchthereafter, to a maximum of five capsules in 1 day. Sideinson, 1999). Eletriptan effectively relieves the symptoms effects include drowsiness and nausea, and it is contrainof an acute migraine attack at both the 40 and 80 mg doses. dicated in patients with hypertension and renal disease, as In clinical trials, therapeutic response to eletriptan is genwell as those taking MAOIs. erally superior to sumatriptan, and the rate of headache Selective serotonin reuptake inhibitors —Sumatrip- recurrence among eletriptan-treated subjects is low (19%) tan, an SSRI, is a mainstay in migraine therapy. A single(Pryse-Phillips, 1999). More investigations and additional subcutaneous dose of 6 mg relieves the majority ofclinical experience with the 5-HT 1B/1D class are needed to determine how the use of these medications can be optimigraine attacks successfully (Subcutaneous Sumatriptan Study Group, 1991); oral and nasal preparations are also mized across the wide range of migraine patients. available. However, because of sumatriptan’ s low oral bioavailability, significant headache recurrence (Goldstein,Symptomatic Treatment When first-line nonprescription and second-line prescrip1996), and contraindication in large subgroups of patients, tion abortive agents fail, symptomatic treatment is indinewer agents have been developed and introduced. cated. Symptomatic agents are sometimes referred to as The migraine drugs being marketed as “next generarescue medications. Transnasal butorphanol, a nasal preption” agents are similar to sumatriptan, 5-HT 1B/1D receptor agonists. As of this writing, there are six new compounds,aration, is one of the more useful drugs in patients with only three of which have been approved for marketing byinfrequent attacks. Pain relief has been demonstrated the FDA: naratriptan, rizatriptan, and zolmitriptan. Threewithin 15 min (Goldstein, Marek, & Winner, 1998), and others, almotriptan, eletriptan, and frovatriptan, should bethe nasal formulation is particularly convenient for patients who are suffering from severe nausea or vomiting. available in the near future. Reports of clinical experience with the approvedOther options for rescue therapy include injectable NSAIDs and butalbital combinations, opioids, and opioidmedications suggest that, although they are effective, response to them is highly individualized. For instance,like combinations. Because of their abuse potential and Freitag, Diamond, Diamond, Urban, & Pepper (2000),the possibility of rebound effects, precautions must be in a retrospective study of clinical experience with observed when using symptomatic medications. naratriptan, rizatriptan, and zolmitriptan, found that all Intractable Migraine the newer acute treatments for migraine were highly Episodic migraine may become incessant and refractory effective, but they observed no clear differences between the 5-HT medications that might distinguish one agentto standard care (Mathew, Reuveni, & Perez, 1987). For as the “best.” However, one trial comparing zolmitriptan many of these patients, drug dependence is a factor; for with sumatriptan found that zolmitriptan (2.5 mg) was others, disabling headaches continue, unabated, seemingly significantly more effective than sumatriptan (50 mg) in indefinitely. In such cases, clinicians should be aware of several approaches to the management of intractable terms of headache response at 2 and 4 h posttreatment (Gallagher, Dennish, Spierings, & Chitra, 2000). In othermigraine. DHE, administered in a protocol developed by work, investigators compared rizatriptan 10 mg with Raskin, can produce a headache-free state in 90% of zolmitriptan 2.5 mg and reported that patients treatedintractable migraine patients within 2 days (Raskin, 1986). with rizatriptan were 31% more likely to be pain free Metoclopramide is used adjunctively with DHE to supand 23% more likely to have pain relief sooner thanpress withdrawal symptoms (Ramaswamy & Bapna, patients who were treated with zolmitriptan (Diener, Pas-1987). Alternative treatments for intractable migraine include dexamethasone (4 mg intravenously) (Gallagher, cual, & Vega, 2000). 1986), ketorolac (30 to 60 mg intramuscularly or intraveIt has been suggested that naratriptan may have the nously), chlorpromazine (0.1 mg/kg intravenously every lowest rate of headache recurrence of the 5-HT oral agents 6 to 8 h) (Newman, 2000). (Ryan, 1998), but headache recurrence remains a problem for all the triptans. Up to one third of patients taking almotriptan (Pascual, et al., 2000), 40% of patients takingCLUSTER HEADACHE sumatriptan, 28% taking naratriptan, 40 to 47% taking rizatriptan, about 30% taking zolmitriptan have experi-Cluster headache is a devastatingly severe type of recurenced recurrence of their migraine symptoms within 24 hrent vascular headache. It also sometimes is referred to as s (Goldstein, Keywood, & Hutchinson, 1999). Preclinical histaminic cephalalgia, histaminic headache, Horton’ s headache, Horton’ s syndrome, or data indicate, however, that frovatriptan may have a pro-cephalalgia, Horton’ longed duration of action, and pharmacokinetic studiesmigrainous neuralgia. Its clinical constellation of sympshow that the elimination half-life is the longest in the toms with the characteristic patient behavioral tendencies

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etiology remains poorly understood. However, it has during attacks should make it easy to recognize and distinguish from migraine or TTH. Of the recurrent headachebeen proposed that vasomotor, hypothalamic, or neurohormonal disturbances may be involved (Moskowitz, syndromes, it is probably the most distressing and brutal 1984; Saper, 1983; Kudrow, 1983). to the afflicted. A cluster attack is characterized by severe unilateral Unlike migraine, diet does not seem to precipitate pain, often described as a burning, boring, or stabbing cluster, although an occasional patient reports that chocsensation in the area of the eye, temple, or forehead with olate can be a factor. The one exception, however, is the radiating to the jaw, ear, or neck. During attacks, sufferers consumption of alcohol during cluster periods. Most, but often pace or become extremely active, similar to patients not all, cluster patients are heavy smokers and drinkers. experiencing renal colic. Frequently associated with theDuring remission periods when patients are not on prepain are ipsilateral lacrimation, eye injection, rhinorrhea,ventive medications, alcohol appears to have no provokcongestion, facial droop, or sweating. The pain usuallying effect. builds quickly over several minutes and lasts approximately 30 to 90 min. TREATMENT Cluster headache attacks can occur numerous times The preferred approach to the treatment of cluster headdaily, sometimes at the same hour each day. Early morning awakening with headache 2 to 3 hours after retiring isache patients is prophylactic. The tremendous pain and common. In its typical form, episodic cluster, the head-relatively short but frequent attacks makes symptomatic treatment less practical and often ineffective. Appropriate aches cluster or group for periods of weeks to months and pharmacological prophylactic regimens can reduce the mysteriously disappear for months to years; thus the name “ cluster headache. ” In its chronic form, which affects frequency and severity of attacks in most patients. When approximately 10 to 15% of sufferers (Ekbom & Olivar- treating cluster patients, the benefits of therapy should be weighed against the hazards of taking medication. Patients ius, 1971), the headaches continue to occur indefinitely, should be monitored closely, because some of the mediaffording the patients few headache-free days. The IHS criteria for cluster headache are shown in Table 18.6cation prescribed in treatment can potentially cause problems. Ergotamine and DHE preparations, methysergide, (HCCIHS, 1988). The typical onset of cluster headache is in the thirdcalcium channel blockers, corticosteroids, and lithium are or fourth decade of life although cluster attacks havecommonly used. Other agents, such as cyproheptadine, indomethacin, chlorpromazine, antidepressants, and been reported from as early as 1 to 3 years to the late 60s (Lance, 1993). Unlike migraine, cluster is more prev-ergonovine have been used with limited success. alent in men; its gender ratio favors men by 5:1. The For cluster patients, ergotamine tartrate is administered orally in divided doses throughout the day and often limits the severity and frequency of cluster attacks. The TABLE 18.6 daily dose should be kept as low as possible (1 to 2 mg IHS Diagnostic Criteria for Cluster Headache daily), and additional ergotamine for breakthrough headaches should not be permitted. Individual tolerance and A. At least five attacks fulfilling B–D sensitivity varies greatly, and patients should be followed B. Severe unilateral orbital, supraorbital, and/or temporal pain closely for untoward reactions and complications. lasting 15 to 180 min untreated Methysergide, an ergotamine derivative, may also be C. Headache associated with at least one of the following signs that have to be present on the pain side: used to treat cluster headache patients. It is administered 1. Conjunctival injection orally in divided doses not to exceed 8 mg/day. On initi2. Lacrimation ation of therapy, some patients experience transient mental 3. Nasal congestion confusion, nausea, vomiting, muscle cramps or takes, and 4. Rhinorrhea insomnia. If the symptoms persist for more than 3 days 5. Forehead and facial sweating or the patient develops evidence of peripheral vasocon6. Miosis striction, claudication, or angina, the medication should 7. Ptosis be stopped. Methysergide is contraindicated in patients 8. Eyelid edema D. Frequency of attacks: from one every other day to eight per day who have peripheral vascular or cardiovascular disease, hypertension, active ulcer, cardiac vascular disease, and E. At least one of the following: hepatic or renal dysfunction; or who are pregnant. History, physical, and neurological examinations not suggesting a secondary disorder Corticosteroids, alone or in combination with methyHistory, physical, and/or neurological examinations suggesting sergide, are frequently effective for ficult dif patients. Their such disorder, but ruled out by appropriate investigations mechanism of action is not completely understood, but it Such disorder present, but cluster headache not occurring for is thought to involve suppression of hormonal mechathe first time in close temporal relation to the disorder nisms. This treatment is more suited for patients with

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episodic cluster headache, because its long-term use could ever, the complete abstinence from alcohol during cluster be hazardous. However, because of the extreme distress periods is imperative. Drinking alcohol, without question, and suffering of some chronic cluster patients, corticos-interfere with prophylactic therapy. Reducing cigarette teroids can provide temporary relief whereas other drugs smoking and caffeine consumption (Gallagher & Freitag, are being introduced. 1987a), as well as avoidance of daytime napping (Stensrud Prednisone or triamcinolone are commonly pre-& Sjaastad, 1980), may benefit some patients. The inhalation of oxygen during a cluster attack is a relatively safe scribed, although others are effective. The steroids are given in divided doses that must be titrated to the indi-and effective treatment. In the majority of sufferers, oxyvidual. The average daily starting dose is 60 mg of pred-gen aborts attacks within 12 min (Kudrow, 1981). Oxygen nisone or 16 mg of triamcinolone. The medication is thenis administered at a rate of 7 l/min by facial mask at the onset of attack continued for up to 15 min. The main tapered over 2 to 4 weeks with adherence to usual steroid precautions. Side effects includeuid fl retention, weight drawback to the use of oxygen is cumbersome equipment, which makes it difficult to transport for patients whose gain, gastrointestinal disturbances, lethargy, and Cushing’s syndrome. Contraindications are hypertension, dia-attacks are unpredictable. betes, peptic ulcer disease, infection, active immuniza- For patients who experienced longer headaches and those who are not suf ficiently controlled by preventive tion, or pregnancy. medication, abortive medication may be needed. This Calcium channel-blocking drugs have been helpful to is generally limited to ergotamine or analgesic/sedamany patients, especially those with the chronic form of tives. Ergotamine and its derivatives can be adminiscluster. It is believed that they alter smooth muscle tone tered early in a cluster attack, sublingually, intramusof cerebral arteries by interfering with calcium ion funccularly, or by inhalation. This may give relief to some, tion (Gallagher & Freitag, 1987a). Verapamil is generally whereas simply delaying the completion of the headwell tolerated and more frequently utilized. It has been ache in others. The usual ergotamine limitations must suggested as a first-line pharmacological treatment for the be observed, which limit the amount that can be taken prevention of cluster headache, although weeks of therapy may be required before control of the condition is estab-and the number of headaches that can be treated. Analgesics and sedatives are a limited help, but they aid lished (Saper, 2000, pp. 76–77). It is given in divided doses certain patients psychologically and reduce the anxiety with an average daily dosage of 360 mg/day. The most frequent side effects with verapamil are constipation andassociated with cluster attacks. Unmonitored use of fluid retention. Verapamil is contraindicated in hypoten-these medications should be avoided, because potential habituation or toxicity can develop. sion, cardiac conduction disease, and significant renal or hepatic disease. Other calcium channel blockers sometimes used are nifedipine (40 to 280 mg/day) and nimoMIXED HEADACHE SYNDROME dipine (30 to 60 mg/day). Lithium carbonate is reported to be affected in reduc-Most headache patients experience one or possibly two ing frequency and severity of attacks in the treatment ofdistinct headache types, with pain-free periods between patients suffering with chronic form of cluster headache.attacks. However, there is a group of patients who Its mechanism of action has been debated, but it may experience intermittent migraine attacks superimposed involve its effect on cyclic changes in serotonin and his-on a daily or near daily, less intense headache similar tamine (Gallagher & Freitag, 1987a) or electrical conduc-to that of the tension type. This pattern is characteristic tivity in the central nervous system (Diamond & Dalessio,of the mixed headache syndrome. The mixed headache 1980). It is administered orally in divided doses with asyndrome is one of the most ficult dif headache patients daily dosage of 600 to 1200 mg. Serum lithium levelto manage. monitoring is necessary to avoid toxicity. Effective theraThe typical mixed headache patient, in many cases, peutic ranges vary greatly, but generally should not exceed has a long history of evaluations and failed therapeutic 1.2 meq/l. Nonsteroidal anti-inflammatory drugs and thi-attempts. Their constant fear of the daily or near-daily azide derivatives should be used with caution; when used headaches worsening sometimes leads to self-treatment concomitantly, these agents raise the potential risks of and excessive medication use. The frequent use of any toxicity. Side effects include fatigue, tremor, sleep distur-immediate-relief medication for head pain can cause bance, diarrhea, decreased thyroid function, goiter, and rebound headache, which perpetuates the problem and fluid retention. Lithium is contraindicated in the presenceoften renders other treatments ineffective until all mediof significant renal or cardiovascular disease. cations are stopped. Psychogenic factors, such as chronic Abortive therapy for cluster patients is a limited effec- stress, anxiety, burnout, or depression, are often present and further contribute to the ongoing problem. tiveness because of the relatively brief headaches and the doctor relationship is critical in the time necessary for medication absorption. Few nonphar- The patient– management of mixed headache patients. Anitive, defi macological measures are helpful to cluster patients. How-

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Gallagher, R.M. (1986). Emergency treatment of intractable comprehensive treatment plan that addresses each elemigraine headache. Headache, 26,74–75. ment of the patient’ s problem must be developed and Gallagher, R.M. (1996). Acute treatment of migraine with dihysupervised by a single physician. The patient must be droergotamine nasal spray. Archives of Neurology, 53, educated as to the nature of his or her headaches and 1285–1291. how each aspect of treatment is expected to contribute Gallagher, R.M., Dennish, G., Spierings, E.L.H., & Chitra, R. to the control of the headaches. Once a plan is begun, (2000). A comparative trial of zolmitriptan and continuity of care with regular follow-up visits is vital. sumatriptan for the acute oral treatment of migraine. The treatment of the mixed headache syndrome usuHeadache, 40,119–128. ally requires prophylactic medications in addition to non-Gallagher, R.M., & Freitag, F. (1987a). Cluster headache: Diagpharmacological measures, such as diet, exercise, stress nosis and treatment. Journal of Osteopathic Medicine, reduction, biofeedback, social adjustments, and counsel1, 10–18. ing. Because these patients, in effect, experience coexistGallagher, R.M., & Freitag, F. (1987b). Muscle contraction heading tension-type and migraine headache, each individual ache: Diagnosis and treatment. Journal of Osteopathic Medicine, 1(6), 8–17. component requires its own appropriate therapy. The manGallai, V., Sarchielli, P., Trequattrini, A., Paciaroni, M., Usai, agement of tension-type and migraine headache has been F., & Palumbo, R. (1994). Neuropeptide Y in juvenile described earlier in this chapter. Patients who do not migraine and tension-type headache. Headache, 34, respond to outpatient therapy or who are unable to with35–40. draw from frequent analgesic or ergotamine use may ben1D receptor efit from hospitalization at dedicated in-patient, tertiaryGoldstein, J. (1996). Current developments in 5-HT agonists.Headache Quarterly, (Suppl. 7 2), 17–20. care facilities (Diamond, Freitag, & Maliszewski, 1986).

Goldstein, J., Keywood, C., & Hutchison, J. (1999, June 22–26). Low 24-hour recurrence during treatment with frovatriptan. Poster session presented at 9th Congress REFERENCES of the International Headache Society, Barcelona, Spain. Buchan, P. (1998). Pharmacokinetics of frovatriptan (VML Goldstein, J., Marek, J.G., & Winner, P. (1998). Comparison of 251/SB 209509) in male and female subjects. Funcbutorphanol nasal spray and Fiorinal with codeine in the tional Neurology, 13,BC3(abstr.), 177. treatment of migraine.Headache, 38,516–522. Diamond, S. (1997). Recommendations for primary care providHeadache Classification Committee of the International Headers: Diagnosis and treatment of migraine. Headache ache Society. (1988). Classification of the diagnostic Quarterly, 8(Suppl.), 6–14. criteria for headache disorders, cranial neuralgias, and Diamond, S., & Dalessio, D. (1980). Practicing physician’s facial pain.Cephalalgia, 8(Suppl. 7), 1–96. approach to headache (2nded.). Baltimore: Williams & Honkasalo, M L., Kaprio, J.A., Heikkilä, K., Sillanpää, M., & Wilkins. Koskenvuo, M. (1993). A population-based survey of Diamond, S., Freitag, F., & Maliszewski, M. (1986). In-patient headache and migraine in 22,809 adults. Headache, 33, treatment of headache: Long-term results. Headache, 403–412. 26, 189–197. Diamond, S., Nursal, A., Freitag, F.G., & Gallagher, R.M. Kruzs, J.C., & Scott, V. (1999). Topiramate in the treatment of chronic migraine and other headaches. Headache, 39,363. (1989). The effects of weather on migraine frequency. Kudrow, L. (1981). Response of cluster headache to oxygen Headache, 29,322. inhalation.Headache, 21,1–4. Diener, H.C., Pascual, J., & Vega, P. (2000). Comparison of Kudrow, L. (1983). Cluster headache. Neurologic Clinic, 1,370. rizatriptan 10 mg versus zolmitriptan 2.5 in migraine Lance, J.W. (1993). Cluster headache. In J.W. Lance (Ed.), (Poster).Headache Quarterly, 11, 51–52. Mechanisms and management of headache (5th ed., pp. Ekbom, K., & Olivarius, B. (1971). Chronic migrainous neural163–187). Oxford: Butterworth Heinemann. gia: Diagnosis and therapeutic agents. Headache, 11, Laska, E.M., Sunshine, A., Mueller, F., et al. (1984). Caffeine 97–101. as an analgesic adjuvant. Journal of the American MedFerrari, M.D. (1993). Biochemistry of tension-type headache. In ical Association, 251,1711–1718. J. Olesen & J. Schoenen (Eds.), Tension-type headache: Lavados, P.M., & Tenhamm, E. (1997). Epidemiology of Classification, mechanisms, and treatment (pp. migraine headache in Santiago, Chile: A prevalence 115–126). New York: Raven Press. study. Cephalalgia, 17,770–777. Freitag, F.G., Diamond, S., Diamond, M., Urban, G.J., & Pepper, Linet, M.S., & Stewart, W.F. (1987). The epidemiology of B.J. (2000). The new treatments in migraine: First year migraine headache. In J. N. Blau (Ed.), Migraine: Clinclinical experience.Headache Quarterly, 11, 33–36. ical and research aspects (pp. 451–477). Baltimore: The Friedman, A.P., Finley, K.H., & Graham, J.R. (1962). ClassifiJohns Hopkins University Press. cation of headache. Archives of Neurology, 6, 173–176. Gallagher, R.M. (1983). Ergotamine withdrawal causing Lipton, R.B., Hamelsky, S.W., Kolodner, K.B., et al. (2000). Migraine, quality of life, and depression: A populationrebound headache. Journal American Osteopathic Assobased case-control study. Neurology, 55,629–635. ciation, 82(9), 677.

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Lipton, R.B., Stewart, W.F., Ryan, R.E., Saper, J., Silberstein,Rolf, L.H., Wiele, G., & Brune, G.G. (1981). 5-Hydroxytryptamine in platelets of patients with muscle contracS., & Sheftell, F. (1998). Ef ficacy and safety of the tion headache.Headache, 21,10–11. nonprescription combination of acetaminophen, aspirin, and caffeine in alleviating headache pain of an acuteRyan, R.E. (1998).Newer modalities for migraine . Presentation migraine attack: Three double-blind, randomized, plato the Diamond Headache Clinic, Orlando, FL. cebo-controlled trials. Archives of Neurology, 55, Saper, J. (1983).Headache disorders: Current concepts and 210–217. treatment strategies . Boston: John Wright-PSG. Lyons, A.S., & Petrucelli, R.J. (1978). Medicine: An illustrated Saper, J. (2000, November 4). Cluster headache[Abstract]. history. New York: Harry N. Abrams. Scottsdale Headache Symposium, American Headache Mathew, N.T., Reuveni, U., & Perez, F. (1987). Transformed or Society, Scottsdale, AZ. evolutive migraine.Headache, 27,102–106. Schoenen, J. (1990). Tension-type headache: Pathophysiologic Migliardi, J.R., Armellino, J.J., Friedman, M., Gillings, D.B., & evidence for a disturbance of "limbic" pathways to the Beaver, W.T. (1994). Caffeine as an analgesic adjuvant brain stem [Abstract].Headache, 30,314–315. in tension headache. Clinical Pharmacology and Ther- Shukla, R., Shanker, K., Nag, D., Verma, M., & Bhargava, K.P. apeutics, 56,576–586. (1987). Serotonin in tension headache. Journal of NeuMoskowitz, M. (1984). The neurobiology of vascular head pain. rology, Neurosurgery, and Psychiatry, 50, 1682–1684. Annals of Neurology, 16, 157–168. Stensrud, P., & Sjaastad, O. (1980). Comparative trial of tenNakano, T., Shimomura, T., Takahashi, K., & Ikawa, S. (1993). ormin (atenolol) and inderal (propanolol) in migraine. Platelet substance P and 5-hydroxytryptamine in Headache, 20,204. migraine and tension-type headache. Headache, 33, Stevens, M.B. (1993). Tension-type headaches. American Family 528–532. Physician, 47,799–805. National Headache Foundation (2000, October). NHF headache Stewart, W.F., Lipton, R.B., Celentano, D.D., & Reed, M.L. facts. http://www.headaches.org/factsheet.html (1992). Prevalence of migraine in the United States: Newman, L.C. (2000, November 3). Inpatient treatment strateRelation to age, income, race, and other sociodemogies for intractable headache[Abstract]. Scottsdale graphic factors.Journal of the American Medical AssoHeadache Symposium, American Headache Society, ciation, 287,64–69. Scottsdale, AZ. Stewart, W.F., Lipton, R.B., Celentano, D.D., & Reed, M.L. Pascual, J., Falk, R.M., Piessens, F., Prusinski, A., Docekal, P., (2000, February).American Migraine Study .IIPaper Robert, M., Ferrer, P., Luria, X., Segarra, R., & Zayas, presented at the Diamond Headache Clinic Research and J.M. (2000). Consistent ficacy ef and tolerability of oral Education Foundation, Palm Springs, CA. almotriptan in the acute treatment of multiple migraine Stewart, W.F., Schecter, A., & Lipton, R.B. (1994). Migraine attacks: Results of a large, randomized, double-blind, heterogeneity: Disability, pain intensity, and attack freplacebo-controlled study. Cephalalgia, 20 (6), 588–596. quency and duration. Neurology, 44, S24–S29. Pradalier, A., Clapin, A., & Dry, J. (1988). Treatment review: Subcutaneous Sumatriptan Study Group. (1991). Treatment of Nonsteroidal anti-inflammatory drugs in treatment and migraine attacks with sumatriptan. New England Jourlong-term prevention of migraine attacks. Headache, 28, nal of Medicine, 325,316–321. 550–557. Pryse-Phillips, W. (1999, June 22–26). A randomised, placebo- Takeshima, T., Shimomura, T., & Takahashi, K. (1987). Platelet activation in muscle contraction headache and migraine. controlled study of eletriptan vs. sumatriptan for the Cephalalgia, 7,239–243. treatment of acute migraine attack . Poster session preTekle Haimanot, R., Seraw, B., Forsgren, L., Ekborn, K., & sented at 9th Congress of the International Headache Ekstedt, J. (1995). Migraine, chronic tension-type headSociety, Barcelona, Spain. ache, and cluster headache in an Ethiopian rural comRamaswamy, S., & Bapna, J. S. (1987). Antagonism of morphine munity. Cephalalgia, 15,482–488. tolerance and dependence by metoclopramide. Life SciTerwindt, G.M., Ferrari, M.D., Tijhuis, M., et al. (2000). The ences, 40,807–810. impact of migraine on quality of life in the general Rapoport, A., & Adelman, J. (1998). Cost of migraine managepopulation: The GEM study. Neurology, 55,624–629. ment: A pharmacologic overview. Americal Journal of Venzmer, G. (1972). Five thousand years of medicine . New York: Managed Care, (4), 4 531–545. Taplinger Publishing. Raskin, N.H. (1986). Repetitive intravenous dihydroergotamine as therapy for intractable migraine. Neurology, 36, Whitty, C.M.W., Hockaday, J.M, & Whitty, M.M. (1966). The effect of oral contraceptives on migraine. Lancet, 1,856. 995–997. Wilkinson, M. (1986). Clinical features of migraine. In P.J. Rasmussen, B.K., Jensen, R., Schroll, M., & Olesen, J. (1991). Vinken, G.W. Bruyn, H.L. Klawans, & F.C. Rose (Eds.), Epidemiology of headache in a general population — Headache(Vol. 48, Handbook of clinical neurology , pp. A prevalence study.Journal of Clinical Epidemiology, 117–133). New York: Elsevier. 44, 1147–1157.

19 Muscular Parafunction of the Masticatory System: Headache, Face, Jaw, and Sinus Pain (Temporomandibular Disorders) James P. Boyd, D.D.S. Some of the most difficult diagnoses to make are those temporalis muscles. Following the opening of the mouth that are without objective signs, that is, conditions that(to capture prey), the role of the temporalis is to forcibly present with subjective symptoms only. Some of the most attempt to elevate the mandible (close the mouth) common pain complaints: headache, face, jaw, and sinus through the objects that are engaged with the canine pain, usually present with no objective signs, and treat-teeth. Conversely, the herbivores have much less develment is based on the patient’s subjective report. The diagopedtemporalismuscles and canine teeth, instead having nosis of parafunction of the masticatory musculature fallsbetter well-developed masseters, which work together into this category (Figure 19.1). with flattened occlusal patterns of the teeth, to facilitate mastication. Before parafunction of any muscle can be addressed, one must become familiarized with the function of that muscle. As with all skeletal muscles, the form of the LATERAL PTERYGOID muscle dictates its function, and the function of the muscle follows its form. This chapter specifically addresses onlyIn 90° opposition to the orientation of the temporalis (i.e., two of the muscles of mastication: the temporalisand the the alignment is horizontal instead of vertical) is the lateral lateral pterygoid. pterygoid muscle. The name is derived from its origin, which is the lateral side of the pterygoid (winglike) plate of the sphenoid bone (which houses the maxillary TEMPORALIS sinuses). The insertion (of its inferior belly) is at the neck The temporalis origin covers the entire side of the skullof the condyle (the superior belly attaches to the articular and resides within the temporal fossa. With the anteriordisc, which rides on top of the condyle). During unilateral portion of the temporal fossa being deepest, the anterior contraction, the lateral pterygoid pulls the condyle in the portion of the temporalis is thickest, and therefore theanterior-medial direction of its fibers (form dictates funcstrongest portion of the muscle. With the insertion of thistion), with the overall effect of the mandible shifting latmuscle as the coronoid process of the mandible, the sole erally. For example, when the right lateral pterygoid confunction of the temporalis is to elevate the mandible.tracts, the mandible moves to the left, and vice versa. Anthropologically speaking, the temporalis functions When both lateral pterygoids contract simultaneously, the closely with the canine teeth. Carnivores who typicallymandible is advanced and the mouth opens as the condyles have prominent canine teeth also have well-developed ride down the articular eminence of the temporal bone.

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mistreatment, but in its misconception of the diagnosis and definition of bruxism. This lack of understanding of the true nature of bruxism has resulted in the current standard of care for chronic temporomandibular disorder (TMD): management of symptoms (McNeil, 1990; Okeson, 1989, p. 160). By using a traditional interocclusal splint, the practitioner has succumbed to the patient’ s intensity of occluding, which plays the largest etiologic role in his or her symptoms (regardless of the patient’ s occlusal scheme). Unfortunately, dentistry has stipulated that treatment with an interocclusal splint results in one of three scenarios: the patient may improve (the intensity of parafunction is disrupted and decreases), remain unchanged (intensity is unaffected), or get worse.(Clark & Solberg, 1987, p. 130; Dao, et al., 1994; Hansson, 1991) (muscle contraction activity intensifi es). Without a full understanding of the nature of bruxism ’s destructive forces, the practitioner cannot inform the patient of the outcome potential when using a traditional interocclusal nightguard/splint (Figure 19.2). One of the problems with treating muscular parafunction has been where to start. Due to the unpredictability FIGURE 19.1 Masticatory musculature. of the outcome of a traditional intraoral splint (which is intendedto reduce muscular parafunction, but may not), FUNCTION VS. PARAFUNCTION varying opinions of TMD treatment have developed within dentistry. Two basic philosophies have evolved: the In humans, these two pairs of muscles work together to bite and tear food, and to position the mandible whilepatient’s jaw orientation is inappropriate and therefore must be altered, or the patient’ s occlusal scheme is inapchewing. Once the jaws have come together and the teeth propriated and therefore must be altered. However, an have occluded, the particular arrangement of the teeth is individual with an ideal jaw relationship (the way the referred to as theocclusion, or occlusal scheme. It is condyle of the mandible seats into the temporal fossa) important to make the distinction between the occlu ding and/or ideal occlusal scheme may suffer from chronic of the teeth (a muscular act) and the scheme of sion occlu (the relationship of the teeth following their occluding). debilitating headaches and/or face and jaw pain (TMD), whereas another with a less-than-ideal jaw relationship During mastication, there is no purpose in having the teeth and/or “improper” occlusal scheme may be completely in occlusion (food is supposed to be in between the upper and lower teeth) for anything more than a fraction ofasymptomatic. (Okeson, 1989, p. 160). When it comes to second. In fact, the instant the teeth occlude with each other, an opening stroke is initiated. Other than chewing and swallowing,any muscular act that occludes the teeth (provided by the temporalis) is considered parafunctional . Symptoms and signs that may develop depend on the intensity, frequency, and duration of the parafunctional muscular contraction.

ETIOLOGY The field of dentistry has obviously been assigned to treat conditions of the masticatory system. Dentistry typicallyFIGURE 19.2 A flat and smooth surface reduces the efforts acknowledges that the activity synonymous with muscularof the lateral pterygoids (green arrows). Eliminating the resistance of occluding cusps reduces the strain on the origins of the parafunction isbruxism, which had traditionally been lateral pterygoid (the pterygoid plate of the sphenoid bone resultdefined as t“eeth grinding. ” However, although the current ing in a reduction of facial symptoms) and insertions (the neck standard treatment for bruxism (an intraoral splint “ nightor of the condyle resulting in a reduction of TMJ strain and sympguard”) may prevent against the signs of teeth grindingtoms). However, the same surface provides a more ficient ef resis(worn and loose teeth), it may not be entirely effective attance to the effort of the temporalis at clenching, therefore resolving thesymptoms . The problem lies not in dentistry’ s increasing the clenching intensity (red arrows).

Muscular Parafunction of the Masticatory System: Headache, Face, Jaw, and Sinus Pain (Temporomandibular Disorders) 209

TMD, etiologic research continues to show that, essentially, it does not matter what a person has or where it is (the occlusal scheme and jaw relationship) (Kahn, et al., 1999; McNamara, Seligman, & Okeson, 1995; RodriguesGarcia et al, 1998). What matters is what one does with what one has (the nature of the muscular activity—the occluding) (Israel, 1999; Ito, et al., 1986).

UNDERSTANDING BRUXISM To gain an upper hand on bruxism, a new understanding of the term, and therefore the condition itself, is necessary. Bruxism is not a condition of the teeth. Teeth do not cause an activity, they are merely being affected by an activity. (Okeson, 1989, p. 160). Dentistry is essentially the art and science of how healthy teeth occlude with each other. Therefore, dentistry has been refl exively treating a condition by FIGURE 19.3 As temporalis contraction increases to maxiaddressing the health of the teeth and their occlusal scheme. mum, lateral pterygoid ability to translate the condyle for poten(Wilkinson, 1991). However, signs and symptoms of brux-tial joint strain is eliminated. As temporalis contraction intensity ism do not result simply from the creation of an occlusalreduces, the opportunity for the lateral pterygoid to translate scheme; they result from the intensity of the occluding of the condyle increases, thereby increasing signs and symptoms the teeth. The resulting scheme of occlusion may modifyof TMD. A: In this example, minimal lateral pterygoid intensity and direct the forces generated during the occlusion, but it produces mild TMD, and minimal temporalis intensity produces mild headache. Traditional splint therapy has a good prognosis. may not alter the intensity of the occluding. B: Intense lateral pterygoid contractions resulting from signifBruxism is best described as a function of clenching . icant occlusal resistance, provided by moderate to severe temThe intensity of clenching dictates the severity of grinding. poralis intensity, allow for severe TMD. C: Intense temporalis There is no teeth grinding unless the jaws are first clenched clenching (nonexcursive) stabilizes the condyles, which pretogether to some degree. The jaws must be clenched sents with tension-type headache without typical signs or symptogether intensely enough to provide adequate resistance toms of TMD. to alternating lateral pterygoid activity, which then grinds the teeth in excursive movements. As the intensity of temporalis contraction (clenching) increases, resistance to or TMD signs or symptoms, may be clenching intensely lateral mandibular movement increases. The required in centric position. Only by recognizing bruxism as a increased efforts of the lateral pterygoids to translate the function of clenching can these patients be accurately condyles (pull them down the articular eminence of thediagnosed and treated (Figure 19.3). temporal bone) provide the strain on the temporomandib- In a study of chronic tension-type headache patients ular joints (TMJs), which is a major source of joint pathol- without signs or symptoms of TMD, clenching during ogy (Israel, 1999). sleep was shown to be, on average, 14 times more intense As the intensity of clenching approaches maximum,than in asymptomatic control subjects (Clark, 1997). the lateral pterygoids ability to move the mandible later-Clenching in centric and balanced position maintains a ally (i.e., translate the condyles) decreases or is prevented stabilized TMJ environment. However, the typical patient entirely. Ultimately, the most intense clenching would pre-with chronic TMD (headaches, face and jaw pain, tooth vent any movement of the jaw or grinding of the teeth.wear) forcibly grinds his or her teeth to an excursive Clenching in a centered position, with a balanced occlusal position, and thenclenches in that position (“grinding to scheme, would provide the most stable and protected envia clench”), placing severe and often damaging strain on ronment for the TMJs. With this observation, the the TMJs (Hannam, 1991). If both lateral pterygoids were appropriate defi nition of bruxism becomes apparent: to maintain an isometric contraction during a centric “Jaw-clenching, with or without forcible excursive move- clench, or even more significantly, with the jaw slightly ments.” The patient who presents with severely worn teeth,advanced, a strain is placed on the pterygoid plates of the obviously a result of vigorous grinding, may have nosphenoid bone (the origins of the lateral pterygoids), symptoms to report because he or she never exerts adethereby generating sinus symptoms (in the absence of quate clenching intensity to become symptomatic (butobjective disease). There exists a dynamic relationship enough to vigorously rub the teeth together). Anotherbetween the temporalis and lateral pterygoids, from which patient with no indication of occlusal wear, but who com-signs and/or symptoms may result. The intensity of the plains of severe headaches and neck pain and has no facial temporalis activity combined with the degree of lateral

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FIGURE 19.4 The relationship between occlusal scheme, joint strain, and muscle contraction intensity. A: Bilateral, posterior equal contact (red dots) allows for maximal clenching (and headache) without joint strain. A unilateral B: posterior contact (maintained by the same side temporalis) provides the opposite lateral pterygoid with resistance to its contraction in a medialthereby direction, straining the joint. Even with a well-adjusted splint, the contortion of the mandible in excursive movement can create this scenario. C: With anterior midline point contact, there is minimal temporalis contraction intensity. Resistance to lateral pterygoid contraction is minimal (therefore minimal contraction intensity) and in an anterior/superior direction, thereby seating the condyle into its optimal orientation.

pterygoid activity (if possible), dictates the presentationare contraindicated for therapeutic use because of the complications caused by excursive (protrusive, retrusive, latof headache, TMD, or tooth wear (Figure 19.4). eral) movements of the mandible. During an excursive movement of the mandible, deprogramming jigs can allow TREATING AND PREVENTING BRUXISM a mandibular canine to contact the device, resulting in Ultimately, to treat and prevent bruxism, clenching inten-ipsilateral near-maximal clenching (Stohler & Ash, 1986) sity must be suppressed. Unfortunately, the traditionaland joint strain. Protrusive movement of the mandible with interocclusal splint, while decreasing resistance to lateral the simple anterior point stop allows for occluding of the movement (thereby relieving lateral pterygoid contractionposterior teeth, again allowing for high-intensity clenchand TMJ strain), provides ideal (or in some cases,ing. All mandibular excursive positions, not just centric, enhanced)resistance to the temporalis, allowing clenchingmust be considered when attempting to suppress tempoto persist or intensify (Clark, Beemserboer, & Rugh, 1981).ralis clenching in a dynamic environment (Figure 19.5). The success or failure of the traditional interocclusal To accommodate for parafunctional, protrusive, and splint is a function of the intensity of clenching. If clench- retrusive movements, an anterior midline point stop can ing intensity persists or increases after using a splint, bruxbe extended anteriorly and distally, providing clenching ism/TMD treatmentbecomes bruxism/TMD management. suppression in all mandibular movements (a prefabricated, Therefore, to treat and prevent bruxism/TMD, clenchingretrofitted device is available commercially through NTIsuppression must be addressed. This is achieved by exploitTSS).* Used primarily during sleep, a modified anterior ing the nociceptive trigeminal inhibition (NTI), refl ex also midline point stop (AMPS) reduces voluntary clenching known as the jaw-opening refl ex (Okesan, 1989, p. 160; intensity to one third of maximum (Becker, et al., 1999). A modified AMPS design allows for the best “musculoskStohler & Ash, 1986), and by creating an occlusal scheme for the least ef ficient muscular contraction (i.e., least eletally stable” (CR) position of the condyles, while supintense). NTI is created by direct pressure stimulation ofpressing hyperactive musculature. In addition, by providthe mandibular incisor periodontal ligament (PDL), acti- ing for no unilateral canine or posterior contacts (as can vating a reflex loop, which suppresses the contractionhappen with a full-coverage splint when the mandible intensity of the temporalis (conversely, anesthetization ofcontorts during excursive movement [Clark & Solberg, the mandibular incisor PDL allows clenching intensity to 1987, p. 130]), the modified AMPS allows for the least Two misconceptions of a modifi ed AMPS are not increase) (Hannam, 1991). uncommon: posterior teeth may supraerupt, and mandibular Historically, an anterior deprogrammer (such as a Lucia jig) or an anterior point stop (Clark, Beemsterboer,* *NTI Tension Suppression System. FDA marketing allowance, July & Rugh, 1981) has been advocated to establish and record 1998: “For the prevention of chronic tension and temporal mandibular optimal condylar position (CR) and to suppress acute musjoint syndrome that is caused by chronic clenching of the posterior cular symptoms on a short-term basis. These are effective mandibular and maxillary teeth by the temporalis muscle. The device is ” NTI-TSS, Inc., Mishawaka, IN. for clenching suppression in a jaw-centered position, butcustom made for the individual.

Muscular Parafunction of the Masticatory System: Headache, Face, Jaw, and Sinus Pain (Temporomandibular Disorders) 211

as symptoms resolve. For example, as chronic tension of the lateral pterygoids resolves, the condyles may seat more posteriorly and superiorly (a tensed lateral pterygoid may have maintained the condyles in a position anterior and inferior to the optimum). Therefore, the mandible may rotate at the last molars, with the anterior mandible rotating inferiorly and posteriorly, possibly resulting in a degree of anterior open bite (depending on the original degree of incisal overlap). After any repositioning of the condyles, some degree of occlusal equilibration or restoration may be necessary. A modified AMPS requires less fabrication and adjustment time than the traditional methods of splint fabrication and delivery (which typically requires impressions, modFIGURE 19.5 Both the anterior deprogrammer (A) and a els, laboratory fees, and potential for several adjustment modified AMPS (B) allow for minimal muscular contraction appointments). The commercially available prefabricated intensity and optimal seating of the condyle. An excursivedevices require one simple chairside procedure where the movement (A1) allows an opposing canine to contact the deprodevice can be retrofitted and delivered (in most cases by grammer, thereby providing an opportunity for intense tempo-a supervised auxiliary) in a 20-min appointment and one ralis contraction on the same side as the translated condyle, follow-up appointment. Compared with the bulky and resulting in significant joint strain. The same excursive move- often irritating traditional splint and the unpredictable outment with a modified AMPS (B1) reduces the possibility of come, the relatively smaller size of a modified AMPS and canine contact, thereby allowing the modifi ed AMPS to be used securefit make for excellent patient compliance. The clintherapeutically. ical efficacy of a modified AMPS makes it a viable treatment alternative for the treatment and prevention of incisors may intrude. However, for a posterior tooth amountocclusal trauma, bruxism, and TMD. of potential joint strain in any excursive or protrusive movements, thereby allowing for optimal joint healing and remodeling (Schames, Boyd, Schames, & King, 2000). REFERENCES To supraerupt, it must go unopposed without any contact for at least 8 days (Kinoshita, et al., 1982). With aBecker, I., Tarantola, G., Zambrano, J., et al. (1999). Effect of modified AMPS in place, mastication is impossible a prefabricated anterior bite stop on electromyographic activity of masticatory muscles. Journal of Prosthetic because of the trauma experienced by the incisors opposDentistry, 82(1), 22–26. ing the device. Therefore, because an AMPS must be removedwhenever the patient eats, the daily masticatoryClark, G.T. (1997). Waking and sleeping temporalis EMG levels in tension-type headache patients. Journal of Orofacial stimulation of the molars prevents their supraeruption Pain, 11(4), 298–306. (Kinoshita, et al., 1982). Clark, G.T., Beemsterboer, P.L., & Rugh, J.D. (1981). Nocturnal As for incisor intrusion, there is no opportunity withmasseter muscle activity and the symptoms of masticatory out a constant apical force, which is required to intrude dysfunction.Journal of Oral Rehabilitation , 8(3), 279–286. teeth (clenching efforts last minutes, and are suppressed). Clark, G.T., & Solberg, V.V.K. (1987). Perspectives in temporoEven in the case of a clinician’ s oversight, where the mandibular disorders . Chicago: Quintessence. discluding element of the modified AMPS (which pro- Dao, T.T., Lavigne, G.J., Charbonneau, A., et al. (1994). The vides the point stop) is not perpendicular to the long axis efficacy of oral splints in the treatment of myofascial of the mandibular incisor, the patient reports a tenderness pain of the jaw muscles: A controlled clinical trial. Pain, 56(1), 85–94. to the tooth immediately after the first night of use. The patient resists wearing the device until the dentistHannam, A.G. (1991). Musculoskeletal biomechanics in the mandible. In C. McNeil (Ed.),Current controversies in addresses the problem, long before there is any orthodontemporomandibular disorders(pp. 72–80) Chicago: tic tipping movement. Quintessence. Although the modified AMPS device itself does not Hansson, T.L. (1991). Orthopedic appliances. In C. McNeil cause any orthodontic movement, it does allow for optimal (Ed.), Current controversies in temporomandibular dis(re)positioning of the condyle, thereby potentially changorders (pp. 159–161). Chicago: Quintessence. ing the occlusal scheme. By providing for the most mus-Israel, H. (1999). The relationship between parafunctional masculoskeletally stable condylar position, a change in ticatory activity and arthroscopically diagnosed temocclusal schemeis most noticeable in patients whose poromandibular joint pathology.Journal of Oral condyles seat more posteriorly and superiorly in the fossa Maxillofacial Surgery, 57(9), 1034–1039.

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Management of temporomandibular disorIto, T., Gibb, C.H., Marguelles-Bonnet, R., et al. (1986). LoadingOkeson, J.P. (1989). ders and occlusion(2nd ed.). St Louis: Mosby. on the temporomandibular joints with five occlusal conditions. Journal of Prosthetic Dentistry , 56(4), 478–484. Rodrigues-Garcia, R.C., Sakai, S., Rugh, J.D., et al. (1998). Effects of major Class II occlusal corrections on temKahn, J., Tallents, R.H., Katzberg, R.W., et al. (1999). Prevalence poromandibular signs and symptoms. Journal of Orofaof dental occlusal variables and intraarticular temporocial Pain, 12(3), 185–192. mandibular disorders: Molar relationship, lateral guidSchames, J., Boyd, J., Schames, M., & King, E. (2000). Theraance, and nonworking side contacts. Journal of peutic motion of the joint. Manuscript submitted for Prosthetic Dentistry , 82(4), 410–415. publication. Kinoshita, Y., Tonooka, K., Chiba, M., et al. (1982). The effect of hypofunction on the mechanical properties of the Stohler, C.S., & Ash, M.M. (1986). Excitatory response of jaw elevators associated with sudden discomfort during periodontium in the rat mandibular first molar. Archives chewing. Journal of Oral Rehabilitation , 13(3), of Oral Biology, 27(10), 881–885. 225–233. McNamara, J.A. Jr, Seligman, D.A., & Okeson, J.P. (1995). Occlusion, orthodontic treatment, and temporomandib-Wilkinson, T.M. (1991). The lack of correlation between occlusal factors and TMD. In C. McNeil (Ed.), Current ular disorders: A review. Journal of Orofacial Pain , 9(1), controversies in temporomandibular disorders (pp. 73–90. 90–93). Chicago: Quintessence. McNeil, C. (1990).Temporomandibular disorders: Guidelines for classification, assessment, and management . Chicago: Quintessence.

20 Complex Regional Pain Syndrome, Types I and II Nelson H. Hendler, M.D., M.S. CLINICAL SIGNS AND SYMPTOMS

Clinically, one can make the distinction between the two disorders on the basis of signs and symptoms.This Complex regional pain syndrome, type I (CRPS I) (for-is a more important set of criteria than results of labomerly known as reflex sympathetic dystrophy [RSD]) ratory tests or response to treatment, because test results and complex regional pain syndrome, type II (CRPSfor this disorder are highly variable, and the accuracy II) (formerly known as causalgia) are symptom com-of diagnosis of this disorder is low. If a disorder is plexes that evoke a great deal of confusion. Very often,misdiagnosed, then how can a physician rely on the physicians do not recognize that these are separate and response to treatment as a way of establishing a diagdistinct entities, and commonly assume that they arenosis? However, sometimes physicians establish a diagdisorders of the same etiology, as well as responsive to nosis based on a response to treatment. This circular the same treatment. Clinically, this has not proven acculogic predicts that all disorders respond equally well to rate. CRPS, type I is a group of symptoms and clinicala given treatment, and those who do not are the fault of signs that usually follows a minor injury to a limb. In the patient. This ego-protective trap is a convenient one contradistinction, CRPS, type II is usually associatedinto which an unsuspecting physician might easily fall. with peripheral nerve injury, classically from a bullet However, there is valuable information that can be wound or some other partial nerve damage. Throughout derived from a patient’s response to treatment, from both this chapter, for the sake of consistency, earlier refer-a retrospective and a prospective research position. ences that used the terms of reflex sympathetic dystroObviously, the variables in clinical research are legion, phy (RSD) are referenced or quoted as CRPS, type and I, include the variable responses patients have to a despite the original nomenclature. This same approach single pathological etiology; the similar manifestations is used for references using the term causalgia, which patients have to diseases of multiple etiologies; the variare changed for the sake of continuity, to CRPS, typeability of accurate diagnosis; the variability of the skill II. In a very fine review article, Payne (1986) clearly of the physician performing a procedure; and the varidefined the distinction between CRPS, type I andable response to a single, well-performed procedure. CRPS, type II, although at the time he called them RSDWithout much trouble, five variables have already been and causalgia, respectively. This has been furthermentioned, giving rise to a 5-factorial analysis, or 120 expanded by the International Association for the Studypossible combinations of factors. Therefore, in analyzof Pain in a supplement edited by Merskey (1986)ing the results of clinical research in humans, one has (Table 20.1). A further expansion of this comparison isto be very circumspect. This is certainly true for CRPS, offered by Baron, Blumberg, and Janig (1996) type I and CRPS, type II. (Table 20.1A).

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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TABLE 20.1 Comparison between CRPS Type I and Type II Definition Site Main features

Associated symptoms

Signs Laboratoryfindings

Usual course Relief

Social and physical disabilities Pathology

Essential features

Definition

Site System Main features

Complex Regional Pain Syndrome Type II (Causalgia) Burning pain, allodynia, and hyperpathia, usually in the hand or foot, after a partial injury to a nerve or one of its major branches In the region of the limb innervated by the damaged nerve, not around the entire limb Onset usually immediately after partial nerve injury or, may be delayed for months; CRPS, type II of the radial nerve very rare; the nerves most commonly involved are the median, the sciatic and tibial, and the ulnar; spontaneous pain; pain described as constant, burning, exacerbated by light touch, stress, temperature change or movement of involved limb, visual and auditory stimuli (e.g., a sudden sound or bright light, emotional disturbances) Atrophy of skin appendages, secondary atrophic changes in bones, joints and muscles Cool, reddish, clammy skin with excessive sweating; sensory and motor loss in structure innervated by damaged portion of nerve Cool, reddish, clammy, sweaty skin with atrophy of skin appendages and deep structures in painful area Galvanic skin responses and plethysmography revealing signs of sympathetic nervous system hyperactivity, roentgenograms possibly showing atrophy of bone If untreated, the majority of patients having symptoms that persist indefinitely; spontaneous remission occurring In early stages of CRPS, type II (first few months) sympathetic blockade plus vigorous physical therapy usually providing transient relief; repeated blocks usually leading to long-term relief; when a series of sympathetic blocks not providing long-term relief, sympathectomy indicated; long-term persistence of symptoms reducing the likelihood of successful therapy Disuse atrophy of involved limb; complete disruption of normal daily activities by severe pain; risk of suicide, drug abuse if untreated Partial injury to major peripheral nerve; actual cause of pain unknown; peripheral central and sympathetic mechanisms involved in an unexplained way Burning pain and cutaneous hypersensitivity with signs of sympathetic hyperactivity in portion of limb innervated by partially injured nerve Complex Regional Pain Syndrome Type I (Reflex Sympathetic Dystrophy) Continuous pain in a portion of an extremity after trauma that may include fracture but does not involve a major nerve, associated with sympathetic hyperactivity Usually the distal extremity adjacent to a traumatized area; all around the limb Peripheral nervous system; possibly the central nervous system The pain follows trauma (usually mild), not associated with significant nerve injury; the pain described as burning, continuous, exacerbated by movement, cutaneous stimulation, or stress; onset usually weeks after injury

Complex Regional Pain Syndrome, Types I and II

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TABLE 20.1 (CONTINUED) Comparison between CRPS Type I and Type II Associated symptoms

Initially there is vasodilatation with increasing temperature, hyperhidrosis, edema, and reduced sympathetic activity also occurring; atrophy of skin, vasoconstriction and appendages, cool, red, clammy skin variably present; disuse atrophy of deep structures possibly progressing to Sudeck’ s atrophy of bone; aggravated by use of body part, relieved by immobilization; sometimes follows a herniated intervertebral disc, spinal anesthesia, poliomyelitis, severe iliofemoral thrombosis or cardiac infarction; may appear as the shoulder–hand syndrome; later vasospastic symptoms becoming prominent with persistent coldness of the affected extremity, pallor or cyanosis, Raynaud’ s phenomenon, atrophy of the skin and nails, and loss of hair, atrophy of soft tissues and stiffness of joints; without therapy these symptoms possibly persisting; not necessary for one patient to exhibit all symptoms together; an additional limb or limbs possibly affected as well Variable; may be florid sympathetic hyperactivity In advanced cases, X-rays possibly showing atrophy of bone, and bone scan changes over time Persists indefinitely if untreated; small incidence of spontaneous remission Sympathetic block and physical therapy; sympathectomy if long-term results not achieved with repeated blocks; may respond in early phases to high doses of corticosteroids (e.g., Prednisone, 50 mg daily) Disuse atrophy of involved limb; suicide and drug abuse if untreated; sometimes spreads to countralateral limb Depression, inability to perform daily activities

Signs Laboratoryfindings Usual course Relief

Complications Social and physical disabilities

Pathology Essential features Differential diagnosis

CRPS I Unknown Burning pain in distal extremity usually after minor injury without nerve damage Unrecognized local pathology (fracture, strain, sprain)

CRPS II Partial nerve lesion Nerve damage Posttraumatic vasospasm, nerve entrapment syndromes radiculopathies, or thrombosis

TABLE 20.1A Criteria for Differential Diagnosis of Complex Regional Pain Syndromes (CRPS) Types I and II CRPS I Etiology Localization Spreading of symptoms Spontaneous pain Mechanical allodynia Autonomic symptoms Motor symptoms Sensory symptoms

Any kind of lesion Distal part of extremity, or entire limb; independent from site of lesion Obligatory Common, mostly deep and superficial orthostatic component Most of patients with spreading tendency Distally generalized with spreading tendency Distally generalized Distally generalized

Note: From Merskey, H. (Ed.). (1986). Pain, 3 Suppl., pp. 28–29. Reprinted with permission.

CRPS II Partial nerve lesion Any peripheral site of body; mostly confined to territory of affected nerve Rare Obligatory, predominately superficial, no orthostatic component Obligatory in nerve territory Related to nerve lesion Related to nerve lesion Related to nerve lesion

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COMPLEX REGIONAL PAIN SYNDROME TYPE I (CRPS I) (REFLEX SYMPATHETIC DYSTROPHY)

Pain Management: A Practical Guide for Clinicians, Sixth Edition

The second stage of CRPS, type I, which usually begins about 3 to 6 months after the injury, is called the dystrophic stage by Payne (1986). During this stage, the patient experiences a burning type of pain, which radiates Following the distinction drawn by Payne (1986), oneeither above or below the site of the injury, and increased considers CRPS, type I as the result of minor trauma;hypersensitivity or hyperalgesia (an exquisite sensitivity inflammation following surgery, infection, or lacerations to touch or temperature—in counterdistinction to alloresulting in some degree of swelling in the affected limb;dynia, a painful response to a normally nonpainful stiminfarctions; degenerative joint disease; frostbite; andulus—a most important distinction that is discussed later burns. One should add to this list the possibility of anyin the chapter). The patient has changes in the nails on compression, such as casting or swelling due to injury,occasion, as well as decreased hair growth. This seems to be a variable finding, and certainly is notsine a qua non that may cause prolonged pressure on peripheral nerves. of the diagnosis of CRPS, type I. Joints may become stiff, As an example of this, we have seen at least two or three with decreased range of motion, and possible thickening, cases per year of CRPS, type I brought about from arthroscopy. The probable etiology is not injury to the nerve fromassociated with some degree of muscle wasting. Edema may be present, as well as bullous skin lesions, that are the use of the arthroscope, but instead from using the tourniquet for a long period of time to create a bloodlessnot related to an autoimmune disease (Baron, et al., 1996). operating field. A differential diagnosis between nerve Osteoporosis may be noted, with proper testing (Payne, 1986). Movement disorders may begin at this stage, with entrapments and CRPS I is critical and based on the distribution of the pain, which follows nerve pathways for either dystonias, or contractures noted (Schwartzman & nerve entrapments, and is circumferencial for CRPS I. Kerrigan, 1990; Webster, Schwartzman, Jacoby, Knobler, According to Schwartzman and McKellan (1987), & Uitto, 1991). Symptoms may vary, and fluctuate from individual to individual. there seem to be three phases to CRPS, type I. Additionally, physicians should recognize that CRPS, type I is a The third stage described by Payne is the atropic stage, which usually occurs 6 months or longer after the injury. symptom complex that is a cluster of symptoms and signs, According to Payne, the patient experiences pain, and that patients do not present with all signs and sympdecreased skin temperature, trophic changes in the skin toms during the course of their disease. In fact, very often associated with a smooth glossy skin, stiff fixed joints they may have only one or two of the signs and symptoms associated with contractures, increased or decreased of the disorder. sweating in the affected extremity, and demineralization As described by Payne (1986) and by Schwartzman and McKellan (1987), the acute stage of CRPS, type I isof the bone associated with wasted muscles and reduced strength (Payne, 1986). Again, the progression to this characterized by spontaneous pain, usually aching or burnstage is highly variable, and may progress, in a rapidly ing, that follows the distribution of blood vessels or fulminating case, in less than 2 to 3 months. As always, peripheral nerves. The acute stage may manifest as in medicine, there are only guidelines, but no hard and “hyperpathia” (this is described as a painful syndrome of fast rules. (A summary of many of the clinical symptoms overreaction to a stimulus or after-sensation following a is shown later in Table 20.2.) stimulus) and may include hypesthesia or hyperesthesia (described as a decreased or an increased sensation to pain stimulation, respectively), or dysesthesia (described as an COMPLEX REGIONAL PAIN SYNDROME, unpleasant abnormal sensation). Associated with these TYPE II (CRPS, TYPE II)(CAUSALGIA) tactile sensations are usually a warm, dry, red skin, or cold, blue, sweaty skin, with some swelling; and, surpris-CRPS type II, is usually associated with peripheral ingly, increased hair and nail growth. A number of authorsnerve injury and severe pain. According to Payne have interjected the notion of allodynia, or a painful (1986), pain occurring in CRPS, type II follows an response to a normally nonpainful stimulus. (Chaplan,injury to a nerve trunk, usually a major proximal nerve Bach, Pogrel, Chung, & Yaksh, 1994; Kim & Chung, branch, and is described as a persistent burning pain, 1995; Lee, Kayer, Desmeules, & Guilbaud, 1994). Addi-but does not necessarily have to be burning in quality. tionally, the patient has dependent redness and reduced It is unrelated to associated damage from surrounding motion in the damaged extremity. This summarizes thetissue, and seems to be worsened by emotional or enviacute stage of this disorder, which may last several weeks, ronmental stimuli. Most importantly, the pain seems to and may begin immediately or several days after the onset persist more than 5 to 6 weeks, which seems to be the of the injury. However, it is possible for CRPS I to remainlength of time needed for surrounding tissue to recover in this stage, and never progress to stage II or stage III. from injury. Typically, the injury is due to damage by a This is a highly individualized response. bullet, a knife, sharpened rocks or parts propelled by a

Complex Regional Pain Syndrome, Types I and II

217

TABLE 20.2 Clinical Symptoms Associated with CRPS, Type II and CRPS, Type I Clinical Symptoms

Mechanism

Diagnostic Studies

Treatment

CRPS, Type II c a a. Unmyelinated C fibers a. Rarely have cold hyperalgesia a. Phenoxybenzamine DREZ (2/7) or heat hyperalgesia sympathectomy 12% to 97% e, (0/9)b; do have mechanical effectivea, clonazepam b f hypersensitivity; use a drop gabapentin of acetone and Von Frey hairs to test a Paroxysms of pain b. Nerve stretch and axon b. Clinical reports b. None disruptiona d Partial motor paralysis (70%) c. Peripheral nerve injury, c. EMG/nerve conduction c. No relief with sympathetic a,b proximal nerve trunk velocity studies blocksb; no success with betablockersd a Worse with stress d. Lots of theory, no proof d. Clinical reports d. Clonidine e. Clinical observation e. Sympathetic blocks Vasomotor changes, but rare e. Unknown d trophic change

a,b a. Burning pain

b. c.

d. e.

CRPS, Type I Hyperalgesia and Allodynia a. Mechanical-hypersensitivity to light touchc

b. Thermal-hypersensitivity

Dystrophy Phase n a. Osteoporosis

a. Ectopic alpha-adrenergic a. All patients have mechanical a. g; chemosensitivity hypersensitivity use Von Frey b sensitization of WDR neurons hairs to test i in the spinal cord; central k; nervous system mediated intact low-threshold mechanoreceptor with A-delta afferentsc b. No mechanism delineated b. Patients having either cold b. b,c,k either heat or cold hyperalgesia (3/4), and/or heat hyperalgesia (4/5); use a b drop of acetone to test

Sympathectomy possibly relieving itc sympathectomy not relieving itj ; low-dose l naltrexone possibly working m f nifedipine ? gabapentin?

6/6 receiving relief with sympathetic blocks or b, nifedipine? sympahtectomy

n,o,p b. Diffuse or patchy, bony r demineralization c. Molted skina,b,r

b. No mechanism delineated

n,o,p a & b. X-ray did not correlate a. & b. Maybe calcitonin well with clinical symptoms, r (abnormal but bone scan did flow images, 83% abnormal r (also true for static images) ); if clinical features c. and ae. clinically had CRPS, Type I, 22/23 had positive delay s image bone scan b. X-ray and bone sscan b. Calcitoninn,o,p,r

c. No mechanism delineated

t,u c. Themography

d. Hair lossb,n r e. Vasomotor instability

d. No mechanism delineated e. No mechanism delineated

f. Nail brittlenessa,n n,v,w g. Muscle spasm

f. No mechanism delineated g. No mechanism delineated

r d. Clinical observation e. History or longitudinal r observation n steroids r f. Clinical observation f. Sympathetic blocks, a g. EMG biofeedback used as g. Trigger point injections testu baclofenl

a. No mechanism delineated

c. Prednisone 60 to 80 mg, taperingr d. Steroidsn,r n steroids r e. Sympathetic blocks,

continued

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

TABLE 20.2 (CONTINUED) Clinical Symptoms Associated with CRPS, Type II and CRPS, Type I Clinical Symptoms a,n h. Contractures

n,w i. Contralateral involvement

j. Edemaa,n

Mechanism

Diagnostic Studies

n h. May be attributed to disuse, h. Longitudinal observation x may be central dystonia i. Cross-communication i. Effective countralateral between sympathetic chain in blockw w 80% of cadavers y j. No mechanism delineated j. History and clinical observation

u k. Lower skin temperature

t,u k. Not vasospasm, but maybe an k. Thermography afferent and efferent reflex arcbb

a,s and l. Joint stiffness r tenderness

l. No mechanism delineated

m. Pathological fractures

m. May be related to osteoporosis or patchy demineralization n. No mechanism delineated

u and n. Pins and needles a dysesthesias q,y,z,dd o. Skin lesions

p. Dystoniax,z myoclonusz

Treatment n h. Physical therapy sympathectomy i. Contralateral w sympathectomy

j. Nifedipine,m spironolactone, acetazolamide, epidural, aa spinal cord stimulation a,b,t,u k. Phentolamine, bb Bier block with reserpine n, guanethidine i.v. b,n sympathetic blocks p l. Maybe calcitonin

l. Proximal interphalangeal joint 12.9 mm greater (average) n affected hand; negative rheumatoid and connective tissue blood studiesr n,o maybe m. 72 hours after a break 95% of m. Maybe calcitonin, cc bone scans are positive Fosamax n. History

o. Disruption of basement o. Observation and electron membrane and destruction of microscopyy y colagenous anchoring fibrils, circulating immune q complexes p. Spinal cord mediated? p. Observation

u n. Sympathectomy

y, o. Prednisone not working y maybe tetracycline

p. Epidural bupivicaine, epidural baclofen, epidural clonidine, ee sympathetic blocks

a

d Ghostine, et al. (1984); e Bouckoms & Litman (1985);f Mellick and Mellick Payne (1986);b Raja, et al. (1996);c Ochoa, et al. (1985); g h i j (1995); Devor (1983); Allen & Morety (1982); Roberts (1986); Hoffert, et al. (1984);k Meyer, et al. (1985);l Gillman & Lichtigfeld (1985); m Prough, et al. (1985); n Schott (1986);o Gobelet, Waldburger, & Meier (1992); p Webster, Iozza, Schwartzman, Tahmoush, Knobler, & Jacoby r Kozin, et al. (1981);s Holder & MacKinnon (1984);t Uematsu, et al. (1981); u Hendler, et (1993); q Van der Laan, Veldman, & Goris, (1998); y Baron, et al. (1996); z Greipp & Thomas (1994); aa Peuschl, al. (1982);v Long (1982);w Kleinman (1954);x Schwartzman & Kerrigan (1990); bb cc dd ee et al. (1991); Janoff, et al. (1985); Matin (1979); Hamamcu, Dursun, Ural, & Cakci (1996);Webster, et al. (1991).

machine, or other such objects. When the injury is assoclearly illustrate the hydraulic effect in soft tissue ciated with a high-velocity missile, one must considercaused by a bullet. not only actual damage to the tissue itself, but also Typically, patients with CRPS, type II report an onset hydrostatic effects caused by shock waves. When one of pain within several hours to a week after the injury, takes into account the fact that the body is made up and describe the pain using words such as stinging, achlargely of water, it is easy to see how a high-velocitying, burning, or tingling. Superimposed on the regular missile can cause damage not only to the actual tissue pain, patients may experience paroxysms of deep pain (Payne, 1986). that has been penetrated by the missile but also to surrounding tissue as a result of hydrostatically transmitted Long (1982) clearly made the distinction between shock waves. If the reader desires additional informationCRPS, type II and CRPS, type I. CRPS, type II is concerning the hydrostatic effects of high-velocity mis- secondary to partial injury to major mixed nerves, siles, he or she is referred to a most amazing book titled caused by low- or high-velocity missiles; and manifests Split Seconds(Dalton, 1984). Photographs in the book as trophic changes in the distribution of the nerve

Complex Regional Pain Syndrome, Types I and II

219

associated with extreme hypersensitivity. The pain isUSING THE CLINICAL HISTORY AND diffuse and burning, and true CRPS, type II almostSENSORY EXAMINATION FOR always responds to sympathectomy. Long suggested DIFFERENTIAL DIAGNOSIS performing three or more sympathetic blocks, sometimes every day for up to a week or longer, with theA number of authors have advanced the notion that there expectation that longer relief should follow each subse-are other types of sensory mechanism, other than hyperquent block. With positive responses to sympatheticalgesia evident in CRPS I and II (Chaplan, et al., 1994; blocks, Long would suggest a sympathectomy; on theKim & Chung, 1995; Lee, et al., 1994; Lee & Yatsh, 1996). other hand, CRPS, type I usually follows a minor injury Unfortunately, the vast majority of the research reports and does not involve a major nerve root. Frequently, theare in animal models, using animals fairly low on the site of injury is the knee, ankles, or wrist; and the painphilogenetic scale. There is always a danger in extraposeems to get worse with cold but not with emotionallating from animal models to clinical work in humans, upset, unlike CRPS, type II. Demineralization of the because there are species-specific differences, and some bone occurs, with brosis fi of tendons and sheaths andof the sensory values assigned to a rat reveal more about spasm of the muscle. Dysesthesia suggests that there the creativity of the researcher than they do about the will be less success with sympathectomy. sensory experience of the rat. However, bearing these caveats in mind, clinicians should be aware of the research observations that may have signifi cant value for their SYMPATHETICALLY MAINTAINED PAIN patients. A sensation called allodynia has been described, a nonpainfulstimThis term has come into use in an effort to further definewhich is a painful response tonormally ulus. It is important to make a distinction between this diagnostic accuracy, which would then allow better selecsensation and hyperalgesia, which is a more intense tion of treatment methods, and have some predictive value response to a normally painful stimulus. This distinction in terms of outcome. Raja and Hendler (1990) report clinical features of sympathetically maintained pain to be (1)bears reemphasis, for this is the most commonly confused terminology in the hands of inexperienced clinicians. spontaneous pain, (2) hyperalgesia to both mechanical and to a cooling stimuli, (3) soft tissue swelling, (4) vasomotor Clinically, hyperalgesia, a more intense responsenormally painful stimulus, is seen in the early phases of nerve disturbances, (5) trophic skin changes, (6) diminished motor function, and (7) pain relief after sympathetic entrapments, and radiculopathies. In counterdistinction, allodynia, a painful response to normally a nonpainful blockade. By using these criteria, one can have sympathetically maintained pain that could have features ofstimulus, is seen in CRPS, types I and II. either CRPS, type I or CRPS, type II because either of Also, it is important to make a distinction between these conditions could have features of sympatheticallycold hyperalgesia, heat hyperalgesia, and mechanical hyperalgesia. Both cold and heat hyperalgesia are rarely maintained pain. Hendler (1982) originally described the use of oralseen in CRPS II (Meyer, Campbell, & Raja, 1985; Raja, et al., 1986). Moreover, it is important to make a distincphentolamine to treat CRPS, type I using the rationale that tion between cold allodynia, and mechanical allodynia. this drug was a postsynaptic alpha-1-blocker. Raja and his Cold thermal allodynia is most often seen in CRPS, types co-workers (1991) later described the use of intravenous I and II, whereas mechanical allodynia is seen commonly phentolamine as a diagnostic test to confirm whether or in CRPS, types I and II; nerve entrapment syndromes; and not the pain a patient had was sympathetic in origin, that is, “sympathetically maintained. ” There is evidence that radiculopathies (Hendler & Raja, 1994). This clinical disthe mechanism of sympathetically maintained pain istinction has led to the use of the Hendler alcohol drop and swipe test to make a distinction between CRPS, types I present not only in CRPS, type I but also in some cases and II, with cold allodynia (which has a painful response of CRPS, type II, however, because various authors have reported the benefit of sympathetic blocks in both disor-to an alcohol dropped on an affected limb [allodynia]); ders (Long, 1982; Ghostine, et al., 1984; Hannington-Kiff,and CRPS, types I and II, nerve entrapment syndromes, 1979). Perhaps the best conceptual framework to use and is radiculopathies, with mechanical allodynia, demonone that takes into account both neurophysiologically (i.e.,strated by lightly stroking the affected limb with the used swab (Hendler, 1995). Concisely stated, mechanical allothe presence or absence of major peripheral nerve injury documented by electromyography [EMG], nerve conduc-dynia is of less use diagnostically, because it may be tion velocities [NCV] studies, and the somatosensory-present in CRPS, types I and II, nerve entrapment syndromes, and radiculopathies; whereas thermal allodynia evoked potential [SSEP]) and response to pharmacological intervention (i.e., response to IV phentolamine testing,is a more useful clinical feature, usually being limited or sympathetic blocks). A physician might consider sixmostly to CRPS, type I and occasionally to CRPS II separate types of disorders, as shown in Table 20.3. (Meyer et al, 1985; Raja, et al., 1986).

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

TABLE 20.3 Diagnostic Considerations Response to IV

Positive Response to Phentolamine IV

EMG/nerve conduction velocity/somatosensory-evoked potential: all negative

CRPS, type I sympathetically maintained pain (SMP)

EMG/nerve conduction velocity/somatosensory-evoked potential: at least one positive Positive response to alcohol drop test Positive response nerve to a local nerve block (radial, ulnar, median, peroneal, saphenous, tibial) with 100% relief of all symptoms Positive response to sympathetic block or (a warm limb and 100% relief of all symptoms) Partial relief of pain with local nerve block

CRPS, type II

CRPS, type I, SMP

No Response to Phentolamine IV

Microvascular damage with Mixed injury swelling and mechanical hyperalgesia; sympathetically independent pain (SIP) Neuroma or nerve entrapment at Mixed injury site of injury; SIP Too low a dose phentolamine

Nerve entrapment syndrome with Nerve entrapment syndrome sympathetic component without any sympathetic component

CRPS, type I, SMP

Mixed injury

Partial Response to Phentolamine IV

Too low a dose phentolamine Nerve entrapment syndrome with sympathetic component

Too low a dose of phentolamine, Too low a dose of phentolamine; or too slow an infusion too slow an infusion Poor nerve block

Mixed injury

Additionally, a cool limb is not diagnostic of CRPS I a peripheral nerve, even if all the sensations for CRPS, and II, despite many reports in the literature to that effecttype I are present, then the clinical syndrome is really a (Hannngton-Kiff, 1979; Prough, et al., 1985). First andnerve entrapment, with the sympathetic sensory compoforemost, for a clinician to hold an affected limb in one nents of it coming from the sympathetic fibers traveling with the sensory nerve. CRPS, type I has a circumfrencial hand, and a normal limb in another, and pronounce that pain distribution (i.e., it is all around the limb, in the the temperatures are either equal or different is a demonstration of arrogance, more than clinical skills. The abilitypattern of the blood flow, not in a discrete nerve distribution or in a radicular distribution). Failure to recognize to detect temperature differences varies due to the ambient temperature of the clinical setting, and the “physiologicalthis distinction has lead to the misdiagnosis of a number of nerve entrapment syndromes, which get mistakenly zero” of the organism sensing the temperature change, which lowers the “threshold of detection for thermal sen-called CPRS, type I (Hendler & Kozikowsku, 1993; Hensation of the opposite quality” (Geldard, 1962, p. 137). Indler, Bergson, & Morrison, 1996). In an article in prepaan extensive report, by Uematsu, Hendler, Hungerford,ration, Hendler and colleagues will report that 70% of the patients sent to Mensana Clinic with the diagnosis of Ono, and Long (1981), reviewing 803 cases at Johns HopCRPS, type I actually have nerve entrapment syndromes. kins Hospital, the authors found that (as expected) patients with CRPS I and II had cold limbs most of the time, with ranges of 0.5° C to more than 3.0° C coldness being TREATMENTS reported for over 79% of the cases diagnosed with CRPS I. However, in 89% of the cases in which there were Appropriate treatments for CRPS, type I and type II abnormal EMG or nerve conduction velocity studies, thehave been described in Consensus Report, sponsored affected limb was also cold, although not to the sameby the International Association for the Study of Pain severity as the patients with CRPS I. These gures fi (IASP) (Stanton-Hicks, et al., 1998). In this report, the included cases of CRPS II, as well as patients with radicparticipants emphasized the need for functional restoulopathies, and nerve entrapment syndromes. ration, and psychological counseling, as well as mediThe anatomic distribution of the pain is another impor-cal intervention. Not only is there disuse as the result tant feature to consider. Sympathetic fibers travel with theof a painful limb, creating multiple disabilities and sensory nerves, so an injured sensory nerve may haveatrophy a but there is also evidence that once the disorder component of sympathetic damage reported, such as coldof CRPS, type I spreads, that there may be a centrally ness, or hyperalgesia. However, the actual location of the mediated muscle disorder, resembling dystonia pain is a critical factor. If the pain is in the distribution of (Schwartzman & Kerrigan, 1990). Therefore, the prob-

Complex Regional Pain Syndrome, Types I and II

221

lem of a painful limb in CRPS, type I and type II is Sympathetic blocks have always been the mainstay of compounded by a real motor disorder. diagnosis and treatment. The important feature of these ef of the block, before The psychological problems associated with bothblocks is to be certain of theficacy interpreting the result. The clinical criterion that best corCRPS, type I and type II have been well described for relates with an ef ficacious block is the report of total limb chronic pain patients in general. Hendler (1982, 1984) has warming. This tells the clinician that the sympathetic long reported that patients with both chronic pain and block did what it was supposed to do (i.e., blocked the depression really have become depressed as the result of sympathetic input to a limb, thereby producing warming their chronic pain. The earlier psychiatric “wisdom” of of the limb). At this point, the next question to ask the feeling that depression manifests as chronic pain has not patient is, “What do you feel?” If the patient has a warm been supported by more care observations (Hendler & limb, and 100% total absolute relief of all pain, then one Talo, 1989). Therefore, the use of group therapy seems to may consider that the block was (1) effective and (2) be the most ef ficient and productive way of providing appropriate for pain relief. From this, a clinician may support for patients with all types of chronic pain problems, and certainly is applicable to patients with CRPS,conclude that the pain is sympathetic in origin. If, howtype I and type II (Hendler, Vierstein, Shallenberger, & ever, the block did not warm the limb, then the clinician Long, 1981). Family counseling and patient education ismust conclude that the block was not effective; and no information of any value can be determined from this type also of great use, when available. of block, except that another block, at a later date, is The pharmacological management of CRPS, type I needed. If the block produces a warm limb, but only partial and type II is complicated (Hendler, 2000). The treatments relief of the symptoms, then the question is, “Where do shown in Table 20.2 are meant to deal with the specific you still have pain?” If the remaining pain is reported in symptoms associated with CRPS, type I and type II. Howa nerve distribution, then the patient has both CRPS, type ever, there is a role for a more generalized pharmacologI and a nerve entrapment syndrome, which coexist, or a ical approach, especially dealing with the issue of depresnerve entrapment syndrome, with a sympathetic composion and pain relief. Antidepressants, in and of themselves, nent. If the limb is warm, and the patient has no relief, provide relief of many of the symptoms by (1) reducing then the chances are the patient has a pure nerve entrapdepression, (2) reducing anxiety, and (3) promoting natument syndrome (see Table 20.3). ral sleep; and actually have some limited pain-relieving After a clinician determines a block is effective, then properties (Max, et al., 1991; Watson, et al., 1991; Watson, the patient should have a series of six to ten blocks. After et al., 1981). For symptomatic relief in CRPS, type I andthis series of blocks, several results are possible: (1) the type II, narcotics are problematic. A number of authorsCRPS, type I or II may go away, (2) the CRPS, type I or have reported reducedficacy, ef or variable effects, of nar- II may temporarily go away for weeks or months, only cotics in the palliative treatment of pain in patients withto return; or (3) the CRPS, type I or II may temporarily CRPS, type I and type II (Arner & Meyerson, 1988; Lee,go away for hours or days, after the blocks, only to return. Chaplan, & Yaksh, 1995; Portenoy, Foley, & Inturrisi, If scenario (1) occurs, the diagnostic blocks have also 1990). The variability and usual lack officacy ef of nar- provided the cure. If scenario (2) or (3) occurs, then the cotics for CRPS, type I and type II may be explained bypatient is a candidate for sympathectomy. This author recent elegant research, which shows only a kappa-2 opifavors the surgical sympathectomy, because direct visuoid agonist blocks the pain of hyperalgesia and allodynia,alization of the sympathetic chain, and pathology reports seen with peripheral neuritis and neuropathy, by inhibitingon the tissue are more reassuring than a blind ablation the activity of theN-methyl-D-aspartate (NMDA) receptor techniques. Moreover, the author has seen disastrous in the spine (Eliav, Herzberg, & Caudle, 1999). Althoughresults in patients, in which phenol was used for a neuthis research is in animals, with all the attendant problems roablative procedure. Despite the obvious bene fit of direct of translating to human use, this avenue seems to holdvisualization a for sympathectomy, there are still some phygreat deal of promise, because the formulation of a kappasicians, mostly anesthesiologists, who continue to use 2 opioid agonist is a feasible endeavor for major drugblind chemoablative techniques, with neurolytic agents, companies. However, as of the date of writing this mate-such as phenol, or radiofrequency lesions (Stanton-Hicks, rial, there is no practical kappa-2 agonist available foret al., 1998). human use; thus the use of narcotics in CRPS, type I and In extreme cases, the use of epidural stimulation has type II for allodynia and hyperalgesia is of limited use- been reported ficacious, ef although there are only a small fulness. Opioids may help pain caused by other symptoms number of cases in the literature ( Barolat, Schwartzman, of CRPS, type I and type II, such as muscle spasm and & Woo, 1989; Peuschl, Blumber, & Lucking, 1991; pathological fractures. A review of other pharmacologicalRobaina, Dominguez, & Diaz, 1989). The epidural infuapproaches for the management of pain can be found sion in of SNX-111 has been suggested as a possible treatseveral chapters by the author (Hendler, 1997, 2000). ment for CRPS, type I or II, as has the infusion of

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baclofen. SNX-111 is a conotoxin that works on specificwide dynamic range (WDR) or multireceptive neurons calcium channels to block the message of pain, whereas results in painful sensation and (2) that a nociceptor baclofen is a gabaminergic muscle relaxer. Epidural opioidresponse is associated with trauma which can produce infusion has been reported (Broseta, Roldan, & Gonzaleslong-term sensitization of the WDR neurons. ” FurtherDarder, 1982), but the absence of a kappa-2 agonist may more, his theory postulates that SMP is mediated by lowhave reduced the potential results (Eliav, et al., 1999).threshold, myelinated mechanoreceptors, and that these Clonidine actually seems more effective than morphine inimpulses, which carry messages to the brain, are the result humans, for deafferentation pain, after spinal cord injuryof sympathetic fibers carrying messages from the spine (Hassenbusch, Stanton-Hicks, & Covington, 1995). Otherand brain to act on the receptors, or to act on the fibers researchers have explained this difference, based on the carrying messages to the brain. The most important part independence of the opioid and noradrenergic pathways of this hypothesis is the fact that Roberts does not postuof the spinal cord (Glynn, Dawson, & Sanders, 1988).late the need for nerve injury or for dystrophic tissue. Opioid receptors exist in only a small group of neuronsBefore one can more fully appreciate Roberts’ theories, in the dorsal horn, and have various subsets, of which only however, one has to explore the basic anatomy of the the kappa-2 subset seems to be effective in reducing the sympathetic chains. allodynia of CRPS, type I (Eliav, et al., 1999). On the Bennett (1991) at the National Institute of Health has other hand, clonidine has multiple sites of action, such as advanced a brilliant theory that integrates clinical obserinhibiting pain transmission in the dorsal horn of the spinalvations with basic neurophysiology. Bennett synthesizes cord, and inhibiting norepinephrine release, due to itsthree theories that show that damaged nerves, when they alpha-2 partial agonist effect, which inhibits the releaseregenerate, have sprouts that are sensitive to norepinephof norepinephrine. rine; they will discharge on exposure to norepinephrine; there is enough norepinephrine produced by sympathetic fibers to trigger firing of damaged nerves; damaged nerves THEORY actually produce norepinephrine receptors at the damaged With the clinical descriptions from Table 20.3 in mind, end; and nociceptors (pain receptors) in intact nerves fire All “of these mechone can then make an effort to defi ne the various ana- more in response to norepinephrine. anisms may be operating in the case of patient nerve tomic, neuroanatomic, and physiological bases for these damage due to physical trauma, ” he says; and these “ two disorders. Ghostine and colleagues (1984) have suggested multiple etiologies for CRPS, type II. Various con-events are likely to sensitize surviving afferent terminals, perhaps to the point of inducing an ongoing discharge …”. siderations include ephapse, in which there seems to be an erosion of the insulation between nerve fibers, allow- Bennett further differentiates between the type of injury: constriction or entrapment vs. partial destruction of a ing for short-circuiting between somatic afferent fibers and sympathetic efferentbers; fi and experimentally pro- major peripheral nerve. The former injury (constriction) does not seem to respond to sympathetic blocks 1 to 2 duced neuromas, with resultant ephapses occurring both acutely and chronically between myelinated fibers. weeks after the injury, and this is attributed to the loss of noradrenergic vasomotor innervation, which takes several Because of the delay in developing the ephapses, which does not correspond to the clinical observations of aweeks to develop. The latter injury (partial nerve destrucrelatively rapid onset of CRPS, type I and type II, how-tion) becomes painful within hours of the injury, remains painful for months, and responds to sympathetic blocks ever, the theory of ephapses as the etiology of CRPS, type II has fallen from favor. To replace this theory, the concepteven months after the injury. Other researchers have expanded on a purely neuron-mediated mechanism, and of nerve sprouts or free nerve endings that are sparsely have suggested that autoimmune factors may be involved. myelinated seems feasible. Axonal sprouting has been noted to occur early after an injury, with a high frequencyThe Schwartzman group, at Thomas Jefferson University and without total axonal disruption. The possibility that School of Medicine, Philadelphia, found inflammatory skin lesions in the late stages of CRPS, type I, and attribute causalgia is produced by these sparsely myelinated fibers is supported by evidence that the blood– nerve barrier, these lesions to a deposition of immune complexes in the which is similar to the blood– brain barrier, has been skin. They believe the skin lesion supports the concept that cytokines and lymphokines such as interleukin-2 (ILdestroyed in the injured nerve. 2) are produced as the result of the activation of complePerhaps the most comprehensive review of the neuroment; this in turn is excited by the progression of events physiological basis of CRPS, type I and type II has been advanced by Roberts (1986). In his extensive review arti-beginning with local injury causing nerve growth factor cle, Roberts dealt with the neural mechanisms associated release, thus activating sympathetic neurons and causing with pain of CRPS, types II and I. He called these disor-recruitment of neutrophils and monocytes, which in turn ders SMP. His hypothesis concerning SMP is based on activate complement (Webster, et al, 1991). Interestingly, two assumptions: “(1) that a high rate of firing in spinalIL-2 has been found to selectively stimulate sympathetic

Complex Regional Pain Syndrome, Types I and II

223

neurons, whereas nerve growth factor (NGF) is produced remains elusive. Therefore, mechanisms other than in high concentrations after injury, which stimulates NMDA inhibition need to be explored. inflammation and in turn activates complement. Knobler To briefly summarize the material presented earlier, (1996) has expanded on this, and advanced the notion three of sensations are associated with CRPS, types I and II: aberrant immunologic mechanism, as a cause for CRPS, (1) pain, which is a sensation usually experienced when type I. He traces trauma, as the cause for the release tissue of damage occurs; (2) hyperalgesia, which is an NGF, which then stimulates inflammation and activatesincreased response to a normally painful stimulus; and (3) the complement components of the immune response, allodynia, which is a painful response to a normally non“promoting the expansion of antibody-producing B cellspainful stimulus. This can be hot, cold, mechanical, or of the immune system. ” He reports that substance P and even chemical. The message of pain is initiated at two the lymphokine IL-2 are released in response to NGF, withreceptor sites: (1) a nosioceptor, which is usually a free both of these factors acting on the sympathetic nerves to nerve ending, or unmyelinated C fiber, which detects tisactivate it. As research progresses, the various factors sue damage such as temperature or chemical changes; (2) described earlier need to be explored, with rigorous cona mechanoreceptor, which is sensitive to pressure, like a trols for (1) the type of lesion (crush vs. cut), (2) the stagePachinian corpusle. When tissue is damaged, it produces of the disease, correlating with anatomic and neurohu-a primary hyperalgesia, which is a sensitivity to pain, at moral changes over time, and (3) the attempt to correlate the site of the pain; and a secondary hyperalgesia, surthe clinical symptoms with response to various treatments.rounding the zone of primary hyperalgesia, in the absence In a discovery that led to her Nobel Prize, Rita Levi- of tissue damage. A sensitized nosioceptor has a lower Montalcini described the effect of NGF on sympatheticthreshold to pain, and produces hyperalgesia, whereas a nerve (Levi-Montalcini, Skaper, Toso, Petrelli, & Leon sensitized mechanoreceptor transmits a message of pain, 1996). In response to an injury or lack of innervation, theto a normally nonpainful stimulus (i.e., allodynia). Both end organ, sensory receptor, releases NGF, which chemohyperalgesia, and allodynia are the result of spinal dorsal taxically stimulates a nerve to grow toward the newlyhorn body sensitization. The afferent fibers carry the sendenervated receptor. This chemotaxic agent was found to sory message to the brain, and the efferent fibers modify be NGF. Clearly, sympathetic ganglion grow profusely inthe sensory input from the brain back to the periphery. response to the addition of NGF to their growth medium.They have their origins in the brain stem, medulla, and This is not limited to just sympathetic nerves. Skin andperiaquaductal gray; and are called descending afferent sensory nerves also have sprouted after injury (Inball,pathways. These pathways modify sensation. At the spinal Rousso, Ashur, Wall, & Devor, 1987). cord level, increased sensory input from the peripheral A study by Ro, Chen, Tang, & Jacobs (1999) showsnosioceptor actually changes cell functioning in the spinal that this process can be reversed, in rats, by the adminiscord, by altering chemical mediators, and receptor activity. tration of anti-nerve growth factor antibodies. PreviousThe persistent sensory stimuli activates NMDA at certain work shows that anti-NGF antibodies prevented collateralcells of the dorsal horn of the spinal cord, called WDR sprouting of dorsal root ganglion in rats (Mearow & Kril, neurons or NS. Phosphorylation of the NMDA receptor 1995). Ro and others (1999) studied the specific sensory is the result of constant sensory input, which then activates response to anti-NGF, which showed that, in a dosage and the NMDA receptor, and this creates central sensitization 2+ is removed, so Ca 2+ time-dependent fashion, heat and cold hyperalgesia can of the receptor ion channel. Mg be reduced, as well as collateral sprouting. enters the channel, which causes cell sensitization. This Finally, one of the most seminal concepts to emergespinal cord change produces allodynia in the peripheral from animals studies is the idea of plasticity of the centralnerves. Therefore, tissue damage produces damage to the nosioceptor in the periphery, causing sensitization, or nervous system (i.e., its ability to change in response to stimuli). Nowhere is this more important than for the hyperalgesia; and the result of this chronic increase in at the spinal cord level produces central sensitiunderstanding of CRPS, types I and II. In response to activity a chronically painful stimulus, the cells of the dorsal hornzation. Likewise, damage to the nerve causes growth horof the spinal cord actually alter their cytoarchitecture (themone to produce nerve sprouts; these are very sensitive, structure of the chemistry of the cell). Hyperalgesia andwhich cause continued input the spinal cord, producing allodynia are largely created by the enhancement ofcentral sensitization. This increased sensory input, which NMDA receptor activity in the spinal cord, and treated produces central sensitization, actually changes the cells by blocking the NMDA receptor (Ren & Dubner, 1993). in the dorsal horn of the spinal cord, which results in The central role of NMDA receptor activity in the cre- allodynia. The damaged nerve produces sprouts, as the ation of allodynia must be emphasized. Unfortunately,result of NGF stimulation. These sprouts have alpha-2 there is not a practical way to modify the NMDA receptoradreno-receptors on them, which are sensitive to norepiin man, so the treatment of hyperalgesia and allodynia nephrine circulating in the bloodstream.

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damage can occur to a nerve. Additionally, there are several sites where chemical intervention is possible, The most startling finding, and one that flies in the facenotably at the synapses that occur along the sympathetic of commonly held beliefs, is a report by Kleinman (1954)pathways. Additionally, the various bers fi that carry in which sympathetic chains were found to have commu-sympathetic messages are important. It has been widely nication between them, in up to 80% of cases. This is an held that C fibers, which are small unmyelinated bers fi importantfinding, because this anatomic consideration iscarrying sensory messages, are responsible for the transrarely, if ever, discussed in surgical textbooks or clinicalmission of pain. Some theories consider that SMP is papers. Thisfinding also explains why some cases of mediated by activity in A bers, fi however, because CCRPS, type I do not respond to sympathetic denervation, fiber blockade fails to eliminate pain in patients with and why, paradoxical as it may seem, some cases do SMP (Roberts, 1986). Therefore, one must start at the respond to countralateral blocks (i.e., if a patient has pain very beginning of the onset of pain (i.e., the receptor in the left leg, blocking the right lumbar sympathetic chainitself) to fully understand SMP and CRPS, types I and may produce relief). II. Originally, it was thought that nociceptor afferents Additional anatomy has been described by Allen and(nerves that carry the message of pain from the periphMorety (1982). When one traces the pathway of the sym-ery to the cord and the brain) were responsible for the pathetic nerves, cell bodies are located in the lateral colcontinuous pain of SMP and CRPS, type I and CRPS, umns of the cervical, thoracic, and lumbar spinal cord.type II (Bonica, 1970; Devo & Janig, 1981; Roberts, Cell bodies then give off axons, which form the pregan-1986). In Roberts’(1986) article, however, he adheres glionic fibers of the sympathetic nervous system. Fromto a theory first advanced by Loh and Nathan (1978) C7 to L2, these fibers are associated with the anterior that indicates low-threshold mechanoreceptors are spinal nerve roots, and leave the spinal cord in this pathresponsible for SMP. Roberts takes this position because way. They then separate from the nerve root and become nociceptor afferents, which are typically considered the white rami communicantes, which then continue onunmyelinated C fibers, do not have appropriate to the paravertebral ganglia, forming a chain running fromresponses to sympathetic activity; therefore, both practhe skull to the coccyx. From the ganglia themselves posttically and conceptually cannot be included as the recepganglionicfibers run back to nerve roots, or become sep-tors that mediate SMP. Roberts (1986) reported that arate nerves supplying various organs. mechanoreceptors do respond appropriately to both It is important to note that some ganglion cells aretouch and sympathetic activity, however. For CRPS, found in the anterior roots, as well as the white and graytype II, others have proposed a neuroma formation as rami. By the same token, some pre- and post-ganglionic the cause of pain. Roberts believes that the sympathetic fibers do not pass through sympathetic trunks, which again action of a neuroma is not capable of explaining why indicates that there is residual sympathetic innervation due treatments that occur distal to the injury (in the form of to either normal variants or aberrant fibers that bypass the either a nerve block or guanethidine infusion) are able sympathetic trunk. This anatomic finding explains the fail-to ameliorate CRPS, type II, however; even so, Roberts ure of some ganglionectomies, and suggests that one (1986) used the summation theory, or convergence themight need to do anterior nerve root sections and preganory, to say that both the peripheral receptors (in this glionic rami sectioning (Smithwick procedure) in patientscase, mechanoreceptors) that arise in the neuroma and in whom ganglionectomy has failed. those that arise in the skin itself are transmitting painful Cervical outflow, coming from the upper portion of the messages to the cord, and that distal blocks eliminate cervical chain, sendsbers fi to the pupils and the eyelids. only the mechanoreceptors from the skin, which is not Thesefibers radiate from the upper stellate ganglion, whichenough to trigger responses in the WDR neurons in the also supplies variousbers fi in the head and face. The upperspinal cord. Additionally, the concept of a neuroma thoracic sympathetic chain receives preganglionic inputcausing prolongation of CRPS, type II-type pain does from upper thoracic roots, and supplies the upper extremity not fit the clinical observation that SMP may occur even through postganglionicbers fi that pass through the brachial in cases in which the nerve is not injured. plexus. The lower extremities receive input from the T11 Ochoa, et al. (1985) advanced the theory that meto L3 nerve roots, forming ganglia; and from the lower twochanical A-delta nociceptor endings become sensitized to lumbar and upper sacral nerve roots, with gray rami (postmultiple sensory inputs. This gives rise to the thermal hypeganglionic) to the lumbosacral plexus. ralgesia that is seen in CRPS, type I. On the other hand, Ochoa believes that there are abnormalities in distal nociceptorfibers that seem to have a low threshold. These lowMICROANATOMY threshold mechanoreceptors reside within large myelinated As described earlier in the gross anatomy portion, there fibers, and are nonsympathetic dependent, because they are various sites along the sympathetic chain where transfer their information to nociceptor pathways proximal

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to the site of injury. These bers fi may account for the the C-fiber nociceptors carry the message to the dorsal mechanical hyperalgesia, manifesting as sensitivity to lightroot ganglion, and then back to the spinal cord neuron, touch. The previously mentioned receptors, which are the where they synapse. After synapsing with the neuron in source of the hyperalgesia seen in CRPS, type I, are difthe spinal cord, these multiple neurons transmit informaferent than the burning pain receptors seen in CRPS, type tion to the WDR neurons, which then send messages, via II. Ochoa and colleagues (1985) believe that the burning their axons, to the central nervous system or higher levels pain of CRPS, type II is mediated by unmyelinated Cof the spinal cord. With use of Roberts’ model, additional fibers, whereas Payne (1986) believes that this pain is due light touch activates the mechanoreceptors, which travel to nerve stretch and axon disruptions. Another considerin the A fibers instead of the C fibers. Because the WDR ation is the fact that such pain may be mediated by nerve neurons are already sensitized by the C fibers nociceptors, fascicles where all three types of C bers fi exit (Ochoa, et they respond to what is usually subthreshold stimuli to the al., 1985). Therefore, in summary, the current thinkingA fiber mechanoreceptors. These mechanoreceptors travel seems to suggest that sparsely myelinatedbers C fi carry in the A fiber, reaching a neuron within the spinal cord, the message of burning pain found in CRPS, type II,which again impinges on the WDR neuron; this, in turn, whereas sparsely myelinated afferent bers fi or the A-delta again sends messages up the spinal cord to the brain. nociceptors may be responsible for pain in CRPS, type I.Sympatheticfibers exist within the lateral portions of the thoracic cord, sending efferent messages to the sensory receptor. These efferent messages (i.e., messages traveling SYNAPSES from the cord to the periphery, mainly to the sensory receptors) may occur in the absence of cutaneous stimuBoth synaptic considerations and axonal considerations lation. According to Roberts’theory, however, the symhave been raised as possible factors controlling both CRPS, types I and II. Ephapses, or artifi cial synapses, pathetic efferent activity requires no cutaneous stimulation, and is the cause of the SMP. In response to this have been demonstrated in normal peripheral nerves. The concept of synaptic factors in CRPS, types I and II painefferent activity, the WDR neurons fire, again sending was first advanced by Granit, Leksell, & Skoglund messages to the spinal cord and brain. The key to Roberts’ (1944) when they found that stimulating the motor roottheory is the fact that the WDR neurons in the spinal cord remain sensitized, and they give a vigorous response to of a damaged mixed motor sensory nerve also produced recordable electrical events in the sensory root. Accord-mechanical stimulation of A-fiber mechanoreceptors even ing to the review by Payne (1986), the formation ofafter healing has occurred. In this schema, multiple synephapses after nerve injury may allow a short circuitingapses occur within the spinal cord, at the WDR neuron, or shunting of current from sympatheticbers fi coming and in the sympathetic ganglion. Therefore, synaptic regulation can occur at the spinal cord level or at the sympafrom the cord to the peripheral nerve into somatic bers fi arising at the site of injury, carrying the message of painthetic ganglion level. When reviewing the actual synapse, one must conceptualize a presynaptic area wherein various back to the cord. Unfortunately, these cross-connections betweenfibers coming from the cord to the periphery, chemicals are formulated, becoming neurosynaptic transand conversely coming from the periphery to the cord,mitters. The two synaptic transmitters that are of most interest to the study of CRPS, types I and II are the have been demonstrated in animal models, but not in indolamines, of which serotonin is an example; and the humans (Payne 1986). Another consideration is the possibility of an ectopic impulse resulting from alterations catecholamines, of which norepinephrine, epinephrine, dopa, and dopamine are examples. In the presynaptic area in calcium, sodium, and potassium channels (Payne, of the nerve, precursor substances are manufactured into 1986). In effect, the damaged nerve becomes epileptic, “ ” neurosynaptic transmitters, which confer a degree of specand the spontaneous discharges from the sensory nerve may give rise to the episodic pain noted in some indi-ificity on nerve transmission. L-Tryptophan becomes 5viduals. This could be dueto lowered threshold or hydroxytryptophan, which becomes 5-hydroxytryptamine (serotonin); dopa becomes dopamine, which can be conheightened mechanical sensitivity. Neurosynaptic mediation of CRPS, types II and I,verted to norepinephrine and epinephrine. holds great promise for the future. When reviewing the The specific type of the neurosynaptic transmitter whether it will occupy a specific postsynaptic synapses that are present within the sympathetic chain, determines it receptor site. Biogenic amines, such as the indolamines is apparent that these provide a potential site of mediation and catecholamines, are constantly being formulated and for sensory input. To understand synaptic mediation, one broken down by monoamine oxidase (MAO). Thus, chemmust review the anatomy of a synapse per se. By borrowing heavily from Roberts (1986), one can define the func-ically, the presynaptic area may be described as an area tional neuroanatomy, and delineate the location of various of high flux, with formulation and degradation of the same synapses. First, the trauma occurs, with receptors in the chemical occurring in the relatively steady state. As elecskin detecting various components of the trauma. Initially,trical impulses travel down the axon, pore diameter

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changes, altering the permeability of the membrane and DIAGNOSIS OF COMPLEX REGIONAL causing the release of neurosynaptic transmitters. These PAIN SYNDROME, TYPE II synaptic transmitters flow across a minute gap between With the foregoing theoretical information, the clinical nerves and occupy postsynaptic receptor sites. The gap, components of CRPS, types I and II should be more of course, is called the synapse. The postsynaptic receptor readily differentiated by appropriate diagnostic studies. sites determine the strength and duration of the electrical According to both Raja, et al. (1986) and Payne (1986), impulse that the synapse propagates. This is done by the degree of specificity that the neurosynaptic transmittersCRPS, type II manifests as a burning pain, which is not a consistent finding of CRPS, type I. Additionally, CRPS, have for a particular receptor site. It also depends on the affinity that a specific neurosynaptic transmitter has for atype II patients may experience paroxysms of pain, especially after stress, whether it be emotional or environmenparticular receptor site, and whether it is easily displaced or forms a tight bond. Almost all neurosynaptic transmit-tal. In an elegant study, Raja, et al. (1986) found that patients with CRPS, type II rarely have cold hyperalgesia ters have their activity ended by presynaptic reuptake; that (two of nine), and they do not have heat hyperalgesia is, the chemical that occupies the postsynaptic receptor (none of nine). Additionally, these patients obtain no relief site is then taken back into the presynaptic area. Acetylfrom sympathetic blocks. Raja, et al. (1986) differentiated choline is an exception, being degraded on the postsynaptic receptor site by acetylcholinesterase. Additionally,various types of hyperalgesia using sensory testing with some small amount of degradation of biogenic amineseither Von Frey hairs for touch, a drop of acetone for cold, occurs in the synapse itself by catechol-O-methyltrans-or laser thermal stimulation for heat. Ochoa, et al. (1985) ferase (COMT). It is thought that less than 5% of thebelieve that CRPS, type II is not always sympathetically chemical degradation of synaptic transmitters occurs inmediated, and instead is mediated by unmyelinated C fibers. Stretch injuries to the nerve or axon disruption of the synapse by COMT, and 95% of the degradation occurs presynaptically, by MAO. Of course, there is constanta major nerve branch is one explanation favored by Payne rebuilding of the neurosynaptic transmitter presynapti-(1986). Usually, the CRPS, type II patient has a history of a nerve injury to a peripheral nerve, or surgery, that has cally, creating the steady state mentioned earlier. Obviously, there are multiple ways to modify the syn- damaged the proximal portion of the nerve trunk (Payne, apse. One can inhibit MAO, thereby enhancing the buildup1986; Raja, et al., 1986). The CRPS, type II may be related to damage of nerve fascicles where all three types of C of a monoamine neurosynaptic transmitter, such as the fibers exist (Ochoa, et al., 1985). indolamines or the catecholamines. In fact, a class of drugs called MAO inhibitors do exactly that. By the same token, certain drugs can function as MAO exciters, which facil-TREATMENT OF COMPLEX REGIONAL itate the degradation of biogenic amine neurosynapticPAIN SYNDROME, TYPE II transmitters, such as the indolamines (serotonin) and the catecholamines (epinephrine, norepinephrine, dopamine, Various authors have reported that sympathetic blocks are and dopa). Because the majority of the neurosynaptic or are not effective, with ficacy ef for sympathectomy being transmitters have their activity ended by presynapticreported to be between 12 and 97% (Payne, 1986). No reuptake, one can enhance the synaptic transmission by relief with sympathetic blocks was reported by Raja, et al. blocking presynaptic reuptake. This is how tricyclic anti- (1986; 1991). Payne has suggested that a dorsal root entry depressants work. Conversely, one can diminish synaptic zone (DREZ) procedure may prove effective. Ghostine, et transmission by facilitation of presynaptic reuptake.al. (1984) have suggested the use of phenoxybenzamine. Finally, one can work at the receptor end by using drugs They reported 40 consecutive cases of CRPS, type II, all that mimic the action of the presynaptic transmitters andof which involved nerve injuries from bullet or shrapnel occupy receptor sites, thereby triggering them as if thewounds. The Ghostine group noted partial motor paralysis actual chemical had been released. By the same token, in the distribution of the damaged nerve in 70% of the other drugs can be used that occupy the receptor sites but cases. Over time these defi cits resolved in many of the have no pharmacological activity other than to inhibit thecases, however. They also noted vasomotor changes, usupresynaptic transmitter from occupying the receptor site.ally severe vasodilatation and sweating and less often vasFor example, curate effects a total blockade of the acetyloconstriction (Dalton, 1984). Rarely were trophic changes choline receptor. In this sense, these drugs become inhibnoted. The majority of the cases involved the sciatic nerve, itors of neurosynaptic transmission. Receptor sites are median nerve, brachial Plexus, cauda equina, and occipital found not only postsynaptically but also presynaptically,nerve, in descending order. The treatment that Ghostine, et very often for the same presynaptic neurosynaptic transal. (1984) used was phenoxybenzamine, which is a mitter. As the number and sensitivity of these receptorspostsynaptic alpha-1-blocker and a presynaptic alpha-2blocker. As mentioned earlier under the etiology of CRPS, change, so does the response to the neurosynaptic transtype II, nerve sprouts, which are one of the theoretical mitter itself.

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origins of this disorder, seem to be highly excitable on thebe present to establish the diagnosis of CRPS, type I. Kozin, et al. (1981) have established the criteria for CRPS, administration of norepinephrine; these can be reversed with alpha-blocking agents such as phentolamine buttype I as a patient presenting with pain and tenderness in an extremity associated with vasomotor instability (parwhich are unaffected by beta-blocking agents. The dosage of the drug used by Ghostine, et al. initially was 10 mgticular temperature or color changes) and generalized three times a day, although this varied from patient toswelling in the same extremity. The second group of patients they consider are those with pain and tenderness patient. Eventually maximum dosages of 40 to 120 mg/day associated with a vasomotor instability or swelling in an were reached, with treatment lasting 6 to 8 weeks. Comextremity; they call this group “probable CRPS, type ” I. mon side effects were orthostatic hypotension in about 45% of the patients and reduced ejaculatory ability in about 8%This system lacks precision, however, because it does not take into account the particular type of pain that patients of the patients. In some instances, treatment lasted as long with CRPS, type I experience. as 16 weeks. It is important to note that the patients were all treated within 2 to 70 days after the onset of their injury, Raja, et al. (1986) define patients as having CRPS, however. type I if they have pain associated with signs of sympaFor this treatment to be effective, it is most importantthetic hyperactivity (i.e., lower skin temperature, skin disthat rapid diagnosis and institution of treatment occur.coloration, increased sweating, and some trophic changes) Another possibility for the pharmacological treatment ofand symptomatic relief after sympathetic blocks; they found that those with CRPS, type I also had thermal hypeCRPS, type II would be the use of clonazepam, which has been reported by Bouckoms and Litman (1985) to beralgesia either to cold or to heat. In contrast, their patients with CRPS, type II did not experience thermal hyperalgeeffective for “burning” pains. Surgical sympathectomy has been recommended assia a to heat, and only two out of seven experienced hyperalgesia to cold. Both the CRPS, type II and CRPS, type treatment for CRPS, type II, after repetitive sympathetic I patients experienced hyperalgesia to mechanical stimublocks. Additionally, guanethidine, which is a ganglionic lation (Raja, et al., 1986). On the other hand, Ochoa, et blocking agent, has proved effective in treating some al. (1985) found mechanical hyperalgesia, which they forms of CRPS, type II. Guanethidine must be used with called allodynia, in their patients with CRPS, type I. Addicaution, however, because it causes the release of tionally, hypersensitivity to temperature was also found in norepinephrine prior to occupying the receptor sites itself; patients with CRPS, type I, whether it be to heat or to and the time course of the cessation of activity is variable. cold (Meyer, Campbell, & Raja, 1985; Ochoa, 1985; Raja, The fact that one may occlude an affected limb below the et al., 1986). site of the CRPS, type II and still achieve effective blocks with guanethidine suggests that its activity is not at the One proposed mechanism for mechanical hypersensiganglion but instead on the peripheral sensory nerves, tivity is ectopic alpha-adrenergic chemosensitivity (Devor, which produces its effect on CRPS, type II (Hannington-1983). Another consideration is a secondary abnormality Kiff, 1979). Surgical intervention, in the form of surgical in distal nociceptor fibers that escaped injury, or intact sympathectomy, has been used to treat CRPS, type II with low-threshold mechanoreceptors with large myelinated variable cure rates, ranging from 12 to 97%. The variabil-fibers that are not sympathetic dependent because of transity may be ascribed to lack of precision and diagnosis,fer of information to nociceptor pathways proximal to the with an overlap of CRPS, type I with CRPS, type II, or site of injury (Ochoa, 1985). Additionally, Ochoa, et al. CRPS, type I mistakenly diagnosed as CRPS, type II;(1985) advanced the concept of alpha-receptor sensitizavarying skills in performing blocks; collateral reinnerva- tion, whereas others believe that the hypersensitivity of tion of postganglionic sympathetic fibers; and delay inthe mechanoreceptors could possibly be a central nervous performing a sympathectomy (Payne, 1986). For CRPS, system event (Meyer, Campbell, & Raja, 1985). type II that is notresponding to sympathectomy, the possibility of a contralateral sympathectomy has been raised TREATMENT OF COMPLEX REGIONAL (Kleinman, 1954).

PAIN SYNDROME, TYPE I

Treatments for the mechanical hypersensitivity or hyperalgesia of CRPS, type I have been advanced by several authors, without clear-cut definition. One group of authors The clinical diagnosis of CRPS, type I is more compli-believes that sympathectomy may relieve mechanical hyperalgesia, whereas another group of authors reports cated than that of CRPS, type II. Some authors believe that sympathectomy does not (Meyer, Campbell, & Raja, that there is a very definite set of criteria to establish the 1985; Hoffert, et al., 1984). Another group has advanced diagnosis, whereas other authors think that only several symptoms from a whole list of symptom complexes needthe notion that nifedipine, a calcium channel-blocking

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agent, may prove effective (Prough, et al., 1985). Finally,motor instability. They also used three other control a group from South Africa suggested that low-dose nalox-groups, including patients with diffuse pain, focal pain, or one, and possibly longer acting naltrexone, may provevascular disease. Holder and MacKinnon (1984) found that 22 of the 23 patients who met their criteria for diageffective for reducing mechanical hyperalgesia, because nosing CRPS, type I had positive delayed image bone of the existence of a hypergesic kappa system of opiate receptors (Gillman and Lichtigfeld, 1985). Again, the areascans, 12 of the 23 patients had positive blood pool images, and 10 of the 23 patients had positive radionucleof mechanical hyperalgesia is quite muddy, because all the patients with either CRPS, type II or CRPS, type I hadotide angiograms. Approximately half the patients with CRPS, type I had positive early phase bone scans, whereas mechanical hypersensitivity (Raja, et al., 1986). Thermal hypersensitivity to either heat or cold (hype-almost all patients with CRPS, type I had positive delayed image bone scans. ralgesia) has been reported by several groups (Meyer, Campbell, & Raja, 1985; Ochoa, et al., 1985; Raja, et al., This study compared favorably with work done by Kozin, et al. (1981), who found that radiography is not a 1986). The mechanism behind the thermal hypersensitivity is not well elucidated, but one can clinically differen- useful tool for diagnosing CRPS, type I (Bonica, 1970). tiate mechanical from thermal hypersensitivity by the useKozin, et al. (1981) did find that 83% of the patients with of a drop of acetone. Patients with CRPS, type I in theCRPS, type I had positive static (delayed) bone scans, however, whereas 69% of the patients had positive flow series studied by Raja, et al. (1986) had hyperalgesia to studies. Therefore, it is apparent that between 50 and 60% cold (three of four, as tested by acetone drop) or to heat (four of five, as tested using a laser thermal stimulator).of patients with CRPS, type I will have positive early phase bone scans, but between 83 and 96% of patients Some patients had hypersensitivity and hyperalgesia to will have positive delayed image bone scans (Holder & both heat and cold; however, these patients did not have CRPS, type II, but instead CRPS, type I. Of the group ofMackinnon, 1984; Kozin, et al., 1981). Treatment for this component of CRPS, type I is ficult dif to assess. Kozin, patients with hyperalgesia to temperature change, six of six got relief with sympathetic blocks or sympathectomyet al. (1981) reported that 90% of patients with a positive bone scan had good to excellent steroid response, begin(Raja, et al., 1986). Other authors have reported that nifedipine is effective for treating hyperalgesia (Prough, et al.,ning with steroids at the level of 60 to 80 mg/day and 1985). Specifically, in 13 patients with pain having a burn-tapering the dosages. ing character, dysesthesia, and cold intolerance, nifedipine Schott (1986) has reported a variety of therapeutic beginning at 10 mg three times a day, and increasing to modalities, including steroids, nonsteroidal anti-inflam30 mg three times a day, proved effective in 7 of 13matory drugs, alpha- and beta-blocking agents, griseofulpatients. Nifedipine is a calcium channel-blocking agent,vin, calcitonin, transcutaneous electrical nerve stimulaand as such may work by dilating blood vessels and antagtion, physical therapy, sympathetic blocks, and onizing the effects of norepinephrine on arterial andintravenous guanethidine. None of these treatments has venous muscle (Payne, 1986). Also, nifedipine may inter-been studied in a systematized fashion, however. fere with ectopic impulse formation that occurs in regen- Nail brittleness has been reported by Schott (1986) erating nerves, by blocking calcium channel protein. and Payne (1986) late in the disorder. The etiology of this The dystrophic component of CRPS, type I is moreis not clear and there is not any clear-cut treatment. Muscle difficult to delineate. Some authors have reported a diffuse spasm has been reported by a number of authors (Kleinor patchy bony demineralization (Kozin, et al., 1981),man, 1954; Long, 1982; Schott, 1986), again without a whereas others have reported frank osteoporosis late clear-cut in mechanism describing the etiology (Payne, the disorder (Schott, 1986). A number of authors have1986). Interestingly, electromyography (EMG) nerve conreported molted skin, again late in the disorder (Kozin, etduction velocity studies seem to be relatively negative in al., 1981; Payne, 1986; Raja, et al., 1986). Some authors CRPS, type I (Uematsu, et al., 1981). The treatments that have reported hair loss, yet again late in the disorder (Raja, seemed most effective for muscle spasm were trigger point et al., 1986; Schott, 1986). Vague terms such as vasomotor injections (Payne, 1986) and the use of baclofen. Baclofen instability have also been reported, as well as trophic skin is a gamma aminobutyric acid (GABA)-minergic drug that changes (Kozin, et al., 1981). The etiology for these com-centrally reduces muscle spasm. The inhibition of subponents is not well defined, but the consensus seems stance to P may be implicated as part of its mechanism for be reduced blood flow to the various involved organs. reducing spasm and the pain associated with spasm (Gillman & Lichtigfeld, 1985). Soma and quinine have also A more precise diagnostic assessment was advanced by Holder and MacKinnon (1984). They evaluated been tried, with only limited success (Hendler, unpubpatients with CRPS, type I, which they defined as diffuselished observations). Contractures, usually in the hand, hand pain, diminished hand function, joint stiffness, andhave also been reported (Payne, 1986; Schott, 1986). The skin and soft tissue trophic changes with or without vaso-etiology of this is unclear, but is probably related to disuse.

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Again, there is an absence of positive EMG-nerve con-to 80 mg) for 2 to 4 days, then 40 to 60 mg for 2 to 4 duction velocity studies (Uematsu, et al., 1981), and thedays, and then 30 to 40 mg for 2 to 4 days, in four equally only treatment seems to be preventative, by the use of divided doses, were the initial therapy. Subsequently, the passive range-of-motion exercises and physical therapy.dose was rapidly tapered using a single morning dose of Contralateral involvement has been reported by sev-40 mg, then 30 mg, 20 mg, 10 mg, and 5 mg over 2 or 3 eral authors (Kleinman, 1954; Schott, 1986). The etiologydays at each dose. By using this regimen, 82% of the for this may be quite direct. In approximately 80% of patients with joint stiffness and tenderness obtained good or excellent relief. examined cadavers there is cross-communication between the sympathetic fibers and the sympathetic chains (Klein- An unusual complication of CRPS, type I is the man, 1954). Countralateral blocks and denervation have appearance of pathological fractures subsequent to been recommended (Kleinman, 1954). Edema of theminor trauma. In patients complaining of persistent pain affected limb (Payne, 1986; Schott, 1986), as well asin the limb that seems to be bony in origin, instead of swelling of a specific joint (Kozin, et al., 1981), has beenpart of the CRPS, type I, it would be imperative to obtain reported. Again, the etiology is unclear. The diagnosis isbone scanning to confi rm the presence or absence of an established by measuring the proximal interphalangeal undetected break. In our experience, one patient with joint, which averages 12.9 mm larger in the affected hand long-standing CRPS, type I received a minor trauma than in the control hand (Kozin, et al., 1981). No treatment(i.e., bumping her ankle while walking in a train) that has been advanced for this, although nifedipine is sugresulted in a chronic intense worsening of pain in the gested to be effective (Prough, et al., 1985). At Mensana heel. Radiographs of this area were within normal limits, Clinic, Stevenson, MD, we have observed some benefit but the pain persisted for several days after the event, from the use of spironolactone, or carbonic anhydrase and a bone scan was obtained. Only on bone scan did inhibitors, but not on a consistent basis. the break in the calcaneus appear, which had been totally missed by routine radiograph. Of any breaks present, Lower skin temperature has been reported by a variety of authors (Hendler, Uematsu, & Long, 1982; Payne,95% will have a positive bone scan after 72 h (Matin, Interestingly, after the fracture is healed, 90% of 1986; Raja, et al. 1996), but it does not seem to be due 1979). to the bone scans have returned to normal 2 years from the vasospasm (Janof, Phinney, & Porter, 1985). Reflex contraction due to altered activity within the afferent anddate of the injury. Therefore, in patients with CRPS, type I who have minor injuries and complain of bony efferent nerves is proposed as the etiology (Janoff, et al., 1985). Thermography is an excellent diagnostic tool topain, it would be prudent to obtain a bone scan, and not rely on radiographs. document the reduced skin temperature (Hendler, et al., 1982; Uematsu, et al., 1981). In fact, very often patients Payne (1986) has enumerated many attempted treatwith CRPS, type I are diagnosed as having psychosomatic ments for CRPS, type I. Unfortunately, there seems to disorders, and thermography can be a most convincing be a lack of systematic investigation for these treatments, diagnostic tool to confirm the otherwise subjective com-and most are based on clinical reports instead of systemplaint (Hendler, et al., 1982). However, nerve entrapments atized trials. Reported pharmacological interventions and radiculopathies can also lower limb temperaturethat may work for CRPS, type II are the use of propra(Uematsu, et al., 1981). nolol, a beta-blocking agent; prazosin, an alpha-1-adrTreatment for lower skin temperature associated withenergic-blocking agent; phenoxybenzamine, both an pain is best effected using regional sympathetic blocksalpha-1- and an alpha-2-blocker; and guanethidine, a sympathectomy. “ ” Physemploying reserpine. It is important to note that thesedrug that produces a chemical reserpine blocks, or Bier blocks, are not effective forical therapy has been advanced for the treatment of CRPS, type I, specifi cally to minimize muscle contracvasospasm, but specifically seem to function best for treatand joint stiffness. It is never a defi nitive treatment, ing CRPS, type I. Therefore, vasospasm does not seem tures to however, and should not be considered such. Electrical be the etiologic mechanism for the coldness noted in the limb in CRPS, type I (Janoff, et al., 1985). Stiffness stimulation of the central nervous system, using either (Holder & MacKinnon, 1984; Payne, 1986) and tender-electrodes centrally implanted into the periaqueductal or periventricular gray or epidural stimulators, may prove ness (Kozin, et al., 1981) of the joints have been reported; again, the etiology is not clear (Payne, 1986). Very often,effective, as might transcutaneous electrical nerve stimthe involvement of the joint leads to misdiagnosis andulation. Tricyclic antidepressants, nonsteroidal anticonfusion with other diseases that can affect the joint,inflammatory drugs, narcotics, and anticonvulsants have all been reported as treating some components of CRPS, notably infective arthritis, rheumatoid arthritis, Reiter’ s type I, with varying degrees of success. syndrome, systemic lupus erythematosus, and arthritides (Kozin, et al., 1981). In one series, 71% of the patients Surgical intervention is a treatment that is reserved with joint tenderness and stiffness had a poor response until to all other modalities of treatment have been attempted. stellate ganglion blocks. Steroids, notably prednisone (60 In all cases, the criterion for surgical intervention would

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TABLE 20.4 Recommended Treatment Flow Sheet Treatment 1. Prednisone 2. Physical therapy 3. Transcutaneous electrical stimulation 4. Sympathetic blocks 5. Sympathectomy

Dosage

Time Course

80 mg to start and taper by 10 mg q.i. 8 days 3 times a week 2 weeks Wear constantly 1 week

Go to 2 Go to 3 Go to 4

3 times a week

If lasting relief, stop; if 100% pain relief but temporary, go to 5 If lasting relief, stop; if no relief, go to 6 If lasting relief, stop; if 100% pain relief but temporary, go to 7, if no relief, go to 8 If relief, stop; if no relief, go to 8 If relief, stop; if no relief, go to 9 If relief, stop; if no relief, try other meds in combination or alone, go to 10 Maintenance

2 weeks

-—

1-week recovery

6. Contralateral blocks

3 times a week

2 weeks

7. Contralateral sympathectomy 8. Epidural spinal cord stimulator 9. Epidural pump

— — Start with clonidine (Rauck, et al., 1993)

1-week recovery 1-week recovery 1-week recovery

10. Psychotherapy (supportive)

If Ineffective, Next Step

Use antidepressants

6 months to 2 years

be repetitive successes with repeat sympathetic blocks. lesions in the dorsal root interrupting the nociceptive The most commonly employed surgical interventions arepathways in the tract of Lissauer and in laminae I-V of resection of the lower third of the stellate ganglion andthe dorsal horn of the spinal cord, may prove to be an resection of the upper two thoracic ganglia; however, some effective modality for treating CRPS, type II for stretch surgeons resect the second through fifth thoracic ganglia injuries (Payne, 1986). A treatment guideline is shown in an attempt to treat upper-extremity ficulties. dif There in Table 20.4. are four surgical approaches to upper extremity sympathectomies (Allen & Morety, 1982):

CONCLUSIONS

1. Above the clavicle (anterior cervical approach) 2. Posterior resection of the transverse processes of ribs 2 and 3, and proximal section of ribs 2 and 3 3. Anterior transpleural entry through the pectoralis muscle to the third intercostal space, pressing the lung, to reach the operative area 4. The axillary approach, which is through a transaxillary incision over the second intercostal space

In summary, it is quite apparent that a great deal of confusion has arisen concerning the diagnosis of CRPS, type I and CRPS, type II. This is evidenced by the lack of uniformity in clinical criteria for establishing the diagnosis. Because of this lack of uniformity, assessment of various articles detailing treatment of CRPS, type I and/or CRPS, type II is dif ficult. What some clinicians take as symptoms of CRPS, type I are not always present in their entirety. Unfortunately, if one adheres rigorously to these criteria, proper diagnosis, and more importantly proper treatment, may be withheld. The various clinical Also, a lumbar approach can be made through the symptoms that have been reported as associated with external and internal obliques, and then the transversalis CRPS, type I and CRPS, type II are shown in Table 20.2. muscle, below the twelfth rib, behind the kidney; othersA patient should be considered to have CRPS, type I if have suggested a thoracolumbar presacral neurectomy. he or she has at least one type of hyperalgesia (either Side effects of surgical approaches are postsympathecmechanical or thermal), lower skin temperature, and the tomy neuralgia, beginning 7 to 10 days after surgery, and sensation of pins and needles. However, the presence of postsympathectomy dysesthesia that may last 2 to 14 allodynia is a more consistentnding. fi At a minimum, weeks, and is described as continuous, severe, and worse diagnostic studies that would facilitate the diagnosis of at night. Anticonvulsants, such as diphenylhydantoin orCRPS, type I would be thermography, sympathetic carbamazepine, may be used to treat this (Allen &blocks, and bone scan. Clinical diagnostic studies that Morety, 1982). Medication, such as valproic acid andwould prove important would be testing with a drop of gabapentin may be useful (Mellick & Mellick, 1995). acetone for cold hyperalgesia and allodynia, and testing Dorsal root entry zone procedures, which produceusing Von Frey hairs for mechanical hyperalgesia and

Complex Regional Pain Syndrome, Types I and II

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allodynia. All patients suspected of having CRPS, typeBennett, G.J. (1991). The role of the sympathetic nervous system in painful peripheral neuropathy. Pain, 45, 221–223. I should have at least three sympathetic blocks. After Bonica, J.J. (1970). Causalgia and other reflex sympathetic dysthat, one should use various diagnostic and treatment trophies. In J.J. Bonica (Ed.), Advances in pain research techniques, including pharmacological intervention, and therapy (Vol. 3, pp. 141–166). New York: Raven depending on the patient’ s type of complaints. Press. To make the diagnosis of CRPS, type II, one certainly Bouckoms, A.L., & Litman R.E. (1985). Clonazepam in the should establish that the symptoms of burning pain are contreatment of neuralgic pain syndrome. Psychosomatics, stantly present, in association with a partial peripheral nerve 26, 933–936. injury. Electromyographic and nerve conduction velocity Broseta, J., Roldan, P., & Gonzales-Darder, J. (1982). Chronic studies should be conducted to detect whether there is an epidural dorsal column stimulation in the treatment of associated nerve injury. Certainly, patients should receive a causalgic pain.Applications in Neurophysiology, 45, peripheral nerve block; sympathetic blocks; and a trial with 190–194. phenoxybenzamine, valproic acid, and gabapentin. Chaplan, S.R., Bach, F.W., Pogrel, J.W., Chung, J.M., & Yaksh, Regardless of whether a patient has CRPS, type I or T.L. (1994). Quantitative assessment of tactile allodynia in the rat paw.Journal of Neuroscience Methods, 53, CRPS type II, one must be aware of the need to make a 55–63. distinction between the two diagnoses, because the treatDalton, S. (1984).Split seconds — The world of high speed ments vary. More importantly, if the patient has even a single photography(pp. 21, 28, 30, 31, 32, 34, 36). Salem, NH: symptom of CRPS, type I, a diagnostic assessment involving Salem House. the previously recommended modalities would be warDevor, M. (1983). Nerve pathophysiology and mechanisms of ranted, and further diagnostic studies should be pursued if pain in causalgia. Journal of the Autonomic Nervous the diagnosis of CRPS type I is not confi rmed. Kozin, et al. System, 7,371–384. (1981) clearly defi ned a number of overlapping conditions that may originally be misdiagnosed as CRPS, type I. OfDevor, M., & Janig, W. (1981). Activation of myelinated afferents ending in a neuroma by stimulation of the sympathe patients who were found not to have CRPS, type I, 25% thetic supply in a rat.Neuroscience Letters, 24, 43–47. had peripheral neuropathy or trapped peripheral nerves, and Eliav, E., Herzberg, U., & Caudle, R. M. (1999). The kappa half the patients misdiagnosed as having CRPS, type I had opioid agonist GR89 696 blocks hyperalgesia and alloinflammatory arthritis (Kozin, et al., 1981). Therefore, labdynia in rat models of peripheral neuritis and neuropaoratory studies, including erythrocyte sedimentation rate, thy. Pain, 79, 255–264. antinuclear antibody, rheumatoid factor, Lyme disease, HIV,Ganit, R., Leksell, L., & Skoglund, C.R. (1944). Fiber interaction and the like, should be conducted in patients thought to have in injured or compressed region of the nerve. Brain, 67, CRPS, type I but in whom the diagnosis is not complete. In 125–140. any event, CRPS, types II and I require clinical acumen toGeldard, F.A. (1962).Fundamentals of psychology . New York: establish the diagnosis, and persistence to effect appropriate John Wiley & Sons. treatment. Aggressively pursuing all the diagnostic studies Ghostine, S.Y., Comair, Y.G., Turner, D.M., et al. (1984). Pheavailable, as well as relying on clinical judgment, provides noxybenzamine in the treatment of causalgia (report of 40 cases).Journal of Neurosurgery, 6, 1263–1268. better care for these patients. Gillman, M.A., & Lichtigfeld, R.J. (1985). A pharmacological overview of opioid mechanisms mediating analgesia and hyperalgesia.Neural Research, 7, 106–119. REFERENCES Glynn, C.J., Dawson, D., & Sanders, R. (1988). A double-blind comparison between epidural morphine and epidural Allen, M.B., Jr., & Morety, W.H. (1982). Sympathectomy. In J. clonidine in patients with chronic non-cancer pain. Pain, Youmans (Ed.),Neurological surgery(2nd ed., Vol. 6, 34, 123–128. pp. 3717–3726). Philadelphia: W. B. Saunders. Arner, S., & Meyerson, B.A. (1988). Lack of analgesic effect of Gobelet, C., Waldburger, M., & Meier, J.L. (1992). The effect of adding calcitonin to physical treatment on reflex symopiods on neuropathic and idiopathic forms of pain. pathetic dystrophy.Pain, 48, 171–175. Pain, 33, 11–23. Greipp, M.E., & Thomas, A.F. (1994). Skin lesions occurring in Barolat, G., Schwartzman, R J., & Woo, R. (1989). Epidural clients with reflex sympathetic dystrophy syndrome. spinal cord stimulation in the management of reflex Journal of Neuroscience Nursing, (6), 26 342–346. sympathetic dystrophy.Stereotactic and Functional Hamamci, N., Dursun, E., Ural, C., & Cakci, A. (1996). CalciNeurosurgery, 53,29–39. tonin treatment in reflex sympathetic dystrophy. A preBaron, R., Blumberg, H., & Janig, W. (1996). Clinical characterliminary study. British Journal of Clinical Practice, istics of patients with complex regional pain syndrome in 50(7), 373–375. Germany, with special emphasis on vasomotor function, in reflex sympathetic dystrophy: A reappraisal. In W. JanigHannington-Kiff, J.G. (1979). Relief of causalgia in limbs by regional intravenous guanethedine. British Medical & M. Stanton-Hicks (Eds.). Progress in pain research and Journal, 12,367–368. management(Vol. 6, pp. 25–48). Seattle: IASP Press.

232

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Hassenbusch, S., Stanton-Hicks, M., & Covington, E.C. (1995).Kozin, F., Ryan, L.M., Carerra, G.E., et al. (1981). The reflex sympathetic dystrophy (RSDS). American Journal of Long term intraspinal infusion of opioids in the treatMedicine, 70,23–30. ment of neurpathic pain. Journal of Pain and Symptom Management, 10,527–543. Lee, Y.W., Chaplan, S.R., & Yaksh, T.L. (1995). Systemic and supraspinal, but not spinal opiates supress allodynia in Hendler, N. (1982). The four stages of pain. In N. Hendler, D. a rat neuropathic pain model. Neuroscience Letters, 199, Long, & T. Wise (Eds.),Diagnosis and treatment of 111–114. chronic pain (pp. 1–8). Boston: John Wright-PSG. Lee, Y.W., Kayer, V., Desmeules, J., & Guilbaud, G. (1994). Hendler, N. (1984). Depression caused by chronic pain. Journal Differential action of morphine and various opioid agoof Clinical Psychiatry, 45 (3, Sec. 2), 30–36. nist on thermal allodynia and hyperalgesia in mononHendler, N. (1995). Reflex sympathetic dystrophy: Clearing up europathic rats.Pain, 57, 233–240. the misconceptions, Journal of Workers Compensation, Lee, Y.W., & Yatsh, T.L. (1996). Pharmacology of the spinal ade5,(1), 9–20. nosine receptor which mediates the anti-allodynic action Hendler, N. (1997). Pharmacology of chronic pain. In R. North of intra-thecal adenosine agonists. Journal of Pharmacol& R. Levy (Eds.),Neurosurgical management of pain ogy and Experimental Therapeutics, 277, 1642–1648 (pp. 117–129). Amsterdam: Springer-Verlag. Hendler, N. (2000). Pharmacotherapy of chronic pain. In P. P.Levi-Montalcini, R. Skaper, S.D., Toso, R.D., Petrelli, L, & Leon, A. (1996). Nerve growth factor: From neurotroRaj (Ed.), Practical management of pain (3rd ed., pp. phin to neurokine.Trends in Neuroscience, 19, 514–520. 145–155). Philadelphia: C.V. Mosby. Hendler, N., Bergson, C., & Morrison, C. (1996). Overlooked Loh, I., & Nathan P.W. (1978). Painful peripheral states and sympathetic blocks.Journal of Neurology, Neurosurphysical diagnoses in chronic pain patients involved in gery, and Psychiatry, 41, 664–671. litigation: Part 2.Psychosomatics, 37 (6), 509–517. Hendler, N., & Kozikowski, J. (1993). Overlooked physical diag- Long, D.M. (1982). Pain of peripheral nerve injury. In J. Youmans (Ed.),Neurological surgery(2nd ed, Vol. 6, pp. noses in chronic pain patients involved in litigation. 3634–3643). Philadelphia: W. B. Saunders. Psychosomatics, 34 (6), 494–501. Hendler, N., & Raja, S. (1994). Reflex sympathetic dystrophyMatin, P. (1979). The appearance of bone scans following fractures, including immediate and long-term studies. Jourand causalgia. In C. D. Tollison (Ed), Handbook of pain nal of Nuclear Medicine, 20, 1227–1231. management(2nd ed., pp. 484–496). Baltimore: Williams & Wilkins. Max, M. B., Kishmore-Kumar, R., Schafer, S. C., et. al. (1991). Efficacy of desipramine in diabetic peripheral neuropaHendler, N., & Talo, S. (1989). Chronic pain patients versus the thy: A placebo controlled trial.Pain, 45, 69–73. malingering patient. In K. Foley & R. Payne (Eds.), Current therapy of pain(pp. 14–22). Philadelphia: B.C. Mearow, K.M., & Kril, Y. (1995). Anti-NGF treatment blocks Decker. the upregulation of NGF receptor mRNA expression associated with collateral sprouting of rat dorsal ganHendler, N., Uematsu, S., & Long, D. (1982). Thermographic glion neurons.Neuroscience Letters, 184, 55–58. validating of physical complaints in "psychogenic pain" patients.Psychosomatics, 23, 282–287. Mellick, G.A., & Mellick, L.B. (1995). Gabapentin in the management of reflex sympathetic dystrophy. Journal of Hendler, N., Vierstein, M., Shallenberger, C., & Long, D. (1981). Pain Symptoms and Management, 265–266. 10, Group therapy with chronic pain patients. Psychosomatics, 22(4), 333–340. Merskey, H. (ed) and the Subcommittee on Taxonomy. (1986). Classification of chronic pain. Pain, 3(Suppl.), 28–29. Hoffert, M.I., Greenburg, P.P., Wolskee, P.J., et al. (1984). Abnormal and collateral innervation of sympathetic and Meyer, R.A., Campbell, J.N., & Raja, S.N. (1985). Peripheral peripheral sensory fields associated with a case of causneural mechanism of cutaneous hyperalgesia. In H.L. algia. Pain, 20, 1–12. Fields, R. Dubner, & F. Cevero (Eds.), Advances in pain research and therapy(Vol. 9, pp. 53–71). New York: Holder, L.E., & MacKinnon, S.E. (1984). Reflex sympathetic Raven Press. dystrophy in the hands: Clinical and scintigraphic criteria. Radiology, 152,517–522. Ochoa, J., Torebjorte, E., Marchetti, H., et al. (1985). Mechanisms of neuropathic pain: Cumulative observations, Inball, R., Rousso, N., Ashur, H., Wall, P.D., & Devor, M. (1987). new experiments and further speculation. In H. L. Collateral sprouting in skin and sensory recovery after Fields, R. Dubner, & F. Cevero (Eds.), Advances in pain nerve injury in man.Pain, 39, 141–154. research and therapy (Vol. 9, pp. 431–450). New York: Janoff, K.H., Phinney, E.S., & Porter, I.M. (1985). Lumbar symRaven Press. pathectomy for lower extremity vasospasm. American Payne, R. (1986). Neuropathic pain syndromes, with special Journal of Surgery, 150, 147–152. reference to causalgia and reflex sympathetic dystrophy. Kim, S.H., & Chung, J.M. (1995). Sympathectomy alleviates Clinical Journal of Pain, 2,59–73. mechanical allodynia in an experimental animal model for neuropathy in the rat. Neuroscience Letters, 134, 131–134. Peuschl, G., Blumber, H., & Lucking, C.H. (1991). Tremor in reflex sympathetic dystrophy. Archives of Neurology, 48, Kleinman, A. (1954). Causalgia: Evidence of the existence of 1247–1252. crossed sensory sympathetic fibers. American Journal of Surgery, 87,839–841. Portenoy, R.K., Foley, K.M., & Inturrisi, C.E. (1990). The nature of opioid responsiveness and its implications for neuroKnobler, R. (1996). The pathogenesis of reflex sympathetic dyspathic pain: A new hypothesis derived from the study trophy: Immune and viral mechanisms. American Jourof opioid infusions.Pain, 43, 273–286. nal of Pain Management,(3), 6 83–85.

Complex Regional Pain Syndrome, Types I and II

233

Prough, D.S., McLeskey, C.H., Poehling, G.G., et al. (1985).Schwartzman, R.J., & Kerrigan, J. (1990). The movement disorder of reflex sympathetic dystrophy. Neurology, 40, Efficacy of oral nifedipine in the treatment of reflex 57–61. sympathetic dystrophy. Anesthesiology, 2, 796–799. Raja, S.N., Campbell J.N., Meyer R.A., et al. (1986, NovemberSchwartzman, R.J., & McKellan, T.L. (1987). Reflex sympathetic dystrophy: A review.Archives of Neurology, 44, 6–9). Sensory testing in patients with causalgia or reflex 555–561. sympathetic dystrophy . Abstract presented at 6th Annual Meeting of American Pain Society, Washington, D.C. Stanton-Hicks, M., Baron, R., Boas, R., Gordh, T., Harden, N., Hendler, N., Koltzenberg, M., Raj., P., & Wilder, R. Raja, S.N., & Hendler N. (1990). Sympathetically maintained (1998). Complex regional pain syndrome: guidelines for pain. In M. Rogers (Ed.), Current practices in anesthetherapy.The Clinical Journal of Pain, 14 (2), 155–166. siology (pp. 421–425). New York: C. V. Mosby Year Uematsu, S., Hendler, N., Hugerford, D., Ono, S., & Long, D.M. Book. (1981). Thermography and electromyography in the difRaja, S.N., Treede R.D., Davis R.D., et al. (1991). Systemic ferential diagnosis of chronic pain syndromes and reflex alpha-adrenergic blockade with phentolarrine: A diagsympathetic dystrophy. Electromyography and Clinical nostic test for sympathetically maintained pain. AnesNeurophysiology, 21, 165–182. thesiology, 74,691–698. Van der Laan, L., Veldman, P.H.J.M., & Goris, R.J.A. (1998). Rauck, R.I., Eisenach, J.C., & Jackson, K. (1993). Epidural Severe complications of reflex sympathetic dystrophy: clonidine treatment for refractory reflex sympathetic Infection, ulcers, chronic edema, dystonia, and myoclodystrophy.Anesthesiology, 79, 1163–1169. nus. Archives of Physical Medicine and Rehabilitation, Ren, K., & Dubner, R. (1993). NMDA receptor antagonists 79, 424–429. attenuate mechanical hyperalgesia in rats with unilateral Watson, C.P., Chipman, M., Reed, K., et. al. (1991). Amitripinflammation of the hindpaw. Neuroscience Letters, 163, tyline vs. maprotiline in post herpetic neuralgia: A ran22–26. domized, double blind, cross-over trial. Pain, 48, 29–36. Ro, L.S., Chen, S.-T., Tang, L.-M., & Jacobs, J.M. (1999). EffectWatson, C.P., Evans, R.J., Reed, K., et. al. (1981). Amitriptyline of NGF and anti-NGF on neuropathic pain in rats folvs. placebo in post herpetic neuralgia. Neurology, 32, lowing chronic constriction injury of the sciatic nerve. 671–673. Pain, 79, 265–274. Webster, G.F., Iozzo, R.V., Schwartzman, R.J., Tahmoush, A. J., Robaina, F., Dominguez, M., & Diaz, M. (1989). Spinal cord Knobler, R.L., & Jacoby, R.A. (1993). Reflex sympastimulation for relief of chronic pain in vasoplastic disthetic dystrophy: Occurrence of chronic edema and nonorders of the upper limbs. Neurosurgery, 24,63–67. immune bulious skin lesions. Journal of the American Roberts, M.A. (1986). Hypothesis on the physiological basis for Academy of Dermatology, (1), 28 29–32. causalgia and related pain. Pain, 24, 297–311. Webster, G.F., Schwartzman, R.J., Jacoby, R.A., Knobler, R.L., & Uitto, J.J. (1991). Reflex sympathetic dystrophy: Schott, G.D. (1986). Neurologic manifestation of bone and joint Occurrence of inflammatory skin lesions in patients with disease. In A. K. Ashbury, G. M. McKham, W. C. stages II and III disease. Archives of Dermatology, 127, McDonald, et al. (Eds.), Diseases of the nervous system 1541–1544. (pp. 1523–1537). Philadelphia: W. B. Saunders.

21 Treatment of Myofascial Pain Syndromes Robert D. Gerwin, M.D. and Jan Dommerholt, P.T., M.P.S. INTRODUCTION

DIAGNOSIS

The treatment of persons with myofascial pain syndromeThe diagnosis of MPS should be suspected when there is (MPS) follows the general principles that apply to all a nonneuropathic pain complaint almost anywhere in the medical disorders. The nature of the pain problem firstbody, including headache. At first glance, such a statement may seem to be so nonspecific as to be meaningless, but must be understood through developing an appropriate differential diagnosis and evaluating the contributions ofit emphasizes the need to be aware of the role of soft tissue coexisting disorders, until a single working diagnosisor muscle in all types of pain. Indeed, MPS has been reported as the most common diagnosis responsible for emerges. Following the initial assessment and formulation chronic pain and disability (Fricton, 1990; Masi, 1993; of diagnostic hypotheses, new data are collected. A regular review at each encounter and modification of the hypoth-Rosomoff, et al., 1989; Skootsky, Jaeger, & Oye, 1989). MPS is often thought of as a regional pain syndrome in eses facilitate a more efficient and effective management of patients with MPS and dictate the actual program com-contrast to fibromyalgia as a widespread syndrome; howponents (Higgs & Jones, 1995; Jones, 1994). Afterever, as many as 45% of patients with chronic MPS have generalized pain in three or four quadrants (Gerwin, addressing the issue of diagnosis, the practitioner must determine the structural or biomechanical functioning of1995b). Patients with widespread MTrPs should be diagthe patient and the contribution that any dysfunction maynosed with MPS and not with fibromyalgia, even though have to the individual’s pain. Medical and psychologicalthe classification criteria for fibromyalgia suggested making the diagnosis of fibromyalgia “irrespective of other disorders that may alter the presentation of MPS or that diagnoses” (Wolfe, et al., 1990). In clinical practice the may predispose to its becoming chronic are assessed. diagnosis of fibromyalgia should not be made without Treatment of persons with MPS addresses each of these issues specifically (Figure 21.1). There must be relief ofconsidering all differential diagnoses (Dommerholt, 2001; pain by the direct inactivation of the myofascial trigger Gerwin, 1999). A survey of members of the American point (MTrP) itself. The mechanical and structural factorsPain Society showed general agreement with the concept that MPS exists as an entity distinct from fibromyalgia that affect or overload the muscle and aggravate the pain (Harden, et al., 2000). must be resolved or alleviated. The medical and psychological problems that affect muscle function, including Muscle pain tends to be dull, poorly localized, and those that alter and impair intracellular metabolism, mustdeep, in contrast to the precise location of cutaneous pain. be identified and corrected where possible. Inactivation ofThe diagnosis of MPS is confirmed when the MTrP is the MTrP may occur with direct intervention at the MTrP identified by palpation. Systematic palpation differentiates itself, through correction of the mechanical factors thatbetween myofascial taut bands and general muscle spasms produced it or through improvement in the underlying(Janda, 1991). An active MTrP is defined as a focus of medical disorders that predispose to the development or hyperirritability in a muscle or its fascia that causes the maintenance of the MTrP. patient pain (Simons & Travell, 1984). The key features 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

235

236

FIGURE 21.1

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Treatment program example.

distinguish an MTrP from any other tender area in muscle of the trigger point have been established by Simons, Travell, and Simons (1999) and are listed in Table 21.1.are a taut band and a tender point in that taut band. The The interrater reliability of the clinical examination has presence of a local twitch response, referred pain, or repros symptomatic pain increases the been established by Gerwin, et al. (1997) for the five majorduction of the person’ features of the trigger point. Individual features of thecertainty and specificity of the diagnosis. trigger point are differentially represented in different Making a diagnosis of MPS may be therapeutic in muscles. For example, the local twitch response is easier itself and may constitute the first step in treatment, because to obtain and therefore more commonly found in themany patients may not have been given a correct diagnosis extensor digitorum communis than in the infraspinatuspreviously. Patients are often depressed, confused, or frusmuscle. One should not expect to find each feature of the trated, as they may not have been given an appropriate trigger point in every muscle by physical examination.explanation of their pain in previous evaluations. They The minimum criteria that must be satisfied in order tooften appear relieved when the practitioner can literally

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point, restoration of normal tissue mobility, and elimination of pain (Dommerholt, 2001; Miller, 1994). The TABLE 21.1 patient and the clinician need to identify appropriate goals Myofascial Trigger Point Characteristics and develop the means to implement them through ther1. Focal exquisite tenderness in a taut band of muscle apy. Inactivation of the trigger point is a means to achieve 2. Referral of pain to a distant site upon activation of the trigger point relief of pain, to improve biomechanical function, and thus 3. Contraction of the taut band (local twitch response) upon to improve the ability of the patient to better perform mechanical activation of the trigger point whatever desired tasks have been selected as goals. Relief 4. Reproduction of the person’ s pain by mechanical activation of of pain or increased range of motion, both of which can trigger point be the result of trigger point inactivation, are not in them5. Restriction of range of motion selves the final goals of treatment. For some individuals, 6. Weakness without muscle atrophy 7. Autonomic phenomenon such as piloerection or changes in loca an initial goal may be to simply sleep through the night. circulation (regional blood flow and limb temperature) in response For another patient, it may be eating out of bed at a table, to trigger point activation or fastening a bra behind the back. For yet another, it may be regaining sexual ability, or returning to work or to a put the finger on the source of the pain, which usuallyrecreational activity. Reasonable goals that can be results in instant rapport between patient and clinician. achieved and measured as being reached or not, are more important to focus on than simply the inactivation of a The introduction of pressure algometers has improved the assessment of sensitivity signifi cantly (Fischer, 1986c; tender point or an increase in the range of a particular movement (Gerwin, 2000 ). Keele, 1954); however, only recently have pressure algometers been applied to the assessment of MTrPs (Fischer, Inactivation of the MTrP can be achieved manually, 1984, 1986a,b). Several studies have confi rmed the reliabil- by correcting structural mechanical stressors, by direct injection of a local anesthetic into the muscle, or by dry ity of pressure measurement for the assessment of pain sensitivity (Jensen, et al., 1986; Merskey & Spear, 1964), forneedle intramuscular stimulation of the MTrP. Treatment pressure sensitivity of MTrPs, and for the detection of theirof the patient with MPS can be very effective when used location (Delaney & McKee, 1993; Jaeger & Reeves, 1986;in the context of a comprehensive diagnostic and treatOhrbach & Gale, 1989; Reeves, Jaeger, & Graff-Radford,ment spectrum (Yue, 1995). After establishing an accurate medical diagnosis with identifi cation of systemic, 1986). Tenderness and the presence of a taut band in muscle may be quantifi ed by pain pressure algometry and tissuemechanical, and psychological perpetuating factors, the patient with chronic MPS is best treated through an intercompliance measurements (Fischer, 1986a,c, 1993). Fischer disciplinary team approach (Turk & Okifuji, 1999). The (1997) discussed the role of algometry and tissue compliterm interdisciplinary is preferred tomultidisciplinary ance testing in the diagnosis of MPSs. He incorporated the ects the coordinated working relationship two main criteria for the diagnosis of MTrPs, local point because it refl between members of the treatment team (Melvin, 1980; tenderness (as quantifi ed by algometry) and recognition of Turk & Rudy, 1994). Essential members of the interdispatient’s symptoms, into his concept of segmental sensitizaciplinary team include the patient, physicians, psycholotion, radiculopathy, and paraspinal spasm. gists, clinical social workers, occupational therapists, Hubbard and Berkoff (1993) identified a characteristic physical therapists, ergonomists, massage therapists, and electrical discharge emanating from the trigger point and others actively involved in patient care (Ghia, 1992; Khaunique to it. Simons, Hong, and Simons (1995) have furlil, et al., 1993). Not every MPS patient necessarily ther studied this activity, whereas Chu (1995) has reported requires such an extensive collaboration. For example, finding it in the trigger points of persons with lumbosacral patients with acute MPS may only require treatment by radiculopathy. Phentolamine infusion reduced the average physicians and physical therapists. The treatment plan can integrated signal of the spontaneous electrical activity by be divided into a pain control phase and a training or about one third in the experimental animal model. This conditioning phase (Saal & Saal, 1991). During the pain result shows that there is a modulating effect of the symcontrol phase, the most essential components are manual pathetic nervous system on the motor activity of the trigger therapy, trigger point injection, dry needling, and elimipoint (Chen, et al., 1998). Thus, an objective electromyonation of mechanical perpetuating factors. Throughout the graphic (EMG) signature of the trigger point is now availtreatment process, much attention should be paid to eduable for diagnostic and research purposes. cating the patient concerning the etiology, perpetuating factors, and self-management. Patients must learn to modify their behaviors and avoid overloading the muscles PRINCIPLES OF TREATMENT without resorting to total inactivity (Simons & Simons, The ultimate goal of treatment of persons with MPS is1994). Following the pain control phase, patients should restoration of function through inactivation of the trigger be introduced to therapeutic exercises, movement reedu-

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cation, and overall conditioning. Too often, patients withtaking up the slack until a barrier is reached. The patient chronic myofascial pain dysfunction are introduced toois then asked to contract the muscle isometrically against soon to isotonic training and conditioning, causing furtherresistance for about 10 s at approximately 10% of maximal aggravation of active trigger points and increase of paineffort. Because it is dif ficult for patients to gauge a level and dysfunction. Likewise, work hardening programsof effort, the clinician presents a force against which the should never be conducted during this phase of treatment. patient pushes. The patient is instructed, “Meet my force, This can lead to further discouragement and depression, but do not exceed ”it.Thus, the clinician is in complete as well as an increase in pain. On the other hand, the pain control of the effort exerted by the patient, and an approcontrol phase must be time limited, and patients mustpriately slight contraction of muscle is achieved. Then the understand that progressing to the conditioning phase patient is relaxes the muscle. Once total relaxation is imperative. If they do not move beyond the pain controlachieved, the slack is taken up again and the process is phase, patients can be restricted in their functional abili-repeated for three to five times (Lewit, 1991; Lewit & ties and be at greater risk of reinjury (Saal & Saal, 1991).Simons, 1984; Simons & Simons, 1994). Respiratory In daily practice, the various aspects of the rehabilitationfacilitation of muscle relaxation utilizes the contraction of process are addressed simultaneously and not treated nonrespiratory as muscles that occurs with inspiration and separate entities. the relaxation of the same muscles during expiration. During the relaxation phase, the patient is asked to exhale and look down to facilitate muscular relaxation (Lewit, 1988). MANUAL THERAPY A variation on Lewit’s approach combines isometric conManual therapy is one of the basic treatment options fortractions, reciprocal inhibition, and stretch (Fischer, MPS. In conjunction with manual therapy approaches,1995). Simons, Travell, and Simons (1999) advocate the stretch Soft tissue mobilization is an essential component of the treatment. Soft tissue biomechanics including and spray technique, which combines use of a vapocoolant ammatory, repair, spray with passive stretching of the muscle. Applicationstress–strain patterns; the normal infl and remodeling stages following soft tissue injury (Carlof vapocoolant spray stimulates thermal and tactile A-beta skin receptors, thereby inhibiting C-fiber and A-delta fiberstedt & Nordin, 1989; Nolan & Nordhoff, 1996; Soderberg, 1992); the reactivity of the tissues; and tolerance afferent nociceptive pathways and muscle spasms, MTrPs, level and comfort of the patient are considered (Ellis & and pain when stretching. Prior to applying the stretch and spray method, the patient is positioned comfortably. TheJohnson, 1996). The intratissue (muscle tone) and intermuscle involved is sprayed with a few sweeps of a vapo-tissue mobility (muscle play) of the structures involved and of the adjacent muscles, fascia, and joints must be coolant spray, after which the muscle is stretched passively. With the muscle in the stretched position, the sprayevaluated and treated as well. Myofascial adhesions may is applied again over the skin overlying the entire muscle,develop with secondary or “satellite” trigger points in nearby muscles. MTrPs appearing in muscles that are part starting at the trigger zone and proceeding in the direction of, and including, the referred pain zone. Following theof a functional unit must be treated together. Muscles that work together as agonists, or that work in opposition to stretch and spray, the area is heated with a moist heat pack for 5 to 10 min. The patient is encouraged to move theeach other as antagonists, constitute a functional muscle body part several times through the full range of motion.unit. The same muscles can be related to each other both as agonists and antagonists, depending on the action being The stretch and spray technique can be used in physical therapy as a separate modality or following MTrP injec-performed. For example, the muscles that move or stabitions. In the United States, Fluori-Methane (Gebauerlize the shoulder form a functional unit. The trapezius and Chemical Co., 9410 St. Catherine Avenue, Cleveland, OHlevator scapula muscles display this relationship well. These two muscles work together as agonists in elevation 44104) has been used, whereas in Europe the use of liquid nitrogen or ethyl chloride is the norm (Dejung, 1988a).of the shoulder, but are antagonists in rotation of the Fluori-methane is being replaced due to its potentiallyscapula, the trapezius rotating the glenoid fossa upward damaging effects on the ozone layer. An environmentallyand the levator scapula rotating it downward. When one of these two muscles contracts to rotate the scapula, the safe substitute is being prepared. Lewit (1991) suggests using the stretch technique forother must relax. If these or some other shoulder muscles short or taut muscles and fascia, while promoting post-become dysfunctional, because of the presence of MTrPs isometric relaxation for treatment of trigger points. Post-that weaken or shorten them and restrict their range of motion, excessive loading on other muscles in the shoulder isometric relaxation is also known as muscle energy technique (Mitchell, 1993) or hold–relax technique (Knott & functional unit may occur. Trigger points in the levator Voss, 1968) and can easily be combined with stretch and scapula limit upward rotation of the lateral border of the spray techniques either in the clinic or as part of thescapula, thereby placing a greater load on the trapezius, patient’s home program. The muscle is gently lengthened,which is unable to accomplish the movement with usual

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effort, or perhaps is not able to accomplish the movement Although it previously has been described ischemic as at all, causing a compensatory lifting of the entire shouldercompression , it is now termedtrigger point pressure to raise the arm. release or trigger point compression . The patient can apply direct compression for self-treatment using a Thera The functional relationships of muscles may differ at ® Cane (Thera Cane Co., P.O. Box 9220, Denver, CO each end of the muscle, because the agonists and antagonists for each muscle may be different at the proximal and 80209; Phone 800–947–1470) or a similar device. Acudistal ends of the muscle. MTrPs may spread from one pressure may be another form of direct compression of region to another because of these relationships. Bilateral trigger points (Kodratoff & Gaebler, 1993). Following the axial muscles like the trapezius, sternocleidomastoid,Simons et al. protocol or using acupressure guidelines, quadratus lumborum, and iliopsoas act as both agonists compression of trigger points is moderately painful. In and antagonists to each other, facilitating the spread of contrast with these relatively gentle compression techMTrPs across the midline. Muscles that bridge regions,niques, Tsujii (1993) suggests using at least 10 to 20 kg like the latissimus dorsi, and those that influence posture, of force over the trigger point and 50 to 60 kg in chronic like the effect of the iliopsoas or quadratus lumborumcases with a strong elbow pressure technique. He premuscles on scoliosis, also facilitate the spread of MTrPs. sumes that successful treatment of chronic muscle pain is Thus, MPS can involve a single region of the body or itdependent on opioid-induced analgesia and that only intercan spread to involve all four quadrants of the body. Effec-mittent painful stimuli for more than 30 min produce such tive treatment should address all the affected areas. Othanalgesia. Because Tsujii’ s approach results in tissue damerwise, remaining dysfunctional muscle units may lead toage, treatments are scheduled with at least 10 days in the recurrence of active or spontaneously painful MTrPs.between appointments to allow the tissues involved to heal Myofascial release techniques and gentle, sustained prior to the next application. pressure may soften or elongate shortened or hardened Trigger points may also be directly related to undermuscles. The principle of the least possible force islying articular dysfunction (Ellis & Johnson, 1996). In the applied, instead of applying high stress to the muscle.treatment of myofascial pain, the practitioner must evalEffective myofascial release techniques include strum-uate and, when indicated, treat both soft tissue and joint ming, perpendicular and oscillating mobilizations, tissuedysfunction. Muscular and joint dysfunction are closely rolling, and connective tissue massage, among others related and should be considered as a single functional (Cantu & Grodin, 2001; Ellis & Johnson, 1996). Deep unit (Janda, 1994). Restrictions in joint capsules inhibit muscle massage consisting offleurage ef (stroking mas- muscle function for those muscles overlying the particular sage technique) and pétrissage (kneading massage techjoint. Conversely, muscle dysfunction results in joint capnique) is also recommended (Lehn, 1990; Vis, Raats, &sule restrictions (Dvorák ˇ & Dvorák ˇ , 1990; Warmerdam, Van der Voort, 1987). After the introductory superficial 1992). Zygopophyseal joints may have referred pain patapproach over the entire muscle and adjacent muscles, terns similar to MTrPs (Bogduk & Simons, 1993; Dwyer, massage therapy can be applied directly to the taut band Aprill, & Bogduk, 1990; McCall, Park, & O’Brien, 1979). and trigger points. Massage and exercise were found to In addition, Butler (2000) suggests that impaired mechanbe effective in reducing the number and intensity of triggerics and physiology of the nervous system may be another points, but the addition of therapeutic ultrasound did notcontributing factor in the overall etiology of various pain improve the outcome (Gam, et al., 1998). problems, including myofascial pain. Somatic dysfunction Soft tissue mobilizations may result in improved local affecting muscle and joint may result in restricted range circulation, normalization of muscle tone and muscle play,of motion and weakness that can be rather quickly and reduction of reflex activity and pain (Vis et al., 1987;reversed by manual therapy. Wells, 1994). By combining gentle approaches with more aggressive techniques, the Swiss physician and psychologist Dejung (1988a) has developed a seven-step treatINVASIVE INACTIVATION OF THE ment approach to myofascial dysfunction. Dejung’ s MYOFASCIAL TRIGGER POINT approach combines sustained compression, stretch and Inactivation of the MTrP by injection appears to be the spray techniques, myofascial release, restoration of musresult of the mechanical action of the needle in the trigger cle play, active and passive movements, and dry needling (Dejung, 1987a, 1988b; Grosjean & Dejung, 1990). Aspoint itself, because it can be successfully accomplished part of Dejung’s protocol, the patient actively moves the by dry needling without the use of local anesthetics or involved muscle, while the physician or therapist main-other materials (Chu, 1995; Gunn, Milbrandt, Little, & tains constant pressure over the trigger point (Dejung,Mason, 1980; Hong, 1994b). When using injection nee1987b, 1994). dles, the use of a local anesthetic is more comfortable for many patients and results in a longer lasting reduction in Simons, et al. (1999) also describe direct manual compression of the trigger point to inactivate trigger points.trigger point pain (Hong, 1994b; Travell, 1976). The use

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of solid acupuncture needles vs. injection needles has not must be released and returned to full length, if possible, been examined at this time. After identifying and manuallyeither by needling or by trigger point compression and stabilizing the tender area in the taut band with the fingers, stretching. Inadequate treatment that leaves critical trigger the needle is quickly passed through the skin and then into points within a functional muscle unit usually results in the trigger zone. A local twitch response or a report ofthe recurrence of trigger points throughout the muscles of referred pain indicates that the trigger zone has been the functional unit. Five to ten different MTrP sites can entered. A small amount, usually 0.1 or 0.2 ml, of localreadily be treated per session, and some physicians skilled anesthetic may be injected into the trigger zone. The neein MPS management treat considerably more in one sesdle is withdrawn to just below the skin, the angle of thesion. Repeat injections or dry needling into the same area needle is changed, and the needle is again passed through are best done after an interval of 1 week to allow the the muscle to another trigger zone. A conical volume ofmuscle to recover. Muscles of the affected functional unit muscle can thus be examined for active trigger pointsmust always be stretched, to their full length if possible, without withdrawing the needle through the skin. Theafter MTrP needling. Moist heat is applied to the muscle trigger zone is explored in this manner until no furtherto improve the local circulation and to reduce postinjection local twitch responses are obtained. At this point, the taut soreness. Otherwise, MTrPs recur because of residual sigband is usually gone, and the spontaneous pain of the nificant muscle dysfunction. Local anesthetic patches can trigger point has subsided. Patients who have previously be applied to reduce the superficial or cutaneous soreness undergone treatment can tell when trigger points remain, from needling. Complications of MTrP injections are and when they have been ficiently suf inactivated. A knowl- listed in Table 21.2. edgeable patient urges the clinician to continue in an area Trigger point injections or dry needling are a highly until a key trigger point is inactivated, at which time thereeffective way to reduce the local pain and contraction of is a noticeable decrease in pain. The process is repeated the taut band. This does not, however, constitute the whole until the symptomatic MTrPs are treated throughout thetreatment of MPS. The causes that led to the condition functional muscle unit (Hendler, Fink, & Long, 1983; must be corrected, when possible. Mechanical, medical, Hong, 1993, 1994a). and psychological perpetuating factors must also be elimTrigger point injections can be performed without inated or alleviated to reduce the chance of recurrence. anesthetic, so-called dry needling, or with a local anes-Inadequate attention to these aspects of treatment leads to thetic (Hong, 1994b). Historically, procaine has been used failure to relieve the pain (Table 21.3). for this purpose, although lidocaine is also commonly used today. Procaine, in a dilute solution of 0.5%, has a short half-life, which is an advantage if the anesthetic solution TABLE 21.2 spreads between tissue planes and produces a nerve block. Complications of Trigger Point Injections Other local anesthetics, such as bupivicaine and etidocaine, are also used, but no study has been conducted 1. Local hemorrhage into muscle to determine whether the longer duration of action of these 2. Local edema latter drugs offers any therapeutic advantage. Glucocorti- 3. Painful contraction of a taut band from inadequate MTrP costeroids and ketorolac have also been used in MTrP inactivation (missing the MTrP) injections, but they too have not been the subject of con- 4. Infection trolled studies comparing their effectiveness against either 5. Perforation of a viscus, most commonly the lung 6. Nerve injury from direct trauma by the needle local anesthetic or dry needling. Steroids have the disad7. Transient nerve block vantage that they are locally myotoxic and that repeated 8. Syncope administration of steroids can produce all the unwanted 9. Allergic reaction from the anesthetic side effects associated with them. Saline or dry needling can be performed on persons allergic to local anesthetics. Botulinum toxin has been tried successfully in MTrP inactivation, although it can cause a flulike myalgia lasting days to a week, and occasionally weakness beyond theTABLE 21.3 area of injection (Cheshire, Abashian, & Mann, 1994; Causes of Trigger Point Injection Failure Childers, 1999; Childers, et al., 1998; Yue, 1995). 1. Missing the trigger point There is no limit to the number of MTrP that can be 2. Injecting the secondary or satellite trigger point and not the needled. Common sense and patient comfort dictate primary trigger point restraint. Nevertheless, when treating a regional MPS, a3. Inadequate stretching of the muscle following the injection in the sufficient number of muscles in the region must be treated clinic to resolve the problem and allow effective postneedling 4. Inadequate stretching of the muscle by the patient at home 5. Failure to correct perpetuating factors stretching. All the muscles in a functional muscle unit

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Acupuncture is used to treat many different types ofhas a diminished height relative to the other or in the pain, including myofascial pain (Baldry, 1993). Acupunc- presence of pelvic obliquity. According to Grieve (1994), ture can be performed by the traditional method of usingthe quadratus lumborum may be less likely to develop predetermined acupuncture points along set meridians or trigger points during the teenage years, and typically, uniby the more recently developed method of placing thelateral low back pain is located on the side of the shorter needle close to the point of pain (Liao, Lee, & Ng, 1994).leg, because of early attenuation of the annulus fibrosis Japanese acupuncture (shallow needling) reduced the pain on that side. In adults, it occurs on the side of the longer of chronic myofascial neck pain in one study (Birch & leg, due to later arthrotic and spondylotic changes and Jamison, 1998). Baldry (1993) has developed a technique shortening of the quadratus lumborum. A true leg length of subdermal needling over the trigger point, while Gunn,discrepancy is corrected by placing a heel lift on the Milbrandt, Little, and Mason (1980) and Gunn, Sola, shorter leg. The asymmetry caused by a small hemipelvis Loeser, and Chapman (1990) use a method of dry needling is corrected by placing an ischial or “butt” lift under the called intramuscular stimulation (IMS). IMS involves the ischial tuberosity. insertion of the needle into the taut band without necessar- A distinction must be made between a true and an ily considering the actual trigger point. It may be combinedapparent leg length discrepancy. An apparent leg length with electrical stimulation delivered through the needlediscrepancy or functional shortening may be caused by a (percutaneous electroneural stimulation). pseudo-scoliosis where the legs are actually of equal or nearly equal length, by hip adductor contractures, by hip capsule tightness, or by posterior innominate rotation, MECHANICAL PERPETUATING FACTORS because the acetabulum is anterior to the iliosacral rotation Biomechanical perpetuating factors have long been known axis (LeVeau, 1994; Mitchell, 1993; Reid, 1992). The to cause persistent musculoskeletal pain (Simons et al., cause must be identified and then corrected where possi1999; Travell & Simons, 1992). Major mechanical factorsble. If the problem is an ilial rotation, the rotation should to be considered in the management of MPS include anabe corrected. If it is combined with a sacroiliac joint tomic variations, poor posture, and work-related stressdysfunction, that should be corrected as well. Quadratus (Simons & Simons, 1994). lumborum or iliopsoas muscles shortened by trigger points, a cause of pseudo-scoliosis, must be inactivated CORRECTION OF ANATOMIC VARIATIONS by stretching or by other means, such as MTrP injections. Placing a heel lift under an apparent shorter leg may According to Simons et al. (1999), the most common anaincrease the leg length discrepancy. Functional shortening, tomic variations are leg length discrepancy and small pseudo-scoliosis, and pelvic obliquity can be corrected via hemipelvis, the short upper arm syndrome, and the long osteopathic mobilizations and muscle energy techniques second metatarsal syndrome. (Fowler, 1994; Greenman, 1991). The leg length inequality syndrome produces a pelvic When clinical determination by physical examination tilt that results in a chronic shortening and activation of a is uncertain, a radiographic study of the pelvis and lumbar chain of muscles in an effort to straighten the head and spine utilizing a plumb line can be useful (Travell & level the eyes. Any asymmetrical position of the pelvis or Simons, 1992). A functional scoliosis can be corrected or spine requires a regulatory adjustment of the neck muscles reduced by a heel lift, even if it has been present for years. to maintain equilibrium and an appropriate head position A fixed skeletal cause of scoliosis does not correct with (Janda, 1994). The quadratus lumborum and paraspinal a heel or butt lift. Functional scoliosis must be distinmuscles contract to correct the deviation of the spine guished from those asymmetries that cannot be corrected caused by the pelvic tilt. This correction in turn causes a before attempting to use a heel or butt lift. Relief of pain tilt of the shoulder in the direction opposite to that of the in the neck, shoulder, low back, and legs can result from pelvic tilt when a simple C-shaped scoliosis occurs. The the complete or partial correction of leg length inequality shoulder and neck muscles then chronically contract and and scoliosis. shorten to correct the subsequent neck tilt. Excessive loading perpetuates MTrPs and may result in low back, head, Saggini, et al. (1996) describe the incomplete resoluneck, and shoulder pain (Gerwin, 1995a). Trigger pointstion of pain in persons with peroneus longus MTrPs and leg length inequality corrected only by a heel lift. The in these chronically shortened and constantly contracted peroneus longus has an increased shear force in the muscles are not readily inactivated until the muscles are medial-lateral plane when loading, which increases eccenunloaded. The combination of trunk muscles that undergo tric muscle involvement, leading to muscle injury. Corshortening as they constantly pull the spine toward one recting abnormal loading associated with leg length disside or the other is more complex in an S-shaped scoliosis, but the problem is the same. A similar loading of trunk,crepancy with a dynamic insole eliminated both the pain shoulder, and neck muscles occurs when one hemipelvis and the trigger points.

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Short upper arms result in forward shoulder roll, pec-posterior cervical muscles and between the anterior and toral muscle shortening, and abnormal loading of neckposterior shoulder muscles. The shoulder girdle protracts, and trunk muscles, as the individual attempts to find aand there is an increase in thoracic kyphosis, a loss of comfortable position when seated. Another cause of bio-lumbar lordosis, and an increase in posterior pelvic rotation. Muscular imbalances may lead to abnormal afferent mechanical stress on muscles that can lead to the persisinput and MTrPs (Cantu & Grodin, 2001). There is a tence of MTrPs is a long second metatarsal bone. In this situation, the normal, stable tripod support of the footstatistically significant relation between the degree of forward head posture, posterior cervical rotation, and pain created by the first and second metatarsal bones anteriorly (Haughie, Fiebert, & Roach, 1995). Poor body alignment, and the heel posteriorly may not be present. Instead, in some individuals with this foot configuration, weight is forward head posture, and muscle imbalances predispose and perpetuate chronic pain problems including MPS. carried on a knife edge from the second metatarsal head to the heel, overloading the peroneus longus that attaches Correcting poor body posture and alignment is an to the first metatarsal bone. Diagnostic callus formationimportant component of treating patients with MPS, even occurs in these individuals in the areas of abnormal loadwhen posture seemingly may not be directly related to the ing, under the second metatarsal head, and on the medial region of musculoskeletal pain. Core (trunk) stabilization aspect of the foot at the great toe and first metatarsal head. as part of a closed kinetic chain rehabilitation allows optiCorrection is accomplished with support under the head mal control of the lumbopelvic complex and improves the of the first metatarsal, restoring the normal tripod supportrecovery of persons with a kinetic chain dysfunction manof the foot (Travell & Simons, 1992 ). ifest as a postural stress syndrome (Clark, Fater, & Reuteman, 2000). Good posture minimizes stress and improves efficiency in the use of muscles (Sahrmann, POSTURE CORRECTION 1988). The physical therapist needs to determine on an In addition to postural deviations due to anatomic varia-individual basis whether manual therapy procedures tions, muscle imbalances and altered movement patterns should precede postural corrections or vice versa. In some play an extremely important role in the etiology andinstances, joint and myofascial restrictions must be management of poor posture. The clinician shouldremoved prior to any postural corrections. Without the become familiar with Vladimir Janda’ s extensive research mobilizations, shortened muscles may restrict movement in posture and muscle dysfunction. Janda distinguished so much that treatment to correct postural abnormalities “ tonic or postural”muscles from phasic “ or dynamic” may not succeed. In other cases, patients may be able to muscles. Postural and phasic muscles are physiologically alter their posture prior to or even without any manual different in their oxidative ability and their ability to therapy (Dommerholt & Norris, 1996). contract over a specifi ed time period. Tonic muscles are Correction and prevention of abnormal postures slow twitch (Type I) muscles. Phasic muscles are fastrequires a comprehensive program that includes exercises twitch (Type II) muscles. MTrPs can develop in both tonicto restore normal dynamic pelvic and vertebral stabilizaand phasic muscles. Tonic muscles include the hamstrings tion and mobility, motor control, muscle balances, muscles, rectus femoris, iliopsoas, quadratus lumborum, strength, endurance, and breathing patterns. Certain activerector spinae muscles, pectorals, sternocleidomastoids, ities of daily living may predispose a patient to chronic descending trapezius muscles, and levator scapulae. Phamusculoskeletal overload, increasing the risk of myofassic muscles include the rectus abdominus, serratus antecial dysfunction. A dynamically stable trunk in neutral rior, rhomboids, ascending and transverse trapezius, deep position is essential, as is normal pelvic mobility (Carrineck flexors, suprahyoid, and mylohyoid (Cantu & Gro- ere, 1996). Paradoxical breathing should be corrected with din, 2001; Carriere, 1996; Janda, 1983, 1993, 1994). functional abdominal breathing. Paradoxical breathing is Tonic muscles have a tendency to tighten in response to a common cause of overload of the auxiliary breathing abnormal stress or dysfunction, whereas phasic muscles muscles, most notably the scalene muscles (Travell & have a tendency to become weak. These typical response Simons, 1983; Carriere, 1996). To improve posture, the patterns result in the upper “ and lower crossed syn- individual components must be integrated into total motor dromes” (Janda, 1993, 1994). The upper crossed syn-patterns (Walpin, 1994). Both the Alexander technique drome or forward head posture is the most common pos(Barlow, 1973; Jones, 1992; Knebelman, et al., 1994) and tural deviation in patients with MPS (Fricton, et al., 1985;the Feldenkrais method (Feldenkrais, 1977; Rywerant, Janda, 1994; Mannheimer, 1994). 1983) aim to restore function to body awareness and In the forward head posture, total body alignment ismovement retraining and can be used in combination with severely affected. There is posterior cervical rotation withphysical therapy (Dommerholt, 2000). hypomobility of the upper cervical and subcranial motion Although posture is usually described in terms of relsegments and hypermobility of the mid and lower cervicalative alignment of body parts, it is important to realize spine. Muscle imbalances occur between the anterior and that a person’ s posture reflects more than just biomechan-

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ical principles. Buytendijk (1964) states that “posture isresulting in impairment of blood circulation, mechanical an individual’s innermost means of expression. ” People overload of the muscles and adjacent muscles, and express their emotions, feelings, and overall well-beingincreased risk for myofascial pain (Järvholm, et al., 1988). through their posture. Therefore, posture must be viewed Particular occupational groups at increased risk include as a physiological, biomechanical, and psychological phedata entry operators, typists (Hünting, et al., 1981), musinomenon. Addressing biomechanical issues without concians (Norris & Dommerholt, 1996), teachers and nurses sideration of a more phenomenological approach to pos(Onishi, et al., 1976), and industrial and assembly line ture reduces the treatment approach to strict mechanistic workers (Amano, et al., 1988; Silverstein, 1985). intervention. Considering work-related aspects of myofascial pain enhances treatment outcomes. Modifying the workplace WORK-RELATED STRESS or the patient’s work habits is critical. If a patient continues to be exposed to certain workplace stress factors withCertain jobs and work-related activities are associated out modification of the conditions, the potential cause of with an increased risk of developing cumulative traumamyofascial dysfunction may not be addressed adequately. disorders or work-related musculoskeletal disordersPhysical therapists and occupational therapists can con(Kuorinka & Forcier, 1995). In certain instances, MPStribute significantly to integrating basic ergonomic prinmay be associated with work exposures (Grosshandler & ciples into therapeutic practice, although specific training Burney, 1979). In the ergonomics literature, the term tenin ergonomics is indicated (Berg Rice, 1995). More comsion neck syndrome is preferred over MPS (Viikari-Juntura, plicated ergonomic problems require the assistance of 1983). Ergonomics is a broad profession and incorporates ergonomists (Ayoub, 1994; Khalil, et al., 1994). knowledge from anatomy, physiology, and psychology. More specifically, ergonomics includes anthropometry and biomechanics, work and environmental physiology,SYSTEMIC MEDICAL FACTORS and skill and occupational psychology (Singleton, 1972). The problem of unresolved or persistent MTrPs can be the Thompson (1991) defines ergonomics as “the application result of systemic medical factors that affect muscle of the human physical and behavioral sciences together with the engineering sciences in the study of humansmetabolism primarily or affect muscle function secondworking with machines and tools. ” Ergonomics is based arily. These factors can be categorized broadly as nutritional, hormonal, metabolic, infectious, autoimmune, etc. on the so-called human-machine system. In designing the An important principle that Janet Travell often emphaideal human-machine system, ergonomics recognizes four sized in her lectures is that insuf ficiency states impair the strategies, namely, stress reduction, machine and task ability of stressed or overloaded muscle to respond adedesign, match between the job demands and human abilities, and education and training (Ayoub, 1994; Khalil, etquately to therapy. Levine and Hartzell (1987) have applied this concept to vitamin C insuf ficiency. They proal., 1993). Pheasant (1991) summarizes the field as “the pose that the optimum concentration of an enzyme cofacscience of matching the job to the worker and the product tor (vitamin or mineral) is that which allows each enzyto the user. ” Awareness of generic risk factors in work-related mus-matic reaction to proceed maximally (not rate limited) culoskeletal disorders is important. They include awkwardwhen required. For example, many vitamin or mineral postures, musculoskeletal loading, task invariability, cog-enzyme cofactors, such as ascorbic acid (vitamin C) or iron, participate in a number of different enzymatic reacnitive demands, and organizational and psychosocial work characteristics (Kuorinka & Forcier, 1995). Prolongedtions that are not all equally active at any one time. However, if a limited concentration of an enzyme cofactor static postures, awkward postures, excessive force, and repetitiveness are the most likely specific risk factors forbecomes rate limiting, then the products of the associated reaction may be insuf ficient, like the underproduction of MPS (Armstrong, 1986a). Several studies havefirmed con that occupational groups with repetitive arm movementshigh-energy organic phosphates for certain iron-dependent enzymes or the underproduction of serotonin or and constrained work postures have high rates of MPS (Amano, et al., 1988; Bjelle, Hagberg, & Michaelsson,norepinephrine for certain vitamin-C-dependent enzymes. 1979; Hünting, Läubli, & Grandjean, 1981). Awkward It is postulated that the needs of the body under physical postures include wrist flexion and extension, ulnar andstress are different than when unstressed and what may radial abduction, forearm supination and pronation,be an adequate concentration of enzyme cofactor under normal conditions may be insuf ficient at times of physical extended reaches beyond the shoulder-reach envelope, and ficiency pinch grips that are either too wide or too narrow (Arm-stress. Hence, the concept of nutritional insuf strong, 1986b; Feuerstein & Hickey, 1992). For example,states is distinguished from that of disease-producing defithe intramuscular pressure in the supraspinatus muscle ciency states like scurvy, the disease associated with vitaexceeds 30 mmHg at 30 degrees flexion or abduction, min C deficiency. Vitamin C taken in the amount of

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10 mg/day prevents scurvy, but 250 mg/day is considered Thyroid hormone supplementation to restore the thyroid the optimum daily intake for good health. state may resolve many myofascial complaints and allow Four nutritional or hormonal factors have repeatedlyresolution of the problem by the usual means of physical been found to be low or in the lower quartile of the normaltherapy and trigger point inactivation. Thyroxine (levothyroxine) is generally used to treat hypothyroidism. Howrange in persons studied in our clinic who have persistent myofascial pain, namely, iron insuf ficiency, folic acid ever, not all tissues are equally able to convert thyroxine insufficiency, vitamin B12 insuf ficiency, and thyroid hor- to triiodothyronine, the active form of thyroid hormone. mone insufficiency. Of women with a chronic sense of The addition of triidothyronine to thyroxine has been coldness and chronic myofascial pain, 65% have a lowshown to result in an improved sense of well-being; an normal or below normal serum level of ferritin, largely improvement in cognitive function and mood; and an from an iron intake insuf ficient to replace menstrual iron increase in serum levels of sex-hormone-binding globuloss. Other causes of low serum ferritin include blood losslins, a sensitive marker of thyroid hormone function associated with chronic intake of mixed cyclooxygenase(Bunevicius, et al., 1999; Toft, 1999). (COX)-1 and -2 nonsteroidal anti-inflammatory drugs, and Other less commonly associated medical problems gastrointestinal blood loss associated with parasitic dis-that are found in patients with chronic MPS and that act ease. Ferritin represents the tissue-bound nonessential iron as perpetuating factors include recurrent candida yeast stores in the body that supply the essential iron for oxygen infections, particularly in women who have been given transport and iron-dependent enzymes. Serum levels of 15 courses of antibiotic therapy for recurrent urinary tract to 20 ng/ml mean that muscle and other storage sites for infections. Persons with myofascial pain dysfunction syniron (liver and bone marrow) are depleted of ferritin. Ane-dromes affecting the temporal mandibular joint often commia is common at levels of 10 ng/ml or less. The disease plain of sore throat or earache and may be given antibiof iron deficiency is anemia. Symptoms of iron insuf fiotics, thereby predisposing them to candida overgrowth. ciency are fatigue, muscle cramps, and coldness. The assoWomen who present with widespread MTrPs resistant to ciation between iron insuf ficiency and chronic myofascial usual treatment should be investigated for candida infecpain suggests that iron-requiring enzymatic reactions liketion. If the history is very suggestive, treatment is indireduced nicotinamide adenine dinucleotide (NADH) cated even if the organism cannot be implicated by hangdehydrogenases and the cytochrome oxidase reaction may ing drop examination or culture. Men and postmenopausal be limited in such persons. This may in turn produce anwomen who have elevated uric acid levels may also have energy crisis in muscle when it is overloaded and thereby persistent MTrPs. Parasitic infections can also be associproduce metabolic stress. MTrPs may not easily resolve ated with widespread MTrPs, often complicated by fatigue in such circumstances. Iron supplementation in persons and an often nonspecific sense of discomfort, and occawith chronic MPSs and serum ferritin levels below 30sionally gastrointestinal distress. Amoebiasis is the most ng/ml prevents or corrects these symptoms. common parasite encountered in MPS in the United Vitamin B12 and folic acid metabolism are closely States, but giardia, trematode, and nematode infection related. They function not only in erythropoiesis but alsohave also been found. Treatment of these infections results in central and peripheral nerve formation. Studies havein an overall improvement, and often in a diminution of the extent of trigger point involvement of muscle. Of shown that in a subset of patients, serum levels of vitamin course, persons with osteoarthritis, rheumatoid arthritis, B12 as high as 350 pg/ml may be associated with a metabolic deficiency manifested by elevated serum or urineSjögren’s syndrome, carpal tunnel syndrome, or periphmethylmalonic acid or homocysteine and may be clini-eral neuropathy caused by diabetes mellitus are more cally symptomatic (Pruthi & Tefferi, 1994). Preliminary prone to develop MTrP. The postlaminectomy syndrome studies show that 16% of patients with chronic MPS eitheris frequently caused by MTrP. Treatment is always were deficient in vitamin B12 or had insuf ficient levels of directed toward the underlying condition, as well as the vitamin B12, and that 10% had low serum folate levelstrigger point where possible. (Gerwin, 1995b). Replacement of vitamin B12 is lifeSleep disturbance can be a major factor in the perpetlong, either orally, transmucosally, or intramuscularly. uation of musculoskeletal pain. Pain is magnified in the Hypothyroidism is suspected clinically in chronic presence of insomnia, whether the insomnia is caused by MPS when there is a complaint of coldness, dry skin orpain or by other factors. There is the rare case in which dry hair, constipation, and fatigue. Hypothyroidism chronic musculoskeletal pain is eliminated by the restooccurred in 10% of chronic MPS subjects in one studyration of normal sleep when caffeine was reduced or elim(Gerwin, 1995b). The MTrPs tend to be widespread ininated from the diet. More often, however, sleep must be hypothyroid persons. The thyroid-stimulating hormoneaddressed directly, noting that sleep disturbance is (TSH) level may only be in the upper range of normal,increased in persons with chronic pain. Attention is paid but, as shown by thyroid-releasing hormone (TRH) stim-to pain control at night, to sleep apnea, and to mood ulation tests, may still be abnormal for a given individual.disorders like depression or anxiety. 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Armstrong, T.J. (1986a). Ergonomics and cumulative trauma pharmacological and nonpharmacological. Pharmacologdisorders: Symposium on occupational injuries. Hand ical treatment utilizes drugs that promote a normal sleep Clinics of North America, (3), 2 553–565. architecture, induce and maintain sleep through the night, Armstrong, T.J. (1986b). Upper extremity posture: Definition, and do not cause daytime sedation. Nonpharmacological measurement and control. In N. Corlett, J. Wilson, & I. treatment emphasizes sleep hygiene, such as using the bed Manenica (Eds.),The ergonomics of working postures: only for sleep and sex, and not for reading, television Models, methods, and cases . Proceedings of the First viewing, and eating (Menefee, et al., 2000). International Occupational Ergonomics Symposium, Psychological stress may aggravate MPS and activate Zadar, Yugoslavia, 1985. London: Taylor & Francis. MTrP (Lewis, et al.,1994; McNulty, et al., 1994). Trigger Ayoub, M.A. (1994). Ergonomic considerations in the workpoint EMG activity has been shown to increase dramatiplace. In C.D. Tollison, J.R. Satterthwaite, & J.W. Tollison (Eds.), Handbook of pain management (pp. cally in response to mental and emotional stress, whereas 640–666). Baltimore: Williams & Wilkins. adjacent nontrigger point muscle EMG activity remained Baldry, P.E. (1993).Acupuncture, trigger points and musculosknormal. Thus, the effect of stress on the trigger point can eletal pain. Edinburgh: Churchill Livingstone. be highly selective, instead of generalized throughout the Banks, S.L., et al. (1998). Effects of autogenic relaxation training muscle. MPS may be the major symptomatic expression on electromyographic activity in active myofascial trigof psychological distress. In addition, pain-related fear and ger points.Journal of Musculoskeletal Pain(4), 6 23–32. avoidance can lead to the development of a chronic musBarlow, W. (1973). The Alexander technique. New York: Alfred culoskeletal pain problem (Vlaeyen & Linton, 2000). A. Knopf. Treatment directed toward reducing stress has been shown Berg Rice, V.J. (1995). Ergonomics: An introduction. In K. to diminish MPS symptoms (Banks, et al., 1998). The Jacobs & C.M. Bettencourt (Eds.), Ergonomics for therclinician must be sensitive to this possibility and refer the apists (pp. 3–12). Boston: Butterworth-Heinemann. patient for psychological counseling when appropriate. Birch, S., & Jamison, R.N. (1998). Controlled trial of Japanese acupuncture for chronic myofascial neck pain: Assessment of specific and nonspecific effects of treatment. SUMMARY Clinical Journal of Pain, 14,248–255. Bjelle, A., Hagberg, M., & Michaelsson, G. (1979). Clinical and In summary, treatment of MPS begins with the identifi caergonomic factors in prolonged shoulder pain among tion of the MTrP as a source of the pain or as a contributing industrial workers.Scandanavian Journal of Work Envifactor, and a delineation of the extent of the problem. The ronment and Health, 5, 205–210. problem may be confi ned to a few muscles or may be more Bogduk, N., & Simons, D.G. (1993). Neck pain: Joint pain or widespread, regional, or generalized. Direct inactivation of trigger points. In H. Værøy & H. Merskey (Eds.), Progress in fibromyalgia and myofascial pain (pp. the MTrP is accompanied by correction of mechanical and 267–273). Amsterdam: Elsevier. systemic medical factors that contribute to the development of the syndrome. Exercise to restore physical conditioningBunevicius, R., et al. (1999). Effects of thyroxine as compared with thyroxine plus triiodothyrinine in patients with reduces the chances of recurrence. Persons with chronic hypothyroidism. New England Journal of Medicine, MPS who have not responded as expected to appropriate 340, 424–429. therapy must be evaluated for further mechanical, medical, Butler, D.S. (2000).The sensitive nervous system . Adelaide, or psychological problems that have been associated with Australia: Noigroup publications. persistent MPS. Attention to the postural and physicalBuytendijk, F.J.J. (1964). Algemene theorie der menselijke houdstresses of work and awareness of the effect that psychoing en beweging . Utrecht, The Netherlands: Het Speclogical stress has on muscle pain identify those areas that trum. need to be addressed. These problems must be corrected Cantu, R.I., & Grodin, A.J. (2001). Myofascial manipulation: or alleviated to effectively treat the MPS. Effective treatTheory and clinical application(2nd ed.). Gaithersburg, MD: Aspen Publishers. ment can be provided through the application of a variety Carlstedt, C.A., & Nordin, M. (1989). Biomechanics of tendons of manual techniques, by invasive inactivation of the trigand ligaments. In M. Nordin & V.H. Frank (Eds.), Basic ger point, and by carefully identifying and correcting the biomechanics of the musculoskeletal system (pp. 59–74). factors that interfered with recovery. Philadelphia: Lea & Febiger. Carriere, B. (1996). Therapeutic exercise and self-correction programs. In T.W. Flynn (Ed.), The thoracic spine and rib REFERENCES cage: Musculoskeletal evaluation and treatment (pp. 287–307). Boston: Butterworth-Heinemann. Amano, M., et al. (1988). Characteristics of work actions of shoe manufacturing assembly line workers and a cross sec-Chen, J.-T., et al. (1998). Phentolamine effect on the spontaneous tional factor control study on occupational cervicobraelectrical activity of active loci in a myofascial trigger chial disorders.Japanese Journal of Industrial Health, spot of rabbit skeletal muscle. Archives of Physical and Medical Rehabilitation, 79,790–794. 30(1), 3–12.

246

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Cheshire, W.P., Abashian, S.W., & Mann, J.D. (1994). BotulinumFeuerstein, M., & Hickey, P.F. (1992). Ergonomic approaches in the clinical assessment of occupational musculoskeletal toxin in the treatment of myofascial pain syndrome. disorders. In D.C. Turk & R. Melzack (Eds.), Handbook Pain, 59, 65–69. of pain assessment (pp. 71–99). New York: The Guilford Childers, M.K., et al. (1998). Treatment of painful muscle synPress. dromes with botulinum toxin: A review. Journal of Back Fischer, A.A. (1984). Diagnosis and management of chronic pain and Musculoskeletal Rehabilitation, 10, 89–96. in physical medicine and rehabilitation. In A.P. Ruskin Childers, M.K., Wilson, D.J. & Simison, D. (1999). Use of (Ed.),Current therapy in psychiatry (pp. 123–145). Philbotulinum toxin type A in pain management (pp. adelphia: W. B. Saunders. 30–50). Columbia, MO: Academic Information SysFischer, A.A. (1986a). Pressure threshold measurement for diagtems. nosis of myofascial pain and evaluation of treatment Chu, J. (1995). Dry needling (intramuscular stimulation) in myoresults.Clinical Journal of Pain, 2 (4), 207–214. fascial pain related to lumbosacral radiculopathy. EuroFischer, A.A. (1986b). Pressure threshold meter: Its use for quanpean Journal of Physical and Medical Rehabilitation, tification of tender spots. Archives of Physical and Med5(4), 106–121 ical Rehabilitation, 67 , 836–838. Clark, M.A., Fater, D., & Reuteman, P. (2000). Core (trunk) Fischer, A.A. (1986c). Pressure tolerance over muscles and stabilization and its importance for closed kinetic chain bones in normal subjects. Archives of Physical and Medrehabilitation.Orthopaedic Physical Therapy Clinics of ical Rehabilitation, 67 , 406–409. North America, 9 (2), 119–135. Fischer, A.A. (1993).Pressure threshold and tolerance meter Dejung, B. (1987a). Die Verspannung des M. iliacus als Ursache (manual). Great Neck, NY: Pain Diagnostics & Therlumbosacraler Schmerzen.Manuelle Medizin, 25, mography. 73–81. Fischer, A.A. (1995). Local injections in pain management; trigDejung, B. (1987b). Verspannungen des M. serratus anterior als ger point needling with infiltration and somatic blocks. Ursache interscapularer Schmerzen. Manuelle Medizin, In G.H. Kraft & S.M. Weinstein (Eds.), Injection tech25, 97–102. niques: Principles and practice (pp. 851–870). PhilaDejung, B. (1988a). Die Behandlung “chronischer Zerrungen. ” delphia: W. B. Saunders. Schweizerische Zeitschrift fur Sportmedizin,16–168. 36, Fischer, A.A. (1997). New developments in diagnosis of myoDejung, B. (1988b). Triggerpunkt-und Bindegewebebehandlung fascial pain and fibromyalgia. Physical Medicine and neue Wege in Physiotherapie und RehabilitationsRehabilitation Clinics of North America,(1), 8 1–21. medizin. Physiotherapeutics, 24 (6), 3–12. Fowler, C. (1994). Muscle energy techniques for pelvic dysfunction. In J.D. Boyling & N. Palastanga (Eds.), Grieve’s Dejung, B. (1994). Manuelle Triggerpunktbehandlung bei chromodern manual therapy(pp. 781–791). Edinburgh: nischer Lumbosakralgie.Schweizerische Medizinische Churchill Livingstone. Wochenschrift, 124(Suppl. 62), 82– 87. Delaney, G.A., & McKee, A.C. (1993). Inter- and intra-rater Fricton, J. R. (1990). Myofascial pain syndrome: Characteristics and epidemiology.Advances in Pain Research and Therreliability of the pressure threshold meter in measureapy, 17, 107–128. ment of myofascial trigger point sensitivity. American Fricton, J.R., Kroening, R., Haley, D., et al. (1985). Myofascial Journal of Physical and Medical Rehabilitation, 72, pain syndrome of the head and neck: A review of clinical 136–139. characteristics of 164 patients. Oral Surgery, Oral MedDommerholt, J. (2000). Posture. In R. Tubiana & P. Amadio icine, and Oral Pathology, 60 (10), 615–623. (Eds.), Medical problems of the instrumentalist musiGam, A.N., et al. (1998). Treatment of myofascial trigger point cian (pp. 399–419). London: Martin Dunitz. with ultrasound combined with massage and exercise in Dommerholt, J. (2001). Muscle pain syndromes. In R.I. Cantu a randomized controlled trial. Pain, 77, 73–79. and A.J. Grodin (Eds.),Myofascial manipulation(pp. Gerwin, R. (1995a). Myofascial back and neck pain. In M.A. 93–140). Gaithersburg: Aspen. Young & R.A. Lavin (Eds.),Physical medicine and Dommerholt, J., & Norris, R.N. (1996). Physical therapy manrehabilitation state of the art reviews(Vol. 9, pp. agement of the injured musician. Orthopaedic Physical 657–671). Philadelphia: Hanley & Belfus. Therapy Clinics of North America, 5, 185–206. Gerwin, R. (1995b). A study of 96 subjects examined both for ˇ J., & Dvorák, ˇ V. (1990). Manual medicine: DiagnosDvorák, fibromyalgia and myofascial pain. Journal of Muscutics. Stuttgart, Germany: Georg Thieme Verlag. loskeletal Pain, (3Suppl. 1), 121. Dwyer, A., Aprill, C., & Bogduk, N. (1990). Cervical zygopo- Gerwin, R.D., et al. (1997). Interrater reliability in myofascial physeal joint pain patterns. 1. A study in normal voluntrigger point examination.Pain, 69, 65–73. teers.Spine, 15 (6), 453–457. Gerwin R.D. (1999). Differential diagnosis of myofascial pain Ellis, J.J., & Johnson, G.S. (1996). Myofascial considerations in syndrome and fibromyalgia. Journal of Musculoskeletal somatic dysfunction of the thorax. In T.W. Flynn (Ed.), Pain 7, 209–215. The thoracic spine and rib cage (pp. 211–262). Boston: Gerwin, R.D. (2000). Management of persons with chronic pain. Butterworth-Heinemann. In M.N. Ozer (Ed),Management of persons with chronic neurologic illness(pp. 265–290) Boston: ButterworthFeldenkrais, M. (1977).Awareness through movement. New Heinemann. York: Harper and Row.

Treatment of Myofascial Pain Syndromes

247

Janda, V. (1993). Muscle strength in relation to muscle length, Ghia, J.N. (1992). Development and organization of pain centers. pain, and muscle imbalance. In K. Harms-Rindahl (Ed.), In P. P. Raj (Ed.),Practical management of pain (pp. Muscle strength(pp. 83–91). New York: Churchill Liv16–39). St. Louis: Mosby-Year Book. ingstone. Greenman, P.E. (1991). Osteopathic manipulation of the lumbar Janda, V. (1994). Muscles and motor control in cervicogenic spine and pelvis. In A.H. White & R. Anderson (Eds.), disorders: Assessment and management. In R. Grant Conservative care of low back pain (pp. 200–215). Bal(Ed.), Physical therapy of the cervical and thoracic timore: Williams & Wilkins. spine (pp. 195–216). New York: Churchill Livingstone. Grieve, G.P. (1994). The masqueraders. In J.D. Boyling & N. Järvholm, U., et al. (1988). Intramuscular pressure in the Palastanga (Eds.), Grieve’s modern manual therapy (pp. supraspinatus muscle. Journal of Orthopaedic Research, 841–856). Edinburgh: Churchill Livingstone. 6, 230–238. Grosjean, B., & Dejung, B. (1990). Achillodynie ein unlosbäres Problem?Schweizerische Zeitschrift für Sportmedizin, Jensen, K., et al. (1986). Pressure pain threshold in human temporal pain. Evaluation of a new pressure algometer. Pain, 38, 17–24. 25, 313–323. Grosshandler, S., & Burney, R. (1979). The myofascial pain Jones, F.P. (1992). Body awareness in action. In M. Murphy syndrome. North Carolina Medical Journal, 40, (Ed.), The future of the body . Los Angeles: Jeremy P. 562–565. Tarcher. Gunn, C.C., Milbrandt, W.E., Little, A.S., & Mason, K.E. (1980). Jones, M.A. (1994). Clinical reasoning process in manipulative Dry needling of muscle motor points for chronic lowtherapy. In J. D. Boyling & N. Palastanga (Eds.), back pain.Spine, 5,279–291. Grieve’s modern manual therapy (pp. 471–482). EdinGunn, C.C., Sola, A.E., Loeser, J.D., & Chapman, C.R. (1990). burgh: Churchill Livingstone. Dry-needling for chronic musculoskeletal pain syn- Keele, K.D. (1954). Pain-sensitivity tests: Pressure algometers. dromes clinical observations. Acupuncture, 1,9–15. . Lancet, 1,636–639. Harden, R.N., et al. (2000). Signs and symptoms of the myofasKhalil, T.M., et al. (1993).Ergonomics in back pain. New York: cial pain syndrome: A national survey of pain manageVan Nostrand Reinhold. ment providers.Clinical Journal of Pain, 16,64–72. Khalil, T.M., et al. (1994). The role of ergonomics in the preHaughie, L.J., Fiebert, I.M., & Roach, K.E. (1995). Relationship vention and treatment of myofascial pain. In E. S. Rachof forward head posture and cervical backward bending lin (Ed.), Myofascial pain and fibromyalgia: Trigger to neck pain.Journal of Manual and Manipulative Therpoint management(pp. 487–523). St. Louis: Mosbyapy, 3(3), 91–97. Year Book. Hendler, N., Fink, H., & Long, D. (1983). Myofascial syndrome: Knebelman, S., Ralson Dressler, P., Mathews Brion, M., et al. (1994). The essentials of the Alexander technique. In H. Response to trigger-point injections. Psychosomatics, Gelb (Ed.), New concepts in craniomandibular and 24, 990–999. chronic pain management(pp. 177–185). London: Higgs, J., & Jones, M. (1995). Clinical reasoning. In J. Higgs & Mosby-Wolfe. M. Jones (Eds.),Clinical reasoning in the health professions(pp. 3–23). Oxford: Butterworth-Heinemann. Knott, M., & Voss, D.E. (1968).Proprioceptive neuromuscular facilitation. New York: Hoeber. Hong, C.-Z. (1993). Myofascial trigger point injection. Critical Kodratoff, Y., & Gaebler, T. (1993).Meridian shiatsu. Basel: Reviews in Physical Medicine and Rehabilitation, 5(2) Sphinx Verlag. 203–217. Kuorinka, I., & Forcier, L. (1995).Work related musculoskeletal Hong, C.-Z. (1994a). Considerations and recommendations disorders (WMSDs): A reference book for prevention . regarding myofascial trigger point injection. Journal of Bristol: Taylor & Francis. Musculoskeletal Pain, 2, 29–59. Lehn, C. (1990). Massage. In W.E. Prentice (Ed.), Therapeutic Hong, C.-Z. (1994b). Lidocaine injection versus dry needling to modalities in sports medicine (pp. 257–285). St. Louis: myofascial trigger point.American Journal of Physical Times Mirror/Mosby. and Medical Rehabilitation, 73, 256–263. LeVeau, B. (1994). Hip. In J.K. Richardson & Z.A. Iglarsh Hubbard, D.R., & Berkoff, G.M. (1993). Myofascial trigger (Eds.), Clinical orthopaedic physical therapy(pp. points show spontaneous needle EMG activity. Spine, 333–398). Philadelphia: W.B. Saunders. 18, 1803–1807. Levine, M., & Hartzell, W. (1987). Ascorbic acid: The concept Hünting, W., Läubli, T., & Grandjean, E. (1981). Postural and of optimum requirements. Third Conference on Vitamin visual loads at VDT workplace. 1. Constrained postures. C. Annals of the New York Academy of Science, 498, Ergonomics, 24 (12), 917–931. 424–444. Jaeger, B., & Reeves, J.L. (1986). Quantification of changes in Lewis, C., et al. (1994). Needle trigger point and surface frontal myocardial trigger point sensitivity with the pressure EMG measurements of psychophysiological responses algometer following passive stretch. Pain, 27,203–210. in tension-type headache patients. Biofeedback and SelfJanda, V. (1983). Muscle function testing. London: Butterworths. Regulation, 3,274–275. Lewit, K. (1988). Postisometric relaxation in combination with Janda, V. (1991). Muscle spasm: A proposed procedure for difother methods of muscular facilitation and inhibition. ferential diagnosis.Journal of Manual Medicine, 6, Manuelle Medizin, 2,101–104. 136–139.

248

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Lewit, K. (1991).Manipulative therapy in rehabilitation of the Pruthi, R.K., & Tefferi, A. (1994). Pernicious anemia revisited. Mayo Clinic. Proceedings, 69, 144–150. locomotor system . Oxford: Butterworth-Heinemann. Lewit, K., & Simons, D.G. (1984). Myofascial pain: Relief by Reeves, J.L., Jaeger, B., & Graff-Radford, S.B. (1986). Reliability of the pressure algometer as a measure of myofascial post-isometric relaxation.Archives of Physical and trigger point sensitivity.Pain, 24, 313–321. Medical Rehabilitation, 65,452–456. Reid, D.C. (1992).Sports injury assessment and rehabilitation. Liao, S.J., Lee, M.H.M., & Ng, L.K.Y. (1994). Principles and New York: Churchill Livingstone. practice of contemporary acupuncture. New York: MarRosomoff, H.L., et al. (1989). Myofascial findings with patients cel Dekker. with “chronic intractable benign pain” of the back and Mannheimer, J.S. (1994). Prevention and restoration of abnormal neck. Pain Management, 3, 114–118. upper quarter posture. In H. Gelb (Ed.), New concepts Rywerant, Y. (1983).The Feldenkrais method: Teaching by hanin craniomandibular and chronic pain management (pp. dling. New Canaan, CT: Keats Publishing. 93–161). London: Mosby-Wolfe. Masi, A.T. (1993). Review of the epidemiology and criteria of Saal, J.A., & Saal, J S. (1991). Rehabilitation of the patient. In A.H. White & R. Anderson (Eds.), Conservative care of fibromyalgia and myofascial pain syndrome: Concepts low back pain (pp. 21–34). Baltimore: Williams & of illness in populations as applied to dysfunctional synWilkins. dromes. In S. Jacobsen, B. Danneskiold-Samsøe, & B. Lund (Eds.),Musculoskeletal pain, myofascial pain syn- Saggini, R., et al. (1996). Myofascial pain syndrome of the peroneus longus: Biomechanical approach. The Clinical drome, and the fibromyalgia syndrome (pp. 113–136). Journal of Pain, 12, 30–37. Binghampton: Haworth Press. TMJ McCall, I.W., Park, W.M., & O’Brien, J.P. (1979). Induced pain Sahrmann, S.A. (1988). Adult posturing. In S. Kraus (Ed.), disorders: Management of the craniomandibular comreferral from posterior lumbar elements in normal subplex (pp. 295–309). New York: Churchill Livingstone. jects. Spine, 4, 441–446. Silverstein, B.A. (1985).The prevalence of upper extremity McNulty, W., et al. (1994). Needle electromyographic evaluation cumulative trauma disorders in industry . Unpublished of trigger point response to a psychological stressor. Ph.D. thesis, University of Michigan, Ann Arbor. Psychophysiology, 31, 313–316. Simons, D.G., Hong, C.-Z., & Simons, L. (1995). Prevalence of Melvin, J. (1980). Interdisciplinary and multidisciplinary activspontaneous electrical activity at trigger spots and conities and ACRM. Archives of Physical Medicine, 61, trol sites in rabbit muscle. Journal of Musculoskeletal 379–380. Pain, 3, 35–48. Menefee, L. A., et al. (2000). Sleep disturbance and nonmaligSimons, D.G., & Simons, L.S. (1994). Chronic myofascial pain nant chronic pain: A comprehensive review of the litersyndrome. In C.D. Tollison, J.R. Satterthwaite, & J.W. ature.Pain Medicine, 1,156–172. Tollison (Eds.), Handbook of pain management (pp. Merskey, H., & Spear, F.G. (1964). The reliability of the pressure 556–577). Baltimore: Williams & Wilkins. algometer.British Journal of Social and Clinical PsySimons, D. G., & Travell, J. G. (1984). Myofascial pain and chology, 3,130–136. dysfunction. In P. D. Wall & R. Melzack (Eds.), Textbook Miller, B. (1994). Manual therapy treatment of myofascial pain of pain (pp. 263–276). Edinburgh: Churchill Livingand dysfunction. In E.S. Rachlin (Ed.), Myofascial pain stone. and fibromyalgia: Trigger point management (pp. Simons, D.G., Travell, J.G., & Simons, L.S. (1999). Myofascial 415–454). St. Louis: Mosby-Year Book. pain and dysfunction: The trigger point manual (Vol. Mitchell, F.L. (1993). Elements of muscle energy technique. In 1). Baltimore: Williams & Wilkins. 2nd edition. J.V. Basmajian & R. Nyberg (Eds.), Rational manual Singleton, W.T. (1972).Introduction to ergonomics.Geneva: therapies (pp. 285–321). Baltimore: Williams & World Health Organization. Wilkins. Skootsky, S.A., Jaeger, B., & Oye, R.K. (1989). Prevalence of Nolan, R.A., & Nordhoff, L.S. (1996). Basic concepts of soft myofascial pain in general internal medicine practice. tissue healing and clinical methods to document recovWestern Journal of Medicine, 151, 157–160. ery. Part 1. Soft tissue injury repair. In L.S. Nordhoff Soderberg, G.L. (1992). Skeletal muscle function. In D.P. Currier (Ed.), Motor vehicle collision injuries(pp. 131–141). & R.M. Nelson (Eds.),Dynamics of human biologic Gaithersburg, MD: Aspen Publishers. tissues(pp. 74–96). Philadelphia: F. A. Davis. Norris, R.N., & Dommerholt, J. (1996). Applied ergonomics: Thompson, D.A. (1991). Ergonomics. In A.H. White & R. Adaptive equipment and instrument modification for Anderson (Eds.),Conservative care of low back pain. musicians. Orthopaedic Physical Therapy Clinics of Baltimore: Williams & Wilkins. North America, 5,159–183. Toft, A.D. (1999). Thyroid hormone replacement-one hormone Ohrbach, R., & Gale, E.N. (1989). Pressure pain thresholds in or two? (Editorial).New England Journal of Medicine, normal muscles: Reliability, measurement effects, and 340, 469–470. topographic differences. Pain, 37, 257–263. Travell, J. (1976). Myofascial trigger points: Clinical view. In J. Onishi, N., et al. (1976). Shoulder muscle tenderness and physJ. Bonica, et l. (Eds.),Advances in pain research and ical features of female industrial workers. Journal of therapy (pp. 919–926). New York: Raven Press. Human Ergology, 5,87–102. Travell, J.G., & Simons, D.G. (1992). Myofascial pain and dysfunction: The trigger point manual. Baltimore: Williams Pheasant, S. (1991). Ergonomics, work and health. Gaithersburg, & Wilkins. MD: Aspen Publishers.

Treatment of Myofascial Pain Syndromes

249

Tsujii, Y. (1993).Myotherapy: Treatment of muscle hardenings. Walpin, L.A. (1994). Posture: The process of body use; principles and determinants. In H. Gelb (Ed.), New concepts Nagoya, Japan: Nagoya University College of Medical in cranio-mandibular and chronic pain management Technology. (pp. 13–76). London: Mosby-Wolfe. Turk, D.C., & Rudy, T.E. (1994). A cognitive-behavioral perArthrokinetic therapy: Improving muscle spective on chronic pain: Beyond the scalpel andWarmerdam, A. (1992). performance through joint manipulation. Paper presyringe. In C. D. Tollison, J. R. Satterthwaite, & J. W. sented at the Proceedings of the 5th International ConTollison (Eds.), Handbook of pain management (pp. ference of the International Federation of Orthopaedic 136–151). Baltimore: Williams & Wilkins. Manipulative Therapists, Vail, CO. Turk, D.C., & Okifuji, A. (1999) Assessment of patients' reporting of pain: An integrated perspective. Lancet, 353, Wells, P.E. (1994). Manipulative procedures. In P.E. Wells, V. Frampton, & D. Bowsher (Eds.), Pain management by 1784–1788. physical therapy(pp. 187–212). Oxford: ButterworthViikari-Juntura, E. (1983). Neck and upper limb disorders among Heinemann. slaughterhouse workers. Scandanavian Journal of Work Wolfe, F., et al. (1990). The American College of Rheumatology Environment and Health, 9, 283–290. 1990 criteria for the classification of fibromyalgia. Vis, A J., Raats, G.J., & Van der Voort, E.J. (1987). MassageReport of the multicenter criteria committee. Arthritis therapie: Een fysiotherapeutische handelen. Zevenaar, and Rheumatism, 33, 160–172. The Netherlands: Van der Voort. Vlaeyen, J.W.S. & Linton, S.J. (2000). Fear-avoidance and itsYue, S.K. (1995). Initial experience in the use of botulinum toxin for the treatment of myofascial related muscle dysfuncconsequences in chronic musculoskeletal pain: A state tions. Journal of Musculoskeletal Pain,(Suppl. 3 1), 22. of the art.Pain, 85, 317–332.

22 Chronic Pelvic Pain Andrea J. Rapkin, M.D. and Julie Jolin, M.D. INTRODUCTION

(sacral) fibers are probably of secondary importance for pain transmission from the pelvic organs. These latter Chronic pelvic pain is, by definition, pain that persists fornerves have their cell bodies in the sacral dorsal root ganmore than 6 months. In its various forms, chronic pelvicglia (Kumazawa, 1986). The innervation of the female pain affects an estimated 12 to 15% of women in thepelvic viscera and somatic structures is depicted in United States, accounting for more than $881 millionFigure 22.1. spent each year on outpatient visits associated with this The lower abdominal wall and anterior vulva, urethra, chronic pain (Mathias, Kupperman, Liberman, Lipschutz,and clitoris are innervated by mixed (motor and sensory) & Steege, 1996). It is one of the most common but taxingsomatic nerves deriving from lumbar 1 and 2 (L1 and L2) problems in gynecologic practice. Even after a thorough(Renaer, 1981). The dorsal rami derived from L1 and L2 workup, the etiology may remain obscure, and the rela-innervate the lower back, often a region of referred pelvic tionship between certain types of pathology and the pain pain. The anus, perineum, and lower vagina are innervated response may be inconsistent and often inexplicable. In by somatic branches of the pudendal nerve, which is the patient who has no obvious pathology, it may be temptderived from the second through fourth sacral root ganglia ing to remove pelvic structures for their physiological (S2 to S4) (Renaer, 1981). variations. Approximately 12% of all hysterectomies are Pain impulses from the upper vagina, cervix, uterine performed for pelvic pain and 30% of patients who presentcorpus, inner one third of the fallopian tube, broad ligato pain clinics have already had a hysterectomy (Chamment, upper bladder, terminal ilium, and terminal large berlain & La Ferla, 1987; Reiter, 1990a). bowel travel with the thoracolumbar sympathetics via the The purpose of this chapter is to outline the anatomyvaginal, uterine, and hypogastric plexes to the hypogastric and physiology of pelvic pain and to explore the differ- nerve, through the superior hypogastric plexus and to the ential diagnosis and management of chronic pelvic pain,lower thoracic and lumbar sympathetic chain (Kumazawa, including the role of surgery, psychotherapy, and the mul-1986). The afferents then pass through the dorsal roots of tidisciplinary pain clinic. thoracic 11, 12 and lumbar 1 (T11, T12, L1) and enter the spinal cord at this level. There is some duplication of afferentfibers in the thoracolumbar and sacral regions and NEUROANATOMY AND NEUROPHYSIOLOGY there are probably some pain impulses from the upper OF PELVIC PAIN vagina, cervix, and lower uterine segment that travel in The pelvic viscera receive afferent (sensory) innervationthe pelvic nerve (nerve erigentes) via pelvic parasympaby way of the autonomic nerve trunks (Kumazawa, 1986).thetics (sacral autotomics) to spinal segments sacral 2 The major neural pathways for visceral pain from thethrough 4 (S2 to S4) (Kumazawa, 1986). Urogenital sinus female pelvic organs travel with the sympathetic nervestructures including the lower vagina, rectum, and lower bundles and have cell bodies in a thoracolumbar distribubladder are innervated by both thoracolumbar and sacral tion. Sensory afferents that travel with the parasympathetic afferents (Kumazawa, 1986). 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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Greater splanchnic nerve Lesser splanchnic nerve

Celiac artery Celiac plexus

Celiac ganglion Least splanchnic nerve

Sup. mesenteric artery, ganglion & plexus

Aorticorenal ganglion Aortic plexus Lumbar splanchnic nerves

Lumbar sympathetic ganglion & chain

Inf. mesenteric artery, ganglion & plexus

Ovarian artery, vein & plexus of nerves

Superior hypogastric plexus Right hypogastric "nerve" Parasympathetic nerves (nervi erigentes)

Ovary

Sacral splanchnic nerves

Fallopian tube

Uterine & vaginal arteries

Round ligament

Uterus

Inferior hypogastric plexus & ganglia

Uterine plexus Vagina

Vaginal plexus

FIGURE 22.1 The innervation of the female pelvic viscera.

Afferents from the ovary, outer two thirds of the fallo- nonmechanosensitive unmyelinated sacral afferents are pian tube, and upper ureter travel along the ovarian artery chemosensitive and can develop de nouveaumechano entering the sympathetic nerve chain at lumbar spinal segsensitivity (Janig, Haupt-Schade, & Kohler 1993). These ment 4 (L4) ascending with the chain to penetrate the cord usually “ silent” fibers may be activated by and sensitized at T9 and T10 (Kumazawa, 1986). The superior hypogastric by inflammation or unusually strong mechanical stimuplexus carries no afferents from the ovary that accounts for lation and may play a role in pelvic pain of urinary tract the failure of presacral neurectomy (the transection of the or gastrointestinal etiology and theoretically from the superior hypogastric nerve) to diminish lateralizing pain orinternal reproductive organs as well. pain of adnexal origin. In sum, the transmission of painful The cell bodies of the afferent axons from the pelvic stimuli from the pelvic organs relies on an intact sympa-organs are located in the dorsal (sensory) ganglia of the thetic nervous system (Cervero & Tattersall, 1986). How-spinal nerves (Fields, 1987). Before entering the spinal ever, the parasympathetic (sacral) system is crucial for urigray matter of the dorsal horn, branches of these afferent nation, defecation, and refl ex regulation of the reproductive axons may extend for two or more segments beyond the organs (Kumazawa, 1986). The role of the sacral autonomlevel at which the original axons entered the cord. Much ics in the genesis of pelvic pain remains to be delineated.of neuronal modulation occurs in the dorsal horn. EviA large proportion of the sacral afferents from thedence from animal studies indicates that supraspinal faccolon and urinary bladder are usually silent. Only 5% oftors interact at the level of the dorsal horn to modulate the colon afferents and 2.5% of bladder afferents can be sensory perception of pain from the pelvic viscera (Berkactivated by mechanical distension. A proportion of theley & Hubscher, 1995; De Groat, 1994).

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The dorsal horn is an important site of modulation of afferent input (Cervero & Tattersall, 1986). The second- TABLE 22.1 order neurons are subjected to excitatory and/or inhibitory Peripheral Causes of Chronic Pelvic Pain interactions. For example, if a visceral structure and a cutaneous (somatic) structure transmitting to the same sec-Gynecologic ond-order neuron in the dorsal horn are stimulated simulNoncyclic taneously, the second-order neuron response may be Adhesions greater than either the cutaneous or the visceral stimulus Endometriosis Salpingo-oophoritis would evoke on its own. These viscero-somatic neurons Acute tend to have larger receptiveelds fi than the somatic neuSubacute rons. There are also many more somatic second-order neuOvarian remnant syndrome rons than there are viscero-somatic neurons (Cervero & Pelvic congestion syndrome (varicosities) Tattersall, 1986). Both of these facts may account for the Ovarian neoplasms vague, poorly localizable quality of visceral pelvic pain. Pelvic relaxation

GENERAL CONSIDERATIONS

OF

VISCERAL PAIN

Cyclic

Primary dysmenorrhea Secondary dysmenorrhea The neurophysiology of pain transmission from the vis- Imperforate hymen cera (internal organs such as bowel, bladder, rectum, Transverse vaginal septum uterus, ovaries, and fallopian tubes) differs from that of Cervical stenosis somatic structures (cutaneous elements, fascia, muscles,Uterine anomalies (congenital malformation, bicornuate uterus, parietal peritoneum, mesentery, external genitalia, anus, blind uterine horn) s syndrome) urethra). Nociceptors receive pain evoked at somatic Intrauterine synechiae (Asherman’ Endometrial polyps nerves, whereas a plentitude of nonspecifi c receptors receive pain induced in the viscera (Berkley, 1994; Uterine leiomyoma Cervero, 1994). Visceral pain, in contrast to somatic pain, Adenomyosis Pelvic congestin syndrome (varicosities) is usually deep; dif ficult to localize; and frequently assoEndometriosis ciated with various autonomic reflexes such as restlessAtypical cyclic ness, nausea, vomiting, and diaphoresis (Procacci, Zoppi,Endometriosis & Maresen, 1986). Early surgical studies performed under Adenomyosis local anesthesia have shown that cutting, crushing, orOvarian remnant syndrome burning the bowel, for example, evokes no pain, whereasChronic functional cyst formation distension of muscular organs or hollow viscera, stretch- Gastrointestinal Irritable bowel syndrome ing of the capsule of solid organs, hypoxia or necrosis of Ulcerative colitis viscera, production of algesic (pain producing) subGranulomatous colitis (Crohn’ s disease) stances, rapid compression of ligaments or vessels, and Carcinoma inflammation may cause severe pain. In contrast, cutting Infectious diarrhea or crushing a somatic structure produces exquisite pain Recurrent partial small bowel obstruction that is well localized (Procacci, et al., 1986). Diverticulitis Hernia Abdominal angina PERIPHERAL CAUSES OF CHRONIC Recurrent appendiceal colic PELVIC PAIN Genitourinary Recurrent or relapsing cystourethritis ADHESIONS Urethral syndrome Interstitial cystitis The differential diagnosis of the peripheral component of Ureteral diverticuli or polyps pelvic pain is listed in Table 22.1. Laparoscopic studies Carcinoma of the bladder for the evaluation of chronic pelvic pain, would suggest Ureteral obstruction that adhesions play a prominent role. However, when these Pelvic kidney studies were performed, nonobvious sources of pelvic painNeurologic Nerve entrapment syndrome such as abdominal wall pain, irritable bowel syndrome, Neuroma and interstitial cystitis (IC) were often not excluded prior Trigger points to laparoscopy. Adhesions were present in 16 to 44% of (continued) the patients undergoing laparoscopy for chronic pelvic

pain (depending on the series) (Rapkin, 1986; Kresch,

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TABLE 22.1 (CONTINUED) Peripheral Causes of Chronic Pelvic Pain Musculoskeletal Low back pain syndrome Congenital anomalies Scoliosis and kyphosis Spondylolysis Spondylolisthesis Spinal injuries Inflammation Tumors Osteoporosis Degenerative changes Coccydynia Myofascial syndrome Fibromyalgia Systemic Acute intermittent porphyria Abdominal migraine Systemic lupus erythematosus Lymphoma Neurofibromatosis

Pain Management: A Practical Guide for Clinicians, Sixth Edition

dysfunction revealed a significant improvement in pain scores in the group without psychosocial dysfunction. The only prospective randomized study of adhesiolysis in the literature revealed no differences in the pain scores between the groups (adhesiolysis vs. no adhesiolysis). Again, post hoc analysis of the data suggested there was a significant improvement (although only on two of the three methods of pain assessment) in pain scores in the subgroup of patients with dense vascular adhesions involving small bowel (Peters, Van Dorst, Jellis, VanZuuren, Hermans, & Trimbos, 1991). Advances using a 3mm laparoscope have enabled development of “conscious pain mapping” whereby patients under local anesthesia and conscious sedation guide in determining which adhesions are those associated with pain (Palter, 1999). In an observational pain mapping study of 50 women under local anesthesia, manipulation of appendiceal and pelvic adhesions was observed to contribute significantly to pelvic pain (Almeida & Val-Gallas, 1997). Though adhesions may be prevalent in patients with chronic pelvic pain, these adhesions may or may not be the cause of pain. No prospective studies of adhesiolysis and outcome based on pain mapping have been published.

Seifer, Sachs, & Barrese, 1984; Lundberg, Wall, & ENDOMETRIOSIS Mathers, 1973; Liston, Bradford, Downie, & Kerr, 1972; Renaer, 1981). Do adhesions actually cause pelvic pain? Another “ peripheral” cause of chronic pelvic pain is Of 100 patients Kresch laparoscoped for chronic pelvicendometriosis. The actual incidence of endometriosis is pain, 38% had adhesions and 10% had bowel adhesions. unknown because many individuals undoubtedly have However, of 50 asymptomatic patients undergoing lap-endometriosis without suf ficient symptomatology to wararoscopy for sterilization, only 12% had adhesions andrant surgical intervention. It seems that the incidence of only 2% exhibited adhesions involving the bowel. Theseendometriosis is increasing. However, this apparent differences were highly significant (Kresch, et al., 1984).increase in prevalence may be a reflection of the more Keltz, et al. in a combined retrospective/prospective studyliberal use of laparoscopy and of the recognition of atypfound colon to side-wall adhesions in a higher proportionical forms of endometriosis. Endometriosis is noted in of patients (93 vs. 13%) with pelvic pain than the controlpatients undergoing laparoscopy for chronic pelvic pain group (sterilization) (Keltz, Peck, Liu, Kim, Arici, & in anywhere from 5 to 37% of the cases (Kresch, et al., Olive, 1995). 1984; Liston, et al., 1972; Lundberg, et al., 1973). In comparison, Rapkin (1986) noted that many inferThe diagnosis of endometriosis is usually made in the tility patients with severe adhesions had no pain and comthird or fourth decade; however, it has been noted to be a pared the results of laparoscopies performed on two prominent diagnosis in adolescents and women in their groups of patients — the first group complained of chronictwenties who are evaluated for chronic pelvic pain (Chatpelvic pain and the second group had infertility, withoutman & Ward, 1982). In fact, endometriosis has been sugcomplaints of pain. When evaluating both the site and gested by one study to be the etiology in up to 70% of density of adhesions, it was notable that there were no adolescents with chronic pelvic pain unresponsive to medsignificant differences between the group with chronicical treatment (Probst & Laufer, 1999). pelvic pain and asymptomatic patients in the infertility The most common symptoms of endometriosis are group. The results of this study question the role of pelvicdysmenorrhea, dyspareunia, infertility, and abnormal uteradhesions as a common cause of chronic pelvic pain (Rapine bleeding, usually from a secretory endometrium kin, 1986). If adhesions cause pain, then lysis of adhesions (Kitchen, 1985). Pelvic pain in women with endometriosis should relieve pain. A prospective noncontrolled nonran-may occur at any time in the menstrual cycle, though domized study of lysis of adhesions did not show signif-dysmenorrhea is the most classic symptom. Dysmenoricantly lower postoperative pain ratings (Steege & Scott,rhea may be so prolonged that the patient may complain of what seems like acyclic, continuous pain; beginning 7 1991). However, post hoc analysis consisting of separation of the subjects into those with and without psychosocialto 10 days before the onset of the menstrual period and

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persisting until 1 week or so after the bleeding has ceased. initially responded at 1-year follow-up (Sutton, Pooley, The patient often describes pressurelike pain and aching Ewen, & Haines, 1997).Patients who do not desire ferin the lower abdomen, back, and rectum. There may be tility may opt for radical surgery for endometriosis, which radiation of pain into the vagina, thighs, or perineum.consists of a total abdominal hysterectomy with bilateral Dyspareunia is common when the disease involves the salpingo-oophorectomy as well as removal of any residual cul-de-sac (pouch of Douglas), uterosacral ligaments, or gastrointestinal (GI), genitourinary (GU), or peritoneal rectovaginal septum. Pain with defecation (dyschezia)disease. It should be noted that patients with endometrimay also be present even in patients without direct bowel osis, who have failed hormonal or conservative surgical wall involvement. These symptoms may be due totherapy, may still benefi t from the pain management endometrial implants near the rectum. Urinary urgency,approach (Rapkin & Kames, 1987). At least 30% of frequency, and bladder pain may also be associated with patients with recurred pain after treatment of endometriurinary tract involvement. Because endometriosis may be osis do not have residual disease at the time of repeat present in unusual locations, the manifestations oflaparoscopy. endometriosis are protean (Kitchen, 1985). Usually the Endometriosis is a common finding in reproductive previously noted common symptoms and signs are present aged women, but it is clear that in many women with but, rarely, patients may complain of rectal bleeding,chronic pelvic pain and endometriosis the latter may not symptoms similar to bowel obstruction, suprapubic pain,be the cause of the pain and may be only a contributing and/or urinary symptoms (such as frequency, dysuria, or factor. There is no signifi cant correlation between the hematuria). If ureteral involvement is present, there mayamount of disease and pain severity although higher stage be flank pain, backache, or hypertension. Signs and sympdisease tends to be associated with a greater prevalence toms of an acute abdomen occur infrequently and are of and increased intensity of pain. Additionally, there is usually related to rupture of an endometrioma. no correlation between location of pain and site of Examination of patients with endometriosis may endometriotic lesions (Fukaya, Hoshiai, & Yajima, 1993) and as many as 30 to 50% of patients regardless of stage reveal tenderness and nodularity on the rectovaginal examination of the uterosacral ligaments and posterior cul-de-have no pain. However, deeply infiltrating lesions, particularly of the uterosacral ligaments, are strongly associated sac (Kitchen, 1985). Progressive disease results in findings of obliteration and fibrosis of the cul-de-sac, and fixedwith pain (Cornillie, Oosterlynck, Lauweryns, & Koninckx, 1990). Vaginal and uterosacral endometriosis has retroversion of the uterus. Enlarged ovaries (endometriobeen associated with complaints of deep dyspareunia (Vermas) with decreased mobility may be noted. Laparoscopy is necessary for definitive diagnosis ofcellini, Trespedi, De Giorgi, Cortesi, Parazzini, & Crosignani, 1996). endometriosis though the diagnosis may be suggested by Clinically it is possible to determine whether there is history and pelvic examination. A study by Ling (1999) a relationship between pain and endometriosis in a specific for the Pelvic Pain Study Group reported the ficacy ef and patient because of the hormonal sensitivity of the disease safety of medical treatment with depot leuprolide before and the potential to surgically cure disease. Clearly, pain laparoscopy based on empirical, clinical diagnosis. Ultrathat does not respond to adequate surgical and medical sound is not diagnostic and cannot differentiate an management of endometriosis should be reevaluated for endometrioma from a benign or malignant ovarian neoanother source, pain, or other contributing central factors. plasm, scattered small implants are not detectable by ultrasound. Laboratory studies are usually not specific. CA 125 and erythrocyte sedimentation rate (ESR) can be elevated PELVIC CONGESTION in women with endometriosis. Endometriosis can be treated hormonally using andro-For the last 100 years there has been waxing and waning ®), progestins, or gonadotro- interest in the role of pelvic congestion in the genesis of genic hormones (Danocrine pin-releasing hormone analogs to create pseudomenochronic pelvic pain without obvious pathology. The conpause and to atrophy ectopic endometrial implants. For cept of autonomic nervous system dysfunction leading those undergoing long-term therapy (12 month or greater), to a vascular disorder affecting the uterine and ovarian hormonal add-back therapy, norethindrone acetate with or veins was outlined by Taylor (1954). Taylor suggested without estrogen, prevents long-term hypoestrogenic side that emotional stress could lead to smooth muscle spasm effects such as bone loss (Hornstein, Surrey, Weisberg, and & congestion of the veins draining the ovaries, uterus, Casino, 1998). Laparoscopic electro- or laser surgery or and vulva. Taylor’s series of 100 cases consisted of laparotomy with resection of disease often is reserved for women in their reproductive years with the chief comtreatment of severe endometriosis. However, in a prospecplaint of lower abdominal pain. Subjects also complained tive randomized double-blinded study of 63 women withof secondary dysmenorrhea, low back pain, dyspareunia, minimal to moderate endometriosis, laparoscopic laserinfertility, and menorrhagia. Their pain was usually bilattreatment was noted to benefit 90% of those women who eral, lower pelvic in distribution, and was exacerbated

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with the menstrual period. Two thirds of the patients alsoresponse reaf firms central factors in this condition. It also complained of nervous tension, chronic fatigue, breastsuggests that hormonal suppression with MPA or gonatenderness, and spastic colon, as well as symptoms simdotropin-releasing hormone (GnRH) agonists with or ilar to the premenstrual syndrome. Personality characwithout low-dose estrogen and progestin hormone addteristics noted by Taylor included immaturity and back may be therapeutic. A few small non-controlled studdecreased sexual drive. ies have assessed the more invasive technique of transcatheter embolotherapy of the ovarian and internal iliac veins On exam, patients manifested tenderness over the uterus. The fundus of the uterus and cervix were oftento treat pelvic congestion, with results revealing good bulky and the ovaries often enlarged with multiple func-short-term success (Capasso, Simons, Trotteur, Dongelinger, Henroteaux, & Gaspard, 1997; Sichlau, Yao & tional cysts. The parametria, especially the uterosacral Vogelzang, 1994; Tarazov, Prozorovskij & Ryzhkov, ligaments, were noted to be tender and indurated. At lap1997). Long-term ef ficacy remains to be evaluated (Venarotomy, the uterus was usually soft, enlarged, and purbrux & Lambert, 1999). plish or mottled. There was increased fluid in the cul-desac and edema of surrounding subserosal connective tissue and occasionally ovarian varicosities were prominentSALPINGO-OOPHORITIS (Taylor, 1954). Salpingo-oophoritis can cause chronic pelvic pain, though The concept of pelvic congestion has been resurrected to explain chronic pelvic pain (Hobbs, 1976). Beard,patients usually present with symptoms and signs of acute or subacute infection before the pain becomes chronic. Highman, Pearce, and Reginald (1984) performed the only blinded study of venograms in patients with chronic pelvicMore commonly, a patient will present with frequent recurrent infections. pain. Larger mean ovarian vein diameters, delayed disappearance of contrast medium, and ovarian plexus conges- Sweet and Gibbs (1985) proposed criteria for making tion were present in a significantly greater proportion ofthe diagnosis of salpingitis on clinical grounds. Patients women with chronic pelvic pain without pathology than should have a history of lower abdominal pain as well as those with pathology or controls. Other diagnostic meanslower abdominal tenderness (with or without rebound), include transvaginal ultrasound, which may reveal uterinecervical motion tenderness, and adnexal tenderness. In addition, they must have one of the following: temperature enlargement, thickened endometrium, cystic ovaries, and dilated pelvic veins (Adams, Reginal, Franks, Wadsworth,greater than 38°C, leucocytosis (greater than 10,500 white blood cells per cubic millimeter); culdocentesis fluid con& Beard, 1990; Stones, Rae, Rogers, Fry, & Beard, 1990), or more recently for more detailed visualization of struc-taining white cells and bacteria on Gram stain; presence tures, magnetic resonance imaging (MRI) (Gupta &of an inflammatory mass; elevated ESR; a Gram stain from the endocervix revealing Gram-negative intracellular McCarthy, 1994). diplococci; or a monoclonal smear from the endocervical Because many patients were noted to have polycystic secretions revealing chlamydia (Sweet & Gibbs, 1985). ovaries, and all were of reproductive age, hormonal suppression consisting of a hypoestrogenic environment was Patients may complain of having had numerous episodes of pain associated with fever and may have been considered as a mode of treatment for pelvic congestion. given the diagnosis of pelvic inflammatory disease. When Medroxyprogesterone acetate (MPA) given in doses of 30 mg daily for 3 months was administered in a randomized,these episodes become recurrent, the patient is often conplacebo-controlled treatment trial for women with chronicsidered to have chronic salpingo-oophoritis, though it is pelvic pain with pelvic congestion (abnormal venograms)not clear that a chronic inflammatory condition exists. Instead, subacute or subclinical disease with recurrent (Farquhar, Rogers, Franks, Pearce, Wadsworth, & Bland, 1989). A study of 84 subjects included four separateacute infections may be present. An additional possibility groups: MPA alone, MPA and psychotherapy, placebois that the patient may not have salpingitis at all. In all plus psychotherapy, and placebo alone. MPA was signif-these situations, laparoscopy with peritoneal fluid cultures icantly more effective after the 3-month treatment periodis diagnostic, though an experienced clinician can often make the diagnosis on the basis of clinical criteria. Broad than psychotherapy or placebo. Patients reported a 50% reduction in pain in the MPA group and 33% reduction inspectrum antibiotics and anaerobic coverage represent the standard treatment of acute or recurrent salpingo-oophorpain score after receiving placebo. However, pain returned in the MPA group after stopping treatment but did notitis. Only rarely is hysterectomy and salpingo-oophorectomy required. return in the placebo group. Psychotherapy did not reduce pain in the short term, but there was a positive interaction between MPA and psychotherapy 9 months after the treatOVARIAN REMNANT SYNDROME ment was concluded. However, 9 months posttreatment, improvement was reported irrespective of the treatmentChronic pelvic pain in a patient who has had a hysterecgroup. This response coupled with a strong placebotomy and bilateral salpingo-oophorectomy for severe

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endometriosis or pelvic infl ammatory disease may be pain of primary dysmenorrhea begins a few hours prior caused by the ovarian remnant syndrome. Ovarian remto or just after the onset of menstrual owfl and usually nant syndrome results from residual ovarian cortical tissue lasts for 48 to 72 hours. The pain is laborlike with that is leftin situ after a difficult dissection in an attempt suprapubic cramping that may be accompanied by lumto perform an oophorectomy (Steege, 1987). Often the bosacral backache, pain radiating down the anterior patient has had multiple pelvic operations with the uterusthighs, nausea, vomiting, and diarrhea. and adnexa removed sequentially. Secondary dysmenorrhea, on the other hand, usually, The diagnosis is suspected on the basis of history and though not always, occurs years after menarche and may physical examination (Price, Edwards, & Buchsbaum,occur with anovulatory cycles (ACOG, 1983). The most 1990). The patient usually complains of pelvic pain thatcommon cause of secondary dysmenorrhea is endometriis often cyclic and may be accompanied by peritonealosis. Other common causes, listed in Table 22.1, include signs. The patient may have a history of flank pain andvaginal, cervical, uterine, fallopian tube, adnexal, and frequent urinary tract infections; and there is on occasionperitoneal pathology. The differential diagnosis of secondintermittent, partial bowel obstruction. The painful symp- ary dysmenorrhea includes primary dysmenorrhea and toms usually arise 2 to 5 years after surgery. Pelvic exam noncyclic pelvic pain and entails ruling out primary dysmay reveal a tender mass in the lateral region of the pelvis menorrhea and confirming the cyclic nature of the pain. and ultrasound following ovarian stimulation with 50 mg The etiology of primary dysmenorrhea has been estabdaily for 5 days of clomiphene usually confirms a masslished to be increased uterine prostaglandin production with the sonographic characteristics of ovarian tissue. In(Filler & Hall, 1970). Prostaglandin synthetase inhibitors a patient who has had bilateral salpingo-oophorectomyare effective for the treatment of primary dysmenorrhea and is not on hormonal replacement, estradiol and follicle-in 70 to 80% of the cases (The Medical Letter, 1979). For stimulating hormone (FSH) assays reveal a characteristic the patient with primary dysmenorrhea who has no conpremenopausal picture, though on occasion the remaining traindications to oral contraceptive agents and desires conovarian tissue may not be active enough to suppress FSH traception, the birth control pill is the agent of choice levels. Laparotomy and removal of residual ovarian tissue(Chan & Dawood, 1980). More than 90% of women with is necessary for treatment (Pettit & Lee, 1988). Impor-primary dysmenorrhea have relief with birth control pills. tantly, it has been shown that those who have achieved If the patient does not respond to prostaglandin synpain relief with GnRH-agonist hormonal therapy prior to thetase inhibitors and does not desire oral contraceptive surgery, are usually those who also receive relief withpills for contraception, or if either of them are contrainsurgical removal of the remnant (Carey & Slack, 1996). dicated, narcotic analgesics should be administered for 2 to 3 days per month. Prior to the addition of narcotic medication, psychological factors and other organic CYCLIC PELVIC PAIN pathology should be ruled out. Other modes of hormonal Cyclic pelvic pain consists of primary and secondary dys-menstrual suppression include high dose progestins (oral or depo intramuscular injection) continuous oral contramenorrhea but also includes atypical cyclic pain, such as pain beginning 1 week prior to menses and lasting for upceptive pill administration, or GnRH agonists with or to 1 week following the cessation of menstrual flow with without continuous low-dose hormone (menopausal dosoccasional midcycle pain as well. Atypical cyclic pain is age) add back. Breakthrough bleeding and associated pain are potential problems with these regimens. a variant of secondary dysmenorrhea. The diagnosis of cyclic pain often depends on the review of a daily pain A patient with dysmenorrhea who does not respond diary that patients should be asked to maintain. With theto prostaglandin synthetase inhibitors and/or birth control availability of nonsteroidal anti-inflammatory agents andpills and in whom organic disease has been ruled out may compounds that alter the female sex steroids, cyclic pelvic also respond to the pain management approach and, in pain has become significantly more manageable. particular, acupuncture or transcutaneous electrical nerve Dysmenorrhea ordifficult “ monthly flow” is a com- stimulation (Helms, 1987; Mannheimer & Whaler, 1985). mon gynecologic disorder affecting up to 50% of men-In one study, Kaplan, et al., (1994) reported a 30% marked struating women (American College of Obstetricianspain relief, 60% moderate pain relief, and 10% no pain and Gynecologists, 1983). Primary dysmenorrhea refers relief in women with primary dysmenorrhea undergoing to pain with menses when there is no pelvic pathology,transcutaneous electrical nerve stimulations (TENS). To whereas secondary dysmenorrhea is painful menses more fully evaluate the evidence for treating primary dyswith underlying pelvic pathology. Primary dysmenor- menorrhea with TENS or acupuncture, a forthcoming rhea usually appears within 1 to 2 years after menarche, study by the Cochrane Library aims to analyze all prowith the establishment of ovulatory cycles. The disorderspective randomized controlled trials comparing those primarily affects younger women with ovulatory cycles, modalities with medical treatment or placebo (Wilson, especially teens, but may persist into the forties. TheFarquhar, Kennedy, & Jin, 2000).

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The distinction between primary and secondary dys-(Ritchie, 1979). Other symptoms include excessive flatulence and alternating diarrhea and constipation. The pain menorrhea requires a thorough history as to the nature and is usually intermittent cramplike and predominantly left onset of the pain, the duration of pain or symptoms, and a pain diary (if on first query the pain does not appear tolower quadrant in location but, occasionally the pain is be cyclic). A complete physical and pelvic examination isconstant. Pain is often improved after a bowel movement. The pain may last for only a few minutes, but 50% of important, with focus on the evaluation of the size, shape, patients may have pain for hours to days, and 20% of and mobility of the uterus and adnexal structures and for nodularity and fibrosis of the uterosacral ligaments andpatients may complain of pain for weeks or longer. Symptoms are usually worse during periods of stress tension, rectovaginal septum. Genital cultures for gonorrhea and chlamydia and a complete blood count (CBC) with ESRanxiety, depression, and with the premenstrual and menare usually warranted. If no abnormalities are found, astrual phases of the cycle (Ritchie, 1979). tentative diagnosis of primary dysmenorrhea may be made The diagnosis of the IBS is usually made on the basis of the history but cannot be made without first excluding and the patient started on oral contraceptive pills and/or other conditions. Sigmoidoscopy or barium enema is often prostaglandin synthetase inhibitors. Having made a diagnosis of primary dysmenorrhea, a 4- to 6-month trial ofnecessary and is routinely negative though there may be mucosal hyperemia on sigmoidoscopy and increased oral contraceptives and/or prostaglandin synthetase inhibitors is warranted before laparoscopy is performed to rulehaustral contractions or loss of haustration on barium enema (Hightower & Roberts, 1981). IBS is a waxing and out secondary dysmenorrhea and, in particular, endometriosis. A strong family history of endometriosis and anywaning disorder and treatment consists of reassurance, education, stress reduction, and antcholinergic or other clinical signs of endometriosis on exam may suggest that antispasmodic pharmaceutical agents. Bulk-forming laparoscopy be performed sooner. ® and high-fiber diet are also agents such as Metamucil Surgical approaches to dysmenorrhea include laparousually added as well (Ritchie, 1979). Low-dose tricyclic scopic uterine nerve ablation, presacral neurectomy, and, antidepressants are also useful. in selected cases of secondary dysmenorrhea, hysterectomy (Malinak, 1980). The uterosacral ligaments carry Patients with chronic diarrhea must be evaluated carethe main afferent supply from the uterus, and if complete,fully, often with a gastroenterologist in consultation. Though symptoms may have become chronic, it is possithe uterosacral ablation should be as effective as the presacral neurectomy, though Doyle (1955) described ble a that the patient may have contracted infectious diarrhea due to any one of a number of bacteria or parasites 70% success rate. Long-term or controlled studies of the including Shigella, Escherichia coli, Salmonella, Camneurectomy procedures are lacking. The management of (Hightower & Roberts, 1981). secondary dysmenorrhea involves treatment of thephylobacter, or Amoeba Though appendicitis is a common cause of abdomiunderlying pathology. nal pain, the abdominal pain of appendicitis is severe enough that the patient presents to the physician within GASTROENTEROLOGIC CAUSES 12 to 48 h after the onset of the symptoms. The practitioner treating a patient for chronic pelvic pain should OF CHRONIC PELVIC PAIN be cautious when the patient suddenly has an increase Many of the patients referred to gynecologists within abdominal pain, especially if it is accompanied by chronic pelvic pain actually have GI pathology (Rapkin localized right lower quadrant pain, as well as anorexia, & Mayer, 1993; Reiter, 1990b). Because the cervix,nausea, vomiting, and peritoneal signs on exam. It is not uterus, adnexa, lower ileum, sigmoid colon, and rectumuncommon that a patient under treatment for chronic share the same visceral innervation, with pain signalspelvic pain develops acute appendicitis or other acute traveling via the sympathetic nerves to spinal cord seg-pelvic condition while in the process of evaluation for ments T10 to L1, it is often dif ficult to determine whether the chronic pain problem. Chronic appendicitis is a conlower abdominal pain is of gynecologic or enterocoelictroversial entity, but in the opinion of Lee, Bell, Griffen, origin (Hightower & Roberts, 1981). In addition, as is & Hagihara (1985), it does exist. true with other types of visceral pain, pain sensation from Another cause of chronic enterocoelic pain is diverthe GI tract is often diffuse and poorly localized. Skillful ticular disease of the colon (Young, Alpers, Norland, & medical history and examination are usually necessary Woodruff, 1976). Of the adult population over 40, 5% to make the diagnosis. have been noted to have diverticulae (Painter, 1970). This Irritable bowel syndrome (IBS) is one of the more percentage increases to 40% in individuals over the age common causes of lower abdominal pain and may account of 70 although most patients never develop diverticulitis. for as many as 7 to 60% of referrals to a gynecologist forThough diverticulosis is usually asymptomatic, diverticuchronic pelvic pain (Reiter, 1990b). The predominantlitis results in severe pain. Diverticulitis results from persymptom of irritable bowel syndrome is abdominal painforation of one or more of the diverticula and usually leads

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to the formation of a pericolonic abscess. The principalnosis is one of exclusion. A negative urine analysis, urine symptom of diverticulitis is left lower quadrant abdominal culture, and urethral cultures, as well as negative evalupain. A tender mass may be palpable on exam. Fever and ation for vulvovaginitis, increase the suspicion for the leukocytosis are usually present. Sigmoidoscopy is diagdiagnosis of urethral syndrome. Treatment consists of a nostic. These symptoms and signs, however, are usually trial of antibiotics, preferably tetracycline for 2 to 3 those of an acute pathological pain process bringing the weeks; and, if without success, urethral dilatation in patient to a physician early in the course of pain. reproductive aged women and vaginal estrogen for periInflammatory bowel disease such as ulcerative colitisand postmenopausal women (Bergman, Karram, & or granulomatous disease (Crohn’ s disease) similarly do Bhatia, 1989). Attention should be paid to psychological factors as well. not usually present as chronic pelvic pain because their presentation is usually more acute with diarrhea, fever, When a patient complains of symptoms of urinary vomiting, and anorexia (Hightower & Roberts, 1981). A frequency, urgency, and suprapubic pain but laboratory sigmoidoscopy or barium enema is diagnostic. studies are negative, the patient may actually have IC Tumors of the GI tract can cause chronic lower(Karram, 1993; Messing & Stamey, 1978). The evaluation abdominal pain in women (McSherry, Cornell, & Glenn, of patients with the preceding symptoms should include 1969). The most frequent and early symptoms of bowelurinalysis and culture, urethral culture for chlamydia, carcinomas are change in bowel habits (74% of patients) mycoplasma, and gonorrhea, and cystoscopy with hydroand abdominal pain (65% of patients). Rectal bleedingdistension and possible biopsy. The consensus criteria for and weight loss may be signs of advanced disease (McShthe diagnosis of IC include at least two of the following: erry, et al., 1969). Most rectal tumors can be palpated on pain or bladder lling fi relieved by emptying; pain in rectal examination. Sigmoidoscopy and biopsy as well as suprapubic, pelvic, urethral, vaginal or perineal region, barium enema are diagnostic. glomerulations on endoscopy; or decreased compliance Included in the differential diagnosis of lower abdom- on cystometrogram (Karram, 1993). Therapy consisting inal pain is hernia though there is a relatively low inci- of intravesical distension with dimethylsulfoxide, intradence of hernia in females (Hightower & Roberts, 1981).vesical instillation of analogs of glycosaminoglycan, Anterior and posterior perineal hernias, usually limited toTENS and biofeedback including pelvic oor fl muscle biocystocele, rectocele, or enterocele, may cause lower feedback training have all reduced pain in uncontrolled abdominal/perineal pain in women though the pain is usu-studies of patients with IC. Because treatment of the ally not severe. This type of pain usually responds to acondition remains empiric and less than optimal, oral pessary though the management is surgical. drugs such as anticholinergics, antihistamines, antispasmodics, nonsteroidal anti-infl ammatories, tricyclic antidepressants, narcotics, and pentosan polysulfate sodium UROLOGIC CAUSES OF CHRONIC (which is Food and Drug Administration [FDA] approved PELVIC PAIN for IC treatment) (Sant, 1998) have all been utilized with some success. Chronic pelvic pain of urologic origin may be related to recurrent cystoureteritis, urethral syndrome, interstitial Very severe chronic suprapubic pain may be caused cystitis (IC), infiltrating bladder tumors, ectopic pelvic by infiltrating carcinomas of the bladder, cervix, uterus or rectum (Vereecken, 1981). These conditions should be kidney, or various ureteral causes of pelvic pain such as apparent after performing the history, pelvic examination, ureteral obstructions or endometriosis (Vereecken, 1981; urine analysis, and cystoscopy, though intravenous pyelSummit, 1993). The patient with cystitis presents with complaints of ogram (IVP) or CT urogram may be necessary. suprapubic pain, dysuria, frequency, urgency; has pyuria on urinalysis; and has a positive urine culture (Vereecken, NERVE ENTRAPMENT OR INJURY 1981). The symptoms usually respond to adequate antibiotic therapy. Relapses and reinfection can be diagnosed Abdominal cutaneous nerve entrapment or injury should with the aid of history, urinalysis, and culture. The anti-always be considered in the differential diagnosis of biotic and duration of therapy may have to be adjustedchronic lower abdominal pain, especially if no visceral and on occasion, if the patient has recurrent cystoureteritis, etiology is apparent. The syndrome most commonly antibiotics may have to be administered postcoitally pos-occurs months to years after Pfannenstiel skin or other sibly for a prolonged period of time (Vereecken, 1981). lower abdominal and even laparoscopic incisions (Sippo, The urethral syndrome is a common condition inBurghardt, & Gomez, 1987) but can also follow trauma or exercise. Commonly involved nerves include ilioinwomen and may present as chronic pelvic pain (Bodner, 1988). Symptoms of dysuria, urinary frequency, supra-guinal (T12 and L1), iliohypogastric (T12 and L1), and pubic pain, and dyspareunia are prominent and the diaggenitofemoral (L1 and L2).

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Symptoms of nerve entrapment include pain that isMYOFASCIAL PAIN typically elicited by exercise and relieved by bedrest ned as p “ ain and/or autonomic (Hammeroff, Carlson, & Brown, 1981; Sippo, et al., Myofascial pain is defi phenomena referred from active myofascial trigger 1987). The pain is described as stabbing, colicky, and points, with associated dysfunction” (Travell, 1976). sudden; and is usually judged as coming from the abdoReports of the prevalence of the syndrome vary, but only men and not from the skin. The pain is located along the two papers assessing chronic pelvic pain patients for trigline of the lateral edge of the rectus margin and may be associated with a burning pain radiating horizontally orger points have been published. Reiter and Gambone found myofascial syndrome in 15% of their patients with diagonally toward the linea alba and back to the ankflor somatic pathology (Reiter, 1990b). [Patients with somatic sacroiliac region. Nausea, bloating, menstruation, and pathology represented 47% of all patients referred to their full bladder may exacerbate the pain of nerve entrapment pelvic pain clinic (Reiter, 1990b).] Slocumb (1984), in (Sippo, et al., 1987). On exam, the pain can usually be localized with thecomparison, noted trigger points in most women presentfingertip (MacDonald, 1993). The maximal point of ten- ing to the pain clinic with chronic pelvic pain irrespective of underlying pelvic pathology. Clinically, myofascial derness is the neuromuscular foramen at the rectus margin medial and inferior to the anterior iliac spine or, in pain is exacerbated by activity within the muscle or musthe case of spontaneous nerve entrapment, at the site cle of group and, in the case of abdominal wall trigger points and pelvic floor muscle, is exacerbated by activity in exit from the aponeurosis of the other thoracic/abdomideeper visceral structures (bladder or rectal fullness, nal cutaneous nerves. A maneuver that helps to make the menses, and cervical motion and intercourse), which diagnosis is to ask the patient to tense the abdominal share the same dermatomal innervation (Slocumb, 1984; wall by raising shoulders or raising and extending the lower limbs in a straight leg raising maneuver. The outerSlocumb, 1990; Travell, 1976). On digital exam of dermatomas of abdomen, back, or vagina, pressure on the side of the rectal muscle is then pressed with a single trigger point evokes local and referred pain. Pain is exacfinger. The pain is exacerbated if nerve entrapment syndrome is present. With the abdominal wall relaxed, theerbated by the straight leg raising maneuver described earlier. Treatment of myofascial trigger points includes pain is relieved and becomes more diffuse. The tentative diagnosis is confi rmed with a diagnostic nerve block injecting the trigger points with local anesthetic, as well consisting of injection of 2 to 4 ml of 1% lidocaine or as treating any physical and psychological factors such 0.25% bupivocaine. Patients usually report immediateas depression, anxiety, and learned behavior patterns that relief with symptoms after injection and many patientsmay accompany and exacerbate the condition (Travell, require no further intervention, though some patients1976; Slocumb, 1984). Medications such as tricyclic antirequire 2 or 3 weekly injections. Only as a last resortdepressants and anticonvulsants or physical therapy may also be useful. should patients be considered for surgical removal of the involved nerves if no other psychological factors predominate and if visceral pathology can be ruled out. CENTRAL (BRAIN) FACTORS IN CHRONIC Deafferentation pain is a probable sequel to surgery and there are no long-term studies of nerve excision. Medi-PELVIC PAIN cations such as low-dose tricyclic antidepressants and Descending pain modulating mechanisms, including those anticonvulsants are also useful for pain control. Physical originating in the brain or spinal cord, probably involve therapy may be necessary to educate the patient concernvarious chemicals such as classical neurotransmitter, ing strengthening other muscles to prevent reinjury. endogenous endorphin and nonendorphin analgesic systems, and excitatory amino acids. Anxiety, depression, and other psychological states may be facilitators or inhibitors MUSCULOSKELETAL CAUSES OF of neurological transmission. Wall (1988) has suggested CHRONIC PELVIC PAIN that it is “necessary to consider the lability of central Women complaining of lower back pain without com- transmission pathways as well as seeking peripheral ” From a psychological plaints of pelvic pain rarely have gynecologic pathologypathology in all painful conditions. perspective, there are various factors that may promote as the cause of their pain; however, low back pain may the chronicity of pain. Described as a “diathesis-stress” accompany pelvic pathology. Back pain may be caused by gynecologic, vascular, neurological, psychogenic, ormodel of pain, a woman is more susceptible in certain social contexts to develop chronic pain based on her prespondylogenic (related to the axial skeleton and its structures) pathology (Morscher, 1981). Musculoskeletalexisting vulnerabilities including those related to cogniabnormalities commonly contribute to the symptoms oftive, affective, biological, and behavioral functioning chronic pelvic pain (Baker, 1993). (Jacobs, 1997).

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Studies on women with chronic pelvic pain have doc-sexual abuse as a child, along with a past history of umented a high level of psychological disturbance. Thedepression, as strongly related to the subsequent persisMinnesota Multiphasic Personality Inventory (MMPI) tence of pelvic pain. conversion“V” profile (elevated scores on the hypochonThe association between prior abuse and pelvic pain driasis, hysteria, and depression scales) was described was by studied by Rapkin, Kames, & Darke (1990). The Castelnuova-Tedesco and Krout (1970) in a survey of 40 study was designed to assess whether prior abuse is more women with pelvic pain. Gross, Doerr, Caldirole, Guzin- likely in pelvic pain patients than in women with chronic ski, and Ripley (1980) reported high levels of psychopa-pain in other sites or a painful control group, and whether thology in women with pelvic pain, as well as a pastthe abuse was specifically sexual or extended to physical exposure to childhood sexual abuse in 90% of their samabuse as well. The prevalence of childhood sexual abuse ple. Studies using the MMPI have failed to find a corre-did not differ significantly between the three groups: 19% spondence between psychological and physiological findof pelvic pain, 16% of other pain patients, and 12% of ings. Renaer, Vertommen, Nijs, Wagemans, and Vancontrols. There was a significant difference in the prevaHemelrijk (1979) compared MMPI profiles of women lence of physical abuse: highest for the pelvic pain patients having chronic pain without obvious pathology with those(39%), compared with 18 and 9% in the other two groups. of women having pain arising from endometriosis and aThis study suggested abuse of any kind is linked to chronic control group. They found the two pain groups differedpain. Walling and colleagues (1994) compared women from controls but not from each other. Interestingly, treat-having chronic pelvic pain with women having nonpelvic ment resulting in subjective improvement in pain severitychronic pain (headache) and pain-free women, finding that and increased activity level produces a signi ficant women suffering pelvic pain reported a higher lifetime improvement in personality profi le (Duleba, Jubnyik, prevalence of major sexual abuse (56%) and physical Greenfield, & Olive, 1998). abuse (50%). By drawing on the learned helplessness Other studies have focused on the specific diagnosis model for depression, abuse may predispose to chronicity of depression and pain (Magni, Salmi, deLeo, & Ceola, of pain because it increases the vulnerability to depression 1984; Walker, Katon, & Harrop-Grif fiths, 1988). Magni, and helplessness in the face of adversity (Abramson, (1984) examined the role of depression and found higher Seligman, & Teasdale, 1978). Toomey reaf firmed the depression scores for women with chronic pelvic pain importance of obtaining sexual and physical abuse histowithout pathology compared with women found to have ries in chronic pelvic pain patients (Toomey, Hernandez, chronic pelvic pain and pathology as established by lapGittelman, & Hulka, 1993). aroscopy. They also found a higher likelihood of depreschronic “ sive disorders in the family histories of women whose pain Renaer (1980) has suggested the diagnosis pelvic pain without obvious pathology” refers to could not be attributed to organic pathology. A comparison patients who lack somatic pathology. Often these of women with pelvic pain of unknown etiology and a have been considered to have psychogenic pain. pain-free control group revealed the pain group to have patients a significantly higher prevalence of episodes of majorAs noted in the previous discussion, the majority of depression. In 12 of the 16 women with a past history ofpatients with chronic pain have abnormal psychogenic profiles, but those patients without pathology do not depression, the depression preceded the onset of the pain (Magni, et al., 1984; Walker, et al., 1988). It has beenappear to be psychologically different from those with disease (Harrop-Grif fiths, et al., 1988; Renaer, suggested that pain may reflect a masked depression, organic in view of the common neurotransmitter pathways mediatinget al., 1979). Furthermore, the potential role of as yet unknown neurophysiological mechanisms on the brain both pain and mood. and spinal cord in the maintenance of chronic pain canStudies have also examined the role of sexual abuse as a specifi c risk factor for chronic pelvic pain. Gross not be ignored. Abdominal wall, lower back, and pelvic floor muscle trigger points; nerve entrapment in surgical and associates (1980) reported a high prevalence (90%) of sexual abuse in their sample. A sample of 25 womenscars; IBS; and IC represent the most common sources with chronic pelvic pain of mixed etiology showed no of nonreproductive system chronic pelvic pain (Reiter differences in psychological functioning when divided 1990a), all of which probably entail alterations of central processing. Interestingly, these patients also have a according to presence or absence of organic ndings fi (Harrop-Griffi ths, et al., 1988). However, when com- high incidence of concurrent psychopathology (somatopared with a control group of gynecologic patients with-form pain disorder), somatization, or depression (Reiter out pain, there was a higher prevalence of prior sub-1990a; Wood, Weisner, & Reiter, 1990). It may be reasonable, therefore, to suggest that chronic pelvic pain stance abuse, functional dyspareunia, inhibited sexual without, or even with, pathology is likely to involve all desire, higher scores on the SCL-90, and greater prevalence of sexual abuse — both as youths prior to age levels of the neuraxis and to direct management 14 and as adults. The authors identifi ed a history of approaches accordingly.

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Abdominal wall pain is augmented and visceral pain is diminished with the preceding maneuvers. The patient should be examined while standing for hernias, abdominal Successful diagnosis and management of patients with (inguinal and femoral) and pelvic (cystocele, enterocele). chronic pelvic pain requires a meticulous yet compassionAn attempt should be made to locate by fingertip palpation ate, multidisciplinary approach. As with the investigationof the tissues (abdominal, pelvic, external genital, and of any other physical symptom, a thorough history shouldlower back) that reproduce the patient’ s pain. The patient be obtained, and often must be acquired in stages. The should be evaluated by, or in concert with, a gynecologist. nature of the pain, location and radiation, aggravating and Laboratory studies to obtain therstfi visit include alleviating factors, timing, effect of menses, exercise,CBC, ESR, urine analysis and culture, cervical and urework, stress, intercourse, and orgasm should be queried. thral cultures (gonorrhea and chlamydia), wet mount of The context in which the pain arose should be ascertained. vaginal secretions, pap smear, stool guaiac, and — if diarDid the pain begin postpartum, postabortal, or postrape? rhea is present — stool culture. If the pelvic or abdominal Have there been previous episodes of pain or inability toexam is confusing or suggestive of a mass, ultrasound perform one’s occupation. Is there pending litigation or evaluation is indicated. If symptoms and signs are suggesworker’s compensation? Other somatic symptoms should tive of other system involvement,beroptic fi or other be noted: genital tract (abnormal vaginal bleeding, dis-appropriate imaging studies of other organ systems should charge, mittelschmerz, dysmenorrhea, dyspareunia, inferbe considered (e.g., upper and lower intestinal barium tility); enterocoelic tract (constipation, diarrhea,atufl studies or computerized axial tomography [CAT] scan, lence, tenesmus, blood, changes in color or caliber of intravenous pyelogram, and MRI of the spine). stool); musculoskeletal system (predominant low back The patient should be given a daily pain diary in which distribution, radiation down posterior thigh, associationto note the onset and intensity of pain. Medication intake with injury, fatigue, postural changes); and urologic tractand aggravating and alleviating factors should be noted in (dysuria, urgency, frequency, suprapelvic pain). Historicalthe diary. A simple diary utilizes a visual analog scale questions specific to all the peripheral pathologies noted from 1 (no pain) to 10 (most severe pain ever). The diary in Table 22.1, should be queried. Past history includingshould be maintained for at least 2 months. Previous medmedical, surgical, gynecologic, obstetric, medicationical records, surgical and pathological reports or scans, intake, and prior evaluations for the pain should be doc-should be requested at the time of, or prior to, this first umented. Operative and pathology reports are important visit. The second visit should be scheduled for approxiif the patient has had surgery. mately 2 weeks later. Current and past psychological history — including During the second visit, one should again pursue the psychosocial factors; history of past (or current) physical,psychosocial and sexual history. The pain diary, laboratory sexual, and/or emotional abuse; history of hospitalization;results, and previous records should be reviewed with the suicide attempts; and chemical dependency — should be patient. Subacute conditions should be treated (e.g., cerasked. The attitude of the patient and her family towardvicitis, salpingo-oophoritis, urethritis, cystitis); and the the pain, resultant behavior of the patient’ s family with abdominal, back, and pelvic exam should be repeated with respect to the pain, and current upheavals in the patient’ s thorough evaluation for abdominal, lumbosacral, and vaglife should be discussed. The part of the history addressing inal trigger points if not performed on the first exam. A sensitive issues may have to be reobtained after establishdescription of the evaluation and treatment of trigger ing rapport with the patient. points is provided by Slocumb (1984). Symptoms of an acute process such as fever, anorexia, At the time of the second visit the patient should be nausea, emesis, signifi cant diarrhea or constipation, evaluated by a psychologist familiar with the evaluation abdominal distension, uterine bleeding, pregnancy, orand management of chronic pain. The psychologist should recent abortion should alert one as to the possibility of an preferably be located within the same fice of or clinic suite. acute condition requiring immediate medical or surgical Psychological referral accomplishes both evaluation, intervention. This is especially called for if accompaniedas well as opens the possibility for introducing cognitive by orthostasis, peritoneal signs, pelvic or abdominal mass, behavioral pain management. The assessment should be abnormal CBC, positive genital or urinary tract cultures,designed to evaluate the pain complaint, its impact on life or positive pregnancy test. circumstances, and the controlling factors and coping One should perform a complete physical examination,mechanisms. Assessment in a chronic context involves a with particular attention to the abdominal, back vaginal,broader range of measures, reflecting social and psychological influences and sequelae, than may apply in the bimanual, and rectovaginal examination. The exam should acute setting. include evaluation of the abdomen with muscles tensed (head raised off the table or with straight leg raising) to Assessment must evaluate the impact of the pain on differentiate abdominal wall and visceral sources of pain.the woman’s lifestyle. Pelvic pain is likely to affect sex-

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ual functioning, which may have additional repercus-ogy and two thirds of patients have findings of adhesions sions in terms of the quality of the patient’ s relationship that may or not play a role in their pain. Furthermore, and self-esteem. As with mood, a careful history isnonsurgical management of chronic pelvic pain (multidisneeded to establish whether the sexual problems existed ciplinary pain clinics or trigger point injections) is sucbefore the pain or developed subsequently. Previous sexcessful in 65 to 90% of patients regardless of presence of ual abuse or trauma should be evaluated, as well as the minimal pathology (Rapkin & Kames, 1987; Reiter, Gamimpact of the pain on day to day functioning. Standard-bone, & Johnson, 1991; Slocumb, 1984). Laparoscopy ized psychological testing is helpful to determine if should probably be reserved for patients in whom other affective disturbance is present, as well as to establish pathology a has been ruled out; and for those with signs baseline against which to measure treatment response and/or symptoms of endometriosis, cyclic pelvic pain, or and guide treatment approaches. infertility. Some retrospective and prospective evidence If somatic pathology is suspected or confi rmed, suggests that laparoscopy provides pelvic pain patients a workup and management should proceed as per treatment positive psychological impact (Elcombe, Gath, & Day, of the somatic condition (see Table 22.1). Consultation1997); however, it is costly and not without surgical and with a urologist, gastroenterologist, orthopedist, or neu-anesthetic risks. rologist should be requested if indicated. The third visit should be scheduled for 1 or 2 weeksLYSIS OF ADHESIONS later. This visit should include another review of the pain diary. Patients with cyclic or atypical cyclic pain should beThe role of pelvic adhesions in the genesis of pain is unclear. Lysis of adhesions at laparotomy is frequently evaluated for primary or secondary dysmenorrhea. Evaluation of pelvic pain, especially cyclic pain, may undermined by a high incidence of adhesion reformation require a diagnostic laparoscopy. Pelvic ultrasound or(Holtz, 1984). Laparoscopic lysis of adhesions may be cant reformation of adhetransuterine venography may be indicated if pelvic con-less likely to result in signifi sions; however, 20 to 90% of adhesions reform or form gestion is suspected, but treatment can proceed on the basis of clinical suspicion. If trigger points were injectedde nouveauafter an adhesiolysis procedure. It is not and pain has persisted, injection should be repeated unreasonable, therefore, to lyse adhesions at the time of weekly or biweekly up to five injections. In addition, diagnostic laparoscopy, but controlled studies have yet consideration should be given to a physical therapy conto be definitive. sultation, especially if activity increases the pain or if low back pain is prominent. HYSTERECTOMY A follow-up appointment (fourth visit) should be scheduled for 1 or 2 weeks later. Before the third andHysterectomy has long been performed to cure pelvic fourth visits, the “pain manager, ” the gynecologist (if not pain. In fact, up to 19% of hysterectomies are performed the pain manager), and psychologist should consult. for the sole indication of chronic pelvic pain (Reiter, If pain persists, the patient should initiate cognitive1990a). However, 30% of patients presenting to pelvic pain clinics have already undergone hysterectomy withbehavioral pain management and various centrally acting pharmaceutical agents should be tried. Tricyclic antide-out experiencing relief of pain (Chamberlain & La Ferla, 1987). Reiter and associates (1991) noted a decline in pressants and anticonvulsants have been used successfully in pelvic pain patients. To date, only one randomizedthe incidence of hysterectomy for the indication of chronic pelvic pain from 16.3 to 5.8% after the initiation controlled trial assessed the effect of selective serotonin reuptake inhibitors on pelvic pain, and the short 14-weekof a multidisciplinary approach to the diagnosis and trial of 23 women failed to show significant difference in treatment of chronic pelvic pain. A prospective cohort measures of pain and functional disability (Engel, Walker,study, the Maine Womens Health Study, revealed 18% Engle, Bullis, & Armstrong, 1998). The patient should of women had a hysterectomy for chronic pelvic pain continue to have scheduled visits with the gynecologistwith significant improvement in pain and associated on a regular basis. symptoms. Their underlying diagnoses, however, were not described (Carlson, Miller, & Fowler, 1994). Hillis, Marchbanks, and Peterson (1995) studied a prospective MANAGEMENT OF CHRONIC PELVIC cohort of 308 women who underwent hysterectomy for PAIN: SURGICAL chronic pelvic pain, thought to be of uterine origin. The outcome revealed a 74% response rate, with observed DIAGNOSTIC LAPAROSCOPY persistent pain associated with multiparity, prior history of pelvic inflammatory disease (PID), lack of pathology, Diagnostic laparoscopy has become a standard procedure in the evaluation of patients with chronic pelvic pain. and Medicaid payer status (Hillis, et al., 1995). HysterBetween 14 and 77% of patients have no obvious patholectomy remains an option for appropriately selected

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patients with pain of uterine origin. In recognition of the MULTIDISCIPLINARY PAIN fact that hysterectomy treats at best only some women, MANAGEMENT the American College of Obstetricians and Gynecologists (1998) established criteria to be met prior to perMULTIDISCIPLINARY PAIN MANAGEMENT forming such invasive surgery for pelvic pain. The criteria include that no remediable pathology is found onMultidisciplinary pain management is an excellent laparoscopic examination and that a 6-month presence approach to chronic pelvic pain. Peripheral factors are of pain occurs with negative effect on the patient’ s qual- managed by the pain manager. Spinal cord and central ity of life. factors related to possible abnormalities of modulation of pain impulses are addressed with trigger point injections, centrally acting medications, acupuncture, or TENS PRESACRAL NEURECTOMY (Helms, 1987; Mannheimer & Whaler, 1985; Rapkin & Presacral neurectomy or sympathectomy (PSN) was rst fi Kames, 1987; Slocumb, 1984). Cognitive behavioral and described by Cotte (1937) for the indication of dysmen-other psychological factors are addressed by the psycholorrhea. As is apparent from the discussion of the neuogist. roanatomy of the pelvic organs, the presacral nerve, One program was successful in reducing pain by at which is actually the superior hypogastric plexus,least 50% in 85% of the subjects (Rapkin & Kames, 1987). receives the major afferent supply from the cervix,Other studies have suggested that similar results may be uterus, and proximal fallopian tubes. Afferents travelingobtained with a multidisciplinary team (Milburn, Reiter, with the sympathetic nerve supply from the bladder and& Rhomberg, 1993; Pearce, Knight, & Beard, 1982; rectum also pass through the superior hypogastric plexus. Peters, et al., 1991; Reiter, et al., 1991; Wood, et al., 1990). Normal micturition and defecation are dependent on anIn a prospective randomized study, the multidisciplinary intact sacral autonomic nerve supply and are relativelyapproach was found to be more effective than traditional unaffected by resection of the superior hypogastricgynecologic (medical and surgical) management (Peters, plexus. The nerve supply to the adnexal structureset al., 1991). bypasses the hypogastric plexus, as the afferents from the ovary travel with sympatheticbers fi accompanying REFERENCES the ovarian artery to the superior mesenteric plexus to enter the spinal cord at T9 and T10. These autonomic Abramson, L.Y., Seligman, M.E.P., & Teasdale, J.D. (1978). relationships constitute the rationale for Cotte’ s (1937) Learned helplessness in human: Critique and reformaemphasis on differentiating dysmenorrhea with the maxtion. Abnormal Psychology, 87 , 49–74. imum intensity of the pain localized to the uterus with Adams, J., Reginal, P.W., Franks, S., Wadsworth, J., & Beard R.W. (1990). Uterine size and endometrial thickness and radiation to the sacrum from lateralizing pain radiating the significance of cystic ovaries in women with pelvic to the lumbar region. pain due to congestion. British Journal of Obstetrics and PSN has been studied in the management of central Gynecology, 97 , 583–587. pelvic pain in the setting of both cyclic and noncyclic Almeida, O.D, & Val-Gallas, J.M. (1997). Conscious pain mappain (Ingersoll & Meigs, 1948; Lee, Stone, Magelssen, ping. Journal of American Association of Gynecologic Belts, & Benson, 1986; Polan & DeCherney, 1980). Laparoscopists, ,4587–590. Though most studies of PSN are uncontrolled, PolanAmerican College of Obstetricians and Gynecologists. (1983). and DeCherney’ s (1980) study did include a control Dysmenorrhea (Vol. 68, pp. 1–5). Washington, D.C.: group of patients who had infertility surgery without American College of Obstetricians and Gynecologists. PSN. In the latter group, only 26% experienced reliefAmerican College of Obstetricians and Gynecologists criteria of pain as compared with 75% of patients who also set. (1998). Hysterectomy, abdominal or vaginal for chronic pelvic pain. Number 29, November 27. Comunderwent PSN. In another randomized controlled mittee on Quality Assessment. American College of study by Tjaden, Schlaff, Kimball, and Rock (1992), Obstetricians and Gynecologists. International Journal the study was prematurely terminated due to the overof Gynaecology and Obstetrics, ,60 316–317. whelming response to PSN compared with resection of Baker, P.K. (1993). Musculoskeletal origins of chronic pelvic moderate to severe endometriosis (Tjaden, et al., 1992). pain. In F. W. Ling (Ed.),Obstetrics and gynecology However, when Candiani, Fedele, Vercellini, Bianchi, clinics of North America: Contemporary management and DiNola (1992) studied PSN vs. resection of modof chronic pain(pp. 719–742). Philadelphia: W. B. Saunerate or severe endometriosis, initial central pain was ders. reduced though 6-month follow-up revealed no signif-Beard, R.W., Highman, J.H., Pearce, S., & Reginald, P.W. icant difference in pain. The value of PSN remains (1984). Diagnosis of pelvic varicosities in women with controversial. chronic pelvic pain.Lancet, 2, 946–949.

Chronic Pelvic Pain

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Bergman, A., Karram, M., & Bhatia, N.N. (1989). Urethral syn- De Groat, W.C. (1994). Neurophysiology of the pelvic organs. In D. N. Rushton (Ed.),Handbook of neuro-urology (pp. drome: A comparison of different treatment modalities. 55–93). New York: Marcel Dekker. Journal of Reproductive Medicine, ,34 157–160. Berkley, K.J. (1994). Communications from the uterus (and otherDoyle, I.B. (1955). Paracervical uterine denervation by transectissues). In J. M. Besson (Ed.), Pharmacological aspects tion of the cervical plexus for the relief of dysmenorrhea. of peripheral neurons involved in nociception, pain American Journal of Obstetrics and Gynecology,, 70 research and clinical management (pp. 39–47). Amster1–16. dam: Elsevier. Drugs for dysmenorrhea. (1979). The Medical Letter on Drugs Berkley, K J., & Hubscher, C.H. (1995). Visceral and somatic and Therapeutics, 21 , 81–84. sensory tracks through the neuroaxis and their relationDuleba, A J., Jubnyik, K J., Greenfield, D.A., & Olive, D.L. to pain: Lessons from the rat female reproductive sys(1998). Changes in personality profile associated with tem. In G. F. Gebhart (Ed.), Visceral pain: Progress in laparoscopic surgery for chronic pelvic pain. Journal of pain research and management (Vol. 5, pp. 195–216). American Association of Gynecologic Laparoscopists, Seattle: IASP Press. 5, 389–395. Bodner, D.R. (1988). The urethral syndrome. Office Urology, 15 , Elcombe, S., Gath, D., & Day, A. (1997). The psychological 699–704. effects of laparoscopy on women with chronic pelvic Candiani, G.B., Fedele, L., Vercellini, P., Bianchi, S., & Di Nola, pain. Psychological Medicine, 27 , 1041–1050. G. (1992). Presacral neurectomy for the treatment ofEngel, C.C., Jr., Walker, E.A., Engel, A.L., Bullis, J., & Armpelvic pain associated with endometriosis: A controlled strong, A. (1998). A randomized, double-blind crossover study.American Journal of Obstetrics and Gynecology, trial of sertraline in women with chronic pelvic pain. 167, 100–103. Journal of Psychosomatic Research,, 203–207. 44 Capasso, P., Simons, C., Trotteur, G., Dondelinger, R.F., HenroFarquhar, C.M., Rogers, V., Franks, S., Pearce, S., Wadsworth, teaux, D., & Gaspard, U. (1997). Treatment of sympJ., & Bland, R.W. (1989). A randomized controlled trial tomatic pelvic varices by ovarian vein embolization. of medroxyprogesterone acetate and psychotherapy for Cardiovascular Interventional Radiology, ,20 107–111. the treatment of pelvic congestion. British Journal of Carey, M.P., & Slack, M.C. (1996). GnRH analogue in assessing Obstetrics and Gynaecology, ,96 1153–1162. chronic pelvic pain in women with residual ovaries. Fields, H. (1987).Pain (p. 41). New York: McGraw-Hill. British Journal of Obstetrics and Gynecology, ,103 Filler, W.W., & Hall, W.C. (1970). Dysmenorrhea and its therapy. 150–153. American Journal of Obstetrics and Gynecology, , 106 Carlson, K.J., Miller, B A., & Fowler, F.J., Jr. (1994). The Maine 104–109. Women's Health Study: I. Outcomes of Hysterectomy. Fukaya, T., Hoshiai, H., & Yajima, A. (1993). Is pelvic Obstetrics and Gynecology, ,83 557–565. endometriosis always associated with chronic pain? A Castelnuova-Tedesco, P., & Krout, B.M. (1970). Psychosomatic retrospective study of 618 cases diagnosed by laparosaspects of chronic pelvic pain. Psychiatry in Medicine, copy. American Journal of Obstetrics and Gynecology, 1, 109–126. 169, 719–722. Cervero, F. (1994). Sensory innervation of the viscera: Peripheral Gross, R.J., Doerr, H., Caldirola, D., Guzinski, G., & Ripley, H. basis of visceral pain.Physiological Reviews, 74 , (1980). Borderline syndrome and incest in chronic pel95–138. vic pain patients.International Journal of Psychiatry Cervero, F., & Tattersall, J.E.H. (1986). Somatic and visceral and Medicine, 10,79–96. sensory integration in the thoracic spinal cord. In F. Gupta, A., & McCarthy, S. (1994). Pelvic varices as a cause for Cervero & J. Morrison (Eds.), Visceral sensation(pp. pelvic pain: MRI appearance.Magnetic Resonance 189–205). New York: Elsevier Science Publications. Imaging, 12, 679–681. Chamberlain, A., & La Ferla, J. (1987). The gynecologist's Hammeroff, S.R., Carlson, G.L., & Brown, B.R. (1981). Ilioinapproach to chronic pelvic pain. In J.D. Burroughs, et guinal pain syndrome. Pain, 10, 253–257. al. (Eds.),Handbook of chronic pain management (Vol. Harrop-Griffiths, J., Katon, W., Walker, E., Helm, L., Russo, J., 33, pp. 371–382). Amsterdam: Elsevier. & Hickok, C. (1988). The association between chronic Chan, W.Y, & Dawood, M.Y. (1980). Prostaglandin levels in pelvic pain, psychiatric diagnoses and childhood sexual menstrualfluid of non-dysmenorrheic and of dysmenabuse.Obstetrics and Gynecology, ,71 589–594. orrheic subjects with and without oral contraceptive or ibuprofen therapy.Advances in Prostaglandin and Helms, J.M. (1987). Acupuncture for the management of primary dysmenorrhea.Obstetrics and Gynecology, ,69 51–56. Thromboxane Research,, 1443–1447. 8 Chatman, D.L., & Ward, A.B. (1982). Endometriosis in adoles-Hightower, N.C., & Roberts, J.W. (1981). Acute and chronic lower abdominal pain of enterologic origin in chronic cents.Obstetrics and Gynecology, ,27 186–190. pelvic pain. In M.R. Renaer (Ed.), Chronic pelvic pain Cornillie, F J., Oosterlynck, D., Lauweryns, J.M., & Koninckx, in women(pp. 110–137). New York: Springer-Verlag. P.R. (1990). Deeply infiltrating pelvic endometriosis: Hillis, S.D., Marchbanks, P.A., & Peterson, H.B. (1995). The Histology and clinical significance. Fertility and Sterileffectiveness of hysterectomy for chronic pelvic pain. ity, 53, 978–983. Obstetrics and Gynecology, ,86 941–945. Cotte, G. (1937). Resection of the presacral nerves in the treatPractitionment of obstinate dysmenorrhea. American Journal of Hobbs, J.T. (1976). The pelvic congestion syndrome. er, 216, 529–540. Obstetrics and Gynecology, ,33 1034–1040.

266

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Holtz, G. (1984). Prevention and management of peritonealMacDonald, J.S. (1993). Management of chronic pain. In F. W. Ling (Ed.), Obstetrics and gynecology clinics of North adhesions.Fertility and Sterility, 41, 497–507. America: Contemporary management of chronic pain Hornstein, M.D., Surrey, E.S., Weisberg, G.W., & Casino, L.A. (pp. 817–838). Philadelphia: W. B. Saunders. (1998). Leuprolide acetate depot and hormonal addback in endometriosis: A 12-month study. Obstetrics Magni, G., Salmi, A., deLeo, D., & Ceola, A. (1984). Chronic and Gynecology, 91 , 702–708. pelvic pain and depression.Psychopathology, 17 , Ingersoll, F.M., & Meigs, J.V. (1948). Presacral neurectomy for 132–136. dysmenorrhea.New England Journal of Medicine, 238 , Malinak, L.R. (1980). Operative management of pelvic pain. 357–360. Clinical Obstetrics and Gynecology, ,23 191–199. Jacob, M.C. (1997). Pain intensity, psychiatric diagnosis, andMannheimer, J.S., & Whaler, E.C. (1985). The ficacy ef of tranpsychosocial factors. In J. Steege, D. Metzger, & B. scutaneous electrical nerve stimulation in dysmenorLevy (Eds.), Chronic pelvic pain: An integrated rhea.Clinical Journal of Pain, 1 , 75–83. approach (pp. 67–76). Philadelphia: Saunders. Mathias, S.D., Kuppermann, M., Liberman, R.F., Lipschutz, Janig, W., Haupt-Schade, P., & Kohler, W. (1993). Afferent innerR.C., & Steege, J. F. (1996). Chronic pelvic pain: Prevvation of the colon: The neurophysiological basis for alence, health-related quality of life, and economic corvisceral sensation and pain. In E.A. Mayer & H.E. Rayrelates.Obstetrics and Gynecology, ,87 321–7. bould (Eds.), Basic and clinical aspects of chronic McSherry, C.K., Cornell, G.N., & Glenn, F. (1969). Carcinoma abdominal pain(pp. 71–86). Amsterdam: Elsevier. of the colon and rectum.Annals of Surgery, 169 , Kaplan, B., Peled, Y., Pardo, J., Rabinerson, D., Hirsh, M., Ova502–509. dia, J., & Neri, A. (1994). Transcutaneous electrical Messing, E.M., & Stamey, T.A. (1978). Interstitial cystitis: Early nerve stimulation (TENS) as a relief for dysmenorrhea. diagnosis, pathology, and treatment. Urology, 12, Clinical Experiments in Obstetrics and Gynecology, , 21 381–392. 87–90. Milburn, A., Reiter, R.C., & Rhomberg, A.T. (1993). MultidisKarram, M.M. (1993). Frequency, urgency, and painful bladder ciplinary approach to chronic pelvic pain. In F. W. Ling syndrome. In M.D. Walters & M.M. Karram (Eds.), (Ed), Obstetrics and gynecology clinics of North AmerClinical urogynecology(pp. 285–298). St. Louis, MO: ica: Contemporary management of chronic pain (pp. Mosby. 643–661). Philadelphia: W. B. Saunders. Keltz, M.D., Peck, L., Liu, S., Kim, A.H., Arici, A., & Olive, Morscher, E. (1981). Low back pain in women. In M.R. Renaer D.L. (1995). Large bowel-to-pelvic sidewall adhesions (Ed.),Chronic pelvic pain in women (pp. 137–154). New associated with chronic pelvic pain. Journal of the York: Springer-Verlag. American Association Gynecologic Laparoscopists, , 3 Painter, N.S. (1975). Diverticular disease of the colon, a 20th 55–59. century problem.Clinical Gastroenterology, 1,3–21. Kitchen, J.D. (1985). Endometriosis. In J. Sciarra (Ed.), GynePalter, S.F. (1999). Microlaparoscopy under local anesthesia and cology and obstetrics (pp. 1–25). New York: Harper and conscious pain mapping for the diagnosis and manageRow. ment of pelvic pain.Current Opinion on Obstetrics and Kresch, A.J., Seifer, D.B., Sachs, L.B., & Barrese, I. (1984). Gynecology, 11 , 387–393. Laparoscopy in 100 women with chronic pelvic pain. Pearce, S., Knight, C., & Beard, R.W. (1982). Pelvic pain — A Obstetrics and Gynecology, ,64 672–674. common gynaecological problem. Journal of PsychosoKumazawa, T. (1986). Sensory innervation of reproductive matic Obstetrics and Gynaecology, I(I), 12–17. organs. In F. Cervero & J. Morrison (Eds.), Visceral sensation(pp. 115–131). New York: Elsevier Science Peters, A.A., Van Dorst, E., Jellis, B., VanZuuren, E., Hermans, J., & Trimbos, J.B. (1991). A randomized clinical trial Publications. to compare two different approaches in women with Lee, A.W., Bell, R.M., Griffen, W.O., Jr., & Hagihara, P. (1985). chronic pelvic pain.Obstetrics and Gynecology, 77, Recurrent appendiceal colic. Surgical Gynecology and 740–744. Obstetrics, 161 , 21–24. Lee, R.B., Stone, K., Magelssen, D., Belts, R., & Benson, W.Pettit, P.D., & Lee, R.A. (1988). Ovarian remnant syndrome: Diagnostic dilemma and surgical challenge. Obstetrics (1986). Presacral neurectomy for chronic pelvic pain. and Gynecology, 71 , 580–583. Obstetrics and Gynecology, ,68 517–521. Ling, F.W., & Pelvic Pain Study Group, (1999). Randomized Polan, M.L., & DeCherney, A. (1980). Presacral neurectomy for pelvic pain in infertility. Fertility and Sterility, 34, controlled trial of depot leuprolide in patients with 557–560. chronic pelvic pain and clinically suspected endometriPrice, F.V., Edwards, R., & Buchsbaum, H.J. (1990). Ovarian osis. Obstetrics and Gynecology, ,93 51–58. remnant syndrome: Dif ficulties in diagnosis and manListon, W. A., Bradford, W. P., Downie, J., & Kerr, M.G. (1972). agement. Obstetrics and Gynecology Surgery, , 45 Laparoscopy in a general gynecologic unit. American 151–156. Journal of Obstetrics and Gynecology, 113 , 672–677. Lundberg, W.I., Wall, J.E., & Mathers, J.E. (1973). LaparoscopyProbst, A.M., & Laufer, M.R. (1999). Endometriosis in adolescents. Incidence, diagnosis and treatment. Journal of in the evaluation of pelvic pain. Obstetrics and GyneReproductive Medicine, 44 , 751–758. cology, 42, 872–876.

Chronic Pelvic Pain

267

Procacci, P., Zoppi, M., & Maresen, M. (1986). Clinical Steege, J.F., & Scott, A.L. (1991). Resolution of chronic pelvic pain after laparoscopic lysis of adhesions. American approach to visceral sensation. In F. Cervero & J. Morrison (Eds.),Visceral sensation(pp. 21–36). New York: Journal of Obstetrics and Gynecology, 165 , 278–283. Elsevier. Stones, R.W., Rae, T., Rogers, V., Fry, R., & Beard, R.W. (1990). Rapkin, A J. (1986). Adhesions and pelvic pain: A retrospective Pelvic congestion in women: Evaluation with transvagstudy. Obstetrics and Gynecology, ,68 13–15. inal ultrasound and observation of venous pharmacolRapkin, A.J, & Kames, L.D. (1987). The pain management ogy. British Journal of Radiology, 63 , 710–711. approach to chronic pelvic pain. Journal of Reproductive Summit, R.L. (1993). Urogynecologic causes of chronic pelvic Medicine, 32,323–327. pain. In F.W. Ling (Ed.),Obstetrics and gynecology Rapkin, A J., Kames, L.D., & Darke, L.L. (1990). History of clinics of North America: Contemporary management physical and sexual abuse in women with chronic pelvic of chronic pain(pp. 685–698). Philadelphia: W. B. Saunpain. Obstetrics and Gynecology, ,76 90–96. ders. Rapkin, A.J., & Mayer, E.A. (1993). Gastroenterologic causesSutton, C.J., Pooley, A.S., Ewen, S.P., & Haines, P. (1997). of chronic pelvic pain. In F.W. Ling (Ed.), Obstetrics Follow-up report on randomized controlled trial of laser and gynecology clinics of North America: Contempolaparoscopy in the treatment of pelvic pain associated rary management of chronic pain (pp. 663–683). Philwith minimal to moderate endometriosis. Fertility and adelphia: W. B. Saunders. Sterility, 68, 1070–1074. Reiter, R.C. (1990a). A profile of women with chronic pelvic Sweet, R.L., & Gibbs, R.S. (1985). Pelvic inflammatory disease. pain. Clinical Obstetrics and Gynecology, ,33 130–136. In R.L. Sweet & R.S. Gibbs (Eds.), Infectious diseases Reiter, R.C. (1990b). Occult somatic pathology in women with of the female genital tract (Part 1, pp. 53–77). Baltimore: chronic pelvic pain.Clinical Obstetrics and Gynecology, Williams & Wilkins. 33, 154–160. Tarazov, P.G., Prozorovskij, K.V., & Ryzhkov, V.K. (1997). PelReiter, R.C., Gambone, J.C., & Johnson, S.R. (1991). Availabilvic pain caused by ovarian varices. Treatment by tranity of a multidisciplinary pelvic pain clinic and frescatheter embolization. Acta Radiologica, 38, quency of hysterectomy for pelvic pain. Journal of 1023–1025. Psychosomatic Obstetrics and Gynaecology, (Suppl.), 12 Taylor, H.C., Jr. (1954). Pelvic pain based on a vascular and 109. autonomic nervous system disorder. American Journal Renaer, M. (1980). Chronic pelvic pain without obvious patholof Obstetrics and Gynecology, ,67 1177–1196. ogy in women: Personal observation and a review of the Tjaden, B., Schlaff, W.D., Kimball, A., & Rock, J.A. (1992). problem.European Journal of Obstetrics and GynecolThe efficacy of presacral neurectomy for the relief of ogy, 10, 415–463. midline dysmenorrhea. Obstetrics and Gynecology, 167 , Renaer, M. (1981).Chronic pelvic pain in women . New York: 100–103. Springer-Verlag. Toomey, T.C., Hernandez, J.T., Gittelman, D.F., & Hulka, J.F. Renaer, M., Vertommen, H., Nijs, P., Wagemans, M., & Van(1993). Relationship of sexual and physical abuse to Hemelrijk, T. (1979). Psychosocial aspects of chronic pain and psychological assessment variables in chronic pelvic pain in women.American Journal of Obstetrics pelvic pain patients.Pain, 53(1),105–109. and Gynecology, 134 , 75–80. Travell, J. (1976). Myofascial trigger points: Clinical view. Ritchie, J. (1979). Pain in IBS. Practical Gastroenterology, , 3 Advances in Pain Research and Therapy, , 919–926. 1 17–23. Venbrux, A.C., & Lambert, D.L. (1999). Embolization of the Sant, G.R. (1998). Interstitial cystitis – a urogynecologic perovarian veins as a treatment for patients with chronic spective. Contemporary Obstetrics and Gynecology , pelvic pain caused by pelvic venous incompetence (pel119–130. vic congestion syndrome). Current Opinion in ObstetSichlau, M.J., Yao, J.S.T., & Vogelzang, R.L. (1994). Transcathrics and Gynecology, 11 , 395–399. eter embolotherapy for the treatment of pelvic congestion syndrome. Obstetrics and Gynecology, ,83 Vercellini, P., Fedele, L., Bianchi, S., & Candiani, G.B. (1991). Pelvic denervation for chronic pain associated with 892–896. endometriosis: Fact or fancy? American Journal of Sippo, W.C., Burghardt, A., & Gomez, A.C. (1987). Nerve Obstetrics and Gynecology, 165 (3), 745–749. entrapment after Pfannensteil incision. American JourVercelini, P., Trespedi, L., De Giorgi, O., Cortesi, I., Parazzini, nal of Obstetrics and Gynecology, 157 , 420–421. F., & Crosignani, P. G. (1996). Endometriosis and pelvic Slocumb, J.C. (1984). Neurological factors in chronic pelvic pain: Relation to disease stage and localization. Fertility pain: Trigger points and the abdominal pelvic pain synand Sterility, 65, 299–304. drome.American Journal of Obstetrics and Gynecology, Vereecken, R.L. (1981). Chronic pelvic pain of urologic origin. 149, 536–543. In M. R. Renaer (Ed.),Chronic pelvic pain in women Slocumb, J.C. (1990). Chronic somatic myofascial and neuro(pp. 155–161). New York: Springer-Verlag. genic abdominal pelvic pain. In R.P. Porreco & R.C. Reiter (Eds),Clinical obstetrics and gynecology (pp. Walker, E., Katon, W., & Harrop-Grif fiths, J. (1988). Relation145–153). Philadelphia: J. B. Lippincott & Co. ship of chronic pelvic pain of psychiatric diagnoses and childhood sexual abuse. American Journal of PsychiaSteege, J.F. (1987). Ovarian remnant syndrome. Obstetrics and Gynecology, 70 , 64–67. try, 145, 75–80.

268

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Wall, P.D. (1988). The John J. Bonica distinguished lecture.Wood, D.P., Weisner, M.G., & Reiter, R.C. (1990). Psychogenic chronic pelvic pain.Clinical Obstetrics and Gynecology, Stability and instability of central pain mechanisms. In 33, 179–195. R. Dubner (Ed.),Proceedings of the fifth world congress on pain (pp. 13–24). Amsterdam: Elsevier Science Pub-Young, S.J., Alpers, D.H., Norland, C.C., & Woodruff, R. (1976). Psychiatric illness and the irritable bowel syndrome: lishers BV. Practical implications for the primary physician. GasWalling, M.K., Reiter R.C., O’Hara,, M.W., Milburn, A.K., Lilly, troenterology, 70 , 162–166. G., & Vincent, S.D. (1994). Abuse history and chronic pain in women: I. Prevalence of sexual abuse and physical abuse.Obstetrics and Gynecology, ,84 193–199. Wilson, M., Farquhar, C., Kennedy, S., & Jin, X. (2000). Transcutaneous electrical nerve stimulation and acupuncture for primary dysmenorrhea [Protocol]. Software Update. Oxford: The Cochrane Library,

Section IV Specialty Approaches to Pain Management through Team Management

23 Pain Medicine and the Primary Care Physician Uday S. Uthaman, M.D., F.A.C.F.P. and Pierre L. LeRoy, M.D., F.A.C.S. Pain is a more terrible lord of mankind than even death itself.

MISSION STATEMENT

FOR

CLINICIANS

We offer the following ten considerations: Albert Schweitzer

This chapter is dedicated to John J. Bonica, M.D., for his outstanding contributions to pain medicine and humanity.

1. 2. 3. 4.

Reduce human pain and suffering Individualize patient care Reduce economic and psychosocial losses Concurrently treat co-morbidity and social productivity Reduce loss of workforce skills Reduce healthcare expenditures Reduce occurrence of preventable disease and injury Pursue educational resources Communicate with the patient with empathy Never give up hope for the patient

5. 6. The dynamics of the present health care system has forced 7. many patients to seek managed care. This has not provided the anticipated results or satisfied the expectations of many 8. to offer individualized care. The current system is largely 9. a pharmacological system-based treatment program that 10. does not address etiology or causation. How can these goals be accomplished? The professional, annual continuing education of phyNEW STATE OF THE ART sicians is now mandated by licensing Medical Boards, but Due to five new considerations, these and other shortcomthe focus on personal selection of pain medicine is elecings can be remedied: tive. Some state Medical Boards are already identifying pain medicine as a subspecialty. 1. New advances in theeld fi of clinical pain medicine 2. Recent advances in diagnoses THE ROLE OF SPECIALTY ASSOCIATIONS 3. New and diversified treatment programs Some specialty scientifi c societies have long recognized 4. Progress in laboratory studies the need for additional specialties in the eldfi of pain 5. Availability of focused integrated studies medicine. For example, the American Association of ve fidiviIndividually and collectively, these provide a new Neurological Surgeons (AANS) has organized sions, of which there is a section on pain management frontier and opportunity for primary care physicians (PCPs) to diversify their clinical practice and acquirethat concentrates on both the medical and surgical treatment of pain. Anesthesiology, orthopedic, and other advanced certifications and degrees.

INTRODUCTION

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societies have also followed this trend, offering educa- may or may not have any correlation with bodily injury or tissue damage. tional course material, conferences, seminars, certifi cation, and accreditation. The world medical community, led by Dr. John J. Bonica, in the 1970s recognized the Later, other definitions evolved to show the definitive need for further research and professional interactionprogress that has been provided by the basic scientist and and founded the International Association for the Studytechnology in neuroanatomy and physiology, which act as of Pain (IASP). Dr. Bonica and several others realizedthe foundation for the improved clinical management of at the first IASP meeting in 1975 in Florence, Italy, that pain medicine. there was no American Pain Society. Thus, it was The fundamental nociceptive stimuli for pain can proquickly organized and became known as the APS. Oth-voke irritation, which is reversible, or can produce tissue ers followed, but remained exclusive in their member-damage that is not reversible and accounts for chronic ship, focus, and formulated regional sections. Realizingspontaneous pain perception, which eventually may be that these organizations were primarily for specialties,interpreted by the limbic-forebrain system as “it hurts”; the American Association of Pain Management (AAPM)and becomes associated with psychological discontent and was organized to be more inclusive, recognizing thedepression. If the inflammatory response, the reaction of need to bring together all health professionals thattissue to an irritation continues, is associated with the of Calor, expressed interest in the complex eldfi of pain medicine, classic, long-known, four characteristicsDolore, Temor, and Rubor (or pain, heat, swelling, and redness). a multidisciplinary approach that brings diversifi cation, interaction, expanding education, and credentialing toThese are discussed later in this chapter and in more detail by Richard S. Materson, M.D., in Techniques for Assessthe field of pain medicine. . The purpose of this chapter is to bring together a syl-ing and Diagnosing Pain labus for the PCP and other interested health professionals, providing a clinical overview of theeld fi and referring to THE INCIDENCE OF PAIN other specific chapters for additional information. Actual, accurate data is not yet available but many estimates have been made that recognize an enormous human THE DEFINITIONS OF PAIN and economic burden in society. It is felt by many colleagues that the incidence of pain is underreported. Data This subject has been a Herculean task and was assigned banks have now been established to correct this. An estito Professor Mersky, on whose committee the co-author mate by The Information Specialists of Tampa, Florida, (Pierre LeRoy) was privileged to be a member. For 5 years, the Taxonomy Committee of the IASP struggled for ais that “pain costs the U.S. economy about 100 billion definition that would satisfy the somatic and psychologicdollars a year, including 515 million workdays lost and ” It is estimated criteria and be translatable into other languages to clarifyabout 410 million office visits to doctors. that one in every five adult Americans experiences chronic the existing Babylonian confusion. pain and seeks relief from a doctor. These staggering estimates are addressed in more MERSKY detail in Pain and Its Magnitude , by Barry Fox, Ph.D. Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Since then, other concepts have emerged.

MOUNT CASTLE Sensory experience evoked by stimuli that injure or threaten to destroy tissue, defined introspectively by every man as that which hurts.

ARNOFF Operational definition of pain is that of a complex, personal, subjective and unpleasant experience which

THE CLASSIFICATION OF PAIN Many classification systems have been proposed, but the acute, chronic, cancer, and psychogenic pain divisions appear practical for clinicians. • Acute: From onset in time of perception, it may be variable, lasting from seconds to months. • Chronic: A consensus is developing that after 6 months, it is considered to be chronic and frequently associated with varied emotional responses. • Cancer: Initially, many malignancies have no symptoms and are silent. Pain perception due to tumefaction, vascular, cytochemical, and pathophysiological changes may develop insidiously

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with symptoms of cancer. Special pain management is needed for this patient population. • Psychogenic pain syndromes: These can be diagnosed when the patient complains of pain, but no physical assessment or laboratory test can corroborate the complaint. It can be considered a symptomatic response, however, that can be managed.

that influence the nerve impulse. These can also be sensitized in injury area cross-talk, interact with other nerves, and produce hyperalgesia. This also explains how a lighttouch stimulus can exacerbate a previously injured area that has not healed, and explains why an acute pain can become chronic and produce regional allodynia. In addition, the autonomic nervous system can produce a transmitted substance under nociceptive stimulation. This helps to explain the sensitization to allodynia in patients with No classification is yet considered complete but Drs. reflex sympathetic dystrophy (now being called Complex Thienhaus and Cole address this in detail in this text. Regional Pain Syndrome), in which patients avoid touch or clothing contacts that produce dysesthesias or disagreeable painful sensations.

PATHOPHYSIOLOGY FOR THE CLINICIAN

THE SPINAL LEVEL

At the spinal level, further modulation takes place prior to sending the messages proximally as well as distally. Sir William Osler Incoming afferent peripheral nerve impulses moving at speeds recorded in milliseconds, from low or high threshBasic anatomical and physiological considerations can be olds, neurons such as A-beta, A-delta, and C-fibers, or simplified. We will review current concepts of incoming from sensitized receptors separating the dorsal horn of the pain signals. They are referred to as afferents or arrival spinal cord into zones called Rexed layers. The outermost sensations. We can identify four fundamental divisionslayer is called Lissauer’ s tract or Substantia Gelatinosa. that can be classifi ed as sensory receptors, peripheralHere, unmyelinated C- and A-delta high-threshold nerve nerve networks, spinal modulation, and central brain dis-fibers transmit specifi c sensations that have burning, crimination and affective correlates. touch, and pressure characteristics. Other A-beta fibers go deeper into the Rexed layer five and transmit non-nociceRECEPTORS FOR PAIN ptive sensations. These fibers integrate with marginal neurons and cross-talk when nociception occurs so that a Receptors for pain are thought to be free nerve endings, but Meissner’s corpuscles and bulbs of Krause, for exam-network discriminates localizing intensity and transmits centrally, temporal-based impulses through the cord prople, have thresholds for pressure and cold temperature portionate to the input stimulus. These clinical characterchanges, as do many other receptor organelles. Such recepistics of the sensory pain signal can be identified by the tors can act like a symphony orchestra and transmit specifi c sensory information, but can also relay to pain networkspatient and communicated to the physician. These deeper when the stimulus becomes nociceptive. In the normalsecond-order neurons are called wide dynamic neurons (WDN). These also ascend and descend, forming the main resting state, receptors are on“ call,” but do not t“alk” pain tract known as the spinothalamic tract — the main unless certain thresholds are reached. This is true for neuropathic, myofascial, vascular, scleral, and visceral pain.pain pathway to the brain for further modulation. He who understands pain, knows medicine.

PERIPHERAL SENSORY NERVES

THE BRAIN

The spinothalamic tract ends superiorly in the basal thalSome peripheral sensory nerves are named but the vast amus. This main tract carries pain and temperature sensory majority remain unnamed. These networks are more comsignals and also has a homunculus, layered localization plex than previously realized because they are not only within the thalamus itself. Non-nociceptive A-beta fibers composed of somatic and autonomic afferents, but also efferent outgoing motor neurons transmitting electro-may now trigger pain perception and help explain central chemical action potentials that regulate many forms ofsensitization. It is this tract — the main pain highway — interactive ionic channel electrolytes such as calcium,that neurosurgeons interrupt by carefully cutting or heating with controlled radio-frequency lesions in order to sodium, and potassium — thus conducting a propagation action potential wave of millivolt energy similar to a small relieve intractable pain. Over the years, neurosurgeons and battery, but which eventually must be recharged. In addi-other scientists realized that pain symptoms temporarily tion, we now know that the ganglion cells produce neu-improved symptoms but the pain sensation returned. It was then realized that other pathways and tracts must be ropeptides, such as catecholamines, bradykinin, histacarrying pain sensations to perceptions not previously mine, cytokines, and many other modulating substances

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realized. Basic scientific research then demonstrated that DIAGNOSIS OF PAIN other tracts, such as in the posterior section of the spinal cord, the medial and lateral tracts ending in gracilis andThe diagnosis of pain can vary from simple to complex, cuneate nucleus, not only transmit light touch, vibrations,but is based on a thorough history, physical and basic neurologic examinations, correlation of appropriate laband proprioception, but also pain. Moreover, they too cross oratory tests, specialty consultations when needed, and in the sensory decussation in the brain stem. In addition, the outcomes of medical, surgical, and alternative treatthe reticular formation and spinal–spinal tracts also transmit pain sensation. Other homologous tracts transmitment programs. facial head and neck pains through the extremely complex In more complex pain syndromes, especially those associated with co-morbidity, the diagnosis cannot be trigeminal network. Thereafter the thalamic afferents relay to the pri-made immediately but may require serial follow-up consultations and this should be communicated to the patient mary somatosensory and secondary cortical centers organized in a homunculus for localization and lateral-and documented in well-kept medical records. It should ization. An example is provided in identifying the left also be remembered that no medical information should s express great toe’s medial aspect as a source of pain. This tractbe sent to requesting agencies without the patient’ integrates with the limbic lobe to generate the discrim-written permission. inatory and affective emotions components of the pain, from which the objective anatomic and physiologic TREATMENT OF ACUTE, CHRONIC, basis for nociception pain and suffering is expressed as AND CANCER PAIN “ I hurt.” In summary, we have reviewed and elucidated theFor successful pain management, individualization by basis for anatomic, discriminatory, and affective psycho-diagnosis, personality traits, intellect, age, and outcome logic responses associated with the the nociceptive, of prior treatments must all be seriously considered. peripheral, central, and psychological components for Based on prior educational/training experience, the your consideration. The types of pain, intensity, duration,PCP is in an excellent position to not only know the and localization due to a focal injury or disease process patient, but also the patient’ s family and supporting friends can have a spreading component by convergence, faciland groups, all of which have assistive value. itation, inhibition, cross-talk, or sensitization responding Administrative managed care and third-party reimto an inflammatory process. For example, when one has bursement programs, however, may place barriers on a sunburn and steps into a warm shower, the pain response model individualized treatment plan and alternatives must is exaggerated and is called hyperalgesia. These be sought, but documentation for the clinical changes must responses are compensated in addition by complex ionic be kept due to the utilization and legal considerations and molecular neurochemical systems providing a self-addressed in other chapters. adjusting, discriminatory-affective defense system. Treatment programs have at least twelve areas to Sometimes, depending on the type of mechanical, therconsider: mal, or chemical stimulus, the intensity can not be modulated sufficiently; and when self-care fails, the patient 1. Self-care seeks medical attention. 2. Pharmacology The pathophysiology of chronic pain perception can 3. Physical modalities also shift from a relatively high threshold stimulus 4. Surgery needed to produce pain sensation to a low mechanical, chemical, or temperature threshold stimulus of any kind 5. Alternative medicine to cause increased pain to be felt and lays the founda- 6. Psychological/psychiatric assessment tion for the sensitization and explanation of pain after 7. Physical medicine and rehabilitation injury when the stimulus has left; this has been referred 8. Management of co-morbidity to as spontaneous pain. The reader is referred to other 9. Specialty consultations chapters for additional information. As technology 10. Occupational and vocational evaluations advances and clinical informational data banks develop, 11. Disability evaluation the progress will continue to close our gap of ignorance 12. Medical/legal considerations so that improvements in the diagnosis and treatment of pain syndromes can be achieved. This basic science SELF-CARE provides the foundation of home care, pharmacology, s cooperphysical therapy, modality, treatment, and improvedIn self-care, is important to involve the patient’ ation, compliance, and motivational initiatives to get well. rehabilitation.

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Lacking these, the treating physician is hard-pressed to This is far from an exhaustive review, but serves as achieve a successful outcome. an outline for more detailed chapters in pharmacotherapeutic, psycho- and immunopharmacology.

PHARMACOLOGIC TREATMENT LABORATORY TESTING

FOR

PAIN MEDICINE

Pharmacologic treatment is usually sought when self-care fails. Pain medicine has four pillars of treatment; however,Laboratory testing for pain medicine includes hematopoiwhen sensitivities, untoward reactions, or complicationsetic, serologic, imaging, and electrodiagnostic tests. Freoccur in each class of drugs prescribed for the patient, quently, functional tests that evaluate impairment and caution must be exercised. related ergonomics that cannot be evaluated by the above are necessary and reasonable to assist in determining medAnalgesics ical impairment and serve as a foundation for legally determined disability ratings. Functional testing comes in two Analgesics are employed for symptomatic pain relief.categories: (1) physical or somatic, and (2) emotional or They include (1) non-narcotic, aspirin-type salicylatepsychological. It should be noted that the latter has gained compounds; and (2) opioids. Opoids are controlled sub-increased credibility because federal mandates direct that stances and require special handling, based on two prindisability be determined by physical or mental impairciples: to benefit the patient and to be in compliance withment, or both. regulatory agencies. Pharmacologic drug selection and The reader is referred to various chapters that relate dosage schedules must be individualized. more specifically to these concerns. Recall that clinical judgment is necessary because, to paraphrase Albert EinAnti-inflammatories stein, “All that is important cannot be measured and all that is measured is not necessarily important. ” The test for Anti-infl ammatories have made signifi cant advances in clinicians is that they be able to provide a basis for their becoming more receptor specifi c in therapy, moving ordered tests (i.e., that the tests be reasonable and necesfrom (COX) cyclooxygenases (with 14 subclasses) to sary) because they may be challenged or adjudicated by the new (COXII) generation with reportedly less undethe legal community. sirable side effects, targeting gastrointestinal, renal, hepatic, and pulmonary organ systems. These individuals still require close monitoring because adverseMODALITIES effects can occur at any time in a treatment program to Modalities are gaining increased use in medical pain manany patient. agement because of the lack of complete ficacy ef of selected chemical compounds we call pharmaceuticals. We are in no way being critical of the pharmacologic approach to pain medicine, but there are limitations of Antispasmodics are prescribed when there isficient suf dosage schedules, intolerance reactions, and lackfi-of ef clinical/objective evidence of involuntary muscle spasm cacy that must be recognized. Some patients are averse to that itself causes pain and limitation of function. The three take medicine. Modalities offer an alternative. classes act: (1) peripherally at myoneural junctures; (2) at Two types of modalities are recognized: the spinal cord level, influencing afferent-efferent modulation; and (3) central inhibition at cortical and possibly 1. Mechanical subcortical levels. 2. Electrical Antispasmodics

Antidepressants

Both prescribed therapies require individualization and outcome documentation. Antidepressants can play a major role in pain management because they are a class of medications that result Mechanical or physical modalities include self-care, rubbing massage, pressure, ultrasound, stretching, tracin several synergistic effects: (1) antidepressant-serotontion, hydrotherapy, and heat and cold techniques. These ergic, (2) antispasmodic, and (3) analgesic. These three can be self-administered, or provided by trained assistants effects vary depending on the type of selective serotonin and professionally experienced physical therapists, and reuptake inhibitor (SSRI) prescribed. also manual medicine techniques performed by osteoThese four classes of medicine can be prescribed singularly or in combination. Frequently, polypharmacy pathic and chiropractic physicians. These offer a variety of options and combinations to assist in the healing results and careful trials of various compounds must be process. All, in various ways, have the potential to accelmade to produce an optimum treatment plan.

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erate the normalization of the pathophysiology of disease The reader is referred to chapters that address these and injury processes. subjects in more detail, permitting the PCP to enter a Electrical modalities are gaining wider acceptance asnew field of electromedicine therapy that we call medical our basic knowledge of physics as applied by medicalenergetics. researchers and bio-engineering has progressed. This progress then lends itself to the clinical practitioner. PHYSICAL MEDICINE AND REHABILITATION Electrical energy used as a therapy has long been Physical medicine and rehabilitation are recommended recognized as beneficial. As we move from a pharmacofor therapies of acute, chronic, and cancer pain because logic-allopathic and homeopathic system of care, we are they provide more than modality treatment. For the using more electronically based therapies. Based on the PCP, it supplements the therapy program in the patient classic research of Gibert, Faraday, Nordenstrom, Becker, Avery, Sheely, Kirsch, and so many others, many clinicalwho continues to have symptoms and impairments of daily activities involving personal and work tasks. It applications are now available to the PCP. Transcutaneous electrical nerve stimulation (TENS)provides a second opinion for the PCP, and it enhances has been available by prescription since the Medicalthe patient’s probability of improving while documenting progress or lack thereof. We refer the reader to the Service Act passed in 1975. There are now probably 100 appropriate chapters on ergonomics by Dr. Sella and types of devices on the market, but great care should be others. exercised in selecting the most suitable modelwith — special attention given to the electrode placement pat- The psychological and psychiatric assessment and tern, electrical settings of waveform, pulse width, andmanagement of the pain patient presents a special field individual tolerance requirements — before prescribing for consideration. Because the discriminatory-affective is complex and is superimposed on a preexista unit. In over 40 years of experience, we recommend component a trial of four to six treatments in the fice of setting with ing emotional character profile, diagnosis of personality physician and clinical assistant supervision before pre-characteristics can be identified as pre- and post-disease and/or injury. Attitude and behavioral components can be scribing home-use units that cost between $200 and s $800. A rental trial is often desirable for home care toevaluated and managed in conjunction with the PCP’ treatment of pain syndromes and co-morbidity. Special see if the patient understands how to use the device. When effective, we found that TENS provided a substan-consideration is made for energizing stress, anxiety, and tial savings (in oral medication) when individualized depression. Reflective care can be offered for lack of complaint; lifestyle and drug abuse without symptom magnifrequency and pulse settings and optimal electrode pad fication must be evaluated very carefully, with further placement were employed. Care must be taken not to prescribe TENS duringfirst and second trimesters of consideration of secondary gain but also secondary losses. Munchausen’ s syndrome and psychogenic pain patients pregnancy, or with cardiac pacemaker patients. Never should be seen in conjunction with specialists in the field. place the electrode adhesive pad over the cervical region of the carotid sinus, due to the possibilities of affectingThe reader is referred to appropriate chapters in this text for further reference. the cardiac rhythms. Electromedicine has made other significant clinical advances in providing relief of physical pain by, probably,OCCUPATIONAL AND VOCATIONAL REHABILITATION closing the spinal gate that hinders the perception of pain by stimulation of the A-beta fibers but also causing a mildOccupational and vocational rehabilitation are important vasodilation (not yet reported in the literature). Thisaspects of pain management for the PCP because they can Alpha-Stim type of stimulation is different from TENS in be made part of the necessary therapy, especially for those with chronic and cancer pain symptoms. Resource serthat it provides a somatic as well as an emotional moduvices are available from both private and state-supported lation pattern mediated by the serotonergic system. Microcurrent electrical therapy (MET) reported by Kir- programs, the latter of which have no service fees. This allows the PCP to be captain of a multidisciplinary team sch and Mercola, is based on bio-electric data and provides, for the first time, a combination therapy for the modulatingto coordinate diagnosis, treatment, and rehabilitation plans the perception of somatic pain and its emotional affectiveand to assist the patient in returning to an economically productive lifestyle. Insurance programs frequently do not symptoms. It has been approved by the FDA. Using probes or clip electrodes applied to the ear-pay for job retraining but are ready to support job modification services in returning the patient to work, thereby lobes, selected patients can use the alpha-stim device for office or home care applications. Not all patientsreducing their monetary outlay. The reader is referred to other chapters that address benefit from these modalities, but they do offer a variety of options for patients who do not, will not, or cannot the challenges and barriers faced by patients returning to the workplace. take medication.

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MEDICAL/LEGAL ASPECTS

277

PAIN MEDICINE

Programs. Periodic reevaluation visits are performed to verify the continuing disability. The reader is referred to The medical and legal aspects of pain medicine presentthe a chapters on disability in this text for more information. different sort of challenge because they are based on the In conclusion, we are of the opinion that: adversarial approach to medical management, in which the PCP is frequently not as experienced as the clinical 1. PCPs are in an eminent position to become medicine physician. Simply stated, the PCP is in a position specialists in pain medicine. to provide both factual and expert witness reports, and, 2. Educational resources are available for inwhen needed, testimony as the treating physician who has office, local, regional, and national services consulted with the patient many times. PCPs are able to offering continuing education credits, certificaprovide credible history, physical examination, treatment, tion, and advanced degrees. pertinent laboratory ndings, fi outcome, and diagnosis. 3. The PCP can become coordinator and captain They can also provide estimates for future medical care, of the ship in pain medicine, providing an indiprognosis, and disability determination by documentation vidualized, humanized treatment program for or oral testimony. These are all subject to challenge by the patient. opposing counsel as well as the medical testimony of 4. Specialty consultations are available to offer secphysicians retained by opposing counsel. These retained ond opinions in complex pain syndromes availphysicians often render reports that tend to minimize findable locally or at academic university centers. ings, testifying about the co-morbidity, preexisting disease 5. The PCPs can concurrently manage co-morbidor injuries, or a contributing cause of the plaintiff ity while practicing pain medicine. (patient’s medical and psychological problems) from a 6. The PCP’s office staff can be trained in special retrospective point of view. techniques for in-of fice care at substantial cost The treating PCP, however, can provide evidencesavings. based opinion and testimony that the diagnosis, treatment, 7. The PCP can provide a supportive and counseland related services being addressed are, in fact, reasoning role in the areas of pain medicine in conable and necessary. The treating physician should also junction with psychological and psychiatric charge for the medical/legal services performed, based on consultations. a usual and customary fee schedule that can be made 8. The PCP can refer the patient with special available to requesting agencies prior to rendering these behavior, abuse, compliance or lifestyle impairadministrative services. Because the rules of testimony ments to specific evaluation and treatment proand evidence change and vary from state to state, the grams and to share the care officult dif patients. reader is referred to the medical/legal chapters of this text 9. The PCP can provide medical testimony that is to update further information. evidence-based and provide impairment ratings OF

for further disability determination.

DISABILITY DETERMINATION

To paraphrase Hypocrites: The future is bright, but Disability determination is a legal concept and has become fraught with difficulty. We will be trained beyond our the purview of the legal community and state and federalintelligences, so the real test for physician is at the bedside . agencies. The PCP, however, is in an eminent position to The ball is in your court. Primary care physicians determine functional impairment. How is this determined?should consider the following value concepts in medical By clinical experience, medical literature, and consulta-decision making. tion, an impairment rating can be determined quantitatively based on mild, moderate, and severe impairment 1. Clinical: Accumulate as much relevant medical classifications. When mild, the patient can perform home, information as possible, employing acceptable self-care, return to usual occupational work and need not services to benefit the patient. Less than that is have professional treatment or see a physician, except on not acceptable. occasion. In the moderate category, the patient has impair- 2. Educational: Every patient encounter proment that interferes with activities of daily living (ADLs) vides an accumulation of data contributing to and must modify these; professional treatments are needed clinical experience, but can also be shared with and physician care is important. Return to work must be others through anecdotal or published peer modified. In severe impairment, the patient has continued review literature. symptoms and needs continued treatment and ongoing 3. Research: Evaluation of unconventional professional medical care. He or she is not able to return approaches to unusual problems adds to the to work and is considered totally and permanently disabled total fund of knowledge and should be shared. as determined by Social Security Disability Entitlement

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4. Administrative: Simplify documentation; it has created a burdensome task for clinicians and staff as well as significantly escalating the cost of medical care. How can this be accomplished? The PCP’s help is needed. 5. Fiscal: Cost constraints instituted by third-party payors have inhibited medical programs. What other options are available? 6. Regulatory affairs: Agencies mandated by legislative actions to maintain and control health care delivery systems often go beyond the spirit of the legislation and are dismantling the nest fi health care system in the world. Together, can PCPs make a difference by acting in an advisory capacity due to the signifi cant advances that produce the gaps in agency updating?

7. Political: Correctness creates a trend toward mediocrity. Having served, can PCPs take a leadership position? 8. Medical/legal: Responsibilities have grown complex and costly, developing an adversarial system in which many health professionals and patients have lost confidence. It still is considered the best we have. How can PCPs help regain credibility? 9. Personal: Has this entire effort of dedicating one’s life and career to the care of others been of value? Guerir quelquefois Soulager souvent Consoler tousjours Anonymous

24 The Impact of Pain on Families James H. Ballard, D.Min., C.R.T. INTRODUCTION: THE IMPACT OF PAIN

abdomen. The attempt to diagnose its origin led to deep depression on my part. All of that resulted in an emerFrom the moment actor Christopher Reeve suffered his gency medical furlough and 6 weeks of hospitalization. accident riding horseback, not only was his life changed,At the end of that time the doctor recommended that we but also the lives of his wife and family. Whether one’snot return to Brazil because of the possibility of the pain is the result of an accident or an illness of spirit, soul,disease returning. Needless to say, my physical and psyor body, its impact is like a rock dropped into a pond …chological pain resulted in emotional and relational pain it has a ripple effect. for my wife and our two preschool-aged children. The Phyllis was referred to me by a local physician. Thetrauma of all that took place sent shock waves through victim of a serious automobile accident, she had spent our family at the time and for several years after our months in physical recovery. In the later phases of herreturn to the U.S. physical therapy, she experienced pain in her body that I agree with Carl McNeely (2000) when he states that could not be traced to any physical cause. She had begun patients, along with family members, may frequently have to have flashbacks to a very painful and abusive past. After adjustment difficulties because of changes in roles and sessions dealing with spiritual and psychological issues, limitations of the functioning of the patient. Look with me I remarked that she had not mentioned the physical pain at the impact of pain on families in the following areas. for which she had entered counseling. Her remark was, “It’s gone!” Relief of pain in spirit and soul had brought PAIN IS INTERGENERATIONAL about physical healing. These sessions took place several years ago and there has been no recurrence of her pain. Karl, in his mid-fifties, has had both heart catherization After years of counseling from a Christian perspec-and bypass surgery. He is presently separated from his tive, I am finding many whom I counsel to be in physicalwife due to repeated martial infidelities on his part. The or psychological pain. Very often, such pain comes fromprobability of reconciliation is very slim. His family of deep spiritual and psychological issues that have not been origin gives evidence of heart trouble for several generafaced and resolved. Rejection, abuse, and abandonment tions. Emotional, relational, and physical dysfunction has often result — not only in spiritual or psychological crises,carried over into his generation and it has become clear but physical ones as well. that, with each succeeding generation, the toxicity has The victim does not stand alone. Family structures are increased. There have been boundary violations within the also vitally involved and affected. Treatment of pain notfamily of origin structure. Karl is not the first to commit only impacts the victim but all those who are part of hisadultery. He is carrying into his generation the lifestyle of or her world. earlier generations. Such behavior ensures that familial A number of years ago, my wife, two children, and pain from the past is carried forward. Karl has two sons. I lived in South Brazil where we served as missionaries.It is Karl’s perspective, however, that his separation and While there, I came down with extreme pain in thedivorce from their mother will not affect his boys because 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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“they are adults. ” It is difficult to move beyond denial. that is self-destructive. These traits can develop in young Often, hurts go deeper in adult children of divorce thanchildren as well as in older ones. Unconditional love and in those who experience that trauma in their earlier years. care within families of origin are extremely vital for There is a probability that Karl’ s sons will continue his healthy relationships to form. Where conditional love or behavior for another generation or else emotionally sepabsence of any type of deep, parental caring is evident, arate themselves from their father’ s irresponsible actions. there is pain within one’ s personhood. I have spent more time counseling George and his Unmet parental needs often find children going into fourth wife, Nora, than most of my other clients. Thereprofessions of parental choosing rather than those of their own choice. Dennis was such a person. His future was was deep-seated anger and personality conflicts between laid out for him by his doctor father who wanted his son them. Nora has a very co-dependent personality. Her to follow in his footsteps. Dennis went to medical school record of failed marriages closely resembles George’ s. They both brought a child into their marriage. These chil-and through medical residency, much to the delight of a doting dad. After Dennis completed his residency and set dren witnessed the pain and anger that permeated their parents’ relationship. Both of these children are now up a medical practice, his father died. Freed from his father’s shadow, Dennis left medicine to become a musiapproaching their teenage years. I am very concerned that the past irresponsibility of their parents may wash overcian, something he had desired to do since childhood. into their lives, thus carrying the toxicity of the past into Warren was the son of a woman who had risen rapidly the present and drastically affecting their futures. in governmental service. She was perfectionistic and controlling in her family. Warren’ s father left the marriage After a number of sessions with George, there was a s dominating personality. Warren, breakthrough. He admitted that much of his anger, whichbecause of the mother’ unable to escape the power of his mother took out his surfaced frequently, was the result of the sexual molestaanger and rage on four different wives. As of this writing, tion and abuse he had experienced as a child. he is allowing his mother to continue to “bail him out. ” Sexual molestation between the ages of birth and 18 years is affecting one out of four women and one out ofHe does not tell his mother where to go; rather, he chooses another woman to become a victim of his dysfunctional five men. The trauma of these events, often many violarelationship with his mother. Warren’ s failed marriages tions over a period years, has devastating effects on the victim and those around him or her. The pain of guilt andhave caused much pain, not only for his ex-wives, but also for their immediate families. shame exacts a high price on the victim. Scars remain with them for years, whereas the perpetrator often does not In the procession of pain within families, whether that pain is spiritual, psychological, or physical, there are other remember actions toward the victim. Traumas from past violations of one’ s personhood can dimensions to consider. have a devastating effect upon one’ s self-esteem. It can affect the victim’s approach to personal intimacy. EviTHE TRAUMA OF THE TEMPORARY dence of the negative effect of such traumas can be seen in many victims of rape. Marriage bonds are strained and Whether it is a broken bone because of an accident or a often broken because of this violation of one’ s person. broken heart that is the result of a failed relationship within Although violation of one’ s physical being may not be teen years, there is trauma that impacts the family structure. evident in many cases, it can be in other areas. Our knowledge and discernment tells us that this, too, shall pass. Yet, during the disconcerting days of its happening, schedules are interrupted and the focus of attenPAIN IS INTERRELATIONAL tion is shifted with the victim leaving other important tasks When a family is healthy in its relationships, it allows undone. Stress often becomes the order of day, particularly appropriate boundaries and personal privacy. There is ifait involves the victim’s hospitalization. Life often seems clear distinction between adults and children. Children areto be filled with times of temporary paining. One knows allowed to be who they are … children. When there isthere will come an end to the hurts, but the journey through the valleys of pain are real while the family member is in dysfunction and enmeshment, children are often the major source of af firmation and affection for the adults. I fre- crisis. There is often a toll on the health of the family. quently hear from clients that they were never allowed to have a positive, happy childhood. They had to continuallyTHE CRISIS OF THE CHRONIC replenish their parents’ sense of well-being. The child in The processing of pain within families of Alzheimer’ s such a relationship often becomes a parent to the parent (or parents). When children grow up in such a toxic envi-patients can be ongoing and often debilitating. The decline ronment, they experience relational pain. The conse-of mental and physical faculties of the patient are often years in duration. Alice was a strong independent woman quence of having to meet parental emotional needs can result in low self-esteem and burnout, or in a perfectionismwho, with her husband Glenn, had a good life on a farm

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in Piedmont, North Carolina. After Glenn’ s death, Alice effect on the family structure. With the severe mood began to show signs of early Alzheimer’ s and began a swings of the victim, there often comes a breakdown of slide into its depths over an 8-year period. Judy, Alice’ s the family structure. Aberrant behavior often causes daughter, took care of Alice at home for the duration ofstrains in a breakup of marriages. Trace this disease back Alice’s life. During that time, Judy worked full-time as a and one often finds genetic links. The same can be true nurse in a regional hospital and spent most of her time with schizophrenia. With both bipolar disorder and schizoaway from work caring for her mother. Alice’ s decline, phrenia, entire families can be affected by the disease of slow at first, began with Alice’ s constant wandering one member. Grace and Harry have a son, Clarence, in around the community and progressed more rapidly withhis early twenties, who has been diagnosed with schizotime. When living with Judy, Alice often set off the house phrenia. When Clarence is on his medication, his behavior alarm at night while attempting to leave the premises. The is stabilized; but like some, he periodically thinks he can possibility of a normal life between Judy and her husbanddo without his medication. When this takes place, the and children became secondary and often nonexistent chronicity of this psychiatric problem takes its toll on the because of the demands of Alice’ s illness. Alice was a family structure. Henry and Grace do not have to tell me large woman and incontinence became an increasing probwhen Clarence is not taking his medication because I can lem that necessitated much lifting and changing. Outside see the pain on their faces and in their eyes. help was difficult to obtain because few people were physically able to manage Alice. The strain of years of dealing with Alzheimer’s had its effect on every family member. PAIN AND PERSONALITY Cancer is another chronic disease that takes its toll on Dick is the older of two boys. William, his younger family members. The Wards were a close-knit family.brother, is 9 years his junior. In his teen years and early Lowell and Ruth, elderly in years, were deeply distressed twenties, Dick acted very immaturely and irresponsibly, when their daughter Carole, with a family of her own, causing his parents to spend an abnormal amount of came down with cancer of the pancreas. For several years, time in rescue mode — devoting time they should have Carole endured an endless series of chemotherapy treatbeen spending with William — coping with Dick’s conments. With each treatment, the quality of Carole’ s life tinuing crises. decreased. Lowell and Ruth spent much of their time and Dick got involved in the drug and alcohol scene and energy caring for her. almost lost his life in a wreck. Seeing the actions of his I recall, during one of my pastoral visits, watching brother, William withdrew into himself and became a Ruth massage Carole’ s back as the cancer spread within very private person, not expressing his feelings to family her body. I do not believe the touching alleviated much or friends. Extremely brilliant, he chose to rebel in pain, but the tenderness of her mother’ s massage had a another way. He refused to attend college and he became soothing effect on Carole’ s mind and spirit. Six weeks extremely critical of societal institutions, particularly in after that scene, Carole died. Just a couple of months later, the areas of education, politics, and religion. William Ruth was diagnosed with a rapidly growing cancer. Refuschose a track opposite to that of his brother. He became ing any treatment, she died within weeks. The pain of a fiercely independent, hardworking, and sought to free double loss so close together had its impact on Lowell, himself from causing anynancial fi drain on his parents. who was 80 years old. The stress of watching his daughter The pain of the problems in the lives of these young men and wife deteriorate, and the grief following their deaths, took a fatal toll on Lowell. He experienced kidney failure had a long-lasting effect on both parents. At one time, and died within weeks of his diagnosis. The impact ofthe strain was so great that the parents contemplated approaches to the such chronic pain exacted the ultimate price on the family.separation and divorce. The parents’ concerns of their children caused them to act in opposite Similar to Alzheimer’s, AIDS takes it toll on family ways. One parent became over-controlling and the other members, often not just psychologically, but physiologipassive-aggressive. cally. I visited John’s hospital room often and every time I went, Mary was there sitting beside her son John who was critically ill with AIDS. As John deteriorated, the PAIN AND PERSONHOOD strain of his illness became more evident on Mary’ s In I Thessalonians 5:23, Paul the apostle prayed that the demeanor. There were two victims of this terrible disease in that room. When John died, I conducted his funeral.Christians at Thessalonica would be preserved complete Not only John’s companion, but members of the gay com-in spirit, soul, and body at the coming of Christ (NASV). munity who had been John’ s friends, gave evidence of Both the Old and New Testaments use separate words in describing these three entities of who we are. their pain from the loss of his life. Whenever we experience pain in one aspect of our Genetics often play a tragic role in the family strucbeing, it affects the other areas. There is often spiritual or ture. Increasingly, bipolar disorders have a devastating

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Not only is the assistance of the family crucial for the psychological pain before physical pain is evident. Stresses within one’ s personality often cause the body to patient, but the family itself has needs that cannot be fall victim to diseases it otherwise has the capability toignored. Caregivers need to have time and energy for their overcome. other varied roles within the structure of family. We are now living in a time where the body is looked Boundaries must be visible. There must be a differat as more than a free-standing mechanistic instrument entiation between caregiving (which has boundaries) and that allopathic medicine can fix. Psycho-spiritual entitiescaretaking (where boundaries are nonexistent). It is crucial must be brought into play as well. that goals be established concerning family involvement. Emotional dysfunction that has been a pattern for sev-Being proactive rather than reactive in this area can be of eral generations may ultimately express itself throughassistance in the ability of the patient to get better. physical symptoms. In a conference sponsored by The It is unwise to treat a complex, chronic pain patient National Institute of Clinical and Behavioral Medicine, separately from his family and social network. This Dr. Paula Reeves (1994) presented a paper dealing with approach could doom or, at best, retard the treatment the effect of somatic belief patterns on emotional, physi-process. ological, and behavioral change. She stated that our biography is our biology, beginning with conception. Her FACING THE FAITH FACTOR belief is that all disease is psychosomatic, with symptoms being one-tenth instinct and nine-tenths metaphor. The In the Old Testament, Job, from the depths of pain that majority of physical illnesses are the result of emotionalencompassed his whole being, states that “… I know that and spiritual crises that occur in lives that experience a my Redeemer lives … even after my skin is destroyed, lack of love and family involvement. yet, from my flesh I shall see God. ” (Job 19:25–26). In Core messages that spring from family concerns result the midst of traumatic testing, Job’ s faith was not in illnesses. Dr. Reeves offers these examples: destroyed, but refined. Several years ago, I visited a lady who was in the terminal stages of cancer. She remarked, “I am so glad I have cancer. ” Taken aback by that stateDon’t feel Phobias, depression ment, I asked, “Why?” Her reply was that through the Don’t think Headache; ear, neck, throat problems pain of cancer she had met many wonderful Christians Don’t be a child Eating disorders, substance abuse, kidney andwhom she otherwise would never have known. Although bowel problems her body was wasting away, due to the disease, her soul Don’t exist Respiratory/circulatory problems, sexual and spirit were at peace. dysfunction, allergies Allopathic medicine seeks the cure and alleviation of Don’t be yourself Skeletal: facial and balance problems pain. There can be healing of soul and spirit without a Don’t be a bother Muscle problems, nerve disorders (multiple cure for the body. You see, we are eternal beings in soul sclerosis, muscular dystrophy) and spirit who live in temporal bodies. All of the above involve pain. Such pain causes fam- A number of years ago, my grandmother developed ily concerns and pain as well. Anyone experiencing thepancreatic cancer. Her disease progressed slowly. My father remarked toward the end of her life that, up until above, according to Dr. Reeves, needs to trust that symptoms have meaning for one spiritually, emotionally, that point, he had emotionally held on to her. When he was able to release her, my grandmother died within a physically, and mentally. short time. And history repeated itself with my father. He almost THE ASSISTANCE OF THE FAMILY died of kidney failure. At that time, my mother prayed, ” Dad lived for 6 Carl McNeely (2000) states that positive interaction“Lord, whatever it takes, let Harold live. more years. My mother, during those years, administered between family members and the person with chronic peritoneal dialysis every other day. As his condition worspain is crucial. Often, when pain levels are high and the ened, mother one day remarked to me, “I am ready for dependency of the patient is great, things can be very your dad to go on home now. ” Dad died a short time later. difficult as well as frustrating. As much as possible, I believe that God, in His mercy, allows loved ones to live clear, open communication is vital to keep at bay the until that time of emotional release by relatives. mounting resentments and counterproductive emotions Core Message

Illnesses

and reactions. The establishment of routines and goals is vital to bothSTRATEGIES FOR POSITIVE ACTION the patient and family, whether the pain is physiological, All of the illustrations set forth in this chapter have a psychological, or spiritual. Family help and assistance are common thread: the faith factor. Christians are not perfect; crucial in up to 70% of patients experiencing pain.

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they are pilgrims. Through painful traumas, both the victim and family members indicated that their faith was often deepened. Andrew knew that he was losing his battle with cancer. His family had put his hospital bed in the living room so that he could see outside. On one of my visits, near the end of his life, Andrew told me that the night before had been a long and painful one. As he lay awake in the midst of his pain, he had begun thinking of how blessed he was with both his family and his faith. And in the midst of the darkness of the night, he had burst out singing. I recalled the scripture from Job 35:10b, “He (God) gives us songs in the night.” A friend of mine, Dr. Ronna Fay Jevne, has Crohn’ s disease. Yet in the midst of her pain, she has ministered to many cancer patients in Edmonton, Alberta, Canada. She is the author of several books centered around the theme of hope. She is also the founder of The Hope Foundation. She shares the following from her book, The Voice of Hope, Heard across the Heart of Life (Jevne, 1994):

“THE VOICE

OF ILLNESS”

Illness is an introduction to the fragility and sacredness of life. With illness we learn we are not immune. Nor are those whom we love. We learn that our sense of invulnerability is an illusion. Illness is the great equalizer. We come to understand that life and death are intimately and ultimately connected. For everyone. Illness comes with a formidable invitation to notice the sacredness of life. It is a wake-up call to slife’ preciousness. A call to notice the everyday, to be present here” “ and “ now.” To place our lives in perspective to others, to our universe. To accept the place we have innity infi and eternity. To ask thebig” “ questions and enjoy the “ simple” answers. To do this, we mustndfi a rightful place for suffering. A perspective that allows room for hope. Serious illness is a journey, a hopeful journey, an unknown destination. In illness the dichotomies are vivid. Hope is the space between symptoms and diagnosis, between diagnosis and prognosis. It is the wrestling match between science and compassion, between body and spirit, between pain and relief. It is the dilemma between fearing to be alone and hungering for privacy. Hoping is waiting: for test results, for appointments, for the organism to heal and the spirit to rekindle. Hoping is walking the line between tolerating constant probing and invasions, and declaringno“ more, not now. ” The hope for survival is not the only hope; many days, not even the overriding hsope. The real hope is not toinvalid.” be “ Hoping is knowing that someone is making an effort to help. That family is never far away. That the system cares. That what happens is the best of technology and the best of humanness. Hoping is being attended by

people who understand that caring makes a difference. An immeasurable difference. Hoping is being treated, not as another case of a particular disease, but as a person. By people who understand, this could happen to them. It is knowing there are no secrets. Being a partner on the treatment team. Being encouraged to do as much as possible for one’ s self. Hoping is trying again. Moving against the odds. Knowing everything that can be done is being done. Knowing the caring will go on when the limits of science are reached. Hoping is denying the statistics. Reaching beyond the traditional. Keeping open the possibility of being the exception. Hoping is listening to the unconscious. Having dreams in the world of sleep and dreams in the world of the consciousness. Wondering if there are miracles. Being fascinated with the little miracles: the words that heal, the memories that let us forget. Hoping is having passion for life. Noticing life. Wanting life. Inching toward life. Being willing to embrace life despite the risks. Hoping is recognizing that death is not the enemy — never living is. Suffering humbles us; hoping takes us forward. We come to understand that we are among many who are ill. Among many who hurt and fear. And who need. We come to trust the unusual experiences we cannot explain. The experiences for which we have no words. There is a knowing that accompanies suffering; a knowing that emerges from deep within us. That speaks from another dimension to life.

Pain affects not only individuals and their family structure, but impacts the human family. We, despite our many differences, are fellow pilgrims on this planet. Perhaps the one thing that is a common factor is pain. The Apostle Paul, writing to the Corinthians, made a statement regarding not only the physical body, but the body of Christ, the Church: “… members should have the same care for one another … if one member suffers, all the members suffer with it; if one member is honored, all the members rejoice with it”(I Corinthians 12:25– 26, NASV). During my years in the ministry, my family and I have experienced periods of pain, either relational or physical. During those times, I questioned why. I now know that those times of trauma were to better equip us to understand and minister to ones trapped in prisons of pain. May it be so with you as well.

REFERENCES Jevne, R. F. (1994). The voice of hope, heard across the heart of life. San Diego: Lura Media. McNeely, C. (2000). The role of the family in the treatment of chronic pain.The Practitioner,10(2), 5.

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Reeves, P. (1994). Spontaneous movement: The effect of somatic belief patterns. National Institute for the Clinical Application of Behavioral Medicine Conference, Vol. A, 482, 493. Mansfield Center, CT: National Institute for the Clinical Application of Behavioral Medicine.

25 The Impact of Nursing on Pain Management Chris L. Algren, R.N., M.S.N., Ed.D. and Mary Romelfanger, R.N., M.S.N. INTRODUCTION

Pain-related guidelines were among the first sets developed by interdisciplinary expert panels representing Pain is the most common reason patients seek out healthmedicine, nursing, pharmacology, psychology, rehabilitacare professionals. The National Institutes of Health (NIH,tion therapy, ethics, and consumers/patients. Nurse clini1987) published a consensus statement in 1987 that cians, educators, researchers, administrators, and professtressed the “caring” and “curing” role in pain manage-sional nursing organization representatives provided ment. Since that time, great strides have been made in the input. The first edition of the Acute Pain Management assessment and understanding of the multiple dimensions Guidelines was published by the AHCPR in February of pain. Advances have been made in both the pharmaco1992 (Acute Pain Management Guideline Panel, 1992). logic and nonpharmacologic methods of treating pain. TheThe American Society of Anesthesiologists promulgated number of multidisciplinary pain centers has grown rap-guidelines for acute pain management in the perioperative idly. Comprehensive, holistic pain management using asetting in 1995 (Ready, 1995). multidisciplinary team of health professionals with an Most recently, the Joint Commission on Accreditaintegrated approach has gained wide acceptance. tion of Healthcare Organizations (JCAHO) published The NIH consensus statement expressed concern that Pain Standards for 2001 (JCAHO, 2001). These new the education of many professionals — including nurses,standards are effective for surveys conducted after Janphysicians, dentists, and physical therapists — did notuary 1, 2001. Aspects of pain management are covered put sufficient emphasis on contemporary pain assessment in six of the eleven chapters of functions or activities and management. The need for communication and colrequired of accredited healthcare organizations. Orgalaborative approaches among professionals was noted nizations — including ambulatory care, behavioral (NIH, 1987). healthcare, home care, hospice, hospitals, and longThe U.S. Congress created the Agency for Health Care term care facilities — now have a mandate to address Policy and Research (AHCPR) in December 1989 as the pain management. federal government’s focal point for health services The integration of the pain management team’s knowlresearch. The agency’s mission is to enhance the quality edge and skill is enhanced through an understanding of of patient care services by generating knowledge that can the perspective and scope of practice of each discipline. be used to meet society’s healthcare needs. The AHCPR Pain manuals specific to nursing practice are available is responsible for developing and updating guidelines that (McCaffery & Pasero, 1999). will be used to manage clinical conditions. To meet these Because “patient” is used by pain management pracchallenges and others, agency activities include database titioners from many disciplines and because “patient” is development, effectiveness and outcome research, and disused in a majority of settings where nurses practice in the semination of research findings and guidelines to providworld, “patient” rather than “client” is used in this chapter. ers, policy makers, and the public (Acute Pain ManageThe rights and responsibilities associated with the use of ment Guideline Panel, 1992). “client” are intended. 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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THE NURSE’S ROLE IN PAIN MANAGEMENT

can only observe signs and obtain information about symptoms. The pain belongs to the patient, not to the practitioner. The person with pain is the best judge of the Nurse decision-making is performed step by step using existence, duration, and severity of the pain and the sucthe nursing process, including assessment, diagnosis, cess of pain management treatments. planning, implementation, and evaluation (Gordon, 2000). The patient as expert rather than the healthcare pracBased on the establishment of a trusting relationship and titioner can be dif ficult for the practitioner to accept. Until a good rapport with the patient and family, this systematicrecently, pain has been viewed as a symptom, not as a process provides a framework for nurses to provide care diagnosis. Pain was thought to be something the healthfor patients with pain in all settings. care provider could cure, or at least control. Many times, The move to multidisciplinary planning and plans of the cause of chronic pain is not discovered quickly or care is supported by accrediting bodies such as the easily. The healthcare provider as well as the patient JCAHO and the American Academy of Pain Management,becomes frustrated. Pain Program Accreditation. Current hospital and home Many healthcare providers had and still have little health JCAHO standards require coordination, collabora-training about pain, particularly chronic pain, and the tion, and continuity of services to each patient by allrelief of pain. Often times, pain management is not condisciplines through an established plan of care. Criticalsidered a priority. pathways are a means of organizing patient care that relate The nurse is a key player on the chronic pain mancare and services by disciplines and time frames to costs agement team, regardless of the setting. Nurses who work and measurable outcomes. Critical pathways are populain community settings are likely to regularly help patients tion specific and provide a database for performance and families manage chronic as well as acute pain. improvement, including outcome-driven, competencyTable 25.1 outlines how home health standards for pracbased staff development. Sample diagnosis-related critical tice and reimbursement can be applied to a diagnosis of paths are available in the literature (Aspen Reference pain (Marrelli, 1994). Group, 1995; Cronin & Bahrke, 1996; Ignatavicius & The nurse, as well as everyone caring for the patient, Hausman, 1995). needs to know the meaning that pain has for the patient. Nurses play an essential role in the assessment of a No chemical or neurophysiological tests exist that can patient’s pain. The information the nurse obtains from accurately measure pain. Because the question of whether assessing the patient’ s pain is used to identify goals for managing that pain. The goals for the patient can be accomplished using a combination of both pharmacologic TABLE 25.1 and nonpharmacologic means. Assessing the effectiveness Home Care Pain Management of interventions and monitoring for adverse effects are important aspects of the nurse’ s role. The nurse serves as • Documentation Guidelines an advocate for the patient when the intervention is not• General considerations effective in relieving pain. The nurse also serves as an• Need for initial visit educator to the patient and family. Teaching about pain• Potential diagnoses and codes (medical-surgical) • Associated nursing diagnoses (e.g., home maintenance management, and measures to relieve it lessens anxiety and gives the impaired) patient and family a sense of control. • Skilled services (e.g., RN to implement nonpharmacological interventions, titrate medication dose to achieve outcome with acceptable level of side effects) NURSING MANAGEMENT OF CHRONIC • Other services (e.g., home health aide to assist with activities of NONMALIGNANT PAIN daily living; MSS to assessnancial fi ability to comply with pain treatment plan; physical therapist to teach energy conservation, One of the most widely accepted definitions of pain is that apply heat or cold) “pain is an unpleasant sensory and emotional experience • Homebound status factors associated with actual or potential tissue damage, or• Short-term goals by discipline (e.g., RN to daily control pain and described in terms of such damage” (IASP, 1979). Pain is other symptoms) not determined by tissue damage alone. Patients with• Long-term goals by discipline (e.g., RN, patient, and/or caregiver knowledgeable about pain management measures) chronic nonmalignant pain (CNP), pain not associated • Discharge plans with a neoplastic process, may have pain for which little• Education needs : patient/family/caregiver or no tissue damage can be found. • Reimbursement tips

Pain is subjective and personal. McCaffery’ s (1968) definition — “Pain is whatever an individual says it is, Adapted from Marrelli, T.M. (1994),Handbook of Home Health Stan(2nd ed., pp. and it occurs whenever he says it does” — seems espe- dards and Documentation Guidelines for Reimbursement 243–248). St. Louis: Mosby, Inc. cially relevant for the patient with CNP. The practitioner

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the patient has “real pain” cannot be answered, healthcare threshold, other factors are known to alter pain perception providers must accept the patient’ s report of pain. The in the elderly. These include peripheral and central nervous nurse must determine what the patient thinks is needed system in impairments, drug therapies, cognitive impairorder to deal with chronic pain. Nurses, particularly thosements, co-existing pathologies, individual psychophysiowho are discharge planners or who work in the commu-logical or cultural experiences, and adaptation (Caird et al., nity, need to know what resources are available to patients 1987; Carpenito, 1999; McConnell, 1988; McCue, 1987). in pain. Support groups established to assist individuals Whether a result of increased pain threshold or other in pain and referral services for patients are needed. One factors, certain conditions are reported to be less painful such group in the United States, with chapters throughout in older adults than in younger persons. Conditions frethe country, is the National Chronic Pain Outreach Asso-quently presenting with significant pain in younger perciation. Nurses and physicians often serve as advisers sons or but with only mild discomfort in the elderly include as coordinators for local chapters. If the practitioners are peptic ulceration, appendicitis, pneumonia, and mesencertified in pain management by the American Academyteric infarction (Charlton & Buckley, 1984). In the elderly, of Pain Management, they bring valuable knowledge andthese events may be heralded only by vague signs such as expertise that might not otherwise be available to manyrestlessness or confusion. members of the group. Another factor confusing the symptom pattern in the Regardless of the setting, the nurse functions as patient elderly is the tendency for pain to be referred to other sites advocate, educator, counselor, provider, and coordinator in the body. Chest pain may be referred from abdominal of care. or esophageal pathologies (Charlton & Buckley, 1984; Dymock, 1985), while abdominal pain may arise from musculoskeletal or spinal problems or abdominal wall NURSING MANAGEMENT OF PAIN entrapment syndromes. Back pain may be the presenting IN THE ELDERLY symptom of a host of pathologies, including disc degenFor purposes of the discussion that follows, the term “eld-eration, arthritis, osteoarthritis, metastatic disease, and Paget’s disease. These conditions may present as lower erly” refers to those persons 65 years of age or older. However, it is important to note that many of the physio-limb pain (Charlton & Buckley, 1984). Spondylosis of the cervical vertebrae may present as pain, muscular spasticlogical changes associated with the aging process have an ity, or paresthesia in one upper limb (Grahame, 1985; onset as early as the fourth decade. Therefore, although Pathy, 1985). this discussion focuses on an age-related cohort, individPerhaps the most frequently cited clinical manifesual variation is a hallmark of any investigation of the tation of paradoxical pain perception in the elderly is sequelae of human aging. The axiom that “aging is not for sissies” may havecardiac pain. Although elderly persons experiencing found its origin in the many factors of aging that supportangina pectoris report the same need to cease exertion the nursing diagnosis “alteration in comfort. ” Carpenito and similar dyspnea and pain radiation patterns as younger persons, they also report much less severe pain. (1999) states unequivocally that pain is omnipresent in the ed severity of pain results elderly. This is a particularly startling revelation in view It is postulated that the modifi of Wolanin’s (1976) observation that pain is primary and,from either the presence of afferent denervation of the until it is relieved, no person functions adequately. Thisheart or the occurrence of disease in the smaller coronary vessels which produces less pain than disease in the discussion explores these concepts in more detail and larger vessels (Caird et al., 1987). addresses other factors that combine to make the elderly In addition to modified chest pain, it is not unusual a population uniquely vulnerable to pain. The myriad physiologic and pathophysiologic changesfor the elderly patient with clinically severe ischemic heart of human aging that result in either acute or chronic paindisease to present totally absent of pain. One study found may manifest themselves in a variety of ways in the eld-that 31% of the elderly patients who experienced myocardial infarction reported no pain, while 40% reported clinerly. Some of these manifestations are obvious and accomically atypical symptoms (Caird et al., 1987; Charlton & panied by typical signs and symptoms of a specifi c probBuckley, 1984). This phenomenon may be the result of lem, while others are subtle, atypical, or even paradoxical (Caird, Dall, & Williams, 1987). Although the mechanisms the presence of multiple pathologies that severely limit of pain have been well described (Thompson, 1984), vari-activity, such as arthritis, parkinsonism, blindness, or ation in pain perception in the elderly remains an area ofhemiplegia. The presence of other pathologies may also contradictory subjective opinion and objective data (Cairdpresent the patient with other symptoms so noxious that et al., 1987; Corso, 1971; Matteson, 1988). However, it ischest pain is not noticed (Caird et al., 1987). generally accepted that pain threshold increases with age Clearly, determining the origin of pain in the elderly (Carpenito, 1999; Charleton & Buckley, 1984; Jacox,presents a challenge to the healthcare practitioner and 1977; McConnell, 1988). In addition to an increased painpatient alike. Pain is a subjective phenomenon. Variables

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such as coexisting chronic pathologies, underreporting of modalities associated with those traditions. As a result, it pain, and the increased incidence of cognitive impairmentappears that we are witnessing the emergence of socioall combine to make pain evaluation much moreficult dif cultural legitimacy of a holistic health paradigm, perhaps among the elderly than among other adult populationsbest described as a renaissance moment. A singular out(Ferrell & Ferrell, 1987). Although practitioners observe come of this ongoing trend is without doubt the consciousthe elderly for behavioral manifestations of pain such asness-raising constellation of external and internal varifacial grimacing, positional guarding, etc., such observa-ables integral to the individual and personal experience of tions, or even the perceptions of the experienced practitiohealth/illness events, such as pain. ner, are not reliable assessments of whether pain is present Seaward (1994) posits that the primary reason for and, if so, how severe that pain may be. As is the case with this readiness to transition originates from the socioecononelderly patients presenting with pain, the elderlynomic reality that the American “ healthcare system is patient’s report of pain must be accepted as the most relicrumbling under its own economic weight. ” The burable clinical description. This requires that the patient withgeoning recognition that Eastern traditions and Western pain be trusted (Wright & Gal, 1987). It has been reportedtraditions are in fact not mutually exclusive but rather that the inability of an elderly patient to walk on a brokencomplementary is perhaps best illustrated by recent thigh was ascribed to hysteria (Pitt, 1982). activities at the federal level of healthcare policy. The fice of Alternative Medicine Although this is an extreme example of failure to trust,NIH is transitioning the Of fing the attributing pain to psychogenic origin may occur in those(OAM) into the mainstream by funding and staf circumstances where no clear-cut etiology for the pain isoffice to serve as the primary agency to engage in and found. In reality, it is not always possible to discover ansupport research in the area of complementary and alteretiology for the discomfort experienced by patients. Thisnative medicine, or CAM (Villaire, 1995). The evolution ected in the creation of six reality can lead to frustration or guilt on the part of theof this new emphasis is refl c clinical practitioner, which in turn can lead to avoidanceto eight additional research centers devoted to specifi of the patient or minimization of the patient’ s pain by the clinical problems, including, but not limited to, stroke, practitioner, neither of which benefi ts either party women’s health, and pain issues. (McConnell, 1988). Compounding the ficulty dif of estabThe readiness of the healthcare community to learn and lishing trust and gathering accurate data from the patient share new realities and awareness of the power of integratis the fact that older persons tend to be more reluctant to ing East and West and high-tech and high-touch has found report pain than younger persons (Charlton & Buckley,a common ground in the search for higher clinical ficacy ef 1984; Matteson, 1988; McConnell, 1988). Additionally, and healthcare cost savings. These were also the discussion due to increased pain tolerance and adaptation, the elderly triggers for the participants in the OAM-sponsored Conindividual also does not tend to demonstrate expected ference on Technology Assessment during the fall of 1995. objective signs of pain as readily as a younger person The two specifi c clinical foci of that conference were treat(Carpenito, 1999). While this adaptive behavior by thement modalities for insomnia and chronic pain, and the elderly patient may be necessary for continued survival,outcome recommendations give new direction for plausible particularly in the presence of chronic pain, it may leadand effi cient modalities for ef ficacious interventions (Chilto inaccurate assessment by the practitioner, ineffective ton, 1996). By nature of the everyday adaptations these pain management, reduced comfort and mobility, andrealities demand of the older adult, the outcome recomincreasing dependence and isolation, anger and frustramendations of this panel have benchmark implications for tion, and, in some cases, confusion on the part of the healthcare providers serving this population. patient (Pitt, 1982). For example, Garner and Kinderknecht (1993) address Clearly, an individual touched by pain experiencesthe responsibility of healthcare workers to empower clithat perception across the broad spectrum of physical, ents in pain by teaching them coping skills that will allow emotional, and spiritual aspects of human experience. The clients to actively engage in the process of ameliorating experience also includes the human diminishments pain pain. In their discussion of the gate theory of pain percepevokes in the individual, both organically and spiritually. tion, the authors provide an overview of pain management This view of the integrated wholeness of the human person and coping modalities designed to insert self-control back experiencing life events is reaching new awareness in into a the equation of health status, even in the face of the healthcare environment and era that had found comfort in reality of illness. This is a most powerful and appealing the high-tech-low-touch approach to problem solving.idea. The concept is a natural evolution of the psychologDuring the past decade, however, the traditional philoso-ical theory of “self-efficacy.” This theory, in turn, is giving phies and healthcare practices of Western society have rise to the model of self-ef ficacy training, which is reportbecome increasingly receptive to a cultural renewal of theedly being proven as an intervention for indigenous ancient and Eastern philosophies of holistic health. Thispeoples in Canada, Latinos in California, and those with openness is resulting in increasingly active interest in the chronic co-morbid conditions (Chilton, 1996).

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Results of scientific investigation into the phenome-cial change in thinking is the clinical foci of control of pain residing with the patient, rather than the individual non of pain experienced by the elderly may assist the elderly in achieving the best possible quality of life. professional whose capacity to address subjective sympAlthough instruments have been developed to quantifytoms may be biased by a host of intellectual, cultural, and qualify pain experienced by the elderly and non-professional, and personal variables which influence effecelderly (Kane & Kane, 1984; Wright & Gal, 1987), this tive treatment interventions for the elderly. remains an area of need for additional nursing research. The awareness of pain and its influence on the quality Unfortunately, until recently, pain research in the elderlyof life has garnered the attention of the graying American has received limited attention. This is despite the fact that public. Thanks to the influences of communications media the special vulnerability to pain experienced by this cohortfrom print to the Internet, the level of healthcare consumer is commonly reflected in the literature as a given. Forknowledge today is more sophisticated than in previous example, the Clinical Practice Guideline for Managementgenerations. Concurrently, the health industry, with its of Cancer Pain states: “The elderly should be considered renewed focus on quality assurance, has found the focus an at-risk group for the undertreatment of cancer painof care delivery once again returning to the patient. Perbecause of inappropriate beliefs about pain sensitivity,formance expectations, measurable behavioral outcomes pain tolerance and ability to use opioids. Elderly patients,of patient care, and other outcome performance tools are like other adults, require aggressive pain assessment and all examples of the shifting model of healthcare service management”(Agency for Health Care Policy and delivery. The shift is consonant with a heightened awareResearch, 1994). ness of the criticality of pain management throughout the Some of the factors that singly and in combinationclinical professions. explain why the elderly population is at high risk for the The clinical discourse on quality assurance of pain nursing diagnosis alteration in comfort are presented incontrol has also translated into a new organizational Table 25.2. awareness. Policy and standard-setting institutions such as the Agency for Healthcare Research and Quality, and the JCAHO are developing new pain management stanTHE LOCUS OF ASSESSMENT: dards (Acute Pain Management Guideline Panel, 1992; THE PATIENT JCAHO, 2001). Significantly, the JCAHO developed new standards for pain control with a radical change in thinking Gratefully, the past decade has brought important changes — that pain management is the responsibility of healthin both the knowledge and performance parameters of pain care organizations. In introducing the new standards management across all health professions. The most cru(effective January 2001), which include the elderly in all care delivery settings, the quality of pain management is addressed through a systematic assessment of pain using TABLE 25.2 a 10-point scale. More detail regarding the specific reviRisk Factors Associated with Nursing Diagnosis: sions in the six standards chapters (Rights and Ethics; Alterations of Comfort in the Elderly Assessment of Persons with Pain; Care of Persons with Pain; Education of Persons with Pain; Continuum of Care, • Pain threshold increases with age. • Physiologic/pathophysiologic changes may alter perception of pain.and Improvement of Organization Performance) is available on the JCAHO Web site (http://www.jcaho.org) (Phil• Pain in the elderly may be referred from site of origin. • Physiologic changes of aging give rise to chronic pain. lips, 2000). • Multiple pathologies may result in the paradoxical absence of pain. • Severe pain and chronic discomfort in the elderly may manifest as NURSING MANAGEMENT OF PAIN confusion. • Cultural/psychological expectations may diminish reporting of pain. IN INFANTS AND CHILDREN • Concern for overmedication may result in insuf ficient pain management modalities. Although pain relief is a primary goal of nurses, pain • Societal acceptance of pain in the elderly leads to avoidance ormanagement in children has often been ignored and has minimalization of pain. received limited attention in the literature. In 1977, Eland • Depression is present and most frequently associated with chronic and Anderson documented the undertreatment of pain in pain. children. Following this study, subsequent research find• Constellation of symptoms in chronic pain states includes behavior commonly associated with maladaptation to the aging process,ings supported the idea that pain in children is an ignored dimension of care (Wong & Hockenberry-Eaton, 2001). including sleep disturbances, appetite disturbances, decreased libido, irritability, withdrawal of interests, weakening of relationships, and Recently, significant advances in the management of chilincreased preoccupation with ill health. dren’s pain have been facilitated by the development of • Underreporting of symptoms occurs frequently. clinical practice guidelines for pain (Acute Pain Manage• Communication difficulties increase history-taking problems.

ment Guideline Panel, 1992) management from the federal

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increased temperature, pulse, and blood pressure; poor tissue perfusion; and dilated pupils may be associated TABLE 25.3 with pain. These signs of autonomic nervous system Myths Associated with the Undertreatment arousal and the body’ s stress response are self-limiting. of Pain in Children The body cannot continue the response. Adaptation • Infants and children are unable to perceive and experience pain. occurs and a state of homeostasis follows, although the • Children have no memory of pain. child is still in pain. These physiological responses, there• Pain produces no harmful effects. fore, are only helpful when they are combined with other • Children become easily addicted to narcotics. assessment data. • Children are more likely to experience respiratory depression. Assessment tools offer a systematic approach to the evaluation of pain. A valid and reliable tool reduces bias. AHCPR and the development of acute pain services inVarious tools exist, and one tool is not appropriate for all hospitals. children. The selection of an assessment tool should be Experts have proposed many explanations for underbased on the child’ s age and developmental level (Wong treatment of pain in children (Table 25.3). The inability to & Hockenberry-Eaton, 2001). assess children’ s pain, however, has presented the biggest A specific assessment form should be used to docuchallenge for pediatric nurses. Preverbal infants, intubated ment assessment findings. Documentation should include patients, and developmentally challenged children are not the location and intensity of the pain, the type of assessable to verbally describe their pain. Pediatric nurses must ment tool used, observed behavioral manifestations, physbe able to assess pain and understand that infants and iological parameters, the pain intervention, and the children respond to pain with reactions based on age and response to that intervention (Lux, Algren, & Algren, cognitive processes. Because of the problems associated 1999). with the measurement of pain in children, assessment The AHCPR publication,“Clinical Practice Guideline requires a multifaceted approach. for Acute Pain Management” (Acute Pain Management Researchfindings indicate that infants and children Guideline Panel, 1992), provides information for the do experience pain and respond to that pain both physioassessment and management of pain in infants, children, logically and behaviorally (Deshpande & Anand, 1996;and adolescents. The goal for pediatric pain management Jorgensen, 1999). These pain cues may be more subtle is preventing or relieving pain as much as possible using than those expressed by adults. Observation of these pharmacological or nonpharmacological strategies, or a responses provides the basis for nursing assessment. Other combination of the two. assessment parameters include: (1) obtaining a thorough Pharmacological agents used to manage pain in chilhistory from the child and/or parents; (2) using a self-dren include both opioid and nonnarcotic analgesics. The report tool, if appropriate; and (3) eliciting parental input ideal analgesic should be easy to administer, have a rapid about the child’s pain. onset, and produce the desired degrees of analgesia. PhysBehavioral changes may indicate pain in children whoiological parameters and respiration should be minimally are unable or unwilling to verbally report pain. Behavioralaltered. The discussion of specific pharmacological agents responses associated with children’ s pain include: is beyond the scope of this chapter. Extensive information can be found in Chapter 39 on the “Management of Pro• Vocal communication, such as moaning, whim- cedural and Perioperative Pain in Children. ” pering, or crying A variety of routes of administration are now being • Facial expressions, such as a grimace utilized in pediatric pain management. Oral and rectal • Body language, such as positioning, posturing, administration are less traumatizing than intramuscular splinting, pushing away, or kicking injection. In fact, injections are strongly discouraged in • Emotional responses, such as withdrawal, most pediatric institutions. Topical anesthetics, regional depression, irritability, and unusual quietness anesthesia and analgesia, and epidural analgesia have also • Changes in daily routines, such as loss of appe- become commonplace in treating children’ s pain (Algren tite and disturbed sleep patterns & Algren, 1994; Wong & Hockenberry-Eaton, 2001). In most children’s hospitals, patient-controlled analBehavioral responses modulate over time and require caregesia (PCA) is the mainstay of pediatric pain manageful assessment throughout a child’ s illness. Parents are ment. Pain resulting from etiologies such as surgery, often the first to detect these subtle behaviors, and their trauma, sickle cell crisis, and cancer can be successfully input is essential. managed by PCA. Using an infusion pump, patients can administer a preset amount of opioid, usually morphine, Physiological parameters that demonstrate the presence of pain include changes in vital signs, skin color,by simply pressing a button. The patient, however, cannot ed period of time, usually sweating, and nausea and/or vomiting. Flushed skin;repeat a dose before a specifi

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8 to 15 minutes. PCA gives the patient control over painthese patients if adequately treated with pharmacological management, permits individual titration, and providestherapy (Jacox et al., 1994). The majority of cancer superior analgesic effect (Lux et al., 1999). patients in the U.S. receive inadequate pain management. The literature suggests that healthcare providers continue Patient-controlled analgesia was first used in adolesto have misconceptions about cancer pain (Pargeon & cents, but its use has quickly spread to younger children. Hailey, 1999). Patients may hamper their own treatment Children as young as 5 years of age can safely and effectively control their own analgesia (Yaster et al., 1997). Adue to misconceptions about pain and fears about opioids. degree of safety is maintained by the patients when they Cancer pain is multifaceted and is generally classified no longer feel the need to “push the button” or when theyas pain from direct tumor involvement, invasive diagnostic become sedated. The key to successful use of PCA in and therapeutic procedures, infection, or toxicity of chechildren is adequate patient and parent education. The motherapy and radiation therapy. Because cancer most control of PCA pumps by a surrogate such as a parent or often occurs at ages when other maladies causing pain nurse is controversial because it compromises the inherent develop (e.g., arthritis and chronic back problems), the safety of PCA. If parents or nurses control the PCA sys-practitioner must attempt to identify the source of the pain tem, frequent assessment and conservative dosing is desirand intervene appropriately. Cancer-related pain may be able (Lux et al., 1999). difficult for the patient to explain. Thorough and accurate Nonpharmacological strategies may be very helpfulnursing assessment is paramount to the diagnosis and in the management of mild to moderate pain and procemanagement of cancer pain. dural pain. These techniques are noninvasive, inexpensive, The Standards of Oncology Nursing Practice emphaand offer some control to the child and parent. Strategies size the systematic and continuous collection of data to plan such as distraction, guided imagery, and relaxation techappropriate interventions with the patient (ANA, 1996). niques decrease anxiety, reduce pain perception, and Cancer patients may underreport pain if they think pain enhance the effectiveness of analgesics (Vessey & Carlindicates their disease is not responding to treatment. Some son, 1996). Guided imagery, such as imagining being at patients simply do not want to complain even if analgesics the beach, can be used in children who are capable of are available to relieve the pain because they think it is part abstract thinking. Relaxation activities such as holding,of the fate of the disease. Other variables suchnancial as fi rocking, reading stories, and listening to music mayconcerns, anxiety, and limited family support may add to reduce the stress associated with pain and thus provide the perceived pain experienced. The absence of standardpain relief. ized assessment tools makes itficult dif for nurses to conCutaneous stimulation can also be used as a noninvasistently and effectively assess the extent of pain, evaluate sive pain relief measure. Activities such as stroking orthe effi cacy of the intervention, and accurately communirubbing an injured area stimulate the large A-alpha periph-cate this information. Lack of knowledge about the cause eral fibers and block the transmission of noxious impulsesof cancer pain, as well as attitudes toward pain and its at the spinal cord. Applications of heat and cold may alsomanagement, can be barriers to adequate assessment. promote analgesia. The Oncology Nursing Society has long recognized In summary, nurses play a vital role in pediatric painthe need for a consistent approach to cancer pain manageassessment and management. Health professionals must ment and barriers to that management. In a recent revision create a climate that makes effective pain managementofa its Position Paper on Cancer Pain Management (Oncolpriority. Developmentally appropriate pain assessmentogy Nursing Society, 2000), emphasis is placed on multools must be utilized in evaluating children ’s pain. Clin- tidisciplinary management that is collaborative and ical practice must be evaluated through research and qualinvolves ongoing assessment, planning, intervention, and ity improvement programs. Finally, all practitioners mustevaluation of pain and pain relief. be advocates for the child and the family for effective The site of the cancer and the stage of the disease pain management. factor into the incidence and prevalence of pain. As the disease progresses, patients with metastatic disease are more likely to experience pain, particularly those with NURSING MANAGEMENT bone involvement from primary infiltration or metastasis. OF CANCER PAIN Interference with organ function or structure or nerve invaApproximately one million Americans are diagnosed withsion intensifies pain. Terminal patients report significant in pain. It is evident that the management of cancer each year. In the early and intermediate stages, increases 30 cancer pain may need to be multimodal secondary to the to 45% experience moderate to severe pain. In the many dimensions of its etiology. However, the treatment advanced stages of cancer, 75% of patients experience of acute and chronic cancer pain continues to remain pain; 25 to 30% of these patients describe their pain as severe. Good to excellent pain relief is possible in 95% ofprimarily within the realm of pharmacologic management.

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Effective cancer pain management has been described in practice quidelines by organizations such as the AHCPR TABLE 25.4 (Jacox et al., 1994). While advocating a team approach, Nursing Therapies for Cancer Pain details such as assessment, pharmacological management, • Rest and sleep adjuvant therapy, and psychological interventions are out• Adequate nutrition lined in the guidelines. • Daily elimination Analgesics are extremely effective in most patients • Activities of daily living when used correctly. In 1986, the World Health Orga• Encourage movement nization recommended a three-step analgesic “ ladder” • Environmental control that emphasizes the use of standard drugs classifi ed as • Encourage independence • Medications nonopioids, weak opioids, and strong opioids. Sequen• Thermal therapy tial use of the drugs is advocated with the addition of a • Communication weak opioid in combination with the nonopioid, or a • Therapeutic touch strong opioid should relief not be obtained. Adjuvant • Relaxation techniques drugs are added if required for specifi c indications, and • Distraction they are often needed in patients with pain secondary • Emotional support to nerve injury. Nonopioid drugs such as the nonsteroi• Availability of spiritual support dal anti-inflammatory drugs interfere with peripheral receptors by inhibiting prostaglandin release, thus reducing pain from resulting infl ammation. Opioid ria for the patient, in relation to comfort, state that the drugs (narcotics) bind to receptors that interfere withpatient will: the transmission of painful stimuli. Because of the dif1. Communicate alterations in comfort level ference in action, a combination of the two types of 2. Identify measures to modify psychosocial, drugs results in ef ficacious pain management. Adjuvant environmental, and physical factors that drugs are used to treat specifi c types of pain and to increase comfort and promote the continuance alleviate other symptoms that may occur in cancer of valued activities and relationships patients. Anticonvulsants, antidepressants, and corticosteroids are used to reduce anxiety and depression, which 3. Describe the source of discomfort, the treatment, and the expected outcome of the prooften exacerbate cancer pain and interfere with other posed intervention activities of the patient. 4. Describe appropriate interventions for potential Other interventions may be useful, particularly for or predictable problems such as pain pain that is not responsive to analgesics. Nerve blocks, transcutaneous nerve stimulation, and neuroablative techTo do so requires a comprehensive approach to pain conniques may benefit cancer patients. Nurses in acute and chronic pain settings can add trol a for the cancer patient. Accountability and responsibility unique perspective to the assessment and care of each of the professionals involved with the care are cancer patient. Changes in a patient’ s comfort that occurs demanded and advocated. The challenge is for the nurse to identify, assess, treat, evaluate at specifi c intervals, every 24 hours can be observed and reported and intermake alterations if necessary, and further evaluate. It is ventions evaluated more closely because of the increased the professional and ethical responsibility of caregivers to contact with the patient. Combining nursing therapies with assist the patient and family in identifying and managing behavioral therapies and pharmacotherapies offers a factors that promote comfort. broader approach to pain management. Comfort measures helpful for patients with cancer pain are summarized in Table 25.4. SUMMARY The Oncology Nursing Society (2000) supports nurse design of individualized physical and psychosocial inter-In conclusion, the AHCPR and other major organizations ventions that are intended to achieve stated outcomes and have widely disseminated pain guidelines. The absence are prioritized according to the patient’ s needs. The nurse of knowledge is no longer a factor in caring for patients also collaborates and communicates with appropriate with pain. Pain management as a multidisciplinary, colmembers of the multidisciplinary team in designing thelaborative practice is still too new for many practitioners plan of care. to be competent, confi dent members of the team. In It is imperative that information be as complete asSeizing the Future , Zey (1994) addresses mentoring as possible and be available to all practitioners involved inan effective developmental tool routed in caring and treating the patient’ s pain or discomfort. Outcome crite- individualized learning that provides the emotional sup-

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port often missing in society’ s high-tech cognitive Corso, J.F. (1971). Sensory processes and age effects in normal adults.Journal of Gerontology , 26, 90–105. approach to solutions. Cronin, Y., & Bahrke, L.S. (1996). An epidural clinical pathway: To assist patients with pain and to help them integrate A new generation for clinical pathways. ASPMN Pathits management into their life, practitioners need cognitive, ways, 5(1), 1, 3–4. affective, and psychomotor practice skills. Formal pain Deshpande, J.K., & Anand, K.J. (1996). Basic aspects of acute mentoring programs established in hospitals and other setpediatric pain and sedation. In J. Deshpande & J. Tobias tings (Kachoyeanos, 1966) and less-formal mentoring (Eds.), The pediatric pain handbook(pp. 1–48). St. through the American Academy of Pain Management, the Louis: Mosby. American Society of Pain Management Nurses, and other Dymock, I.W. (1985). The gastrointestinal system-the upper gaspain organizations can develop practitioners to better serve trointestinal tract. In J.C. Brocklehurst (Ed.), Textbook patients and mentor other colleagues in the future. of geriatric medicine and gerontology (3rd ed., pp. Nurses are ubiquitous, just as pain and the need for 508–519). Edinburgh: Churchill Livingstone. pain management is ubiquitous. Nurses have more conEland, J., & Anderson, J. (1977). The experience of pain in children. In A. Jacox (Ed.),Pain: A sourcebook for tact with patients in pain than any other practitioner. nurses and other health professionals (pp. 453–473). Nursing practice, research, and mentoring are vital comBoston: Little, Brown & Company. ponents of pain management practice, and nurses are valuable participants who help determine how the health-Ferrell, B.R., & Ferrell, B.A. (1997). Care of elderly patients with pain. In Expert pain management . Springhouse, care systems in the U.S. and throughout the world deal PA: Springhouse Corporation. with pain management.

Garner, J.D., & Kinderknecht, C. (1993). Living productively with arthritis. In J.D. Garner and A. Young (Eds.), Women and healthy aging (pp. 61–81). Binghamton, REFERENCES NY: Haworth Press. Gordon, M. (2000).Manual of nursing diagnosis (9th ed.). St. Acute Pain Management Guideline Panel (1992). Acute pain Louis: Mosby. management: Operative or medical procedures and Grahame, R. (1985). The musculoskeletal systemæ disease of trauma (AHCPR Publ. No. 92-0032). Rockville, MD: the joints. In J. C. Brocklehurst (Ed.), Textbook of geriAgency for Health Care Policy and Research, U.S. atric medicine and gerontology (3rd ed., pp. 795–819). Department of Health and Human Services Public Ignatavicius, D., & Hausman, K. (1995). Clinical pathways for Health Service. collaborative practice . Philadelphia: W.B. Saunders. Agency for Health Care Policy and Research. (1994). Management of cancer pain . Clinical guideline number 9. International Association for the Study of Pain (IASP) Subcommittee on Taxonomy (1979). Pain terms: A list with (AHCPR Publication No. 94-0592). Rockville, MD: definitions and notes on useage. Pain, 6(2), 249. Agency for Health Care Policy and Research. Jacox, A. (1977). Sociocultural and psychological aspects of Algren, C.L., & Algren, J.T. (1994). Pain management in chilpain. In A. Jacox (Ed.),Pain: A sourcebook for nurses dren. Plastic Surgical Nursing , 14(2), 65–70. and other health professionals (pp. 57–87). Boston: LitAmerican Nurses Association: Oncology Nursing Society tle, Brown & Company. (1996).Standards of oncology nursing practice . Kansas Joint Commission on Accreditation of Healthcare Organization City, MO: American Nurses Association. (2001). 2001 Accreditation manual . Oakbrook Terrace, Aspen Reference Group (1995). Pain management: Patient eduIL: Joint Commission on Accreditation of Healthcare cation manual(S. Neimeyer & S. N. DiLama, Eds.). Organizations. http://www.jcaho.org/standard/pm.html Gaithersburg, MD: Aspen Publishers. Jorgensen, K. (1999). Pain assessment and management in the Caird, F.L., Dall, J.C., & Williams, B.O. (1987). The cardiovasnewborn infant. Journal of Perianesthesia Nursing , cular system. In J.C. Brocklehurst (Ed.), Textbook of 14(6), 349–356. geriatric medicine and gerontology(3rd ed., pp. Kachoyeanos, M.K. (1966). Establishing a pain mentoring pro230–267). Edinburgh: Churchill Livingstone. gram. ASPMN Pathways,(1), 5 7–8. Carpenito, L.J. (1999). Nursing diagnosis: Application to cliniKane, R., & Kane, R. (1984). Assessing the elderly: A practical cal practice(8th ed.). Philadelphia: Lippincott, Williams guide to measurement . Lexington, MA: Lexington & Wilkins. Books. Charlton, J.E., & Buckley, F.P. (1984). Management of chronic pain. In J.G. Evans & F.I. Caird (Eds.), Advanced geriat- Lux, M., Algren, C., & Algren, J. (1999). Management strategies for ensuring adequate analgesia in children. Disease ric medicine(Vol. 4, pp. 17–32). London: Pittman Press. Management and Health Outcomes , 6(1), 37–47. Chilton, M. (1996). Panel recommendations integrating behavioral and relaxation approaches into medical treatment ofMarrelli, T.M. (1994).Handbook of home health standards and documentation guidelines for reimbursement (2nd ed.). chronic pain, insomnia. Alternative Therapies , 2(1), 18–28. St. Louis: Mosby. Cleary, B.L. (1997). Age-related changes in the special senses. In M. A. Matteson, E.S. McConnell, & A.D. Linton McCaffery, M. (1968).Nursing practice theories related to cognition, body pain, and man-environment interaction . Los (Eds.), Gerontological nursing: Concepts and practice Angeles: University of California, Students’ Store. (2nd ed., pp. 385–405). Philadelphia: W. B. Saunders.

294

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Ready, L.B. (1995). Practice guidelines for acute pain manageMcCaffery, M., & Pasero, C. (1999). Pain: Clinical manual.St. ment in the perioperative setting: A report by the AmerLouis: C.V. Mosby. ican Society of Anesthesiologists Task Force on Pain McConnell, E.S. (1988). Nursing diagnoses related to physioManagement, Acute Pain Section. Anesthesiology, 82 , logical alterations. In M.A. Matteson & E.S. McConnell 1071. (Ed.), Gerontological nursing concepts and practice Seaward, B.L. (1994, September). Alternative medicine comple(pp. 331–428). Philadelphia: W. B. Saunders. ments standard. Health Progress , 52–57. McCue, J.D. (1987). Medical screening of the relatively asymptomatic elderly patient. In C. S. Rogers & J. D. McCue Thompson, J.W. (1984). Pain: Mechanisms and principles of management. In J. G. Evans & F. I. Caird (Eds.), (Eds.),Managing chronic disease (pp. 391–399). OradAdvanced geriatric medicine (Vol. 4, pp. 3–16). London: ell, NJ: Medical Economics Books. Pittman Press. National Institutes of Health Consensus Development ConferVessey, J.A., & Carlson, K. (1996). Nonpharmacological interence. (1987). The integrated approach to the manageventions to use with children in pain. Issues in Comprement of pain: Consensus development conference hensive Pediatric Nursing , 19, 169–182. statement.Journal of Pain and Symptom Management , Villaire, M. (1995). A fresh start: OAM charts its course for the 2(1), 35–44. future. Alternative Therapies , 1(5), 18–20. Oncology Nursing Society. (2000). Position paper on cancer Wolanin, M.O. (1976). Nursing assessment. In L.M. Burnside pain. Pittsburgh: Oncology Nursing Society. (Ed.), Nursing and the aged (pp. 398–420). New York: Pargeon, K, & Hailey, B. (1999). Barriers to effective cancer McGraw-Hill. pain management: A review of the literature. Journal of Wong, D., & Hockenberry-Eaton, M. (2001). Wong’s essentials Pain and Symptom Management , 18(5), 358–368. of pediatric nursing(6th ed.). St. Louis: Mosby. Pathy, M.J. (1985). The central nervous system. Clinical presenCancer pain relief . Geneva, tation and management of neurological disorders in oldWorld Health Organization. (1986). Switzerland: World Health Organization. age. In J. C. Brocklehurst (Ed.), Textbook of geriatric medicine and gerontology (3rd ed., pp. 795–819). Edin- Wright, A.B., & Gal, P. (1987). Assessment and treatment of pain. In C.S. Rogers & J.D. McCue (Eds.), Managing burgh: Churchill Livingstone. chronic disease(pp. 28–34). Oradell, NJ: Medical EcoPhillips, D. (2000). JCAHO pain management standards are nomics Books. unveiled.Journal of the American Medical Association , Yaster, M., et al. (1997). Pediatric pain management and seda284(4), 428–429. tion handbook . St. Louis: Mosby. Pitt, B. (1982).Psychogeriatrics: An introduction to the psychi. New York: Simon & atry of old age(2nd ed., pp. 2–14, 31–38). Edinburgh: Zey, M.G. (1994). Seizing the future Schuster. Churchill Livingstone.

26 The Psychiatrist’s Role in Pain Diagnosis and Management Nelson H. Hendler, M.D., M.S. INTRODUCTION

histrionic personality disorder, who has surgical excision of a disc and does not get well, may run afoul of the The role of a psychiatrist in chronic pain management issystem. His or her lack of recovery is ascribed to “secmultiple. He or she must be a diagnostician, a pharmacoloondary gain” or “dependency needs, ” but not to retained gist, a sociologist, a psychotherapist, and even, on occasion, disc material missed by the first surgery patient advocate. Therefore, by definition, the psychiatrist The integrated response model. Using this model, the must have an eclectic orientation, and be broadly schooled psychiatrist tries to establish both medical and psychiatric in all forms of diagnostic and therapeutic interventions. diagnoses, not only from the point in time at which a patient There are at least three approaches to chronic pain is seen, but also based on the historical perspective of the that a psychiatrist can use. Each has its own advantages patient, that is, thepre-morbid” “ or “pre-pain” personality. and disadvantages. In this fashion, one can determine the appropriateness of The medical model. Using this paradigm, pain is response to pain, and to treatment. This approach is timedefined as a manifestation of a disease. This approac lends consuming and involves a multidisciplinary approach, with clarity to the problems of pain, and offers predictive capa-multilevel diagnoses and integration of material. In this bilities for outcome. It may offer a cure where none existedmodel, both medical and psychiatric diagnoses can exist. before. As an example, “pain in the back and the leg” is a description, but “a herniated disc with radiculopathy” isMEDICAL MODEL a diagnosis. Surgery on the disc may cure the pain. However, should the surgery not work, or should there beAdherence to the medical model is often found within pain psychological problems or social problems compoundingtreatment centers or in clinical practices that utilize only the recovery, response to surgery may not be as predicted. medical evaluation of the patient. The absence of a psyThe psychiatric model. Using this approach, a psy- chiatric or psychological professional to assist in evaluachiatrist tries toestablish a psychiatric diagnosis to explain tion and diagnosis limits the evaluation of the chronic pain the behavior of a pain patient who is troublesome or notpatient to only medical assessment. It disregards the posresponding in the predicted fashion. Using this tack, per-sibility that a patient may have psychiatric problems, the sonality disorders, affective disorders, or anxiety traits thatresult of chronic pain, which can lead to diagnostic overmight be the source of a patient’ s complaints are identified sight. Indeed, some authors believe that the incidence of and treated. Unfortunately, the use of psychiatric interven-depression, in dissociation with chronic pain, is remarkably tion in this fashion very often leads to an “either-or” typehigh (Hendler, 1984b; Krishnan, et al., 1985; Pilowsky & of thinking, with psychiatric diagnosis being establishedBassett, 1982). Other authors have advanced the theory to the exclusion of medical diagnosis. A person with athat chronic pain may be a manifestation of an underlying 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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dromes under the description of somitizing disorders. He depression (Engel, 1959; Maruta, Swanson, & Swanson, describes hard-working individuals who have an accident, 1976). Therefore, the medical assessment of chronic pain and then fall apart. This inability to function allows the without psychiatric assessment (to determine the preexisting personality characteristics and motivations that mayindividual to have support and secondary gains, and allows an underlying dependency to manifest itself. lead to an exaggerated response to chronic pain, or may, in fact, lead to the expression of psychiatric disease as a chronic pain process) would compromise any medicalPSYCHIATRIC MODEL diagnostic endeavor. By the same token, severe and chronic In a superb review article, Drs. Turk and Flor (1984) illness certainly produces depression, and perhaps other psychiatric disorders, which would benefi t from therapeu- reviewed the psychological models contributing to chronic tic intervention. The use of a purely medical model cannotback pain. In this article, they discuss theoretical constructs, which explain the transition from acute to chronic be endorsed. Likewise, the purely psychiatric model suffers from back pain, with the exception of the psychoanalytic many of the same problems. aInmost thorough review of approach. Inthis approach, unexplained back pain is considered a conversion neurosis, a manifestation of underthe problem, Dr. Charles Ford (1986) discusses what has been called “ somatizing disorders. ” In this article, Ford lying tension, and manifess as increased muscle activity discusses the concept of the sick role, which allows the illand spasm. Using this model, various authors have suggested that pain of unexplained origin should be treated person to be released from regular duties and obligations. He further differentiates illness from disease, describingas depression with the use of antidepressant drugs. Another explanation for unexplained back pain advances the latter as objectively measured, while illness discusses the change in functioning of an individual. He further clar-the family system theory. In this approach, the basic idea is that “symptoms of the patient fulfill the emotional needs ifies the point, indicating that disease can occur in the ” They suggest that the sick role absence of illness, while conversely, illness can occur inof other family members. is used for confl ict avoidance. Another theory that is the absence of disease. Dr. Ford further describes somatization as t“he process by which an individual uses the body,advanced is the observational learning theory based on or bodily symptom, for psychological purpose or personalcognitive behavioral assumptions. In this model, the patient expresses feelings of helplessness aand hopelessgain.” However, Ford does concede that somatization can occur in the presence ’ofdemonstrable physical disease, ness, and loss of control over his or her environment. with amplification of the response to a real physical disor-Another theory, originally advanced by Flor, discusses the der. Ford then lists nine reasons why people somatize: diathesis-stress model of chronic back pain. In this model, interactions lead to the development of chronic back pain. 1. To avoid unpleasant tasks, or to achieve primary This is an attempt to integrate the physical, psychological, and social factors that lead to the development of illness. or secondary gains, in the form of payment In this diathesis-stress model, hyperactivity of the back 2. To solve family problems muscles may be due to (1) the existence of a response 3. To allow an individual to focus on physical symptoms rather than psychological problems stereotypy (diathesis) involving the back muscles, (2) recurrent or very intense adverse situations perceived as 4. As a form of communication of displeasure 5. As a way of expressing oneself when they are stressful, and/or (3) inadequate coping abilities of the indinot capable of expressing themselves otherwise vidual. Another attempt to explain pain of unknown etiology 6. A culturally determined response utilizes the diagnostic manual of the American Psychiatric 7. Using a physical symptom because is it more Association (1994). Reich, Rosenblatt, and Tupin (1983) culturally acceptable than a psychiatric one have attempted to explain the use of this diagnostic system 8. Focusing on physical problems that are manifor chronic pain patients. They indicate that attempts to festations of underlying stress categorize chronic pain patients “merely in terms of the 9. Utilizing the fashionable diagnosis to explain prime physical complaints has obvious shortcomings. ” underlying/psychiatric disease, such as They describe the prime physical complaints as having hypoglycemia five categories, or axes, the in Diagnostic and Statistical Manual of Mental Disorders (DSM-III), that correspond Ford further feels that patients may utilize somatic to five major areas of concern: symptoms instead of expressing depression, and further indicates that these depressions are unrecognized. Anxiety Axis I: used to describe thought disorders, such as may also manifest as a somatic complaint, which he also schizophrenia and manic depressive disease, believed could go undiagnosed. According to Ford, and drug abuse; “chronic pain syndromes are one of the more common forms of somatization. ” He also includes disability syn- Axis II: used to describe personality characteristics

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chological Factors and General Medical Conditions (DSM-IV code 307.89). Most noteworthy is the addition of a concept of Pain Disorder Associated with a General Medical Condition, divided into acute (less than 6 months) or chronic (greater than 6 months). This category is not considered a mental disorder and is coded under Axis III to facilitate differential diagnosis, and then uses the ICD9 codes of the medical disorder to classify the diagnosis. Reich and colleagues (1983) feel that an entire category of diagnoses, “the somatoform disorders, ” can be This is a major advance in psychiatric thinking; it advances the notion that chronic pain can produce psychiused to categorize chronic pain patients, in whom there is a strong psychological component that could explain aatric disorders, rather than the reverse. (APA,1994). pain unexplained by physical diagnosis. The major diagnosis within this group is “psychogenic pain disorder. ” INTEGRATED RESPONSE MODEL The criteria for utilizing this diagnosis are (1) the absence The third approach to diagnosing chronic pain patients, of appropriate physical findings, and (2) the presence of psychological factors that may explain the etiology of theutilizing an integrated response model, avoids the diagcomplaint. Attendant to this diagnosis are a variety ofnostic dualism of the previous two models. In this model, an attempt is made to study the normal response to chronic subjective assessments, such as the severity of the pain, the inability of the pain to conform with anatomical dis- pain in a previously well-adjusted individual, and then these responses as a benchmark against which other tribution, and, perhaps the most subjective assessment using of responses can be measured. Only by thoroughly underall, that the severity of the pain be out of proportion to standing the normal patterns of response can one deterwhat one might anticipate. Further diagnostic categories mine what is abnormal. It is for this reason that a medical under the somatic disorders include hypochondriasis and student studies anatomy before he or she studies patholconversion disorder. In the former, the patient is concerned ogy, physiology, or pathophysiology. This approach also with the development of a severe, debilitating illness, attempts to integrate responses, taking into account physdespite the lack of objective findings. In this instance, the ical, psychological, and environmental factors, including patient’s concerns are considered inordinate because the sociological and legal considerations. One such attempt organic condition was not substantiated. In conversion at integration has been advanced by Richard Black, M.D. disorders, the physical condition suggests an underlying (1982). Black asserts that a patient with a chronic pain organic disease, but the basis of the illness is purely psysyndrome must be assessed simultaneously for physical, chological. The authors then offer several examples of DSM-III diagnoses, in which the predominate features aremental, and environmental factors. He believes that sociohighly subjective, and the use of words “inconsistent withlogical and economic factors rarely get considered, except when litigation is involved. physicalfindings” or “pain, etiology unknown, ” and prior surgeries with residual pain. The authors advocate the use In an effort to further clarify this issue, Hendler and Talo of DSM-III taxonomy because it has achieved better reli-(1989a) offer a diagnostic system that takes into consideration (1) the pre-morbid (pre-pain) adjustment of the indiability than previous psychiatric diagnostic systems. With the advent of the Diagnostic and Statistical Man-vidual (pathological or well-adjusted), (2) the response to ual of Mental Disorders, fourth edition, which was pub- the pain (pathological or appropriate), and (3) the actual physical diagnosis (the presence or absence of objective lished in 1994, there have been some modifications to the approach to pain, with a wide range of options. At onefindings). Central to this formulation are two basic concepts: extreme, there is a group of patients who actually fabricate symptoms for subconscious psychological, but not finan- 1. Chronic pain can create psychological problems in apreviously well-adjusted individual cial gain. These patients have factious disorders, with predominantly physical signs and symptoms (DSM-IV code 2. Regardless of the pre-morbid (pre-pain) person300.19) or with combined psychological and physical ality characteristics, if a person has a normal signs and symptoms (DSM-IV code 300.19). An entire response to chronic pain, then the chances of a chapter is devoted to “Somatoform Disorders, ” and convalid organic basis for the complaint of pain are tains a wide-ranging list. Included are Hypochondriasis quite high. This would be true even in the (DSM-IV code 300.7), Somatization Disorder (DSM-IV absence of objective laboratory studies or physcode 300.81), Undifferentiated Somatoform Disorder ical finding. Restated for emphasis, if a patient’ s (DSM-IV code 300.81), Conversion Disorder (DSM-IV response to pain is appropriate but there are no code 300.11), Pain Disorder with several subtypes: Pain objective physical ndings, fi it is incumbent Disorder Associated with Psychological Factors (DSM-IV upon the physician to keep looking for the code 307.80), or Pain Disorder Associated with both Psyorganic basis of the patient’ s complaints.

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Hendler (1981) has divided chronic pain patients into Hendler (1982b) further expands upon the objective pain patient, indicating that this individual goes through four groups, based on the three factors mentioned previously; that is: (1) pre-morbid adjustment, (2) response tofour stages in response to the chronic pain: pain, and (3) the presence or absence of objective upon physical findings in laboratory studies or physical exam- 1. The acute stage, anywhere from 0 to 2 months, ination. These four categories are: is when the individual expects to get well and has no psychological problems. Psychological testing administered during this time is within 1. Objective pain patient, defined an as individual normal limits. with: 2. The subacute stage, which occurs anywhere a. Good pre-morbid adjustment, from 2 to 6 months, is when the individual b. Normal response to chronic pain begins to experience somatic concerns and may c. A definable organic lesion have elevated Scales 1 and 3 on the Minnestoa 2. Exaggerating pain patient, defined as an indiMultiphasic Personality Inventory (MMPI). vidual with: 3. The chronic stage of chronic pain occurs anya. Pathology as part of a pre-morbid adjustment where from 6 months to 8 years after the acquib. An unusual response to pain, in that there sition of the pain. The previously well-adjusted might be an absence of anxiety, or depression individual then develops depression and has c. Minimal organic findings elevated scales 1, 2, and 3 on the MMPI, with 3. An undetermined pain patient, defined as an Scale 2 depression being higher than Scales 1 individual with: and 3 (hypochondriasis and hysteria). a. Good pre-morbid adjustment 4. The subchronic stage of chronic pain occurs b. A normalresponse to pain anywhere from 3 to 12 years after the acquisic. An absence of objective physical findings or tion of the pain, during which time the depresphysical examination (it is this individual sion resolves, but hypochondriacal and who warrants further investigation) hysterical Scales of the MMPI remain elevated 4. Affective or associative pain patient, defined as as one might expect, because the patient still an individual with: has somatic concerns. a. A poor pre-morbid adjustment If all of the above occurs in an individual with afinde b. An unusual response to chronic pain c. A total absence of objective physical findings able organic lesion and with positive objective testing, then one categorizes this type of patient as an objective pain or positive laboratory studies patient. If all of the above psychological features are By studying the normal response to chronic pain, onepresent, but no objective testing is positive, then one considers this individual an undetermined pain patient who can then compare any patient against a known standard. still needs further medical investigation (Hendler, 1981). In this case, the objective pain patient serves as the “normal” model against which all other responses to chronic To facilitate diagnosis using the four categories previously, Hendler and co-workers (1985b) pain should be judged. The objective pain patient has described a good pre-morbid adjustment, which can be defined (Hen-have devised the Mensana Clinic Back Pain Test. Using a simple, 15-question screening test, chronic pain patients dler, 1982a) as: can be divided into the four diagnostic categories, as described by Hendler. The screening test had good pre1. A good work record dictive values because womenscoring in the objective pain 2. A stable family background patient category (17 points or less) had positive findings 3. A negative psychiatric history, with no previous on electromyogram (EMG), nerve conduction velocity suicide attempts or depression studies, thermography, CT scan, myelogram, or X-ray 4. The absence of alcohol or drug abuse 77% of the time. If women scored in the exaggerating 5. A good marital history pain patient category (21 points or greater), none of the 6. Lack of financial difficulties prior to the pain 53 women studied had objective physical findings, which 7. A good sexual adjustment is in counter-distinction to the MMPI, which had a great 8. No sleep difficulties deal of scatter, with only the Depression Scale correlating 9. No radical changes in weight, other than con- with all with the absence or presence of physical findings. scious attempts to change it Hendler, et al., (1985a) also published results for the premen, showing that in 3l men 10. The absence of any anti-social or sociopathic dictive volume of the test for there was a 91% chance of organic pathology if the patient behavior

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scored inthe objective pain patient range. Overall, theshould facilitate selection of an appropriate therapy. predictive value of the test was 85% (Hendler, Mollett,Although many types of psychotherapy are available, Talo, & Levin (1988).The usefulness of the four diagnos- treatment results are not well documented for any of the tic categories for chronic pain patients is highlighted byforms of therapy. This chapter deals with the more conthe ability to predict the presence or absence of objective ventional modalities, such as physicalfindings, based on the pre-morbid adjustment to the response to chronic pain and the description of the 1. Individual psychotherapy pain itself. The fact that the MMPI, which measures per- 2. Biofeedback sonality traits, was not a useful predictor of organic pathol- 3. Family therapy ogy lends support to the belief that personality character- 4. Group psychotherapy istics and physical abnormalities are independent events, 5. Pharmacotherapy which reduces the accuracy of the DSM-III diagnostic 6. Narco-synthesis manual, for validating the complaints of pain (Hendler 7. Hypnosis. and Talo, 1989a). Patients with chronic pain are often misdiagnosed. This PSYCHOTHERAPY is neither a local nor regional phenomenon. Data from research reports from the Mensana Clinic, in Stevenson, Very few reports in the psychiatric and medical literaMaryland, reflect a national picture because 75% of theture support the contention that individual psychotherreferrals to the Clinic are from 42 states and 8 foreignapy is a useful treatment for chronic back problems, or countries. Hendler and Kozokowski (1993) and Hendler,pain of any sort. For the purpose of defi nition, one Bergson, and Morrison (1996) found that 40 to 67% of theshould consider psychotherapy as an individual session, patients referred to Mensana Clinic arrived with over-conducted between a patient and a therapist without the looked physical diagnoses, which were later diagnosed and use of specialized techniques, such as hypnosis, biotreated at Mensana Clinic. Failure to have a diagnosis for feedback, or narcosynthesis. Likewise, group psychomedical conditions, and even worse, having a psychiatric therapy (or conditioning therapy) is separate and disdiagnosis assigned to a patient to explain the symptoms, tinct from individual, insight-oriented, dynamic leads to frustration, resentment, and certainly a well-justi-psychotherapy. When one imposes these parameters on fied psychological response in a previously well-adjustedthe definition of psychotherapy, reports on itsficacy ef individual. In these instances, chronic pain certainly leadsare sparse indeed. However, some components of indito depression, as described previously. Moreover, after the vidual psychotherapy have therapeutic benefi ts, proper diagnoses are found at Mensana Clinic, 50 to 55% although it is diffi cult to substantiate their ficacy. ef of the patients are referred for surgery. Finally, once proper Rutrick (1981) reports that psychotherapy can be effecdiagnosis and treatment are obtained, the patients get bettive if the therapist directs his or her activity toward ter. This is amply demonstrated by objective measures, understanding thepsychosomatic” “ personality, which such as return to work rates. Liberty Mutual, one of theis described as those individuals who (1) have ficulty dif largest workers’compensation insurance carriers in thewith psychological thinking, (2) have dif ficulty exU.S., reports that when a claimant is out of work for 2pressing emotion, and (3) are impulsive. years or more on a workers’ compensation claim, the Very often, psychotherapy is administered in conjuncreturn-to-work rate is less than 1%. At Mensana Clinic, fortion with other modalities of therapy. As such, eclectic the same group of patients, the return-to-work rate is 19.5% studies employing numbers of interventions provide some for workers compensation patients and 62.5% for autoevidence for the usefulness of comprehensive treatment accident cases (Hendler, 1989). This is in stark contrast to programs. However, the lack of control groups, the lack the results of the more psychologically and behaviorallyof a comprehensive pain assessment, and the uncertainty oriented pain treatment centers, very few of which haveabout the effective component do not allow definite conany published statistics on these outcome measures. clusions to be drawn. Here too, a wide variety of patients The preceding lengthy preamble regarding the psychi-have been treated with a lack of or widely divergent samatric diagnosis is critical in defining the role of a psychi-ple descriptions. It needs to be determined which patients atrist in treating chronic pain patients. It is essential toprofit from what treatment. Component analysis of eclechave a diagnosis of an individual before instituting the tic and cognitive behavioral treatments are needed to therapy. By offering a clinician a variety of diagnostic determine the effective interventions and thus reduce cost systems from which to choose, the selection of appropriate and treatment time and enhance the effectiveness of the therapy becomes a less formidable task. Whether one treatment (Turk & Flor, 1984). strictly adheres to DSM-IV diagnoses or less conventional One element of psychotherapy, which is present diagnostic systems is a matter of which system gives the whether an individual therapist recognizes it or not, is the best results in the hands of a particular practitioner. Thiscomponent of modeling. This process occurs when

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patients observe another person with chronic pain who is on at least 4 out of 5 days of EMG biofeedback training, functioning despite their physical damage. This otherbut 11 of the 13 were unable to alter EMG biofeedback individual serves as a model for the patient ’s behavior in the affected muscle group. EMG relaxation consisted and straddles the bridge between individual psychotherof reduction of muscle tension in the forehead. Therefore, apy, and behavioral therapy. Some therapists have used one might conclude that specific muscle relaxation was videotapes of patients in pain coping with their problem,not the therapeutic component of the EMG biofeedback. while others have used a directive approach, actuallyThere were no significant differences between either the instructing a patient about which behaviors are acceptable starting EMG muscle tension levels or the final levels and which are not (Webb, 1983). between the two groups. However, the response rate (i.e., 6 out of 13) was double what one might expect from a placebo response alone on a consistent basis (Hendler & BIOFEEDBACK Fernandez, 1980). The difference between the two groups was thought to be due the stagewhich at the patient was The use of biofeedback as a modality for assisting patients in his or her chronic pain process; that is, whether they with chronic pain has created much controversy. Some were in the acute stage, subacute stage, chronic stage, or authors feel that biofeedback does not offer any advantage subchronic stage. The difference between the patients who over relaxation techniques, and attributed its ficacy ef to responded and those who did not respond was the presence its placebo effect (Webb, 1983). Other authors have conof depression in the responders. Those who did not ducted a more comprehensive review and concluded that respond did not have elevated depression scales, using the EMG biofeedback may be a promising treatment modality SCL-90. for chronic back pain (Turk & Flor, 1984). In their most fi- ef evenhanded review of biofeedback techniques, Turk and Another component that might contribute to the cacy of biofeedback therapy is the issue of the patient’ s Flor report only the results of EMG biofeedback. This motivation or preparedness for change (Large, 1985). modality seems to have the most usefulness for patients for “ illness attitudes”in an with muscle tension-type pain. Turk and Flor found thatLarge utilized a measure effort to determine which patients might respond to therthere were three types of reports in the literature: (1) apeutic interventions. He used an illness behavior quesanecdotal or systematic case studies, (2) group outcome tionnaire, developed by Pilowsky and Spence, and or comparison studies, and (3) controlled group studies. expanded upon this by using a repertory grid technique, The efficacy of EMG biofeedback was further complicated which has been described by Bannister and co-workers. by the fact that in a review of over 20 articles, all Seven of the 18 patients did not experience overall relief researches— save one — utilized concomitant medicaof symptoms, while 11 did. In this report by Large tion, and not biofeedback exclusively. In the two con(1985), 48 ratings were analyzed to determine the distrolled studies reviewed by Turk and Flor, both showed crepancy between how patients perceived themselves, strong effects of EMG biofeedback on reducing pain and and how patient wished they would be. Correlating these tension levels. In one study, a decrease of 60% in pain findings with response to biofeedback showed that peointensity and duration, as suffered by the patients, was ple who were dissatisfi ed with their condition (i.e., noted. As expected, as muscle tension levels drop, pain intensity also drops. However, interestingly, at 3-monthchronic andpersistent pain) were more likely to respond follow-up, although muscle tension increased, pain reduc-well to biofeedback. tion was maintained. In the other study reviewed, EMG biofeedback was compared to medical treatment and “psyFAMILY THERAPY chotherapy. ” In this study, conducted by Flor and coworkers, they found that EMG biofeedback was moreThe role of the family in the maintenance of chronic pain behavior may be one factor to consider when dealing with efficacious than psychotherapy and control groups receiving just medical treatment alone. They noted that EMGtreatment failures. The poorest outcome among patients with chronic pain was found in families with the greatest readings decreased and the patients sought less medical degree of agreement when rating the severity of the attention when utilizing EMG biofeedback. Turk and Flor patient’s pain (Webb, 1983) Webb interprets this as “terconcluded that muscle relaxation alone does not necessarily contribute to the beneficial effects of EMG biofeed- tiary gain,” indicating that the pain is maintained because back, but rather that a cognitive process is important.of the psychological importance to other family members. Hendler, et al. (1977) attributed EMG biofeedback effec-A more likely explanation is the fact that a person with dif concealtiveness to other factors. In their study, they found twosevere debilitating disease would haveficulty ing the deficit from the family members and that they groups of patients: (1) those who responded to biofeedwould be in agreement with his assessment of the pain. back and (2) those who did not respond to biofeedback. In this study, 13 patients were evaluated using EMG bio-Webb describes family studies in which it is clear that the spouse and children of patients with chronic pain experifeedback. Six of the 13 reported that they had less pain

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ence distress, as might be expected. This is particularly of pain or illness inthe family, and location of the pain true in families where the patient is unemployed, whilecorresponding to that of the family member. Depression less so in familieswhere the patient is retired. Webb in the family member has also been explained in psycho(1983) feels that families can reinforce the pain anddynamic terms, which are equally asficult dif to substanworsen the prognosis. tiate. No doubt, patients with chronic pain have reduced A more empathetic study involved that of the spousesexual activity and poor sexual adjustment, which may contribute to poor marital relationships. Unfortunately, the of chronic pain patients. Two nurses (Rowat & Kna fl, majority of studies in this area discuss only the patient, 1985) studied the impact of pain on 40 spouses of chronic pain sufferers (21 males and 19 females). They found that and they appear at the time that they are seen by the 60% of the spouses were uncertaintoasthe cause or physician, without an adequate historical perspective. One dif develop as persistence of the pain in their partners. Additionally,questions whether or not marital ficulties the result of the chronic pain, or if marital ficulties dif 83% of the spouses reported experiencing emotional, predated the chronic pain and if the chronic pain became physical, or social disturbances that they directly attriba convenient excuse to avoid further sexual contact. When uted to the pain in their spouses. And 69% of the spouses chronic pain patients with depression were compared to felt that they were experiencing emotionalficulties dif as patients with just depression, the former group had a more a result of their partners’ pain. The most frequent forms disturbed marital relationship than the latter. In another of emotional disturbance were sadness or depression, fear, irritability, and nervousness; 40% ofthe spousesstudy, pain patients with no documented organic lesion were found to have more frequent “upsets, blows, conreported that there was a sense of helplessness because flicting interests, or separation” than those patients with they were unable to effect any change in their partner ’s pain, and they were uncertain about how to proceed in definable organic lesion. Payne and Norfleet (1986) further report that 91% of couples interviewed at the Chronic doing so. They expressed feelings of loss of control. Some 75% of the spouses felt that they could delineate whichPain Treatment Center reported sexual problems and a factors influenced their mate’ s pain, such as increased decline in their social lives since the onset of their pain problems. This was confirmed by other researchers. The activity that reduced or increased the pain, and medicaauthors conclude that studies on marital relationships tions reducing the pain. In a very fine review article, Payne and Norfleet (1986)involving chronic pain patients consistently indicate high examined the factors influencing family relationships andrates of sexual and marital maladjustment, even in previbelieve that certain family characteristics and behaviorsously stable relationships. However, they also advance the contribute to the problem of chronic pain, as well as influ-notion that the family can maintain the pain of an indis review of encing outcome. In their review, Payne and Norfleet foundvidual patient. Based on Payne and Norfleet’ the literature, they feel there are four factors that contribthat some authors believe that there might be a relationship ute to the persistence of chronic pain in a patient: between the maintenance of pain and large family size. The rationale for this is obvious. In a large family, one of s pain is an expression of dysfuncthe only ways to get attention and reduce tension would 1. The patient’ tion within the family system, and it is easier be the expression of disability or invalidism. Some authors to utilize the complaint of pain rather than say have reported that the majority of their patients come from there are dif ficulties with the relationships. families with four or more children. Birth order was also considered as a factor influencing the complaint of pain. 2. The family acts as a reinforcer for pain behavior by nurturing and caring for the injured member. One author found that the youngest or the oldest child complained, while another author found that the complaint 3. The patient may use the symptom of pain to control his or her family members and is reinof pain might even effectively reduce tension for younger forced when this works. children in large families. These findings have not been supported by other authors. 4. The stresses of family life may produce physiological effects that predispose an individual to Socioeconomic status may also influence the expresstress and disease. sion of pain. The fact that a majority of pain patients are blue-collar workers has been interpreted as the inability of working-class people to express emotional conflict, The review article considers the three approaches to thereby using somatizing terms. Of course, one must take family therapy: (1) behavioral, (2) transactional, and (3) into account that there are probably more blue collar work- systems approach of structural family therapy. The behavers than there are professionals, and it is the blue-collar ioral approach has been discussed in previous chapters in workers who have the physically strenuous jobs that putthis volume. The transactional approach tries to make them at higher risk. Other equivocally substantiated the-family members aware of the ways a patient can use pain ories have been offered, such as the quality of relationships for psychological “payoffs” and how they might foil these with parents, early loss of a family member, maintenanceattempts. The systems approach deals with the family as

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an organization and tries to change the structure so that deal with depression and frustration including (Hendler, no one family member has to be in the sick role. Mostet al., 1981): articles report that family therapy is a combination of behavioral, transactional, and systems approaches. Unfor- 1. The feeling that treatment in a pain treatment tunately, it is quite dif ficult to assess theficacy ef of family center is a last resort therapy. However, follow-up studies designed to reassess 2. Expression of displeasure and anger toward the recurrence of symptoms are the best way to determine physicians for not helping efficacy. One study, conducted at the Northwest Pain Cen- 3. A willingness to do anything to get rid of the pain ter, compared 25 successful patients with 25 patients who 4. A feeling of helplessness and guilt, compounded did not maintain gains made at the pain treatment center. by feelings of inadequacy and frustration Interestingly, they found that there were more divorced or because of an inability to function with the pain separated people in this success group, while the failure 5. Indications about the relationship between the group had done little to change the patterns of behavior patient and his or her family that clearly indiin their environment. They concluded that the role of the cate whether the family is supportive of the family in maintaining pain behavior contributed to the patient behavior, or in conflict with it failures. Payne and Norfleet (1986) concluded that family 6. A questioning of religious faith and the selecmembers contribute to treatment outcome by reinforcing tion process (why me?) or not reinforcing pain behavior. They suggested that if a 7. Explorations regarding feelings of dependency, patient has a family that is appropriately supportive, and 8. Resentment towards the disbelief of family has learned not to reinforce pain behavior, the chance of members, physicians, and associates success with pain treatment is greatly improved. If family 9. A fear about the origin of the pain and its promembers have not participated in the program, or resist gression change to their own behavior, then the family member with pain will probably persist. When compared to these These same authors then described outpatient group resistant family groups, a single (unmarried) pain patienttherapy that was more protracted and allowed exploration will probably have a better chance at success although of different themes including: they do not have family support. 1. Feelings of physical inability or handicaps 2. Resentment toward vocational rehabilitation GROUP PSYCHOTHERAPY 3. Difficulty in readjusting life goals Group psychotherapy has been an adjunctive treatment for 4. Concern about other group members patients with terminal disease, rheumatoid arthritis, and 5. Frustration regarding the slowness of the process of rehabilitation chronic, intractable benign pain. These three groups of patients share four common features (Hendler, Viernstein, 6. Fear regarding the loss of a spouse because of the chronic pain Shallanberger, & Long, 1981): 1. They have not had success with conventional therapy. 2. They feel isolated and burdensome to their family and friends. 3. They are angry at physicians and disappointed about treatment failure. 4. They have reactive depressions, frustration, and reduced physical activity.

As with all forms of psychotherapy, it is ficult dif to access the ficacy ef of group treatment. However, Ford (1984) utilized an objective measure officacy ef (i.e., the amount of medical care sought by patients prior to and after group psychotherapy) and reviewed the literature on this topic. Ford offers a cogent argument for psychotherapy — if it able to reduce the number of medical visits, on a cost-effective basis, if for no other reason. Various authors have reported between a 50 and 75% reduction in Group therapy can be utilized on both an inpatientmedical clinic visits while patients with somatic illness and outpatient basis, although the structure and format were undergoing group psychotherapy concomitantly. for these two groups is somewhat different (Hendler,Ford’s own experience was not quite as dramatic, but he 1981). In the inpatient setting, the patient is involved inattributes this to patients belonging to a low socioecogroup therapy for a relatively short period of time, usuallynomic group, and underscores the need for very long-term 8 to 12 sessions. In this context, the group psychotherapy group treatment before any benefit was noted. The most format more closely resembles a mixture of educationalimportant patient benefit appeared to be in the area of and free-interaction group psychotherapy, with more ofgaining control over his or her life. Other authors have a focus on the depressive components of the chronic pain advanced the notion that “peer modeling” and “interaction process. The most common themes of inpatient groups with other group members” allow patients to more freely

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express their emotions, to learn new coping methods, and ies, Slater (1965) did a 9-year, follow-up study on 85 to be more verbal when soliciting help (Gamsa, Braha, &people originally diagnosed as having hysterical converCatchlove, 1985). Although these authors conclude that sion reaction, who had been seen at the Queens Square group psychotherapy is a useful adjunct to their chronicHospital in London. At the time of follow-up, only 19 of pain treatment program, they do not offer any objectivethe 85 patients were free of symptoms. Of these 85 evidence. Hendler, et al. (1981) studied patients assigned patients, 7 were found to have recurrent endogenous to group therapy or individual therapy. In their study, 8 ofdepression, 2 were schizophrenic, 3 had undetected neothe 11 patients assigned to group therapy had remained plasms, in and of the 4 who committed suicide, 2 had atypical therapy, and 7 of the 8 had abstained from narcotic and myopathy and disseminated sclerosis. Each died of natural hypnotic use. This was contrasted with a group of 12causes. Two of the patients were found to have trigeminal patients, 7 of whom continued to use hypnotics, narcotics, neuralgia and one woman was finally diagnosed as having or benzodiazepines prescribed by other physicians. At the thoracic outlet syndrome. Three people were finally diagend of 3 months, 6 of the 12 had discontinued sessions. nosed as having early, previously undetected, dementia, A much more comprehensive report (Hall, Hall, & Gard- while one woman, who had pain in the right shoulder and ner, 1979) compared theficacy ef of combined group ther- arm, was later diagnosed as having Takayasu’ s syndrome. apy and tricyclic antidepressants vs. supportive individualThe remainder had a multiplicity of organic diseases, therapy, analytically oriented therapy, and management by including epilepsy, vestibular lesions, and total block of surgical specialists, using narcotics or antidepressants. the spinal cord. Of the 85 patients with the original diagUsing the Zung Rating Scales as an indication of thenosis of “hysteria” meaning conversion reaction, only 7 severity of depression, Hall’ s group found that group psy- were really found to have an acute psychogenic reaction chotherapy combined with tricyclic antidepressants wasresulting in formation of a conversion symptom, while 14 the most ef ficacious modality of therapy, while individual were diagnosed as having Briquet’ s syndrome, which is a psychotherapy and surgical management, using narcotics polysomatic hysterical neurosis more compatible with or antidepressants, were least effective. hypochondriasis, or somatizing disorders. Although it is difficult to accurately assess theficacy ef In a most thorough review of the literature, encomof group therapy, and many reports do not have objective passing nearly a 50-year period of time, Stephens and measures of outcome, the technique is cost-effective and Kamp (1962) found that the incidence of hysterical conprovides a degree of modeling and social reinforcement version reaction at a psychiatric hospital (Phipps Clinic that is not available from other forms of therapy. Theof Johns Hopkins Hospital) was approximately 2% of all effectiveness of other self-help groups, such as Alcoholics psychiatric admissions. Therefore, one must be quite cauAnonymous, would lend credence to the contention thattious in assigning the diagnosis of conversion neurosis, or group therapy is an effective modality for treating chronichysterical conversion disorder. Additionally, many clinipain patients. cians have dif ficulty differentiating between histrionic personality disorders, and a hysterical personality disorder resulting in many somatic complaints, which has been NARCOSYNTHESIS called Briquet’s syndrome. These two disorders are difSeveral recent articles in the psychiatric literature, as wellferent from a hysterical conversion reaction because the last of these three disorders can occur in a previously wellas in the chronic pain literature, suggest that many undiadjusted individual subjected to extreme stress (Hendler, agnosed chronic pain problems are really conversion reactions or hysterical conversion disorders. Most of these1981). A review of histrionic personality disorders vs. polysomatic Briquet syndrome vs. hysterical articles are unsubstantiated, or deal with single cases orhysterical, a conversion reactions vs. malingering can be found in Henfew cases, after which the authors attempt to apply their limited experience to the broad range of chronic paindler’s book (Hendler, 1981). Also, Hendler and Talo patients. In reality, the number of conversion disorders(1989a) published a chapter in which the differential diagpresenting as chronic pain problems is probably verynosis of these disorders is summarized. small. In this author’ s experience (more than 25 years), If hysterical conversion reaction is suspected in the after treating over 7000 chronic pain patients at thedifferential diagnosis, amobarbital narcosynthesis can Chronic Pain Treatment Center of Johns Hopkins Hospi-be quite useful in assisting in the diagnosis. One of the tal, while under the direction of the Department of Neu-leading proponents of this technique, Dr. Walters rosurgery, and at the Mensana Clinic, the incidence of(1973), of the University of California School of Medhysterical conversion disorders was three cases. Of course, icine, has recommended dosages between 200 and 500 these cases are quite memorable and represented enormg, taking a patient through the surgical pains of anesmous therapeutic challenges. thesia, including loss of corneal refl ex which produces One must be quite careful in making the diagnosis offull relaxation of “psychogenic tissue pain. ” Indeed, hysterical conversion reaction. In one of the classic studusing too small a dose of amobarbital may contribute

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to many of the failures associated with the lack of effec-(Krishnan, et al., 1985). France and co-workers believe tiveness of this technique (Hendler, Filtzer, Talo, Pan-that one can differentiate various subtypes of depression zetta, & Long, 1987). In fact, Hendler and co-workersin chronic low-back pain patient, and distinguish between specific ally found that a diagnostic failure, using (1) major depression, (2) minor depression, (3) intermitamobarbital narcosynthesis, was directly related to antent depression, (4) chronic low back pain patients without depression. One way of making this distinction is the use inadequate dosage of amytal (dosage range 200 to 250 of the dexamethasone suppression test. The former chairmg). When the dosage was increased to between 450 man of the Department of Psychiatry at Duke University, and 600 mg,effective narcosynthesis was obtained. Bernard Carroll, first advanced the notion of elevated plasma cortisol, resistant to suppression by dexamethaHYPNOSIS sone, in severe depressive illness (Carroll, Martin, & When considering hypnosis for the patient in pain oneDavies, 1968). Subsequent to this original article in 1968, Carroll and co-workers published extensively about the must make a distinction between acute pain and chronic pain. There is no question that hypnosis is an effectiveuse of the dexamethasone suppression test. Randall France, formerly of Duke University, and later the Unitreatment for acute pain problems. Scott (1974) has disversity of Utah, studied a group of 80 chronic back pain cussed the usefulness of hypnotic techniques for treating badly burned patients and for surgical candidates. How-patients, with and without depression, using the dexamever, even Scott admits that the effectiveness of thisethasone suppression test (DST) (France & Krishnan, technique is variable and unreliable. In theory, hypnosis1985). France and co-workers selected a uniform group can be used to treat the patient with acute pain, byof chronic low-back pain patients, that is, those with altering his or her perception of the amount of time thechronic low-back pain associated with organic pathology, pain is experienced. In this fashion, Teitelbaum (1965)and divided them into two groups based on the presence or absence of major depression, using DSM-III criteria. has proposed that hypnosis can be used for hypnoanalThey then examined the cortisol response to dexamethagesia and calls this phenomenon time “ distortion.” sone in each group. Of this group of 80 patients, 35 For chronic pain states, generalized relaxation therapy, patients were diagnosed as having major depression, while as described by Jacobson (1964) seems to be quite useful. 45 patients did not satisfy the criteria for major depression. As with biofeedback, hypnotic relaxation techniques seem However, of the 45 patients who did not have major to work best with chronic pain patients who have myodepression, 10 satisfied the criteria for dysthymic disorder. fascial pain or chronic muscle tension. Unfortunately, it In the group of patients with the diagnosis of major depresis difficult to assess the efficacy of hypnosis , especially in sion, 14 of the 35 had a positive dexamethasone suppreschronic pain states, and the technique does not lend itself sion test, while none of the 45 patients who did not have to controlled studies. The question of the ficacy ef of hypmajor affective disorder had a positive dexamethasone nosis with chronic back pain awaits controlled empirical suppression test. Again, of this group of 45 patients, 10 research(Turk & Flor, 1984). The major objection to were diagnosed as having a dysthymic disorder, which hypnosis lies in the fact that it might provide temporary might be more appropriately described as reactive depresrelief for the patient with chronic pain, but long-term relief sion. France very appropriately concluded that the abnorhas not been adequately documented. However, hypnosis mal dexamethasone suppression test is in response to a may be a useful diagnostic tool for uncovering underlying major depressive disorder, and not to chronic pain itself. hysterical conversion reactions, although it may be less Additionally, France noted that the incidence of anormal than narcosynthesis, as previously discussed. cortisol response to dexamethasone is higher in depressed patients without organic findings. As a conclusion, France and co-workers stated that the “difference in the rate of DIAGNOSIS AND TREATMENT non-suppression in chronic back pain patients with and OF DEPRESSION without depression suggests that the notion of conceptua variant of depression or as No discussion about the psychotherapy of chronic painalizing chronic back pain as a marked (sic) (masked) depression might be an oversimpatient would be complete without a thorough understandplification” (France & Krishnan, 1985). ing of the depression associated with chronic pain. One of the major difficulties one encounters in diagnosing In another study of 63 patients, conducted at the Unichronic pain patients with depression pertains to the eti-versity of Washington Pain Clinic, 49% of the sample met ology of the depression. France and Krishnan (1985) make the DSM-III criteria for major depression (Haley, et al., a distinction between despondency, or grief reaction in1985). In this study, depressed patients did not differ sigresponse to serious physical disease, and depression, statnificantly from nondepressed patients in the ratio of male ing that despondency is similar to grief reaction and mustvs. female, use of narcotics, use of sedative-hypnotics or be differentiated from depression in chronic pain statesantidepressant medication, number of years in chronic

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pain, age, or number of surgeries. However, for women,and adhering rigorously to DSM-IV diagnostic criteria, depression was more closely related to subjective reports one can identify a group of chronic pain patients who will of pain; while in men, depression was more closely related respond to interventions for depression. There is no doubt to impairment of activity. In a review of 454 chronic pain that the use of antidepressant medication in the chronic patients at Columbia-Presbyterian Medical Center,pain patients with major depression will prove the most Department of Anesthesiology Pain Treatment Service,efficacious modality of therapy. To appropriately prescribe NewYork, 100 patients were selected at random, and evenmedication, physicians should understand the pharmacotually 82 patients were contacted by telephone for long-logical contributions to normal sleep, pain perception, term follow-up of a sub-sample of the original number ofanxiety, and depression. aInreview of the literature, Henpatients (Dworkin, Richlin, Handlin, & Brand, 1986). In dler (1982a) describes the common pharmacological subevaluating the original 454 chronic pain patients, 79 ofstrate of normal sleep, pain perception, and antidepressant these patients were found to be depressed, while 375 were activity within the central nervous system as being elevanot considered depressed. Between the two groups, there tion of serotonin levels. Therefore, drugs that enhance was no significant difference in the percentage of males, serotonin activity within the central nervous system are females, age, marital status, education, or compensation. beneficial, and these include tricyclic antidepressants as The only significant differences existed between the per-well as the newer bicyclic and tetracyclic antidepressants. centage of patients undergoing litigation or beingThus, an antidepressant given at bedtime may promote employed. The depressed patients had a higher percentage natural sleep, reduce the perception of pain, and reduce of litigation and a lower percentage of employment whenanxiety and depression. Unfortunately, the selective serocompared with nondepressed chronic pain patients. When tonin reuptake inhibitors (SSRIs), which would be thought compared with pain-related characteristics, chronic painto be ideal for augmenting the treatment of pain, have not patients with depression more often had constant pain, and been as effective as the tricyclic antidepressants (Hendler, a higher self-reported scale of pain than the non-depressed 2000). Moreover, there seems to be a paradoxical worspatients. In non-depressed patients, significant variables ening, or even creation of anxiety with the use of certain contributing to the ability to predict treatment outcomeSSRIs, in certain sensitive individuals (Hendler, 2000). were number of treatment visits, compensation, number Antidepressant dosage should be individually tailored of previous therapies, and the location of pain. Into suit the patient’ s age and tolerance for medication, but depressed patients, the predictors of treatment outcome as a starting dose, one might recommend 50 to 100 mg were employment and duration of pain. amitriptyline, or doxepin, in patients who are both anxious Atkinson and his group in San Diego have definedand depressed, while one might consider using nortriptyline or desipramine at dosages between 25 and 75 mg three subgroups of chronic pain patients based on MMPI in patients who are depressed and report lack of energy scores and the type of depression they experience (Atkinson, Ingrani, Kremer &Saccuzzo, 1986). Using Research or a feeling of sluggishness. Dosage can be escalated in s Diagnostic Criteria, Atkinson, et al. found that 44% of the25- to 50-mg increments, depending on the patient’ response to the medication. It should be noted that the 52 patients examined had major depression, 19% had anti-anxiety effects of medication usually occur within the minor depression, 13% had other psychiatric disorders, first 2 days, as does enhancement of sleep. However, it and 22% had no mental disorder. Patients with a major depression were found to have a discrete MMPI profile,usually take 2 to 4 weeks before the antidepressant effect of these medications are fully appreciated. This seems to with Scales F, Hs, D, Hy, Pd, Pa, Pt, Sc, Ma, and Si being significantly higher, and Scale K being significantly lower correlate well with the amount of time it takes for the down-regulation of the post-synaptic serotonin receptors than the other three groups. The best predictors were (Hendler, 2000). If the use of antidepressants does not Scales Sc, Pt, and D. When the patients were divided by clinical characteristics of somatization, depression, orprove productive by the end of 4 weeks, therapeutic monhypochondriasis, patients with major depression fell intoitoring, using serum levels, will allow adjustment of the three depression MMPI profile groups (2, 1, 3, for rankdosage into the proper range. The use of specialized treatments for depression, such order elevation of MMPI scales, or D, Hs, Hy). Despite as monoamine oxidase inhibitors or electroconvulsive these distinctions, there wasan“ even distribution of therapy, is best left in the hand of psychiatrists, and the objective evidence for pain across all MMPI subgroups. ” selection of patients for these types of therapies should be This supports the contention that Hendler, et al. (1985a,b) done only after psychiatric consultation has been obtained. have long maintained, that is, the MMPI cannot predict the validity of the complaint of pain, and patients with psychiatric problems can also have real physical problems RESULTS at the same time. By using a psychiatric diagnostic system for delineat-Describing a pain patient can be likened to the famous fable of the five blind men describing an elephant for their king. ing the various types of depression in chronic pain patients

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Each clinic, each physician, and each hospital sees a difand eight foreign countries, as of the year 2000. Thereferent type of patient. Therefore, to assess results properly, fore, the need to accurately diagnose patients, both medthe demographics of the chronic pain patient populationically and psychiatrically is of paramount concern for the under study must be defi ned. On this point, the literature is psychiatrist. The psychiatrist cannot rely on the medical in shambles. Even more chaotic is the reporting of results. diagnosis of nonpsychiatric physicians. If he or she feels Few, if any, individual psychiatrists have published the patient merits further diagnostic evaluations, it is any results documenting theficacy ef of their intervention. incumbent upon the psychiatrist to order additional diagnostic studies and to obtain consultation with top-quality Reporting is hampered by the absence of objective criteria surgical colleagues. for improvement. What parameters should be measured to determine if a patient has benefi ted from the intervention of a psychiatrist? How do you measure pain? Is pain THE PSYCHIATRIST AS EDUCATOR relief or improved activity the desired goal? Can they exist independently? How long has the patient had pain? Patients with chronic pain are frightened because, very Is litigation involved? often, they do not know or understand what is wrong Hendler and Talo (1989) reviewed the literature ofwith them. Once an accurate diagnosis has been estabchronic pain clinics that had published results of treatinglished, the psychiatrist should explain in — simple and their pain patient population. Most clinics were eitherconcise terms —the anatomic origin of the pain problem, multidisciplinary or behavior modifi cation clinics. Of the options for treatment, the expected treatment outnote, 1 year after discharge from the clinic, most clinicscome, and alternatives to treatment. Chronic pain is a reported that only 25% of their patients had maintaineddevastating problem; but once a patient is fully informed the improved level of activity they had experienced atabout his or her options, anxiety is reduced and the discharge from the clinic. Pain relief ranged from slightpatient has been given an active role in the decisionto great in only 33 to 63% of the patients. That is, onlymaking process. Patients appreciate this involvement and about half the patients experienced any relief, even slight respond in a positive fashion. Little has been written relief, and only 25% maintained any improvement in theirabout the educator role for a psychiatrist; but in the level of activity (Hendler & Talo, 1989a). Using a more author’s opinion, it is one of the most benefi cial interobjective set of criteria, Hendler (1989) reviewed 60ventions that he or she performs. patients who had been diagnosed and treated at the Mensana Clinic. All 60 patients were involved in litigation PSYCHOLOGICAL TESTS and had been out of work an average of 4.9 years. By all accounts, this group of patients was considered to be difficult to treat because of the involvement of litigation Simply put, if a psychiatrist wants to measure personality and the chronicity of their problem. Although 90% of the traits, then he or she should use the MMPI or the Millon. patients had no dif ficulty discontinuing narcotics, hyp- If one wishes to measure psychological states, then the notics, and/or tranquilizers, only 50% had pain relief, butSCL-90, Beck Depression Test, Stress Vector Analysis, 91% improved their sleep and levels of activity. However, and Holmes-Rahe Life Events tests should be used. To measure the validity of the compliant of pain, only the the most startling statistic was the number of undiagnosed surgical problems; 50% of the patients were referred onMensana Clinic Back Pain Test is designed to do so, for further surgery (one to four additional operations)independent of preexisting personality traits or psychological states (Hendler, et al., 1979, 1985a, b, 1988). The because they had not been properly diagnosed before fact that not one single scale of the MMPI ever correlates referral (Hendler, 1989). Subsequent reports by Hendler with the presence or absence of organic pathology clearly and colleagues show that 40 to 67% of the patients are illustrates the need to use the proper test to measure the misdiagnosed, and the referral to surgery rate is 50 to 55% (Hendler & Kozokowski, 1993; Hendler, et al., pathology of interest. 1996). Referral diagnosis was very often a vague or descriptive one in 41% of the cases (25/60), with suchSUMMARY terms as psychogenic “ pain, ” “ pain neurosis, ” “ low-back dif task pain,” “ chronic muscle strain, ” etc. being used instead of Psychotherapy of chronic pain patients is aficult at best. In part, the process is complicated by the lack of any attempt at diagnosis. Because 96% of the referrals precision of diagnosis within the realm of psychiatry, but came from orthopedic or neurosurgeons, internists, rheumatologists, and physical medicine and rehabilitationalso within the realm of medicine. For this reason, chronic medicine physicians, the failure to diagnose surgicallypain patients engender controversy. Improved treatment correctable lesions is especially troubling. This was notcan be achieved by improved precision of diagnosis, both in the medical and psychiatric realms. Unfortunately, the a local or regional phenomenon because 75% of Mensana ficult to establish, but Clinic patients came from around the country (43 states)efficacy of psychotherapy is dif

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Helping improved levels of functioning, less depression, betterHendler, N. (1984a). Chronic pain. In H. Roback (Ed.), patients and their families cope with medical problems family relationships, and improvements in sleep and pain (pp. 79–106) . San Francisco: Jossey-Bass. levels can all be achieved with appropriate interventions. Hendler, N. (1984b). Depression caused by chronic pain. ClinMost important, the psychiatrist should serve as an objecical Journal of Psychiatry, 43 (3), 30–36. tive observer and recorder of patient complaints and be a Hendler, N. (1989). Validating the complaint of pain: The Mendiagnostician. Without accurate diagnosis, all treatments sana clinic approach . Clinical neurosurgery, 35 , are doomed to fail.

385–397. Hendler, N. (2000). Pharmacological management of pain. In P. Prithvi Raj (Ed.), Practical management of pain (3rd REFERENCES ed., pp. 145–155). Philadelphia: Mosby. Hendler, N., Bergson, C., & Morrison, C. (1996). Overlooked American Psychiatric Association (APA). (1994). Diagnostic physical diagnoses in chronic pain patients involved in and statistical manual of mental disorders (4th ed.). litigation, Part 2.Psychosomatics, 37 (6), 509–517. Washington, D.C.: APA. Atkinson, J.H.,Ingram, R., Kremer, E., & Sacctizzo, D. (1986). Hendler, N., Derogatis, L., Avella, J., & Long, D. (1977). EMG biofeedback in patients with chronic pain.Diseasesof MMPI subgroup:Affective disorders in chronic pain the Nervous System , 38, 505–509. patients. Journal of Nervous and Mental Disease, Hendler, N., & Fernandez, P. (1980) Alternative treatments for 174(7), 408–413. patients with chronic pain . Psychiatric Annals, 10 (12), Black, R.G. (1982).The clinical managment of chronic pain. In 25–33. N. Hendler, D. Long, & T. Wise (Eds.), Diagnosis and Hendler, N., Filtzer, D., Talo, S., Panzetta, M., & Long, . D treatment of chronic pain (pp. 211–224).Littleton, MA: (1987). Hysterical scoliosis treated with amobarbital John Wright–PSG. narcosynthesis.The Clinical Journal of Pain, (3), 2 Carroll, E.J., Martin, F.R., & Davies, B. (1968) Resistance to 179–182. suppression by dexamethasone of plasma II–OHCS in Hendler, N., & Kozokowski, J. (1993). Overlooked physical severe depressive illness. British Medical Journal, 3, diagnoses in chronic pain patients involved in litigation. 285–287. Psychosomatics, 34 (5), 494–501, Dworkin, R., Richlin, D., Handlin, D., & Brand, I. (1986). Predicting treatment response in depressed and non-Hendler, N., Mollett, A., Viernstein, M., Schroeder, D., Rybock, J., Campbell, J., Levin, S., & Long, D. (1985a). A comdepressed chronic pain patients. Pain, 24(3), 343–353. parison between the MMPI unit the "Hendler back pain Engel, G. (1959). Psychogenic pain in the pain prone patient. test" for validating the complaint of chronic back pain American Journal of Medicine, 26, 899–918. in men. The Journal of Neurological & Orthopaedic Ford, C.V (1984). Somatizing disorders . In H. Roback (Ed.), Medicine & Surgery, (4), 6 333–337. Helping patients and their families cope with medical Hendler, N., Mollett, A., Viernstein, M., Schroeder, D., Rybock, problems(pp. 39–59). San Francisco: Jossey-Bass. J., Campbell, J., Levin, S., & Long, D. (1985b). A comFord, C.V. (1986). Somatizing disorders. Psychosomatics, 27(5), parison between the MMPI and the "Mensana Clinic 327–337. back pain test" for validating the complaint of chronic France, R., & Krishnan, K.R.R. (1985). The dexamethasone back pain inwomen.Pain, 23(3), 243–252. suppression and a biological marker of depression and Hendler, N., Mollett, A., Talo, S., & Levin, S. (1988). A comchronic pain. Pain, 21(1), 49–55. parison between the Minnesota multiphasic personality Gamsa, A., Braha, R., & Catchlove, R. (1985). Theofuse strucinventory andthe "MensanaClinic back pain test" for ture group therapy sessions in the treatment of chronic validating the complaint of chronic back pain. Journal pain patients.Pain 22(1), 91–96. of Occupational Medicine, 30 (2), 98–102. Haley, W., Turner, J., & Romano, J. (1985). Depression in chronic pain patients: Relation to pain, activity, and sexHendler, N., & Talo, S. (1989a). Chronic pain patients versus the malingering patient. In K. Foley & R. Payne (Eds.), differences.Pain, 24(3), 343–353. Current therapy of pain(pp. 14–22).Toronto: B. C. Hall, R.C., Hall, A.K., & Gardner, E.R. (1979). Comparison of Decker. tricyclic antidepressants and analgesic: The manageHendler, N., & Talo, S. (1989b). Role of the pain clinic . In K. ment of chronic post-operative surgical pain . Paper preFoley & R. Payne (Eds.), Current therapy of pain(pp. sented at the Annual Meeting of the Academy of 23–32).Toronto: B. C. Decker. Psychosomatic Medicine, San Francisco. Hendler, N. (1981).Diagnosis and nonsurgical management of Hendler, N., Viernstein, M., Gucer, P., & Long, D. M., (1979). A pre-operative screening test for chronic back pain chronic pain.New York: Raven Press. patients.Psychosomatics, 20 (12) 801–808. Hendler, N. (1982a). The anatomy and psycho-pharmacology of Hendler, N., Viernstein, M., Shallanberger, C., & Long, D. chronic pain.Journal of Clinical Psychiatry, 43, 15–20. (1981). Group psychotherapy with chronic pain patients. Hendler, N. (1982b) . The four stages of pain. In N. Hendler, D. Psychosomatics, 22 (4), 332–340 . Long, & T. Wise (Eds.),Diagnosis and treatment of Anxiety and tension control (pp. 108–111). chronic pain (pp. 1–8). Littleton, MA: John Jacobson, E. (1964). Philadelphia: J. B. Lippincott. Wright–PSG.

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Krishnan, K.R.R., France, R.D., Belton, S., McCann, U.D., Rutrick, D. (1981). Psychotherapy with chronic intractable benign pain patients. Pain, Suppl.1(331), S271. Davidson, J., & Urban, B.J. (1985). Chronic pain and depression 1, Classification of depression and chronicScott, D.L. (1974).Modern hospital hypnosis. Chicago: Yearlower back pain patients. Pain, 22(3), 279–287. book Medical Publishers. Large, R. (1985). Prediction of treatment response in painSlater, E. (1965). Diagnosis of "hysteria." British Medical Jourpatients: The illness self-concept repertory grid and nal, 1, 1395–1399. EMG biofeedback.Pain, 21(3), 279–287. Stephens, J. & Kamp, M. (1962). On some aspects of hysteria: Maruta, E., Swanson, D., & Swanson, W. (1976). Pain as a A clinical study, Journal of Nervous andMental Dispsychiatric symptom: Comparison between low back ease, 134 , 305–315. pain and depression. Psychosomatics, 17 , 123–127. Teitelbaum, M. (1965).Hypnosis induction techniques (pp. Payne, B., & Norfleet, M. (1986). Chronic pain and the family: 22–24). Springfield, IL: Charles C Thomas. A review. Pain, 26(1), 1–22. Turk, D., & Flor, H, (1984). Ideological theories and treatments Pilowsky, I., & Bassett, D. L. (1982). Pain and depression. Britfor chronic back pain, II: Psychological models and ish Journal of Psychiatry, 141, 30–36. interventions.Pain, 19(3), 209–233 Reich, J., Rosenblatt, R., & Tupin, J. (1983). DSM-III: A new Walters, A. (1973). Psychiatric consideration of pain . In J. Younomenclature for classifying patients with chronic pain. mans (Ed.),Neurological surgery(1st ed., Vol. 3, pp. 1516–1645). Philadelphia: W. B. Saunders. Pain, 16(2),201–206. Psychosomatics , 24(2), Rowat, K.M., & Knafl, K.A. (1985). Living with chronic pain: Webb, W., Jr. (1983). Chronic pain. 1053–1063. The spouse's perspective. Pain, 23(3), 259–271.

27 A Rheumatologist’s Perspective on Pain Management Thomas J. Romano, M.D., Ph.D., F.A.C.P., F.A.C.R. INTRODUCTION

patient with chronic (i.e., incurable and probably progressive) disease. Pain can be defined as an unpleasant sensation that is Rheumatologists are concerned with many problems thought to originate from a particular body part and and/or potential problems that affect the clinical course of which is usually associated with processes that are capathe patients under their care. Patients need to be kept ble of causing damage to body tissue. Pain can be acute, ambulatory, if possible, or at least their ability to care for such as one might experience in the case of a fractured themselves must be maximized to prevent progressive bone. If pain persists beyond the customary time it takes joint and spine deformity. Physicians want to minimize or the affected part to heal or recuperate, the pain is termed “chronic.” Acute pain typically occurs when a noxious eliminate the chance that the patient’s underlying disease stimulus activates sensitive peripheral endings of pri-(e.g., systemic lupus erythematosus, rheumatoid arthritis) mary afferent nonciceptors. The noxious stimulus is thenwill affect their internal organs (e.g., nephritis in systemic lupus erythematosus, Felty’s syndrome [splenomegaly turned into a form of electrochemical energy by a process and neutropenia] in RA), and optimize the length and called transduction, whereupon the message is then quality of the patient’s life. transmitted via peripheral nerves to the spinal cord and then on to the brain, where the inputs are modulated and When the vast majority of patients first present for pain is consciously perceived (reviewed in great detailconsultation and treatment, it is the complaint of pain, by Fields, 1987). It is clear that pain is more than just aabove all other symptoms, that dominates the initial patient-physician encounter. Certainly, the fear of having sensation. It has two components: sensory and affective. a potentially crippling disease or of not being able to Regardless of the cause of the pain, both components perform certain tasks because of weakness, stiffness, or must be considered. loss of dexterity comes to the forefront after the impact No greater interplay between the sensory and affecof the illness is explored. However, it is the worsening tive aspects of pain can be found than in the rheumatic diseases. Not only is the central nervous system of of a pain or the fear of increased pain that has brought the patient suffering from arthritis bombarded by afferent patient for treatment at that particular time, although signals from inflamed swollen tissue, but the consciousother symptoms may have been present for months or (or unconscious) interpretation of the significance of theeven years. To better appreciate how the rheumatologist painful stimuli (perhaps the harbinger of crippling, loss approaches the problem of pain, and to gain an underof independence, etc.) may influence pain perception, standing of the role of pain control in the rheumatic disas can other factors such as the development of a secondary fibromyalgia syndrome or psychiatric/psycho-eases, one must first know what a rheumatologist is, how logical problems that may complicate the course of ahe/she was trained, and what concerns him/her when con0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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fronted with a patient who is in pain and who often has other symptoms/problems. Frequently, the rheumatolo- TABLE 27.1 gist’s patient is confused as to the diagnosis and prognosis, Possible Causes of Secondary Osteoarthritis often having seen numerous other health professionals A. Joint damage due to: before contacting the rheumatologist. • Infectious (septic arthritis) A rheumatologist typically treats many types of mus• Hemophilia culoskeletal diseases. The spectrum of rheumatologic dis• Neuropathy (Charcot joint) ease is vast, and classifi cations are constantly being • Gout and other crystal-induced arthritis updated. The most recent classification can be found in • Rheumatoid or other inflammatory arthritis the latestPrimer on Rheumatic Diseases (Schumacher, B. Multiple epiphyseal dysplasia 1997). In his/her day-to-day practice, the rheumatologist C. Congenital dislocation of the hip • Slipped capital epiphysis typically encounters patients with inflammatory condiD. Inherited metabolic disorders tions such as rheumatoid arthritis (RA), systemic lupus • Wilson’s disease erythematosus, and the like, or degenerative joint disease • Hemochromatosis such as osteoarthritis and myofascial pain syndromes of • Alkaptonuria both the regional and generalized (i.e., fibrositis/fibromy• Morquio’s disease algia) forms. Quite frequently, he/she is also confronted E. Paget’s disease of bone with musculoskeletal problems that arise out of or comF. Acromegaly plicate other diseases. Infectious diseases (e.g., AIDS, G. Other processes that damage articular cartilage tuberculosis, rheumatic fever), endocrine abnormalities (e.g., diabetes mellitus, thyroid disease, hyperparathyroidbone, and other connective tissue by repeated trauma or ism), malignancy, and other pathologic conditions may inflammation; and low back pain that usually arises from first manifest themselves as neuromuscular or musculoa combination of factors. skeletal problems. Therefore, the rheumatologist must use his/her acumen as an internist to understand and treat Degenerative arthritis or osteoarthritis (OA) (osteoarthrosis in Great Britain and The Commonwealth) is probpatients thus af flicted. ably the most common rheumatic disease affecting bones It would be easier to understand the treatment of rheuand joints (Creamer & Hochbery, 1997). It may be primary matologic diseases if general categories were established (idiopathic) or secondary to other diseases (Table 27.1). and analyzed separately. For purposes of clarity and trying to follow general pathophysiologic guidelines, I proposeIt is characterized by the narrowing of joint space by dividing rheumatologic diseases into four main groups: progressive loss of articular cartilage, usually accompanied by reactive changes at the joint margins and underlying subchondral bones. Many patients describe a “bone1. Degenerative diseases on-bone” sensation in weight-bearing joints, such as the 2. Inflammatory conditions knees and/or hips, especially during exercise or simply 3. Myofascial pain syndromes 4. Other (e.g., infectious, neoplastic, endocrine, upon ambulation. It must be remembered that OA is a disease of the joints and it has no systemic component congenital) conditions (Bergstrom, 1985; Forman, Malamet, & Kaplan, 1983). Naturally, there may be considerable overlap, and any one The prevalence of OA increases with age and some form of OA is present in almost all patients 65 or older. patient may have several of the above conditions, but these distinctions should prove useful in systematically analyz-Many times, the patient experiences transient and/or mild ing and treating patients with either simple or complexto moderate discomfort and does not see a rheumatologist. problems. Conspicuous in its absence in the above format Often, over-the-counter analgesics, combined with resting is the impact of psychological forces that may play a partof the affected area, tend to provideficient suf relief. Other in the suffering of rheumatologic disease patients.patients have more prolonged symptoms or have more Although rheumatologists do not primarily treat psycho-severe pain than they can control themselves, so they logical disease, its presence is recognized in some initially seek relief from their family doctor. Many such patients. Therefore, problems such as depression and anxpatients obtain relief with the chronic use of nonsteroidal iety will be discussed in terms of their impact on specificanti-inflammatory drugs (NSAIDs) such as prescriptiondiseases, as opposed to creating a separate category. strength aspirin preparations (Zorprin, Easprin), nonsalicylate medications such as ibuprofen (Motrin, Rufen), diclofenac (Voltaren), naproxen (Naprosyn), flurbiprofen DEGENERATIVE DISEASES (Ansaid), ketoprofen (Orudis), piroxicam (Feldene), indomethacin (Indocin, Indocin SR), and many others. The category of degenerative diseases contains, but is not limited to, degenerative joint disease; degradation of joint,These have been amply reviewed (Fowler and Arnold,

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1983) and their effectiveness has been established. A word from weeks to months, it can aid the patient in taking of caution: if a patient with OA on an NSAID obtains advantage of exercise or physical therapy that previously objective improvement (e.g., decreased swelling, redness, may have been dif ficult to endure. More recently, warmth) but still complains of pain, a secondary myofas-viscous/elastic intra-articular preparations composed of cial pain or fibromyalgia syndrome should be consideredmixtures of hyaluronic acid and saline such as sodium ® ) (Altman & Moskowitz, 1998) (Romano, 1996). Many OA patients also suffer fromhyaluronate (Hyalgan regional (e.g., anserine bursitis) or generalized (e.g., fibrohave been employed to treat painful knee OA. While these myalgia) soft tissue myofascial pain syndromes. Unlessvisco-supplementation medications are superior to oral these are addressed separately and treatment initiated, the NSAID treatment alone, their role in the long-term manpatient will continue to complain of pain — which is the agement of OA remains to be determined. Other regimens primary reason he/she sought medical attention in the first to help reduce pain and relieve mechanical stress on place— despite a good response to OA treatment. These affected (especially weight-bearing) joints are weight loss, are the types of patients whom the rheumatologist is apt muscle strengthening, use of orthotics (e.g., cane, walker, to see. These OA sufferers who do well with NSAIDs orcrutches), and local heat/massage. other therapy prescribed by their family doctor have no A word of warning: NSAIDs should be given with reason to visit a rheumatologist’ s office. While NSAIDs great caution in patients taking oral anticoagulants, sulare excellent medications, they should not be used in phonylurea a anti-diabetes medication, or other highly procavalier fashion, due to potentially severe and even life-tein-bound drugs because NSAIDs compete with such threatening side effects. The potential gastrointestinal toxmedication for plasma protein binding sites and often icity of these medications is very well-known (Huskisson,displace a suf ficient amount of the drug in question to Woolf, Balme, Scott, & Franklin, 1976), as are the effectscause untoward effects (e.g., a further prolongation of the of these drugs on renal plasmaowfl (Brezin, Katz, prothrombin time or an exaggerated hypoglycemic Schwartz, & Chintz, 1979) and platelet aggregation (Rothresponse). In addition, NSAIDs can interfere with diuretic & Majerus, 1975). These effects are the result of prostagtherapy, and adjustments in type or dosage of these medlandin inhibition and seem to affect patients in a directications may need to be made (Day, Graham, Champion, proportion to their age and the presence of other disease & Lee, 1984). (e.g., peptic ulcer disease, liver disease, kidney disease). When the pain or deformity of OA become overOne way to prevent the untoward effects of prostag-whelming, consideration should be given to orthopedic landin inhibitors is the use of anti-inflammatory medica-consultation, especially if the patient has symptoms tions that are selective prostaglandin inhibitors, such as involving a weight-bearing joint like the hip or knee. The salsalate (Disalcid, Salflex, Monogesic) or choline magtechnology for the replacement of these joints is superior nesium trisalicylate (Trilsate). Misoprostol (Cytotec) can than for other joints, and orthopedists generally have more be introduced to prevent NSAID gastropathy (Graham, experience with this type of replacement. However, not Agranval, & Roth, 1988) because it is a synthetic prosevery patient with recalcitrant knee OA needs total knee taglandin E analog that allows the stomach to proceed replacement. High tibial osteotomy and other corrective with its endogenous cytoprotective mechanisms even in procedures may be more appropriate in selected patients. the presence of NSAID-induced prostaglandin inhibition. It is generally prescribed for patients who are elderly or Often, patients with OA develop associated painful conditions, such as carpal tunnel syndrome, fibromyalgia, who have had upper gastrointestinal problems in the past. or a local myofascial pain syndrome, all of which need to Patients using nonacetylated salicylates do not need to use be identified and treated. misoprostol. Recently, a new class of NSAIDs has been Joints under increased mechanical stress would seem approved for use for arthritis sufferers (Osiris & Moreland, ® to be likely candidates for the development of OA, ) (Simon, et al., 1999) and 1999). Celecoxib (Celebrex ® although the medical literature is far from clear on this rofecoxib (Vioxx ) (Langman, et al., 1999) selectively issue, as illustrated in recent papers regarding runners inhibit cyclooxygenase-2 (COX-2), thus minimizing (Lane, et al., 1986; Panush, et al., 1986). potential adverse effects on the gastrointestinal tract. FurSome studies have found that there is a relationship thermore, topical capsaicin (McCarthy, & McCarthy, between prolonged stress and OA (e.g., spine OA in coal 1992) and topical preparations of NSAIDs (Russell, 1991) miners [Schlomka, Schroter, & Ocherwal, 1955] and (Ginsberg & Famaey, 1991) have been shown to be effecshoulder OA in bus drivers [Lawrence, 1969]), while other tive in relieving symptoms in OA patients. studies have not found this to be the case (Burkle, Fear, Often, topical and NSAID therapy is not enough to & Wright, 1977; Puranen, Ala-Ketola, Peltokallio, & relieve the pain in a particular joint. In such cases, the use of intra-articular injections of a local anesthetic-corticos-Saarela, 1975). teroid mixture can provide prompt, dramatic relief (HolEach patient’ s problem must be evaluated individulander, 1972). While the relief is usually temporary, lastingally, and aggravating factors minimized or removed if and

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when they are identifi ed. This is particularly true for dramatic relief. Age alone should not be a deterrent in patients with back problems. cases of spinal stenosis, especially since medical manageBack pain may come from a single problem or ament of this condition is far from ideal and the quality of combination of pathologic processes. Spinal OA is a dis-life can be greatly enhanced by a relatively safe and effective procedure. ease of the apophyseal joints. It is frequently associated with disc disease and the terms degenerativedisc andjoint disease, or spondylosis, are often used. While anatomic INFLAMMATORY CONDITIONS changes may be well-defined by an X-ray or CT scan showing osteophytic lipping and sclerosis, often these corUnlike degenerative diseases such as OA, inflammatory relate poorly with the clinical picture. The developmentconditions, such as systemic lupus erythematosus (SLE), of spondylosis is probably inevitable in most patients withrheumatoid arthritis (RA), and vasculitis (e.g., polyarterimicrotrauma where everyday activities contribute to thetis nodosa, giant cell arteritis, or cryoglobulinemia), are symptoms. However, preventive measures, such as the not only painful conditions, but can be life-threatening. maintenance of ideal weight, good posture, moderate exerThe musculoskeletal manifestations of these systemic discise, and proper methods of lifting and carrying, can doeases can be quite severe, and can affect the nervous much to ease symptoms. The use of NSAIDs, as well as system directly through the deposition and activity of adequate rest and the use of heat or cold applications immune to complexes. the affected areas, may be helpful. In some patients, trac- Rheumatoid arthritis (RA) is a chronic inflammatory tion and/or bracing may be needed (Lee, et al., 1989). Ifconnective tissue disease that can be potentially crippling the cervical spine is involved, the use of a cervical pillowand even life-threatening (Harris, 1990). It typically (preferably a four-in-one cervical pillow or Wal-Pil-O affects diarthrodial joints, but can also cause such extra[Roloke Co., 8919 Sunset Blvd., Los Angeles, CA articular manifestations as scleritis, pericarditis, lymphad90069]), which prevents neck flexion and hyperextension,enopathy, arteritis, nodulosis, splenomegaly, neutropenia, is helpful in relieving night pain. Using chairs with a anemia, and pleural effusions/pleuritis. The systemic headrest and avoidance of reading or watching television nature of RA is reflected by the presence of an increased while recumbent can also help. Posterior neck muscles erythrocyte sedimentation rate, the presence of rheumacan be strengthened by isometric exercises (Thiske, 1969). toid factor, antinuclear antibody, other autoantibodies, The patient tightens the muscles in the back of the neck anemia (usually chronic disease, but iron deficiency aneand makes a double chin (military posture) to the countmia may also be present), or low plasma albumin in some, of five; this is repeated 10 times. Patients are encouraged but not necessarily all patients. to do this four or five times per day. Rheumatoid arthritis is found worldwide and is As far as the lumbar area is concerned, pain in the extremely common (approximately 1% of the U.S. popubuttocks, thighs, and legs is caused by a combination of lation is believed to be affected) with a female to male entrapment of nerve roots by discs, apophyseal joints, and ratio of 3:1. Peak incidence is between the ages of 40 and adjacent soft tissue. There is often a long-standing history 60. Mild cases are usually treated symptomatically by of recurrent low back pain related to a congenital narrow-patients using over-the-counter preparations, while more ing of the neural canal. Aging and degenerative changes seriously afflicted individuals seek the services of their bring on further narrowing and the clinical syndrome ofprimary care doctor. Rheumatologists usually see more spinal stenosis. severe cases, especially when disease-modifying antirheuSpinal stenosis, especially of the lumbar spine, mostmatic drugs (DMARDs) or remittive agents are needed in commonly occurs in elderly patients with spondylosisaddition to NSAIDs and/or oral glucocorticosteroids. DMARDs are slow-acting agents whose function is to with encroachment of osteophytes into the spinal canal or prevent RA from crippling and are also helpful in controlexit foramina. This causes a phenomenon known as neurogenic claudication in which the patient experiences calfling systemic problems (Furst, 1990). Gold salts (injectand/or thigh/buttock pain while walking. Relief typically able or oral), d-penicillamine, and hydroxychlorogorine occurs when the patient sits down, which helps to differ-have been used in the past, over a decade ago, with some entiate the problem from vascular claudication. The symp-success; but recently, immunosuppressive agents such as toms of vascular claudication are often alleviated whenmethotrexate, azathioprine, and cyclosporin have been successful in halting the ravages of RA. However, even ambulation ceases, but sitting down is not usually necessary for relief. The presence of the above history in anthe immunosuppressive agents were less than ideal, either elderly patient (or one who suffers from Paget’ s disease) due to unacceptable side effects (e.g., bone marrow failure, ef with strong distal pulses, should make the clinician veryhepatotoxicity, nephrotoxicity, etc.) or the lack officacy. More recently, leflunomide (Arava® ), etanercept suspicious. A CT scan of the spine should be taken and, ®), have been intro(Enbrel®), and infliximab (Remicade if stenosis is present, orthopedic or neurosurgical consultation should be obtained. Corrective surgery often givesduced. Each works differently but all have been shown to

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art icu lar

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Int

tic

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be effective in treating many RA patients already on methotrexate (Smolen, et al., 1999; Weinblatt, Kremer, & Bankhurst, 1999; Maini, Breedveld, & Kalder, 1998). Leflunomide inhibits pyrimidine synthesis while etanercept blocks the action of tumor necrosis factor (TNF), a Experimental Treatments substance necessary for the autoimmuneammatory infl synovitis in RA. Infliximab, a monoclonal antibody, neutralizes the activity of TNF, thus reducing disease activity. NSAIDs plus a For patients with particularly severe RA that is unrecombination of DMARDs sponsive to various combinations of one NSAID and a single DMARD, combinations of DMARDs have been NSAIDs plus DMARDs used with success (McCarty, Harman, Grassanovich, Qian, & Klein, 1995b). The treatment pyramid for RA is shown in Figure 27.1. NSAIDs Lately, many rheumatologists have chosen to treat RA much more aggressively, initiating treatment with Education; Avoidance of Aggravating Factors NSAIDs plus DMARDs earlier rather than later (Wiske Physical Therapy & Healey, 1990). Suf fice it to say, the rationale regarding RA therapy has undergone some changes recently (Mikuls & O’Dell, 2000). Each patient is unique and, given theFIGURE 27.1 Treatment pyramid for RA. variety of medications and techniques now at our disposal, leukocytes. Complement levels in RA synovial uidfl are it is more likely than ever that a safe, individualized treatgenerally low and rheumatoid factors are often found; ment can be designed to fit each patient. however, this testing tends to be of only limited benefi t A word of caution: DMARDs with NSAIDs tend to as it usually does not affect the course of treatment. A have potentially more serious side effects than NSAIDs more dramatic, convenient, and inexpensive test is the used alone. Alopecia, lowering of blood count (red blood fl is watery compared count and/or white blood count and/or platelet count),observation that RA synovialuid fl found in joint fluid from OA hepatotoxicity, gastrointestinal upset, and oral ulcerationto the more viscous uid patients and normal controls. This is because the hyaluare common to all DMARDs. Gold salts can cause renal ronic acid and other macromolecular synovial uidflcomproblems and rashes, as can d-penicillamine, which can ponents have been degraded by the ammatory infl medialso cause such bizarre problems as polymyositis (a myasators (e.g., superoxides, enzymes, lymphokines) present thenia gravis-type syndrome) and obliterative bronchioliin the affected joint. tis. Cyclosporin use can cause renal failure. Leflonamide can cause hepatotoxicity and other side If an inflamed RA knee develops a large effusion that becomes chronic, a popliteal or Baker’ s cyst may develop. effects such as rash, diarrhea, and reversible alopecia. EtanMost of the time, the communication between the joint ercept must not be given to patients at risk for serious space and the cyst is one-way and this valve effect can infection because it is immunosuppressive and may exaccause high pressures in the popliteal space. Because fluid erbate infectious processes. One disadvantage in using etanis incompressible, a rupture of the cyst can occur. The ercept is that it needs to be injected subcutaneously (25 mg) release of a large volume of fluid that contains inflammatwice a week. Another is cost — the wholesale price for tory mediators posteriorly between the medial head of the 6 months of treatment would be $6000 to $7000. For severe gastrocnemious muscle and the tendinous insertion of the refractory RA, intravenous infl iximab has been given in biceps muscle can cause the affected calf to become swolmultiple administrations. The cost of three doses for a 70-kg len, red, and intensely painful. The patient thus involved patient would easily cost several thousand dollars. This cost must be weighed against the potential benefi t and, of course, can present to the physician with a problem that resembles acute thrombophlebitis. The Homan’ s sign is frequently potential life-threatening side effects. Like OA, RA can involve weight-bearing joints in positive, thus causing some confusion. A positive arthroaddition to its capacity to involve the small joints of the gram (with or without a negative venogram, depending on the circumstances) can confirm the presence of a Baker’ s hands, wrists, feet, ankles, and elbows in a symmetrical cyst. Treatment with intra-articular steroids, rest, elevamanner. Often when knees are involved, large effusions result and aspiration and injection can be dramaticallytion, and attention to the underlying rheumatological coneffective (McCarty, Harman, Grassanovich, & Quin, ditions should be effective in the vast majority of cases. 1995). Analysis of synovial uid fl generally shows an Surgical synovectomy may occasionally be necessary. A s cyst elevated white cell count (usually 10,000 to 50,000 perword of caution: treating a patient with a Baker’ microliter) with a predominance of polymorphonuclear using an intravenous anticoagulant, such as heparin (the

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preferred treatment for acute thrombophlebitis), is notpresent at a site distant from the painful area and often only ineffective, but may be counterproductive, causingpossess taut myofascial bands which may even restrict painful ecchymoses in the calf tissues that have become movement. These are amply illustrated (Travell & hyperemic from the inflammation. Simons, 1983; Sheon, Moskowitz, & Goldenberg, 1982) Although many reports of improved and “unorthodox” (see Figure 27.2). The trigger point has been shown to treatments for RA are sprinkled throughout the lay presshave a characteristic pattern on needle electromyoand touted by some health care professionals, it is imporgraphic testing (Hubbard & Berkoff, 1993; Romano & tant to remember that testimonials and endorsements are Stiller, 1997). Furthermore, some patients with myofasnot a substitute for sound scientific research. However, cial pain syndrome have been shown to have magnesium one must keep an open mind regarding new RA therapies. deficiency (Romano, 1994). Trauma, especially susThree recent studies offer examples of the utility of treat-tained repetitive trauma, can bring on these syndromes, ments not ordinarily thought of as antirheumatic but haveand part of therapy is to avoid aggravating conditions. been shown to be effective in treating RA: fish oil (Kremer, et al., 1995) and the antibiotic minocycline (Kloppenburg, Breedveld, Terwiel, Mallee, & Dijkmans, 1994; Tilley, et al., 1995). The clinician must weigh what he/she feels is the potential benefit vs. the possible risks/toxicities of each therapeutic intervention and prescribe accordingly. RA may be unpredictable and often periodic reassessments of the patients’conditions need to be made with attendant adjustments in therapeutic regimen changes in therapy. Other painful problems that can occur in RA are the development of fibromyalgia, severe metatarsalgia (often helped by wearing 3/8-in. metatarsal bars on the outside of the shoes), carpal tunnel syndrome (median nerve compression neuropathy), chest pain due to either pleuritis or pericarditis, and Sjogren’ s syndrome (a chronic autoimmune/inflammatory disorder that results in keratoconjunctivity sicca and xerostomia). The dry eyes associated with the latter condition are painful and annoying, and other mucous membranes can also become affected. The lack of vaginal secretions can make sexual intercourse painful. If food is not chewed well and eaten with frequent sips of water, it may become lodged in the throat. The paucity of saliva (with its attendant antibacterial activity) can lead to painful dental caries and frequently loss of teeth. Other complications of RA are legion but their enumeration and description fall outside the scope of this chapter.

MYOFASCIAL PAIN SYNDROME It is important for the rheumatologist to realize that, in terms of the general population, the majority of patients with musculoskeletal complaints do not have arthritis. The pain usually results from problems (i.e., disease or injury) in structures near or around the joint, such as nerves, muscles, tendons, fascia, ligaments, bursae, or bones (Simons, 1990). This section focuses on pain caused by these non-articular areas. The problem may FIGURE 27.2 Zones of reference: Upon palpating the trigger be localized or generalized (reviewed in Fricton & point, pain is produced at some distant point. This zone is quite Awad, 1990). Localized myofascial pain syndromescharacteristic for each trigger point. (From Shoen, R.P., Markowitz, R.W., & Goldberg, V.M. (Eds.) (1987). Soft tissue have plagued man since the beginning of time. These rheumatic pain: Recognition, management and prevention syndromes are characterized by complaints of regional (p. 224). Philadelphia: Lea & Febiger. Copyright ©1987. pain (e.g., neck, shoulder, hip) that can be reproduced by palpation of specifi c trigger points that may be Reprinted by permission.)

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Men and women appear to be affected equally. Treatment usually consists of local trigger point injections TABLE 27.2 with a local anesthetic —long-acting corticosteroid The American College of Rheumatology 1990 preparation followed by massage of the affected area.Criteria for the Classification of Fibromyalgia This can cause a dramatic response with prompt relief and better range of motion. The use of a moist heating1. History of widespread pain Definition: Pain is considered widespread when all of the pad several times a day for 5 to 15 minutes is encouraged following are present: pain in the left side of the body, pain in the as is trying to get family members involved in the treatright side of the body, pain above the waist, and pain below the ment scheme, because recurrences may be preempted waist. In addition, axial skeletal pain (cervical spine, anterior chest, with easily learned acupressure techniques (Prudden, thoracic spine, or low back) must be present. In this definition, 1980) before the pain becomes unbearable. Education shoulder and buttock pain is considered as pain for each involved and reassurance are extremely helpful and usually result side. “low back” pain is considered lower segment pain. in fewer visits and a diminished requirement for trigger 2. Pain in 11 of 18 tender point sites on digital palpation. point injections. Definition: Pain, on digital palpation, must be present in at least 11 of the following 18 tender point sites: For the patient with chronic myofascial pain that is recalcitrant or recurrent (and for the generalized myo- • Occiput: Bilateral, at the suboccipital muscle insertions fascial pain patient), a counselor/psychologist trained in • Low cervical: Bilateral, at the anterior aspects of the intertransverse spaces at C5-C7 biofeedback, relaxation techniques, and a cognitive• Trapezius:Bilateral, at the midpoint of the upper border behavioral approach to pain may prove invaluable. Often, • Supraspinatus:Bilateral, at origins, above the scapula spine such patients benefi t from treatment by a physical thernear the medial border apist with interest and training in myofascial release • Second rib:Bilateral, at the second costochondral junctions, techniques or spray and by a chiropractor who is able to just lateral to the junctions on upper surfaces manipulate certain muscle groups that are in spasm or • Lateral epicondyle:Bilateral, 2 cm distal to the epicondyle very taut. In so doing, pain can be relieved and postural • Gluteal: Bilateral, in the upper outer quadrants of buttocks in anterior fold of muscle problems corrected.

FIBROMYALGIA SYNDROME

• Greater trochanter:Bilateral, posterior to the trochanteric prominence • Knee: Bilateral, at the medial fat pad proximal to the joint line Digital palpation should be performed with an approximate force of 4 kg. For a tender point to be considered “positive,” the subject must state that the palpation was painful. “Tender” is not to be considered“painful.”

The epitome of a widespread soft tissue pain syndrome is fibromyalgia (previously termedfibrositis) syndrome (FS). Intense research efforts over the past decade have provided good evidence that FS is a distinct rheumatolog, 33, ical disorder, and widely accepted definitive criteria for Adapted from Wolfe, et al., 1990,Arthritis and Rheumatism its diagnosis were published in early 1990 (Wolfe, et al.,160–172. 1990). The 1990 criteria are given in Table 27.2. FS occurs predominantly (80 to 90%) in women from their teens to(Romano & Stiller, 1988; Cohen, Arroyo, & Champion, mid-thirties, but in the Upper Ohio Valley area, the 1990; Romano & Govindan, 1996) testing. This may help female:male ratio is 3:1 (Romano, 1988b). Children haveexplain the presence of such neuritic complaints as paresthesias, lancinating pains, and headache that affect also been diagnosed as having FS (Yunus & Masi, 1985; over 50% of FS sufferers (Wolfe, et al., 1990). Fatigue Romano, 1991a). FS is a very common problem, and it confronts rheu-is an extremely common symptom in FS patients and matologists on a daily basis (Bohan, 1981; Mazenac,many have been shown to have FS and chronic fatigue 1982). FS patients usually complain of musculoskeletalsyndrome (Goldenberg, Simms, Geiger, & Komaroff, pain, stiffness, and easy fatigability, often linked to non-1990). Fatigue may be the major reason why some FS patients are impaired. A defect in stage 4, non-REM, restful sleep. Generalized achiness and diffuse musculoskeletal pain are very common and, although jointdelta-wave sleep is often present (see Figure 27.3) leadswelling cannot be documented, it is often a complaint.ing to a nonrestorative sleep after which the FS patient feels as tired, or more tired, upon arising than when he Feelings of weakness cannot be documented, but are commonly encountered. They cannot be correlated withor she retired. Nocturnal myoclonus has been found to be very common in FS patients (Romano, 1999). This the usual tests of muscle strength and routinely available disturbing symptom often responds to clonazepam tests (e.g., blood muscle enzyme levels, routine muscle (Klonopin®) taken at bedtime. biopsies, and electromyographic studies) are normal. However, more sophisticated testing has demonstrated Patients with FS are reported to have a poor quality abnormalities in histochemical (Awad, 1990), immuno- of life (Burkhardt, Clark & Bennett, 1993; Bernard, logical (Caro, 1986; Romano, 1991b), and neurologicalPrice, Edsoll, 2000) and may become so impaired that

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FIGURE 27.3 (A) Frequency spectra and raw EEG from non-REM (stage 4) sleep in a healthy 25-year-old subject. The spectrum shows that most amplitude is concentrated at 1 cps (delta). (B) Non-REM sleep in a 42-year-old “fibrositis” patient. The spectrum shows amplitude at both 1 cps (delta) and 8–10 cps (alpha). (C) Non-REM sleep of a healthy 21-year-old during stage 4 sleep deprivations. In the EEG, there is a clear association between the external arousal (auditory stimulation) and alpha onset. Again, the frequency spectrum (obtained by 10-second analysis from stimulus onset) shows amplitude concentrated in the delta and alpha bands. (From Primer on the rheumatic diseases (9th ed.). Copyright ©1988. Used by permission of the Arthritis Foundation.)

they are disabled from gainful employment (Bennett,tion is the presence of typical tender points at character1993). This may be because the central nervous system istic locations (Wolfe, et al., 1990). A dolorimeter examis affected. Yunus (1992) postulated a pathophysiologicalination is not necessary for diagnosis, but helps in model of FS that described aberrant central pain mechachieving more objectivity in the analysis of tender points anisms with peripheral modulation. Recent studies lend(Campbell, Clark, Forehand, Tindall, & Bennett 1983; support to this hypothesis. Abnormalities of regionalFischer, 1987). Not all FS patients are aware of the prescerebral blood ow fl have been demonstrated in FS ence of many of these discrete points of tenderness and patients (Mountz, et al., 1995; Romano & Govindan,often express surprise when the trained physician seems 1996). Cognitive difficulties have also been demon- to locate these points with relative ease. The examination strated in patients with FS (Clauw, Morris, Starbuck,of the primary FS patient often does not reveal any other Blank, & Gary, 1994), as has abnormal central processabnormalities. There is no synovitis or joint swelling. ing of nociceptive stimuli (Bradley, et al., 1995). Range of motion of all appendicular joints is usually Many modulating factors affect the FS sufferer. Mostnormal, and edema is absent. Neurological examination reveals no abnormalities in gait or station (although poor FS patients report worsening symptoms due to cold damp posture may be present). There is normal sensation to weather, loud noises, emotional stress, anxiety, and/or refl are normal. If overexertion. Patients seem to report improvement inpinprick and vibratory sense, and exes a localized myofascial pain syndrome also flicts af the FS symptoms in warmer, dryer months, and after hot baths, patient, then a trigger point or constellation of trigger mild to moderate activity, and/or vacations. Often, numerpoints is usually present. As opposed to a tender point ous medications (e.g., NSAIDs, analgesics) have been tried without success. Many patients report that chiro-that causes local pain when palpated, pressure on a trigger practic help gives relief, albeit temporary. A completepoint causes pain to be referred to nearby regional sites. history should help the clinician in making diagnosis ofThe rheumatologist needs to be aware that many conditions may present with FS-like symptoms. These include, FS in that the physical examination would defi nitely include a tender point count, as well as good general but are not limited to, early SLE or RA, polymyalgia examination. The hallmark of the FS patient ’s examina- rheumatica, polymyositis, Sjogren’ s syndrome, metabolic

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myopathies, regional myofascial pain syndromes,as an important treatment for these patients. As FS is still hypothyroidism, hyperparathyroidism, and widespreadincompletely understood and treatment far from ideal, successful management of FS patients requires a good generalized OA. Before initiating treatment, the physician needs tophysician-patient relationship, with the realization that progress can be made through mutual trust and effort. As stress that patients must be actively involved in their treatis the case with other rheumatic diseases, cookbook” a“ ment and not just a passive recipient of health care (Benapproach has little chance of success and shortchanges nett, 1986; Romano, 1988a). Patients need to understand both the physician and the patient. that FS does not kill or cripple; it can nonetheless be very painful, and they must minimize stress in their lives and be compliant with the treatment plan. TRAUMA AND SOFT TISSUE The treatment of FS consists of prompt symptomatic relief, along with a plan for long-term management.RHEUMATISM CONDITIONS NSAIDs are not very useful, except as analgesics.It is important to realize that there are three types of FS. Because of a paucity of potential adverse reaction (espeThe first is idiopathic FS or FS that occurs for a reason cially important in those FS sufferers who also have irri-but one that cannot be readily identifi ed. Another form of table bowel syndrome, irritable bladder, tension head-FS is called secondary or concomitant FS, where the FS aches, temporomandibular joint syndrome, migraine, and comes as a direct consequence of a chronic medical condysmenorrhea), use of one of the nonacetylated salicylates dition, such as rheumatoid arthritis, chronic lung disease, (salsalate: Disalcid, Monogesic, Salfex; choline magne-chronic heart disease, etc. The third type of FS, known sium trisalicylate: Trilisate) prescribing up to 3 g/day in as post-traumatic FS, comes as a result of an accident, divided doses is preferred. FS patients may get temporary such as a motor vehicle accident or fall. In terms of benefit from heat therapy, massage, acupuncture, sprayseverity, a recent study has shown that reactive FS (either and-stretch techniques, injection of tender points withpost-traumatic FS or secondary/concomitant FS) is more local anesthetic (such as 1% procaine or 1% xylocaine severe and more disabling than the idiopathic variety with or without a corticosteroid preparation), transcuta-(Greenfield, Fitzcharles, Esdaile, 1992). There is no doubt neous nerve stimulation, physical therapy, and/or postural that fibromyalgia (also known asbrositis) fi can be caused correction. Medications that help restore normal sleepby trauma (Bennett, 1989; Smythe, 1989). The question patterns, such as amitriptyline, nortriptyline, chlorprom-is whether a specifi c trauma caused a specifi c FS in a azine, doxepin, trazodone, or cyclobenzaprine, can be specific patient at a specifi c time. To determine that, a very useful if taken in the evening. The dosages may need careful history and physical examination must be obtained to be individualized to each particular patient, but typicalso that a conclusion based on the facts as opposed to starting doses are: amitriptyline (Elavil), 10– 50 mg; prejudice or bias can be reached. However, because many nortriptyline (Pamelor), 10– 25 mg; chlorpromazine physicians are unfamiliar with FS and/or myofascial pain (Thorazine), 25– 100 mg; doxepin (Sinequan), 10– 50 mg; syndromes, their relationship to a traumatic event can be trazodone (Desyrel), 50– 150 mg; and cyclobenzaprine overlooked. Dr. David Simons (1987) wrote, Myofascial “ ®) (Neville, (Flexeril), 10–20 mg. Gabapentin (Neurontin trigger points are one of three musculoskeletal dysfunc2000) at 100 to 3600 mg/day in divided doses helps many tions that are commonly overlooked and deserve particuFS patients who have prominent neuritic symptoms.lar attention. The other two arebrositis/fi fi bromyalgia and Tramatol (Ultram®) 50 mg q 4–6h prn) has been reported articular dysfunction. None has a diagnostic laboratory by many FS researchers to be helpful as a safe and effecimaging test at this time. All three conditions presently tive analgesic. Other strategies, including the use of narrequire diagnosis by history and physical examination cotic analgesics and growth hormones have been reviewed alone. In each case, the diagnosis would probably be by Bennett (1999). Brand-name medications instead ofmissed on routine conventional examination. The examgeneric drug preparations are preferred, despite the cost iner must know precisely what to look for, how to look savings. Too many questions have been posed concerning for it, and then must carefully be looking for” it. Since the quality control and bioavailability of generic drugs to this was written, techniques such as dolorimetry, tissue have confidence in them, and therefore, their use is dis-compliance testing, etc., have aided the pain practitioner, couraged. Narcotic preparations that provide moderate but it is ultimately the hands-on” “ examination by an analgesic effect may be helpful in some patients, but the experienced examiner that can correctly diagnose a given need for their use should diminish with time. Recentsituation. This is incredibly important in dealing with studies have demonstrated a ciency defi of magnesium in patients who suffer from these nonarticular or soft tissue some FS patients (Clauw, Blank, Hewitt-Moulman, & rheumatism conditions especially when such patients and Katz, 1993; Romano & Stiller, 1994) and dietary supple-their advocates are criticized for maintaining that these patients are in a great deal of pain when diagnostic studies mentation has been suggested (Abraham & Flechas, 1992)

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such as MRI, CT, etc., are negative or normal. An article If asked to testify in court regarding soft tissue injuin a law journal (Smiley, Cram, Margoles, Romano, ries, the physician must remember that the court needs to Stiller, 1992) underscores the importance of obtaining aknow (1) what the patient is suffering from; (2) if the soft tissue problem (e.g., FS, myofascial pain syndrome, etc.) good history, performing a methodical and accurate physical examination, and obtaining the appropriate tests tocould be precipitated or caused by trauma; (3) if the proballow the pain practitioner to determine the presence orlem was precipitated or caused by the accident/incident in question (i.e., if the trauma would not have occurred, absence of one or another soft tissue pain syndrome. The would the patient have this problem); (4) if the problem jury can then determine the extent of compensation based is permanent; and (5) the cost of future care for the patient on the manner in which these tools are used to describe the patient’s injuries (or lack of them). Once a patient is for the injuries sustained in the accident/incident. The court needs to know these things to a reasonable degree diagnosed as having post-traumatic FS, he/she is likely to return for treatment even when litigation is over (Romano,of medical probability or certainty. How this standard applies to testimony given by a rheumatologist was out1990), a phenomenon that has also recently been observed lined in a paper authored by several prominent FS in patients with post-traumatic headache disorder (Packresearchers (Yunus, et al., 1997). A method to assess the ard, 1992). contribution of several different traumas regarding To understand how a local injury can cause FS, one patients’ painful medical problems has been determined needs to understand that most patients with soft tissue s trauma, and even with fractures, recover uneventfully after(Romano, 1998). Ultimately, however, the physician’ education, training, and experience, as well as his knowla reasonable period of time, usually several months. Howedge of the particular patient in question, should be the ever, some patients do not recover and have widespread basis for giving such opinions. pain that seems to get worse with time. Several noted rheumatologists have described the connection between trauma and FS. Smythe (1989) wrote, “Trauma may ini-MISCELLANEOUS CONDITIONS tiate a chronic fibrositis syndrome with a frequency of Perhaps in no other area is the skill of the rheumatologist 25% in one study of 92 patients. ” In addition; “injury to (vis-à-vis internist) put to more of a test than in the realm the neck was described in 40% before the onset of symptoms and in the low back in 31%. ” More recently, several of such miscellaneous conditions as endocrine, metabolic, infectious, or neoplastic diseases that present with musrheumatologists described an increased incidence of FS after cervical spine injury as opposed to injuries to theculoskeletal signs and symptoms. The patient with a dislower extremity (Buskila, Neumann, Vaisberg, Alkalag, & ease that fits into one of the above categories has more than a muscle, joint, bone, or soft tissue problem, but this Wolfe, 1997). Bennett (1989) described how a sequence may not be obvious early in the course of the disease, less of events can take place to generate a widespread FS from so if the condition behaves in an atypical manner. One a local myofascial pain syndrome. must remember, however, that FS can coexist with any of FS can be as painful and disabling as rheumatoid these disorders (Hudson, Goldenberg, Pope, Keck, & arthritis (Russell, 1990). It can adversely affect lifestyleSchlesinger, 1992). In fact, FS has even been described in (Burkhart, Clark and Bennett, 1993), so much so that FS patients infected with human immunodefi ciency virus patients consistently scored among the lowest in all(Simms, et al., 1992). domains measured compared with patients with RA, OA, The musculoskeletal problems attendant to certain permanent ostomies, chronic obstructive pulmonary dis-endocrine diseases may be the first clue that an endocrinease, insulin-dependent diabetes, and health controls. This opathy is present. The rheumatological signs and sympmay be a surprising finding for the uninitiated, but this istoms are often eminently treatable and even curable if the absolutely true and is something that is seen on an almostunderlying endocrine abnormality is rectified (Bland, Frydaily basis. moyer, Newberry, Revers, & Norman, 1979). If the patient Because traumatically induced FS usually starts as presents a with myofascial pain (especially fibromyalgia), local myofascial pain syndrome (Bennett, 1989) orcarpal tunnel syndrome, shoulder capsulitis (i.e., periar“regional fibromyalgia” (Yunus, 1993), and then spreadsthritis), crystal deposition disease (e.g., pseudogout due to involve other areas of the body, possibly as the result to calcium pyrophosphate deposition disease), proximal of expanded receptive fields (Dubner, 1992) and neuromyopathy, or osteopenia (osteoporosis and/or osteomalaplasticity of the nervous system (Mense, 1994), it is nocia), the presence of an underlying endocrine disorder surprise that the resultant FS is intensely painful and dif-should be strongly considered. Endocrine problems ficult to treat. These “persistent pain syndromes can draincluding, but not limited to, parathyroid disease (both matically affect the patient’ s life, leading to long-term hypo- and hyperparathyroidism), adrenal disorders, and disability and a significant decrease in quality of ”life. diabetes mellitus can be causative or contributing to the (Ashburn & Fine, 1989). development of the above rheumatologic problems.

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3 The patient suffering from hyperparathyroidism often highly viscous, with white cell counts of 1000 cells/mm presents with back pain and even vertebral fractures that or less). Thyroid replacement often results in dramatic mimic osteoporosis senilis (Dauphine, Riggs, & Schlotz,resolution of the above rheumatic problems. 1975). Generalized muscular aching and stiffness, joint If a patient has an overactive thyroid, rheumatic problaxity (and accompanying arthralgia from hypermobility), lems often manifest. Diffusely swollen and painful hands erosive OA (Resnick, 1974), spontaneous tender avuland feet associated with periositis (thyroid acropachy) can sion/rupture, and neuromyopathy (Patten, et al., 1974) can be seen in Graves’ disease, as can thyrotoxic myopathy, also raise the suspicion of the presence of hyperthyroidbone pain caused by osteopenia, shoulder periarthritis, and ism, especially if serum calcium determinations are ele-shoulder-hand syndrome complicating adhesive capsulitis vated. Some 35% of hyperparathyroidism patients have (Wohlgethan, 1987). Musculoskeletal pain may also occur chondracalcinosis (Pritchard & Jessop, 1977). Acutewith Hashimoto’s thyroiditis. This disorder has been seen arthritis in the setting of an acute myocardial infarctionwith increased frequency in association with RA and posor postoperatively may be due to gout or pseudogout. Asibly other connective tissue disease (Smiley, Husain, & synovial fluid analysis, which includes a crystal examina- Indenbaum, 1980; Gordon, Klein, Dekker, Rodnan, & tion, helps establish this diagnosis. Medsger, 1981). Ironically, one of the treatments of hyperAt the opposite end of the spectrum, the patient withthyroidism, the administration of propylthiouracil, has hypoparathyroidism may present with signs and symp-been reported to cause such rheumatic diseases as SLE toms (typically back pain) of ankylosing spondylitis (Amrheim, Kenney, & Ross, 1970) and vasculitis (Hous(Chaykin, Frame, & Sigler, 1969), carpopedal spasmton, Crouch, Brick, & DiBartolomeo, 1979). with tingling due to the low serum calcium, as well as Diabetes mellitus, probably the most common endomuscle cramps. crine disease, also has numerous rheumatologic manifesMusculoskeletal complaints seem to be associated tations (Gray & Gottlieb, 1976). Painful neuropathy may with adrenal overactivity and adrenal underactivity, thefirst bring the diabetic patient to the attention of the pain latter condition (Addison’ s disease) frequently manifest- specialist. Other problems, such as Charcot joints (Sinha, ing itself as severe muscle cramping. Munichoodappa, & Kozak, 1972) (often not completely Cortisol excess (Cushing’ s syndrome) can be idio- painless and confused with osteomyelitis, another condipathic or due to treatment with glucocorticosteroids, andtion to which diabetic patients are susceptible), shoulder in severe osteoporosis may ensue with compression fracperiarthritis (Bridgman, 1972), carpal tunnel syndrome tures of the spine and ribs, proximal muscle wasting, and and palmar flexor tendinitis (Jung, et al., 1971), and a possible aseptic necrosis of bone (especially the femoral scleroderma-like digital sclerosis (Seibold, 1982), can head). When exogenous corticosteroids are withdrawn, plague the diabetic patient. The rheumatologist often pseudorheumatism (diffuse muscle, joint, and bony ach-encounters patients with both adult and juvenile onset ing) may occur. It is imperative to be aware of this, asdiabetes who have painless contractures of the proximal such a problem can have the same symptoms as a flareand of distal interphalangeal joints; recognition of these concertain types of arthritis for which the medication mayditions is important because such microvascular complihave been prescribed. When and if such symptoms occur, cations as nephropathy and retinopathy may parallel the their interpretation in light of the patient’ s clinical course development and progression of these contractures (Fitzis crucial for optimal management, because pseudorheucharles, Duby, Waddell, Banks, & Karsh, 1984). matism usually abates gradually with a slowing down of Excess pituitary secretion of growth hormone, which the steroid tapering schedule and the administration of causes acromegaly, can result in a characteristic arthropmild non-narcotic analgesics. However, a flare of RA, forathy that mirrors the enhanced action of this hormone on example, could entail a much more thorough reassessment bone, cartilage, and periarticular soft tissue. With regard and revision of the treatment plan. to the diarthrodral joints, early cartilage hypertrophy Thyroid disease often affects the musculoskeletal syscauses the joint space to be abnormally wide, as seen on tem and its manifestations are protean. HypothyroidismX-ray. This cartilage tends to break down more easily than often presents with a myopathy, with profound musclenormal cartilage and such patients develop OA at a relaweakness and elevated serum muscle enzymes. It can tively be early age. Carpal tunnel syndrome is also common. confused with inflammatory disorders of muscles, such as The spinal pain and polyarthritis have been reported to polymyositis or dermatomyositis. The peripheral joints ofrespond dramatically when the underlying pituitary disorhypothyroid patients with myxedema may be swollen inder is treated successfully (Lachs & Jacobs, 1986). This a symmetrical fashion much like the joints in rheumatoidprinciple (i.e., the importance of the identification and arthritis (Dorwart & Schumacher, 1975). treatment of the underlying endocrine problem) is crucial In contrast to the joint fluid from RA patients, the in alleviating the pain and suffering of patients with endosynovial fluid aspirated from the joints of hypothyroid crine disease in whom musculoskeletal manifestations patients is definitely not inflammatory (i.e., it is thick and may be severe.

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eletal conditions. Osteopenia can also occur in patients who have other rheumatic diseases, especially those TABLE 27.3 receiving long-term glucocorticosteroid treatment (Hahn Differential Diagnosis of Generalized Osteopenia & Hahn, 1976). The scope of the problem is so vast that in Adults a chapter devoted to it could not even begin to outline the Osteoporosis Parallel loss of mineral and matrix problem and discuss therapy. However, some major facPredisposing factors include aging, tors need to be considered. The patient with osteopenia menopause, female sex, white or Asian usually has osteoporosis (loss of bone mineral and matrix race, immobilization, low physical in parallel), osteomalacia (accumulation of unmineralized activity, inadequate dietary calcium, smoking, alcohol, corticosteroid therapy, matrix after loss of bone mineral), hyperparathyroidism with osteitis fibrosa (replacement of bone bybrous fi family history tissue), or cortisteroid-induced osteopenia. The last probOsteomalacia Inadequate mineralization of bones, matrix lem is often unavoidable due to the patients’ need for such Differential diagnosis includes: medication, but the ability of steroids to interfere with • Vitamin D deficiency: Inadequate calcium absorption from the intestine may be partially intake, low sunlight exposure, drugovercome by the administration of calcium and vitamin D induced catabolism of vitamin D, supplementation (Hahn, Halstead, Teitelbaum, & Hahn intestinal malabsorption 1979). The use of these medications is recommended for • Phosphate-wasting syndrome: patients with osteoporosis senilis, as is estrogen, fluoride, Acquired renal tubular defects, with calcitonin, or a combination of these agents based on the isolated phosphate loss, combined individual patient’s needs. The best method of treating tubular defects (Fanconi’ s syndrome), osteoporosis is prevention, if feasible. Patients at risk (typrenal tubular acidosis, antacid abuse ically sedentary, small-framed women approaching menoOsteitis fibrosa PTH-induced increase in mineral and matrix reabsorption pause who smoke and drink alcohol and who have low Differential diagnosis includes: calcium and vitamin D intake) should use preventative • Primary hyperparathyroidism measures such as regular exercise, adequate intake of cal• Secondary hyperparathyroidism: cium and vitamin D (Matkovic, et al., 1979; NIH ConsenVitamin D deficiency states, primary sus Conference, 1984), and consultation with a physician decrease in intestinal calcium who may feel that other measures, such as estrogen therabsorption with age, reduced renal apy, are necessary. mass (chronic renal insuf ficiency) The most common causes of osteomalacia in adults Glucocorticoid-induced Differential diagnosis includes: are decreased absorption of vitamin D due to intestinal or osteopenia • Iatrogenic • Adrenal corticosteroid overproduction: biliary tract disease, accelerated catabolism of vitamin D Indiopathi (Cushing’ s syndrome) due to drug-induced increases in hepatic oxidase activity, Other disorders • Hyperparathyroidism and acquired renal tubular defects with phosphate wasting. • Diffuse osteolytic malignancies (e.g., Correcting the cause of the metabolic problem is necesmultiple myeloma) sary for reversal of the osteomalacia. • Congenital disorders: Osteogenesis While not as common as osteopenia, Paget’ s disease imperfecta tarda, vitamin D–resistant of bone is a frequent cause of bony pain, and is estimated rickets to affect 1 to 3% of people over the age of 45 in the U.S. It is usually polyostotic, and men tend to predominate. From Seminars in Arthritis and Rheumatism. While the cause of Paget’ s disease (osteitis deformans) is It should be noted that FS often coexists with endo-unknown (late manifestation of viral infection has been crine problems (Crofford, 1996; Griep, Buersmat, & desuggested), it is characterized by excessive bone resorption Kloet, 1993), necessitating even more vigilance and cir-followed by excessive bone formation, culminating in a cumspection on the part of the clinician. Clearly, the mostbizarre mosaic pattern of lamellar bone associated with common metabolic disease that causes musculoskeletal increased local vascularity and increased brous fi tissue in pain in the general population is osteopenia. The scope of adjacent marrow (Smiger, et al., 1977). The disease is a this problem is enormous and the differential diagnosisfocal disorder as normal bone exists even in patients lengthy (see Table 27.3). Acute bone fracture can result severely affected. The sites most commonly involved are from osteopenia, and thousands of patients suffer from hip the pelvis, skull, femur, tibia, and spine. In addition to pain, fractures annually, making it a major public health prob-gross deformity, compression of neural structures, fracture lem with high morbidity and mortality. Metabolic bone of involved bone, and alteration of joint structure/function, disease can also cause muscular pain and weakness, sympoften result. Increased serum alkaline phosphatase and uriect the increased bone turnover in toms of which are often confused with other musculosk-nary hydroxproline refl

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this disease. An infrequent (300 kHz, short wavelengths 3–30 m. Typically, 27.12 MHz, 65–400 mS, 32 W average (< 200 W).

Indications Amenorrhea Brachial plexus neuritis Bronchiectasis Bronchitis Bursitis (subacute and chronic) Colic Contusions Dislocations Diverticulitis Dysmenorrhea Epicondylitis Fibrositis Fibrous fixation/ankylosis

Absolute Contraindications Fractures (recent) Hearing aids Hemoptysis, epitaxis, melena, and other hemorrhagic tendencies Malignancy Menstruation Metallic dental appliances and fillings Metallic implants On a metal table Over adhesive strapping

Relative Contraindications Areas of decreased vascularity Arteriosclerosis (advanced) Hypothermesthesia Infants and debilitated elderly Intrauterine device (metallic) Metallic buttons, zippers, hairpins, buckles, clasps, keys, knives, etc. Nondraining cellulitis Osteomyelitis

Electromedicine: The Other Side of Physiology

Furuncle/carbuncle Hypertonia Intercostal neuralgia Ischialgia (chronic) Intervetebral disc syndrome Low back pain Mastitis Myalgia Myositis Neuritis Osteoarthritis Pelvic inflammatory disease (subacute, chronic) Pleurisy Prostatitis Pyelitis (subacute, chronic) Rheumatoid arthritis (subacute, chronic) Sprains and strains Tenosynovitis

Over casts Over moist dressings Pacemakers Peptic ulcers Pregnancy Pyretic states Rheumatoid arthritis (acute) Septic arthritis (acute) Tuberculosis (pulmonary or joint)

Pain Ankle pain Foot pain Fractures Joint mobilization Knee pain Sciatica Sprains and strains Tendonitis Thrombophlebitis

Pain Carpal tunnel syndrome Epicondylitis Frozen shoulder Hand pain Peripheral nerve injury Sprains and strains Subdeltoid bursitis Wrist pain

Osteoporosis (advanced) Over growing epiphyseal plate Patients on anticoagulants, cortisone, gold therapy Peripheral vascular disease (occlusive) Poliomyelitis (acute stage) Polyneuritis with impaired circulation Suppurating inflammatory process Thrombosis Transcranially Varicose veins

757

Ultrasound Promotes blood circulation; improves metabolism, muscle relaxation, pain control; increases elasticity of connective tissues. Used to treat tendon adhesions and scars, post-traumatic injuries, binding tissue contractions (scars), Dupuytren’ s Contracture, bursitis, capsulitis, tendonitis, and chronic open wounds. Micromassage, microdestruction, and heat generation. May cause mechanical or thermal tissue damage. Overdose may decrease blood sugar levels, cause fatigue, nervousness, irritability, constipation, and a tendency to catch cold. Do not use over pregnant uterus, heart, testicles, spine, areas of thrombophlebitis, infections. High frequency mechanical vibrations using piezoelectricity > 20 kHz (typically between 0.8 and 3 Mhz) 2. and 0.1–3 W/cm

Indications Bursitis (subacute, Sprains and strains chronic) (subacute, chronic) Calcific bursitis Sudeck’s atrophy Causalgia Tendonitis Decubital ulcers (subacute, chronic) Transcutaneous Electrical Nerve Stimulation Fibrositis (subacute, Trigger points chronic) Varicose ulcers (TENS) Fibrotic (chronic) Acute, chronic, and post-operative pain. polymylosis Uses low-frequency biphasic currents of 75–400 mS, Herpes zoster Joint contractures 50–150 Hz, < 100 mA. Myalgia Neuralgia Osteoarthritis Indications Painful neuroma Systemic Pain Abdominal Pain Back Pain Periarthritis Bursitis Bladder pain Coccydynia (nonseptic) Cancer Bowel stasis Intercostal neuralgia Radiculitis Causalgia Diverticulosis Intervertebral disc (subacute, chronic) Ischialgia Dysmenorrhea syndrome Raynaud’s disease Neuralgia Labor Low back pain Rheumatoid Osteoarthritis Post-operative pain Lumbrosacral pain arthritis (subacute, Passive stretch pain Radiculitis chronic) Rheumatoid arthritis Sprains and strains Scars Synovitis Thoracodynia Shoulder–hand Whole back pain syndrome Spondylitis Lower Extremity Upper Extremity Contraindications Metallic implants Metastatic carcinoma Near carotid sinus area Over or through heart Pacemakers Pregnancy Transcranially

Contraindications Acute infection Areas of thermohypersthesia Near hearing aid Near malignant lesions Near metallic implants Near pacemakers Occlusive vascular disease Over bony prominences Over epiphyseal plates of growing children Over nerve plexuses Over suspected embolus Over the eye Over the heart Over a pregnant uterus Over the reproductive organs Over spinal cord after laminectomy Radiculitis (acute) Tendency to hemorrhage Transcranially

SUMMARY One must stray from the routine procedures of today in order to create the advances of tomorrow. There is still a lot to learn about bioelectricity and electromedicine. In

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Kitchen, S., & Bazin, S. (1996). Clayton’s electrotherapy(10th order to do so, we must first acknowledge that there is ed.). London: W.B. Saunders Company, Ltd. another side of physiology. Everyone concerned about Low, J., & Reed, A. (1994). Electrotherapy explained: principles health should demand widespread access to conservative, and practice (2nd ed.). Oxford: Butterworth Heinesafe, alternative care. To lessen human suffering is a notamann. ble goal. That we have not been able to achieve enough Lyte, M., et al. (1991). Effects of in vitro electrical stimulation of this to date without causing undo harm is a good indion enhancement and suppression of malignant lymcation that the answers must lie elsewhere. Biophysics phoma proliferation.Journal National Cancer Institute, must be better understood to realize the actual basis for 83, 116–119. the control of the regulatory processes of life. Morris, D.M., et al. (1992). Electrochemical modification of Even at its present state of evolution, electromedicine tumor growth in mice.Journal of Surgical Research 53, offers an unprecedented conservative, cost-effective, fast, 306–309. safe, and powerful tool in the management of the painNelson, R.M., & Currier, D.P. (1991). Clinical electrotherapy (2nd ed.). Norwalk, CT: Appleton & Lange. patient. As such, it should be the first priority on the list Nordenström, B.E.W. (1983). Biologically closed electric cirof treatment options. cuits: Clinical, experimental and theoretical evidence for an additional circulatory system . Stockholm: Nordic Medical Publications. REFERENCES Nordenström, B.E.W. (1984). Biologically closed electrical circuits: Activation of vascular interstitial closed electric Bauer, W. (1983). Neuroelectric medicine. Journal of Bioeleccircuits for treatment of inoperable cancers. Journal of tricity, 2, 2–3. 159. Bioelectricity, 3, 137–153. Becker, R.O. (1981). Mechanisms of growth control . Springfield, Nordenström, B.E.W. (1989). Electrochemical treatment of canIL: Charles C Thomas Co. cer. Variable response to anodic and cathodic fields. Becker, R.O. (1982). Electrical control systems and regenerative American Journal of Clinical Oncology(CCT), 12, growth. Journal of Bioelectricity , 1(2), 239–264. 530–36. Becker, R.O. (1983). The role of the orthopaedic surgeon in the Nordenström, B.E.W. (1998).Exploring biologically closed development of bioconductivity. Journal of Bioelectricelectric circuits. Stockholm, Sweden: Nordic Medical ity, 2(1), 77–81. Publications. Becker, R.O. (1990).CrossCurrents: The perils of electropolluLo que he descubierto en el tejido cantion, the promise of electromedicine . Los Angeles, CA: Pallares, D.S. (1998). ceroso. Col. Pedregal de San Nicolás, Tlalpan, Mexico Jeremy P. Tarcher, Inc. (in Spanish), 1–275. Becker, R.O., & Marino, A.A. (1982). Electromagnetism and Palmer, D.D. (1910).The science, art and philosophy of chirolife. Albany: State University of New York Press. practic: The chiropractor’s adjuster. Portland, OR: PortBelehradek, J., Orlowski, S., Poddevin, B., et al. (1981). Elecland Printing House. trotherapy of spontaneous mammary tumors in mice. Segel, I.H. (1975)Biochemical calculations , (2nd ed.). New European Journal of Cancer , 27, 73–76. York: Wiley, 414–415. Benton, L.A., Baker, L.L., Bowman, B.R., & Waters, R.L. (1981). Functional Electrical Stimulation: A Practical Sersa, G., et al. (1992). Anti-tumor effect of electrotherapy alone or in combination with interleukin-2 in mice with sarClinical Guide (2nd ed.). Downey, CA: Rancho Los coma and melanoma tumors. Anti-Cancer Drugs,3, Amigos Hospital. 253–260. Chang, N., Van Hoff, H., & Bockx, E., et al. (1982). The effect of electric currents on ATP generation, protein synthesis,Smith, S.D. (1981). Biological control of growth – A retrospective look. In Becker, R.O. (Ed.), Mechanisms of growth and membrane transport in rat skin. Clinical Orthopecontrol. Springfield, IL: Charles C Thomas. dics, 171, 264–272. New frontiers in transcutaneJaskoviak, P.A., & Schafer, R.C. (1993). Applied physiotherapy Tapio, D. & Hymes, A.C. (1987). ous electrical nerve stimulation . Minnetonka, MN: (2nd ed.). Arlington, VA: The American Chiropractic LecTec Corp. Association. Kirsch, D.L. (1978).The complete clinical guide to electro- Thuile, C., & Kirsch, D.L. (2000).Schmerzen Linden ohne Chemie: CES, die Revolution in der Schmerztherapie . acutherapy(2nd ed.). Glendale, CA: National ElectroIGEM, Austria (in German). Acutherapy Foundation. Kirsch, D.L. (1999).The science behind cranial electrotherapy Walker, M.J. (1993).Dirty medicine: Science, big business, and the assault on natural health care . London: Slingshot stimulation. Edmonton, Alberta, Canada: Medical Scope Publications. Publishing.

61 A Practical Protocol for Electromedical Treatment of Pain Daniel L. Kirsch, Ph.D., D.A.A.P.M. If there were pharmaceutical products that could controllearned to appreciate the power of physics in our lives people’s physical pains more than 90% of the time andwith convenient technologies such as microwave ovens were safe enough to use as often as necessary without and cellular telephones. Today, our daily lives are increascausing any significant side effects, physicians would pre-ingly more influenced by electronics than chemistry. scribe them often. If those drugs could also calm people As we begin this new millennium, we rely on various who were seriously clinically anxious or depressed, whileforms of technology to diagnose our patients, both locally being safe enough for people who are only a bit stressed, through an ever-increasing armamentarium of devices, they would be the most widely prescribed drugs on Earth.and even over long distance with telemedicine. But we If those same drugs could also heal broken bones and close also can treat our patients with new technologies for a wounds, the pharmacies could not possibly stock enough variety of disorders with remarkable and unprecedented of them. safety and efficacy. What if there is something that could do all these Most systems of healthcare have historically been things and so much more, but is not a drug? What if there based on biophysics. Acupuncture is an obvious example. is a treatment that is so safe it could be used daily to Chinese call the electrical properties of life Chi energy, control pain and stress-related diseases. What if it is also Japanese call Ki, it Indians call itPrana, and chiropractors so inexpensive that once purchased for a fraction of the call it “innate intelligence. ” Even homeopathy is based on cost of conventional care, it will cost almost nothing tothe energetic residual of the chemical after it has been so use? There is. New forms of electromedicine offer all thisdiluted that chemists question its continued existence. and more. Western allopathic medicine stands alone in reliance on synthetic chemical treatments and invasive procedures, Change has always fought its way into the healthcare many of which impose a risk worse than the disease for system slowly. A mere 100 years ago it would have been considered quackery to propose that invisible little germswhich it is offered. In fact, conventional medical care is the third leading cause of death in the United States with could cause disease. Even after the discovery of bacteria, at least 225,000 people dying annually from iatrogenic for 35 more years most doctors refused to believe that washing their hands before surgery would make much ofconditions (Starfield, 2000). a difference. Yet progress in medicine occurred as we Change takes time in medicine as in any established system. There are strong controlling economic influences developed tools to look deeper into the body, and to see and long-standing institutions that will always argue for smaller particles. We even speak of subatomic particles, the status quo. Yet people are more educated and informed such as electrons, which could both cause disease in the about healthcare than ever before. With that comes conform of free radicals and cure known diseases as well as functional disturbances of the body and mind. We havecern over side effects of dangerous treatments. Why do

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moist environment (Kulig, Jarski, Drewek, et al., 1991). we not try the most inexpensive and conservative treatThe moisture may allow endogenously produced current mentsfirst, instead of last? When that treatment is based to flow more readily through the injury, and thus promote on sound electromagnetic principles, most physicians are wound healing. Electrical stimulation of the wound has surprised to discover that, while not a drug, the results are a similar effect, and also tends to increase the amount often more immediate and spectacular than one can imagine. Also, unlike drugs, the results are usually long lastingof growth factor receptors, which increases the amount of collagen formation (Falanga, et al., 1987). and cumulative. While electromedicine has been practiced in some Electricity was first used to treat surface wounds over form for thousands of years, research and clinical usage 300 years ago when charged gold leaf was found to prein electromedicine are expanding as never before in hisvent smallpox scars (Robinson, 1925). There are several tory. Perhaps even more than any other therapeutic option, recent studies supporting the beneficial effects of treating electromedicine is now used routinely by a growing num-wounds with an artificial current (Goldin, et al., 1981; ber of practitioners from all of the healthcare professions,Ieran, et al., 1990; Jeran, et al., 1987; Mulder, 1991). as well as by patients themselves at home. Only the United Experimental animal wound models in the 1960s demonStates Food and Drug Administration (FDA) restricts thestrated that electrical intervention results in accelerated sale of electromedical devices for use by or on the order healing with skin wounds resurfacing faster, and with of licensed healthcare practitioners. All other countriesstronger scar tissue formation (Assimacopoulos, 1968; allow people to purchase therapeutic electromedicalCarey & Lepley, 1962). devices over the counter for their own personal use. Elec- Assimacopoulos (1968a) published the first human tromedical modalities are easy to use, relatively safe, and study using direct current for wound healing. He docuthe newer technologies, such as microcurrent electrical mented complete healing in three patients with chronic therapy and cranial electrotherapy stimulation, haveleg ulcers due to venous stasis after six weeks of electrical proven efficacy unprecedented by any prior form of med- therapy. One year later Wolcott, Wheeler, and Hardwicke ical intervention. (1969) published the most frequently cited work in the One word of caution, though: Medicine is still a history of electrical wound healing. They used direct curscience. Modern electromagnetic therapies haverents of 200 to 1000 µA on 67 patients. Gault and Gatesn attracted many charlatans. Simply said, not everything(1976) repeated the Wolcott and Wheeler protocol on 76 is equally safe and effective. Rely only on evidence-additional patients with 106 ischemic skin ulcers. Rowley, based technologies. McKenna, Chase, and Wolcott (1974) studied a group of patients having 250 ischemic ulcers of various types. These included 14 symmetrical control ulcers. The elecMICROCURRENT ELECTRICAL THERAPY trically stimulated ulcers had a fourfold acceleration in Joseph M. Mercola and Daniel L. Kirsch (1995) coinedhealing response compared to the controls. Carley and the term “microcurrent electrical therapy” (MET) to define Wainapel (1985) performed one of the only studies on this a new form of electromedical intervention using biocom-subject with equal and randomized active and control groups. All of these studies documented significant accelpatible waveforms. Patrick DeBock (2000), a physiotherapist at the Uni-erated healing from electrical stimulation. One additional consistent observation in these studies versity of Antwerp in Belgium, recently compared MET with TENS based on the Eight Parameter Law whichwas a reversal of contamination in the wounds. Wounds Pseudomonas and/or covers every possible influence in electrotherapy. In histhat were initially contaminated with conclusion, DeBock states, “MET has a completely dif-Proteus were usually sterile after several days of MET. ferent mechanism, which at this time is not fully under-Other investigators also have noticed similar improvestood, but works on a cellular level … It looks as if TENSments and encourage the use of this therapy as the preis going to lose this competition … MET will, in most ferred treatment for indolent ulcers (Alvarez et al., 1983; Barron & Jacobson, 1985; Kaada, Flatheim, & Woie, cases, be much more satisfying than TENS because of the 1991; Lundeberg, Eriksson, & Malm, 1992). Additionally, longer lasting and more intense effects. ” A growing body of research shows the effectivenessno significant adverse effects resulting from electrotherof MET to do more than control pain. It can actually apy on wounds have been documented (Weiss, et al., 1990). A review of the literature by Dayton and Palladino accelerate and even induce healing. When a wound is dry, its bioelectric current ow fl is shut off. Eaglstein and (1989) shows that MET is clearly an effective and safe Mertz (1978) have shown moist wounds to resurface upsupplement to the nonsurgical management of recalcitrant leg ulcers. to 40% faster than air-exposed wounds. Falanga (1988) found that certain types of occlusive dressings, like Duo- Some of these studies used unipolar currents that were derm, accelerate the healing of wounds. It is probablealternated between negative and positive based on various that these dressings achieve their effects by promoting criteria. a Some researchers initially used negative current

A Practical Protocol for Electromedical Treatment of Pain

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to inhibit bacterial growth and then switched to positive Becker theorizes that primitive organisms used this current to promote healing. To date no study has compared analog type of data transmission and control system for this variable of MET. However, there is some compellingrepair. He postulates that we still have this primitive nerbasic science research, and one animal study, suggesting vous system in the perineural cells of the central nervous that a biphasic waveform, which provides both negativesystem. These cells comprise 90% of the nervous system. and positive current, may be better in that it both sterilizesThe perineural cells have semiconductor properties that the wound and promotes wound healing (Stromberg,allow them to produce and transmit nonpropagating DC 1988; Windsor, Lester, & Herring, 1993). signals. This system functions so vastly differently from In the 1960s Robert O. Becker (1985) demonstratedthe “ all or none” law of propagation of the nerve action that electrical current is the trigger that stimulates healing,potentials that Becker called this the fourth nervous system. growth, and regeneration in all living organisms. He found This analog system senses injury and controls repair. that repair of injury occurs in response to signals that come It controls the activity of cells by producing specific DC from an electrical control system, and suggested that this electrical environments in their vicinity. It also appears to system became lessficient ef as we age. be the primary primitive system in the brain, controlling Becker developed his theory of biological control sys-the actions of the neurons in their generation and receipt of nerve impulses. Accordingly, as knowledge of this tems based on concepts derived from physics, electronics, and biology. He postulated that the rstfi living organisms aspect of our nervous system is uncovered, another mystery of brain physiology may be explained, including the must have been capable of self-repair, otherwise they never regulation of our consciousness and decision-making prowould have survived. The repair process requires a closedloop system. A specifi c signal is generated, called the cur- cesses. Given this understanding, the application of the rent of injury, which causes another signal to start repair.correct form of electrical intervention is a powerful tool The injury signal gradually decreases over time with thefor treating pain, initiating the endogenous mechanisms repair process, until it nally fi stops when the repair is for healing, and altering states of consciousness. complete. Such a primitive system does not require demon- Chang, Van Hoff, Bockx, et al. (1982) proposed strable consciousness or intelligence. In fact, many animals another mechanism for MET. Their research showed that actually have a greater capacity for healing than humans. microcurrent stimulation increased adenosine triphosphate (ATP) generation by almost 500%. Increasing the Science has amassed a vast amount of information on how the brain and nervous system work. Most of thislevel of current to milliampere levels actually decreased the results. Microcurrent also was shown to enhance research involves the action potential as the sole mechanism of the nerve impulse. This is a very sophisticatedamino acid transport and protein synthesis in the treated and complex system for the transfer of information. It isarea 30 to 40% above controls. helpful to compare this conceptualized concept of the It would be helpful to review the cellular nature of an nervous system to a computer. injury to fully appreciate the importance of Chang’ s The fundamental signal in both the computer and theresearch. Becker (1985) has shown that trauma will affect the electrical potential of cells in damaged tissues. Initially nervous system is a digital one. Both systems transfer the injured site has a much higher resistance than that of information represented by the number of pulses per unit of time. Information also is coded according to where thethe surrounding tissue. Basic physics dictates that electricity tends to flow toward the path of least resistance. pulses originate, where they go, and whether or not there Therefore, endogenous bioelectricity avoids areas of high is more than one channel of pulses feeding into an area. resistance and takes the easiest path, generally around the All our senses (e.g., smell, taste, hearing, sight, and touch) injury. The decreased electrical flow through the injured are based on this type of pulse system. Like a computer, area decreases the cellular capacitance (Windsor, et al., the nervous system operates remarkably fast and can transfer large amounts of information as digital on-and-off data.1993). As a result, healing is actually impaired. This may It is unlikely that the first living organisms had such be one of the reasons for inflammatory reactions. Pain, heat, swelling, and redness are the characteristics of a sophisticated system. Becker believes they must have had a much simpler mechanism for communicating infor-inflamed tissues. Electricity flows more readily through fluids. mation because they did not need to transmit largethese hot inflammatory amounts of sophisticated data. Accordingly, they probably The correct microcurrent application to an injured site used ananalogsystem. An analog system works by meansaugments the endogenous current flow. This allows the of simple DC currents. Information in an analog systemtraumatized area to regain its capacitance. The resistance is represented by the strength of the current, its direction of the injured tissue is then reduced, allowing bioelectricof flow, and slow wavelength variations in its strength.ity to enter the area to reestablish homeostasis. Therefore, This is a much slower system than the digital model.microcurrent electrical therapy can be viewed as a catalyst However, the analog system is extremely precise and helpful in initiating and sustaining the numerous chemical works well for its intended purpose. and electrical reactions that occur in the healing process.

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When a muscle experiences trauma it goes into spasm Ten patients discontinued treatment because they thought it was not helping them, and three more disconto protect itself. This decreases its blood supply, reducing the amount of oxygen and nutrients that reach it. Thetinued due to undesirable side effects. An additional 13 terminated treatment when their insurance ran out and they decreased circulation causes an accumulation of metabolic could no longer pay for treatment; 20 patients moved out waste products. This acts as noxious input resulting in pain. Adenosine triphosphate is an essential factor in theof the area while treatment was in progress or discontinued healing process. Large amounts of ATP, the scell’ main treatment for other, unstated reasons. energy source, are required to control primary functions Negative adverse effects were all rare, mild, and selfsuch as the movement of vital minerals, like sodium,limiting, with 472 (94.4%) reporting none. Six (1.2%) reported vertigo as a side effect and 2 (0.4%) reported potassium, magnesium, and calcium, into and out of the nausea, either of which normally occurs when the current cell. It also sustains the movement of waste products out is set too high or in patients with a history of vertigo. Only of the cell. Injured tissues are deficient in ATP. As MET restores circulation and replenishes ATP,3 (0.6%) reported skin irritation, and 1 (0.2%) each nutrients can again flow into injured cells and waste prod-reported anger, a metallic taste, a heavy feeling, or intensified tinnitus. These generally receded or disappeared as ucts can flow out. This is necessary for the development soon as the current was reduced. of healthy tissues. As ATP provides the energy tissues require for building new proteins, it also increases protein The most important aspect of this survey was the results reported as a degree of improvement in the seven synthesis and membrane transport of ions. symptoms present in most patients for which MET and/or CES is prescribed; i.e., pain, anxiety, depression, stress, SURVEY RESULTS insomnia, headache, and muscle tension. The treatment Two surveys were recently conducted on a total of 3000outcome was broken down into response categories beginpeople using Alpha-Stim™technology employing the ning with [it made the condition] “Worse, ” and progresscombined treatment protocols of MET and CES as pre-ing up to “Complete” improvement or cure. As in pharsented here. maceutical studies, a degree of improvement of 25% or Healthcare practitioners completed a post-marketingmore was considered to be clinically significant. The data survey of 500 patients in 1998 (Kirsch, 1999). Therefor all 500 patients reporting on multiple symptoms are summarized in Table 61.1. were 174 males, and 326 females, ranging from 5 to 92 years old. Outpatients accounted for 479 of the forms, In addition, 2500 patients were surveyed through a while 21 were hospitalized at the time of treatment.form attached to warranty cards (Smith, 2001); 1411 Treatment was satisfactorily completed by 197 (41%) of(72.40%) of the patients were female; ages ranged from the patients with 207 (43%) still receiving treatment at15 to 92 years old with a mean of 50.07 years. The length of use ranged from the minimum of 3 weeks which was the time of the survey.

TABLE 61.1 Results of Using Alpha-Stim™ Technology for MET and CES as Reported by Healthcare Practitioners Condition

N

Pain

286

Anxiety

349

Depression Stress

184 259

Insomnia

135

Headache

151

Muscle tension

259

Worse

No Change

Slight < 24%

Fair 25–49%

Moderate 50–74%

Marked 75–99%

Complete 100%

Significant > 25%

1 0.35% 0 0.00% 0 0.00% 0 0.00% 0 0.00% 1 0.66% 2 0.77%

5 1.75% 8 2.29% 8 4.35% 6 2.32% 16 11.85% 8 5.30% 6 2.32%

20 6.99% 14 4.01% 11 5.98% 12 4.63% 12 8.89% 6 3.97% 6 2.32%

48 16.78% 39 11.17% 31 16.85% 37 14.29% 17 12.59% 25 16.56% 42 16.22%

77 26.92% 89 25.50% 38 20.65% 70 27.03% 34 25.19% 32 21.19% 76 29.34%

108 37.76% 181 51.86% 82 44.57% 124 47.88% 45 33.33% 63 41.72% 111 42.86%

27 9.44% 18 5.16% 14 7.61% 10 3.86% 11 8.15% 16 10.60% 16 6.18%

260 90.91% 327 93.70% 165 89.67% 241 93.05% 107 79.26% 136 90.07% 245 94.59%

Note: Total N = 500 patients with multiple symptoms.

A Practical Protocol for Electromedical Treatment of Pain

763

the only inclusion criterion, to a maximum of 5 years in ADJUST THE SETTINGS two cases. The average period of use reported was 14.68 weeks or approximately 3.5 months. Of 1949 primary painUse 0.5 Hz frequency most of the time. It is unusual ever to need other frequency settings. However, if 0.5 Hz does patients, 1813, or 93.02% rated their improvement as significant, and these findings correlate well with the physi-not work, and a number of electrode placements sites have cians’ survey of 500 patients where 90.91% of 286 painbeen attempted, try 1.5 Hz; 100 Hz sometimes produces faster results when treating infl ammatory articular problems patients were observed to have significant improvement. (e.g., arthritis, bursitis, tendonitis, etc.). However, 100 Hz The data for all 2500 patients reporting on multiple sympdoes not contribute much to long-term results so treatment toms are summarized in Table 61.2. should always be completed using a low frequency. Set the current intensity level at the highest comfortable position, BASIC TREATMENT PROTOCOL which is usually 500 to 600 µA for probes, although sometimes less for the silver electrodes used with MET. Do not FOR MICROCURRENT use standard TENS electrodes except in the initial treatment ELECTRICAL THERAPY (MET) of hypersensitive patients. Carbon TENS electrodes have a The following section is intended as a practical guide forresistance of about 200 ohms, while silver electrodes have clinicians to utilize the principles discussed in this chapter.a resistance of about 20 ohms. Only silver electrodes will The methods of treatment provided herein have been work effectively with MET devices. developed by the author based on 3 decades of experience When using probes, firstfix af new felt electrodes and in electromedicine. The reader is cautioned to remember saturate them with an appropriate electromedical conductthat not all brands of microcurrent devices are equallying solution. Then apply firm pressure, but less than what efficacious. Always check the manufacturer’ s specific would cause more pain. Tap water does not work well in instructions before using a medical device. As medicinesome places anymore because of recent advances in is not an exact science, the author cannot assume respondesalination during water processing. Saline solution may sibility for the clinical efficacy of, or liability for, the be used if a conducting solution is not available. methods and treatments found in this text. For extremely hypersensitive people, such broas fi myalgia patients, it is better to start with a minimal STEP ONE: HISTORY AND BRIEF EXAM amount of current. Even low-level MET currents may be uncomfortable in some patients. For these patients it may It is important to take a comprehensive history and do be necessary to initially reduce the conductivity by using a brief analysis of the patient’ s current condition before more resistive electrodes. Over the course of a few beginning each session of MET treatment. A diagnosis weeks, the therapeutic dosage of electricity can gradually is not enough. One should determine when the pain rst fi be increased. Start with standard carbon electrodes, folpresented, its frequency, duration, intensity, limitationslowed by silver electrodes, then probes with tap water, of-motion, positions which exacerbate the pain, and any until the area is desensitized enough to use probes with precipitating factors. Ask about the specifi cs of previous conducting solution. Fortunately, this is rarely necessary. treatments and details all of surgical scars and traumatic Most people will not even feel MET stimulation at a injuries. Microcurrent electrical therapy is a very holiscurrent of 600µA. tic procedure. It may be necessary to clear the body of any and all electrical blocks” “ in order to achieve the BASIC TREATMENT STRATEGY best results. Even brief 10- to 20-second treatments of other problems and/or old injuries may reverse a refrac-There are only a few principles one must remember when treating patients with MET. The patient should be in a tory case. Immediately before each treatment determine therelaxed position to receive maximum beneficial effects. patient’s present pain level, and positions that exacer- For example, do not let patients help with the treatment of their hands by holding up their arms, which would bate the pain. Ask the patient to rate his or her present pain on a scale of 0 (no pain) to 10, with 10 beingcause the arm muscles to tense. In this case, it is better to excruciating, debilitating pain. Tell the patient to con- place both hands on a table. The most important variable is the position of the sider 10 as the “ worst this condition has been. ” Also note any immediate limitations-of-motion, positive probes, or silver electrode pads. Place the probes, or pads, orthopedic and neurologic testndings, fi and objective in such a way that if a line were drawn between them, the line would travel through the problem area. Keep in mind signs of psychological distress. Because the results of MET can be seen after only a minute or so of treatmentthat the body is three-dimensional. Therefore, many possible lines can be drawn through the problem area. Some in most people, these indicators are necessary reference lines will work much better than others. The correct elecparameters to determine effectiveness throughout a sintrode location is the one that works! However, the one gle treatment session.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

TABLE 61.2 Results of Using Alpha-Stim™ Technology for MET and CES for at Least 3 Weeks as Reported by Patients Condition

N

Pain (all cases)

1949

Back pain

403

Cervical pain

265

Hip/leg/foot pain

160

Shoulder/arm/hand pain

150

Carpal tunnel syndrome

25

Arthritis pain

188

TMJ pain

158

Myofascial pain

62

RSD

55

Fibromyalgia (alone)

142

Fibromyalgia (with other)

363

Migraine

118

Headaches (all other)

112

Psychological (all cases)

723

Anxiety (alone)

128

Anxiety (with other)

370

Anxiety/depression

58

Depression (alone)

53

Depression (with other)

265

Stress

123

Chronic fatigue

50

Insomnia

163

Slight < 24%

Fair 25–49%

Moderate 50–74%

Marked 75–100%

Significant > 25%

136 6.98% 20 4.96% 18 6.79% 6 3.75% 13 8.67% 0 0.00% 11 5.85% 17 10.76% 6 9.68% 10 18.18% 13 9.15% 33 9.09% 2 1.69% 20 17.86% 61 8.44% 13 10.16% 33 8.92% 3 5.17% 7 13.21% 29 10.94% 6 4.88% 3 6.00% 10 6.13%

623 31.97% 109 27.05% 69 26.04% 43 26.88% 41 27.33% 5 20.00% 51 27.13% 60 37.97% 18 29.03% 16 29.09% 53 37.32% 131 36.09% 49 41.53% 30 26.79% 175 24.20% 29 22.66% 85 22.97% 19 32.76% 11 20.75% 61 23.02% 30 24.39% 30 60.00% 47 28.83%

741 38.02% 157 38.96% 125 47.17% 53 33.13% 63 42.00% 17 68.00% 88 46.81% 60 37.97% 18 29.03% 19 34.55% 52 36.62% 152 41.87% 30 25.42% 24 21.43% 237 32.78% 42 32.81% 122 32.97% 19 32.76% 23 43.40% 93 35.09% 39 31.71% 10 20.00% 47 28.83%

449 23.04% 117 29.03% 53 20.00% 58 36.25% 33 22.00% 3 12.00% 38 20.21% 21 13.29% 20 32.26% 10 18.18% 24 16.90% 47 12.95% 37 31.36% 38 33.93% 250 34.58% 44 34.38% 130 35.14% 17 29.31% 12 22.64% 82 30.94% 48 39.02% 7 14.00% 59 36.20%

1813 93.02% 383 95.04% 247 93.21% 154 96.25% 137 91.33% 25 100.00% 177 94.15% 141 89.24% 56 90.32% 45 81.82% 129 90.85% 330 90.91% 116 98.31% 92 82.14% 662 91.56% 115 89.84% 337 91.08% 55 94.83% 46 86.79% 236 89.06% 117 95.12% 47 94.00% 153 93.87%

Note: Total N = 2500 patients with multiple symptoms. From consecutive warranty cards analyzed as of July 2000.

that works may be transient, working well one day, but A common mistake made by clinicians familiar with ineffective another day. As the problem begins to resolve,traditional TENS is placing the electrodes on each side of the electrode locations may require frequent adjustments. the spine for back pain. This is a two-dimensional

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approach. With such a placement, microcurrent will travel If the pain is gone, stop for the day. If it is reduced, just under the skin between the electrodes and never reach ask the patient to point to where it hurts with one nger fi the spine. Nor can the electrodes be effectively placed and treat for another minute or so directly through the “between the pain and the brain. ” These are common area of pain, which may have moved after the original placements for TENS electrodes, but MET is not TENS.2-minute treatment. A better way is to place one electrode next to the spine at Think in terms of symmetry. Look, palpate, and oththe level where the problem is, and the other on the conerwise examine areas above, below, and to the left and tralateral side, anteriolaterally (front and opposite side).right of the primary area undergoing treatment. Always A line drawn between those will go right through the treat the opposite side and connect both sides. spinal nerves. Next, reverse the sides. Then follow up by doing another set of contralateral placements one spinal SILVER SELF-ADHESIVE ELECTRODES level above, and one below the problem to accommodate overlap in the dorsolateral fasciculus. These are used following the same strategy as the probes, Always treat bilaterally. Bilateral treatment includes except for a longer period of time. The probes and brief electrode treatments assume MET is working as a catalyst the spinal cord, thereby involving dermatomes, myotomes, and sclerotomes. Also, if the problem is within the axialfor the patient’s own bioelectrical system, whereas keepskeleton and the contralateral side is ignored, there is ing a electrodes in place can be viewed as using MET to good chance that the primary location of a pain problemaugment endogenous bioelectricity. For optimum results, silver electrodes also may be moved around the problem will be missed. Pain often presents itself on the tense side, area. Whereas the probes are used for 10 seconds a site, which may be compensating for muscular weakness on silver electrodes should be left at each locationatfor least the other side. 5 to 10 minutes. Some cases will require an hour or even several hours of stimulation daily. Accordingly, silver QUICK PROBE TREATMENTS electrodes are best used for home care. However, if brief When using probes, set the timer on a probe setting, or stimulation if works, do not continue treatment at that sesone is not available, treat about 10 seconds per site. In sion. More is not better when using MET technology to other words, move the probes to the next location every manage pain! 10 seconds. Consider one treatment “set” to be 12 to 20 of these 10-second stimulations, each at a different angle WHEN TO STOP of approach. The first set should take about 2 minutes, but then additional treatment may be done at 1-minute inter-Reevaluate the patient after the 2-minute protocol using vals. The patient should be reevaluated between each set. the original criteria. It is not enough to ask if the patient The protocol involves four steps: feels better, ask for a specifi c percentage of how much better. If the patient has dif ficulty with a 0-to-10 scale, 1. First treat in a large “X” manner over a wide to facilitate communication, ask,If “you had a dollar’s area holding the probes so that the current is worth of pain when we began, how many cents do you directed through the problem area. An example have left?”Also, reexamine for improvement in objective of this strategy for knee pain would be to first signs, such as range-of-motion increases, etc. Stop when make the large X by treating from the medial, the pain is completely gone, or when the improvement superior thigh to the lateral foot, then lateral at has reached a plateau after several treatment sets. Conthe hip to the medial foot. tinuing to treat the area at this time may cause the pain 2. Treat with smaller Xs, or a “star” (*) closer and to return! If the pain is gone, it is far better to stop directly around the involved knee (e.g., two treatment for that day even if the patient only had 1 or obliques, one or two medial–lateral, one or two 2 minutes of treatment. anterior–posterior, etc.). If the patient can no longer identify any pain, but 3. Treat the opposite knee for at least 20 seconds complains of stiffness, this indicates that it is time to stop (one X), even if it is asymptomatic. treatment for the day. Microcurrent may not reduce resid4. Connect the two knees by placing a probe on ual stiffness. Post-pain stiffness usually wears off by itself. Yoga, Tai Chi, or simple stretching exercises are good each knee at least four times. means of controlling chronic stiffness. The above example takes 2 minutes. A big X beyond Although most patients will have an immediate response to treatment, in some the effects will be the area (20 seconds), a star through the chief complaint delayed, continuing to improve over a day or two after (40 seconds), treat the opposite side with one small X (20 the treatment. In these patients relief will generally seconds), and connect the two sides (40 seconds). Then occur 1 to 3 hours post-treatment or even as late as the reevaluate the pain based on the original criteria.

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next morning. Some patients will experience a cumu- Also, preliminary observations suggest that people lative effect, continuing to improve over time. Patientswho have had a significant exposure to strong electrical current may be poor candidates for MET. This means that who experience a delayed effect are moreficult dif to treat due to lack of immediate feedback. Usually,they either have been held by electrical current at some patients who experience a delayed effect fromtime in their life, or have been treated with mA TENS or microcurrent treatment also have a delayed effect withsimilar modalities for a prolonged period of time, usually years. There have even been a few reports of failures in anesthetics. Ask the nonresponsive patient if his or her dentist had to wait more than 10 minutes after injectingpatients who were struck by lightning. Brief exposure to very high levels of electricity is not as bad as longer anesthetic prior to doing dental procedures. Because exposure to any level of electricity. Such patients need to treating patients who exhibit delayed responses can be viewed as a type of blind” “ treatment, one must rely be treated for a longer period of time. on experience with other patients who exhibited an Aside from hydration and nutrition and electrical immediate response in order to develop the skills toshock, the primary reversible reason patients fail to treat those few who have a delayed response. A postrespond to treatment is that they have some sort of a treatment diary is also helpful in analyzing the responseblockage somewhere on or in their body that is resisting of these patients. endogenous electricalow. fl This is usually something superficial, like a scar or old injury. It need not be anywhere near the patient’ s primary problem. Identify FOLLOW-UP all scars by taking a very thorough, persistent history, and examining the patient completely. All scars are Most patients should be given at least three to seven treatments before evaluating their responses toimportant no matter how old or how far they are from microcurrent electrical therapy. It helps to explain to thethe chief complaint. Scar tissue impedes the systemic patient that the effects of MET treatment are cumulative.flow of endogenous bioelectricity because it is a poor Like antibiotics, one must take several doses over aconductor of electricity. Accordingly, scar tissue may s entire bioelectrical system. period of time to get results. Although results will usu- interfere with the patient’ ally be seen during or subsequent to the rst fitreatment, If scars are present they should be treated with silver the longevity of the results can only be evaluated afterelectrodes for 10 minutes per scar, at least four times. a series of treatments. Fortunately, most patients willSimply cover the scars with the electrodes, or for large scars, place the electrodes on the ends of the scars. This experience long-lasting results. However, in some cases the results will plateau to a similar time period regard-may be done 4 days in a row or there can be a short less of treatment. For example, a patient may only getinterval of up to a few days between the treatments. 1 or 2 days of relief no matter what combination of Some people report that it helps to repeat this procedure after a month or so. treatment strategies is employed. For these, and cases of severe pathology, the effectiveness may be only short- During treatment for scars the person may experience lived, so a MET device should be prescribed for homea significant surge of energy. This can be viewed as if an care. After an initial series of up to ten clinical treat- electrical “bioresistor” has broken down, reestablishing ments, a good rule of thumb is to prescribe a unit forthe normal flow of bioelectricity. After scar therapy, anyone with a chronic condition who requires more thanpatients will often report feeling half their age. Because one or two palliative treatments per month, and forpeople have nothing with which to compare their life experiences, they usually attribute the subtle effects of patients who have progressive pathologies. When used at home, after an initial series of 1 or 2 weeks of dailyscars on their electrical system as normal aging. Be aware that this treatment will often also increase pain, because treatments, treatment every other day usually provides the whole body and mind “wake up, ” including the painful better results than daily treatment. part. However, in nearly all cases, when this happens the painful area can then be successfully treated. Always TIPS FOR LIMITED OR POOR RESULTS schedule enough time to treat the pain after a scar treatWhile a good MET device will be at least somewhatment, so the patient will not need to endure even a temefficacious on more than 90% of the population whenporary increase in pain. used correctly, MET will not work for everyone. In cases If all the scars are treated and there are still no results, where there are no results at all, a few things should be or if there are poor results, a few other options still exit. considered. Dehydrated patients may not respond well. Question the patient about old injuries that may not have Patients should be advised to drink at least eight to ten healed properly. These also could be electrical blocks glasses of water daily. Nutrition is certainly a factor. A and should be approached in the same way as scars. poor diet does not provide the necessary building blocks Consider treating the primary complaint at a lower curto reinstate homeostasis. rent setting of 100µA with silver electrodes for 60

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minutes or more. Slightly higher pulse repetition rates Balance out contralateral side by treating any mirror (e.g., 1.5 Hz) may produce results in some people when areas not already covered. the 0.5 Hz fails, but this is rare. For more informationNote: Reduce the current as necessary to avoid vertigo. about treating scars, or how to determine which scars to Treating near the eyes may cause the patient to see flashtreat, physicians and dentists may contact the American ing lights due to stimulation of optic nerve. Patient may Academy of Neural Therapy through their Web site atalso taste metal fillings when treating across oral cavity. www.neuraltherapy.com. None of these conditions is harmful.

SINUS

SAMPLE PROTOCOLS

AND

OCULAR PAIN

The following illustrated sample protocols may be usedSAMPLE 2 (See Figure 61.2): Sinus and as a guide for treatment using MET. Ocular Pain Begin sinus and ocular pain treatment using the above protocol for head pain.

HEAD PAIN PROTOCOL SAMPLE 1 (See Figure 61.1): Head Pain Include the temporomandibular joint (TMJ), neck, and shoulders. 1. Above the ear to the tip of the contralateral shoulder. Reverse sides. 2. Across the shoulders by treating bilaterally across the distal tips of the acromions. 3. A few “X” patterns across back of neck. 4. From one TMJ to the other. 5. Temple to ipsilateral masseter muscle. Reverse sides. 6. About 1 minute through the primary area of involvement.

1

2

7. Treat sinuses when indicated, above and below eyes, or from side to side (see notes in head pain section). The patient should be able to breathe more clearly immediately after treatment. 8. For ocular headaches, treat behind eyes by placing probes on each temple, lateral to the lateral canthus of the eyes, and across each eye (one at a time) at the bridge of the nose to the lateral canthus.

7

8

FIGURE 61.2 Sinus and ocular pain protocol.

4

3

TEMPOROMANDIBULAR DISORDER SAMPLE 3 (See Figure 61.3): Temporomandibular Disorder (TMD) Begin temporomandibular disorder treatment using the above protocol for head pain.

5

FIGURE 61.1 Head pain protocol.

6

7. A star pattern across TMJ. Reverse sides. 8. Connect the TMJ with the sternocleidomastoideus (SCM) muscles, below the mastoid, and along the clavicular and sternal branches. Reverse sides.

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7

to the webs between the fingers in addition to local treatment at the wrist. 3. Treat the area corresponding to the area of pain on the other upper extremity for 20 to 40 seconds. 4. Connect the two upper extremities by placing one probe on each in several symmetrical places encompassing the pain area for 40 seconds to 1 minute.

8

LOWER EXTREMITY PAIN PROTOCOL FIGURE 61.3 Temporomandibular disorder (TMD) pain protocol. SAMPLE 5 (See Figure 61.5): Lower Extremity

1. First make the large “X” by treating from the medial, superior thigh to the lateral foot, then the lateral hip to the medial foot. 2. Complete 40 seconds to 1 minute of smaller Xs closer to and directly around the hip, knee, ankle, foot, or other area of pain. 3. Treat the area corresponding to the area of pain on the other lower extremity for 20 to 40 seconds. 4. Connect the two lower extremities by placing one probe on each in several symmetrical places encompassing the pain area for 40 seconds to 1 minute.

UPPER EXTREMITY PAIN PROTOCOL SAMPLE 4 (See Figure 61.4): Upper Extremity 1. First make the large “X” by treating from the anterior shoulder to the posterior hand, and the posterior shoulder to the anterior hand. 2. Complete 40 seconds to 1 minute of smaller Xs closer to and directly around the shoulder, elbow, wrist, hand, or other area of pain. For carpal tunnel syndrome (CTS) or repetitive strain injury (RSI), treat superior to the elbow

1

2

3

4

FIGURE 61.4 Upper extremity pain protocol.

1

2

FIGURE 61.5 Lower extremity pain protocol.

3

4

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BACK PAIN PROTOCOL

leg at 4- to 6-inch intervals with the last, most inferior placement at the lateral foot (or just past where the pain radiates).

SAMPLE 6 (See Figure 61.6): Back Pain 1. Anterior between the trapezius muscle and the clavicle connected to the contralateral posterior hip. Reverse sides. 2. Then place one probe next to the spine at the level where the problem is, and the other on the contralateral side, anteriolaterally (front and opposite side). A line drawn between those will go right through the spinal nerves. Reverse the sides. Repeat contralateral placements one spinal level above, and one below the problem. 3. Also treat across the vertebrae, from each side of the body through the problem area, above, and below. 4. For low back pain with sciatic radiculitis, connect various levels from L3 to L5 about 1 inch lateral to the spine with the ipsilateral, posterior

CRANIAL ELECTROTHERAPY STIMULATION Cranial electrotherapy stimulation (CES) is the application of low-level, pulsed electrical currents (usually not exceeding 1 mA), applied to the head for medical and/or psychological purposes. It is used primarily to treat both state (situational) and trait (chronic) anxiety, depression, insomnia, stress-related and drug addiction disorders, but it is also proving indispensable for treating pain patients (Kirsch & Smith, 2000; Lichtbroun, Raicer, & Smith, 2001; Thuile & Kirsch, 2000). Drs. Leduc and Rouxeau of France were the first to experiment with low-intensity electrical stimulation of the brain in 1902. Initially, this method was called electrosleep

1

2

3

FIGURE 61.6 Back pain protocol.

4

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

as it was thought to be able to induce sleep. Since then, as operating a motor vehicle or heavy machinery, for up it has been referred to by many other names, the most to several hours after treatment. popular being transcranial electrotherapy (TCET) and At present, there are over 100 research studies on CES neuroelectric therapy (NET). Research on using what isin humans and 20 experimental animal studies (Kirsch, now referred to as cranial electrotherapy stimulation1999). No significant lasting side effects have ever been (CES) began in the Soviet Union during the 1950s. reported. Occasional self-limiting headache (1 out of 450), Cranial electrotherapy stimulation is a simple treat- discomfort or skin irritation under the electrodes (1 out of ment that can easily be administered at any time. The 811), or lightheadedness may occur. A rare patient with a current is applied by easy-to-use clip electrodes thathistory of vertigo may experience dizziness for hours or attach on the ear lobes, or by stethoscope-type electrodes days after treatment. placed behind the ears. In the 1960s and early 1970s, Most cranial electrotherapy stimulators are limited to electrodes were placed directly on the eyes because 600 it µA. To put this into perspective, it takes one half of was thought that the low level of current used in CESan ampere to light an ordinary 60-watt light bulb. To truly could not otherwise penetrate the cranium. This electrode compare the work done per second by these two different placement was abandoned more than 20 years ago. currents, we must multiply the currents by the respective Recent research has shown that from 1 mA of current, voltages that drive them. The product of current × voltage about 5 µA/cm2 of CES reach the thalamic area at ais a measure of the rate of generation of energy, and is radius of 13.30 mm which is suf ficient to affect the referred to as the power output. By definition, when a manufacture and release of neurotransmitters (Ferdjaldevice outputs 1 ampere of current with a 1-volt driving lah, Bostick, Jr., Francis, Jr., & Barr, 1996). force, the power output of the device is 1 watt. Therefore, Anxiety reduction is usually experienced during a a device producing a maximum output of 600 µA is limtreatment, but may be seen hours later, or as late as 1 day ited to about 11,000 times less power than the light bulb: after treatment. Although in some people it may require(600/1,000,000) amperes × 9 volts = 0.0054 watts. Some a series of 5 to 10 daily treatments to be effective. Severe people do not even feel this amount of current. depression often takes up to 3 weeks to establish a ther- As in many areas of biology and therapy, the evidence apeutic effect. of CES effectiveness is empirical. It is generally believed Cranial electrotherapy stimulation leaves the user that the effects are primarily mediated through a direct alert while inducing a relaxed state. Psychologists callaction on the brain at the limbic system, the hypothalamus this an alpha state . The effect differs from pharmaceu- and/or reticular activating system (Brotman, 1989; Gibson tical treatment in that people usually report feeling that& O’Hair, 1987; Madden & Kirsch, 1987). The primary their bodies are more relaxed, while their minds are more role of the reticular activating system is the regulation of alert. Most people experience a feeling that their bodies electrocortical activity. These are primitive brainstem are lighter, while thinking is clearer and more creative.structures. The functions of these areas and their influence A mild tingling sensation at the electrode sites also mayon our emotional states were mapped using electrical stimbe experienced during treatment. The current should ulation. Electrical stimulation of the periaqueductal gray never be raised to a level that is uncomfortable. One 20matter has been shown to activate descending inhibitory minute session is often all that is needed to effectivelypathways from the medial brainstem to the dorsal horn of control anxiety for at least a day, and the effects arethe spinal cord, in a manner similarβ-endorphins to (Ng, usually cumulative. If the patient can only tolerate aDouthitt, et al., 1975; Pert, Dionne, Ng, et al., 1981; Salar, small amount of current (< 200 µA) due to vertigo or Sob, et al., 1981). Cortical inhibition is a factor in the nausea, more time is required. Cranial electrotherapy Melzack-Wall Gate Control theory (Melzack, 1975). stimulation also may be used as an adjunct to anxiolyticToriyama (1975) suggested it is possible that CES may or antidepressive medication, but the dosage of medicaproduce its effects through parasympathetic autonomic tion should then be reduced by approximately one third.nervous system dominance via stimulation of the vagus It is also proven to be an effective complimentary treat-nerve (CN X). Taylor (1991) added other cranial nerves ment along with psychotherapy, biofeedback training,such as the trigeminal (CN V), facial (CN VII), and glosand surgical anesthesia (Kirsch, 1999). For people who sopharyngeal (CN IX). Fields, Tacke, and Savana (1975) have diffi culty falling asleep, CES should be used in theshowed that electrocortical activity produced by stimulamorning to avoid the possibility of increased alertnesstion of the trigeminal nerve is implicated in the function that may interfere with sleep. of the limbic region of the midbrain affecting emotions. Most people can resume normal activities immedi-Substance P and enkephalin have been found in the ately after treatment. Some people may experience trigeminal a nucleus, and are postulated to be involved in euphoric feeling, or a state of deep relaxation that maylimbic emotional brain structures (Hokfelt, Ljungdahl, et temporarily impair their mental and/or physical abilities al., 1977). The auditory-vertigo nerve (CN VIII) must also for the performance of potentially hazardous tasks, such be affected by CES, accounting for the dizziness one

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experiences when the current is too high. Ideally, CESMoore, Mellor, Standage, & Strong, 1975; Overcash, electrodes are placed on the ear lobes because that is1999; a Patterson, 1988; Smith, 1999; Turaeva, 1967; convenient way to direct current through the midbrain andWeiss, 1973). Sixteen of 16 (100%) reported that at least brain stem structures. some of the subjects had continued improvement after a From studies of CES in monkeys, Jarzembski, San-single CES treatment, or a series of CES treatments. The other follow-up report only commented on safety (Forford, and Sances, Jr. (1970) measured 42 to 46% of the current entering the brain, with the highest concentrationster, et al., 1963). None of the 17 studies revealed any in the limbic region. Rat studies by Krupisky (1991) long-term harmful effects. showed as much as a threefold increase β-endorphin in When restricted to anxiety populations or studies that concentration after just one CES treatment. Pozos, Richmeasured for physiological and/or psychological changes ardson, and Kaplan (1971) conducted mongrel dogin anxiety, there are 40 scientific studies of CES involving research that suggests CES releases dopamine in the basal 1835 patients. Thirty-four of the 40 (85%) studies reported ganglia, and that the overall physiological effects appearefficacious results in the treatment of anxiety. Five of the to be anticholinergic and catecholamine-like in action.studies on CES (all using the Alpha-Stim) support the Richter, Zouhar, Tatsuno, et al. (1972) found the size,effectiveness for managing anxiety during or after a single location, and distribution of synaptic vesicles were alltreatment (Gibson, & O’ Hair, 1987; Heffernan, 1995; within normal limits after a series of ten, 1-hour treatmentsSmith, 1999; Voris, 1995; Winick, 1999). in Rhesus monkeys. Several studies in stump-tailed None of the 6 of 40 (15%) anxiety studies categorized macaques and humans revealed a temporary reduction by in the authors as having negative or indeterminate results gastric hypersecretion (Kotter, Henschel, Hogan, et al.,were recent; 5 were done in the 1970s, and one in 1980. 1975; Reigel, Dallmann, Christman, et al., 1970; Reigel,Three showed both actual treatment and sham groups to Larson, Sances, Jr., et al., 1971; Wilson, Reigel, Unger, et improve significantly, most likely because both groups al., 1970). were also taking medications (Levitt, James, & Flavell, A recent review by Kirsch (1999) of 106 human stud-1975; Passini, Watson, & Herder, 1976; Von Richtofen, & ies involving 5439 subjects (4058 receiving cranial elec-Mellor, 1980). One was a depression study in which the trotherapy stimulation, while the remainder served asauthor noted that acute anxiety was not relieved and again, sham-treated or placebo controls) revealed signifi cant the study did not control for medications (Hearst, et al., changes associated with anxiolytic relaxation responses, 1974). One reported no significant change on anxiety or such as lowered reading on electromyograms (Forster, depression scales, but subjective insomnia improved Post, & Benton, 1963; Gibson, & O’Hair, 1987; Hef- (P < .05) during active treatment (Moore, et al., 1975). fernan, 1995; Overcash, & Siebenthall, 1989; Voris, 1995),Only one study conducted on a population of insomniacs, slowing on electroencephalograms (Braverman, Smith,with an average duration of symptoms for almost 20 years, Smayda, & Blum, 1990; Cox, & Heath, 1975; Heffernan,did not show any significant change at all in any param1996; Heffernan, 1997; Krupitsky, 1991; McKenzie, eters (Frankel, Buchbinder, & Snyder, 1973). [Perhaps the Rosenthal, & Driessner, 1971; Singh, Chhina, Anand, etdevice used in Frankel’ s study was defective.] al., 1971), increased peripheral temperature, an indicator Cranial electrotherapy stimulation has been well of vasodilatation (Brotman, 1989; Heffernan, 1995),researched and clearly proven to be the most effective, reductions in gastric acid output (Kotter, Henschel, Hogan,and safest method of treatment for anxiety, and anxietyet al., 1975), and in blood pressure, pulse, respiration, and related disorders. It is also highly effective for depression heart rate (Heffernan, 1995; Taylor, 1991). and insomnia, muscle tension, fibromyalgia, and headThe efficacy of CES has also been clinically confirmed aches. As an increasing number of patients seek alternathrough the use of 27 different psychometric tests. Thetives to the side sfects and potential addiction to moodsignificance of CES research for treating anxiety has been altering pharmaceuticals and controlled substances, CES reconfirmed through meta-analyses conducted at the Unioffers a viable solution. It is easy enough to offer CES in versity of Tulsa by O’Connor, Bianco, and Nicholson a psychologist’ s, dentist’s or physician’ s office, clinic, or (1991), and by Klawansky, Yeung, Berkey, Shah, et al.hospital, and chronically stressed patients will find it cost(1995) at the Department of Health Policy and Manage-effective over time to own their own CES device. ment, Harvard School of Public Health. Seventeen studies conducted follow-up investiga-INDICATIONS tions from 1 week to 2 years after treatment (Brotman, 1989; Brovar, 1984; Cartwright, & Weiss, 1975; Flemen-In addition to the primary claims for anxiety, depression baum, 1974; Forster, et al., 1963; Hearst, Cloninger,insomnia, and pain, CES has been researched with sigCrews, & Cadoret, 1974; Heffernan, 1995; Hochman,nificant results for many other conditions. Smith and 1988; Koegler, Hicks, & Barger, 1971; Magora, Beller, Shiromoto (1992) showed it to be highly effective in Assael, & Kenazi, 1967; Matteson, & Ivancevich, 1986;blocking fear perception in phobic patients. Favorable

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results also have been reported for labor, epilepsy, The ideal treatment time is 20 to 60 minutes, but some hypertension, surgery, spinal cord injuries, chronic pain,patients may achieve the full benefits of a CES treatment within 10 minutes. Many dentists use it instead of nitrous arthritis, cerebral atherosclerosis, eczema, dental pain, oxide gas to help relax patients during dental procedures asthma, ischemic heart disease, stroke, motion sickness, (Winick, 1999). Sometimes these dental procedures last digestive disorders as well as various addictive disorders including cocaine, marijuana, heroin and alcohol abusefor hours with the patient undergoing CES treatment the (Brovar, 1984; Daulouede, 1980; Feighner, Brown, & entire time. Olivier, 1973; Gomez & Mikhail, 1978; Overcash & Although CES treatment is indicated for insomnia, Siebenthall, 1989; Patterson, 1983; Schmitt, Capo, Frabecause of the increased alertness some patients find it zier, & Boren, 1984; Smith, 1975; Smith, 1982; Whar- difficult to fall asleep immediately after a treatment. ton, McCoy, & Cofer, 1982). Accordingly, it is recommended that CES be used at least 3 hours before going to bed. Also, in most cases after daily Reflex sympathetic dystrophy (RSD) and bromyalfi gia syndrome (FS) are two signifi cant pain diagnoses treatments for the first week or two, treating every other from primary central and autonomic nervous system eti-day is usually more effective than daily treatment. ologies that respond best to CES (Alpher & Kirsch, 1998; Lichtbroun, Racier, & Smith, 1999). Adding somatic THE CES EXPERIENCE treatment with MET to these two conditions does not During the treatment, most patients will experience a seem to improve the outcomes. change in body weight. They may feel Besides specific pathological disorders, there are subjective a heavier at fi rst and then lighter, or they may feel lighter growing number of studies being conducted that show initially. The patient may feel worse during the heavy increases in cognitive functions. Michael Hutchison cycle and this feeling can last for hours or even days (1986) discussed several mind-enhancement techniques in in rare cases unless extra treatment time is given. Therehis book Megabrain,devoting Chapter 9 to CES as a tool fore, it is important to continue the treatment if the for attaining higher levels of consciousness. Sparked by patient feels heavier at the end of the allotted time, even Hutchison, Madden and Kirsch (1987) completed a study if it has already been 20 minutes or more. Continue for that demonstrated CES is a useful tool for improving at least 2 to 5 minutes after the patient feels lighter. psychomotor abilities. Smith (1999) demonstrated that Not all patients will be aware of these weight-percepCES significantly improved stress-related cognitive dysfunction, such as attention deficit disorder (ADD), aftertion changes. only 3 weeks of treatment, and maintained the effect Following CES, most people feel better, less distressed, and more focused on mental tasks. They generally through an 18-month follow-up assessment. sleep better and report improved concentration, increased learning abilities, enhanced recall, and a heightened state METHODOLOGY of well-being. Cranial electrotherapy stimulation devices are generally Psychologistsfirst described these general feelings similar in size and appearance to TENS units, but pro-during the 1970s as an alpha state of consciousness. Medduce very different waveforms. Standard mA-current itation, biofeedback training, relaxation instructions, TENS devices must never be applied transcranially.chanting, hypnotherapy, and certain religious rituals also CES electrodes can be placed bitemporally, forehead produce such states. This is not the same as the alpha brain to posterior neck, bilaterally in the hollow just anterior wave frequency of 8 to 13 Hz. Often, practitioners are to the mastoid processes, or through electrodes clipped confused by device representatives who claim that their to the earlobes. The ear clip method, developed by the particular devices will output and entrain a brain to the author, is the easiest and possibly most effective elecalphafrequency . There is no evidence to support that CES trode placement. devices work on an entrainment principle. The electrodes mustrst fi be wet with an appropriate conducting solution. When using ear clip electrodes, applyCONTRAINDICATIONS them to the superior aspect of the ear lobes, as close to the jaw as possible. Start with a low current and graduallyThere have not been any significant lasting harmful side increase it. If the current is too high the patient may experi-effects reported in any of the research literature from either ence a painful stinging sensation at the electrodes, dizziness, MET or CES. As with all electrical devices, caution is or nausea. If any of these three symptoms arise, immediately advised during pregnancy, and with patients using an older reduce the current and the symptoms will subside in a few model (pre-1998) demand-type pacemaker. In addition, it moments. After a minute or two, try increasing the currentis recommended that patients do not operate complex again, but keep it at a comfortable level. It is okay for themachinery or drive automobiles during and shortly after patient to feel the current as long as it is not uncomfortable. a CES treatment.

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Brovar, A. (1984). Cocaine detoxification with cranial electrotherapy stimulation (CES): A preliminary appraisal. Microcurrent electrical therapy and cranial electrotherInternationalElectromedicine Institute Newsletter , 1(4). apy stimulation are electromedical modalities that useCarey, L.C., & Lepley, D. (1962). Effect of continuous direct electric current on healing wounds. Surgical Forum, 13, low level currents that usually do not exceed 1 mA. 33–35. Beneficial effects have been reported for a wide variety of pain, psychological distress, and addiction-relatedCarley, P.J., & Wainapel, S.F. (1985). Electrotherapy for acceleration of wound healing: Low intensity direct current. disorders. Archives of Physical Medicine and Rehabilitation , 66, Pain is a complex process encompassing the entire 443–446. nervous system. To achieve optimal results through elecCartwright, R.D., & Weiss, M.F. (1975). The effects of electrostromedical intervention, the peripheral and central nerleep on insomnia revisited. Journal of Nervous and Menvous systems should both be treated. Cranial electrotal Disease, 164(2), 134. Chang, N., Van Hoff, H., Bockx, E., et al. (1982). The effect of therapy stimulation induces a relaxed, alert state. It is a electric currents on ATP generation, protein synthesis, primary modality effective for controlling anxiety, and membrane transport in rat skin. Clinical Orthopedepression, insomnia, and generalized stress ubiquitous dics, 171, 264–272. in pain patients. In addition, there is mounting evidence Cox, A., & Heath, R.G. (1975). Neurotone therapy: A prelimithat CES can enhance cognitive functions. Because of nary report of its effect on electrical activity of forebrain its safety and effectiveness, the combination of MET structures. Diseases of the Nervous System , 36, and CES used with the protocols described here is highly 245–247. recommended for a broad range of pain and stressDaulouede, J. (1980). Une nouvelle methode de sevrage des related disorders. toxicomanes par utilisation du courant de Limoge (A new method of eliminating drug addiction using Limoge’s current). Annales Medic-Psychologiques , 138(3), 359–370. REFERENCES Dayton, P.D., & Palladino, S.J. (1989). Electrical stimulation of cutaneous ulcerations: A literature review. Journal of the Alpher, E.J., & Kirsch, D.L. (1998). Traumatic brain injury and American Podiatric Medical Association , 79, 318–321. full body reflex sympathetic dystrophy patient treated DeBock, P. (2000). A comparison between TENS and MET. with cranial electrotherapy stimulation. American JourPhysical Therapy Products , September, 28–33. nal of Pain Management , 8(4), 124–128. Alvarez, O.M., et al. (1983). The healing of superficial skin Eaglstein, W.H., & Mertz, P.M. (1978). New method for assessing epidermal wound healing: The effects of triamcinowounds is stimulated by external electrical current. lone acetonide and polyethylene film occlusion. Journal Journal of Investigative Dermatology , 81, 144–148. of Investigative Dermatology , 71, 382–384. Andersson, et al. (1976). Effects of conditioning electrical stimulation in the perception of pain. ACTA Orthopaedica Falanga, V., et al. (1987). Electrical stimulation increases the expression of fibroblast receptors for transforming Scandinavica , 47, 149–162. growth factor-beta (abstracted). Journal of Investigative Assimacopoulos, D. (1968). Low intensity negative electric curDermatology, 88, 488. rent in treatment of ulcers of leg due to chronic venous Falanga, V. (1988). Occlusive wound dressings. Archives of Derinsufficiency: Preliminary report of three cases. Amerimatology, 124, 872–877. can Journal of Surgery , 115, 683–687. Feighner, J.P., Brown, S.L., & Olivier, J.E. (1973). Electrosleep Assimacopoulos, D. (1968a). Wound healing promotion by the therapy: A controlled double-blind study. Journal of use of negative electric current. Annals of Surgery , 34, Nervous and Mental Disorders , 157, 121. 423–431. Ferdjallah, M., Bostick, F.X., Jr., & Barr, R.E. (1996). Potential Barron, J.J., & Jacobson, W.E. (1985). Treatment of decubitus and current density distributions of cranial electrotherulcers: A new approach.Minnesota Medicine , 68, apy stimulation (CES) in a four-concentric-spheres 103–105. model. IEEE Transactions on Biomedical Engineering , Becker, R.O. (1985).The body electric . New York: William 43(9), 939–943. Morrow and Co. Fields, W.R., Tacke, R.B., & Savana, B.S. (1975). Pulpal anodal Braverman, E., Smith, R., Smayda, R., & Blum, K. (1990). Modblockade of trigeminal field potentials elicited by tooth ification of P300 amplitude and other electrophysiological stimulation in the cat.Experimental Neurology , 47, parameters of drug abuse by cranial electrical stimulation. 229–239. Current Therapeutic Research , 48(4), 586–596. Flemenbaum, A. (1974). Cerebral Electrotherapy (Electrosleep): Brotman, P. (1989). Low-intensity transcranial electrostimulaAn open clinical study with a six month follow-up, tion improves the ef ficacy of thermal biofeedback and Psychosomatics , 15, 20–24. quieting reflex training in the treatment of classical Forster, S., Post, B.S., & Benton, J.G. (1963). Preliminary observations on electrosleep. Archives of Physical and Medmigraine headache. American Journal of Electromediical Rehabilitation, 44, 81–89. cine, 6(5), 120–123.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

Frankel, B.L., Buchbinder, R., & Snyder, F. (1973). Ineffective- Klawansky, S., Yeung, A., Berkey, C., & Shah, N., et al. (1995). Meta-analysis of randomized controlled trials of craness of electrosleep in chronic primary insomnia. nial electrotherapy stimulation: ficacy Ef in treating Archives of General Psychiatry , 29, 563–568. selected psychological and physiological conditions. Gault, W.R., & Gatesn, P.F. (1976). Use of low intensity direct Journal of Nervous and Mental Diseases , 183(7), current in management of ischemic skin ulcers. Physical 478–485. Therapy, 56, 265–269. Gibson, T.H., & O’Hair, D.E. (1987). Cranial application of low Koegler, R.R., Hick, S.M., & Barger, J. (1971). Medical and psychiatric use of electrosleep (transcerebral electrotherapy). level transcranial electrotherapy vs. relaxation instrucDiseases of the Nervous System , 32(2), 100–104. tion in anxious patients. American Journal of ElectroKotter, G.S., Henschel, E.O., Hogan, Walter J., et al. (1975). medicine, 4(1), 18–21. Inhibition of gastric acid secretion in man by the tranGoldin, H., et al. (1981). The effects of Diapulse on the healing scranial application of low intensity pulsed current. Gasof wounds: A double-blind randomized controlled trial troenterology, 69, 359–363. in man.British Journal of Plastic Surgery , 34, 267–270. Gomez, E., & Mikhail, A.R. (1978). Treatment of methadone Krupitsky, E.M., Burakov, G.B., Karandashova, JaS., et al. (1991). The administration of transcranial electric withdrawal with cerebral electrotherapy (electrosleep). treatment for affective disturbances therapy in alcoBritish Journal of Psychiatry , 134, 111–113. holic patients.Drug and Alcohol Dependence , 27, Hearst, E.D., Cloninger, R., Crews, E.L., & Cadoret, R.J. (1974). 1–6. Electrosleep therapy: A double-blind trial. Archives of Krupisky, E.M., Katznelson, Ya.S., Lebedev, V.P., et al. (1991). General Psychiatry , 30, 463–466. Transcranial electrostimulation (TES) of brain opioid Heffernan, M. (1995). The effect of a single cranial electrotherstructures (BOS): Experimental treatment of alcohol apy stimulation on multiple stress measures. The withdrawal syndrome (AWS) and clinical application. Townsend Letter for Doctors and Patients , 147, 60–64. Presented at the Society for Neuroscience Annual MeetHeffernan, M. (1996). Comparative effects of microcurrent stiming, New Orleans, November 10–15. ulation on EEG spectrum and correlation dimension. Kulig, K., Jarski, R., Drewek, E., et al. (1991). The effect of Integrative Physiological and Behavioral Science , microcurrent stimulation on CPK and delayed onset 31(3), 202–209. muscle soreness. Physical Therapy , 71, 6(suppl.). Heffernan, M. (1997). The effect of variable microcurrents on EEG spectrum and pain control. Canadian Journal of Levitt, E.A., James, N., & Flavell, P. (1975). A clinical trial of electrosleep therapy with a psychiatric inpatient sample. Clinical Medicine. 4(10), 4–11. Australia and New Zealand Journal of Psychiatry , 9, Hochman, R. (1988). Neurotransmitter modulation (TENS) for 287–290. control of dental operative pain. Journal of the American Lichtbroun, A.S., Raicer, M.S., & Smith, R.B. (1999). The use Dental Association , 116, 208–212. of Alpha-Stim cranial electrotherapy stimulation in the Hokfelt, T., et al. (1977). Immunohistological analysis of peptide treatment of fibromyalgia. Presented at the 15th annual pathways possibly related to pain and analgesia: International Symposium on Acupuncture and ElectroEnkephalin and substance P. Proceedings of the Therapeutics, Columbia University, New York City, National Academy of Science , 74, 3081–3085. October 21–24. Hutchison, M. (1986).Megabrain. New York: Beech Tree Books, Lichtbroun, A.S., Raicer, M.S., & Smith, R.B. (2001). The William Morrow. treatment of fibromyalgia with cranial electrotherapy Ieran, M., et al. (1990). Effect of low frequency pulsing electrostimulation. Journal of Clinical Rheumatology , 7(2), magnetic fields on skin ulcers of venous origin in 72–78. humans: A double blind study. Journal of Orthopedic Lundeberg, T.C., Eriksson, S.V., & Malm, M. (1992). Electrical Research , 8, 276–282. nerve stimulation improves healing of diabetic ulcers. Jarzembski, W.B., Sanford, J.L., & Sances, A., Jr. (1970). EvalAnnals of Plastic Surgery , 29(4), 328–331. uation of specific cerebral impedance and cerebral current density. Annals of the New York Academy of Madden, R.E., & Kirsch, D.L. (1987). Low intensity transcranial electrostimulation improves human learning of a psySciences , 170, 476–490. chomotor task.American Journal of Electromedicine , Jeran, M., et al. (1987). PEMF stimulation of skin ulcers of 2(2/3), 41–45. venous origin in humans: Preliminary report of a double Magora, F., Beller, A., Assael, M.I., & Askenazi, A. (1967). Some blind study.Journal of Bioelectricity , 6, 181–188. aspects of electrical sleep and its therapeutic value. In Kaada, B., Flatheim, E., & Woie, L. (1991). Low-frequency F.M. Wageneder, & St. Schuy (Eds.) (pp. 129–135). transcutaneous nerve stimulation in mild/moderate Electrotherapeutic sleep and electroanaesthesia . hypertension.Clinical Physiology, 11, 161–168. Amsterdam: Excerpta Medica Foundation, International Kirsch, D.L. (1999).The science behind cranial electrotherapy Congress Series No. 136. stimulation. Edmonton, Alberta, Canada: Medical Scope Matteson, M.T., & Ivancevich, J.M. (1986). An exploratory Publishing. investigation of CES as an employee stress management Kirsch, D.L., & Smith, R.B. (2000). The use of cranial electrotechnique. Journal of Health and Human Resource therapy stimulation in the management of chronic pain: Administration, 9, 93–109. A review. NeuroRehabilitation , 14, 85–94.

A Practical Protocol for Electromedical Treatment of Pain

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Reigel, D.H., Larson, S.J., Sances, A., Jr., et al. (1971). Effects McKenzie, R.E., Rosenthal, S.H., & Driessner, J.S. (1971). Some of electrosleep currents on gastric physiology. In D.V. psychophysiologic effects of electrical transcranial stimReynolds & A. Sjoberg (Eds.). Neuroelectric research . ulation (electrosleep). American Psychiatric Association, Springfield, IL: Charles C Thomas. Scientific Proceedings Summary . Also in The nervous system and electric currents (1976). N.L. Wulfsohn, and A. Richter, W.R., Zouhar, R.L., Tatsuno, J., et al. (1972). Electron Sances, (Eds.). New York: Plenum. 163– 167. microscopy of the macaca mulatta brain after repeated Melzack, R. (1975). Prolonged pain relief by brief, intense tranapplications of electric current. Anesthesiology , 36(4), scutaneous somatic stimulation. Pain, 1, 373–375. 374–377. Mercola, J.M., & Kirsch, D.L. (1995). The basis for microcurrent Robinson, K.R. (1925). Digby’ s receipts.Annals of Medical electrical therapy (MET) in conventional medical pracHistory, 7, 216–219. tice. Journal of Advancement in Medicine , 8(2), Rowley, B.A., McKenna, J.M., Chase, G.R., & Wolcott, L.E. 107–120. (1974). The influence of electrical current on an infectMoore, J.A., Mellor, C.S., Standage, K.F., & Strong, H. (1975). ing microorganism in wounds. Annals of the New York A double-blind study of electrosleep for anxiety and Acadamy of Science , 238, 543–551. insomnia.Biological Psychiatry,10(l), 59–63. Salar, G., et al. (1981). Effect of transcutaneous electrotherapy Mulder, G.D. (1991). Treatment of open-skin wounds with elecon CSF β-endorphin content in patients without pain tric stimulation. Archives of Physical Medicine and problems.Pain, 10, 169–172. Rehabilitation, 72, 375–377. Schmitt, R., Capo, T., Frazier, H., & Boren, D. (1984). Cranial Ng, L.K.Y., Douthitt, T., et al. (1975). Modifi cation of morphineelectrotherapy stimulation treatment of cognitive brain withdrawal syndrome in rats following transauricular elecdysfunction in chemical dependence. Journal of Clinical trostimulation: An experimental paradigm for auricular Psychiatry, 45, 60. electroacupuncture. Biological Psychiatry , 10, 575–580. Singh, B., China, G.S., Anand, B.K., et al. (1971). Sleep and O’Connor, M.E., Bianco, F., & Nicholson, R. (1991). Metaconsciousness mechanism with special reference to analysis of cranial electrostimulation in relation to the electrosleep. Armed Forces Medical Journal(New primary and secondary symptoms of substance withDelhi), 27(3), 292–297. drawal. Presented at the 12th Annual Meeting of theSmith, R.B. (1975). Electrosleep in the management of alcoholBioelectromagnetics Society, June 14. ism. Biological Psychiatry , 10, 675. Overcash, S.J. (1999). A retrospective study to determine the Smith, R.B. (1982). Confirming evidence of an effective treateffect of cranial electrotherapy stimulation (CES) on ment for brain dysfunction in alcoholic patients. Journal patients suffering from anxiety disorders. American of Nervous and Mental Disorders , 170(5), 275–278. Journal of Electromedicine , 16(1), 49–51. Smith, R.B. (1999). Cranial electrotherapy stimulation in the Overcash, S.J., & Siebenthall, A. (1989). The effects of cranial treatment of stress related cognitive dysfunction with an electrotherapy stimulation and multisensory cognitive eighteen month follow-up.Journal of Cognitive Rehatherapy on the personality and anxiety levels of subbilitation, 17(6), 14–18. stance abuse patients. American Journal of ElectromedSmith, R.B. (2001). Is microcurrent stimulation effective in pain icine, 6(2), 105–111. management? An additional perspective. American Passini, F.G., Watson, C.G., & Herder, J. (1976). The effects of Journal of Pain Management , 11(2), 62–66. cerebral electric therapy (electrosleep) on anxiety, Smith, R.B., & Shiromoto, F.N. (1992). The use of cranial elecdepression, and hostility in psychiatric patients. Journal trotherapy stimulation to block fear perception in phobic of Nervous and Mental Disease , 163(4), 263–266. patients.Current Therapeutic Research , 51(2), 249–253. Patterson, M. (1983). Getting off the hook . Wheaton, IL: Harold Starfield, B. (2000). Is U.S. health really the best in the world? Shaw Publishers. Journal of the American Medical Association , 284(4), Patterson, M., Firth, J., & Gardiner, R. (1984). Treatment of 483–485. drug, alcohol and nicotine addiction by neuroelectric Stromberg, B.V. (1988). Effects of electrical currents on wound therapy: Analysis of results over 7 years. Journal of contraction.Annals of Plastic Surgery , 21, 121–23. Bioelectricity, 3(1/2), 193–221. Pert, A., Dionne, R., & Ng, L.K.Y., et al. (1981). Alterations in Taylor, D.N. (1991). Effects of cranial transcutaneous electrical nerve stimulation in normal subjects at rest and during rat central nervous system endorphins following transstress. Doctoral dissertation, Brooklyn College of the auricular electroacupuncture.Brain Research , 224, City University of New York. 83–94. Pozos, R.S., Richardson, A.W., & Kaplan, H.M. (l971). Electro- Thuile, C., & Kirsch, D.L. (2000).Schmerzen Linden ohne Chemie: CES, die Revolution in der Schmerztherapie (in anesthesia: A proposed physiologic mechanism. In D.V. German). IGEM, Austria. Reynolds & A. Sjoberg (Eds.), Neuroelectric research Toriyama, M. (1975). Ear acupuncture anesthesia. Ear Throat, (pp. 110–113). Springfield, IL: Charles C Thomas. 47, 497–501. Reigel, D.H., Dallmann, D.E., Christman, N.T., et al. (1970). Physiological effects of electrotherapeutic currents inTuraeva, V.A. (1967). Treatment of eczema and neurodermatitis by electrosleep. In F.M. Wageneder, & St. Schuy (Eds.). the primate and man. In F.M. Wageneder & St. Schuy Electrotherapeutic sleep and electroanaesthesia . (pp. (Eds.). Electrotherapeutic sleep and electroanesthesia . 203–204). Amsterdam: Excerpta Medica Foundation. (Vol. II) pp. 158–165). Amsterdam: Excerpta Medica.

776

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Von Richthofen, C.L., & Mellor, C.S. (1980). Electrosleep ther- Wilson, A.S., Reigel, D., Unger, G.F., et al. (1970). Gastric secretion before and after electrotherapeutic sleep in apy: A controlled study of its effects in anxiety neurosis. executive monkeys. In F.M. Wageneder & St. Schuy Canadian Journal of Psychiatry, (3), 25 213–229. (Eds.). Electrotherapeutic sleep and electroanesthesia . Voris, M.D. (1995).An investigation of the effectiveness of cra(Vol. II, pp. 198–206). Amsterdam: Excerpta Medica. nial electrotherapy stimulation in the treatment of anxiety disorders among outpatient psychiatric patients, Windsor, R.E., Lester, J.P., & Herring, S.A. (1993). Electrical stimulation in clinical practice.Physician and Sports impulse control parolees and pedophiles (pp. 1–19). Medicine, 21, 85–93. Dallas: Delos Mind/Body Institute. Weiss, D.S., et al. (1990). Electrical stimulation and woundWinick, R.L. (1999). Cranial electrotherapy stimulation (CES): A safe and effective low cost means of anxiety control healing.Archives of Dermatology , 126, 222–225. in dental practice.General Dentistry,47(1), 50–55. Weiss, M.F. (1973). The treatment of insomnia through use of electrosleep: An EEG study. Journal of Nervous and Wolcott, L.E., Wheeler, P.C., & Hardwicke, H.M. (1969). Accelerated healing of skin ulcers by electrotherapy. Southern Mental Disease,157(2), 108–120. Medical Journal, 62, 795–801. Wharton, G.W., et al. (1982; 1983). The use of cranial electrotherapy stimulation in spinal cord injury patients. A poster study presented at the American Spinal Injury Association Meeting, New York, and at the Texas ASIA meeting in Houston.

Section IX Behavioral, Social, and Spiritual Concerns and Aspects of Pain Management

62 Pain, Disease, and Suicide Blake H. Tearnan, Ph.D. NATURE OF THE PROBLEM

suicide in all populations (Williams, 1997). For example, it is a well-established fact that suicidal behavior is parINCIDENCE ticularly associated with major depression. Other findings have shown suicidal risk is greater in Protestants than There are over 30,000 completed suicides in the United other religious af filiations including Catholics and Jews. States each year. Most successful suicides are carried out However, in general, churchgoing is associated with by men, but women attempt suicide more often (National decreased risk of suicide, possibly related to increased Center for Injury Prevention and Control, 1999). Suicide social supports (Williams, 1997). is currently the third leading cause of death among young adults ages 15 to 34, and in the United Kingdom, suicide The incidence of suicide in various social classes also has been studied. One investigation of social classes in is the second most common cause of death in this age group after motor vehicle accidents (Williams, 1997).England and Wales found the risk of suicide was greater in the professional and unskilled classes (Charlton, Kelly, Recently, the Surgeon General identified suicide as one of Dunnell, Evans, Jenkins, & Wallis, 1992). Comparatively the top public health concerns in the United States (Parker, 1998). Overall, suicide accounts for nearly 9% of malesfewer suicides were found in lower-level professional and and 4% of females in loss of years of life before the ageexecutive, skilled and partially skilled classes. However, of 65. This figure is similar for most Western countriesthe highest risk was found among individuals who had no (Williams, 1997). Clearly, suicide represents a majoroccupation at all. Studies conducted in the United States have shown that people in the lower classes living in health concern. substandard housing have proportionately higher rates of suicide (Charlton, et al., 1992). The exception is AfricanRISK FACTORS Americans living in poor communities. Williams (1997) Extensive research has been done to identify risk factors concluded that this result was possibly related to the strong associated with suicide in the general population. Some social ties within the African-American community. of the more consistent findings include increased rates for It is clear economic conditions, particularly unemmen by a factor of nearly 2 to 1 in most countries and 5ployment, increase the risk of suicide. Generally, men who to 1 in Finland (Sainsbury, Jenkins, & Baert, 1981).are unemployed and seeking employment are at two to Whites in the United States are also approximately twicethree times greater risk. Boor (1980) found that among as likely to commit suicide as blacks or other nonwhitesuicide victims, the rate of unemployment was 50% across groups, and this difference is particularly associated withseveral studies. the older age group. The exception to this finding is that There have been numerous studies on suicide related suicide is particularly high in young Native Americans to lifespan issues. In most all Western countries, suicide (Williams, 1997). is extremely uncommon in young children but rises Most studies have found the presence of psychiatricsteadily after puberty with the risk increasing with age disturbance and/or substance abuse increases the risk (Buda of & Tsuang, 1990). Recent studies have confirmed 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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earlier investigations, but in men rather than women,between 1991 and 1996. The patients’ medical charts where the rates actually have decreased in recent years were examined to identify patients who had committed (Kaplan & Sadock, 1996). The rates of suicide in youngersuicide, had expressed suicidal intent, or refused therapy men appear to be rising, and recent studies have shownpreferring a to die. The results showed 1.2% of their sample slight decline in the suicide rate among older people.committed suicide. Two patients admitted to suicidal Williams (1997) explains the rise in suicide in young intent and an additional four patients refused treatment. males as caused by the increase of working class men who They concluded that head and neck cancer patients have are unemployed and may be experiencing significant ecosome of the same risk factors as other cancer patients but nomic hardship. This group is also most likely to abuseappear particularly prone to suicide because there is often alcohol and other drugs. significant disfigurement after treatment, and many of these patients use alcohol, have poor social support and may become socially isolated because their speech appaMEDICAL ILLNESS AS A RISK FACTOR ratus interferes with speaking. In addition, these patients Perhaps more than any other factor, medical illness is also report other changes in quality of life including associated with an increased risk of suicide (Druss &decreased smell, interference in taste for foods, and Pincus, 2000). Psychological autopsies performed on inability to chew foods and swallow. completed suicides have found general medical disorders It is interesting to speculate that some somatic dissubstantially raise the risk for completed suicide. Severaleases, like cancer, may pose a greater risk of suicide other studies have shown certain medical illnesses are because of the alteration of certain neurochemical proassociated with unusually high rates of suicide. For examcesses such as the availability of serotonin or by some ple, the risk of suicide among epileptic patients is 4 timesother mechanism (Stenager, Stenager, & Jensen, 1994). greater than the general population and 25 times greater The problem is compounded by the use of various medifor temporal lobe epileptics (e.g., Rosenfeld, Breitbart,cations that can precipitate mood disturbance and cogniStein, et al., 1999; Chochinov, Wilson, Enns, & Lander,tive impairment and by various medical illnesses that can 1998). Also, people suffering from peptic ulcer, Hunting- cause an organic mood disturbance, not necessarily by ton’s chorea, spinal cord injuries, AIDS, and those under-altering brain chemicals but by some other pathway. going renal dialysis experience higher rates of suicide Studies have shown the risk of suicide rises in patients compared to the general medical population. with a general medical illness, even when co-morbid Cancer is particularly associated with an increase infactors, such as depression or pain, are controlled for. In suicide. Although the overall incidence is low, patientsone study, Druss and Pincus (2000) showed a ficant signi with cancer are at two times increased risk for committingassociation between various medical conditions and suisuicide when compared to the population at large (Fox,cidality that persisted after adjusting for depressive illness Stanek, Boyd, et al., 1982). One study examining maleand alcohol use. In this investigation, the authors examcancer patients (Marshall, Burnett, & Brasure, 1983)ined the presence of a medical illness in more than 7500 showed there was a 50 to 100% greater likelihood ofindividuals, ages 17 to 39 years of age. They administered suicide among male cancer patients when compared to the the Diagnostic Interview Schedule as part of a national general population. For women, the risk was increased by survey. The information collected from this survey 30 to 50%. Suicidal behavior is particularly prevalentincluded any incidence of lifetime suicidal ideation and immediately following the diagnosis of cancer and in thesuicide attempts. Also assessed were common medical beginning of treatment for men (Fox, Burnett, & Brasure,illnesses, presence of major depression and alcohol usage. 1983). Apparently this difference in sexes disappearsOne purpose of the study was to determine if there was roughly 2 years after the diagnosis. a relationship between medical illness and suicidality Investigations have identified several factors that areafter controlling for psychiatric morbidity. The results likely to increase the risk of suicide in cancer patients.show 16% of the respondents without medical illness These include significant disability, delirium, prognosis,described suicidal ideation at some point in their lives; disfigurement, feelings of hopelessness, and pain (e.g., whereas, individuals with a general medical condition Allebeck & Bolund, 1991; Hietanen & Lonnqvist, 1991; reported a 25% lifetime incidence of suicidal ideation. Chochinov, et al., 1998). History of psychiatric distur- The figure was as high as 35% in those individuals who bance, poor family support, psychological disorder, espereported two or more medical illnesses. The sample on cially depression, substance abuse, pain, and family histhe whole reported a 5.5% incidence of attempted suicide tory of suicide all may be additional risk factors for cancerwhereas 9% of the respondents with a medical illness patients but are not specific to cancer. made a suicide attempt and 16% of those with two or In a recent study, Henderson and Ord (1997) studied more medical conditions had attempted suicide. After 241 patients who were diagnosed with head and neck controlling for major depression and alcohol use as well cancer. They studied these patients over a 5-year period as certain demographic characteristics, the results showed

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that the presence of a medical condition predicted a 1.3 patients. Studies have shown that these patients are at times increase in the likelihood of suicidal ideation. Cer-greater risk for depression and suicide than the general tain medical illnesses showed a much higher increase in population. Fishbain, Cutler, Rosomoff, and Rosomoff the incidence of suicidal ideation. For example, cancer(1997) examined 18 studies that looked at the association and asthma were each associated with more than a fourof chronic pain and suicide. He concluded that suicidal fold increase in the likelihood of a suicide attempt. ideation, suicidal attempts, and suicide completions are Although medical illness by itself is associated with commonly found in chronic pain populations. He also an increased risk of suicidality, clearly when co-morbidnoted that chronic pain patients usually show other suipsychiatric conditions, such as depression and substance cidal risk factors, especially depression. He concluded that abuse are present, along with a number of demographic chronic pain is a significant suicide risk factor. He cauand lifespan issues, the risk increases dramatically (Will-tioned that a careful search for co-morbid risk factors iams, 1997). Persistent pain is another factor in the medneeds to be accomplished when evaluating the chronic ically ill patient that can raise suicidal risk. This was pain patient. demonstrated clearly by Stenager et al. (1994) who exam- In summary, it is well-established that one of the most ined a sample of suicide attempters admitted to a departsignificant risk factors for suicide is somatic illness. Medment of psychiatry. Each patient underwent a structured ical illness is associated with 30 to 50% of attempted and interview examining a multitude of factors that may havesuccessful suicides. Certain medical conditions such as led up to the suicide attempt. The results show 52% of the cancer epilepsy, AIDS, spinal cord injuries, and chronic patients were shown to have a somatic disease, and 21% pain pose increased risk. In most cases, the co-occurrence were taking analgesics daily for pain. The patients expeof depression, especially associated with feelings of riencing a physical illness differed from other suicide hopelessness, increases the risk of suicide. Evidence from attempters on a variety of measures including depression various studies indicates that although medical illness scores, age, pain, and the presence of psychoses. The poses a signifi cant risk factor for suicide, rarely does the authors noted fewer of the physically ill subjects reportedpatient attempt or commit suicide in the absence of a significant psychopathology, and those with significantpsychiatric disorder. pain were more often depressed and abused medications. They concluded the risk of parasuicide for subjects withUNDERSTANDING PAIN, SUFFERING, AND SUICIDE a physical illness, but without depression, was signifiMedical illness increases the risk for suicide. There are a cantly less. In a smaller sample of successful suicides, number of factors that appear to compound the problem they noted the subjects were older and there was also a including pain, especially chronic pain, and depression tendency toward painful somatic diseases and depression, associated with feelings of hopelessness. Efforts to underincreasing the risk for suicidality. stand the relationships among pain, depression, and suiVenkoba (1990) reviewed the literature on the relacide have traditionally relied upon the biomedical model. tionship between somatic disease and suicide. The invesThis disease model of pain has been useful for promoting tigation included examining the association between pain the development of various analgesic medications and from physical illnesses, like duodenal ulcer, and suicide. neuroablative techniques that have shown some success Some of the conclusions reached indicated patients sufin pain management. fering from physical illnesses associated with pain, especially when scores on depression and hopelessness were BIOMEDICAL MODEL high, were associated with signifi cantly increased suicidal behavior. In the strictest sense, the biomedical model posits that In a 5-year follow-up study, Nielsen, Wang, and Bille- pain results from a disturbance in nerve pathways, and Brahe (1990) also concluded that depression and physical pain intensity is presumed to be a function of the degree illness represented the greatest risk for suicide. In addiof physical damage. Pain is conceived as a closed, tion, they showed that subjects reporting no depression unmodulated, unidirectional system. The affective qualand pain contacted their primary care providers more often ity of pain is thought to be incidental to the underlying before attempting suicide. Obviously, patients with adisease and strongly correlated to the signal intensity of somatic illness and depression are especially susceptible pain. The degree of disability associated with pain is to suicidal behavior. This is particularly true for older considered directly proportional to the underlying patients with painful somatic diseases and depression. impairment, and changes in disability, depression, and The relationship between somatic disease and suicidsuffering occur by reducing the signal intensity of pain. ality is clear. Patients with a variety of illnesses are atDramatic displays of pain behavior associated with few increased risk, and the problem is compounded by a numphysical findings are often attributable to psychological ber of factors including depression, pain, and lifespan.overlay, and pain is viewed as symptomatic and never a Thesefindings also extend to chronic, nonmalignant painproblem in and of itself.

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Limitations of the biomedical approach are numerous, Suffering is defined as “a state of severe distress assoespecially when applied to the understanding of persistent ciated with events that threaten the intactness of the perpain of a nonmalignant nature. Studies conducted as far son. It occurs when an impending destruction of the person as back as the 1950s show pain and the disability and is perceived; suffering continues until the threat has suffering associated with it, are often poorly correlated topassed” (Cassell, 1982). According to Fordyce (1988), this biological disturbance (Melzack & Wall, 1983). How definition emphasizes the anticipatory nature of suffering patients interpret and apply meaning to their pain, and the and events that are likely to precipitate threats to the self social and environmental factors with which they come inor the intactness of the person. In other words, suffering contact also have been shown to affect pain and the sufis an emotional experience triggered in anticipation of fering associated with it (Melzack & Wall, 1983). events the person perceives as potentially threatening. Although related to the signal intensity of pain, suffering is independent. For example, a patient with chronic pain BIOPSYCHOSOCIAL MODEL may experience persistent pain related to a number of The biopsychosocial model (Turk & Waddell, 1992) main-underlying pain mechanisms, including disc disruption. tains that pain usually is initiated by nociception with The suffering expressed by the patient is related to the accompanying sensory perception, but pain is also influ-sensory experience of pain triggered by the disc pathology, enced by emotional, social, and environmental factors. Inbut is also affected by the understanding the patient has this conceptualization, each factor interacts in complexabout the pain, fear of pain and re-injury, possibly the type ways to affect pain. It carries with it the overriding of job to which the patient is expected to return, and what assumption that changing the pain experience requires the patient thinks may happen in the future as long as the attention to multiple influences. pain persists. Suffering is diminished not simply by affectThe biopsychosocial model also assumes that the ing a change in pain intensity, which is often not possible, affective quality of pain is not simply an incidental but by reducing the perceived threat associated with pain response to pain, but is related to multiple factors such as the patient is experiencing. This could be as direct as how the pain is interpreted, the social consequences of the educating the patient more effectively about the underlypain, pre-morbid psychological vulnerabilities, perceiveding nature of the pain problem and offering reassurances loss of self, and so forth. that being bound to a wheelchair is not likely to happen if a modicum of activities are initiated. Fordyce (1988) observed that clinicians often conDISABILITY AND SUFFERING DEFINED found pain and suffering. This carries with it important Disability and suffering are often poorly related to under-implications because it places paramount importance on lying physical impairment, especially in chronic pain correcting the physical disturbance before the relief of (Turk & Waddell, 1992). According to the biopsychosocial pain, as well as suffering, can occur. As Fordyce wrote, model, this finding can be easily assimilated because non“Suffering behaviors may occur for many reasons and may physiologic influences are recognized to affect disabilityhave little or no relationship to nociception. ” and suffering, such as fear of pain or type of job. Clearly, Like suffering, disability, or the patient’ s diminished reducing pain does not always decrease disability and capacity, is frequently unrelated to nociception, especially suffering. Because physical disturbance, disability, andin chronic pain (Turk & Waddell, 1992). Patients are dissuffering are often poorly related due to multiple physical,abled for a variety of reasons including physical impairenvironmental, and social factors, it is erroneous toment. But, patients are also disabled because of fear, attribute the lack of any clear relationship to so-calleduncertainty associated with pain, and co-morbid factors psychological overlay. such as depression. Turk and Waddell (1992) in a series Suffering and the disability associated with pain fromof studies showed that the correlation coef ficients were the perspective of the biopsychosocial model exert indeminimal to modest at best among various medical condipendent influences on pain and, as emphasized above, are tions and expressed disability. In lower back pain, they not incidental to physical impairment. This has importantfound a 0.5 correlation and in arthritic conditions only a implications for the understanding of pain and in the treat-0.3 correlation between underlying damage and disability. ment of depression and prediction of suicidal risk associated with pain. If suffering and disability are simply con- THE ROLE OF COGNITIONS AND EMOTIONS sequences of underlying organic pathology and related proportionally to the degree of physical disturbance, thenIt should be clear by now that cognitive factors play an treatment efforts directed at symptomatic relief of pain toimportant role mediating in pain perception and the affect a change in suffering and disability would be effec-expression of suffering and disability. One of the first studies demonstrating the influence of beliefs, including tive. However, clearly this has been shown not to be the attributions in pain, was conducted by Henry Beecher case (Turk & Waddell, 1992).

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(1959). He showed wounded soldiers requested far fewer number of studies including investigations showing a narcotics and reported less intense pain experiences when strong link between pain and the later development of compared to civilian post-surgery patients. Beecher condepression (Fishbain, et al., 1997). Suffering as it relates cluded after interviews with the soldiers that the meaningto the expectation of threat was first talked about in the of pain was entirely different for them. If they survived pain literature by Fordyce (1988), but was borrowed origthe battle, it meant a ticket home and out of the range of inally from social psychology (Higgins, Bond, Klein, & danger. In other words, they attached a different meaning Strauman, 1986) and work by Cassell (1982) suggesting to the pain experience than civilians who may have inter-psychological distress and emotional upheaval occur when preted the pain as a nuisance and a disruption of daily events threaten the intactness of the person. activities (Fordyce, 1988). The relationship between psychological distress and There are countless other studies showing howsuffering also was demonstrated by Tearnan and Lewanpatients interpret their pain experiences and that the meandowski (1992). They showed that chronic pain patients ing they give to their pain affects not only pain perception,consistently identified certain factors when asked to report but also disability and suffering levels (c.f., Wall, 2000). what they were most concerned about when their pain In particular, patients who perceive greater levels of threat, increases. These included the expectation that the pain more ambiguity, and feel more vulnerable, possiblywill negatively impact others, contribute to a loss of prorelated to a loss of self-control and the inability to cope,ductivity, cause physical harm, lead to psychological probexpress more distress. This can translate into heightened lems, and cause more pain. These five groupings were levels of pain-related suffering and disability (Chapmansupported in factor analytic studies sampling over 600 & Gavrin, 1999). pain patients. The patients scoring high on all concerns, Underlying the experience of pain and uencing infl conceptualized collectively as pain suffering, expressed in part all the different facets of the pain experience,more depression and distress in general. They also especially levels of suffering, is the emotional tone ofreported more problems associated with overall pain and the patient. Patients who are more anxious and depressed disability, especially activity interference. cope more poorly with pain and with the problems a According to Chapman and Gavrin (1999), suffering medical illness presents. Depression is a common conrepresents“a disparity between what one expects of onesequence of persistent pain (Fishbain, 1999). It com-self and what one does or is. A serious disruption in the pounds the problem of pain by heightening a sense of psychosocial trajectory of human life, such as the onset threat leading to increased levels of suffering (Tearnanof uncontrolled pain, can cause such a disparity and & Lewandowski, 1992). Depression also increasesthereby compel changes in a sense of”self. For example, fatigue and contributes to lowered self-confi dence for the development of a painful shoulder would probably managing day-to-day problems. have little impact on a man working in a sedentary capacity but could be devastating to a professional football player “because it affects what he or she is and can hope CONCEPTUAL FRAMEWORK to be in the future” (Chapman and Gavrin, 1999). Medical illness raises the risk for suicide because somatic Patients with persistent pain, largely as a result of disease, especially associated with persistent pain, strains trying to cope with the various stressors a somatic illness coping abilities. This increases the likelihood that thecan cause, can become consumed by negative events they patient will attribute failures to cope to personal inade-anticipate will occur in the future (Fordyce, 1988). This quacies, and uncertainty about the future and worries is fueled by the often ambiguous nature of physical illness about the medical condition will cause further loss andand the inability of the medical system to assist patients deterioration of the self. This often leads to feelings ofin coping more effectively with a pain problem that is depression, especially in individuals sensitive to loss ofunlikely to dissipate completely. control (Duggleby, 2000). Depression heightens the sense The suffering that results from medical illnesses with of vulnerability because a failure to cope is thought to bepersistent pain occurs as a consequence of self-blame for more probable. Threat is judged more significantly whenfailure to adequately cope and for trying to fight against a sense of vulnerability increases, leading to increased the onslaught of numerous stressors patients frequently suffering. Feelings of hopelessness result from the belief feel ill equipped to manage (Chapman & Gavrin, 1999), that suffering will never stop and, as a result, nothingparticularly those patients prone to feel out of control. positive will ever come of the future. Suicide is in response It should be mentioned that even though depression to a belief of hopelessness (Chochinov, et al., 1998). Death resembles suffering because both are associated with negis seen as an option to end the suffering and prevent ative a thoughts, feelings of exhaustion, and general psyfuture without hope. chological impairment, suffering is not a pathologic state Evidence for this conceptual understanding of how(Chapman & Garvin, 1999). Depression, unlike suffering, suicide may result from a medical illness is based on a is associated with self-blame and self-depreciation.

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A considerable body of research has shown that hopepast decade (Cohen, Steinberg, Hails, Dobscha, & Fischel, lessness is correlated highly with suicidal ideation in gen-2000). Disagreements largely revolve around whether eral medical patients and is a significant predictor of evenpatients who request end-of-life measures have reached tual completed suicide (Chochinov, et al., 1998). Physicalthis decision through rational thought processes or are disease by itself is seldom decisive for the suicidal acttheir requests triggered by pathological depression (Williams, 1997). Also, depression has been defined dif-(Cohen, et al., 2000). The available data are not conclusive ferently by various investigators but is generally associ-enough to settle the issues physicians must confront in ated with measures of discouragement and pessimism and deciding whether or not to actively end a patient’ s life or is not based fully on medical prognosis. Chochinov et al.discontinue treatment. However, several well-controlled (1998) defined hopelessness as encompassing the capacity studies have recently shown that patients who request to find purpose in living. Patients experiencing medicalphysician-assisted suicide score high on formal measures illnesses who have lost the capacity to believe the future of depression and hopelessness (Shuster, Breitbart, & will change will generally express hopelessness and are Chochinov, 1999). Unfortunately, physicians often place at increased risk for suicide. very little emphasis on ruling out depressive illness, conIn an important review by Hall, Platt, and Hall sidering depression a natural consequence to terminal ill(1999), 100 patients who made severe suicide attempts ness (Haghbin, Streltzer, & Danko, 1998). This is particwere studied. They were interviewed by the authors, and ularly disconcerting because a substantial minority of their charts carefully reviewed. All patients required physicians report a lack of confi dence in diagnosing treatment in the emergency room or were admitted todepression, and many admit to discomfort making a psyintensive care or a surgical unit of a large urban hospital. chological referral (Haghbin, et al., 1998). Results from the study suggested that the symptoms most There are many healthcare professionals who believe predictive of severe suicide attempts were beliefs ofthe rational decision to end life occurs in only a minority hopelessness and insomnia; severe, relentless anxiety, of patients and palliative care efforts need to be made often with intermittent panic attacks, depressed mood,before any decision to hasten death is reached. This recent conflict or loss, and alcohol abuse. The majority includes assessment of depression and hopelessness. of the patients developed symptoms within 3 monthsStudies in Oregon show that patients who died through before the suicide attempt, and most had experienced physician-assisted a suicide were 7.3 times more likely significant loss. The majority of the patients attemptedthan controlled patients to be concerned about loss of suicide impulsively. Interestingly, the majority of the independence and 9 times more concerned about loss of patients describedeeting, fl intermittent, transient but not bodily function, suggesting anxiety and possibly depresdisturbing thoughts of suicide and no persistent thoughts sion in the generation of decisions to end life (Cohen, of a plan. Particularly relevant to this discussion was thatet al., 2000). 41% of patients had some type of chronic medical illness. In the area of pain control, studies have shown patients Most of the patients had never attempted suicide before who request physician-assisted suicide do so because of and 88% had sought counseling from a healthcare prodepression and helplessness rather than from physical pain vider in the month prior to the attempt. (e.g., Emanuel, Fairclough, & Emanuel, 2000; Emanuel, 1997). Depression can be caused in part by poor pain control but is often related to a multitude of other factors PHYSICIAN-ASSISTED SUICIDE supporting discussions made earlier on pain, suffering, End-of-life issues have become increasingly importantand disability. In one large study van der Maas, van as attention shifts from curative to palliative care forDelden, and Pijnenborg (1992) showed only 5% of the patients nearing the end of life. Issues of withdrawingeuthanasia cases were motivated solely by pain. Another or withholding life support treatment and the legalizationstudy by Emanuel and Emanuel (1998) found patients of physician-assisted suicide in Oregon have stimulated experiencing pain were no more likely to request euthadiscussions among many health professionals and reprenasia than those without pain. sent a significant challenge to groups traditionally concerned with preserving rather than facilitating death. TheDISCUSSION AND TREATMENT IMPLICATIONS ethical and moral dilemmas faced by healthcare profesMedical illness is a significant risk factor for suicide, sionals are outside the scope of this discussion. Instead, a brief review of issues important to pain, depression,particularly in patients who are depressed and expressing beliefs of hopelessness. The presence of pain compounds and hopelessness are presented as explanations for why the problem and may increase the likelihood of suicide. patients request assistance from the physician to end It is important healthcare providers learn to formally their lives prematurely. Physician-assisted suicide remains a controversialassess and screen for depression and beliefs of hopelessness in general medical populations, particularly in issue, but one that has been discussed more openly in the

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patients with medical conditions where persistent painwith the pain, eliminating medications likely to precipitate is present. Studies have shown that when less formal depression and confusion, and encouraging the patient to screening is provided, even professionally trained mental increase levels of activity using the skills of pacing. health professionals often haveficulty dif recognizing the It is important that under certain circumstances presence of depressive symptoms and hopelessness extraordinary measures be taken to prevent the possibility (Haghbin, 1998). of suicide, particularly when patients express depression, It is important to also recognize in the assessmentbeliefs of hopelessness, excessive alcohol use, and are process that a general medical illness increases the likelireporting severe levels of anxiety and/or panic attacks. hood of suicide but having more than one physical illnessRecent losses of close personal relationships, global raises the risk of suicide substantially (Druss & Pincus,insomnia, and a sense that the medical condition is dete2000). Even when depression and alcohol use are adjusted, riorating are signs of which the clinician needs to be the relationship between medical illness and suicidalityparticularly aware. In addition, patients out of work and persists. As Druss and Pincus suggest, perhaps depression unable to find jobs, patients who are unskilled and feel and alcohol use do not necessarily mediate the relationship disenfranchised, and mothers with few social supports are between suicide and medical illness. Possibly other interparticularly prone to attempt suicide (Williams, 1997). mediate factors, such as disability, disruption of social An examination of the many risk factors for suicide supports, and chronic pain, may make an individual regard reveals the prevalence of these signs within the pain his life as no longer worth living. population. Although single-modality, unidimensional It is worth emphasizing that while studies have showntreatment approaches might be appropriate for shortthat depression and suicide are related, most patients term transient pain, they are inappropriate for persistent admitting to suicidal behavior do not meet criteria for pain, especially because pain is rarely a symptom that major depression. This strongly suggests assessing for exists in isolation. For the nonmalignant chronic pain suicidal ideation and intent, aside from examining forpatient, education, attention to emotional factors, focus signs of depression (Druss & Pincus, 2000). on function rather than cure, and attention to other probIt is imperative that healthcare professionals, not justlems such as sleep disturbance, are important in managmental health professionals, talk openly about depresing pain and should reduce the risk of suicide. These sion, death, and suicide with their patients. There is nosame general treatment recommendations are suitable for evidence these discussions will trigger suicidal behaviorthe cancer patient, except the physician should make (Henderson & Ord, 1997). In fact, more evidence existsevery effort to prevent the pain and to relieve it promptly. that these discussions help correct misconceptions, Also, fears about cancer need to be addressed and, like establish a strong rapport between the clinician andthe nonmalignant pain patient, what patients think about patient, and improve a patient’ s sense of personal control is important, especially in efforts to alleviate their fears (Henderson & Ord, 1997). and correct misconceptions. In cases where a patient admits to thoughts of suicide, It is helpful to conceptualize pain as a stressor that either through formal screening or in discussions with thecan promote a destructive stress response, leading to a patient, referral to a psychologist, psychiatrist, or othervariety of physiologic, cognitive, and behavioral conseappropriate mental health professional should be made. quences such as fatigue, myalgia, and impaired cognitive The discomfort many health professionals feel about ini-functioning (Chapman & Gavrin, 1999). Addressing the tiating this type of referral needs to be addressed, mostly pain problem by reducing the stress of pain and its conby the professional, because, as the author generally has sequences can involve reducing the unpleasant sensation found, if talked about in an open and honest manner, of pain, altering the perception of unpleasantness or the patients are not offended or upset but generally see the consequences of loss that are associated with pain, and importance of addressing psychosocial issues. modifying the body’s response to the stress through medThoughts of suicide and the risk of suicide should beications or relaxation. Developing skills to manage the assumed by the clinician when working with the medicalstressors more effectively, including pacing of activities, patient experiencing persistent pain. Addressing the probinteracting more effectively with physicians to participate lem directly, assessing for it aggressively in an open and in care, and understanding the mechanism of pain also honest manner, and applying solid pain management techmay be important. niques in an interdisciplinary setting, including attention The essential focus of treatment, however, starts with to behavioral medicine issues, are appropriate measures the recognition that the problems medical patients in pain for dealing with the potential problem of suicide. This present with are not alleviated by attention just to the requires attention to effective pain management practices sensation of pain. They are best dealt with when attention including educating the patient about better ways to manis directed to a multitude of other factors. It is up to the age and cope with pain, reducing the ambiguity and uncerclinician to formulate what problems are best managed to tainty about the future and the medical illness associated affect a change in patients. For example, in certain

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Emanuel, E.J., & Emanuel, L.L. (1998). The promise of a good patients, treating the depression and beliefs of hopelessdeath.Lancet, Suppl. 2,SII21–9. ness with cognitive restructuring techniques might be the Fishbain, D.A. (1999). The association of chronic pain and suimost effective approach, whereas other patients might cide. Seminars in Clinical Neuropsychiatry, (3), 4 benefit more from reducing their fears through simple 221–227. physical therapy activities. Still, in other patients, attention Fishbain, D.A., Cutler, R., Rosomoff, H.L., & Rosomoff, R.S. to social factors and isolation might be the best approach (1997). Chronic pain-associated depression: Antecedent to affect change in mood, pain, sleep, and hopefully suior consequence of chronic pain? A review. Clinical Jourcidal risk. nal of Pain, 13(2), 116–137. Whatever specific treatment measures are applied to Fordyce, W. (1988). Pain and suffering: A reappraisal. American affect change, it is important that they sustain hope, reduce Psychologist, 43(4), 276–283. uncertainty, contribute to pain acceptance and, in some Fox, B.H., Stanek, E.J., Boyd, S.C., et al. (1982). Suicide rates among cancer patients in Connecticut. Journal of cases, encourage patients to turn their attention to spiritual Chronic Disease, 35 , 89. needs (Duggleby, 2000). Haghbin, Z., Streltzer, J., & Danko, G. (1998). Assisted suicide and AIDS patients: A survey of physicians’ attitudes. Psychosomatics, 39 , 1, 18. REFERENCES Hall, R., Platt, D., & Hall, R. (1999). Suicide risk assessment: A review of risk factors for suicide in 100 patients who Allebeck, P., & Bolund, C. (1991). Suicides and suicide attempts made severe suicide attempts. Psychosomatics, 40 :1, 18. in cancer patients. Psychological Medicine, 21 , Henderson, J., & Ord, R. (1997). Suicide in head and neck 979–984. cancer. Journal of Oral and Maxillofacial Surgery, 55 , Beecher, H.K. (1959).Measurement of subjective responses. 1217–1221. New York: Oxford University Press. Annals Boor, M. (1980). Relationship between employment rates andHietanen, P., & Lonnqvist, J. (1991). Cancer and suicide. of Oncology, 2 , 19–23. suicide rates in eight countries: 1962–1967. PsychologHiggins, E.T., Bond, R.N., Klein, R., & Strauman, T. (1986). ical Reports, 47,1095–1101. Self-discrepancies and emotional vulnerability: How Buda, M., & Tsuang, M.T. (1990). The epidemiology of suicide: magnitude, accessibility, and type of discrepancy influImplications for clinical practice. In S. Blumenthal & ence affect.Journal of Personality and Social PsycholD. Kupfer (Eds.),Suicide over the life cycle: Risk facogy, 51,5–15. tors, assessment and treatment of suicidal patients . Kaplan, H.I., & Sadock, B.J. (1996). Pocket handbook of clinical Washington, D.C.: American Psychiatric Press. psychiatry (2nd ed.). Baltimore, MD: Williams & Cassell, E.J. (1982). The nature of suffering and the goals of medWilkins. icine. New EnglandJournal of Medicine, 306, 639–645. Marshall, J.R., Burnett, W., & Brasure, J. (1983). On precipitatChapman, C.R., & Gavrin, J. (1999). Suffering: The contribuing factors: Cancer as a cause of suicide. Suicide and tions of persistent pain. Lancet, 353 , 2233–2237. Life-Threatening Behavior, 13, 15. Charlton, J., Kelly, J.S., Dunnell, R., Evans, B., Jenkins, R., & . New Wallis, R. (1992). Trends in (factors associated with) Melzac, R., & Wall, P.D. (1983).The challenge of pain York: Basic Books. suicide deaths in England and Wales. Population Trends National Center for Injury Prevention and Control. (1999). Ten (London), 10–16 and 34–42. leading causes of death by age group. Atlanta: Centers Chochinov, H.M., Wilson, K.G., Enns, M., & Lander S. (1998). for Disease Control and Prevention. Depression, hopelessness, and suicidal ideation in the Nielsen, B., Wang, G.A., & Bille-Brahe, U. (1990). Attempted terminally ill. Psychosomatics, 39, 366–370. suicide in Denmark: Five years follow-up. Acta PsychiCohen, L., Steinberg, M., Hails, K., Dobscha, S., & Fischel, S. atrica Scandinavica, 81,250–254. (2000). Psychiatric evaluation of death-hastening Parker, S. (1998, October). Seeing suicide as preventable: A requests: Lessons from dialysis discontinuation. Psychonational strategy emerges. Christian Science Monitor , 3. somatics, 41,3, 195. Rosenfeld, B., Breitbart W., Stein K., et al. (1999). Measuring Druss, B., & Pincus, H. (2000). Suicidal ideation and suicide desire for death among patients with HIV/AIDS: The attempts in general medical illnesses. Archives of Interschedule of attitudes toward hastened death. American nal Medicine, 160,1522. Journal of Psychiatry, 156, 94–100. Duggleby, W. (2000). Enduring suffering: A grounded theory analSuicide trends ysis of the pain experience of elderly hospice patientsSainsbury, J., Jenkins, J., & Baert, A.E. (1981). in Europe. Copenhagen: World Health Organization, with cancer.Oncology Nursing Forum, 27 (5), 825. Shuster, J., Breitbart, W., & Chochinov, H. (1999). Psychiatric Emanuel, E. (1997). The painful truth about euthanasia. Wall aspects of excellent end-of-life care. Psychosomatics, Street Journal, 23 , 1, 123. 40:1, 1. Emanuel, E.J., Fairclough, D.L., & Emanuel, L.L. (2000). AttiStenager, E.N., Stenager, E., & Jensen, K. (1994). Attempted tudes and desires related to euthanasia and physiciansuicide, depression and physical diseases: A 1-year folassisted suicide among terminally ill patients and their low-up study.Psychotherapy and Psychosomatics , 61, caregivers.Journal American Medical Association, 284 65–73. (19), 2460–2468.

Pain, Disease, and Suicide

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Tearnan, B.H., & Lewandowski, M.J. (1992). The Behavioral Venkoba, R. (1990). Physical illness, pain, and suicidal behavior. Crisis, 11(2), 48–56. Assessment of Pain Questionnaire. Journal of the AmerWall, P. (2000). Pain: The science of suffering. New York: ican Academy of Pain Management, (4),2 181–191 . Columbia University Press. Turk, D.C., & Waddell, G. (1992). Clinical assessment of low Williams, M. (1997).Cry of pain: Understanding suicide and back pain. In D.C. Turk & R. Melzack (Eds.), Handbook self-harm. London: Penguin Books. of pain assessment (pp. 15–36). New York: Guilford. van der Maas, P., van Delden, J., & Pijnenborg, L. (1992). Euthanasia and other medical decisions concerning the end of life. Amsterdam: Elsevier.

63 Assessing the Veracity of Pain Complaints and Associated Disability Michael F. Martelli, Ph.D., Nathan D. Zasler, M.D., F.A.A.P.M.&R., F.A.A.D.E.P., C.I.M.E., D.A.A.P.M., Keith Nicholson, Ph.D., Treven C. Pickett, A.B.D., Psy.D., and V. Robert May, Rh.D. INTRODUCTION

pain patients, but there are significant problems with the reliability of any such estimates and an absence of reliable Evaluation of pain complaints and pain-related disabilitiesmethodologies for detecting malingering in chronic pain presents a significant diagnostic challenge. In cases of patients. However, it should be noted that pain evaluation clear, severe, and/or functionally disabling physicalreferrals also frequently involve such contexts as healthpathology and pain, the evaluations and opinions of most care insurance policy coverage, disability insurance policy healthcare practitioners are fairly consistent. In mostapplication, social security disability application, personal cases, however, where physical findings are less, clear injury litigation, worker’s compensation claims, funcpractitioners who specialize in pain and disability assesstional capacity evaluations, and determination of capacity ments may express widely varying opinions. Medical evi-for work. In these medicolegal situations, the incidence dence is often problematic or disputable and the relationof symptom exaggeration and malingering may be signifship between physical findings and subjective report isicantly higher (Rohling & Binder, 1995; Binder & frequently weak. Pain, ultimately, is a subjective com-Rohling, 1996). plaint that is difficult to verify or refute (Hall & Pritchard, Importantly, the evaluation of pain complaint and 1996; Merskey, 1986). Finally, despite recent biopsycho-pain-associated functional impairment and disability may social and psychophysiologic advances in terms of underbe one of the more confounded and misunderstood areas standing, simplistic and dichotomous conceptualizationsof healthcare-related work. The task of making determiremain overly represented (Martelli, 2000). nations regarding pain severity, impact, and related funcTraditionally, pain and pain-related disability evalua- tional impairment and disability is fraught with potential tions have been conducted by such specialists as physiaobstacles and pitfalls. This is, of course, due to the poorly trists, orthopedists, neurologists, neurosurgeons, psychiaunderstood and complex nature of the deficits involved, trists, psychologists, and neuropsychologists. Further,as well as the lack of formal, scientifically validated condiagnosis and treatment are the presumed reasons for ceptual models and “rating systems. ” Disentangling the assessment, and the estimation of frank malingering, as multiple contributors to subjective pain experience and well as significant exaggeration of symptoms, is generallyassociated functional disability requires careful scrutiny. estimated to be less than 20% (Martelli, Zasler, Mancini, Chronic pain patients may present with some response & MacMillan, 1999). A recent review by Fishbain, Cutler, bias to report pain or related disability. In the present Rosomoff, and Rosomoff (1999) indicates that malinger-chapter, response bias is defined as a class of behaviors ing might be present in between 1 and 10% of chronicthat reflects less than fully truthful, accurate, or valid 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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symptom report and presentation. Importantly, response responses, can take several forms. Bias ranges from bias is a ubiquitous phenomenon affecting almost anyinterpretations of symptoms that may be minimized to domain of human self-report. However, in the context ofexaggerated or feigned, and that may be accurately or medicolegal or insurance presentations, with which thisinaccurately attributed to different events. For instance, chapter is primarily concerned, the prevalence or impor-pre-existing symptoms may suddenly be attributed to an tance of such bias becomes more acute (Rohling & Binder, accident, symptoms previously not noticed suddenly may 1995; Binder & Rohling, 1996; Youngjohn, Burrows, & be given such vigilant attention that attention and anxiety Erdal, 1995). Given frequent financial and other incentivesalone produce signifi cant increases, or an accident may to distort symptoms and performance during examinations cause an aging person to do a self-inventory of health conducted in medicolegal or insurance contexts (i.e.,that reveals symptoms due to aging that were present but healthcare policy coverage, disability insurance, socialpreviously minimized. Further, a heightened awareness security disability, personal injury litigation, worker ’s or vigilance effect can lead to focusing and sensitization compensation claims, functional capacity, and work eval-to problems which would otherwise be innocuous. In uations), assessment of examinee veracity and motivation addition, environmental realities also exert uence infl to provide accurate and full effort during assessmentover response to injury and symptoms. For example, the becomes critical. The importance of detecting response vastly different consequences for diagnoses of cancer vs. biases or invalid symptoms is crucial with regard tomild traumatic brain injury or back injury produce difincreasing the likelihood of diagnostic accuracy. Accurateferential reinforcement; the former is clearly undesirable diagnosis is prerequisite to provision of appropriate andand negative, while the latter can result in highly desirtimely treatment and prevention of iatrogenic impairmentable monetary compensation. and disability reinforcement; it is also critical to approMartelli et al. (1999) reviewed the literature and found priate legal compensation decisions. that the following injury context variables were associated Medicolegal and insurance assessments, with their with poorer post-injury adaptation and recovery, and significant consequences of determination decisionsincreased likelihood of response bias. regarding impairment and disability, require the following in order to ensure validity: (a) an accurate assessment of 1. Anger or resentment or perceived mistreatment possible response bias to report pain or related disability; 2. Fear of failure or rejection (e.g., damaged (b) an accurate assessment of attribution, i.e., whether pain goods; fear of being fired after injury) and related problems are correctly being attributed to the 3. Loss of self-confidence and self-ef ficacy assocompensable cause; and (c) sensitivity, specificity, utility, ciated with residual impairments and ecological validity of assessment measures. 4. External (health, pain) locus of control Blau (1984; 1992) has expounded on the importance 5. Irrational fear of injury extension, reinjury, of determining response biases and measuring true levels or pain of impairment in medicolegal situations. Essentially, in 6. Discrepancies between personality/coping style this arena, an alleged victim of a wrongful act or omission and injury consequences (e.g., very physically attempts to establish (a) causality in order to demonstrate active person with few intellectual resources entitlement to compensation for damages, which is who has a back injury) awarded based on (b) level of damages suffered. In cases 7. Insufficient residual coping resources and skills of less obvious, clear-cut, and significant trauma with 8. Prolonged inactivity resulting in disuse atrophy psychologic, neurologic, or soft tissue damage, causality 9. Fear of losing disability status, benefits, and and level of current and future damages are more ficult dif safety net to prove and expert evaluation and opinion are heavily 10. Perceptions of high compensability for injury relied upon for making legal determinations. In the paral- 11. Preinjury job (task, work environment) dissatlel insurance situation, the insured attempts to access entiisfaction tlements to healthcare treatment and disability benefits, 12. Collateral (especially if “silent”) and expert evaluation and opinion are relied upon for 13. Inadequate and/or inaccurate medical information making policy determinations. In both cases, financial and 14. Misdiagnosis, late diagnosis, or delays in instiother incentives clearly represent motivational factors that tuting treatment increase the likelihood of response bias in the form of 15. Insurance resistance to authorizing treatment or exaggerated or feigned symptoms. delays in paying bills 16. Retention of an attorney 17. Greater reinforcement for “illness” vs. “wellEXAMINING PATIENT RESPONSE BIASES ness” behavior Examinee response bias, or predilections toward less 18. Dichotomous (organic vs. psychologic) conceptualizations of injury and symptoms than fully valid, accurate, and effortful behavioral

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help and who, upon confronting tests that seem These variables represent vulnerability factors that can different and maybe easier than the real-life reduce effective coping with post-injury impairments and situations where they have problems, reduce increase the likelihood of maladaptive coping and effort to highlight their problems. response bias. Importantly, these variables are not mutually exclu5. Sociopathic, Manipulative, and Opportunistic sive, and, as with the variables presented below, more than (SMO) types. These rather self-explanatory one can contribute to symptom report and presentation styles can be found in all groups. Additional review of the literature, balanced with clin6. Passive Aggressive or Impatient or Rebellious ical experience, identifies the following significant sources types, representative of those who resent othof response bias that can be seen during examinations ers not listening to them and believing them (Martelli, 2000). at face value, and resent imposed evaluations or doctor’s visits, especially ones that examine psychological function or motivation. They 1. Cultural Differences. For example, many nonmay play games with doctors by withholding Western cultures mix emotional and physical or undermining procedures or treatments, and pain and symptoms at a conceptual and phemay especially alter performance or play nomenological level. Also, some cultures see games on tests that seem nonchallenging or failure to impose severe penalty/extract signifunrelated to real life situations. icant compensation for harm as a sign of weakness and disgrace in God’ s eyes. 7. Psychologically Decompensated types, i.e., the extremely dysfunctional patient who is usually 2. Reactive Adversarial Malingering (RAM) easily recognizable. based on fear, mistrust of the opposing ’s side honesty, or mistreatment (e.g., from assumed 8. Those who don’ t take our examinations or tests “ facts” in many work settings and cultures, as seriously as we do. The authors have some including plaintiff attorney groups) resulting very limited but relevant survey data suggesting in a deliberate pendulum-like overplaying of that plaintiffs may take our examinations a little symptoms. This may be especially charactermore seriously than defendants. In contrast, istic in persons/groups with tendencies weathermen seem to be taken more seriously toward suspiciousness, including immigrants, than independent examiners by persons who outsiders, or those who feel chronically have not graduated high school, while indepenunderprivileged. dent examiners seem to fare better with those who have been to college. 3. Conditioned Avoidance Pain-Related Disability (CAPRD), or, roughly, phobic or extreme anxiety reactions wherein activity (mental or physImportantly, a too often overlooked form of bias is ical) is associated with anticipation of an one that is iatrogenic to the nature of the insurance and exacerbation of pain, with such stress possibly adversarial legal system. In an effort to elucidate expectresulting in an actual exacerbation. Kinesiopho- ancy influences and bias for persons sustaining injuries, bia and cogniphobia are two types. Martelli, Zasler, and Grayson (2000) collected survey atti4. Desperation Induced Malingering (DIM) or tudinal data from professionals who work with injured Desperation Induced Symptom Exaggeration Worker’s Compensation (WC) patients. A summary of the (DISE), e.g., insecure immigrant workers, preliminary data is offered in Table 63.1, broken down by aging workers, tired workers, workers insecure the three sample groups: (1) disability evaluators, comabout work changes, immigrants who tried prised of physicians, chiropractors, physical therapists, introjection and feel resentful that they were not and vocational evaluators; (2) staff from a rehabilitation rewarded, persons who recently climbed back neuropsychology service; (3) attendees at a case manageon the horse only to get knocked off again with- ment conference, including over 50% WC case managers. out belief they can climb back in the saddle one These data are quite compelling. Overall, approximately more time, workers fearing their own limited 25% of WC patients are believed to be exaggerating or or declining abilities, real or imagined abuse malingering, with higher rates evidenced by WC case from employers, family, etc., immigrants who managers. This suggests a general skepticism and distrust feel rejected by the culture and feel entitled, faced by injured persons during evaluations. In contrast, immigrants who feel disillusioned because the the majority of professionals filling out the survey believed new land was not everything they had hoped — they would be treated unfairly by the WC system if they i.e., those who believe this to be a viable solu- were injured, suggesting a general skepticism and distrust tion to a desperate situation. Probably also of the extant systems that fund evaluation and treatment included are those making desperate pleas for of injury and disability.

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TABLE 63.1 Survey of Attitudes Regarding Worker’s Compensation (WC) Respondent Sample (%)

Question % Injured workers who fake/exaggerate/malinger % Injured workers that WC insurance treats < fairly % Employers who treat injured workers < fairly Likelihood your employer would treat you < fairly Likelihood WC would treat you if injured < fairly

Disability Evaluating Professionals (N = 17) 19.2 49.2 53.5 43.75 60.0

Medical Psychology Service Staff (N = 7) 24.7 62.5 41.2 54.2 65.9

Case Managers (N = 16) (including 7 WC employees) 28.5 23.2 32.7 46.4 48.9

Despite the preliminary nature of these data derivedas primarily suggestive of simulated or exaggerated incafrom small samples and the fact that generalizabilitypacity included across situations cannot be assumed, they nonetheless seem compatible with the levels of diffuse distrust 1. Failure to comply with reasonable treatment observed by the authors in medicolegal situations. These 2. Report of severe pain with no associated psydata highlight the importance of considering the much chological effects different set of motivational factors that operate on exam- 3. Marked inconsistencies in effects of pain on inees that present to independent evaluation. In addition, general activities they strongly argue for deliberate and thorough prepara- 4. Poor work record; history of persistent appeals tion of examinees prior to the examination. against awards 5. Previous litigation In an interesting theory about a major type of response bias in chronically disabled workers, Matheson Features identifi ed as not primarily suggestive included (1988; 1990; 1991a; 1991b) conceptualizedsymptom a“ magnification syndrome”based on a careful analysis of injured industrial workers. He defi ned this syndrome as 1. Mismatch between physical findings and a conscious or unconscious self-destructive (e.g., blocks reported symptoms return to productive activity) and socially reinforced pat2. Report of severe or continuous pain tern of symptoms, which are intended to control life 3. Anger circumstances of the sufferer, but which impede health- 4. Poor response to treatment care efforts. He further defi nes three major subtypes, and 5. Behavioral signs/symptoms provides classifi cation guidelines for evaluation via observation during performance of simulated work tasks A brief review of important sources of bias, or threats completed within functional capacity evaluations. Theto objectivity, which require assessment during evaluaType I “refugee”is defined as displaying illness behavior tion of physical, sensory, and neurocognitive impairthat provides escape or avoidance of life situations perments follows. ceived as unsolvable. Somatization, conversion, psychogenic pain, and hypochondriacal disorders are conATTRIBUTION AND BIAS ceptualized as extreme subcategories for this type. The Type II “game player”employs symptoms for positive Examinee attribution bias can confound accurate diagnogain. Although this type seems associated with the psysis. Examples include mistaking clinical entities like chiatric diagnosis of malingering, Matheson argues thatdepression or sleep disturbance and concomitant physical, true malingering is a medicolegal concept, while Typememory, or motivational problems for physical injury and II symptom magnifying is a treatable self-destructivepain-related sequelae. This can occur due to misattribution syndrome. The Type III“ identified patient”is motivated or over-attribution or retrospective attribution, or illusory by maintenance of the patient role as a means of lifecorrelation, or heightened awareness due to vigilance survival. Associated psychiatric diagnoses include facti-biases. Importantly, conditions like depression and sleep tious disorder (May, 1999). disturbance are reversible and may have even been present Main and Spanswick (1995) also examined simulatedpre-injury without producing significant limitations. Furor exaggerated incapacity in persons claiming physicalthermore, these factors may be interacting with true physdisability. They identified a list of features associated withical injury symptoms to increase distress, prolong impairment, and interfere with recovery. Finally, such factors as simulated or exaggerated incapacity. Features identified

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presence of vigilance to symptoms can increase physio- Symptom magnification, in contrast, refers to exaglogic arousal and lead to increased symptomatology and geration of impairment and can occur in relation to mulperceptions of impairment, in a vicious cycle. tiple factors and serves a wide range of psychological Examiner misattribution can similarly occur. Only needs (e.g., efforts to legitimize latent dependency needs, resolve pre-existing life confl icts, retaliate against methodical medical and psychological assessment can difemployer or spouse or other, reduce anxiety, exert a “plea ferentiate sequelae secondary to, for example, brain injury for help, ” or solicit acknowledgment of perceived ficuldif from chronic pain. Tendencies toward over-diagnosis of ties). Symptom exaggeration always promotes passivity brain injury-related disorders by brain injury specialists and helplessness and an external locus of control and is a given abnormal neurocognitive findings and/or nonspesignificant impediment to rehabilitation (Martelli, Zasler, cific somatic complaints not exclusively pathognomonic of brain injury can be avoided only through careful dif- & Grayson, 1999b). ferential diagnosis. Brain injury specialists sensitized to Symptom exaggeration also can occur in patients with premorbid histories of psychologic problems who “latch neurologic symptoms have been observed by the authors on” to a specific diagnosis that not only becomes responto misdiagnose chronic pain sequelae as post-concussive symptoms, which may result in iatrogenic impairmentsible for all life problems, but also promotes passivity and helplessness and an external locus of control. When associated with an escalation of medical costs, prolongation of inappropriate treatment, and eventual failure thatpatients are assessed for claims of major disability following uncomplicated mild whiplash or soft tissue injuries, produces helplessness and chronic disability (e.g., nonrenonorganic contributors should be closely scrutinized. solving post-concussive disorders) and misperceptions in Depression, post-traumatic stress disorders, anxiety conthe injured person. Conversely, similar observations have ditions, and other psychiatric syndromes generally have a been made for psychiatrists and psychologists prone to infer psychiatric etiologies for all pathology, including favorable psychological and functional prognosis given pain and physical injury sequelae (Main & Spanswick,timely and appropriate assessment and treatment. Misdiagnosis of these conditions serves to promulgate misper1995; Martelli, Zasler, & Grayson, 1999a). ceptions and amplify functional disability and healthcare costs. THE RESPONSE BIAS CONTINUUM Malingering, as defi ned in the DSM-IV (p. 683) As indicated above, for the purposes of this chapter,(American Psychiatric Association, 1994) is “…the intenresponse bias is defined as any behavioral predisposition tional production of false or grossly exaggerated physical involving less than fully truthful, accurate, and valid or psychological symptoms, motivated by external incensymptom report and presentation. This includes less than tives such as avoiding military duty, avoiding work, fully effortful behavioral responses displayed on formalobtaining financial compensation, evading criminal prosand informal interview and examination procedures. For-ecution, or obtaining drugs. ” Malingering should be susmal assessment of response bias, which is frequently lackpected if any combination of the following is noted: ing or only haphazardly attended to in most clinical examinations, represents the only assurance that clinical exam 1. Medicolegal context of presentation findings are accurate and valid reflections of pain severity, 2. Marked discrepancies between claimed stress frequency, and functional impairment levels. Response or disability and objective findings bias appears best conceptualized on a continuum that 3. The presence of Antisocial Personality Disorder extends from Therefore, measures of malingering, or deliberate symp1. Denial and unawareness of impairments, tom production for purposes of secondary gain, should 2. Symptom minimization, always be administered in cases of medicolegal presenta3. Symptom magnification/exaggeration to tion, suspicion of any disincentive to exhibit full effort, or 4. Frank malingering. suspicion of sociopathic personality disorders. According to Lipman’s typology (1962), malingering Denial and unawareness refer to either psychologiccan be categorized into four categories: (1) fabrication of or organic phenomenon wherein impairments are undernonexistent symptoms; (2) exaggeration of symptoms that appreciated due to dysfunction of brain operations subare presented as worse than in actuality; (3) extension of serving awareness or psychological repression to guard symptoms that have actually improved or resolved; and against distressful realizations. Symptom minimization(4) misattribution or fraudulent attribution of symptoms is a related, but more consciously motivated desire, and to an injury when they actually preceded, postdated, or usually involves an attempt to minimize the impact of are otherwise unrelated. Notably, exaggeration is considundesirable functional restrictions or distress (Martelli,ered much more frequent than fabrication, while more et al., 1999a). than one category can occur in a single person. Finally,

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Some major exam findings that are inconsistent with as Miller (2001) notes, different combinations of types can occur in persons with more than one problem (e.g., structural lesions include patchy sensory loss, pain in a chronic pain, PTSD, post-concussion syndrome), whichnondermatomal distribution, nonpronator drift, and/or can further co-occur with other psychological syndromesastasia-abasia. Motor and other impairment inconsisten(e.g., somatoform and personality disorders). cies that fluctuate or disappear under hypnosis, drugassisted interviews or “presumed” nonobservation may certainly increase the index of suspicion regarding nonIDENTIFYING RESPONSE BIAS organicity, although exceptions to this rule do exist. Faked The difficulty with defining pain, actual accentuation of hemiparesis is typically more common on the left side, the pain response (e.g., hyperpathia) seen in some chronic perhaps due to the fact that most persons are right-hand pain problems, response bias to reported pain, and its posdominant. Consistency regarding laterality of symptoms, sible deception, makes the assessment of pain-related comparticularly with referred pain and/or neurologic impairplaints extremely challenging. Pain, defi ned as an unpleas- ment, should be evaluated. ant sensory and emotional experience associated with Clinicians evaluating chronic pain must be familiar actual or potential tissue damage (Merskey, 1986), is a with psychosocial syndromes that may present as pain, complex multidimensional subjective experience mediated including by emotion, attitude, and perception. Unlike other modalities, it is not possible to devise simple signal detection 1. Factitious disorder , or the intentional producparadigms for the evaluation of response bias given that tion or feigning of physical symptoms, or exagthis is a subjective experience with no clear objective refgerated expression of physical conditions in erents, especially in the case of chronic pain associated order to adopt a sick role with actual injury and nociception or abnormal function of 2. Somatoform disorders , characterized by preocthe nervous system. Clearly, multiple variables may impact cupation with physical symptoms and pain that on pain reporting and behavior. For example, arousal, exceeds possible organic pathology stress, tension, and anger all may exacerbate subjective , or preoccupation with pain as reporting of pain and pain behavior, as may depression, 3. Hypochondriasis part of a conviction that it is a part of a pernithrough effect on physiologic function. Psychoemotional cious disease process and psychosocial concomitants of chronic pain must also , or the expression of frank be appreciated, including loss of self-esteem, lowered frus- 4. Conversion disorder psychiatric disorder via some symbolic transtration tolerance, depression, sexual dysfunction and formation decreased libido, and anger and guilt. Further, situational factors make additional contributions to pain-related complaints. The context of an exam, however, typically requires Clinicians should also be familiar with symptoms related to pain imperception. Pain complaints should that psychological and physical pain factors be addressed be assessed, in part, when of CNS origin as opposed individually, despite the fact that these components are typically inextricably intertwined with one another, as well to psychogenic, by concurrently assessing temperature as such affective conditions as depression and anxiety. perception, given that the same neural pathways mediPhysicians should be familiar with exam strategiesate these sensations. When temperature sensation is designed to evaluate disorders with (a) probable “func-preserved in the presence of a loss of pain sensation, after either brain or spinal cord injury, theficit de is not tional” components, or symptoms that seem more strongly likely to be organic (the loss should occur contralateral associated with psychosocial vs. structural factors, as well to and below the level of the lesion). This point also as (b) feigned symptoms, including bedside exam techbelabors the fact of understanding the neuropatholniques for physical and cognitive “malingering. ” Examples include such strategies as Hoover’ s test for evaluation ogy/pathology of the lesion based on imaging studies fi have for anticof malingered lower extremity weakness, sideways/back-and the implications that thesendings ipated clinical exam ndings. fi Alleged pain impercepward walking for assessment of feigned gait disturbance, and a positive Stenger’ s test on audiologic assessment for tion can be evaluated, as can any impairment for that matter, with appropriately designed forced choice testnonorganic hearing loss. Other tests that might be of value ing. Additionally, examiners should realize that alleged in the context of response bias detection on the physical dif to examination include Mankopf ’s maneuver, strength reflex pain imperception or loss of sensation isficult test, arm and/or wrist drop test, hip adductor test, axialfake upon repeated bilateral stimulation. This is due to loading test, Gordon-Welberry toe test, Bowlus and Cur-the fact that examinees who exaggerate rely on subjecrier test, Burns bench test, Magnuson’ s test, among others tive strategies rather than truly responding to the [(Babitsky, Brigham, & Mangraviti, 2000); see also strength of the stimuli. Therefore, assessments such as Table 63.3 for a relatively comprehensive listing]. Von Frey hairs could be utilized in the aforementioned

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scenario to provide further objective evidence of response bias during exams should, therefore, be emphafeigned sensory defi cits. sized with regard to optimizing accurate performance It is worth emphasizing that the presence of structuraland assessment. Clinicians should familiarize themselves with the wide variety of simple yet effective anxiety inconsistencies, a nonorganic syndrome and/or response management interventions. bias does not necessarily exclude the diagnosis of another organic syndrome. This certainly complicates the process With regard to assessment of psychological/psychiatof disentangling multiple clinical entities that sometimesric, somatic, and neuropsychological impairments, includcoexist. Unfortunately, the science and art of methodicing chronic pain, response bias represents an especially important threat to validity. Because these assessments differential diagnosis are too often underappreciated in the usually begin with an interview about self-reported sympevaluation process (Martelli, et al., 2000). A relevant screening procedure frequently used bytoms and subsequently rely heavily on standardized measures of performance on tests which are variably normed, physical therapists, doctors, and chiropractors for estimating when psychological factors are significantly influenc-their validity requires the veracity, cooperation, and motivation of the patient for obtaining valid performance ing pain-related responses is the assessment for Waddell’ s Nonorganic signs (Waddell & Main, 1984; Waddell, Main, measures. Recent evidence, however, strongly suggests Morris, Paoloa, & Gray, 1984; Waddell, 1999). These arethat patients seen for presumptive injury-related impairments over-report preinjury functional status (Lees-Haley, listed below: Wil-liams, Zasler, Margulies, English, & Steven, 1997). This is especially true with post-concussive and pain Screening for Nonorganic Response Bias: Waddell Signs related deficits because these symptoms often appear with 1. Overreaction similar frequency in the general population (Lees-Haley Guarding/limping, bracing, rubbing affected area, grimacing, & Brown, 1993). In addition, the demonstrated ability of sighing. physicians and psychologists to accurately detect malin2. Tenderness gering in examinations and test protocols has been less Widespread sensitivity to light touch of superficial tissue. than impressive (Hall & Pritchard, 1996; Loring, 1995). 3. Axial loading Light pressure to skull of standing patient should not significantly Nonetheless, various instruments, techniques, and strategies are available that have demonstrated at least some increase low back symptoms. utility in detecting response bias, especially malingering, 4. Rotation Back pain is reported when shoulders and pelvis are passively as a means of increasing confidence in appropriate motirotated in the same plane. vation during examination, and hence the validity of 5. Straight leg raising assessment findings. Marked difference between leg raising in the supine and seated In Table 63.2, a general summary of hallmark and position. selected signs of response bias are presented. The signs 6. Motor and sensory are predicated on examination of inconsistencies and can Giving way or cog wheeling to motor testing or regional sensory certainly be applied to most aspects of comprehensive loss in a stocking or nondermatomal distribution (rule out medical and psychological evaluations for chronic pain. peripheral nerve dysfunction). In Table 63.3, a summary of some very specifi c response bias detection measures and strategies, along Additional nonorganic signs include lower extremity with guidelines, is presented in an integrated format. giving way, no pain-free spells in the past year, intolerance Importantly, these strategies are presented as illustrations of treatments; and emergency admissions to hospital with of indicators of important information for interpreting back trouble. examinationfindings and test data within a larger context Importantly, the presence of Waddell’ s or other non- of multidisciplinary evaluation for chronic pain. This organic signs does not exclude physical components as approach integrates contextual information, history, the cause of low back pain. Rather, they suggest only behavioral observation, interview data, collaborative data, that psychological factors appear to be uencing infl the and personality data with measures of effort or perforpatient’s responses and behavior. Notably, physical andmance (or symptom exaggeration or malingering) and psychologicalfindings are not mutually exclusive, and physical examination, medical and neuropsychological psychological factors may more often be a result of lowexamination performance data. This approach potentially back pain than a cause (Simmonds, Kumar, & Lechelt,offers increased reliability with regard to estimating the 1998). Further, recent reports strongly demonstrate the degree to which an examinee is responding truthfully and relationship between high levels of anxiety and nonor-exerting full effort or withholding or distorting effort or ganic responses during physical exams in chronic lowperformance, and the degree to which specific and general back pain (Hadjistauropoulos & LaChapelle, 2000). Astest results from multiple assessment areas are reliable and such, the importance of minimizing anxiety-related valid and reflect true abilities.

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TABLE 63.2 Response Bias: Hallmark Signs 1. Inconsistencies within and between the following (given absence of significant psychiatric, attentional, comprehension, or other disorders where inconsistencies are not uncommon): a. Reported symptoms b. Examination/test performance c. Clinical presentation d. Known diagnostic patterns e. Observed behavior (in another setting) f. Reported symptoms and exam/test performance g. Measures of similar abilities h. Similar tasks or tasks within the same exam or test (especially when ficultdif tasks are performed more easily than easy ones) i. Different examination sessions 2. Grossly impaired performance and extreme complaints a. Poorer performance and more extreme complaints vs. established expectancies or normative data for similar injury/illness b. Very poor performance on easy tasks (especially when presented ficult) as dif c. Failing tasks that all but severely impaired perform easily 3. Lack of specific diagnostic signs of impairment 4. Specific signs of exaggeration/dissimulation/malingering on psychological testing a. Minnesota Multiphasic Personality Inventory (MMPI/MMPI-2) Original and additional validity scales: L, F, Fb, Fp, Ds, K,TRIN, VRIN, F-K, Fake Bad, etc. b. Personality Assessment Inventory (PAI) Validity scales (inconsistency, infrequency, positive and negative impression management) and 8 malingering and 6 suspected malingering patterns c. Pain Assessment Battery (PAB): Symptom magnification, extreme beliefs frequency and other “validity” indicators d. Millon Behavioral Health Inventory (MBHI) validity scales (3) e. Hendler (i.e., Mensana Clinic) Back Pain Test: scores of 21–31 (exaggerating) f. Cognitive malingering detection tests (e.g., memorization of 15 items test, Digit Recognition Tests, Computerized Assessment of Response Bias, Word Memory Tests, Word Memory Test, Word Completion Memory Test, etc.). 5. Interview evidence a. Nonorganic temporal relationship of symptoms to injury b. Nonorganic symptoms, or symptoms that are improbable, absurd, overly ficspeci or of unusual frequency or severity (e.g., triple vision) c. Disparate examinee history/complaints across interview or examiners d. Disparate corroboratory interview data vs. examinee report 6. Physical exam findings a. Nonorganic sensory findings b. Nonorganic motor findings c. Pseudoneurologic findings in the absence of anticipated associated pathologic findings d. Inconsistent exam findings e. Failure on physical exam procedures designed to specifically assess malingering

Empirical support exists indicating that each of theseas an optimal method for estimating the degree of effort indicators has some utility in detecting dissimulation oror performance and the degree to which test results are * Examining the pitfalls and limitations reliable and valid and reflect actual abilities. Notably, in suboptimal effort. of each of these procedures, both conceptual and methodevaluation of response bias and malingering, as in evaluological, is well beyond the scope of this chapter. How-ation of pre- and post-injury status, the following investiever, increasing evidence exists for improved discrimina-gative tools may be used in conjunction with interviews tion and increased reliability when multiple measures areand examination and testing: (1) school records; (2) medemployed. The conceptual approach offered by the proical records; (3) driver records; (4) service and criminal posed Motivation Assessment Profi ling (MAP) is one records; (5) employment records; (6) psychological/psywhere behavioral observation, interview, collaborative,chiatric records and reports; (7) interviews with family historical, personality, and contextual data with neuropsy-members, friends, teachers, and employers, etc.; (8) any chological and medical performance data and measures other available materials (e.g., from attorneys through forof effort or performance (or response bias) are integrated mal discovery). Importantly, the strategies and guidelines offered in Table 63.3 are presented as important indicators for * See starred references.

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TABLE 63.3 Response Bias Detection Measures and Strategies Pain Assessment Measures with Built-In Response Bias Indicators Pain Assessment Battery (PAB), Research Edition Symptom Magnification Frequency (SMF) > 40% Proposed clinical hypothesis procedure evaluating Extreme Beliefs Frequency (EBF) > 35% Four other “validity” indicators (i.e., alienation, rating percent of max, % extreme ratings (2 scales)) Millon Behavioral Health Inventory (MBHI) Elevations on 3-item validity scale Hendler (i.e., Mensana Clinic) Back Pain Test Scores of 21–31 (Exaggerating) Scores > 31 (Primary psychological influence) Medical Indicators Test for malingered lower extremity weakness associated with normal crossed extensor response Astasia-abasia “Drunken type” gait with near-falls but no actual falls to ground Nonorganic sensory loss Patchy sensory loss, midline sensory loss, large scotoma in field, visual tunnel vision Nonorganic upper extremity drift Long tract involvement results in pronator type drift; proximal shoulder girdle weakness and malingering typically present with downward drift while in supination Stenger’s Test Test for malingered hearing loss during audiologic evaluation Gait discrepancies when observed vs. not observed If organic, should be consistent regardless of whether observed or not Gait discrepancies relative to direction of requested ambulation Gait for a patient with hemiparesis should present similarly in all directions; malingerers do not as a rule practice a feigned gait in all directions Forearm pronation, hand clasping, and forearm supination test for Malingeredfinger sensory loss is dif ficult to maintain in this perceptually digit/finger sensory loss confusing, intertwined hand/finger position Pain vs. temperature discrepancies Because both sensory modalities run in the spinothalamic tract, they should be found to be commensurately impaired contralateral to the side of the CNS lesion Lack of atrophy in a chronically paretic/paralytic limb Lack of atrophy in a paralyzed/paretic limb suggests the limb is being used or is getting regular electrical stimulation to maintain mass Impairment diminishes under influence of sodium amytal, hypnosis All these observations are most consistent with nonorganic presentations or lack of observation including consideration of malingering or conversion disorder Incongruence between neuroanatomical imaging and neurologic Lack of any static imaging findings on brain CT or MRI in the presence examination of a dense motor or sensory deficit suggests nonorganicity Arm drop test An aware patient malingering profound alteration in consciousness or significant arm paresis will not let his own hand, when held over his head, drop onto his face Presence of ipsilateral findings when implied neuroanatomy would An examinee claiming severe right-brain damage who claims right-eye dictate contralateral findings blindness and right-sided weakness and sensory loss Tell me “when I’m not touching” responses An examinee with claimed sensory loss who endorses that he does not feel you touch him when you ask him to tell you “if you do not feel”this. Lack of shoe wear in presence of gait disturbance An examinee with claimed longer term gait deviation due to orthopedic or neurologic causes should demonstrate commensurate wear on shoes (if worn with any frequency) Calluses on hands in “totally disabled” examinee An examinee who is unable to work should not present with signs of ongoing evidence of physical labor Assistive device “wear-and-tear” signs In any examinee using assistive devices for any period of time, e.g., cane, crutches, there should be commensurate wear on the device consistent with the claimed impairment and disability Mankopf’s maneuver Increase in heart rate commensurate with nociceptive stimulation during exam (some controversy exists on whether this always occurs) Lack of atrophy in a limb that is claimed to be signi ficantly impaired If side-to-side measurements and/or inspection do not bear out atrophy consider other causes aside from one being claimed

Hoover’s test

continued

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TABLE 63.3 (CONTINUED) Response Bias Detection Measures and Strategies Sudden motor give-away or ratchitiness on manual strength testing Considered to normally be a sign of incomplete effort omor sympt exaggeration Weakness on manual muscle testing without commensurate Suggests simulated muscle weakness if longstanding asymmetry of DTRs or muscle bulk Toe test for simulated low back pain Flexion of hip and knee with movement only of toes should not produce an increase in low back pain Magnuson’s test Have examinee point to area several times over period of examination; inconsistencies suggest increased potential for nonorganicity Delayed response sign Pain reaction temporally delayed relative to application of perceived nociceptive stimulus Wrist drop test In an examinee with claimed wrist extensor loss, have him pronate forearm, extend elbow, and flex shoulder … if upon making a fist in this position he also extends wrist, then nonorganicity should be suspected Object drop test Examinee claims inability to bend down yet does so to pick up a light object “inadvertently” dropped by examiner Hip adductor test Test for claimed paralysis of lower extremity, similar to Hoover ’s test yet looks for crossed adductor response Disparity between tested range of motion (ROM) and observed range When ROM under testing is significantly disparate (e.g., less) from of motion of any joint observed, spontaneous ROM, suspect functional contributors Straight leg raise (SLR) disparities dependent on examinee Differences in SLR between sitting, standing, and/or bending may positioning suggest a functional overlay to low back complaints Grip strength testing via dynamometer Three repetitions at any given setting should not vary more than 20% and/or bell-shaped curve should be generated if all 5 positions are tested Sensory“flip” test Sensory findings should be the same if testing upper extremity in supination or pronation or lower extremity in internal vs. external rotation, differences may suggest a functional overlay Pinch test for low back pain Pinching the lumbar fat pad should not reproduce pain due to axial structure involvement; if test is positive, suspect a functional overlay Personality Instruments with Built-In Response Bias Designs Personality Assessment Inventory (PAI) Inconsistency (INC), Infrequency (INF), Positive Impression Management (PIM), and Negative Impression Management (NIM) scales. 8 score patterns thought to comprise a Malingering Index (Morey, 1996). > 2 patterns malingering suspected > 4 patterns likely malingering Minnesota Multiphasic Personality Inventory (MMPI-2) Validity indices (L, F, Fb, Fp, Ds, K, VRIN, TRIN), F-K (Gough, 1954) The Fake Bad Scale (Lees-Haley, 1991) Compare subtle to obvious items Rogers et al. (1994) – cutoff scores: Liberal: 1. F-scale raw score > 23 2. F-scale T-score > 81 3. F-K index > 10 4. Obvious– subtle score > 83 Conservative: 1. F-scale raw > 30 2. F-K index > 25 3. Obvious– subtle score > 190 Qualitative Variables in Assessing Response Bias Time/response latency comparisons across similar tasks Inconsistencies across tasks Performance on easy tasks presented as hard Low scores or unusual errors Remote memory report Difficulties, especially if less than recent memory, or severely impaired in absence of gross amnesia

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TABLE 63.3 (CONTINUED) Response Bias Detection Measures and Strategies Personal information Very poor personal information in absence of gross amnesia Comparison between test performance and behavioral observations Discrepancies Inconsistencies in history and/or complaints, performance Inconsistencies across time, setting, interviewer, etc. Comparisons for inconsistencies within testing session (quantitative A. Within tasks (e.g., easy vs. hard items) and qualitative) B. Between tasks (e.g., easy vs. hard) C. Across repetitions of same/parallel tasks (rule out fatigue) D. Across similar tasks under different motivational sets Comparisons across testing sessions (qualitative, quantitative) Poorer/inconsistent performance on re-testing Symptom self-report: complaints High frequency, severity of complaints and higher frequency, severity vs. significant other report or other collaborative report Main & Spanswick, 1995 Failure to comply with reasonable treatment Report of severe pain with no associated psychological effects Marked inconsistencies in effects of pain on general activities Poor work record and history of persistent appeals against awards Previous litigation Symptom self-report: early/acute vs. late/chronic symptom complaint Early symptoms reported late or acute symptoms reported hronic as c Response to typically helpful pain interventions Failure to show any pain relief to at least one of the following: biofeedback, hypnosis, mild analgesics, psychotherapy, relaxation exercises, heat and ice, mild exercise Failure to show any pain relief in response to TENS Assessment of Cognitive Effort: Performance Patterns on Existing Psychological/Neuropsychological Tests Full scale IQ Low (vs. expected, estimated, etc.) Arithmetic and orientation scale performance “Near-miss” (Ganser errors) WMS-R Malingering Index: Attention/Concentration Index vs. Attention–concentration index score < general memory index (AC-GMI) Memory Index Grip strength Unusually low w/o gross motor deficit Recognition memory (California Verbal Learning Test (CVLT)) < 13 Rey Complex Figure and Recognition Trial Atypical recognition errors (> = 2); recognition failure errors Word Stem Priming Task Performance Poor or unusual performance Specific Cognitive Effort/Response Bias Measures Word Memory Test (WMT) < 50% chance responding Test of Memory Malingering (TOMM) < 50% chance level responding Dot Counting Test (DCT) Correct/incorrect responses Computer Assessment of Response Bias (CARB) < 89% raises suspicion Rey Memory for 15 Items Test (MFIT) Lezak (1983), < 3 complete sets, < 9 items Symptom validity testing (SVT) < 50% chance level responding

interpreting examinee data. Integration of contextualassessment procedures regarding malingering. Further, information, history, behavioral observation, interview some alarming trends have appeared that do not objectively data, collaborative data, personality data, with measures or critically evaluate the weaknesses, as well as strengths, of effort or performance (or symptom exaggeration orof these procedures. Based on a critical evaluation of the malingering) and examination and test performance data current state of the art, it appears that many common provides the best information for estimating, for assumptions about response bias detection and malingering instance, the degree to which a person was responding measures should be considered myths (Martelli, Zasler, truthfully and exerting full effort, and the degree to Mancini, et al., 1999). Importantly, malingering (1) should which test results are reliable and valid andect reflactual not be considered dichotomous, or EITHER/OR (i.e., abilities and current status. present/not; malingering/not); (2) should not be considered something that clinicians can reliably or validly assess with It also should be noted that the necessary recent any high degree of certainty, even when serious efforts are increase in attention to response bias assessment has been made; and (3) should not be considered a discrete entity accompanied by frequently haphazard and overzealous application of poorly validated detection models and singlethat symptom validity tests (SVT) measure.

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TABLE 63.4 General Weaknesses of Response Bias Assessment Measures 1. Psychometric research inadequacies (e.g., basic test construction issues such as reliability, validity, as well as convergent and divergent validity studies are poorly addressed). 2. Limited generalizability of analogue research (i.e., simulated malingerers vs. externally or criterion-validated malingerers, unknown differences between simulated and real malingerers; cf. studying serial killers this way), as well as tendencies for measures with good discrimination to show less effectiveness in cross-validation and follow-up studies. 3. Variable group membership (i.e., wide variability in samples for both simulators and symptom/disorder groups). 4. Differential vulnerability to response bias (i.e., some tests are more obvious while others are more subtle). 5. Questionable generalizability of findings (i.e., from one measure to any other (response bias or real) test, or to actual symptoms, or across time; conversely, good effort on a response bias measure does not necessarily predict response on any other measure). 6. Absence of mutual exclusivity (i.e., poor effort can occur in presence of real disorder, symptoms). 7. “Law of the instrument” operational definitions wherein malingering becomes what malingering tests measure. Specifically, the definitions of “effort,” and validation studies to examine the construct are missing. Further effort cannot be assumed uniform for mild traumatic brain injury (TBI), chronic pain, and depression diagnoses, for nonlitigating and litigating, etc. 8. Effects of fatigue, pain, disinterest, non-attended (computer) administration, mixing real tests and SVTs in a battery with unknown face validity, and other factors, on response bias tests, are not understood and have not been addressed. 9. Exclusive or even primary reliance on any current SVT/Index or combination potentially violates APA ethics APA and Standards for Educational and Psychological Tests with regard to making a diagnosis of malingered pain or n making decisions about recommending treatment termination, due to limited reliability and validity data. 10. Frequently high misclassification rates (i.e., false positive) when these are assessed through record review and detailed analysis. 11. Problems associated with inaccurate assumptions of nonorganic conditions based on inconsistencies or absence findings. of peripheral Notably, recent advances in our relatively poor understanding of pain and its mechanisms and associated sequelae have implicated central nervous system effects in many such cases. A growing body of evidence strongly associates central nervous system effects, especially central sensitization phenomenon, in cases where peripheral findings are inconsistent, weak, or even apparently nonexistent (Jay, Krusz, Longmire, & McLain, 2000; Miller, 2000; Nicholson, 2000; Nicholson, in review; Mailis, Papagapiou, Umana, Cohodarevic, Nowak, & Nicholson,).in press

A specific method of response bias assessment that is A summary of some of the major problems with extant response bias procedures is offered in Table 63.4 worth mentioning is SVT, which typically refers to a to (1) emphasize the necessary caution with regard to forced-choice technique originally designed for assessing effort or symptom validity with respect to nonorganic overinterpretation of response bias procedures; (2) emphasize the importance of employing multiple data blindness (Pankratz, 1988). This technique has been sources and making thoughtful inferences only after inteextended to assess effort in purported sensory loss and, more recently, memory complaints (Colby, 2000). The typ-gration of thorough historical information, interview, ical SVT paradigm involves presentation of a stimulus,assessment, behavioral observations, collaborative interfollowed by a distraction, and then presentation of theview, and data sources, and so on (Martelli, 2000). original stimulus with a novel stimulus with instruction to Table 63.5 is presented to further caution against simidentify the original stimulus. With regard to memory plistic and dichotomous conceptualizations with regard to assessment, a series of words is presented for recall and, diagnosis, Table 63.5 is presented. Notably, this table repfollowing a delay, each word is presented with a sham,resents just 64 of the possibilities with regard to injury with the subject instructed to select the previously pre-related presentations. The range of possibilities represented span from (a) persons with real, uncomplicated sented word. In the case of visual or sensory assessment, with impairments on exam and in functional the simplest procedure entails exposing the subject to disorders a series of visual or sensory stimuli (e.g., pinpricks whilestatus, without exaggeration on either (but possibly minblindfolded, asking whether or not he or she perceivedimization or denial) to (b) persons with no real physical pathology or impairments, but who exaggerate or feign each. Performance is then compared with chance, which impairments on exam and functional status. is the worst possible expected performance if sensory function or ability is completely absent. Below chance (i.e., Necessarily, a cautious approach is indicated with below 50%) performance across a sample of numerous regard to estimating the probabilities regarding presence trials indicates negative bias and indicates that the symptom or absence of physical impairment and response bias. is feigned. Such performance provides strong and unamHowever, in many cases, it is not ficient suf to integrate biguous evidence of conscious dissimulation or symptomdata from multiple sources and make inferences about malingering, because worse- than-chance performance which of the 64 possible combinations is most likely. requires recognition and suppression of true responses. Descriptive characterization is often relevant. For

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TABLE 63.5 Diagnostic Realities in Assessment of Chronic Pain Real Physical Pathology 1. 2. 3. 4.

Yes Mixed Indeterminate No 4

Residual Impairments On Exam, Testing

Residual Functional Impairments 1. 2. 3. 4. ×

Yes, and exaggerated Yes, and not exaggerated No, and exaggerated No, and not exaggerated 4

1. 2. 3. 4. ×

Yes, and not exaggerated Yes, and exaggerated No, and exaggerated No, and not exaggerated 4

= 64

instance, if a person has both physical pathology and an optimal method for estimating the degree of effort or exaggeration, inferences must be generated about not performance and the degree to which examination findings only the degree of physical impairment, but also theare reliable and valid and reflect actual abilities; and (e) degree of awareness of exaggeration on the part of the allows estimation of motivation by incorporating currently subject. Has the person adopted a sick role, and talked available instruments and methods and the available pubthemselves into believing they cannot perform certainlished research for direct and indirect measurement of tasks or lack certain abilities (e.g., somatoform disorder),motivation and response bias. with conscious withholding of effort due to intending to Notably, these strategies are not offered individually demonstrating what they believe to be true disabilities?and, again, are not intended to support a simple dualistic Or, are they less conscious and aware, as in a conversion model that assumes examinees either try hard or malinger, disorder? Or are they completely aware, but coping in aor that evidence of less-than-full effort on any one test way that may be adaptive as in the case of an aging necessarily implies absence of impairment in other areas worker with a chronic history of back failures who may of examination or in real world abilities. Although they be shy, have low self-esteem and self-confi dence; be also are not offered with specific guidelines (e.g., failure disconnected from or less than well liked by his/heron any one, or any two, or any three, etc. represents employer, against the backdrop of believing that anotherinadequate performance, or symptom exaggeration or back injury is inevitable and cumulatively painful and malingering), they are offered with the suggestion that (a) disabling, that uncomfortable interactions with othersexamination performance can be influenced by multiple may be required, that the company sometimes res fipre- factors including a desire to be completely truthful and viously injured workers, that the company did not makeperform with full effort; (b) the degree of truthfulness and obvious safety precautions to prevent the individual’ s effort exerted on examinations exists on a continuum (vs. injury; and that no other job options are realistic? a dichotomy) and can be estimated by the extent to which indicators of unreliable report and poor/inconsistent effort are present; (c) reliability and validity of examination CONCLUSIONS findings are dependent on relative assurances of full effort; and (d) interpretation and diagnostic impressions are To summarize, the major response bias detection strategies presented in Table 63.3 provide an illustrative summarydependent upon reliable and valid examination results. of a constellation or profiling approach to response bias It should be emphasized that “failure” on one measure of response bias or malingering does not mean that the detection strategy use that relies on assessing relevant information for interpreting examination data. This con- entire set of complaints is biased or malingered. Ethical guidelines universally caution against overzealous interceptual model is also a methodological approach for constructing a profile of motivation and response bias, whichpretation of limited test data. In fact, the only reasonable (a) incorporates a wide array of findings from commonevidence of certain or definite malingering is confession or admission. A secondary form of evidence, although instruments and procedures during evaluation; (b) summarizes empirically supported indicators with at leastsomewhat less than perfectly reliable, is when the person some purported utility in detecting suboptimal effort; (c) or examinee is detected, via surveillance, performing an despite numerous pitfalls and limitations of each of theseact he or she reported was absolutely impossible to perform under any circumstance. procedures, both conceptual and methodological, offers improved discrimination and increased reliability given It should be noted further that a great disparity exists multiple measures; (d) integrates behavioral observation, between the adversarial legal process and the responsiinterview, and collaborative, historical, personality, andbility of attorneys to be client advocates vs. the dispascontextual data with medical examination and psycholog-sionate, objective scientifi c ethics expected and required ical performance data and measures of response bias, of aspsychologists and physicians. The danger of attorney

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“ coaching” based on utilization of this material cannot attitude. We can’ t assume that everyone takes be underestimated. This, of course, would then represent our tests seriously, will be as forthcoming, hona form of “stealth” threat to the validity of examination est, or effortful as we would like, will not doubt data. This threat, or expected consequence of collision our procedures or try to emphasize their probbetween disparate legal and scientifi c ethics, has recently lems, or that we won’ t have to work at getting been documented in a national publication noting a case them optimally motivated. of attorney–client coaching (Youngjohn, 1995). How4. Ensure that important general situational and ever, compared to simpler models where only a couple psychosocial variables affecting motivation are of isolated response bias measures are used, it seems adequately assessed during an interview that is extremely unlikely that the multiple measures, such as concluded prior to examination procedures. those outlined in the MAP approach, could be underSpecifically, assess the impact of anger or blame stood and manipulated. and feelings of resentment or victimization (Rutherford, 1989), as well as the other variables Finally, enhancing response bias detection as a means shown in the literature to be associated with poor of optimizing interpretability of examination results, critrecovery and adaptation to impairments (Marical as it is, should not be considered the nalfi step. telli, Zasler, & Grayson, 2000). Decreasing response bias must certainly be considered a more efficacious and economic approach to enhancing 5. In addition to emotional and motivational issues, always assess interest/disinterest in the utility of medical and psychological assessments. examination and testing procedures process, The following explicit and comprehensive recomand any obstacles or impediments to optimal mendations for enhancing motivation, assessing effort and performance. Always assess anxiety response bias, and increasing ficiency, ef utility, and ecolevel and ensure that measures are taken to minlogical validity of examination procedures are offered imize its effect and potential interference with (Martelli, et al., 1999b). valid assessment. 6. Rely primarily on M.D.s and Ph.D.s for all RECOMMENDATIONS FOR ENHANCING VALIDITY aspects of examination, including interviewing IN CHRONIC PAIN ASSESSMENTS and testing, with limited use and reliance on technicians. Experienced M.D.s and Ph.D.s 1. Establish rapport and attempt to establish a who conduct interviews, examinations, and test working relationship with patients. Even in administration are infinitely more capable of cases of independent examinations where the a. Integrating history, interview, personality, referral source and expectation are extremely and emotional assessment data and inferadversarial, valid data collection requires a colences, with more sophisticated clinical laborative effort. Be on guard by addressing observations during examination; potential sources of bias directly, and providing b. Adapting more creative modifications of feedback, education, and clarification. testing procedures given suspicion of low 2. Prepare patients and examinees before beginmotivation, as well as modifications to the ning examination and testing. Employ undertesting process (e.g., provision of corrective standing, as well as education, in order for feedback, instruction, anxiety reduction examinees to be prepared to respond truthfully interventions) to increase motivation and and to the best of their abilities. Emphasize that optimize effort; the procedures and tests don’ t always measure c. Benefiting from the probability that examineverything, but that they do assess poor motiees will be less likely to believe they can vation or effort. Emphasize that interview data, “fake out the doctor”; corroborative data, and functional abilities are d. Avoiding the possibility of symptom exagjust as important as examination data. geration owing to fear that a technician or inexperienced clinician will miss legitimate 3. Spend time with patients/examinees and try to problems. get to know them from a motivational, emotional status, personality, and coping style per7. Differentially utilize instruments with built-in spective. If motivation seems poor, confront and response bias or symptom validity measures. attempt to elicit more valid responses vs. ignore Most major objective personality measures, some and/or proceed with collecting invalid data of the newer domain-specifi c pain assessment and/or attempting to interpret data of questionmeasures, and some neuropsychological measable validity. Such questioning of motivaures (e.g., Memory Assessment Scales (Williams, tion/effort should not involve a gotcha” “ 1992), and the Rey Complex Figure Test and

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9.

10.

11.

12.

13.

803

cutting scores for one or two measures. Note Recognition Trial (Meyers & Meyers, 1995)) provide simulator performance data. that cutting scores by their nature (Dwyer, 1996) always entail judgment, inherently result Apply multiple strategies for assessing motivain misclassification, impose an artificial dichottion, especially when cutoff score approaches are employed, and include qualitative and qualomy on essentially continuous variables, and itative measures. Integration of contextual “true” cut scores do not exist. information, history, behavioral observations, 14. Promote utilization of independent examinainterview and collaborative data, and personaltions by clinicians who actually spend a sigity and coping data with measures of effort or nificant portion of their time treating the type performance and current test data, provides the of patient being assessed. This helps assure best information for estimating the degree of more adequate clinical skills for accurate effort exerted, and the degree to which test diagnosis and understanding, including results are reliable and valid. detection and appreciation of suboptimal performance, as well as collection of internalVary the response bias measures and procedures ized tracking data to validate previous that are employed in order to prevent dilution inferences across time, and continuous selfof utility. Notably, publicizing of these tests has correction and increased collection of interled to increased recognition by potential defennalized norms regarding ecological and predant attorneys, litigants, support groups, Interdictive validity of available assessment net groups, etc. measures. Promote development of assessment procedures with built-in response bias or symptom validity measures and develop built-in measREFERENCES ures for existing assessment procedures. Employ more sophisticated and less dichoto* Allen, C.C., & Ruff, R.M. (1990). Self-rating versus neuropmous continuous conceptualizations of motisychological performance of moderate versus severe vation and response bias using multiple head-injured patients. Brain Injury, 4(1), 7. independent measures and estimated effort. * Allen, L.M., & Cox, D.R. (1995).Computerized assessment Employ a reasonably sophisticated model of response bias(revised ed.). Durham, NC: Cognithat conceptualizes motivation and effort as Syst, Inc. continuous variables that can vary across * Allen, M. (1985). Review of Millon Behavioral Health Inventory. In J.V. Mitchell (Ed.),The ninth mental measuretests, settings, and occasions. Utilize and ments handbook (p. 1521). Lincoln, NE: University of devise models that measure degree of apparNebraska Press. ent motivation and effort, using multiple data American Psychiatric Association (1994). Committee on sources, and estimate confi dence levels in Nomenclature and Statistics. Diagnostic and statistical inferences given consideration of the multiple manual of mental disorders (4th ed.). Washington, D.C.: factors that contribute to test results. Employ American Psychiatric Association. similarly sophisticated models for assessing * American Psychiatric Association (1994). Diagnostic and stapersistent impairments, adaptation to impairtistical manual of mental disorders, (4th ed. revised). ments, disability, and so on. Probability stateWashington, D.C.: American Psychiatric Press. ments based on multiple meas-ures are * Arnett, P.A., Hammeke, T.A., & Schwartz, L. (1995). Quantiprobably best. tative and qualitative performance on Rey’ s 15-Item Test Do not freely share relevant trade secrets (e.g., in neurological patients and dissimulators. Clinical Neuropsychologist , 9(1), 17. information about response bias tests, or known patterns of performance on procedures and Babitsky, S., Brigham C.R., & Mangraviti, J.J. (2000). Symptom magnification, deception and malingering: Identification instruments) with referral sources, attorneys, through distraction and other tests and techniques (VHS and nonphysicians and nonpsychologists. They video). Falmouth, MA: SEAK, Inc. often adhere to a completely different set of * Beetar, J.T., & Williams, J.M. (1995). Malingering response professional ethics. styles on the memory assessment scales and symptom Remain aware that in science and medicine validity tests. Archives of Clinical Neuropsychology , things are rarely either–or, clear cut, or uni10(1), 57. dimensional. Avoid simplistic conceptual mod* Bernard, L.C., Houston, W., & Natoli, L. (1993a). Malinels that are compatible with dichotomous gering on neuropsychological memory tests: Potential approaches to assessing motivation/effort and objective indicators.Journal of Clinical Psychology , malingering. Such approaches usually rely on 49(1), 45.

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* Bernard, L.C., McGrath, M.J., & Houston, W. (1993b). * Hayes, J.S., Hilsabeck, R.C., & Gouvier, W.D. (1999). Malingering traumatic brain injury: current issues and caveats Discriminating between simulated malingering and in assessment and classification. In N.R. Varney, and closed head injury on the Wechsler memory R.J. Roberts (Eds.),The evaluation and treatment of scale–revised.Archives of Clinical Neuropsychology , mild traumatic brain injury. Mahwah, NJ: Lawrence 8(6), 539. Erlbaum Associates. * Berry, D.T., Baer, R.A., & Harris, M.J. (1991). Detection of * Hendler, H.H., & Eimer, B.N. (in press). Psychological tests malingering on the MMPI: A meta-analysis. Clinical for assessing chronic pain and disability. Psychology Review , 11, 585. Binder, L.M., & Rohling M.L. (1996). Money matters: A meta- * Hendler, N.H., Viernstein, M., Gucer, P., & Long, D. (1979). A preoperative screening test for chronic back pain analytic review of the effects of financial incentives on patients.Psychosomatics , 20(12), 301. recovery after closed-head injury. American Journal of * Iverson, G.L. Qualitative aspects of malingered memory defPsychiatry, 153(1), 7. icits. Brain Injury, 9(1), 35, 1995. * Binder, L.M., & Pankratz, L. (1987). Neuropsychological eviJay, G.W., Krusz, J.C., Longmire, D.R., & McLain, D.A. (2000). dence of a factitious memory complaint. Journal of ClinCurrent trends in the diagnosis and treatment of chronic ical & Experimental Neuropsychology , 9(2), 167. neuromuscular pain syndromes . Las Vegas: American Blau, T. (1984).The psychologist as expert witness . New York: Academy of Pain Management and Elan PharmaceutiJohn Wiley & Sons. cals. Blau, T. (1992). The psychologist as expert witness. Presented at the National Academy of Neuropsychology annual Lees-Haley, P., & Brown, R.S. (1993). Neuropsychological complaint base rates of 170 personal injury claimants. meeting, Reno, Nevada. Archives of Clinical Neuropsychology , 8, 203. * Brandt, J. (1988). Malingered amnesia. In R. Rogers (Ed.), Lees-Haley, P.R, Williams, C.W., Zasler, N.D., Margulies, S., Clinical assessment of malingering and deception (pp. English, L.T., & Steven, K.B. (1997). Response bias in 65–83). New York: Guilford Press. plaintiff ’s histories.Brain Injury, 11(11), 79–99. Colby, F. (2000). Does the binomial distribution stand falsely Lezak, M. (1965).Neuropsychological assessment , (3rd ed.). accused?Brain Injury Source , 4(4), 18–21. New York: Oxford University Press. * Cullum, C., Heaton, R., & Grant, I. (1991). Psychogenic factors Teminfluencing neuropsychological performance: Somato-Lipman, F.D. (1962). Malingering in personal injury cases. ple Law Quarterly , 35, 141. form disorders, factitious disorders and malingering. In H.O. Doerr, & A.S. Carlin (Eds.),Forensic neuropsy- Loring, D.W. (1995). Psychometric detection of malingering. Presented at the annual meeting of the American Acadchology. New York: Guilford Press. emy of Neurology, Seattle. Dwyer, C.A. (1996). Cut scores & testing: statistics, judgment, Mailis, A., Papagapiou, M., Umana, M., Cohodarevic, T., truth, and error.Psychological Assessment , 8(4), 360. Nowak, J., & Nicholson, K. (in press). Unexplainable * Elmer, B.N., & Allen, L.M. (1995).User’s guide to the pain widespread somatosensory deficits in patients with assessment battery (Research ed.). Durham, NC: Cognichronic nonmalignant pain in the context of litigaSyst, Inc. tion/compensation: A role for involvement of central * Faust, D. (1995a). The detection of deception. Special issue: factors.Journal of Rheumatology . Malingering and conversion reactions. Neurologic ClinMain, C.J., & Spanswick, C.C. (1995). Functional overlay, and ics, 13(2), 255. illness behaviour in chronic pain: distress or malingerFishbain, D.A., Cutler, R.B., Rosomoff, H.L., & Rosomoff, R.S. ing? Conceptual dif ficulties in medico-legal assessment (1999). Chronic pain and disability exaggeration/malinof personal injury claims.Journal of Psychosomatic gering research and the application of submaximal effort Research , 39(6), 737. research to this area: A review. Poster presented at International Association of Pain 9th World Congress, Martelli, M.F. (2000). Psychological Assessment of Response Bias in Impairment and Disability Ratings. Presentation Vienna, Austria. as part of Symposium #2031 (The Psychologist’ s Role * Franzen, M.D., & Iverson, G.L. (1998). Detecting negative in the Social Security Disability Process) at the Amerresponse bias and diagnosing malingering: The dissimican Psychological Association 2000 Convention, Washulation exam. In P.J. Snyder & P.D. Nussbaum (Eds.), ington, D.C. Clinical neuropsychology – A pocket handbook for Martelli, M.F., Zasler, N.D., & Grayson, R. (1999a). Ethical assessment (pp. 88–101). Washington, D.C.: American considerations in medicolegal evaluation of neurologic Psychological Association. injury and impairment.NeuroRehabilitation: An Inter* Green, P., Iverson, G., & Allen, L. (1999). Detecting malindisciplinary Journal, 13, 1, 45. gering in head injury litigation with the Word Memory Martelli, M.F., Zasler, N.D. & Grayson, R. (1999b). Ethical Test. Brain Injury, 13(10), 813. considerations in impairment and disability evaluations Hadjistavropoulos, H.D., & LaChapelle, D.L. (2000). Extent and following injury. In R.V. May & M.F. Martelli (Eds.), nature of anxiety experience during physical examinaGuide to functional capacity evaluation with impairment tion of chronic low back pain.Behavior Research and rating applications. Richmond: NADEP Publications. Therapy, 38(1), 13. Hall, H.V., & Pritchard, D.A. (1996).Detecting malingering and deception: Forensic distortion analysis . Delray Beach, FL: St. Lucie Press.

Assessing the Veracity of Pain Complaints and Associated Disability

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Martelli, M.F., Zasler, N.D., & Grayson, R. (2000). Ethics and * Mittenberg, W., Arzin, R., Millsaps, C., & Heilbronner, R. (1993). Identification of malingered head injury on the medicolegal evaluation of impairment after brain injury. Wechsler Memory Scale. Psychological Assessment , 5, In M. Schiffman (Ed.),Attorney’s guide to ethics in 34. forensic science and medicine . Springfield, IL: Charles * Morey, L.C. (1996).An interpretive guide to the personality C Thomas. assessment inventory (PAI). Odessa, FL: Psychological Martelli, M.F., Zasler, N.D., Mancini, A.M., & MacMillan, P. Assessment Resources. (1999). Psychological assessment and applications in impairment and disability evaluations. In R.V. May & Nicholson, K. (2000). At the crossroads: Pain in the 21st century. NeuroRehabilitation , 14, 57. M.F. Martelli (Eds.),Guide to functional capacity evaluation with impairment rating applications . Richmond: Nicholson, K., Psychogenic pain: Review of the construct, a NADEP Publications. novel taxonomy and neuropsychobiological model (in review). Matheson, L. (1988). Symptom magnification syndrome. In S. Isernhagen (Ed.),Work injury, Rockville, MD: Aspen * Nies, K.J., & Sweets, J.J. (1994). Neuropsychological assessPublishers. ment and malingering: A critical review of past and present strategies. Archives of Clinical NeuropsycholMatheson, L. (1990). Symptom magnification syndrome: A ogy, 9(6), 501. modern tragedy and its treatment. Part one: Description and definition.Industrial Rehabilitation Quarterly , 3(3), Pankratz, L. (1988). Malingering on intellectual and neuropsy1, 5, 8–9, 12, 23. chological measures. In R. Rogers (Ed.), Clinical assessment of malingering and deception . New York: Matheson, L. (1991a). Symptom magnification syndrome: A Guilford Press. modern tragedy and its treatment. Part two: Techniques of identification. Industrial Rehabilitation Quarterly , * Rogers, R. (Ed.). (1988). Clinical assessment of malingering 4(1), 1–17. and deception . New York: Guilford Press. Matheson, L. (1991b). Symptom magnification syndrome: ARohling, M.L., & Binder, L.M. (1995). Money matters: A metamodern tragedy and its treatment. Part three: Techniques analytic review of the association between financial of treatment.Industrial Rehabilitation Quarterly , 4(2), compensation and the experience and treatment of 5–6, 22–24. chronic pain.Health Psychology , 14(6), 537. May, R.V. (1999). Symptom magnification syndrome. In R.V. Rutherford, W. (1989). Postconcussion symptoms: Relationship to acute neurological indices, individual differences, and May & M.F. Martelli (Eds.),Guide to functional capaccircumstances of injury. In H.S. Levin, H.M. Eisenberg, ity evaluation with impairment rating applications . and A.L. Benson (Eds.). Mild head injury(p. 229). New Richmond: NADEP Publications. York: Oxford University Press. Merskey, H. (1986). Classification of chronic pain, descriptions of chronic pain syndromes and definitions of pain terms.Simmonds, M.J., Kumar, S., & Lechelt, E. (1998). Psychosocial factors in disabling low back pain: Causes or consePain, 3, S10–S11, S13–S24. quences?Disability and Rehabilitation , 18, 161. * Meyers, J., & Volbrecht, M. (1999). Detection of malingerers using the Rey complex figure and recognition trial. Waddell, G. (1999). Nonorganic signs or behavioral responses to examination in low back pain. Hippocrates’Lantern, Applied Neuropsychology , 6, 4, 201. 6(3), 1. * Meyers, J.E., & Meyers, K.R. (1995). Rey complex figure and recognition trial. Odessa, FL: Psychological Assessment Waddell, G., & Main, C.J. (1984). Assessment of severity in low back disorders.Spine,9, 204–208. Resources. Miller, L. (2000) Neurosensitization: A model for persistent Waddell, G., Main, C.J., Morris, E.W., Paoloa, M.D., & Gray, I.C. (1984). Chronic low back pain, psychologic disdisability in chronic pain, depression, and posttraumatic tress, and illness behavior. Spine, 9, 209. stress disorder following injury.NeuroRehabilitation , 14(1), 25–32. * Williams, J.M. (1992).The memory assessment scales . Odessa, FL: Psychological Assessment Resources. Miller, L. (2001). Not just malingering: Syndrome diagnosis in traumatic brain injury litigation.NeuroRehabilitation, * Youngjohn, J.R. (1995). Confirmed attorney coaching prior to 16, 1–14. neuropsychological evaluation. Assessment , 2(3) 279. * Millis, S. R. (1994). Assessment of motivation and memory Youngjohn, J.R., Burrows, L., & Erdal, K. (1995). Brain damage or compensation neurosis? The controversial post-conwith the recognition memory test after financially comcussion syndrome.Clinical Neuropsychologist , 9(2), pensable mild head injury. Journal of Clinical Psychol112. ogy, 50(4), 601.

64 Psychoneuroimmunology Jan M. Burte, Ph.D., D.A.A.P.M. Historically, the study of mind/body interaction can be natural killer-cell levels, etc.) that are affected by environtraced to early Greek physicians. Indeed, when one begins mental and internally mediated stress? Second, to restate a search of its earliest origins, one inevitably is led tothe question often raised by clinicians, “Does statistical Hippocrates and Galen of ancient Greece. To the ancient significance (i.e., changes in hormone levels) assume clinGreeks, emotions were seen to play a significant role in ical relevance (i.e., a clinical change in the immune systhe progress and maintenance of diseases. What todaytem’s is protective potential)?” Third, if we accept that stresknown as tuberculosis was described symptomologicallysors experienced through conscious awareness and by Hippocrates and prescribed to have its etiology injudgment impact the immune system, what can be done stress. However, the importance of the role of the mind into reduce those stressors? maintaining health has passed through many significant A discussion of treatment modalities is offered, and perceptions since that time. Until recently, post-Descartianfinally, hope for a united direction for future research thinking resulted in the mind’s role in immune functioning unifying the basic sciences (statistical analyses) and the being allocated to the periphery of medicine. applied sciences (clinical relevance). What then do we Masek, Petrovicky, Sevcik, Zidek, and Frankova know about the integrative reaction of the CNS and the (2000) pointed out that psychoneuroimmunology (PNI)immune response? was comprehensively described only as recently as 20 Stress, via bidirectional interactions between the cenyears ago. They go on to define PNI as the bidirectional tral nervous system, endocrine system, and immune syscommunication between the central nervous system tem, impacts the hypothalamic, pituitary, adrenal (HPA), (CNS), neuro-endocrine system, and immune system. and the sympathetic adrenal medullary (SAM) axes, can With a return to examination of the interactive role of theinduce modulation of the immune system and, thereby, central nervous system, the endocrine and immune sysdefense against infectious agents and health (Yang & Glatems came a new field currently labeled PNI. Many defi-ser, 2000). nitions of PNI are available, depending on the emphasis In a review of research articles, Sali (1997) notes that or direction of the pathways particular fields of researchers stress increases the risk of viral infection. Stress and choose to emphasize. depression can depress immunity, whereas stress reducOne definition offered by Paul Martin (1998) is “the tion enhances immunity. Sali points to outcome data on field of scientific research that is concerned with theimproved cancer prognosis by enhanced immunity resultcomplex interrelationship between the psychologicaling from stress reduction. Spiegel (1999) found increased and emotional factors, the brain, hormones and immu-survival rates in breast cancer patients who attended stress nity and disease.” reduction groups or programs. Further, Van der Pompe, The purpose of the chapter is to offer the following: Anoni, Visser, and Garsseri (1986) suggested the imporFirst, a basic understanding of precisely which pathwaystance of psychotherapy and psychological resiliency in are considered in PNI. For example, what are the biologbreast cancer survival. Utilizing a twin study model (124 ical immune responses (cortisol levels, cytokines levels,normal adult twin pairs; Hickie, Bennet, Lloyd, Heath, 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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and Martin 1999) found a positive genetic relationshipchanges in state anxiety, systolic blood pressure, diastolic between psychological distress and immunity. They con-blood pressure, and CD4+ lymphocyte numbers were assocluded that genotype may play a significant role in theciated with levels of perceived pain intensity to a cold pressor test. reactivity of the immune system to stress. Garssen and Goodkin (1999) suggest that some evidence has been In extreme situations where physical trauma and pain found that a low level of social support and a tendencyare severe, the body releases endogenous opioids which reduce the perception of pain and have pain-relieving toward helplessness and repression of negative emotions actions. However, as a result, the immune activity of natare factors that promote cancer progression but not cancer ural killer cells and lymphocytes is reduced. initiation. These same factors are also symptoms commonly associated with depression. Further, Christiansen, This raises the issues of placebos and other treatments s perception of pain Edwards, Wiebe, Bonotsch, McKelvey, Andrews, andthat work by altering the individual’ Lubaroff (1996) found that immunosuppression (NKC without actually providing an external source of analgesia. activity) could be positively impacted by self-disclosure If, in fact, they operate as some believe by triggering painrelieving opioids, do they then represent a two-edge sword of traumatic or stressful experiences. A question is then raised: “Does a correlation existwhich offers pain relief, thus, diminishing the immunosuppressant levels of IL-6 and cortisol while possibly between depression, suppressed immunological functiontumor suppression by lowering NKC and cering, and the elevation of underlying disease processes decreasing to tain lymphocyte activities? a level above threshold (i.e., the symptomatic expression of herpes or the increase in joint counts in rheumatoid Another issue about pain is its controllability. Laudenslager (1983) found that lack of control vs. control over arthritic patient)?” Research continues to support the conpain induced by electric shock determined lymphocyte cept that stress plays a significant role in exacerbating pathophysiology. Berin and Perdue (1997) note thatresponsiveness of rats. This may also explain the more recent findings of researchers that depression (learned reported stress often precedes relapses in patients with inflammatory bowel disease or irritable bowel syndromehelplessness) with regard to pain may be significantly related to dysfunctional reciprocal relations between and that CNS and immune-mediated pathophysiology as neuroendocrine and immune function (Geiss, Varodi, expressed by changes in the epithelium may exist. Steinback, Bauer, & Anton, 1997). Stress and pain also have been demonstrated to adversely affect endocrine and immune function in regard The patient’s perception of the controllability of pain and level of optimism may also play a significant role in to postsurgical wound healing, with greater fear or distress prior to surgery being associated with slower and morethe impact that pain has on immune functioning. In an complicated postoperative recovery (Kiecolt, Glaser,examination of pain patients suffering with temporomanPage, Marucha, MacCallum, & Glaser, 1998) and to smalldibular pain and dysfunction syndrome, immune functionpunch biopsy wound healing in caregivers as demon-ing was not impacted compared to controls. However, strated by increased healing time and lower cytokinespatients who scored high on measures of “demoralization” (IL–1) levels (Glaser, 1996). In regard to posttraumatic(low self-esteem and perceptions of helplessness and hopelessness) demonstrated signifi cant decreases on patients, Klapheke (2000) suggested that their depression (Marbach, Schleifer, & Keller, 1990). should be seen as a contributory factor to the net state measures of In a review article, Page and Ben-Eliyahu (1997) note immunosuppression in transplant patients that the immune system plays a role in controlling the spread of cancer and that perio-operative pain relief PSYCHONEUROIMMUNOLOGY improves immune status and health outcomes. They sugAND PAIN gest that suf ficient evidence exists to view pain as a pathogen in and of itself that is capable of facilitating the proThe impact of pain on immune functioning has been studgression of metastatic disease via immunosuppression. ied extensively in animals, but more recently the role of Along similar lines, a study by Parker, Smarr, various types of pain on immune function has been examAnglone, Mothersead, Lee, Walker, Bridgers, and Caldined. Kremer (1999) notes that surgery negatively affects well (1992) utilizing the Beck Depression Inventory, the immune function, and that pain has a deleterious effect on Arthritis Helplessness Index, and the Arthritis Impact immune function. Via neuroendocrine pathways, depresMeasurement Scales (AIMS) pain score in conjunction sion, stress, and pain can be viewed as psychoneurological with immunophenotypic analyses of peripheral blood phenomena. He suggests that treatment of postoperative lymphocytes found that the percentage of HLApain must be included in the recovery process because of DR + cells in the peripheral blood and helplessness its psychoneural immunological impact on the patient. related to joint count in rheumatoid arthritis (RA) In a study to assess acute pain impact on immune levels + – in 10 HIV and 10 HIV patients, Eller (1998) found no patients. Further, joint count had an effect upon depression and depression affected the perception of pain, significant difference between groups. However, signi ficant

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demonstrating the interrelationship among psychologi-(PHA and DWM) and NK cell cytotoxicity than those who cal factors, immunologic activation, and disease activityhad more severe reactions or who repressed their stress in RA. Zautra, Hoffman, Potter, Matt, Yocum, and Cas-reactions. tro (1997) also found that interpersonal stressors were Adaption to stress and its impact on the immune sysassociated with increased disease activity in a study of tem may be somewhat more complicated. Kelly, Hertz41 rheumatoid arthritic women. man, and Daniels (1997) have suggested that PNI measAffleck, Urrows, Tennen, Higgins, Pav, and Aloisi ures may act as markers to adaption to socioeconomic and (1997) examined sedimentation rates, an indication of syspsychosocial stressors. temic inflammation and soluble interleukin-II receptors (a There appears to be significant evidence that psychomarker of immune system activation known to correlatelogical stress contributes to immunological suppression with the RA disease activity). For RA patients, they found(Biondi & Annino, 1997). However, there is less compelthat daily event stressors were associated with increased ling evidence suggesting that immunosuppression may joint pain (regardless of mood) and decreased joint inflam-result in mental disease. However, recent research identimation (reduced levels of soluble interleukin-II receptors).fies the hypersecretion of IL-2 in schizophrenia and IL-6 Another issue that often is raised is the impact of acute in depression. Muller (1997) suggests that cytokine stressors on individuals who are experiencing chronic lifechanges resulting from stress impacting the immune sysstressors. It would seem that individuals who are experi-tem may play a role in psychiatric disorders. Further, encing chronic life stress might be more vulnerable to theDabkowska and Rybakowski (1994) suggest that the impact of acute stressors. The importance of this is apparimmune system may play a role in increasing vulnerability ent when we look at disease onset rates in more vulnerable to psychiatric disorders. populations, such as the infirmed, ill, or impoverished, Given the interactive nature of PNI, it is evident that who may be experiencing higher levels of chronic lifea relationship exists between emotional disorders such as stress. Indeed, Pike, Smith, Hauger, Nicassio, Patterson, depression and alterations in the response of the immune McClintick, Costlow, and Irwin (1997) found that indi- system. However, as Kaye, Morton, Bowcutt, and Maupin viduals experiencing chronic life stress demonstrated(2000) point out, the associations and relevance of these greater subjective stress, higher peak levels of epinephalterations with regard to health and illness are not yet rine, lower peak levels of beta endorphin and of NK cellfully determined. lysis and NK cell distribution to a mild acute stressor than Anyone who has spent a night in pain or stressed did controls. These changes persisted beyond termination knows the impact that either can have on sleep. Hall, of the stressor and sympathomedullary recovery. It rein-Baum, Buysse, Prigerson, Kupfer, and Reynolds III (1998) forces the concept that those already suffering, often the report that sleep has been demonstrated to be a significant case in chronic illness or injury patients, are most vulner-factor in the stress/immune relationship of NKC number able to further immunosuppression from acute stressors. and functions. In the case of traumatic injury, Schrader (1996) suggests Severity of pain was also a factor. This suggests that that the individual’s psychologic and physiologic states clinicians must be aware of the patient’ s mental state may alter the immune system and decrease immunity as and take into account immunological susceptibilities in measured by serum cortisol levels, and further, that the those patients who present with signifi cant levels of perception of diminished control and subjective stress may emotional demoralization (chronic pain syndrome) contribute to immune changes when combined with thewhen invasive potentially immunosuppressant intervenimmunosuppressive effects noted with regard to pain, sugtions are considered. gesting that the state of significantly decreased immunity In fact, an optimistic outlook may protect the immune needs to be addressed from a psychological, controlled system from the negative impact of stress. First-year law coping skill, and pain management approach. students evaluated at the onset of the semester who were Interestingly, research suggests when the stress is confound to manifest a more optimistic attitude had more sistent with the stressor (perhaps demonstrating better helper T-cells (T-cell increased 13%) and higher naturalcoping skills by the individual), immunological changes killer cell cytotoxicity mid-semester than their pessimistic are less severe than when the stress experienced is greater peers (T-cell dropped 3%). This led to the suggestion that than expected from the trauma. Solomon, Segerstrom, the optimist’s attitude protected their immune functioning Grohr, Kemeny, and Fahey (1997) found that earthquake (Segerstrom, 1998). survivors who manifested acute psychological reactions Another important question often asked is, Does “ to a realistic degree given the life stress experienced less stress impact suf ficiently enough on the immune system disruption of an aspect of immunity (lymphocyte subsetsto create a health risk?” Glaser (1996) found studying – total T[CD3+] helper T[CD4+] cytotoxic T[CD3+ and antibody responses tou-vaccinated fl Alzheimer’ s disease CD8+] 19+) and natural killer cell (NK; CD3– , patients’caregivers and to Hepatitis B-vaccinated medCD16+ sign CD56+) as well as lymphoid cell mitogenesisical students that the ndings fi indicated psychological

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nology techniques in use are aimed at alleviating stress stress may be able to alter a person’ s response to a vaccine and, therefore by implication, his or her risk to effects on the immune system rather than at direct infection by a live virus. Koenker (2000) states that psy- augmentation of immunity by the brain. They raise the question as to whether the mind can, via conditioning, chological stress suf ficiently impacts the immune system to raise catecholamine and CD9 levels and increases the be trained to remember an output pathway to raise immunity. risk of viral infection-released histamines which trigger severe bronchoconstriction in asthmatics. It also alters If so, then it lends increased credibility to the mindinsulin needs, increasing the risk for diabetes mellitus; control components promoted in Eastern philosophies and alters acid concentrations in the stomach contributing to healing arts. peptic and stress-ulcers and ulcerative colitis; and Further, as we break down the concept of training increases plaque buildup in arteries thus adding to the pathways, one is presented again with questioning to what risk of angina and heart attack. (Elliott & Eisdorfer, extent conditioning is behaviorally mediated via the build1982; Lieberman, 1974). up of neural pathways or unconsciously mediated via As we continue to learn about complex PNI interacimagery-based internal experiences. tions our views of the forms of intervention and pharmoLet us first examine the different modalities utilized cotherapies may significantly change. Masekt, Petrovicky, and presented in the literature concerning stress reducSevcik, and Zidek (2000) point out that the data strongly tion as a means of enhancing immune function. Stress suggest that in the very near future we will not only better management represents a broadly ned defi treatment oriunderstand the very complex communication between entation encompassing a huge variety of treatments. The mind and body, but also have completely new types of singular underlying common goal is to bring about either compounds become available. objectively or subjectively reported changes in the Vedhara, Fox, and Wang (1999) raised the question as patient’s experience of stress. However, as has been freto whetherin vitro statistically significant results can be quently noted in the literature from Selye (1956; 1976) equated toin vivo immune outcomes. Although not yet to the present, not all stress is negative, and although completely answered, signifi cant in vivo research is general stress values have been numerically quantifi ed present, as evidenced by the plethora of treatment outcome (Holmes and Rahe 1967), not all events maintain equal studies represented in the literature. These studies suggest stress values for all individuals. In addition, factors such the presence of a PNI effect. as the ability to control the stressors (Schrader, 1996; Kiecolt, et al., 1998; Kaye, et al., 2000; Laudenslager, TREATMENT 1983), support systems (Spiegel, 1999), chronicity of the stressor (Pike, et al., 1997), and adaptation to the stresHaving reviewed the mechanisms and correlations sors (Kelly, et al., 1997) may play a signifi cant role in between the psyche (mind), and neuro (brain/endocrine) the impact of stress on immunological functioning and and immune system, and seeing that a bidirectional relaresponsiveness to treatment. tionship exists, we next should review what forms of interSome of the treatments that have sought to address vention have been applied in treating various conditions. the effects of stress include biofeedback, hypnosis, cogOne might feel initially tempted simply to try to correlate nitive behavioral, behavioral approaches, exercise, nutritreatments with conditions/diseases, but this would undertion, physical manipulation, yoga, and a host of other mine the very essence of the psychoneuroimmunological techniques including laughter therapy, dance, and the arts. model which seeks to approach immunosuppression from What almost all of these approaches have in common is a more holistic framework. Perhaps the best title for all that they seek to change the patient’ s (assuming he or she interventions which utilize this model is the one proposed is ill at this point) appraisal of the stressors that preceded by Biondi and Zannino (1997) who refer to such interventhe influence of immunodepression, the stressors associtions as psychoimmunotherapy, namely, the application of ated with his/her appraisal of the illness and treatment. conjoint psychological intervention in pathologies such as This typically includes the patient’ s ability to control pain tuberculosis, herpes simplex virus, and HIV. Coyle (1996) and the degree to which he or she is limited or disabled offers a similar concept of psychoneuroimmunology in by the illness or pain, as well as the stressors associated the treatment of multiple sclerosis. with the patient’ s appraisal of future functioning and/or An important issue rises, however, but the point of mortality. intervention. Hiramoto, Solvason, Hsueh, Rogers, Demissie, Hiramoto, Gauthier, Lorden, and Ghanta (1999) state In essence, stress combined with a stress-prone personality leads to physiological and hormonal consequences which deplete the immune system. This opens Psychoimmunology has been credited with using the the door for possibly increased susceptibility to or mainmind as a way to alter immunity. The problem with tenance of illness. Ultimately, the presence and impact of this concept is that many of the current psychoimmu-

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that consequent illness, especially if pain is concomitant,NKC activity and possibly reducing mutagenic effects), can easily become a stressor unto itself and further mitihelps the patient tangibly connect with intervening in his or gate stress-induced immunosuppression. In this model her own treatment (Davis, 1986). then, a downward spiral of health requiring significant multimodal intervention is required if we are to reverseCRANIAL ELECTROTHERAPY STIMULATION (CES) its direction. With patients having dif ficulty achieving therapeutic levels of alpha states, even with biofeedback, cranial elecBASIC STRATEGIES OF CHANGE trotherapy can assist by passing microcurrents through the cranial area via electrodes attached to the earlobes. BIOFEEDBACK CES stimulation has been shown to be helpful when Biofeedback as a form of intervention provides the patientutilized for emotional distress such as depression and with an increased sense of control over physiologicalanxiety by teaching the patient how to achieve a relaxed, responsivity to stressors. Through monitoring their EMG,quieted but alert state. While CES has not been found traditionally to be useful in treating stress-related disorEEG, and/or thermal responsiveness to covert and/or overt stimuli, patients can learn to significantly reduce physio-ders, recent studies have begun to demonstrate its effeclogical reactivity. Biofeedback can be especially useful intiveness. Research has also demonstrated utility in pain management. By passing microcurrents through affected reducing arousal responses to conditioned stressors such pain regions, patients report signifi cant reductions at the asfinger sticks, nausea associated with chemotherapy, and sites of their pain. By combining CES with microcurrent stress-induced cervical headaches associated with envistimulation at pain sites patients can reduce emotional ronmental queues (i.e., entering a hospital). distress and physical discomfort (Kirsch, 1999), thereby In addition, by experiencing feedback on their physipositively impacting upon the pain and emotional comological functioning, patients who have been educated ponents of the PNI triad. The pain relief associated with about the concept of PNI can gain an increased sense of microcurrent stimulation may provide the patient with an control (previously noted as extremely important) over increased sense of control over pain and a smoothing of their physiological responsiveness and, thereby, over their EEG peaks (associated with pain) when emotional and environmental stressors. It provides for the generally posphysical complaints are conjointly present (Hefferman, itively perceived concept oflearning “ and master”to be placed back into the patient’ s hands. For example, even 1997). Because this treatment can often be self adminispatients who feel little control over their illness and/or paintered by the patient, it further enhances their sense of can gain some emotional and/or pain relief by focusing onself-effi cacy. It has little or no documented negative interminor successes in controlling physiological changes dur-actions with other forms of treatment. ing biofeedback. Immediate biological biofeedback may VISUALIZATION/IMAGERY be especially helpful with patients who evidence low to moderate levels of hypnotizability, whereas highly hypno-Visualization has been conceived as the active process tizable patients appear to benefi t more from delayed bio- by which we “voluntarily and intentionally instruct the logical feedback. In delayed biofeedback, information isbody.” Whereas imagery is the spontaneously occurring provided after several minutes of self-hypnosis training in“ appearing in unconsciousness” modifier, qualifier, or order to shape and confi rm the effi cacy of the self-hypnosis belief emerging from the unconscious (Norris, 2000). training (Wickramasekera, 1999). Visualization represents how we ingest the world around Within the thermal biofeedback approach, one goal isus and what we then transfer to our unconscious or to teach the patient to lower sympathetic nervous system cognitive processing mind. Imagery represents how we activity level through autogenic hand warming. Additionally, interpret that information from the perspective of our a quieting of the muscular armoring through EMG biofeed-internal beliefs and knowledge base. It represents, What “ back can benefi t patients by reducing stress-induced pain asdoes that visualization mean to me?” Perhaps more sucwell as pain-induced stress. The relaxing of the physiologycinctly stated, as clinicians, we can guide patients into and musculature is then enhanced with EEG biofeedback varying visualizations but the imagery is the process where patients can induce increased alpha and beta wave within them, their “experience” of the visualization. activity, thereby seeking to incur a quieter mental and emoThrough the use of imagery, patients can learn to change tional state. Alterations of cognitions, beliefs, and percep-their outlooks for the future, and for the illness process. tions can be achieved via the association of altered physioThis has been shown to be tremendously helpful in logical states with new concepts and coping thoughts.improving clinical outcomes. Bibliotherapy in conjunction with the biofeedback, which Pioneering in the use of imagery in fighting cancer in includes educating the patient about the benefi ts controlling works such asLove, Medicine, and Miracles(Siegel, stress responses has upon their limbic system (increasing 1986) helps patients develop a sense of personal ficacy ef

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in dealing with their illnesses, and enhancing the PNIin turning over control to the therapist (i.e., pain mantriad. Visualization can help patients focus on the events agement) or where the patient enters the therapeutic they are experiencing in the process of working throughsetting with significantly impaired feelings of selftheir illnesses. empowerment or self-ef ficacy. An excellent example of the use of imagery applied The need to feel thatthe “ therapist is hypnotizing to the treatment of severe and chronic illness, especially them” provides an initial sense of being taken care of, cancer, is the program developed by Mitchell Gaynor,which may be critical to some patients, especially those M.D. In his book,Healing E.S.S.E.N.C.E. , he details the deeply ingrained in the medical model. Issues of suggestuse of imagery throughout seven steps toward healing: ibility and susceptibility are often raised when arguing the experiences, see, surrender, empower, nurture, create, effectiveness of traditional hypnotherapeutic interventions. embody (Gaynor, 1995). Even patients with no prior With regard to pain management, significant support experience with imagery can develop a practical andexists for the importance of the hypnotic suggestibility of useful means of controlling illness and enhance the healpatients. Highly suggestible patients demonstrate signifiing process. cantly greater pain tolerance (DePascalis, Magurano, & Whatever the name, mental imagery (Moye, Richard-Bellusci, 1999; Farthing, Venturino, Brown, & Lazer, son, Post-White, & Justice, 1995), guided imagery (Giedt,1997; Rainville, Carrier, Hofbauer, Bushnell, & Duncan, 1997), relaxation imagery (Andrews and Hall, 1990), and1999; Sandrini et al., 2000; Zachariae, Anderson, Bjerring, autogenic training (Benor, 1996) have been shown to be Jorgensen, & Arendt-Nielsen, 1998) and postoperative immuno-enhancing. In a somewhat more extreme example recovery than less suggestible patients (Defechereuz, of drug-induced imagery states, Roberts (1999) found that Meurisse, Hamior, Gollogly, Jorus, & Faymonville, 1999; entheogen-induced mystical and peak experiences may Mauer, Burnett, Oullette, Ironson, & Dandes, 1999). Other boost the immune system. studies have demonstrated that the ability to be hypnotized may be less of a factor especially in emergency room settings where an increase in hypnotic susceptibility may HYPNOSIS be induced by the trauma (Pebbles-Kleiger, 2000). Hypnosis is arguably the most effective approach in unifying the different aspects of the PNI triad. In ways, Indirect Approaches hypnosis may encompass many of the other approaches previously mentioned. Hypnosis can have a positiveCurrently, one of the most commonly utilized indirect effect on illness by intervening at several levels includinghypnotic approaches is Ericksonian hypnosis. Ericksonian symptom alleviation, emotional stabilization, stresshypnosis promotes the idea of trusting in the patient’ s reduction, self-image enhancing, and self-ef ficacy unconscious to deal with issues that arise. By its very empowering. It also can be employed in directly attempt-nature, Ericksonian hypnosis employs a psychoimmunoing to enhance endocrine responsiveness and CNS reactherapeutic bent. Through the use of metaphor, storytelling tivity as well as pain control. Kalt (2000) states that techniques, and indirect suggestion, the patient is asked “ techniques which attempt to infl uence the mind fall into to seek what internal images or associations arise while the theoretical categories of passive, active, or targeted in a hypnotic state in order to bring about emotional and approaches, each of which may carry varying degrees of psychotherapeutic change (Erickson, 1980). Distraction importance in immuno-enhancement. ” and dissociative suggestions have been utilized with pain Hypnosis has often been segregated into three general patients within the Ericksonian model (Burte, Burte, & orientations. These include direct, indirect, and nondirec-Aroaz, 1994). The therapist often acts in a reflective mantive approaches. The following is a brief discription of ner, guiding the patient into a deepening understanding of each approach and its utility in PNI intervention. the spontaneously generated images by applying metaphors or stories to relay the hypnotic suggestion while Traditional Approaches of Direct Suggestion allowing the patient to integrate the message into his or her own schema. The therapist helps the patient to underwith Formal Induction stand the nature and origin of his or her symptoms, In these approaches, general trance depth is considered whether emotional, physical, or physiological. Ericksoto be important in symptomological change, or behav-nian approaches have been extensively employed in the ioral changes are given as a directive from the therapist. treatment of medical illness both symptomologically and Although imagery may be employed, it is often the etiologically (Erickson, 1986). hypnotherapist’ s conceptualizations that direct the Simonton and Henson (1992) utilize hypnotic patient’s internal experience. Direct hypnotic approaches in helping patients learn how to increase their approaches have been effectively used, especially in ability to heal (enhance their PNI triad).Visualizing their situations where the patient either is strongly investedbodiesfighting illness by generating increased T-cells (i.e.,

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little white Pac men eating the cancer) or visualizing bron-promising results. Perhaps of most significance in PNI is chial dilation or shunting off blood flow to a tumor are the concept of repressed trauma as a possible precursor to examples of but a few of the plethora of indirect hypnoticimmunosuppression. applications patients can utilize. Group Therapy Nondirective Approaches Extensive work has been conducted on the impact of group The new hypnosis initially developed by Araoz (1985) therapy and stress management on immunosuppression. presents a somewhat different model than either the traDavid Speigel’s (1999) work with breast cancer patients ditional (direct suggestion) or Eriksonian models (indirectdemonstrates theficacy ef of group support as does the work suggestion). The new hypnosis utilizes the symptomsof other researchers who have found subsequently that brought to the session by the patient as the means of group therapy can enhance life expectancy and functioning entering the patient’ s “inner state. ” A process of observing of patients with HIV and other immunosuppressant disorthe patient’s somatopsychic behaviors (i.e., hair twirling, ders. It appears that group therapy offers patients a sense fist clenching), and psychosemantic expressions (i.e., “he of cohesiveness and an opportunity to express their negative turns my stomach”) within the framework of how theseemotions and beliefs while simultaneously helping them actions are manifested through the visual, auditory, olfac-develop a better mental attitude and coping skills which, in tory/taste, proprioceptive, and kinesthetic senses is initi-turn, appears to enhance immune system functions. ated. Patients are then led into their own inner aware- Societal isolation and self-imposed feelings of family nesses. They are encouraged not to judge or critique what isolation (even at times when under the best of supportive arises. Often the patients gain new insights into the proconditions) negatively impact the PNI triad in the chronic cess, which affects their interpretations or reactions topain and chronically ill patient (Hitchcock, 1998). Lack stressors. of family coherence, at times present with severely ill At this point, patients are given the opportunity to patients, emphasizes the importance of group therapy as “visualize and introduce changes that promote greater well an outlet for these patients. It provided a sense of coherbeing.” Perhaps most critical in the PNI framework is the ence and support that they cannot obtain from their famconcept of negative self-hypnosis (NSH). Patients oftenilies or personal support networks. A review of the literfind that they maintain negative self-hypnotic statementsature appears to suggest that a diverse range of such as broad concepts of “I can never overcome this therapeutic/support groups may be effective, and, in fact, illness, it is going to kill me” to more minute specific it may be merely the intangible element of not facing beliefs about their illnesses or stressors. adversity alone that enhances immune functioning. Stress The goal in applying the new hypnosis or any hypnoticmanagement, pain management, coping skills developintervention is to be able to intervene and exchange those ment, dance, acting “as ”if,group laughter, supportive negative self-hypnotic beliefs for positive self-hypnotic nondirective groups, all appear to contribute positively to beliefs (PSH). This is best accomplished when, throughpatient well-being and demonstrate PNI enhancement. the hypnotic experience, the patient feels a change that comes from changes in his or her inner awareness and Meditation belief system. For example, a patient who was experiencRole Play and Dance ing chest pain of a nonorganically based nature, reported Another technique found to impact the immune system that in trance, due to unresolved issues with his father he includes meditation, which via the pineal gland fluences in became aware of the pain as an image of his father’ s fist melatonin levels, which, in turn, have been shown to modsqueezing his heart. Upon imaging a conversation where he resolved these issues and could see his father’ s hand ulate the progression of breast and prostate tumors (Coker, 1999). In addition to covert techniques such as meditation, stroking his heart, the pain abated (Burte, 1989). the mere outward expression or acting/modeling “ of happy In situations where pain or stress has a clear etiologbehaviors have been found to stimulate endorphins and ical basis, the new hypnosis has been employed in devel(Anderson, 1997). This oping coping skills, visualizing analgesia, or promotingenhance immune system function” dif to convince positive internal representation for changes in biophysiol-may be especially helpful when it is ficult patients of the impact of their negativistic thinking. At such ogy (Burte et al., 1994). times, perhaps we can encourage them “ act to as if” they were happy in order to bring about immunological changes. Eye Movement Desensitization and Still other researchers have found that dance therapy Reprocessing (EMDR) (Hanna, 1995) may improve patient immune functioning An interesting new approach, known as EMDR, has been possibly by providing proprioceptive feedback and feelings employed with trauma patients. It demonstrates some of self-effi cacy and physical self-control during those times.

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. New York: BrunA variety of other modalities too far reaching to encom-Araoz, D.L. (1985). The new hypnosis ner/Mazel Inc. pass in this brief chapter also deserve mentioning as they Benor, R. (1996). Autogenic training. Complementary Therapy are represented in the PNI literature. Behavioral approaches in Nursing and Midwifery , 2(5), 134–138. (Caudell, 1996; Cottraux, 1993; ), diet and psychological health (Miller, 1996; Norris, 2000), healing energy (Wright Berin, M.C., & Perdue, M.H. (1997). Effect of psychoneural factors on intestinal epithelial function. Canadian Jour& Sayre-Adams, 1999), laughter and music (Bittman, 2000; nal of Gastroenterology , 11(4), 353–357. Strickland, 1993), and exercise (LaPierriere, Ironson,Biondi, M., & Zannino, L.G. (1997). Psychological stress, neuroAntoni, Schneiderman, Klimas, & Fletcher, 1994) have immune-modulation and susceptibility to infectious disbeen demonstrated to provide positive changes, although eases in animal and man: A review. Psychotherapy and further investigation of their mechanisms is necessary. Psychosomatics, 66 (1), 3–26. Physical manipulative techniques that directly affectBittman, B. (2000, September) Psychoneuroimmunology of laughter and music. Paper presented at the 11th annual clinical the physiology and nerve transmission, such as chiropracmeeting of the American Academy of Pain Management. tic massage therapy (Homewood, 1981; Rich, 1999) may . S. bring physical and restorative relief and provide pain con-Burte, J.M. (1989, October).Internally directed hypnosis Rosenberg (Ed.), New York Society of Clinical Hypnotrol (with or without opioids). These are but a few sis course workbook. approaches that may promote healing via reducing stress, Burte, J.M., Burte, W., & Aroaz, D.L. (1994). Hypnosis in the reducing pain, or enhancing patientficacy. ef treatment of back pain. Australian Journal of Clinical A word of caution is raised by Greer (1991), who notes Hypnotherapy and Hypnosis, (2), 15 93–115. that within the PNI model of intervention, one must be onBurte, J.M., & Aroaz, D.L. (1994). Cognitive hypnotherapy with guard that a blaming “ the victim”mentality is not promulsexual disorders.Journal of Cognitive Psychotherapy gated inadvertently. Emphasis should be on positive change, Winter, 8, 299–311. not responsibility for creating one’ s own impaired status. Burte, J.M. (2000). Psychoneuroimmunology. Paper presented at the 11th annual meeting of the American Academy Any intervention that increases the individual ’s sense of of Pain Management, Sept. 21, 2000. control of his or her environment or pain level reduces stress, enhances optimism and self-ef ficacy, impacts the Caudell, K.A. (1996). Psychoneuroimmunology and innovative behavioral interventions with leukemia. Oncology NursPNI triad proactively, and may promote increased health by ing Forum, 23(3), 493–502. reducing immunosuppression (Burte, 2000). Christensen, A.J., Edwards, D.L., Wiebe, J.S., Benotsch, E.G., “Goodbye” said the fox.And “ now here is my secret, McKelvey, L., Andrews, M., & Lubaroff, D.M. (1996). a very simple secret. It is only with the heart that one can Effect of verbal self-disclosure on natural killer cell see rightly. What is essential is invisible to the ”eye. “What activity: Moderating influence of cynical hostility. Psyis essential is invisible to the eye” the little prince repeated chosomatic Medicine, 58 (2), 150–155. so that he would be sure to remember (Antoine de SaintCoker, K.H. (1999). Meditation and Prostate Cancer: integrating Exupéry, 1943). a mind/body intervention with traditional therapies. Seminars in Urologic Oncology, (2), 17 111–118. Cottraux, J. (1993). Behavioral psychotherapy applications in ACKNOWLEDGMENTS medically ill. Psychotherapy and Psychosomatics, 60(3–4), 116–128. I would like to acknowledge Michele Underwood, Steve Coyle, P.K. (1996). The neuroimmunology of multiple sclerosis. Bonomo, and Theresa Barle for their assistance. Advances in Neuroimmunology,(2), 6 143–154. Dabkowska, M., & Rybakowski, J. (1994). Stress, depression and schizophrenia in view of psycho-immunology. PsyREFERENCES chiatria Polska, 28 (3 Suppl.), 23–32. Davis, H. (1986). Effects of biofeedback and cognitive therapy Affleck, G., Urrows, S., Tennen, H., Higgins, P., Pav, D., & on stress in patients with breast cancer. Psychological Aloisi, R. (1997). The dual pathway model of daily Reports, 59 (2), 967–974. stressor effects on rheumatoid arthritis. Annals of Behav- Defechereux, T., Meurisse, M., Hamoir, E., Gollogly, L., Joris, ioral Medicine, 19(2), 161–170. J., & Faymonville, M.E. (1999). Hypnoanesthesia for Altman, F. (1997). Where is the “neuro” in psychoneuroimmuendocrine cervical surgery: A statement of practice. nology? A commentary on increasing research on the Journal of Alternative Complementary Medicine, (6),5 “neuro” component of psychoneuroimmunology. Brain, 509–520. Behavior, and Immunity, 11 (1), 1–8. DePascalis, V., Magurano, M.R., & Bellusci, A. (1999). Pain Andersen, D.L. (1997). Nurses: act now! Journal of Practical perception, somato-sensory event related potentials and Nursing, 47(1), 16–18. skin conductance responses to painful stimuli in high, Andrews, V.H., & Hall, H.R. (1990). The effects or relaxation/imagmid, and low hypnotizable strategies. Pain, 82(2), ery training on recurrent aphthous stomatitis: a preliminary 159–171. study.Psychosomatic Medicine , 52(5), 526–535. de Saint-Exupéry, A. (1943). The Little Prince. New York: Harcourt Brace (reprinted 1982).

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Eller, L.S. (1998). Testing a model: Effects of pain on immunity Holmes, T.H., & Rahe, R.H. (1967). The social readjustment rating scale.Journal of Psychosomatic Research,(2), 11 in HIV + and HIV– participants.Scholarly Inquiry for 213–218. Nursing Practice, 12 (3), 191–124. Erickson, M.H. (1980). Hypnotic alteration of sensory percep-Homewood, A.E. (1981).The neurodynamics of vertebral sublaxation. St. Petersburg, FL: Valkyrie Press. tual and psychological process. In E. Rossi (Ed.), The Kalt, H.W. (2000). Psychoneuroimmunology: An interpretation collected papers of Milton H. Erickson on hypnosis (Vol. of experimental and case study evidence towards a parII). New York: Irvington Press. adigm of predictable results. American Journal of HypErickson, M.H. (1986). Mind-body communication in hypnosis. nosis, 43(1), 41–52. In E. Rossi & M. Ryan (Eds.), The seminar, workshops Kaye, J., Morton, J., Bowcutt, M., & Maupin, D. (2000). Stress, and lectures of Milton H. Erickson (Vol. 1). New York: depression and psychoneuroimmunology. Journal of Irvington Press. Neuroscience Nursing, 32 (2), 93–100. Farthing, G.W., Venturino, M., Brown, S.W., & Lazar, J.D. (1997). Internal and external distraction in the control Kelly, S., Hertzman, C., & Daniels, M. (1997). Searching for the biological nature of pain.Seminars in Oncology of cold pressor pain as a function of hypnotizability. Nursing, 13(1), 10–15. International Journal of Clinical Experimental HypnoKiecolt-Glaser, J.K., Page, G.G., Marucha, P.T., MacCallum, sis, 45(4), 433–446. R.C., & Glaser, R. (1998). Psychological influences on Garssen, B., & Goodkin, K. (1999). On the role of immunologsurgical recovery. Perspectives from psychoneuroimmuical factors as mediators between psychosocial factors nology. American Psychologist, 53 (11), 11209–11218. and cancer progression. Psychiatry Research, 85 (1), Kirsch, D. (1999).The science behind cranial electrotherapy 51–61. stimulation: An annotated bibliography . Edmonton, Gaynor, M. (1994).Healing E.S.S.E.N.C.E. A cancer doctor’s Canada: Medical Scope Publishing Company. practical program for hope and recovery . New York: Klapheke, M.M. (2000). Transplantation psychoneuroimmunolKodansha International. ogy: Building hypotheses. Medical Hypotheses , 54(6), Geiss, A., Varodi, E., Steinbach, K., Bauer, H.W., & Anton, F. 969–978. (1997). Psychoneuroimmunological correlates of persisting sciatic pain in patients who underwent discec-Koenker, H. Stress and the Immune System. http://www.econ.uiuc.edu/~hanko/bio/stress.html. tomy. Neuroscience Letters, 237 (2–3), 65–68. The Giedt, J.F. (1997). Guided imagery. A psychoneuroimmunolog-Kremer, M.J. (1999). Surgery, pain and immune function. Clinical Forum for Nurse Anesthetists , 10(3), 94–100. ical intervention in holistic nursing practice. Journal of LaPerriere, A., Ironson, G., Antoni, M.H., Schneiderman, N., Holistic Nursing, 15(2), 112–127. Klimas, N., & Fletcher, M.A. (1994). Exercise and psyGlaser, R. (1996). The effects of stress on the immune system: choneuroimmunology.Medicine and Science in Sports Implications for health. Summary of presentation on and Exercise, 26 (2), 182–190. Dec. 17, Science Writers Briefings, OBSSR and APA. Laudenslager, M.L. (1983). Coping and Immunosuppression. http://www/.od.nih.gov/obssr/stresimn.htm Science, 221 , 568. Greer, S. (1991). Psychological response to cancer survival. PsyMarbach, J.J., Schleifer, S.J., & Keller, S.E. (1990). Facial pain, chological Medicine, 21 (1), 43–49. distress, and immune function. Brain, Behavior, and Hall, M., Baum, A., Buysse, D.J., Prigerson, H.G., Kupfer, D.J., Immunity, 4(3), 243–254. & Reynolds, C.F. III. (1998). Sleep as a mediator of the stress-immune relationship. Psychosomatic Medicine, Martin, P. (1998).The healing mind: The vital links between brain and behavior, immunity and disease . New York: 60(1), 48–51. St. Martin’s Press. Hanna, J.L. (1995). The power of dance: health and healing. Journal of Alternative and Complementary Medicine, Masek, K., Petrovicky, P., Seucik, J., Zidek, Z., & Frankova, D. (2000). Past, present and future of psychoneuroimmu1(4), 323–331. nology. Toxicology,142(3), 179–188. Hefferman, M. (1997). The effect of microcurrent of EEG spectrum and pain control.Canadian Journal of Clinical Mauer, M.H., Burnett, K.F., Oullette, E.A., Ironson, G.H., & Dandes, H.M. (1999). Medical hypnosis and orthopedic Medicine, 4(10), 4–11. hand surgery: Pain perception, postoperative recovery Hickie, I., Bennet, B., Lloyd, A., Heath, A., & Martin, N. (1999). and therapeutic comfort. International Journal of ClinComplex genetic and environmental relationships ical and Experimental Hypnosis, (2), 47 144–161. between psychological distress, fatigue and immune Alternative functioning: A twin study. Psychological Medicine, Miller, M. (1996). Diet and psychological health. Therapies in Health and Medicine,(5), 2 40–48. 29(2), 269–277. Hiramoto, R.N., Solvason, H.B., Hsueh, C.M., Rogers, C.F.,Moye, L.A., Richardson, M.A., & Post-White, J.B. (1995). Research methodology in psychoneuroimmunology: Demissie, S., Hiramoto, N.S., Gauthier, D.K., Lorden, rationale and design of the IMAGES-P clinical trial. J.F., & Ghanta, V.K. (1999). Psychoneuro-endocrine Alternative Therapies in Health and Medicine,(2),1 immunology: perception of stress can alter body tem34–39. perature and natural killer cell activity. International Muller, N. (1997). Role of the cytokine network in the CNS and Journal of Neuroscience, (1–2), 98 95–129. psychiatric disorders. Nervenarzt, 68(1), 11–20. Hitchcock, L.S. (1998). The role of self-help groups in easing chronic pain. In R. Weiner (Ed.). Pain management: A Norris, P. (2000). Self-regulation for immune system disorders. http://www.cjnetworks.com/~lifesci/immu.htm practical guide. Boca Raton: CRC Press.

816

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The healing journey. New Overcash, S.J. (1999). A retrospective study to determine fi- ef Simonton, O.C., & Henson, R. (1992). York: Bantam. cacy of cranial electrotherapy stimulation (CES) on Solomon, G.F., Segerstrom, S.C., Grohr, P., Kemeny, M., & patients suffering from anxiety disorders. American Fahey, J. (1997). Shaking up immunity: psychological Journal of Electromedicine, 16 (1), 49–51. and immunologic changes after a natural disaster. PsyPage, G.G., & Ben-Eliyahu, S. (1997). The immune-suppressive chosomatic Medicine, 59 (2), 114–127. nature of pain.Seminars in Oncology Nursing, (1), 13 Spiegel, D. (1999). Embodying the mind in psycho-oncology 10–15. research.Advances in Mind and Body Medicine,(4), 15 Parker, J.C., Smarr, K.L., Angelone, E.O., Mothersead, P.K., Lee, 267–273. B.S., Walker, S.E., Bridges, A.J., Caldwell, C.W. (1992). Today’s OR Psychological factors, immunologic activation and dis- Strickland, D. (1993). Seriously, laughter matters. Nurse,15(6), 19–24. ease activity in rheumatoid arthritis. Arthritis Care Turk, D., Merchenbaum, D., & Genest, M. (1983). Pain and Research, (4), 5 196–201. behavioral medicine: A cognitive-behavioral perspecPeebles-Kleiger, M.J. (2000). The use of hypnosis in emergency tive. New York: Guilford Press. medicine.Emergency Medicine Clinics of North AmerVan der Pompe, G., Antoni, M., Visser, A., & Garssen, B. (1996). ica, 18(2), 327–338. Adjustment to breast cancer: The psychobiological Pike, J.L., Smith, T.L., Hauger, R.L., Nicassio, P.M., Patterson, effects of psychosocial interventions. Patient Education T.L., McClintick, J., Costlow, C., & Irwin, M.R. (1997). and Counseling, 28 (2), 209–219. Chronic life stress alters sympathetic, neuroendocrine and immune responsibility to an acute psychologicalVedhara, K., Fox, J.D., & Wang, E.C. (1999). The measurement of stress-related immune dysfunction in psychoneurostressor in humans.Psychosomatic Medicine, (4), 59 immunology. Neuroscience and Biobehavior Reviews, 447–457. 23(5), 699–715. Rainville, P., Carrier, B., Hofbauer, R.K., Bushnell, M.C., & Duncan, G.H. (1999). Dissociation of sensory and affec-Watt, D., Verma, S., & Flynn, L. (1998). Wellness programs: A review of the evidence. Canadian Medical Association tive dimensions of pain using hypnotic modulation. Journal, 158(2), 224–230. Pain, 8(2), 159–171. Wickramasekera, I. (1999). How does biofeedback reduce clinRich, G.J. (1999). Healing hands. Psychology Today , 32(2), 23. ical symptoms and do memories and beliefs have bioRoberts, T.B. (1999). Do entheogen-induced mystical experilogical consequences? Toward a model of mind–body ences boost the immune system? Psychedelics, peak healing. Applied Psychophysiology and Biofeedback, experiences and wellness. Advanced Mind and Body 24(2), 91–105. Medicine, 5(2), 139–147. Wright, S.G., & Sayer-Adams, J. (1999). Healing energy and Sali, A. (1997). Psychoneuroimmunology: Fact or fiction. Jourthe complementary therapies. Complementary Therapy nal of the Family Physician, 26 (11), 1291–1294, in Nursing and Midwifery , 5(4), 95–97. 1296–1299. Sandrini, G., Mianov, I., Malaguti, S., Nigvelli, M.P., Moglia, Yang, E.V., & Glaser, R. (2000). Stress induced immunomodulation: Impact on immune defenses against infectious A., & Napp, G. (2000). Effects of hypnosis on diffuse disease. Biomedicine and Pharmacotherapy, (5), 54 noxious inhibitory controls.Physiological Behavior , 245–250. 69(3), 295–300. Schrader, K.A. (1996). Stress and immunity after traumaticZachariae, R., Andersen, O.K., Bjerring, P., Jorgensen, M.M., & Arendt-Nielsen, L. (1998). Effects of opioid antagonist injury: The mind-body link.American Association of on pain intensity and withdrawal reflexes during inducClinical Nursing Clinical Issues, (3), 7 351–358. tion of hypnotic analgesia in high and low hypnotizable Segerstrom, S. (1998). Optimism is associated with mood, copvolunteers.European Journal of Pain,(1), 2 25–34. ing and change in response to stress. Journal of PersonZautra, A.J., Hoffman, J., Potter, P., Matt, K.S., Yocum, D., & ality and Social Psychology, (6), 74 1646–1655. Castro, L. (1997). Examination of changes in interperSelye, H. (1956).The stress of life . New York: McGraw Hill. sonal stress as a factor in disease exacerbation among Selye, H. (1976).Stress in health and disease . Woburn, MA: women with rheumatoid arthritis. Annals of Behavior Butterworth. Medicine, 19(3), 279–286. Siegel, B. (1998).Love, medicine and miracles. New York: Harper and Row.

65 Variables in the Sensation and Perception of Pain Richard H. Cox, M.D., Ph.D., D.Min. and John Essman, M.A., R.E.E.G./E.P.T., R.P.S.G.T. to see that physical pain can be reduced or increased by emotional and spiritual pain and vice versa. The latest version (1995) ofRoget’s Thesaurus classifies pain as a Albert Schweitzer physical experience, as does the Sixth Edition (2000) of The Columbia Encyclopedia. Our definitional literature has not caught up with the experiential world. INTRODUCTION Practitioners are now challenged to preserve goodpain Pain is doubtless one of the most illusive and complicated while attempting to eliminate bad pain. Someone has said aspects of life, particularly for the practicing health pro-that without pain we could die without knowing that we fessional. From the inception of recorded human historywere sick. Therefore, there is good pain, i.e., that pain everyone from the afflicted to sages, philosophers, theowhich triggers action to protect the body and mind. Howlogians, and magicians have attempted to enlighten us ever, there is also bad pain that produces more pain and regarding this condition. We are now wise enough to knowsuffering. Sometimes the signals of these two kinds of that what we are currently recording will no doubt alsopain become confused and produce even greater suffering be shown to be just as naive in years to come. Yet, despite and actually escalate simple neuropathic pain into allothis, we must try to consolidate what we know in andynia, the normally nonpainful stimulus that is perceived attempt to help those living in this era of history. We nowas painful, and is probably psychologically mediated. The know enough to see pain as more than a result and more possibility that such pain is psychologically mediated does than a syndrome. It is doubtless an illness all its own.not, however, mean that the pain is psychosomatic (psyPortenoy (1996) conceptualized longstanding pain assochologically induced) or only imagined. The etiology of ciated with tissue damage as far more disabling than the pain and the mediation of pain are not the same. The origin injury itself. of a neurological message and the transmission of that caused be by Whereas “pain” has traditionally been thought of asmessage are not the same thing. Pain may psychological stimuli or the stimulus may be transmitted a result of distress, usually with physical etiology, we now neurologically, or in variations and combinations. Allorecognize many kinds of pain arising from multiple, sindynia may truly be somatopsychic and real regardless of gular, and combined sources. Whereas physical pain conthe mechanism that produced the final perceived sensation tinues to be our greatest challenge in the medical world, other disciplines have joined to remind us of emotional(Iadarola & Caudle, 1997). pain and spiritual pain. We have come to recognize the Because pain is highly individualized and individuinterconnection of these kinds of pain and the reciprocalally reported, it is possible that a practitioner could nature of the origins and amplifiers of pain. We have come unwittingly create a state for future serious injury Whosoever is spared personal pain must feel himself called to help in diminishing the pain of others.

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designated intrinsic properties of conscious experience. because of neuropathic reporting and the subsequent alleviation of good pain. Illustrative of this are the per- However, any health service provider who has worked with unconscious patients knows that even in the state of sons who have been delivered from headache only to die from undiagnosed brain tumors. When healers aredeep coma patients respond to deep pain, proving that consciousness is not a necessary requirement for pain instructed by the Oath of Hippocrates to do“ no harm, ” they must first recognize that the remediation of pain, in perception. The qualia become beneficial in diagnosis and and of itself, although seemingly a noble gesture, maytreatment of illness because they provide us with the in truth not always be the most benefi cial goal of treat- descriptors, and the descriptors have common and frequent relationships to certain physiological conditions. ment. Every quadriplegic knows that the absence of pain Certainly the more accurately a patient can describe the is a serious detriment to one’ s health. Pain is a multichannel warning system within the pain, the more likely the physician will be able to provide human body. It is transmitted via many different pathwaysthe correct remedy. and culminates in the body’ s awareness that something is Descarte believed that pain was a simple mechawrong. However, pain is more than a warning system. Itnism of action–reaction. As simplistic as this descripis frequently an entity in itself that precludes normaltion is, the vast majority of persons who adhere to thought and physiological functions. Illustrative of this areWestern medical thought maintain a view that is not conditions such as post-herpetic neuralgia, a condition in very different. The rapidly growing body of literature which the nervous system continues to emit painful mes-regarding pain is proving that pain is not simply an sages long after the actual viral infection has been arrested. action–reaction phenomenon but a complex neural, When this is the case, the pain becomes both the etiology chemical, anatomical, emotional, and cultural mixture. and the result of a condition that is definable as a separate Most health service providers, even in the Western and distinct illness. world, have given up the Cartesian mind/body separation, but we as yet have insuf ficient practitioner understood knowledge of the complex mechanisms we know THE CHALLENGE OF PAIN are present but as yet unexplained. MEASUREMENT AND ASSESSMENT Pain and suffering are not synonymous although often companions. Culturally mediated experiences of One of our greatest unsolved problems in dealing with the same kind of stimuli produce different levels of perpain is our inability to see or measure it. We are getting ceived suffering. Athletes, martyrs, and mentally ill and closer to understanding substance P and its binding recephypervigilant persons have been reported to experience tor NK-1. The release of neuroactive substances such as severe traumatic stimuli that under other conditions and glutamate, calcitonin, along with substance P and subin other cultures are reported as very different levels of stance K combines with biochemical mediation of nocisuffering. There is no absolute correlation between the ceptive neurons, producing a perceived and probable actual stimulus of pain and the reported level of sufferactual change in the neurogenic recognition and transmising. Persons experiencing coma, yoga, hypnosis, and sion of the stimulus, which is ultimately experienced as other states of altered consciousness have shown the pain. Good pain and bad pain are by all probability “attenpresence of pain stimulus without the recognition of such uated by different toxin-ligand molecules” (Iadarola & by the person experiencing it. The attempt to measure Caudle, 1997). pain by its consequent manifestations of suffering are, There have been several attempts to measure pain; therefore, without scientifi c or experiential bases however, none has proven valid. The Gaston-Johansson (McQuillen, 1991). Pain-O-Meter and the Gaston-Johansson Pain-O-Meter Visual Analogue Scale are attempts to quantify and iden- The aspect of suffering has been coupled with the tify levels of pain (Sittner, Hudson, Grossman, & Gaston-degree to which the etiology of the pain is perceived to be a threat to the patient as a person. This has also been Johansson, 1998). In the final analysis, the only reliable called one’s “ Total pain” (Cassel, 1982). It stands to measurer of pain is the person experiencing it. Pain is most reason that a threat of change or loss of life can markedly accurately measured by descriptors such as “burning ,” “lancinating,” “stabbing,” “aching,” “throbbing,” etc. The impact the meaning and, therefore, the attention paid to said stimulus, with the ultimate stakes of an impaired perception of pain measurement on a scale of one to ten quality of life, which could result in social isolation, is probably as beneficial to most practitioners as anything. The patient can then indicate if the remediation is provid-occupational difficulties, and financial hardship to name s ing a lesser or greater scale score. Perception, in truth, but is a few. This can stand as a true test of a person’ everything when it comes to the phenomenon of pain. character, possibly adding kindling to underlying dysDoubtless one’ s level of consciousness is related to functional character traits, which could lead to a multione’s perception of pain. Qualia are the philosophicallytude of poor choices.

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Pain is more strongly linked with emotion than any other area of perception (Matlin, 1988). A visual perception, There are only minor and poorly substantiated differences in each gender’ s perception of pain. These vague andsuch as a beautiful sunset, exists out there in the environment and, therefore, can be a common or shared experinonscientifically based reports tend to indicate that much ence with another individual. In contrast, a perception of additional study is needed before one can conjecture regarding gender-related pain (Marble, 1999). Kellypain, such as a toothache, is a much more in here experience, within the confines of our bodies; therefore, such an (1999) asserts that because women probably experience ficult to convey to others (Verillo, 1975). pain more frequently than most men, they feel pain moreexperience is dif keenly, yet women have a lower threshold for pain than Pain is a subjective experience depending on the men. The research is scant and far from scientificallynature of the perception of the individual; therefore, the experience of and response to a given painful stimuli can based on this subject. Children are most interesting in their reactions tochange as the perception changes. Cornock (1996) pointed s pain. They tend to relate pain to various actions doneout a few of the many factors that may affect a person’ perception of any given painful stimulation. He included to them, and they tend to see all pain as bad. As children mature, differentiate pain and its severity into variouscultural factors, the context in which the pain occurs, categories. Young children see pain as having anexpectations, emotions, motivations, personality, past “ owie,” or being “stuck or poked, ” or simply that it experiences, and preparations. To understand these as “ stings” or “burns.” We, of course, know that young some of the contributing influences of the net experience a person has provides the clinician with key elements for children do not relate causality to consequence in the addressing a person’ s past experiences to help change the same fashion as do older children or adults. It only goes present perception of a painful process. to reason that they would perceive pain as whatever is present in the end state. Much the same as the child Interestingly, pain research has investigated essentially every aspect covered in a basic college psychology who spills the milk says, the “ milk spilled,” the child in pain says simply that it“ hurts” (Woodgate & course, including learning and motivation, psychophysics and perception, brain and behavior, memory and cogniKristjianson, 1996). The same ambiguity is present in attempting to dif-tion, individual differences, development, personality, ferentiate the experience of pain by ethnicity. A recentpsychological disorders, and social behavior (Craig & study reported that white persons reported less“ severe Rollman, 1999). To truly understand a pain process holisdisabling pain and withstood more pain for longer inter-tically, one must understand physiology, psychology, socivals than blacks”(Pirisi, 2000). Numerous studies have ology, and spirituality. Since Melzack and Wall (1965) published their Gate Control theory, a watershed of difdemonstrated that responses and expressions differ greatly from one ethnicity to another; however, studiesferent types of nontraditional treatment methods has been ficacious ef moddo not exist that clearly demonstrate that the variationsforthcoming because of the suggestion of ulation of pain in concert with traditional allopathic medof response are due solely or primarily to ethnicity icine. For the first time, it became apparent that the suf(Chapman, Toru, Martin, Tanaka, Okazaki, Colpitts, ferer had some degree of control over the pain processes Mayero, & Gaghardi, 1982; Clark & Clark,1980; Morse af with proper edu& Morse, 1988; Woodrow, Friedman, Seigelaub, & Col- associated with his/her givenfliction, cation and work. len, 1972). Generalizations abound regarding certain ethbody nic responses to pain, however, solid research is lacking A greater sense of personal control over sone’ can have great infl uence on the impact of his/her percepto establish any such claims. There is an emerging literature regarding thetion. Much like the elephant who has learned he tcan’ responses of older people to pain. Ruzicka (1998)break free from his shackles, even though the claims are reports that the beliefs of elders modify the experienceoftentimes much smaller chains than what were origiof pain considerably. She found that Pain “ is common nally used, the individual with an external locus of control, dependent on others to take care of his/her ills, often and older people are expected to put up with ” and it, nes “ Searching for the meaning in the pain experience iswill lack the confidence to break free from the confi important, and often a review of past personal experi-of the condition. This often will lead to a less proactive and sedentary, unhealthy lifestyle, which does not proence is the method used to attach meaning to the experience,” and that elders are reluctant to express pain.mote healing. ficacy is closely related to There is doubtless a critical element present regarding Likewise, a sense of self-ef ficacy originated with the experience of pain and the willingness to complainan internal sense of control. Self-ef s sense about it. This is most probably a result of culture ratherAlbert Bandura and is defined as “an individual’ of their abilities, of their capacity to deal with the particthan age.

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ular sets of conditions that life puts before them” (Reber,and causes some degree of tissue damage. This injury to 1995). Obviously, learned helplessness can be the net tissues produces the release of algogenic (pain-causing) result of a poor sense of self-ef ficacy. Knowing this may substances that promote immune functioning and inflambe a normal reaction of individuals suffering from painful mation responses, and activate pain receptors. The algoconditions, work geared toward self-confidence, personal genic substances include serotonin, bradykinin, and hiscontrollability, and an internal locus of control may prove tamine, but this process also involves the production of fruitful for many patients. It is important to remember, other substances such as substance P and prostaglandin. however, that some individuals need their pain. It gives This nociceptive pain process triggers an action potenthem focus, attention, and reinforcement that may betial, sending messages toward the central nervous system. beyond the scope of the clinician to understand. Transmissionis the movement of pain impulses from the Cornock (1996) outlined four major nonpharmaceuti-site of transduction to the brain. This phase begins in the cal approaches that can be used to help alter the pain dorsal horn of the spinal cord, triggers the release of patient’s perception of pain. Please refer to the psycho-substance P among other chemicals, sending this impulse logical technique chapter of this text for a more compre-to the brain.Perception is the process of recognizing, hensive understanding of these concepts. These includedefining, and responding to pain, our conscious experience of the pain. Last,modulationis the activation of descend1. Information control. Through open communiing pathways that exert inhibitory effects on the cells cation of pain and its underlying conditions, responsible for pain transmission. This occurs, in part, some of the mystery is eliminated, thus allevi- with the release of endogenous opioids, serotonin, and ating the fear of the unknown. norepinephrine (Pasero, et al., 1999). 2. Behavior methods. Through operant models of The second major type of pain is neuropathic pain, conditioning, desirable behavior is reinforced defined as pain initiated or caused by a primary lesion or and positive change is rewarded. Relaxation dysfunction in the nervous system. Within neuropathic and biofeedback also may be used to reduce pain, there are two distinctive types: centrally generated tension and stress that may contribute to pain. pain, initiated or caused by a primary lesion or dysfunction 3. Cognitive approaches. These work to replace in the central nervous system, and peripherally generated maladaptive thoughts, provide nonpain imag- pain, caused by primary lesion or dysfunction in the ery, and refocus attention. peripheral nervous system (Pasero, et al., 1999). Science 4. Hypnosis. A modality used for many different has explained fairly effectively the physiology of pain problems through relaxation, the placebo effect, processes, although work is certainly not complete in this and possibly the effect of the clinician on the area. Modern theories such as Melzack’ s Neuromatrix patient. theory may be more thoroughly understood through a working knowledge of preceding basic theories. With the successful use of one or several of these techniques, pain can be managed effectively by changing THEORIES OF PAIN the perception of the ongoing physiological pain.

SPECIFICITY THEORY TWO MAJOR TYPES OF PAIN

The specificity theory was greatly infl uenced by the writNociceptive pain was defi ned by Pasero, Paice, and ings of RenéDescartes. Pain and touch sensors on the McCaffery (1999) as “pain resulting from the ongoing skin are wired to a pain center in the brain through activation of primary afferent neurons by noxious stimuli.specific receptors and pathways, similar to the visual The nervous system is intact. ” Furthermore, Portenoy system (Matlin, 1988). The painful stimulus was theo(1996) added, it tends to becommensurate “ with the rized to travel directly to the brain, and any emotions displayed as part of the experience were in response to degree of ongoing tissue damage from an identi fiable peripheral lesion that involves either somatic or visceralthe original stimulus. The theory assumes the intensity structures. ” Somatic pain is generated from muscle, skin,of the pain is directly proportional to the amount of damage and because pain is neural, it results in triggering joint, connective tissue or bone, oftentimes has an achy or throbbing quality and is often easily localized. Visceralirritation of specific neural pathways. pain arises from visceral organs such as the pancreas and There is a fundamental fault with this theory regarding the denial of the emotional aspect of the pain experience, the GI tract. Nociceptive pain (visceral or somatic in nature) hasand considers only biological factors. Chemical blocking four basic processes. Transductionis the conversion from and surgical severing of nerve tracts oftentimes fail to eliminate pain. Additionally, the existence of pain in conone energy to another. This is a peripheral process that begins with a mechanical, thermal, or chemical stimulus,ditions with no apparent physiological bases cannot be

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explained. For example, there is no way to account for the the family or support system plays in the manifestation soldier who feels no pain from injuries until after an of a chronic pain condition. The major emphasis conintense battle. There is an organic basis for pain; there cerns is the social context in general and the family context just no conscious awareness until the person has time in to particular. Just as in the Stress– Diathesis model, a focus on it. framework exists in every individual, including the biological (CNS neurobiological), behavioral, cognitive, and affective domains, that results in coping techniques PATTERN THEORY by the individual that may be positively or negatively This theory suggests that the pattern of nerve endings reinforced by the family or support system. This is simdetermines sensation due to pain spots in the tissue ilar to the operant conditioning model regarding the which, through summation, produce nerve activation.importance of signifi cant others, but the family is viewed The intensity and frequency of a stimulus (known asas a more active participant in the evaluative response pattern of the stimulation) determine to what extent (ifto the adequacy of coping strategies and the individual’ s at all) it will consciously be perceived as painful. Eachability to effectively meet the challenges of his or her receptor does respond to many different types of stim-given condition. ulation, but that response is greater to some stimuli than Schemas, described as relatively xed fi beliefs about others. Therefore, a receptor, which responds vigor-the world, develop in family systems. These have a sigously to touch, may still respond to a hot stimulus, butnificant effect in specifi c appraisals regarding the pain less vigorously, even less so to painful stimuli and verypatient’s condition, and may affect the individual’ s abillittle to cold stimuli. Ultimately, the brain was thought ity to deal effectively with the condition and help deterable to interpret a code in terms of the relative strengths mine the level of adaptation. Past failure to deal effecof the receptors’responses (Matlin, 1988). The weak- tively with one’s condition can enhance the perceived ness of this theory has to do with the fact the focus was threat of the condition, which could lead to intensifi ed on sensation, while ignoring the variables of the perfocus on the symptoms, heightening the level of perception of pain. ceived pain, and increasing disability and affective distress (Turk & Gatchel, 1996). OPERANT BEHAVIOR MODEL The cornerstone of the Stress– Diathesis model, as Fordyce (1976) introduced this new mindset by describ-previously mentioned, includes biological, psychologing the operant factors that occur in chronic pain. Centralical, and social factors. Simply put, preexisting personality features place the individual at risk of maladaptive to this theory are behavioral manifestations rather than response to a painful condition. This places stress on the sensation of pain. It suggests pain behavior, such as the person, thus infl uencing the interrelationship excessive rest, overuse of pain medications, verbal complaints, protective behaviors, limping and bracing,between the neurobiological and psychological varialthough initially useful in combating pain, may be pos-ables, which can lead to vulnerability. This vulnerabilitively reinforced by spouses and healthcare providers.ity can result from the crossover of several domains, ficacy, The behavior may be maintained further by the avoid-including cognitive perceptions of control/ef ance of activity which may test the waters too much,affective depression which leads to anxiety and fear, finally, putting the individual at risk of having the noxious stim- behavioral declines in functional activity and, family and social interactions that may signi ficantly ulation return. Well behaviors, such as exercise and work, may notinfluence pain expression. be sufficiently reinforcing and the pain behaviors may, therefore, be maintained.The “ operant conditioning STIMULATION-PRODUCED ANALGESIA (SPA) model focuses on overt manifestation of pain and suffering This is a pain modulation theory largely based on stimuexpressed as pain behaviors such as limping, moaning and avoiding activity. Emphasis is placed on the communica-lation-produced analgesia through the production and utitive function of these behaviors” (Turk & Gatchel, 1999). lization of endogenous opiates, such as endorphins and The psychological factors involved in the chronic painenkephalins, for the modulation of pain. The opioid peppatient are considered only reactions to painful stimuli,tides largely associated with pain are enkephalins, betaendorphins, and dynorphins. It is thought SPA as well as rather than affecting the perception directly. opiate analgesia operate in part through descending control of spinal and trigeminal nociceptors (Basbaum, 1983). COGNITIVE BEHAVIOR-TRANSACTIONAL With discovery of these endogenous opiate-like subMODEL/STRESS–DIATHESIS MODEL stances, the scientifically based suggestion could be made This more recent theory is heavily infl uenced by social that the brain itself can produce substances that can act to learning and cognitive theories and the great importance modulate the perception of pain.

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THREE DIMENSIONS

determined neurosignature patterns of nerve impulses. These patterns may be triggered with or without actual sensory inputs; therefore, providing an explanation for the A multitude of different theories about pain and its pro-mystery of the perception of pain sometimes present in cesses has existed since antiquity. It was not until Melzack individuals devoid of pathology or injury. and Wall published their Gate Control Theory in 1965 that It proposes thatthe “ output patterns of the neuromascience could understand the pain process from the pertrix activate perceptual, homeostatic, and behavioral prospective of descending nerve pathways originating fromgrams after injury or pathology or as a result of multiple higher regions and acting via the midbrain and medulla,other inputs that act on the neuromatrix” (Melzack, affecting the perception of pain by inhibiting the trans-1999b). Pain then can be viewed as an output of an mission of signals through the substantia gelatinosa of the extensive neural network in the brain instead of as a dorsal horn in the spinal cord. much more complicated process than simple injury, They considered pain to have three dimensions: seninflammation, or other pathology. Stress is a major trigsory-discriminative (thought to provide information gering factor in this theory, due to the complex processes regarding the nature of the noxious stimulus), motiva-required for the body to restore homeostasis. Chrousos tional-affective (the reactive component of the process,(1992) defined stress as a state of threatened homeostawith importance in both acute and chronic pain andsis, that is, a disruption by stressors of physiological medicated by polysynaptic afferent pathways thought toprocesses such as blood sugar level and body temperature fi delicately balbe interconnected between the brain stem’ s reticular acti- that are normally maintained at axed, vating system and the limbic system), and cognitive-anced set point. Therefore, a disruption of homeostasis evaluative (the meaning of a given pain can profoundlydue to a stressor (physical or psychological) activates programs of neural, hormonal, and behavioral activity. alter its sensory experience) (Portenoy, 1996). It is these three areas that are the bases of the widely used McGill Indeed, the neuromatrix theory considers five basic types of inputs that produce the unique neurosignature Pain questionnaire. “(1) sensory inputs (cutaneous, Physiologically, three variables control the gate.δ A- outputs. These include visceral and other somatic receptors); (2) visual and other fibers (sharp pain), are small fibers and travel at a slower sensory inputs that influence the cognitive interpretation conduction velocity than those of theβA-fibers. C fibers of the situation; (3) phasic and tonic cognitive and emo(dull pain) are unmyelinated afferent neurons, with slow tional inputs from others areas of the brain; (4) intrinsic conduction velocity. Both the C and δA-fibers tend to neural inhibitory modulation inherent in all brain function; open the gate by obstructing or inhibiting the special gate (5) the activity of the body’ s stress-regulation systems, neurons of the substantia gelatinosa. Finally, β Afibers including cytokines as well as the endocrine, autonomic, (messages of light touch) are large fibers with much faster immune and opioid systems” (Melzack, 1999a). conduction velocities than the previous two. It is theorized that besides the modulation of the pain signal by the stimulated Aβ nerve fibers our conscious PAIN THRESHOLD VS. PAIN TOLERANCE experience of pain intensity is affected not only by the There is no denying the subjectivity of pain. The response magnitude of the pain stimulus but also by concentrations of chemical regulators, namely, the endogenous opiates a in given individual has is an intensely personal experience, and therefore, cannot be predicted with certainty. There two major classes: enkephalins and endorphins (Coren, Ward, & Enns, 1999). Willer, Dehen, and Cambier (1981)are times when seemingly innocuous stimuli are perceived as excruciating, whereas quite severe injuries can produce found the effects of psychological stress when subjects anticipating painful shocks triggered the endogenous opi-almost no perceived sensation to the individual. ate system to protect the individual from the forthcoming Obviously, this poses a great challenge to the healthpain. Similarly, it has been that found women have ancare professional during the assessment. It is important to be mindful of the inherent difference of pain threshold increased pain tolerance in the last 2 weeks of pregnancy, presumably to ready them for the upcoming painful eventsvs. paintolerance.When considering pain and sensation as a process, there are many aspects, which are fairly (Cogan & Spinnato, 1986). consistent and reproducible from person to person, and from the same person over time. Pain threshold is sciNEUROMATRIX entifically based, quantifi able and reliable. It has been Neuromatrix as proposed by Ronald Melzack in the 1990s defined as the intensity of a stimulation at which a subject expounded upon the infl uential gate control theory. It con- says,“ It’ s painful” half the time and It’ “ s not painful” siders pain a multidimensional experience characterized by half the time (Matlin, 1988). Threshold is variable across the “ body–self neuromatrix”in the brain, which are con- the body as evidenced by neurologists’ two point dissidered genetically (but modifi ed by sensory experience) crimination test. More pain receptors means greater disAND

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crimination of the presented stimulus, and a lower painCassel, E.J. (1982). The nature of suffering and the goals of medicine. New England Journal of Medicine , 306, 639–645. threshold. Chrousos, G.P. (1992). Regulation and dysregulation of hypoThe great challenge is that pain tolerance has so thalmic-pituitary-adrenal axis. Endocrinology and many variables and elements. Not only does it vary Metabolism Clinics of North America, ,21 833–858. between individuals, but within the same individual at Clark, W.C., & Clark, S. (1980). Pain responses in Nepalese different times. What possible factors can account for porters,Science , 209, 410–412. the high variability in the tolerance of pain over time? Cogan, R., & Spinnato, J.A. (1986). Pain and discomfort threshTurk and Flor (1999) point out that an injury to the olds in late pregnancy. Pain, 27, 63–68. nociceptive transmission system or to the activity of theCoren, S., Ward, L.M., & Enns, J.T. (1999). Sensation and permodulatory system can lower pain intensity. There may ception (5th ed., p. 248). New York: Harcourt Brace. also be abnormal neural activity, which may produceChapman, C., Toru, S., Martin, R., Tanaka, A., Okazaki, N., Colpitts, Y., Mayero, J., & Gaghardi, G. (1982). Comhypersensitivity creating a self-sustaining process started parative effects of acupuncture in Japan and the United by the original injury. Examples of such processes may States on dental pain perception. Pain, 12, 319–328. be seen in phantom limb pain, neuropathic pain, or comCornock, M.A. (1996). Psychological approaches to cardiac plex regional pain. pain. Nursing Standard , 11, 34–38. Finally, psychological factors may affect normal Craig, J.C., & Rollman, G.B. (1999). Somesthesis. Annual responses to pain, and yield quite variable and unpredictReview of Psychology, ,50 305–331. able responses. One of the most important factors when Fordyce, W.E. (1976). Behavioral methods for chronic pain and considering the tolerance and general perception of pain illness. St. Louis: Mosby. is themeaningof the pain to the sufferer. Needless to say,Gale Group Staff (Eds.). (2000) The Columbia encyclopedia (6th ed.). Mt Kisco, NY: Visible Ink Press. a painful condition associated with a minor injury or temporary illness will likely be a much different experience Iadarola, M.J., & Caudle, R.M. (1997). Good pain, bad pain. Science, 278 , 5336, 239. than similar pain levels associated with more severe lifeKelly, A.L. (1999). The painful truth.Walking Magazine , 14, 2, altering conditions.

30. Kerns, R.D., & Payne, A. (1996). Treating families of chronic pain patients. In R.J. Gatchel & D.C. Turk (Eds.), PsychologCONCLUSION ical approaches to pain management, a practitioner’ s handbook.New York: Guilford. There is considerable evidence that the expression of pain Women’s follows social modeling, cultural expectations, and reli-Marble, M. (1999). Gender differences (pain response). Health Weekly , October, 19. gious beliefs. Stoicism, hysteria, athletic endurance, and Matlin, M.W. (1988).Sensation and perception (2nd ed.). Bosnumerous other designations of discomfort accompany ton: Allyn & Bacon. lifestyles and life expectations. It has been observed that McQuillen, M.P. (1991). Can people who are unconscious or in wealthy persons expect to be able to “buy relief” from the ‘vegetative state’perceive pain.Law and Medicine, pain, and that athletes view pain as the only way to gain. 6, 4, 373. Winners in athletic endeavors often express the pain of Melzack, R. (1999a). Pain and stress: A new perspective. In R.J. overexertion or injury differently if they win or lose the Gatchel & D.C. Turk (Eds.),Psychosocial factors in contest. The pain from muscular irritation and other physpain: Critical perspectives.New York: Guilford. ical states resulting from “practice” becomes dissociatedMelzack, R., (1999b). Abstract. From the gate to the neuromatrix. Pain (Suppl. 6), S121–126. a part of their experience. Religious persons have been Melzack, R., & Wall, P.D. (1965). Pain mechanisms: A new known to welcome pain as a believed prelude to rewards theory. Science, 150 , 971–979. in the after life. Pain is not universally perceived the same, Morse, J.M., & Morse, R.M. (1998). Cultural variation in the expressed the same, nor is it treated the same. For these inference of pain.Journal of Cross-Cultural Psychology, and myriad other reasons, pain continues to be our most 19(2), 232–242. illusive encounter with human existence. Pasero, C., Paice, J.A., & McCaffery, M. Basic mechanisms underlying the causes and effects of pain. Pain, clinical manual (2nd ed.).St. Louis: Mosby. REFERENCES Pirisi, A. (2000). The color of pain. Psychology Today, 32 , 4, 22. Portenoy, R.K. (1996). Control of pathological pain. In L. Kruger American Heritage Publishing Staff. (1995). Roget II: The new (Ed.), Pain and touch(pp. 343–386). San Diego, CA: thesaurus . Boston, MA: Houghton Mif flin. Academic Press. Basbaum, A.I. (1983). The generation and control of pain. InReber, A.S. (1995). Penguin dictionary of psychology (2nd ed.). R.N. Rosenberg & W.D. Willis (Eds.), The clinical neuNew York: Penguin Books. rosciences: Neurobiology(Vol. V, p. 313). New York: Ruzicka, S.A. (1998). Pain beliefs. Journal of Holistic Nursing , 16, 3, 369. Churchill Livingstone.

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Verillo, R.T. (1975). Cutaneous sensations. In B. Scharf (Ed.), Sittner, B., Hudson, D., Grossman, C., & Gaston-Johansson, F. Experimental sensory psychology . Glenview, IL: Scott, (1998). Adolescents perceptions of pain during labor. Foresman. Clinical Nursing Research,(1), 7 82. Turk, D.C., & Flor, H. (1999). Chronic pain: A biobehavioral Willer, J.C., Dehen, H., & Cambier, J. (1981). Stress-induced analgesia in humans: Endogenous opioids and naloxPerspective. In R.J. Gatchel & D.C. Turk (Eds.), Psyone-reversible depression of pain reflexes. Science, 212 , chosocial factors in paincritical perspectives(p. 28). 689–690. New York: Guilford. Turk, D.C., & Gatchel, R.J. (1996). Psychological approaches Woodgate, R. & Kristjianson, L.J. (1996). My hurts: Hospitalized young children’ s perceptions of acute pain. Qualito pain management: A practitioner’ s handbook . New tative Health Research,, 62, 184. York: Guilford. Turk, D.C., & Gatchel, R.J. (1999). Psychosocial factors in pain: Woodrow, K., Friedman, G., Seigelaub, M., & Collen, M. (1972). Pain tolerance: Differences according to age, sex, and Critical perspectives . New York: Guilford. race.Psychosomatic Medicine, ,34 548–556.

66 Screening for Alcohol and Other Substance Use Disorders* Nick J. Piazza, Ph.D. Alcohol and other drug use are primarily or secondarilyCHARACTERISTICS OF A GOOD SCREEN implicated in a large number of medical problems, includThere are a number of characteristics that help determine ing pain (Kitchens, 1994). Undetected and untreated alcowhether a screening procedure is of value. The most hol or other substance use disorders can have a significant important characteristics are sensitivity, specificity, valideffect on a patient’s response to treatment as well as treatity, reliability, and cost-ef ficiency. ment compliance. Adger and Werner (1994) stated that healthcare professionals “should screen all patients for [subSENSITIVITY AND SPECIFICITY stance] use and determine the need for further assessment and intervention.” Failure to at least screen for a substance Sensitivityrefers to the proportion of individuals correctly use problem could lead to misdiagnosis, and failure to proidentified as positive for a particular condition or disorder. vide the patient with the most appropriate care. In this case, sensitivity would refer to the percent of indiAdger and Werner state that the goal of screening is to determine the likelihood that a problem exists andviduals correctly identified by a particular screen as having a substance use disorder. A screen with good sensitivity whether further assessment is needed. They believe that all patients should undergo screening for alcohol or otheris important because it can tell us who needs to be referred for a more complete evaluation, who may not respond to drug problems. If a screen is positive, then the Health Care Provider (HCP) should refer the patient for a detailedmedications or therapies as expected, or who may be malingering or drug-seeking. substance use assessment, and initiate prevention or treatSpecificityrefers to the proportion of individuals corment measures where appropriate. rectly identified as negative or as not having a substance Assessment is a lengthier, more involved process usuc screen is that it ally conducted by personnel specifically trained in sub-use disorder. The value of a highly specifi stance use disorders. The purpose of assessment is can to tell us who is least likely to have a substance use city can tell us when it “determine the extent of the problem, explore coexistingdisorder. A screen with good specifi medical and psychiatric conditions, and assist in treat-is unnecessary to expend valuable time or resources evalument planning” (Adger & Werner, 1994). Most HCPs feel ating patients for a condition they most likely do not have. competent to screen for a substance use disorder; how- Salaspuro (1994) noted that a good screen should not overidentify individuals as having a problem (i.e., false ever, they may prefer to refer the patient to a specialist positives) nor should it overidentify individuals as being for assessment. problem-free (i.e., false negatives). A high false-positive *

Portions of this chapter were excerpted from Piazza, N.J., Martin, N., & Dildine, R. (2000). Screening instruments for alcohol and other drug problems.Journal of Mental Health Counseling, 22, 218–227. With permission.

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rate would mean that valuable time and resources were Fleming (1993) identified four useful laboratory measures. expended on individuals who, in fact, did not have a sub-These include measuring levels of gamma-glutamyl transstance use disorder, while a high false negative rate means ferase (GGT), mean corpuscular volume (MCV), alanine that individuals went untreated because they were not aminotransferase (ALT), and aspartate aminotransferase detected by screening. (AST). Fleming (1993, p. 231) selected these tests because they “measured direct hepatic and hematopoietic cellular alcohol toxicity.” Fleming notes that the sensitivity of VALIDITY AND RELIABILITY these screens ranges from 20 to 90%, with GGT levels Validity refers to a screening instrument’ s ability to meas- the most sensitive of the four measures. ure what it purports to measure. Valid screening proce- O’Connor and Schottenfeld (1998) recommend testdures for substance use disorders should accurately dising for carbohydrate-deficient transferrin in addition to the criminate true positives and true negatives from falsemeasures listed above. They report that carbohydrate-defipositives and false negatives. A number of threats to validcient transferrin levels have a “sensitivity of 58 percent to ity exist including standardization on a too small sample,70 percent and a specificity of 82 percent to 98 percent using a screen on individuals who were not part of thefor the detection of heavy drinking or alcohol abuse” standardization group, using a screen for purposes other (O’Connor & Schottenfeld, 1998). than those for which it was developed. A perfectly valid instrument would achieve a value of 1.0. Screening instru-BLOOD-ALCOHOL CONCENTRATION (BAC) ments for substance use disorders can range from lows of BAC is a measure of the percent of alcohol concentrated about 0.4 to highs of 0.9 or better. Reliability refers to the consistency with which an in a volume of blood. The BAC is sometimes alternatively referred to as the blood-alcohol level or BAL. The proceinstrument measures the variable or condition of interest. A reliable screen will yield consistent results across indi-dure involves drawing a sample of blood and analyzing the viduals and, more importantly, across time. Conversely,sample to determine how much alcohol is present. Persons an unreliable instrument yields different results each timewith a BAC of 0.1% or higher are considered too intoxiit is administered. Technically, it is not possible to havecated to drive in 34 states, the District of Columbia, and an unreliable screening procedure that is valid. Validity isPuerto Rico; 16 states and all the provinces in Canada have set their legal intoxication limit at 0.8% (Harley Owners dependent on the stability of the results obtained. As with validity, reliable screens should approach aGroup, 2000). The validity and reliability for this test are sufficiently high that BAC is accepted as evidentiary of value of 1.0. Most screening instruments report–retest test intoxication in a court of law. It has been the author’ s reliability because this measures the stability of results over experience that any BAC over 0.15% in an adult is sugrepeated administrations of the procedure. Questionnairegestive of alcohol abuse or dependence, while a BAC of based screens often will report internal consistency or alpha reliability. High internal consistency or alpha values mean0.2% is almost always associated with alcohol dependence. that the items on the questionnaire are highly intercorrelated and most likely measure the same variable or condition. URINALYSIS Many drugs are broken down or metabolized in the liver. The by-products of liver metabolism are called metaboCost-efficiency implies that the benefi ts of using the lites. The kidneysfilter these metabolites from the blood screening procedure are greater than the costs. Using supply, an and then dump them in the urine where they are inexpensive but poorly constructed screen with low sen-expelled during urination. It is possible to determine sitivity and specificity may prove to be more costly overwhether a patient has recently ingested a drug by examtime because resources are wasted on false positives and ining the urine for the presence of these metabolites. This false-negative patients go undetected and untreated. procedure In is commonly known as urinalysis. addition, screening all persons in a population for a low Urinalysis actually consists of two tests. The first test prevalence disorder may add considerable cost to treatis known as the enzyme multiplied immunoassay techment while benefiting only a few individuals. nique or EMIT. The strength of an EMIT is its specificity. A negative EMIT fairly conclusively indicates that the patient’s urine is relatively free of drug metabolites. An LABORATORY OR BIOLOGICAL EMIT’ s sensitivity, however, is suf ficiently poor that a SCREENING PROCEDURES significant proportion of individuals will be false positives. Consequently, it is necessary to run a second measure—a LABORATORY TESTS gas chromatography/mass spectrometry (GC/MS)— to Laboratory tests, especially liver enzyme tests, have long confirm the results of the EMIT. GC/MS accuracy been used as a means to screen for potential alcohol abuse. approaches 100% and is considered evidentiary in courts

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of law. It is possible that a patient may test positive onscreen can tell the HCP is that the individual has recently urinalysis because he or she is taking a legitimately preused; biological screens cannot determine why the drug ®]). These scribed medication (e.g., meperidine [Demerol is present or the nature of the use. This led Fleming individuals should be considered false positives, and many (1993) to recommend that laboratory testing be limited urinalysis laboratories employ Medical Reviewficers Of to assessing toxicity, while questionnaires and patient (MROs) to eliminate these cases. reports were more valid for differentiating problem from nonproblem users.

OTHER BIOLOGICAL SCREENS Procedures have been developed to test a patient’ s hair, PSYCHOSOCIAL SCREENING breath, sweat, and saliva for the presence of alcohol, INSTRUMENTS drugs, or their metabolites. The best known is probably ® test, which provides a highly accu- Piazza, Martin, and Dildine (2000) noted that psychosothe Breath-a-lyzer cial screening instruments for detecting substance use disrate estimate of BAC. Instruments that look like a child’ s orders fall into one of two categories. The first category sucker change color when exposed to saliva containing logically derivedinstruments. Logitraces of drugs. Finally, hair analysis can determine ifconsists of so-called contentor face an individual has used drugs any time in the weeks orcally derived screens typically have good months prior to testing. Obviously, the longer the indi- validity in that the items obviously measure substance usevidual’s hair, the farther back in time detection will be related behaviors and problems. The greatest asset of logically derived screens is that a positive result is a strong possible. indication that a problem is present. The greatest liability for logically derived screens is that the items are so obviADVANTAGES AND DISADVANTAGES ous that anyone motivated to deny or conceal a problem OF LABORATORY OR BIOLOGICAL can easily “fake good. ” In fact, it can be said that logically SCREENS derived screens are best at detecting those individuals who wish to be identified. Despite this inherent weakness, howADVANTAGES ever, O’Connor and Schottenfeld (1998) noted that selfreported information regarding substance use is “reliable Biological and laboratory screens are most useful and ” most valid for those situations where evidence of sub-and reproducible. stance use or impairment is required. Urinalysis, espe- A second category described by Piazza et al. (2000) cially when combined with a GC/MS and an MRO, hasis comprised of what are known as empirically derived an especially high sensitivity rate with almost no falseinstruments. Empirically derived instruments use positives. Because of the high sensitivity combined withresearch and statistical analysis to identify items that can a low false-positive rate, urinalysis is most often employeddiscriminate individuals with substance use disorders in situations where it is important to determine if an indi-from individuals who are problem-free. Generally, the vidual is drug-free. Examples of such situations includecontent of the item is unimportant. What is important is es who is a member of the following an accident or injury in the workplace; compli- that the item correctly identifi ance with drug-free workplace policies; fitness for workcriterion group (i.e., that group of individuals with a determinations; and compliance with the terms of absti-substance use disorder). Items on empirically derived nence-based treatment programs, probation, or parole. screens often have poor content or face validity; however, they should have good to excellent predictiveor criterion validity. Empirically derived screens appear to be best at DISADVANTAGES identifying individuals who are motivated to deny or A number of limitations exist to using biological screensminimize a substance use disorder because item content to determine who may or may not have a substance use appears unrelated to substance use. Unfortunately, disorder. The principle disadvantage is that individualsbecause most empirically derived screens do not ask need only abstain for a few days to test negative onquestions related to substance use, they frequently do urinalysis. Conversely, some procedures such as hair not give any indication of the severity or extent of a analysis will yield positive results weeks or even monthsdrinking or other drug problem. after use has stopped. Liver enzyme tests often have high false-negative rates for young, healthy, or early stage MICHIGAN ALCOHOLISM SCREENING TEST (MAST) users who do not have a many-year history of heavy or abusive drinking. Laboratory procedures also can beThe MAST was originally developed by Selzer (1971) expensive and time consuming. Finally, laboratory andand consists of 24 face valid items. Pokorny, Miller, biological screens cannot differentiate legitimate usersand Kaplan (1972) and Selzer, Vinokur, and van Roofrom recreational or problem users. All a biological ijen (1975) later developed abbreviated versions of the

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questionnaire with 13 items each. The most discrimi-final concern is that like the MAST questions on the nating items are SAAST are specifi c to alcohol and do not address problems with other drugs. 1. Have you ever attended a meeting of AA? 2. Have you ever sought help about your drinkCAGE, T-ACE, AND TWEAK ing? 3. Have you ever been in a hospital because of These three logically derived instruments were developed your drinking? as brief screens that could be administered orally during a clinical interview. All three are very similar and share Items are scored 1, 2, or 5 points according to theirmany of the same strengths and weaknesses. The CAGE diagnostic utility. The MAST is designed to assign respon-was specifically developed for use by primary care phydents into one of three categories: no drinking problemsicians. Kitchens (1994) noted, however, that the CAGE (score of 0 to 3), possible problem (score of 4 to 6), andhad not been standardized for use with pregnant women. alcohol dependent (score of 7 or higher). The T-ACE and the TWEAK are variations of the CAGE The MAST is one of the best known and most widelythat were specifically developed to “ascertain drinking in used logically derived screens. Its wide acceptance and pregnant women” (Nilssen & Cone, 1994). use, however, are inconsistent with the problems associated with the instrument. Selzer (1971) acknowledgedTHE CAGE that because the items are so obvious, alcoholics wishing to avoid detection could easily do so. To correct for this,Nilssen and Cone (1994) report that the CAGE is probably ” It consists Selzer set the cutoff scores lower to improve sensitivity.the “most widely used test in clinical practice. of four items, answered with either yes or no: This resulted in a false-positive rate of about 33% and lowered the overall accuracy rate to about 75% (JacobCut down on son, 1983; Creager, 1989). Correlations between MAST 1. Have you ever felt you should your drinking? results and counselor diagnoses reveal a concurrent 2. Have peopleAnnoyed you by criticizing your validity of r = .65 (Mischke and Venneri, 1987). Finally, drinking? the MAST only assesses for alcoholism and cannot disGuilty about your criminate between alcohol abuse and problems with 3. Have you ever felt bad or drinking? other drugs. 4. Have you ever had a drink first thing in the The MAST’s applicability to women and minorities morning to steady your nerves or get rid of a is also questionable. Jacobson (1983) reports that there is hangover E ( ye opener)? little information on female norms, and nothing in the literature addressing minority norms. The high false-positive rate and low overall accuracy Two or more yes answers are interpreted as a positive led Popkin, Kannenberg, Lacey, and Waller (1988) to con-screen, suggesting the need for further assessment. The clude that the MAST “may be useful in detecting personsprinciple advantages of the CAGE are that it is easy to remember, easy to administer during a clinical interview, who acknowledge having an alcohol problem. ” Russell and takes only about a minute to complete. The reported (1994, p. 58) described the MAST as lengthy,ficult dif to accuracy rates of the CAGE are quite variable, ranging score, and “impractical for clinical use. ” anywhere from 40 to 95% (Sokol, Martier, & Ager, 1989). O’Connor and Schottenfeld (1998) reported that lifetime SELF-ADMINISTERED MICHIGAN ALCOHOLISM sensitivity for patients with an alcohol problem ranges SCREENING TEST (SAAST) from 60 to 95%. This is a modified version of the MAST that has been Despite its advantages, a number of problems have developed for self-administration. The SAAST is a 35-been associated with using the CAGE. Nilssen and Cone item questionnaire that correlates highly (r = .83) with(1994) noted that the CAGE is specific to alcoholism and the MAST. Davis, Hurt, Morse, and Brien O’ (1987) does not assess for problems with drug use. They also note reported that the SAAST correctly identifi ed 92.1% of that the CAGE assesses lifetime use instead of focusing 520 alcoholic participants and only incorrectly classifi ed on current drinking history. Fleming (1993) reports that 1.3% of 636 controls. It was not clear in the Davis, etthe CAGE’s lifetime approach results in a false-positive al. study, however, whether the alcoholic group con-rate of over 50%. Kitchens (1994) pointed out that while tained individuals who were attempting to deny a prob-the CAGE is “reasonably accurate at identifying those lem on the instrument. A 92.1% accuracy rate shouldindividuals who are alcohol dependent or heavy drinkers, ” not be surprising in a group of alcoholics who are beingthe CAGE is “not at all sensitive to detecting the lower open and honest about their drinking experiences. Alevels of consumption that may be dangerous. ” In addition,

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the items on the CAGE are very obvious and can be easily stages” (Nilssen & Cone, 1994). The developers intended denied by someone motivated to do so. for the AUDIT to be used to identify harmful drinking rather than alcohol use disorders. However, Russell (1994) believes that the AUDIT “also can detect alcohol disorders THE T-ACE with a high degree of accuracy. ” The T-ACE is similar to the CAGE, except that it drops The AUDIT is a logically derived, paper-and-pencil the CAGE question on guilt and replaces it with a question screen consisting of ten items. The items relate to three on alcohol tolerance (Sokol, et al., 1989). Russell (1994) areas of harmful drinking: (a) amount and frequency of reportedfinding sensitivity and specificity rates for the Talcohol consumption, (b) dependency symptoms, and ACE of about 79%. Russell stated that the T-ACE per(c) harmful effects. Items are scored on a scale from 0 to formed about the same as the MAST and slightly better 4, with a maximum possible score of 40. A score of 8 or than the CAGE with a sample of pregnant women. Despite higher is positive for harmful drinking. Russell (1994) the improvement in performance, the T-ACE still suffers claims the AUDIT has a sensitivity rate of 92% and a from the same limitations as the CAGE, i.e., specificity to alcohol, lifetime focus, inability to detect early stagespecificity rate of 93% for identifying harmful drinking. problems, and easy deniability. Another problem is that itIsaacson, Butler, Zacharek, and Tzelepis (1994) reported sensitivity and specificity rates of 96% for patients in a has only been standardized on pregnant women and not general medical clinic. The AUDIT would appear to be a on the general population. very strong instrument for identifying harmful or at-risk drinkers within a multicultural population. THE TWEAK The TWEAK “ combines questions from the MAST, SUBSTANCE ABUSE LIFE CIRCUMSTANCES CAGE, and T-ACE tests that have been found most effecEVALUATION (SALCE) tive” (see Table 66.1) (Russell, 1994). Russell reports that the TWEAK is superior to the CAGE or the MAST The SALCE was developed to use with people arrested and equivalent to the T-ACE when used with pregnantfor driving under the influence (DUI). The intended use women. Because the TWEAK is a derivative of thefor the SALCE is to differentiate those individuals needing MAST, CAGE, and T-ACE, it shares the same liabilities to alter their use of alcohol or other drugs from individuals as these instruments. In addition, the TWEAK is morewho may have a more serious substance use disorder. complicated to score. Popkin, et al. (1988) report that the SALCE “was not designed to differentiate alcoholics from nonalcoholics. ” The SALCE is a logically derived screen consisting of an THE ALCOHOL USE DISORDERS 85-item questionnaire that is to be used in conjunction IDENTIFICATION TEST (AUDIT) with a 20-minute interview. Total screening time is estiThe AUDIT was developed under the auspices of themated to be approximately 40 minutes. Applicability of the SALCE is probably limited to use World Health Organization (WHO) to serve as a multicultural screening instrument (Babor & Grant, 1989). Thewith DUI offenders as it has never been standardized on AUDIT “was specifically designed to be used in primaryother populations. Internal consistency reliability for the care settings to screen for alcohol problems at earlier SALCE is reported to be r = .93; no test–retest reliability

TABLE 66.1 Tweak T W E A K(C)

Tolerance: How many drinks can you hold? Have close friends or relatives Worried or complained about your drinking in the past year? Eye-opener: Do you sometimes take a drink in the morning when you first get up? Amnesia: Has a friend or family member ever told you about things you said or did while you were drinking that you could not remember? Do you sometimes feel the needCut to down on your drinking?

The TWEAK uses a 7-point scale. The Tolerance item scores 2 points if the respondent reports she can consume five or more drinks without falling asleep or becoming unconscious. A positive response to the Worry item scores 2 points. Positive responses to the remaining items are scored 1 point each. A total of 2 or more points indicates a positive screen. (Adapted by permission from Russell, M. Alcohol (1994). Health and Research World, 18, 55–61.)

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was reported (Popkin, et al., 1988). Popkin, et al. (1988)“are suggestive of persons who are socially extroverted report a 61% agreement rate between the SALCE and [ sic], exhibitionistic, and willing to take risks. ” There is assessment based on professional interviews. no mechanism for determining if a high score has been s substance use or these conPopkin, et al. (1988) noted that the SALCE “appearsproduced by a respondent’ founding personality and behavioral variables. to be reasonably well constructed, includes a measure of response bias (truthfulness), and has the automated capa- Greene (1991), Butcher et al. (1989), and Graham (1990) all state that validity, reliability, and accuracy bility for updating norms specific to DUI offenders. ” Popkin, et al. (1988) felt the SALCE had considerable poten-problems preclude using the MAC and the MAC-R to tial for use in DUI programs. They did note, however, thatdiagnose substance-related disorders. Graham (1990) no independently published evaluations of the SALCEstated that an elevated MAC-R score is only indicative of the “possibility of substance abuse, ” while Butcher, exist and that the publishers consider their data to be associated “ proprietary and not available for independent evaluation.et al. (1989) believed that high scores are with addiction-proneness rather than with alcoholic tendencies alone. ” Greene (1991) went so far as to suggest THE MACANDREW SCALE that professionals might want toavoid “ using the MAC The MacAndrew Scale (MAC) and the MacAndrew Scale-scale to predict whether a client will abuse substances, Revised (MAC-R) consist of 49 true/false items embeddedwhich has been the standard use of the MAC scale since in the Minnesota Multiphasic Personality Inventory it was first developed. ” (MMPI) and the Minnesota Multiphasic Personality Inventory-2 (MMPI-2), respectively. Greene (1991) wrote SUBSTANCE ABUSE SUBTLE SCREENING INVENTORY that the MAC scale was originally developed to differen(SASSI) tiate alcoholic outpatients from nonalcoholic psychiatric outpatients. The MAC and MAC-R are empirically The SASSI has gone through two revisions since its derived scales designed to be indirect measures of alcorelease in 1985 (Miller, 1985). The current version is holism, because neither version of the scales contains any referred to as the SASSI-3 (Miller, Roberts, Brooks, & questions obviously related to actual alcohol consumptionLazowski, 1997). The SASSI-3 actually consists of two or alcohol-related problems. separate screens: one logically derived, the other empiriButcher, Dahlstrom, Graham, Tellegen, and Kaemmercally derived. The logically derived portion is comprised (1989) stated that “raw scores of 28 or above stronglyof 26 face valid items formerly known as the Risk Presuggest substance abuse. Scores between 24 and 27 diction are Scales (RPS). Items on the RPS are scored on a somewhat suggestive of substance abuse, … [and] scores scale from 0 to 3. The second portion is made up of 67 below 24 contraindicate a substance-abuse problem. ” Gratrue/false empirically derived items. The 93 items of the ham (1990) also noted that drug addicts and alcoholics SASSI-3 are divided into ve fi clinical subscales, two obtained similar scores on the MAC. defensiveness subscales, one validity scale, and two supReliability and validity are problems for both the plementary scales. The SASSI-3 is written on a sixthMAC and the MAC-R. Graham (1990) observed that “Nograde reading level and takes 15 to 20 minutes to cominternal consistency data were reported for the originalplete. Hand scoring takes an additional 5 to 10 minutes. MAC scale, but the MAC-R scale does not seem to have The SASSI-3 is interpreted using decision rules for particularly good internal consistency. ” Butcher, et al. a configural analysis of the scores on the different sub(1989) reported coef ficient alphas of .56 for males and .45 scales. The publisher claims a 93.8% correspondence for females. One week test–retest reliability coef ficients rate between the SASSI-3 and a professional diagnosis, for the MAC-R were .62 for males and .78 for femaleswith a sensitivity rate of 94.1% and a specifi city rate of (Graham, 1990). Sensitivity rates for white males ranged92.7% (F. Miller, personal communication, May, 1997). around 80%, with false positive rates approximating 20%A separate study (Piazza, 1996) found that the adolescent (Greene, 1991). Accuracy rates for the MAC and theversion of the SASSI had similar accuracy rates. A plus MAC-R scales for adolescents, women, and minorities can for the SASSI-3 is that accuracy rates are about the same be much poorer. Greene (1991) reported that true positive whether respondents are being honest about their suband false positive rates for African-American males werestance use or are attempting to deny or conceal a probboth nearly 60%, while true positive rates for white ado-lem. Additionally, the norm sample of 2800 individuals lescents and women “ranged around 75%, with approxi-was comprised of about 30% African- and Native-Amermately 35% false positives. ” icans. This means that the SASSI-3 should be valid for Another validity problem common to both the MAC these groups. and the MAC-R is that the scales are not independent of Reliability coeffi cients are equally impressive. other personality characteristics or psychopathology.Test–retest reliability coef ficients for the clinical and Butcher, et al. (1989) noted that high scores on these scales defensiveness scales ranged from .92 to 1.00, while the

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Cronbach alpha coef ficient for the overall SASSI-3 was before attempting to use the SASSI-3. The advantage of 0.94 (F. Miller, personal communication, May, 1997). improved accuracy, however, would appear to make the cost of additional training well worth it. The SASSI-3 appears to be a compact and ficient ef marriage of the advantages to the two types of screens. Persons who are motivated to provide an honest report of their alcohol and drug use can reveal this on the RiskREFERENCES Prediction Scales. These data can be very useful in Adger, H., & Werner, M.J. (1994). The pediatrician. Alcohol assessing the severity of a substance use disorder and Health and Research World, 18, 121–126. for treatment planning. Persons who are in denial or who are deliberately being deceptive are typically iden-Babor, T.F., & Grant, M. (1989). From clinical research to secondary prevention: International collaboration in the tifi ed through a confi gural analysis of the clinical and development of the Alcohol Use Disorders Identification defensiveness scales. While information on the severity Test (AUDIT). Alcohol Health and Research World, 13, of the problem is lost, the SASSI can provide informa371–374. tion on the degree of denial or defensiveness exhibited Butcher, J.N., Dahlstrom, W.G., Graham, J.R., Tellegen, A., & by the examinee. Kaemmer, B. (1989).Minnesota Multiphasic Personality Inventory-2: Manual for administration and scoring. Minneapolis: University of Minnesota Press. DISCUSSION Creager, C. (1989). SASSI test breaks through denial. Professional Counselor , 65. Logically and empirically derived screens each have theirDavis, L.J., Hurt, R.D., Morse, R.M., & O’Brien, P.C. (1987). own strengths and limitations. Choosing a screen involves Discriminant analysis of the self-administered alcoholtrading off between ease of administration and accuracy. ism screening test. Alcoholism: Clinical & Experimental Research, 11,269–273. Selecting a screen should be based on the provider’ s needs, Fleming, M.F. (1993). Screening and brief intervention for alcopatient factors, and the circumstances under which the hol disorders.The Journal of Family Practice, 37, screen is to be used. 231–234. Logically derived screens seem to be best employed Graham, J.R. (1990). MMPI-2: Assessing personality and psyin situations where the motivation to provide an honest chopathology.New York: Oxford University Press. self-report is high. Typically, this means a situation where Greene, R.L. (1991). The MMPI/MMPI-2: An interpretive manthe patient is well known to the provider and a good ual. Boston: Allyn & Bacon. working relationship exists. A positive relationship can Harley Owners Group. (2000). America’s touring handbook . lower defensiveness and denial, which should lead to a Milwaukee, WI: Harley Owners Group. more honest self-appraisal. When these conditions are Isaacson, J.H., Butler, R., Zacharek, M., & Tzelepis, A. (1994). met, using an instrument like the CAGE, T-ACE, Screening with the Alcohol Use Disorders Identification Test (AUDIT) in an inner-city population. Journal of TWEAK, or AUDIT can be productive. All four of these General Internal Medicine, 9, 550–553. screens are brief and easily administered, scored, and Jacobson, G.R. (1983). Detection, assessment, and diagnosis of interpreted. It should be noted, however, that denial is a alcoholism: Current techniques. In M. Galanter (Ed.), defining characteristic of alcohol and other drug use disRecent developments in alcoholism: (Vol. 1, pp. 377– 413). orders. The motivation to deny or minimize a substanceNew York: Plenum Press. related disorder may be strong even in the presence of a Kitchens, J.M. (1994). Does this patient have an alcohol probpositive relationship. lem?Journal of the American Medical Association, 272, Empirically derived screens should probably be 1782–1787. employed in situations where the client is unknown toMiller, G.A. (1985).The substance abuse subtle screening inventhe provider, where there is a diverse client population, tory manual.Bloomington, IN: The SASSI Institute. or where clients are likely to be motivated to concealMiller, G.A., Roberts, J., Brooks, M.K., & Lazowski, L.E. (1997). SASSI-3: A quick reference for administration their problems. Generally, this would include situations and scoring. Bloomington, IN: Baugh Enterprises, Inc. such as intake, diagnostic, or evaluative interviews where Mischke, H.D., & Venneri, R.L. (1987). Reliability and validity clients may be motivated to present themselves in the of the MAST, Mortimer-Filkins questionnaire, and most favorable light. It is probably best to use the CAGE in DWI assessment. Journal of Studies on AlcoSASSI 3, or a comparable instrument, in these circumhol, 48, 492–501. stances. Using the SASSI-3 should yield valid and reliNilssen, O., & Cone, H. (1994). Screening patients for alcohol able results even if the examinee is trying to defeat the problems in primary health care settings. Alcohol Health screen. The disadvantage to using any of the empirically and Research World, 18, 136–139. derived screens, however, is they are more complicated O’Connor, P.G., & Schottenfeld, R.S. (1998). Patients with alcoto administer, score, and interpret. In fact, we would hol problems.The New England Journal of Medicine, recommend completing the 3- to 4-hour training program 592–602.

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Russell, M. (1994). New assessment tools for risk drinking durPiazza, N.J. (1996). Dual diagnosis and adolescent psychiatric ing pregnancy.Alcohol Health and Research World, 18, inpatients.International Journal of the Addictions, 31, 55–61. 215–223 Piazza, N.J., Martin, N., & Dildine, R.J. (2000). Screening Salaspuro, M. (1994). Biological state markers of alcohol abuse. Alcohol Health and Research World, 18, 131–135. instruments for alcohol and other drug problems. JourSelzer, M.L. (1971). The Michigan Alcoholism Screening Test: nal of Mental Health Counseling, 22, 218–227. The quest for a new diagnostic instrument. American Pokorny, A.D., Miller, B.A., & Kaplan, H.B. (1972). The brief Journal of Psychiatry, 127, 1653–1658. MAST: A shortened version of the Michigan Alcoholism Screening Test.American Journal of Psychiatry, 129, Selzer, M.L., Vinokur, A., & van Rooijen, M.A. (1975). A selfadministered Short Michigan Alcoholism Screening 342–345. Test (SMAST).Journal of Studies on Alcoholism, 36, Popkin, C.L., Kannenberg, C.H., Lacey, J.H., and Waller, P.F. 117–126. (1988). Assessment of classification instruments designed to detect alcohol abuse (DOT Publication No.Sokol, R.J., Martier, S.S., & Ager, J.W. (1989). The T-ACE questions: Practical prenatal detection of risk-drinking. HS 807 475). Springfield, VA: National Technical InforAmerican Journal of Obstetrics and Gynecology, 160, mation Service. 863–870. Russell, M. (1994). New assessment tools for risk drinking during pregnancy.Alcohol Health and Research World, 18, 55–61.

67 Interactive Guided Imagery in Treating Chronic Pain David E. Bresler, Ph.D., L.Ac. and Martin L. Rossman, M.D. Chronic pain has become the Western world’s most expenourselves. They strongly infl uence our beliefs and attisive, disabling, and common disorder. It is estimated that tudes about how we fall ill, what will help us get better, 8 to 10% of the population of most Western countriesand whether or not any medical and/or psychological suffer from chronic headaches. Arthritis afflicts over 50interventions will be effective. million Americans, of whom 20 million require medical Imagery has powerful physiological consequences care. Low back pain generates nearly 20 million doctorthat are directly related to the healing systems of the body. visits per year and has disabled 7 million AmericansResearch on the omnipresent placebo effect, the standard (National Center for Health Statistics). Add facial andto which we compare all other modalities (and find reladental pain, neuralgia, cancer pain, chronic neck and tively few more powerful), has provided some of the stronshoulder pain, fibromyalgia, and other common pain syn-gest evidence for the power of the imagination and positive dromes, and it’s easy to understand why chronic pain is expectant faith in healing. It is well documented that 30 estimated to cost the nation’s economy $60 billion dollarsto 55% of all patients given inactive placebos respond as per year. The cost in human suffering is incalculable. well or better than those given active treatments or agents Our focus in this chapter is on the uses of a particular(Frank, 1974). form of mental imagery, called Interactive Guided ImagIf people can derive not only symptomatic relief, but ery, to relieve chronic pain, increase pain tolerance, reduce actual physiologic healing in response to treatments that the emotional toll and amplification of pain, and relieveprimarily work through beliefs and attitudes about an suffering. In the past 30 years of treating patients withimagined reality, then learning how to better mobilize and chronic pain and other chronic illnesses, we have found amplify this phenomenon in a purposeful, conscious way Interactive Guided Imagery to be unusually effective inbecomes an important, if not critical, area of investigation relieving symptoms, enhancing tolerance, relieving feel-for modern medicine. ings of hopelessness and helplessness, promoting healing, In addition to its potential for stimulating physical and increasing functional abilities in our patients. healing, imagery provides a powerful window of insight into unconscious processes, rapidly and graphically revealing underlying psychological dynamics that may WHAT IS INTERACTIVE GUIDED support either health or illness. To the clinician, this “winIMAGERY? dow” is invaluable for quickly identifying opportunities Mental images, formed long before we learn to under-for positive change, manifestations of resistance to stand and use words, lie at the core of who we thinkchange, and ways to work effectively with both. we are, what we believe the world is like, what we feel Guided imageryis a term variously used to describe a range of techniques from simple visualization and direct we deserve, and how motivated we are to take care of

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imagery-based suggestion, through metaphor and storythe more effective analgesic agents also carry a high risk telling. Guided imagery is used to help teach psychophysof dependency. iologic relaxation, to relieve symptoms, to stimulate heal- As a result, it is common to find patients with chronic ing responses in the body, and to enhance tolerance pain to taking large amounts of ineffective medications that procedures and treatments. produce significant side effects, many of which even conInteractive Guided Imagery (IGI) is a service-marked tribute to the pain experience. When patients or their docterm coined by the Academy for Guided Imagery to rep-tors attempt to reduce these medications, withdrawal resent its highly interactive, nonjudgmental, content-freesymptoms make pain even less tolerable, and they return style of using guided imagery to evoke patient autonomy.in desperation to their former regimes. This approach allows patients to draw upon their own When medications fail, patients are often told, “Nothinner resources to support healing, to choose the most ing more can be done. You’ ll have to learn to live with it. ” appropriate adaptations to changes in health, and to find But in our opinion, there isalways hope for someone in creative solutions to challenges that they previouslypain. Until everytherapeutic approach has been attempted, thought were insoluble. IGI is particularly useful in our no one should ever be told, “Nothing more can be done. ” current healthcare climate, where cost-effective This statement has two iatrogenic implications: mind/body medicine, improved medical self-care, andFirst, it destroys the most signifi cant healing asset that briefer yet more empowering approaches to healthcare are victims of chronic pain (or other chronic illnesses) posbecoming more highly valued by patients, providers, andsess, namely, hope or positive expectant faith. Second, insurers alike. it conveys the subtle message that if you have “ to learn Before explaining the principles and practices of IGI,to live with it,” the only time you won’ t have it is when let’s briefly examine some of the unique aspects of chronic you are no longer alive. This may add to the signifi cant pain that demonstrate why a sophisticated mind/bodysuicidal ideation already experienced by many people approach that utilizes techniques such as IGI is critical toin chronic pain. long-term success. The way we communicate with patients in pain has important effects and implications. As we discuss below, such negative communications may actually retard the CHRONIC PAIN DEMANDS DIFFERENT body’s intrinsic healing abilities, while more positive, TREATMENT THAN ACUTE PAIN imagery-based suggestions may enable patients to unlock the door to the most potent and varied pharmacy yet disModern technology has created a huge variety of pharmaceutical products for pain relief, many of which are avail-covered— the one in our own brain. able over the counter. For acute or self-limiting pain, these agents are usually highly effective, for they provide tem-THE IMPORTANCE OF THE PAIN porary relief while the body heals itself. With the devel- EXPERIENCE opment of neural blockade and other modern anesthetic One of the greatest challenges in researching and treating techniques, patients who undergo operative or other invachronic pain is to resolve ambiguity in the terms and sive procedures are generally spared all but the slightest concepts we use to describe it. For example, it is helpful degree of pre- or post-surgical discomfort. to distinguish between a painful sensation(mental awareYet, the pharmacological approaches that have proven ness of an unpleasant stimulus) and the pain experience so successful in the management of acute pain are often ineffective or even counter-intentional for controlling (the total subjective experience of pain). Furthermore, it chronic or long-term pain. Although acute pain usuallyis important to recognize that there is not necessarily any gets better by itself as the body heals, chronic pain typi-direct relationship between the sensation and experience cally becomes worse with time. As a rough rule of thumb,of pain. chronic pain refers to any pain problem that lasts longer This is seen in a study reported by Beecher, who than 6 months. Victims are referred endlessly from doctorfound that soldiers seriously wounded in battle reported to doctor, for even if temporary relief can be obtained, theonly mild discomfort compared to civilians with similar injuries because they were elated to learn that the war pain inevitably returns. was over for them and they were to be sent home. In For example, when analgesic medications are used over a prolonged period of time, pharmacologic toler-contrast, patients with phantom limb pain often report agonizing discomfort even though the entire stump has ance begins to develop and effectiveness is progressively reduced. As tolerance develops, patients typicallybeen anesthetized. Many individuals think of pain primarily as a tangible increase their dosages with the idea that if a“ little is good, a lot will be even better. ” Unfortunately, higher thing, much like a splinter is a thing, that is, an object or substance from outside that infiltrates the body. Thus, if dosages only produce greater amounts of side effects, for tolerance continues to develop. In addition, most ofyou accidentally strike your thumb with a hammer, you

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might say that you “feel pain in your thumb that is radi- and despair, sleep and appetite disturbances, irritability, ating to your hand. ” decreased interests and libido, erosion of personal relaSuch a notion is totally inaccurate, for there is no paintionships with family and friends, as well as increased “in” your thumb, any more than there is pleasure “in” your somatization of complaints. Thus, acute pain and anxiety mouth when you eat something that tastes good. You probbecome chronic pain and depression. ably wouldn’t say, “Umm. My mouth is full of pleasure It is well known that the most notable emotional that is radiating to my stomach. ” change in patients with chronic pain is the development When you injure your thumb, you stimulate neural of depression. This may be overt or masked to both patient receptors that send a barrage of electrical and chemical and health practitioner. In a sense, depression can be conmessages up through the nerves in your hand and arm sidered to a type of emotional pain, and when it is effectively your spinal cord and brain. Whether or not a given sen-treated, the chronic pain experience is also often relieved. sation becomes “painful” depends upon the way it is inter- It is important to emphasize the psychophysiological preted by the nervous system. If you’ ve ever scratched an basis of chronic pain, for it is a complex subjective expeitch really hard, you know that sometimess it’ hard to tell rience that involves physical, perceptual, cognitive, emoif something hurts or feels good. If, for all sorts of reasons,tional, and spiritual factors. When a patient with low back the nervous system decides that the messages from the pain complains that “my back hurts, ” his/her pain experithumb are urgent and require immediate action, it creates ence also may involve anxiety or depression (producing an experience of pain that is identified with the thumb soinsomnia, loss of appetite, and decreased sexual desire), that you’ll give it proper attention. However, it is important drug dependence or addiction, separation from work, famto note that the main pain receptor is between the ears, ily, and friends, loss of avocational interests and hobbies, and that’s where pain resides. numerous secondary gains, and a host of other problems. Like many perceptions, pain is well known to be influ- These may remain indelibly associated with the experienced by learning and early developmental predisposience of back pain, even after the entire spine has been tions. For example, animals raised in a pain-free environ-chemically anesthetized. ment show insensitivity to noxious stimuli in later life. Thus, it is easy to see why no simple pill or shot can Social, cultural, and ethnic differences in the experiencecure chronic pain. The most common error made by cliof pain also are well documented. A vivid example is thenicians is to evaluate and treat only the physical aspect of elective initiation rituals of many primitive tribes, which the problem, for they assume that the objective of therapy would be considered nothing short of torture if practicedis to treat pain in people. To us, however, the objective of by members of Western cultures. therapy is to treat people in pain, which takes a much Aristotle was the rst fi to suggest thatpain “ is an broader perspective. From this point of view, it is nonsenemotion,” as pervasive as anger, terror, or joy. The emo-sical to wonder if a patient has real vs. unreal pain, organic tional component of pain is inexorably bound to othervs. psychologic pain, or legitimate vs. hysterical pain. Pain aspects of the pain experience, for anxiety and agitation is an intensely subjective and personal experience, and are the natural consequences of a painful sensation that even if no physical explanation for it can be found, all tells higher cognitive centers that something is wrong.pain is real. If the “something” can be clearly identifi ed and appropriate corrective action can be taken, the (acute) pain PAIN VS. SUFFERING experience is terminated. However, for most patients with chronic pain, the In our culture, pain is usually considered an enemy to be “ something” is vague, and fear of continued pain in anfought and overcome, and our first approach is to search unknown future produces even greater anxiety. On afor a pain killer. This approach overlooks and ignores the physiologic level, sympathetic hyperactivity develops, assurvival value of pain, which can be a warning signal, a manifested by increased heart rate, blood pressure, resprotector, a potential teacher, guide, motivator, or even an piration, palmar sweating, and muscle tension. Inincentive for change. While some believe that chronic pain patients with musculoskeletal pain, this increased muscle is a symptom that has lost its meaning, this is the result tension often augments the sensation of pain, which fur-of our healthcare system’ s tendency to medicalize and ther increases anxiety, which, in turn, produces evenexternalize symptoms rather than to examine their meangreater muscular tension and more pain. The amplifyinging in a holistic context. relationship between pain and anxiety is well known to Whatever the cause, when one cannot tolerate or cope clinicians, for treatment of one frequently provides reliefeffectively with pain, he or she suffers, which is manifested of the other as well. as an inability to sleep, eat, work, or fully enjoy one’ s life. Over time, exhaustion of sympathetic hyperactivity isLife, in the most personal, meaningful sense, stops. As we inevitable, and more vegetative signs and symptoms soon discuss below, suffering is primarily an epiphenomenon of emerge, such as feelings of helplessness, hopelessness, one’s attitude and beliefs, and we are convinced that it is

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message that something is wrong, and it encourages the possible to have pain, and yet not suffer, depending upon body to take action to prevent further injury. From an evohow we relate to the pain we experience. In the more traditional psychological literature, a dis-lutionary point of view, it is one of the most powerful ways tinction is often made between pain sensitivity and painto insure the survival of an organism in a dangerous world. While most authorities acknowledge the positive tolerance. To illustrate the clinical importance of pain tolerance when teaching fellows and residents at UCLA,aspects of acute pain, many believe that chronic pain is a one of us (DB) found it helpful to compare X-ray films biological mistake or obsolete symptom that serves no useful purpose. In order to correct this mistake, they recof two patients with knee pain. The first patient was a professional football player ommend strong drugs or surgical procedures to obliterate who had undergone six prior knee surgeries. Whilethe sensation of pain. It is interesting to note that the exact reviewing his films, we wondered how this individual technique utilized will depend more upon the type of s unique needs. could walk, much less continue to play football. However,specialist consulted than upon the patient’ For example, an internist may prescribe medication; he reported little pain or discomfort, took no pain medications (they made him “feel less ferocious”), and onlya psychologist, psychotherapy; an acupuncturist, needles; a chiropractor, manipulation; and so forth. Abraham desired treatment that would increase stability and range Maslow used to say, “When all you have is a hammer, of motion in his knees. ” The second patient was injured on the job and had led fi you tend to look for nails. In our opinion, the best long-term interests of the extensive worker’ s compensation litigation. Although his knee X-rays were completely normal, he suffered greatlypatient often are not served when the major goal of therapy is to artificially mask or suppress pain without attempting and was unable to climb stairs, drive a car, or sleep for more to understand its ultimate message. To do so is like than 2 to 3 hours at a time. He was totally disabled, desponresponding to a ringing fire alarm by cutting its wires to dent and depressed, and dependent on his family, four medstop the annoying clamor, rather than by leaving the burnical doctors, and seven different pain medications. The first patient had significant pathology but high ing building. tolerance and barely complained of pain. The second had We invite patients to consider the notion that like the minimal if any pathology, but little tolerance to the pain oil light in a car, their nervous systems are generating the experience of pain for a reason. We invite them to explore he experienced. In the clinical situation, we often confront limitations in the possibility that chronic pain is usually not a disease or mistake but a symptom generated through the wisdom our ability to reverse severe physical pathology (e.g., degeneration of cartilage in a joint). However, our ability to help of the body. patients enhance their tolerance of pain seems to have no We then teach them about the extraordinary self-balupper limit. Thus, practitioners who help patients embraceancing, regeneration, and repair systems of the body and remind them that symptoms are the way that the body tries a more positive belief or attitude about pain can be successful to heal itself or prevent further injury. Like the oil light in helping to reduce suffering and enhance tolerance, even and the fire alarm, once their message is heard and approwhen nothing more (medically) can be done. Increasing pain tolerance is, after all, the basis ofpriate action is taken, symptoms usually will disappear, for they are no longer needed. effectiveness of our most potent pain medications. When Much of contemporary medicine is based on an sympa patient is given an injection of morphine (which mimics the effects of endorphins), he or she will often state. “Ittomatic adjustment model of therapy designed to reduce still hurts, but it doesn’ t bother me. ” This represents or suppress symptoms. If a patient has high blood presantihypertensives are prescribed to reduce it. If a enhanced central tolerance, not reduced sensation, yetsure, it enables the patient to become more highly functional. patient is unable to sleep, medications are given for sedaThe extent to which a patient’ s suffering can be tion at night. If a patient has excessive anxiety, tranquilizers are often utilized. But why does a given patient have reduced through psychophysiological approaches such as IGI depends upon many complex variables including thehypertension, sleep disorders, or anxiety neurosis? What patient’s belief systems and attitudes, early life experi-is the message that the symptoms are trying to convey? Exploring this question in a nonjudgmental way can be ences, the degree of physical pathology, and perhaps most importantly, the meaning of pain in the context of thethe key to relieving or modulating many symptoms, including chronic pain. patient’s life. Pain is a message that alerts us to danger. Through the primitive, survival-oriented wisdom of the nervous THE MEANING OF PAIN system, it motivates us to correct the situation by changing Since the dawn of creation, pain has provided criticallyand adapting to the shifting demands of the world in which important information concerning our relationship to ourwe live. Through pain, we are warned about all of the dangers we face, and if we continue to ignore them, the inner and outer environments. Pain strongly conveys the

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intensity of pain will increase in an attempt to get our Imagery serves simultaneous a information processing attention and/or elicit some change. system, which underlies the holistic, synthetic, pattern Perhaps this is why many chronic pain patients receive thinking of the unconscious mind, and can reveal to us how only temporary relief after symptomatic treatment. seemingly disparate areas of our lives are intimately related. Although the nervous system can be fooled for a short A brief clinical example from Dr. Bresler’ s practice time by drugs or surgical treatment, if it believes that someserves to focus on the importance of this relational quality subtle danger still remains, pain will attempt to breakto life. through and, over time, continue to return until the mes- A 52-year-old cardiologist named John was suffering sage is heard and properly responded to. from excruciating low back pain following treatment for rectal cancer. Although surgery and radiation therapy apparently had eradicated the cancer, he described the pain PRINCIPLES OF INTERACTIVE GUIDED that remained as unbearable. Because the area had been IMAGERY (IGI) so heavily irradiated, neither repeated nerve blocks nor further surgery could be used to help relieve his terrible HEALING BENEFITS FROM RESPECTFUL ATTENTION discomfort, and he had long ago developed tolerance to Although no one really knows what consciousness is, we his pain medications. believe that it is critically related to the process of atten- When John first came in, he already had narrowed tion, for we only experience what we attend to. There isdown his personal alternatives to three: (1) successful an old saying that “whatever you give your attention totreatment, (2) voluntary commitment to a mental institugrows,” whether it be your garden, your children, your tion, or (3) suicide. John was convinced that under no worries and fears, or your pain. circumstances could he continue to live with pain and, at Over the years, most of us learn to give our attentionthe same time, maintain his sanity. to the conscious, verbal part of our mind that narrates a In reviewing his medical records, I noticed that during linear logical, rational, analytic monologue describing itsa psychiatric workup, John had described his painaas “ perspective of the world and how we think about it. s It’ dog chewing on my spine. ” This image was so vivid that the little voice inside your head that talks all the time, theI suggested we make contact with the dog, using guided person most of us think we are. imagery. With his training in traditional medicine, he However, who we really are is much more than justthought the idea was silly, but he was willing to give it a try. what we think. We are also the richness of our intuitions, In John’s case, our initial goal was to have the dog emotions, feelings, memories, drives, fantasies, goals, stop chewing on his spine. Over the next few sessions, the appetites, aspirations, expectations, ambitions, values, dog began to reveal critically important information. passions, beliefs, perceptions, and sensations. Any or all According to the dog (named Skippy), John never had of these aspects of self may require and even demand wanted to be a physician, his own career choice was archiattention,finding ways to compete by intruding on every- tecture, but he had been pressured into medical school by day consciousness through physical, cognitive, emotional, his mother. Consequently, he felt resentment not only or even behavioral symptoms, if need be. toward his mother, but also toward his patients and colRather than suffer the results of neglecting these parts leagues. Skippy suggested that this hostility had, in turn, of ourselves, we can focus attention on them in a relaxed contributed to the development of his cancer and to the state of mind and invite images that represent them to subsequent pain problem as well. come to mind. By properly dialoguing interactively with During one session, Skippy told John, “You ’re a damn these images, we can reconnect with important and powgood doctor. It may not be the career you wanted, but s it’ erful inner resources that are deeply dedicated to protecttime you recognized how good you are at what you do. ing us and improving the quality of our lives. When you stop being so resentful and start accepting yourself, I’ll stop chewing on your spine. ” These insights were accompanied by an immediate alleviation of the IMAGERY IS THE PRIMARY ENCODING LANGUAGE pain, and in only a few weeks’ time, John became a new OF THE BODY’S HEALING SYSTEMS person, and his pain progressively subsided. Imagery can be thought of as one of the brain ’s two This type of experience demonstrates how powerfully higher-order information processing and encoding sys-the imagery process can reveal meaning in a supposedly tems. The system we are most familiar with is that whichmeaningless symptom, and show the way to healing. usessequential information processing , and it underlies While imagery does not always lead so dramatically to linear, analytic, and conscious verbal thinking. Mostrelief, and disease remission from such dialogues does not health professionals are highly educated and highlyalways occur, they almost always lead to better self-underrewarded for their abilities in using this mode of infor- standing and enhanced coping skills for dealing with a mation processing. chronic illness or condition.

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IMAGERY HAS PHYSIOLOGICAL CONSEQUENCES

PATIENT AUTONOMY IS MOST SUPPORTED BY USING A TWO-WAY INTERACTIVE GUIDING STYLE Numerous research studies have shown that imagery is able to affect almost all major physiologic control systemsOne key to the extraordinary clinical effectiveness of of the body, including respiration, heart rate, blood pres-Interactive Guided Imagery is the unique interactive comsure, metabolic rates in cells, gastrointestinal mobility andmunications component that it incorporates. By working secretion, sexual function, and even immune responsiveinteractively instead of simply reading an imagery script, ness (Sheikh & Kunzendorf, 1984). the Interactive Imagery Guide ensures that the experience Imagery is essentially a way of thinking that useshas personal meaning for the client, and that it proceeds sensory attributes, and in the absence of competing senat a pace determined by the client’ s actual needs and sory cues, the body tends to respond to imagery as it would abilities rather than the guide’ s best guess estimate. to a genuine external experience. For example, imagine For example, an Interactive Imagery Guide might that you have a big, fresh, yellow, juicy lemon in your ask,“ Of all the different problems, symptoms, and chalhand. Experience it in your mind’ s eye until you sense its lenges now going on in your life, allow an image to form heaviness and fresh tartness. Now, imagine taking a knife that represents the single most important and critical and slicing into the lemon. Carefully cut out a thick, juicy issue for us to work on now, and then describe it to” me. section. Now take a deep bite of the lemon slice andThe guide can then facilitate a dialogue between the imagine tasting the sour lemon juice, saturating every taste client and the image tond fi out what the image wants, bud of your tongue so fully that your lips pucker and yourneeds, and has to offer. tongue begins to curl. Because the content, direction, and pace are set by If you were able to imagine this vividly in your mind’ s the client, not the guide, it is the client who actually eye, the image probably produced substantial salivation, (unconsciously) guides the process to the resources most for the autonomic nervous system easily understands and needed to support healing, change, and positive theraresponds automatically to the language of imagery. peutic results. Here is the crux of the matter: If imagining a lemon makes you salivate, what happens when you imagine PATIENT AUTONOMY IS MOST ENCOURAGED BY you’re a hopeless, helpless victim of chronic pain?USING CONTENT-FREE LANGUAGE AND Doesn’t it tell your nervous system to give up? Isn’ t it NONJUDGMENTAL GUIDING likely to create neural and biochemical signals that go along with being defeated rather than actively healing?We often like to say that “the guide provides the setting, And, in the other direction, might not resolving seriouswhile the client provides the jewel. ” Whenever possible, life problems, improving communications and relation- the Interactive Imagery Guide uses nonjudgmental, conships, and learning to modulate pain create a healthier and tent-free language, because it encourages clients to tap more functional physiology in the body? their own inner resources to find solutions for solving their own problems. At a time when there is so much concern about false IMAGERY IS THE LANGUAGE OF THE EMOTIONS memory syndrome (Pope, 1996), this type of content-free Imagery also is a powerful tool in the healing arts because guiding also insures that the client’ s experience is not of its close relationship to the emotions. Imagery is theunduly contaminated or influenced by the suggestions of expressive language of the arts — poetry, drama, painting, the guide. sculpture, music, and dance, and thus of the emotional self. Emotions show us what’ s personally important to us PATIENT AUTONOMY IS ENCOURAGED BY SPECIFIC and they can be either potent motivators or barriers to QUALITIES AND SKILLS UTILIZED BY THE GUIDE changing lifestyle habits. As clinicians, we have concluded that, by and large, if an issue doesn’ t affect you There are important personal qualities that the Interactive emotionally, it probably won’ t make you sick nor is it Imagery Guide brings to the therapeutic experience, likely to help you get well. including a nonjudgmental attitude, patience, and trust in Emotions motivate us to action and they also producethe client’s own abilities. The consistent emphasis on characteristic physiologic changes in the body, includingresources and solutions, the repetitive inner focus as a varying patterns of muscle tension, blood flow, respiration,source for solutions and strengths, and the modeling prometabolism, and neurologically and immunologically vided by the guide’ s belief that the clients have within reactive peptide secretions. Modern research in psychothem more resources than they had imagined, leads to neuroimmunology points to the emotions as key modula-minimal transference, greater opportunities for effective tors of neuroactive peptides secreted by the brain, gut, and client self-care, an enhanced sense of self-ef ficacy, and immune systems (Pert & Chopra, 1997). the rapid development of patient autonomy.

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Typically, patients are initially seen one to three times to explore the potential benefits of working with IGI. After three sessions, clients may have solved the problem, may PATIENT ASSESSMENT PROCEDURES have found a successful way to work it out by themselves, may have identified an issue that will require additional The Interactive Imagery Guide must first decide whether work, or may have found that the method or practitioner there are any contraindications to introducing imagery to is not suitable for them. the patient, such as a medical or surgical condition requirWhile imagery may bring psychological material to ing emergency treatment, or mental illness precluding its light that was not previously perceived to be part of the use. Having decided that imagery may offer benefit, a medical equation, it also can provide ways to work with history is taken regarding the client’s prior experience with this material that do not create unnecessary dependence imagery, hypnosis, relaxation, meditation, or related on a therapist. Many medical or nursing professionals will approaches. This allows the guide to utilize prior positive work with patients if the situation appears it will yield to experiences or to address relevant issues in the case of a brief course of teaching and counseling, while referring negative experiences. those with more complex issues to therapists who are more If the client has no prior experience with relaxation highly trained in the method. or imagery, the guide usually invites the client to relax while being guided through a brief relaxation techTREATMENT OPTIONS nique. The client is then invited to imagine him or herself in a beautiful, safe, and peaceful place and then Because imagery is a natural way we think, and can almost to describe what he or she sees, heasr, smells, and feels always be helpful, there are virtually an unlimited number there. The guide may suggest that this special place has of situations where it can be used in healthcare settings. other qualities that also might be uniquely helpful to For simplicity, it may be helpful to consider three major the client. For example, a fearful client might be categories of use: encouraged to imagine hi or herself in a powerful place, a sanctuary, or a place where you are completely safe 1. Relaxation and stress reduction, which are easy and beyond harm. A client who feels he or she is too to teach, easy to learn, and almost universally exhausted to deal with a situation might be encouraged helpful. to imagine a place of great energy and vitality, or a 2. Visualization, or directed imagery, where the place of rest, renewal, and refreshment. client/patient is encouraged to imagine desired Imagining a quiet, safe place is one of the quickest outcomes in a relaxed state of mind. This ways to teach most people to relax and it powerfully affords the patient a sense of participation and illustrates the profound effects a simple imagery expericontrol in his or her own healing, which itself ence can have. is of significant value. In addition, it also may Occasionally, a client cannot imagine such a place, or relieve or reduce symptoms, stimulate healing gets more anxious as the eyes close and he or she begins responses in the body, and/or provide effective to relax. If this anxiety doesn’t respond to reassurance that motivation for making positive lifestyle the person is in control, and gentle encouragement to see changes. what comes next, it may be a signal that the person has 3. Receptive or insight-oriented imagery, where not experienced such a place or that relaxing may be images are invited into awareness and explored psychologically dangerous to them. Relaxation-induced to gather more information about a symptom, anxiety may also be a marker for early trauma, as is the illness, mood, situation, or solution. experience of having an imaginary safe place suddenly turn dangerous or foreboding. Another set of options to consider is whether the client Alternatively, clients may be invited to turn their atten- will be able to use imagery most effectively as a self-care tion to specific symptoms, to allow images to form for technique, in a group or class, or as part of an individual them, and to invite healing imagery to come to mind. Theycounseling or therapy relationship. Self-help books and may be invited to have an imaginary dialogue with antapes are another inexpensive option for many clients who image of a symptom, or with a kind, wise “Inner Advisor” are capable of utilizing these techniques on their own. who can provide previously inaccessible information In practice, most patients and practitioners will about their issues or illness. explore all of the above options and utilize the ones that In this relaxed state, we can invite images to form forsuit a given client the best, given the unique nature of the almost anything we want to know more about, and sys-issue, patient coping responses and approach to life, and tematically explore the images to expand awareness and the amount of time, energy, and funds the patient is willing identify new options that promote healing. or able to invest in the process.

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This interactive technique can be used with an image that The list of techniques utilized in IGI is quite extensive, represents anything the client or therapist wants to know more about, and in many ways, it is the quintessential and this approach has been applied to problems ranging insight technique. We use it to explore an image of a from severe depression and chronic pain, to post-traumatic stress, to relationship conflicts, to enhance creativity, tosymptom (whether physical, emotional, or behavioral), an image representing resistance that arises anywhere in the search for life purpose. However, some of the more the process, an image for an inner resource that can help basic techniques include the following. the client deal with the current problem, or an image of the solution. Conditioned Relaxation When using Interactive Imagery, the point is not to This powerful, relaxation technique is based on Pavloviananalyze the images, but to communicate with them as if classical conditioning techniques and utilizes imagery-they are alive (which of course, they are). This is not to linked breathing and body awareness techniques to train say they have an existence apart from the client, but rather the patient to relax automatically by taking a special “sig-that the images represent complexes of thoughts, beliefs, nal breath. ” Instead of tensing when pain starts to flare,attitudes, feelings, body sensations, expectations, and valpatients become conditioned to relax and gently move the ues that at times can function as relatively autonomous painful symptoms out of their bodies. aspects of the personality. These constellations have been referred to as subpersonalities by Assagioli, or ego states Symptom Suppression Techniques by Watkins and Watkins.

Symptomatic imagery techniques reduce the physical sympThe Inner Advisor toms of pain without concern for their causes. They are a useful alternative to analgesic medications, and are particuAfter relaxing in his or her own safe place, a client is larly helpful when discomfort is so intense that the patientinvited to dialogue with an imaginarygure fi who is cannot concentrate enough to use other guided-imagery designed to be both wise and loving, or as characterized approaches. They include a wide variety of scenarios and in analytic terms, an “Ego Ideal. ” We call this figure the techniques, such asglove “ anesthesia, ” a two-step imagery “Inner Advisor,” and it is often referred to as the “Inner exercise in which patientsrst fi are taught to image develop- Guide,” “Inner Healer,” “Inner Wisdom,” “Inner Helper,” ing feelings of numbness in the hand, as if it were being“Inner Physician, ” “Higher Self,” or any other term that placed into an imaginary anesthetic glove. Next, they learn is meaningful and comfortable for the client. As the client to transfer these feelings of numbness to any part of the body is invited to imagine a figure with these qualities, a diathat hurts, simply by placing theanesthetized” “ hand on it. logue with whatever figure arises is usually meaningful Glove anesthesia often helps to take the edge off the pain and helpful. sensation, thus permitting patients to explore other aspects of the pain experience more fully. In addition, glove anes-Evocative Imagery thesia provides a dramatic illustration of the power of selfThis state-dependent technique helps clients shift moods control. When patients realize that they can produce feelings and affective states at will, thus making new behaviors of numbness in their hands at will, they recognize that they may be able to control their discomfort, too. This is pro-and insights more accessible to consciousness. Through foundly therapeutic for pain sufferers who feel totally help-the structured use of memory, fantasy, and sensory recruitment, the client is encouraged to identify a personal qualless and unable to affect their discomfort. ity or qualities that would serve him or her especially well in the current situation. For instance, a client may need Symptom Substitution Techniques more calmness or peace of mind in order to deal more Symptom substitution is another symptomatic techniqueeffectively with pain. that permits the nervous system to move the discomfort The guide then invites clients to relax and recall a to a new area of the body where it will be less disruptive.time when peace of mind was actually experienced. For example, patients can learn to experience their headThrough the use of sensory recruitment and present tense aches in, say, their little finger instead of their head. Thisrecall, the clients are encouraged to imagine they are there technique does not ask the nervous system to stop the again now, feeling that peace of mind. Once this peaceful experience of pain (or to cover up the message it is trying feeling state has been well established and ampli fied, the to communicate). Rather, it moves the symptom to a less patients are invited to let the past images go, but to come traumatized area so that patients can work more effectively back to the present, bringing the feelings of peace of to identify what is wrong. mind. As they now become aware of their pain problems

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while strongly in touch with this feeling, they are usually After this evaluation, an agreement is made to terminate treatment, to continue for another period of time, to refer able to tolerate it far more effectively. ne a period of time in Evocative imagery was researched by Dr. Sheldonto another practitioner, or to defi “ wnwork” and then return to Cohen at Carnegie-Mellon University (personal commu-which the client will do o nication) and found to be highly effective in shifting report progress. affective states. Research aimed at assessing the effects of those altered affective states on subsequent behavior, TREATMENT APPLICATIONS IN ADDITION TO PAIN problem-solving, and self-ef ficacy remain to be done and offers a fertile field for future psychological and behav- Since imagery is a natural language of the unconscious and the human nervous system, its potential uses in the ioral research. healing professions are protean. We think that imagery is essentially a way of working with the patient, rather than Grounding: Moving from Insight to Action a way of treating particular disease entities. Thus, it is This is the process by which the insights evoked by imag-almost always useful as an adjunctive therapy, while it is ery are turned into actions, and increased awareness and rarely, if ever, utilized as a sole therapy. motivation are focused into a specific plan for attitudinal, Table 67.1 lists some of the major applications of emotional, and/or behavioral change. This process of addimagery in the healing professions. ing the will to the imagination involves clarification of insights, brainstorming, choosing the best option, firmaaf tions, action planning, imagery rehearsal, and constantTABLE 67.1 reformulation of the plan until it actually succeeds. It is Applications of Interactive Guided Imagery often the missing link in insight-oriented therapies, for it in the Health Professions connects the new awareness to a specific action plan. s It’ where the “rubber meets the road, ” and imagery can be In Medicine used to enhance this process by providing creative options for action and by utilizing imagery rehearsal to trouble- • Relaxation and stress reduction • Pain reduction and symptom relief shoot and anticipate obstacles to success. • • TREATMENT EVALUATION • We refer to the time spent before entering into a formal • guided imagery exploration as the “foresight” part of the • • process. Along with evaluating the appropriateness of •

using imagery with the client or patient, the guide works with the client to establish the desired goals and objectives • for their work together. As with any medical or psychological situation, goals • can be defined in physical, emotional, or behavioral terms,• and a reasonable trial period of exploration is agreed upon.• We often ask patients to do three exploratory sessions and• • then decide whether this approach seems useful to them, • whether they can best use it as self-care in a brief, time-• limited period of work (10 to 15 sessions), or whether it • looks like a longer-term piece of work will be needed. • Many physicians and nurses work for a defined period • of time with patients in a psycho-educational or counsel- • ing model, with well-defined symptomatic or behavioral goals, and refer patients to mental health practitioners if • their work becomes psychologically complex. At the same • time, we urge that mental health practitioners take precau-• tions to ascertain the medical status of any patient to make• certain they are also aware of the medical options. • At the end of each session, and at the end the agreed-• upon time period, the goals of the work are reviewed • and progress assessed (we call this phase hindsight”). “

Increasing compliance with treatment regimens Tolerating difficult procedures Preparing patients for surgery Stimulating healing responses (immunity, blood flow) Insight and affect recognition Engaging patients in their own self-care Finding meaning in illness

In Psychotherapy Relaxation and stress reduction Systematic hyposensitization for phobias Conflict clarification and resolution Shift of locus and control and relief of powerlessness Positive suggestion, firmation, af and enhanced self-esteem Finding vision and meaning Action planning Values clarification Increased creativity and enhance problem-solving Modulation of mood and affect Insight and awareness development Grieving In Nursing Relaxation and stress reduction Deepening rapport Enhancing compliance Tolerating procedures Pain and symptom relief Engaging patients in self-care Addressing emotional needs of patients

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PRECAUTIONS

1. Do not substitute imagery for necessary medical or surgical interventions. The primary danger in using imagery to augment healing in medical situations is when it is used in lieu of appropriate medical diagnosis and/or treatment. We emphasize the necessity of an accurate diagnosis prior to using any psychophysiologic approach so that the patient also is aware of the medical options for treatment. At times, patients may decide that they do not have acceptable medical options available and will then choose to use imagery and mind/body/spirit approaches as their firstline treatment. Although there are some situations in which this makes perfect sense, each situation must be evaluated individually to ascertain the patient’ s ability to judge for him or herself and to make such choices. 2. Do not use imagery inappropriately with patients with unstable or unmanaged psychopathology. There are several diagnostic categories of mental illness where the practitioner must use extreme care when utilizing exploratory receptive imagery techniques. In particular, patients who are psychotic or who are on the verge of psychotic breaks, patients with dissociative identity disorders, and patients with borderline personality disorders must be handled with care, and only by welltrained and experienced practitioners. While these diagnoses do not represent absolute contraindications for imagery work, they absolutely require treating health professionals to have appropriate training and expertise in these areas. While many clients with these diagnoses may benefit from certain uses of imagery (usually directed imagery scripts focusing on centering, calmness, self-control, safety, etc.), great caution should be taken when using potentially disorganizing receptive imagery techniques. In proper therapeutic hands, imagery techniques can be one of the most effective ways to work with clients who are survivors of traumatic abuse and who tend to pathologically dissociate. However, such treating practitioners must be well trained and experienced in working with both survivors of abuse and with exploratory IGI approaches. 3. Do not confuse responsibility with blame. The fact that an illness can be helped through mental processes does not necessarily suggest that it was caused by mental means. When

using exploratory techniques such as imagery dialogue with symptoms, or working with an inner advisor, there is a tendency to confuse the ability to learn from illness with blame for causing the illness. This issue needs to be handled with skill and sensitivity, and while the practitioner may not be able to prevent certain clients from self-blaming (this may be an important issue to address with them), they can help most people realize that using positive images to stimulate healing does not necessarily mean that their negative images caused their illness. 4. Do not underestimate the holotropic principle and the innate resources of the patient. Imagery is a potent form of communication and suggestion. Whenever possible, we advocate using the patient’ s own imagery and an interactive guiding style because we are convinced that the client has within him- or herself a great deal of information, experience, knowledge and problem-solving resources that have not yet been used most effectively. While there are certainly places and situations where a guide needs to supply suggestions and images, these are relatively rare when utilizing IGI, and may even rob clients of the opportunity to learn an important way to help themselves. This creates or sustains a sense of dependency on the expertise of the guide, rather than attention to the inner abilities that have always been available to help them to help themselves.

SCOPE OF PRACTICE FOR INTERACTIVE GUIDED IMAGERY This has been an important and problematic area for the Academy for Guided Imagery. As we considered the criteria for formal certification in IGI, we decided to exercise caution and restrict certifi cation eligibility to professionals licensed to provide counseling services in their states of residence. We soon found out that many states have no such licensing for therapists, and people of various levels of quality were providing counseling, psychotherapy, hypnosis, and guided imagery. As a result, we evaluate each candidate on an individual basis, assessing him or her for both competence and ethical standards as we observe them in clinical supervision as part of the Academy’ s training. Health professionals must practice within the scope of their licensure, education, experience, and competence. Within these guidelines, certifi cation in IGI can signifi cantly help make professionals more effective at what they already do. Using guided imagery or IGI does not turn a physician into a psychotherapist, or a psychotherapist into a physician.

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usually centrally involved, primarily because it is a funInstead, it gives each a greater range of skillfulness in works healing systems. As ing with issues that involve both mind and body, and withdamental language of the body’ this is better recognized, we are hopeful that health issues involving emotions and behavioral change. Certified IGI practitioners must discriminate betweenprofessionals will learn more about the best ways to utilize this potent form of thinking to support optimal psychotherapy and psychoeducation, and between health and healing. enhancing healing responses and the practice of medicine. They must ethically practice each within their scope of Feedback from the thousands of health professionals who have taken IGI training confirms that it is a rapid licensure, training, experience, and competence. route to insight, growth, and change. One constant piece Because our approach is holistic, there is more crossof feedback we get is that learning to use imagery interover in these areas than is immediately apparent. If we actively has improved the listening, communicating, and can effectively activate healing responses through essentherapeutic skills of our graduates, whether they are mentially psychological means, how does this affect the scope of practice of mental health practitioners who are well-tal health professionals, physicians, or nurses. We feel that competence in effectively yet respectfully versed in IGI? Shouldn’ t they be critical members of every guiding the imagery process should be a fundamental part primary healthcare team? We believe so. of every health professional’ s education and training, and the Academy for Guided Imagery is working toward that TRAINING, CERTIFICATION, AND ISSUES goal by co-sponsoring many of its professional training OF COMPETENCE programs with well-established schools of medicine, nursMany health professionals utilize guided imagery in theiring, and psychology. work, although they may have only learned to lead some- In addition to professional training and Certification one by reciting a noninteractive script. The quality of theirin Interactive Guided Imagery, the Academy for Guided training and competence with this approach is highly vari-Imagery is a resource for self-help books and tapes and reliable information on imagery. The Academy also is able. Because the potential for doing harm always exists participating in research studies exploring the uses of when these techniques are used inappropriately or without imagery in pain control, surgical preparation and recovery, adequate skills, standards of practice and quality control and cancer chemotherapy, and it recently established the are an issue of critical importance. The Academy for Guided Imagery has establishednonprofit Imagination Foundation to support further research in these and other areas. The Imagination Founspecific standards of competence and ethical behavior that must be met before Certification in Interactive Guideddation is currently soliciting both funds and research proposals investigating imagery in healing. Imagery is awarded. Quality assurance is based largely Humans have always used their imaginations to solve upon direct observation of clinical work in small group and individual supervision sessions during the trainingproblems that threatened their survival. Our times program. Over 52 hours of supervision, four to six differ-demand that we now learn to use this powerful information-processing and problem-solving mechanism even ent faculty members carefully observe each candidate, and more effectively to help heal ourselves, our families, our provide specific feedback to enhance his or her skills. We communities, and our planet. A sustainable future know of no other such standards of quality assurance depends in part on our ability to imagine it in both established for imagery practitioners. personal and global terms, and we are committed to supporting the healing potential of this much underREIMBURSEMENT STATUS utilized resource —the human imagination. Imagery practitioners usually bill and are reimbursed for their work in the same way as for other professional services RESOURCES they render. Sessions are usually billed as psychotherapy, counseling, stress reduction training, or medical hypnosis. PROFESSIONAL TRAINING When applied for medical purposes, medical practitioners may ethically bill for medical services, although insurance The Academy for Guided Imagery companies may challenge this if services are lengthy and Martin Rossman, M.D. and David Bresler, Ph.D. repetitious. There are currently no separate billing codes for Professional Certifi cation Training in Interactive ™, Public Education, Healthguided imagery or IGI. Guided Imagery care Consulting, Speakers, Books, and Tapes P.O. Box 2070 PROSPECTS FOR THE FUTURE Mill Valley, CA 94942 When you look closely at almost every form of human 1-800-726-2070; FAX 415-389-9342 therapeutic interaction and communication, imagery is http://www.interactiveimagery.com

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Imagery for Health and Healing Jeanne Achterberg, Ph.D. 369 Montezuma, Ste. 342 Santa Fe, NM 87501-2626 505-986-826

PROFESSIONAL ASSOCIATIONS International Association for Interactive Imagery™ P.O. Box 124 Villa Grande, CA 95486 Imagination Foundation P.O. Box 2070 Mill Valley, CA, 94942 1-800-726-2070; FAX 415-389-9342

TAPES, VIDEOS, BOOKS,

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RELATED MATERIALS

The Imagery Store (Academy for Guided Imagery) P.O. Box 2070 Mill Valley, CA 94942 1-800-726-2070 Health Journeys (BelleRuth Naparstek, Ph.D.) 891 Moe Drive, Suite C Akron, OH 44310 1-800-800-8661 Source Cassettes (Emmett Miller, M.D.) P.O. Box W Stanford, CA 94309 1-800-528-2737

REFERENCES Academy for Guided Imagery, 1-800-726-2070. www.interactiveimagery.com Cohen, S. Personal communication. Frank, J. (1974).Persuasion and healing . New York: Schocken Books. Imagination Foundation, POB 2070, Mill Valley, CA 94942. www.imaginationfoundation.org Inventory of Pain Data from the National Center for Health Statistics. Washington, D.C.: U.S. Government Printing Office. Pert, C.B., & Chopra, D. (1997). Molecules of emotion: Why you feel the way you feel . New York: Scribner. Pope, K.S. (1996). Memory, abuse, and science. American Psychologist, 957–974. Sheikh, A., & Kunzendorf, R.G. (1984). Imagery, physiology and psychosomatic illness. In A. Sheikh (Ed.), International review of mental imagery . (Vol. 1, pp. 95–138). New York: Human Services Press. Vargiu, J. (1974).Subpersonalities, synthesis(pp. 1 57–90). Redwood City, CA: Synthesis Press. Watkins, J.G., & Watkins, H.H. (1979). The theory and practice of ego-state therapy. In H. Grayson (Ed.). Short-term approaches to psychotherapy . New York: Human Sciences Press

68 Behavioral Protocols for Burning and Cramping Phantom Limb Pain* Richard A. Sherman, Ph.D. CONCEPTUAL INTRODUCTION

RELATIONSHIPS BETWEEN PHANTOM LIMB PAIN AND MUSCLE TENSION Behaviorally oriented treatments for phantom limb pain have been in use at least since the late 1970s (e.g., SherChronholm (1951) quotes Amyot, Livingston, and others man, 1976). Use of behavioral interventions is predicated as having noted increased muscle tension and spasms in on the supposition that amputees can learn to recognize the stumps of amputees. He found that 51 of 99 amputees and then control incorrect levels of physiological functionsquestioned about stump muscular activity reported sponrelated to their phantom pain. taneous hyperactivity. This idea requires that (1) there are specific physi- Onset and intensity of cramping and squeezing ological parameters which are directly related to specificdescriptions of phantom pain are related to muscle tension descriptors of phantom pain and (2) people can, indeed, in the residual limb. A variety of studies have demonlearn to control them. Over the past several decades, strated that intensity of cramping phantom pain and data have accrued that strongly infer that the extent ofamount of muscle tension in the residual limb change near-surface blood flow in the residual limb is inverselytogether from day to day (Sherman & Arena, 1992) and correlated with intensity of burning/tingling descrip- from moment to moment (Sherman, Grif fin, Evans, & tions of phantom limb pain and that many amputees can Arena, 1992). learn to control blood flow in the residual limb suffiChanges in surface electromyographic (sEMG) repreciently to reduce or eliminate these sensations. Data also sentations of muscle tension in the residual limb precede show that cramping/twisting descriptions of phantomchanges in cramping and squeezing phantom pain by up limb pain are related to increased muscle tension and to several seconds. This relationship does not hold for any spikes/spasms of the major muscles in the residual limb other descriptions of phantom pain. The critical point is and that amputees learning to eliminate these abnormalthat the amputee only shows changes in muscle tension ities also eliminate their cramping phantom pain. Therein the painful residual limb. Surface EMG in the pain-free are no known physiological correlates of shockingresidual limb does not change significantly. If the change shooting phantom pain and none of the behavioral inter-in EMG was simply a reaction to the change in pain, the ventions appears to be effective for this description ofchange in EMG would have followed, rather than prephantom pain. ceded, the change in pain and at least some change in

*

Adapted fromPhantom Pain , Sherman, Devor, Jones, Katz, and Marbach (1997).

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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residual limbs were cooler muscle tension in the pain-free limb should have beenstudy found that amputees’ at the distal end than paired points on the opposite observed as would be expected from a generalized withdrawal reflex from pain. extremity and that the cooler areas did not warm up when ow fl Relationships between overall muscle tension in theattempts were made in increase cutaneous blood through such mechanisms as giving the subjects whiskey residual limb and cramping phantom pain have also been to drink. Wahren (1990) reviewed the propensity nof fi shown to hold throughout the day in subjects’ normal enviger amputees to be very sensitive to the cold and for ronments (Sherman, Evans, & Arena, 1993). The device their pain to be aggravated by cold environments. They used to establish the relationship was capable of recording ngers fi were cooler surface EMG from the residual limb and button press rep-found that the residual areas of the than corresponding areas on the intact hand and were resentations of pain intensity (Sherman, Arena, Searle, & Ginther, 1991). The relationship between cramping phan-more sensitive to pain in response to cooling. Kristen, tom pain and muscle tension in the residual limb is sup-et al. (1984) reported using videothermographic recordported by the consistent success of treatments resulting ings in of temperatures in the residual limbs of 50 amputees reduction of residual limb muscle tension for crampingto detect phantom pain. They found that most amputees phantom pain but not for other descriptions (Shermanhaving phantom pain showed different patterns of temperature than those who had none. 1976; Sherman et al., 1991; Sherman et al., 1992). Numerous amputees report that cramping phantom Consistent, inverse relationships between intensity of phantom limb pain and temperature in the residual limb pain decreases with any activity that tends to decrease muscle contraction levels in the residual limb andrelative to that of the intact limb have been demonstrated increases with activities increasing overall levels of con-for burning, throbbing, and tingling descriptions of phantom pain but not for any other descriptions (Sherman & traction. Thus, such activities as phantom exercises, which result in changes in muscle tension in the residual limb,Bruno, 1987). can result in temporary changes in intensity of phantom pain. Gessler (1984) reported that when the muscles of It has also been established that (a) for these descriptors the residual limb of 10 amputees with chronic cramping of phantom pain there is a day to day relationship between the relative amount of blood owfl in the stump phantom pain were relaxed, the phantoms felt as though and pain intensity and that (b) there is an immediate they were opening. change in pain when bloodow fl changes. However, this does not mean that the changes in blood ow flcause the change in pain. It is possible that a change in pain intenBURNING-TINGLING-THROBBING sity causes a physiological chain reaction which evenPHANTOM LIMB PAIN tually causes a decrease in blood owflto the stump. This is improbable for several reasons. Although videotherReduced near-surface bloodowfl to a limb has been mographs normally record only near-surface blood ow fl implicated as a predictive physiological correlaterst(fi patterns, hands are thin enough so that thermographs cousin to a cause) in many pain conditions including can record blood ow fl patterns throughout the hand. In causalgia and refl ex sympathetic dystrophy (Karstetter four cases of burning or tingling phantom pain following & Sherman, 1991). Return of bloodow fl to normal pata finger amputation, bloodow fl changed only in the area terns through any intervention, including time alone, just proximal to the amputation site. The rest of the hand usually results in either the complete cessation or signif- was essentially unchanged and there were no changes flow was icant decrease of the pain (Sherman et al., 1991). If in the paired area of the intact hand. If blood changing as a result of a refl ex, we would have expected phantom limb pain is a referred pain syndrome, anything a bilateral change or, if unilateral, a change related to affecting the nerve endings in the residual limb is likely dermatomal distribution patterns in which an entire derto affect phantom pain as well. A number of excellent matome would have cooled off. This was not the case studies have demonstrated that (a) the ends of the nerves ex reaction is not likely. The that used to serve the amputated limb are still sensitive so we conclude that a refl subjects were taught to increase blood ow flin the stump to stimuli; (b) cooling the nerve ends causes increased by using temperature feedback to relax, and thus dilate, firing rates; and (c) reducing bloodowfl to the extremity the peripheral blood vessels. Increasing peripheral blood results in cooling it (Campbell, 1987; Harber, 1955; flow to the cool area of the stump resulted in a decrease Janig, 1987; Koschorke, Meyer, & Campbell, 1987; in the pain intensity. If the decrease in blood owflwas Matzner & Devor, 1987; Sherman & Arena, 1992). due to an increase in pain, blood owfl would decrease Chronholm (1951) quotes Pitres (1897) as having for all descriptors of phantom pain, not just a consistent stated that the perceived temperature of the phantom is few (Sherman & Arena, 1992).

related to the temperature of the stump. Measurements of skin temperature in amputees have been made since Numerous thermograms form the key evidence that at least 1952 (Berkeley Medical School, 1952). Thethe decreased blood flow associated with burning phantom

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pain is not the subsequent result of a general sympathetic and spasms in the stump were related to episodes of reaction because only the painful residual limb showscramping phantom pain, muscle relaxants and muscle tendecreased blood flow —the other residual limb maintains sion biofeedback were used to control the pain (Sherman its temperature. This tight, progressive relationship haset al., 1997). been replicated numerous times (e.g., Sherman & Bruno, In the most recent cases, EMG biofeedback was effec1987) and indicates that there is more than a casual relative for 13 of 14 trials for cramping phantom pain. EMG tionship between the two. biofeedback had minimal success with 2 and no success “ The existence of a vascular related mechanism forwith 10 of 12 trials for burning phantom pain. It had no burning phantom pain is also supported by the short term success with 8 trials of shocking phantom pain. Tempereffectiveness of those invasive procedures, such as sympaature biofeedback was ineffective for 4 trials of cramping thetic blocks and sympathectomies, which increase blood phantom pain, was effective for 6 of 7 trials with burning flow to the limb and reduce the intensity of burning phan-phantom pain, and had no success with 3 trials for shocktom and stump pain but not other descriptors (Sherman ing phantom pain. Nitroglycerine ointment (a topical 1980; Wall, 1981). It is indirectly supported by the virtual vasodilator) was ineffective for 1 trial of cramping phanineffectiveness of every surgical procedure involving sev-tom pain and 1 trial of shocking phantom pain but sucering nerves either in the spinal cord or running between cessful for 2 trials of burning phantom pain. Trental (a the amputation site and the spinal cord (Sherman & Sherblood viscosity enhancer) was ineffective for 2 trials of man, 1985; Wall 1981). Beta blockers such as propranolol cramping phantom pain and 1 trial of shocking phantom cause dilation of peripheral blood vessels and have been pain. Nifedipine (a systemic vasodilator) was effective for reported to be successful in ameliorating phantom pain at 3 trials of burning phantom pain but ineffective for 1 trial least in the short term (Marsland, Weekes, Atkinson, &of cramping and 2 trials of shocking phantom pain. FlexLeong, 1982)” (Sherman & Arena, 1992). Relationships eril (a muscle relaxant) was effective for 2 trials of crampbetween muscle tension and burning phantom limb pain ing phantom pain but ineffective for 1 trial of shocking (Sherman & Bruno, 1987) have been shown to be due phantom pain. Indocin (an anti-inflammatory agent) was largely to the change in near-surface blood flow that ineffective for 2 trials of cramping phantom pain. These accompanies increased muscle tension (Laughlin & Arm-medications have potential side effects and cannot be used strong 1985; Richardson, Schmitz, & Borchers, 1986). by patients with a variety of medical problems. Thus, the use of “self-control”-oriented strategies is encouraged to avoid these limitations. RECOMMENDED PROCEDURE It is clear that burning phantom pain responds to interFOR BEHAVIORAL INTERVENTIONS ventions that increase bloodow fl to the residual limb while TO PATIENTS WITH CHRONIC cramping phantom pain responds to interventions that PHANTOM LIMB PAIN* decrease tension and spasms in major muscles of the residual limb. Shocking– shooting phantom pain does not As early as 1979 it became apparent that different descriprespond well or consistently to either type of intervention. tions of phantom pain responded to different treatments It is strongly recommended that biofeedback of appro(Sherman, Gall, & Gormly, 1979). Initial attempts to treat priate parameters be used in conjunction with other selfphantom limb pain with a combination of biofeedback and control training strategies to treat cramping/squeezing and relaxation techniques showed excellent success up to 6burning/tingling phantom limb pain. It is important for month to 3-year follow-ups with 14 of 16 successive phanclinicians to recognize that biofeedback as utilized for tom pain patients. The major difference between those patients who succeeded in learning to control their paincontrol of phantom limb pain is not some kind of black and those who did not was the ability to control theirbox psycho-magic. Rather, it is simply the process of physiology in any measurable way. The two failures neverrecording the physiological parameters (such as muscle (a) demonstrated the ability to relax or (b) reported sub-tension in the residual limb) that precede changes in phanjective feelings which would be associated with learningtom pain, and showing the signals to patients. The patient uses the information to change the signal. The patient also to relax or to control their muscle tensions. In an attempt to align behavioral and medical treat-learns to associate sensations related to onset of phantom ments of phantom pain with underlying physiological cor-pain with tension in the muscle, decreased blood flow, etc. and to use the learned ability to control the parameter to relates, amputees who showed increased burning phantom prevent the onset of or to stop it if it has already begun. limb pain in response to decreased blood flow in the residual limb were treated with peripheral vasodilators and Unfortunately, the large, controlled studies with longterm follow-ups needed to clearly show that burning and temperature biofeedback. When increased muscle tension cramping phantom pain are amenable to behavioral inter* Modified from Sherman & Arena, 1992 and Sherman, et al., 1997. ventions have not been conducted.

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Laughlin, M.H., & Armstrong, R.B. (1985) Muscle blood flow during locomotory exercise.Exercise and Sport Sciences Reviews, ,13 95–136. CRAMPING PHANTOM PAIN Marsland, A.R., Weekes, J.W.N., Atkinson, R., & Leong, M.G. The existent data (e.g., Sherman, 1994) support the (1982). Phantom limb pain: a case for beta blockers? contention that nearly all amputees with cramping Pain, 12, 295–297. phantom limb pain, who can learn to recognize theMatzner, O., & Devor, M. (1987). Contrasting thermal sensitivity of spontaneously active A- and C-fibers in experimental relationship between their pain and spikes in the surface nerve-end neuromas. Pain, 30, 373–384. EMG of the residual limb and can learn to prevent the McKechnie, R. (1975). Relief from phantom limb pain by relaxspikes from occurring, can prevent their phantom pain ation exercises. Journal of Behavior Therapy and Experto the extent they can prevent the spikes. If the spikes imental Psychiatry ,6262–263. continue, so will the cramping phantom pain. If the Richardson, D., Schmitz, M., & Borchers, N. (1986). Relative spikes can be voluntarily stopped once an episode of effects of static muscle contraction on digital artery capphantom pain begins, the episode can nearly always be illary blood flow velocities.Microvascular Research, 31 , almost entirely aborted. The small studies showed that 157–169. the vast majority of people can learn to control nearlySherman, R.A. (1976). Case reports of treatment of phantom all of their cramping phantom pain. Again, no learning, limb pain with a combination of electromyographic biofeedback and verbal relaxation techniques. Biofeedback no control. Follow-ups of 1 to several years showed and Self Regulation,, 1353. that the results are sustained. Sherman, R.A. (1980). Special review: Published treatments of phantom limb pain.American Journal of Physical MedBURNING PHANTOM PAIN icine, 59, 232–244. Sherman, R.A. (1994). What do we really know about phantom The same premise holds true for burning as for cramping limb pain?Pain Reviews, (3), 1 261–274. phantom pain. If patients can learn to increase blood flow Sherman, R.A., & Arena, J.G. (1992). Phantom limb pain: Mechto the residual limb, burning phantom pain will decrease anisms, incidence, and treatment. Critical Reviews in to the extent that blood flow is normalized. The burning Physical and Rehabilitation Medicine,, 1–26. 4 will remain away as long as blood flow remains normal.Sherman, R., Arena, J., Searle, J., & Ginther, J. (1991). DevelUnfortunately, about half of the patients have not been opment of an ambulatory recorder for evaluation of musable to learn to raise the blood flow in their residual limbs cle tension and movement in soldiers’ normal to a significant extent. environments.Military Medicine, 156, 245–248. Sherman, R.A., & Bruno, G.M. (1987). Concurrent variation of burning phantom limb and stump pain with near surface blood flow in the stump.Orthopedics, 10,1395–1402. REFERENCES Sherman, R., Devor, M., Jones, C., Katz, J., & Marbach, J. (1997) Phantom pain , New York, Plenum Press. Campbell, J. (1987). Painful sequelae of nerve injury. Pain, 34, Sherman, R., Evans, C., & Arena, J. (1993). Environmental334. temporal relationships between pain and muscle tension: Cronholm, B. (1951). Phantom limbs in amputees. Acta PsychiRamifications for the future of biofeedback treatment. atrica et Neurologica Scandinavica, (Suppl), 72 1–310. In M. Shtark & T. Sokhadze (Eds.), Biofeedback: Theory Gessler, M. (1984). Relief of phantom pain by stimulation of and practice. Novosibirsk: Nauka Publishers. the nerve supplying the corresponding extensor-musSherman, R., Gall, N., & Gormly, J. (1979). Treatment of phancles. Proceedings of the International Society for the tom limb pain with muscular relaxation training to disStudy of Pain, meeting held in Hamburg, Germany. rupt the pain-anxiety-tension cycle. Pain, 6, 47–55. Haber, W.B. (1955). Effects of loss of limb on sensory function.Sherman, R., Grif fin, R., Evans, C., & Grana, A. (1992). TemJournal of Psychology, 40 , 115–123. poral relationships between changes in phantom limb Janig, W. (1987). Pathophysiology of nerve following mechanpain intensity and changes in surface electromyogram ical and ischemic injury.Pain, S4, 335. of the residual limb.International Journal of PsychoKarstetter, K., & Sherman, R. (1991). Use of thermography for physiology, 13 , 71–77. initial detection of early Reflex Sympathetic Dystrophy. Sherman, R., & Sherman, C. (1985). A comparison of phantom Journal of the American Podiatric Medical Association, sensations among amputees whose amputations were of 81, 198. civilian and military origins.Pain, 21, 91–97. Kristen, H., Lukeschitsch, G., Plattner, F., Sigmund, R., & Resch,Studies relating to pain in the amputee. (1952). A progress report P. (1984). Thermography as a means for quanititative from the prosthetic devices research project at the Instiassessment of stump and phantom pains. Prosthetics and tute of Engineering Research, Department of EngineerOrthotics International, ,8 76–81. ing, U of C Berkeley Medical School, Series II, Issue 23. Koschorke, G., Meyer, R., & Campbell, J. (1987). Myelinated Tsushima, W. (1982). Treatment of phantom limb pain with EMG and temperature biofeedback: A case study. Amerafferents that innervate neuromas display marked sensiican Journal of Clinical Biofeedback,, 5150 - 153. tivity to stimuli. Pain, S4, 281.

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Wahren, L. (1990). Changes in thermal and mechanical pain Wall, P.D. (1981). On the origin of pain associated with amputhresholds in hand amputees. A clinical and physiologtation. In J. Siegfried & M. Zimmermann (Eds.). Phanical long-term follow-up.Pain, 42, 269–277. tom and stump pain , (pp. 2–14). New York: SpringerVerlag.

69 Hypnotherapeutic Advances in Pain Management Jan M. Burte, Ph.D., D.A.A.P.M. Historically, pain reporting was by necessity There is little doubt that the induction of hypnoidal states heavily relied upon as part of the initial diagutilizing chanting and breathing exercises dates back to nostic procedure, where severity, location, and earliest history. The earliest clinical records of hypnosis nature of the pain often assisted in proper diagare attributed to John Elliotson (1792 to 1869), an English nosis. Although pain reporting maintains a sigsurgeon, who used hypnosis for pain management in his nificant role in diagnosis, the advent of practice. James A. Esdaile (1808 to 1859) performed more additional diagnostic procedures (i.e., CAT, than 300 operations using hypnosis as analgesia while MRI scans) goes beyond pain reports and practicing in India (Bassman & Wester, 1992). One such reduces their unique significance. The reliance operation reportedly entailed the removal of a 103-pound on pain reports was especially true in certain tumor (Jackson, 1999). Hypnosis and trance represent an acute pain situations although not as much in age-old treatment for a variety of conditions including chronic pain situations where a diagnosis had pain; hypnosis has been embraced as a legitimate therapy been reached (Bonica, 1990). It was postulated consequent to continuing research only over the past 50 that hypnosis could mask the symptoms of pain years (Hrezo, 1998). and might interfere with obtaining a proper Hypnosis as a form of pain management fell in and diagnosis and treatment (i.e., hypnosis utilized out of favor from the early 1940s until the 1960s when to mask pain associated with appendicitis could Milton H. Erickson demonstrated its utility with acute and result in delaying care until the appendix had chronic pain control (Erickson, 1986). The application of ruptured). hypnosis within the medical and pain setting has continued to develop from the work of Hilgard and Hilgard 2. Pain was seen as evolving from either a physical (1975), Hilgard and LeBarron (1982), Barber and Adrian or a psychological origin rather than from both. (1982), and Melzack and Wall (1965; 1983). Pain was perceived to have either a “real/organic” Zohaurek (1985) points out two historical misconcepbasis or a “functional/imaginary” basis (Fordyce, tions of pain that have affected the role of hypnosis in 1976, Sternbach, 1978). Current thinking might treating pain. view the impact of pain as an etiological factor that by its bidirectional psychoneuroimmunolog1. Pain was considered only to be a symptom of ical role (on the psychological, endocrinological, an underlying disease or trauma. Therefore, and immunological systems) may contribute to research and treatment focused on the etiologthe maintenance of illness (Burte, 2000) or ical cause and ignored the pain, assuming it enhance the progression or metastasis of certain would disappear when the cause was addressed. illnesses (Paige and Ben-Eliyahu, 1997).

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Since 1958, hypnosis has been recognized by the Where this may be signifi cantly prevalent is in the nonAmerican Medical Association as a legitimate form of pharmacological strategies employed in managing cancer medical treatment when administered by an appropriately pain. As Zaza, Sellick, Willan, Reyno, and Browman (1999) trained practitioner (Simon & James, 1999). Fortunately,point out, while pharmacological treatments are appropriwith the resurgence of integrative, mind/body, psycho-ately the central component of cancer pain management, neuroimmunological approaches, current thought andthe under-utilization of effective nonpharmacological stratresearch have begun to view hypnosis as a potentially egies may contribute to the problem of pain and suffering significant modality in the treatment of pain and illness. among cancer patients. In a study of 214 health professionIn this section, I focus on the hypnotherapeuticals, Zaza, et al. (1999) found that the healthcare professionals recommendedimagery” “ exercises 54% of the time and advances in pain management. In the next section, I discuss the applicability of hypnosis in the treatment of spe-meditation 43% of the time. They expressed interest in cific illnesses. Due in part to its historical misportrayal inlearning more about hypnosis and other nonpharmacologthe popular media, patients referred for hypnosis oftenical strategies suggesting its under-utilization as a compleask, “But does it really work?” Contemporary popular mentary or adjunctive treatment to standard care. In a critical review of the literature, Sellick and Zaza (1998) found media portray hypnosis as an effective means of pain control (Foderaro, 1996). Currently, ficient suf experimen- that in randomized controlled studies of hypnosis in mantal and clinical research exists to allow clinicians toaging cancer pain, substantial evidence exists for its effecrespond af firmatively to the question. However, certain tiveness when nonpharmacological pain management approaches are being sought. caveats, discussed later, still exist. What then is medical or clinical hypnosis and what are This concept, then, of unifying both the confidence of the contemporary views of both practitioners and the pub-the practitioner and the trust and belief of the patient, may ficacious ef lic, especially within the realm of pain management? Onerepresent the components necessary to obtain recent survey indicates,that “ most people have a positive pain relief. Barber (1998) aptly delineates a two-compoview of the therapeutic benefi ts with a vast majority of nent model as to why hypnosis may work for pain management. He suggests that in the first component the “clirespondents believing that it reduces the time that is usually required to uncover causes of a person’ s problems, and that nician communicates specific ideas that strengthen the patient’s ability to derive therapeutic support and to hypnotized persons can undergo dental and medical prodevelop a sense of openness to the unexplored possibilities cedures without pain”(Johnson and Hauck, 1999). of pain relief within the security of a nurturing therapeutic Retrospectively, it is important to recognize that “ pain,” relationship.” In so doing, the patient is led to relax in the until the 20th century, was considered an untreatable consequence of illness or injury. Indeed, Chaves and Dworkinclinician’s confidence in hypnosis. In the second compo(1997) astutely point out that hypnoanalgesia did not fullynent,“the clinician employs posthypnotic suggestions that s particular pain experiences emerge until the 19th century, due largely in part to thecapitalize on the patient’ societal belief that, at that time, did notfine de pain relief which simultaneously ameliorate the pain experience and which, in small repetitive increments, tend to maintain and reduced suffering as the primary goal in treatment. Prior ” This to effective clinical techniques for pain management, painpersistent pain relief over increasing periods of time. second component offers the patient a sense of voluntary was an accepted aspect of life. One might wonder whether the introduction of pharmacological forms of pain relief learned control over his or her pain, thereby reducing such as analgesia and anesthesia altered patients ’ percep- anxiety and learned helplessness. tions and ultimately their thresholds for pain. A somewhat more constructionistic view is offered by If pain can act as a mediator in trance production withChapman and Nakamura (1998) who suggest that hypnosis alters the learned pain experience (pain schemata) by pain patients, then did our progenitors and do perhaps third world cultures who had/have limited access to vari-interacting with feedback processes that prime the assoous forms of pain relief intuitively rely on hypnosis and ciations and memories tied to the pain, thereby shaping the formation of pain expectations and processes and ultiself-hypnosis to alter their pain thresholds? For these individuals, pain, whether from childbirth, dental procedures,mately reducing the experience of pain. illness, or injury, was anticipated. As mentioned previously, hypnosis has fallen in and Today, the application of hypnotic analgesia in acuteout of favor over the years due in part to arguments and chronic pain treatment has grown substantially. Bothconcerning the lack of hard scientifi c data to support its patients and clinicians are demonstrating increased knowlefficacy or pathophysiology. With increasing frequency edge and experience with hypnosis. In many cases, studies are demonstrating the impact of hypnosis on pain patients bring clinical experiences with hypnosis forfrom the perspective of changes occurring in the brain related or unrelated issues to the treating physician itself. Rainville, et al. (1997) demonstrated that positron (Lynch, 1999), thereby opening a door to increased comemission tomography revealed signifi cant changes in plementary approaches to standard interventions. pain-evoked activity within the anterior cingulate cortex

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is a psychoneurologically learned behavior? The concept consistent with the encoding of perceived unpleasantness, thereby linking frontal lobe limbic activity with pain sus- of the existence of a “neural signature of pain” that acts as a progenitor of subsequent pain experiences is offered ceptible to hypnotic suggestion. In an examination of exposure to noxious stimuli pre-by Melzack (1983). If this is so, we should teach patients sented to subjects, Faymonville, Laureys, Degueldre,how to communicate more positively when in acute pain DelFiore, Luxen, Franck, Lamy, and Maguet (2000) foundstages before they develop chronic pain. Meta-analyses of 18 studies revealed a moderate-to-large hypnoanalgesia that hypnosis could reduce the intensity and unpleasantef of hypnotic technique for ness of the exposure. By examining cerebral blood floweffect supporting the ficacy of subjects both with and without hypnotic intervention, pain management in both clinical and experimental pain they concluded that hypnotic modulation of pain appearssettings (Montgomery, Dultamel, & Redd, 2000). to be mediated by the anterior cingulate cortex. When we speak of pain patients and hypnosis, another Rainville (1999a) in their examination of cerebral important question is raised. Does hypnosis work equally blood flow utilizing PET scans found that the hypnotic well for all patients? The literature seems to suggest that numerous variables must be considered in drawing any experience may result in increased occipital regional cerehypnotic susceptibility, bral blood flow (RCBF) and delta activity (EEG) by alter- conclusions. Issues of patients’ chronic vs. acute pain, and the origin and etiology of the ing the consciousness associated with decreased arousal via facilitation of visual imagery. Frontal increases in pain are relevant factors. RCBF may be associated with verbal mediation of sug- In the realm of hypnosis, the question of the imporgestions, working memory, and top– down processes tance of hypnotic susceptibility and trance depth has long involved in re-interpreting the perceptual experience ofbeen debated (Frankel, Apfel, Kelly, et al., 1979; Hilgard the noxious stimuli. They concluded that specific patterns& Hilgard 1979; Perry, Gelfand, & Marcovitch, 1979) of cerebral activation appear to be associated with the especially with regard to pain (Hilgard and LeBaron hypnotic state. 1982). Recent studies that have examined the importance of hypnotic susceptibility of pain patients (as opposed to Other researchers have demonstrated the effectiveness non-pain patients) appear to indicate that when dealing of hypnotic analgesia on raising pain thresholds by examining the nociceptive flexion (RIII) reflex and EEG pat- with acute pain issues, hypnotic susceptibility is very important. Sandrini, et al. (2000) examined subjects rated terns (Danziger, et al., 1998). as either high or low susceptibles on the Harvard Group However, the real question for clinicians is, “ Can learning to develop hypnoanalgesia to noxious stimuli inScale of Hypnotic Susceptibility (Shor & Orne, 1963) a laboratory (an acute short-term artificial environment)and the Stanford Hypnotic Susceptibility Scale (Weitzenbe generalized to a patient’ s ability to control real nocio- hoffer & Hilgard, 1959). Utilizing a noxious stimulus, “ susceptibility of the subject is ceptive acute or chronic pain. Crawford (1998) found thatthey concluded that,the chronic back pain patients could be trained to utilize hyp-critical in hypnotically induced analgesia. Similarly, high hypnotic but not low hypnotic subjects demonstrated signotic analgesia on a noxious stimulus and then generalize nificant reductions in pain intensity and reduced nocicethe hypnotic analgesia to their back pain. They concluded ptive receptive refl exes during hypnotic analgesia that “hypnotic analgesia is an active process that requires an inhibitory effort dissociated from conscious awareness(Zachariae, et al., 1998). where the anterior frontal cortex participates in a topo- Increased hypnotizability was also found to positively graphically specific inhibitory feedback circuit that coop- affect sensory and pain thresholds during dissociated erates in the allocation of the thalamocortical activities. ” imagery and focused analgesia as measured by skin conThey further point out that the subjects could successfullyductance responses, somatosensory event-related potentransfer the experimental pain reduction to reduction oftials, and pain perceptions (De Pascalis, Maguarano, & their own chronic pain and, in so doing, also experienceBelluschi, 1999). The ability to modulate pain was greater increased well-being and increased sleep quality. when subjects demonstrated higher hypnotic suggestibilUtilizing a modulated form of pain, patients can learnity (Rainville, 1999b). Controlled associative ability the hypnotic skill of pain control or the raising of their (Agargun, Tegeoglu, Kara, Adak, & Ercan, 1998) and the ability to utilize internal (guided imagery), and external pain thresholds. They can then be taught to generalize this skill to pain situations that are more a function of theirdistractors (word memory and pursuit of motor tasks) were also found to be effective only in high susceptibility subillness or injuries. jects fulfilling analgesic suggestions (Farthing, Vonturino, Hypnotic analgesia has also been shown to reduce subjective pain perceptions and the nociceptive flexionBrown, & Lazar, 1997). reflex in high-hypnotizable subjects (Sandrini, Mianov, Is then the low suggestibility patient subjugated to not Malaguti, Nigrelli, Moglia, & Nappi, 2000). This raises being able to utilize hypnosis or is suggestibility trainable? yet another question. If pain can be unlearned via hyp-In a brief training experience Milling, Kirsh, and Burgess noanalgesia, does it imply that at least to some degree (1999), it utilizing the Carlton Skill Training Program, found

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that training failed to increase overall suggestibility scores Another area where hypnosis has been extensively or to enhance the effects of a suggestion for pain reduction. utilized is in the arena of surgical intervention. HypnoHowever, pain reduction was more highly correlated withanesthesia, the use of hypnotic suggestion rather than genpost-traumatic levels of suggestibility than to pre-treat-eral anesthesia to mediate pain during surgical intervenment suggestibility. tion, has been successfully employed for endocrine cerviMany authors have thought that hypnotizability is acal surgery (Defechereux, Meurisse, Hamoir, Gollogly, skill that is enhanced with practice but occurring at a rateJoris, & Faymonville, 1999; Meurisse, Hamoir, Defechereaux, Gollogly, Derry, Postal, Joris, & Faymonset by the patient. It has been further suggested that “hypville, 1999). Hypnosedation (hypnosis in combination nosis may be best conceived as a set of skills to be deployed by the individual rather than as a state” (Aldenwith conscious IV sedation and local anesthesia) has been employed as an alternative to traditional anesthetic techand Heep, 1998). Others have suggested that hypnotic susceptibility may not be a factor in treatment. In a studyniques (Faymonville, Meurisse, & Fissette, 1999; of hypnotic susceptibility and the treatment of irritable Meurisse, et al., 1999). bowel syndrome, hypnotic susceptibility to suggestion Hypnosis has also been shown to provide propriocepwas not a factor in the positive effect found for hypnosistive pain and anxiety relief, reduced Alfenta and Mida(Galovski and Blanchard, 1998). Utilizing the Hypnotic zolam requirements and increased patient satisfaction and Induction Profile as part of the hypnotic experience, cli-surgical conditions when compared to other surgical stress nicians can within 5 to 10 minutes assess a patient’ s hypstrategies in patient receiving conscious sedation (Faynotic response capabilities and provide the patient with an monville, Mambourg, Joris, Vrijens, Fissette, Albert, & initial first-hand experience (skill acquisition trial) of what Lamy, 1997). Audiotaped hypnotic instructions produced hypnosis is like (Spiegel and Spiegel, 1978/87). Anyreduced anxiety (Ghoneim, Block, Sarasin, Davis, & patient, but especially pain patients, may spontaneously Marchman, 2000) while pre-operative hypnosis resulted shift to an altered state of awareness increasing their sugin a reduction of consumption of analgesics (Engvist and gestibility merely as a function of their motivation to Fischer, 1997) in third molar surgeries. develop rapid rapport and trust in the clinician in an effort Self-hypnosis has been employed as an anesthesia for to escape the pain (Araoz, 1985). liposuction surgery (Botta, 1999) and for postoperative A simple but effective means of incorporating the levels of pain control and relaxation in coronary artery patient’s willingness to accept suggestion is presented by bypass surgery (Ashton, Whitworth, Seldonridge, Shapiro, Eimer (2000) who, at the end of an induction concludes,Weinberg, Michler, Smith, Rose, Fisher, & Oz, 1997) and “As you go deeper and deeper into relaxation and hypnoarteriotomies (Austan, Polise, & Schultz, 1997). It is sis, the door way to your unconscious opens and, with attributed to reduced reported pain and anxiety and your permission, I have the opportunity to talk directly toimproved hemodynamic stability during invasive medical your unconscious and give it the information it needs tointerventions such as percutaneous vascular and renal prohelp you make the changes you want to make”(p. 20). cedures (Lang, Benotsch, Fick, Lutgendorf, Berbaum, A review of the literature points to an increasingly Berbaum, Logan, & Spiegel, 2000). In particular, hand broadening range of applications of hypnosis in treatingsurgery that requires painful rapid remobilization of the hand is especially benefi ted by hypnosis. Hypnosis medical conditions with associated pain. One area where reduces perceived pain intensity allowing patients to be hypnosis has been utilized for both acute pain and healing is with burn victims. Hypnosis has been shown tomore compliant and able to withstand physical rehabilitareduce pain even in situations where opioids fail to bringtive interventions (Mauer, Burnett, Ouelette, Ironson, & relief (Ohrbach, Patterson, Carroughen, & Gilbram,Dandes, 1999), as well as increased rates of anatomical and functional healing (Ginandes & Rosenthal, 1999). 1998). Treatment and dressing changes can be an extremely painful part of burn care. Wright and DrumHypnosis also has demonstrated its ficacy ef with chilmond (2000) found that rapid induction analgesia (RIA)dren dealing with the pain and anxiety associated with was effective in reducing pain and anxiety associatedinvasive medical procedures (Hilgard & LeBaron, 1984), with dressing changes, and Ewin (1986) found that hyp-including bone marrow aspiration (Liossi & Hatira, nosis positively reduced pain in adults during debride-1999), resulting in lower levels of reported pain, reduced ment. Similar findings were also found with pediatric anxiety, and shorter hospital stays (Lambert, 1996; Smith patients (Foertsch, O’ Hara, Stoddard, & Kealey, 1998). & Barabasz, 1996). Distraction and imagery techniques Indeed, burn victims may demonstrate enhanced recephave been shown to be highly effective in reducing pain tivity to hypnotic suggestion secondary to issues of moti-in painful procedures (Broome, Lillis, McGahee, & vation, dissociation, and regression (Patterson, Adcock, Bates, 1992). Scripts and metaphors for children with & Bobardier, 1997), especially within the subset of burnpainful conditions are readily available to the pediatric patients who report high levels of baseline pain (Patter-pain practitioner (Wester & O’ Grady, 1991; Mills & son and Ptacek, 1997). Crowley, 1986).

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Another significant area where hypnosis has continuedorthopedic emergency room care (Ginandes & to demonstrate its utility is cancer intervention. NumerousRosenthal, 1999). books and articles on the use of imagery and healing Hypnotically induced glove anesthesia with transfer(Gaynor, 1994; Siegel, 1998) have discussed the psychoence to the pain site for acute pain relief is a commonly neuroimmunological benefi ts of hypnosis (see Chapter 64 utilized technique. This is accomplished by using suggeson psychoneuroimmunology in this volume). For manytions of creating a numbing sensation in the hand. Patients years hypnosis has also been shown to providefic speci pain may be asked to imagine their hands in a bucket of anesrelief and reduced suffering for cancer patients (Sacerdote, thetic gel or a glove or other such images. This numbing 1966; Hilgrad & Hilgard, 1975; Hilgard and Le Barron or pleasant sensation is then transferred to the pain site 1984) and more recently, by employing physical relaxationwith a pleasant increase in numbness. An excellent examcoupled with imagery that provides a substitute focus ofple of this technique is offered by Basserman and Wester attention for painful situations (Spiegel and Moore, 1997).(1984). Other techniques include distraction techniques Patients demonstrate an increased awareness of the willingand dissociative techniques (Burte, 1999; Eastwood, ness to employ hypnosis adjunctively to their standard medGaskowski, & Bowers, 1998). In all cases, a trusting rapical care resulting in new programs that incorporate hypno-port with the clinician appears to be a critical factor in sis into their treatment protocols (Lynch, 1999). As recentlyachieving the desired goals. In addition, as has been noted as 1996, the NIH Technology Assessment Panel presented earlier, pain may act as a mediator toward an altered state its conclusion inJAMA that strong evidence exists for the of increased suggestibility to pain alleviation. Acute pain use of hypnosis in alleviating pain associated with cancer.patients may willingly and rapidly transfer their pain to Vidakovic-Vukic (1999) notes that irritable bowel syn- the hypnotherapist or anyone willing to accept the pain. drome (IBS) is a frequently observed painful disorder, butPatients should be reassured that proper medical care is its etiology and pathogenesis are still unknown. However,forthcoming and they can let go of their pain. As Schafer it is clear that individual perceptions may play an impor-(1996) points out, perhaps as many as half the patients in tant role in its pathogenesis. Vidakovic-Vukic points outan emergency room may be in spontaneous trance. An that in recent years hypnotherapy has been shown to be alternative approach is to focus on the imagery the patient successful in the treatment of IBS, resulting in eitherspontaneously reports associated with the pain. Psychoreduced or complete disappearance of pain and flatulence semantics and somatopsychic queues are observed when and a normalization of bowel habits. Similar results withutilizing the patient’s perceptions, internal representations, a hypnotic treatment where the focus of intervention wasand understandings of the pain to alter the cognitive, emo“gut directed” and “symptom driven” found that abdom- tional, and sensory experience (Burte and Araoz, 1994). inal pain, constipation, and flatulence improved, while Utilizing the New Hypnosis Model developed by anxiety scores decreased (Galovski & Blanchard, 1998).Daniel Araoz (1985), patients are helped to achieve an McGrath (1999), based on the studies of P.J. Whorwellaltered state of internally directed experiencing of their and those of O.S. Palsson, presents hypnosis as a signifisymptomology. By focusing on the way they interpret and cant component in the treatment of IBS with success rates communicate their pain through any or all of their five approaching 80% reported in the literature. The focus ofsenses, patients are led to a reinterpretation and underhypnosis for IBS should be on the gut-directed and assostanding of their ability to modulate their pain. How ciated symptomology. In a review article, Camilleri (1999) patients integrate pain sensations will impact their pain points out that in addition to various medicinal interven-thresholds. Positive suggestions to pain altered the amount tions and fiber intake, hypnosis may play an importantof time that patients could keep their hands immersed in role in relief of pain in IBS patients. ice water (Staats, Hekmat, & Staats, 1998). For example, Hypnosis also has been shown to be effective in acute in the case of an individual with recently cracked ribs, he pain care settings such as emergency room settings with may be asked to experience or visualize the ribs as they burn pain, pediatric procedures, psychiatric presentaappear to him. He is then asked to visualize ways to tions, and obstetric situations (Peebles-Klieger, 2000;soothe, protect, or heal the ribs (i.e., an anesthetic band Zahourek, 1985). Iserson (1999) describes a simple wrapped around the chest, relaxing, protecting, and healmethod of hypnosis utilized in pediatric fracture reduc-ing the area of injury), while communicating calming, tion on four cases of angulated forearm fractures using relaxing, and possibly in“ control of the situation” distraction techniques when no other form of analgesiathoughts. At times, visualizing being in a safe or pleasant was available. Interestingly, fracture healing also may besituation helps induce a hypnoidal form of relaxation or enhanced utilizing hypnosis. Faster edge healing,mild dissociation. Though creating relaxation has often improved ankle mobility, greater function mobility to been seen as an important element-inducing trance for the descend stairs, lower use of analgesic, and trends toward pain patient, it may be a secondary goal with the imaging lower self-reported pain were found in patients whoor individualized experience of the pain as the primary received hypnotic intervention in addition to standardpathway to the hypnotic state.

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Acute pediatric pain represents a somewhat differentlost wages and medical care (Burte, Burte, & Araoz, 1994; issue in that children often lack clinical insight regardingMiller & Krauss, 1990). Unlike acute pain, chronic pain their condition, an understanding of the etiology, potentialmay result in signifi cant changes in individuals, personalilongevity, or plausible interventions available for amelio- ties, and clinical presentations as evidenced by performance rating their pain, concepts that help adults cope with acute on MMPI profiles (Strassberg, Tilley, Bristone, & Oei, pain more effectively. Patients provided appropriate pre-1992). operative information demonstrate less acute pain Chronic pain patients clinically demonstrate elevated (Stevensen, 1995). Hypnosis may represent a complemenlevels of feelings of hopelessness, helplessness, and tary treatment in conjunction with other forms of inter- despair. They often report ongoing struggles with depresvention such as pharmacological pain management (Rusy sion, somatic preoccupations, and obsessive concerns with & Weisman, 2000). By providing cognitive and behavioral fatal illness (Miller & Krauss, 1990). When chronic pain schemata via modalities easily accessed by children (i.e., becomes a central issue in the individual’ s life, it may imagery, fantasy), the acute pediatric pain patient can be function as a coping mechanism altering the patient’ s empowered similarly to the way adults utilize reason tocapacities, both psychopathophysiologically and etiologiempower coping ability with pain. cally (Kuhn, 1984). In addition to its direct impact on pain Hypnosis may be a means of reducing both pain and alleviation, it is with the depression and hopelessness the pain-related distress (Chen, Joseph, & Zeltzer, 2000). For chronic pain patient experiences that hypnosis can play a example, Adam, a young cancer patient was treated utikey role. Metaphors and hypnotic scripts can address both lizing hypnosis for pain. First he was taught glove anes-the pain and psychological distress (Havens & Walters, thesia which he applied to areas where he was to have 1989). Individuals who are diagnosed with what would finger sticks, Broviac changes, and later bone marrowtoday be referred to as chronic pain syndrome (CPS) often aspirations. He was taught to visualize himself as a cartoon are overwhelmed by the impact of their pain. For CPS super hero named He-Man. By lifting his crutch and laterpatients the pain often takes on an all-encompassing life his finger into the air and reciting the words, “By the of its own, dictating the patient’ s quality of life both psypower of Grey Skull I am He-Man, ” Adam was magically chologically and physically. The CPS patient’ s pain alle(hypnotically) transformed into He-Man, the strongestviation is often complicated by issues of learned behaviors, man in the universe. At such times, he could withstandconditioned avoidances, and conscious and unconscious increased levels of pain and invasive procedures. secondary gains. Hypnotherapy represents a complementary component in a multidisciplinary approach that should Recurrent pediatric headaches appear to show a positive response to hypnotic intervention when relaxationfirst acknowledge that the CPS patient is not primarily a psychiatric patient but rather a composite of both psychoand/or thermal feedback techniques are employed (Holden, Deichman, & Levy, 1999). The use of autogeniclogical and physical distress. Melzack (1990) points out training (hand warming) with imagery has also been usefulthe advantages of a multidisciplinary approach inclusive in reducing or eliminating pediatric migraines when doneof narcotics, for the purpose of rescuing people in chronic cant early into the migraine episode at the first signs of visualpain. As Hitchcock (1998) points out, there are signifi myths and misconceptions about the chronic pain patient aura or muscular discomfort. Crawford, Knebel, Kaplan, Vendermia, Xie, Jamison,that the pain practitioner must address in formulating a and Primbam (1998), in drawing attention to the transitiontreatment plan. She further points out that in many ways the patient is a valuable contributor to the understanding of the acute pain to the chronic pain patient, note that by utilizing hypnosis, patients could alter acute pain experi-of his or her own condition. As such, hypnosis may assist patients in that understanding via uncovering techniques ences. They further suggest that learned hypnotic analgeand experiential insights into various aspects of their pain. sia resulted in reported chronic pain reductions, increased psychological well-being, and increased sleep quality. The In addition to low back pain, many other conditions “neurosignature of pain” can influence subsequent paincan result in CPS. Patients experiencing temporomandibexperiences (Melzack, 1983). Specific pain reduction hyp-ular disorders who underwent hypnotic intervention demnotic skills may indeed be essential in developing lastingonstrated significant decreases in pain severity and frepain relief, especially in situations where chronic painquency which were maintained for at least 6 months after treatment (Simon and Lewis, 2000). based on medical conditions (i.e., cancer tumors, herniated discs) is anticipated. In this context, hypnotic pain control Self-hypnosis has been used adjunctively in dealing may be conceived as a set of skills rather than a state with pain associated with sickle-cell anemia (Dinges, (Alden & Heap, 1998). Whitehouse, Onre, Bloom, Carlin, Bauer, Gillen, Shapiro, Chronic pain patients clearly represent a different pop-Ohene-Frempong, Dampier, & Orne, 1997). Hypnosis has ulation than acute pain patients. The most common form helped adolescent teens and adults with cystic brosis fi (CF) of chronic pain, other than from illness, is chronic low backdevelop improved attitudes about health and a sense of pain, accounting for $50 to $100 billion dollars a year inindependence and decreased anxiety (Belsky & Kahanna,

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. Northvale, 1994; Olness & Kohen, 1996). Utilizing a technique intro-Araoz, D.L. (1998).The new hypnosis in sex therapy NJ: Jason Aronson Inc. duced by Bressler (1990), Anbar (2000) taught CF patients . New York: Brunto seek an inner advisor while in self-hypnosis to uncoverAraoz, D.L. (1985). The new hypnosis ner/Mazel. information pertaining to their physical or psychological symptoms. In so doing, they achieved greater levels ofArargun, M.Y., Tegeoglu, I., Kara, H., Adak, B., & Ercan, M. (1998). Hypnotizability, pain threshold and dissociative physical comfort and reduced anxiety levels. experiences.Biological Psychiatry, 44 (1), 69–71. Hypnotic intervention resulted in improvement in Ashton, Jr., C., Whitworth, G.C., Seldonridge, J.A., Shapiro, symptoms resulting from multiple sclerosis (Sutcher, P.A., Weinberg, A.D., Michler, R.E., Smith, C.R., Rose, 1997); fibromyalgia syndrome, especially when utilized E.A., Fisher, S., & Oz, M.C. (1997). Self-hypnosis as part of a multidisciplinary treatment (Berman & reduces anxiety following coronary artery bypass surgery. A prospective randomized trial. Journal of CarSwyers, 1999); and phantom limb-pain (Sthalekar, 1993; diovascular Surgery (Torino), 38 (1), 69–75. Muraoka, Komjama, Hosoi, Mine, & Kubo, 1996). The list of illnesses, disease conditions, and injury-inducedAustan, F., Polise, M., & Schultz, T.R. (1997). The use of verbal expectancy in reducing pain associated with arteriotopain conditions for which hypnosis has historically been mies. American Journal of Clinical Hypnosis, (3), 39 utilized and for which its application may apply is beyond 182–186. the scope of one chapter. A review of the literature sugBarber, J. (1998). The mysterious persistence of hypnotic analgests that its clinical application is continually expanding. gesia.International Journal of Clinical and ExperimenAnother arena where hypnosis may play a signifi cant tal Hypnosis, 46 (1), 28–43. role in pain management and suffering is with patientsBarber, J. & Adrian, C. (1982). Psychological approaches to the experiencing psychogenic and psychosomatic pain. management of pain. New York: Brunner/Mazel, Inc. Through the use of the affect bridge (Watkins, 1971) andBasserman, S.W., & Wester, W.C. (1984). In W.C. Wester & A.H. Smith, Jr. (Eds.),Hypnosis and pain control in clinical listening to the patient’ s somatopsychic language (Burte, hypnosis: A multidisciplinary approach . Philadelphia: Burtre, & Araoz, 1994) patients can gain insight into the Lippincott. range and variety of symptoms they are experiencing. The Bassman, S.W., & Wester, II, W.C. (1992). Hypnosis, headache psychosemantics the patient utilizes in describing his or her and pain control, an integrated approach . Columbus, life situations or pain offers insight into the nonorganic OH: Psychology Publications Inc. etiology of the conditions. Queues associated with past Belsky, J., & Kahanna, P. (1994). The effects of self-hypnosis trauma may maintain the patient’ s symptoms, whereas refor children with cystic fibrosis: A pilot study. American associating those symptoms to positive images may result Journal of Clinical Hypnosis, 36, 282–292. in symptom reduction or alleviation (Burte, 1993). With theBerman, B.M., & Swyers, J.P. (1999). Complementary medicine psychosomatic patient with no known organic etiological treatments for fibromyalgia syndrome. Baillieres Best basis for the pain the exploration of the negative self-hypPractical Research in Clinical Rheumatology,(93), 13 487–492. notic (NSH) statements associated with the condition will (Vol. 1, 2nd ed.). lend insight into the symptom output. This is especiallyBonica, J.J. (1990).The management of pain Philadelphia: Lea & Febiger. relevant with patients experiencing sexual dysfunction assoBotta, S.A. (1999). Self-hypnosis as anesthesia for liposuction ciated with pain (Araoz, 1998; Burte & Araoz, 1994). surgery.American Journal of Clinical Hypnosis, (4), 41 Techniques and case histories are presented in the 299–331. above noted works, but the essence of the hypnotherapy Bressler, D.E. (1990). Meeting an inner advisor. In D.C. Hamis to have the patient, by experiencing these NSH statemond (Ed.),Handbook of hypnotic suggestion and metments in trance, identify the bridges between his or her aphors. New York: W.W. Norton. psychic conflicts (semantic input) and the pain or dysfunc-Broome, M.E., Lillis, P.P., McGahee, T.W., & Bates, T. (1992). tional symptoms (somatic output). The use of distraction and imagery with children during painful procedures.Oncology Nursing Forum , 19, 499–502. ACKNOWLEDGMENT Burte, J.M. (1993). The role of hypnosis in the treatment of tinnitus. Australian Journal of Clinical Hypnotherapy I thank Lea Racioppi for her assistance. and Hypnosis, 14 (2), 41–52. Burte, J.M. (1999). Introduction for creating a dissociative state. In S. Rosenberg, (Ed.), Course workbook.New York: REFERENCES New York Society of Clinical Hypnosis. Burte, J.M. (2002). Psychoneuroimmunology. In R. Weiner Alden, P., & Heap, M. (1998). Hypnotic pain control: Some (Ed.), Pain management : A practical guide for clinicians theoretical and practical issues. International Journal of (6th ed.). Boca Raton, FL: CRC Press. Clinical and Experimental Hypnosis, (1), 46 62–67. Burte, J.M. & Araoz, D.L. (1994). Cognitive hypnotherapy with sexual disorders.Journal of Cognitive Psychotherapy , Anbar, R.D. (2000). Hypnosis, Theodore Roosevelt and the 8(4), 299–312. patient with cystic fibrosis. Pediatrics, 106 (2), 339–346.

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

Erickson, M.H. (1986). Mind-body communication in hypnosis. In E. Rossi & M. Ryan (Eds.), The seminars, workshops Burte, J.M., Burte, W., & Araoz, D.L. (1994). Hypnosis in the and lectures of Milton H. Erickson (Vol. III). New York: treatment of back pain. Australian Journal of Clinical Irvington Publishers Inc. Hypnotherapy and Hypnosis , 15(2), 93–115. Camilleri, M. (1999). Review article: Clinical evidence to sup- Ewin, D.M. (1986). The effect of hypnosis and mental sets on major surgery and burns. Psychiatric Annals, 16 (2) port current therapies of irritable bowel syndrome. Ali115–118. mentary Pharmacology and Therapeutics, 13, Suppl. Farthing, G.W., Vonturino, M., Brown, S.W., & Lazar, J.D. (2), 48–53. (1997). Internal and external distraction in the control Chapman, C.R., & Nakamura, Y. (1998). Hypnotic analgesia: A of cold pressor pain as a function of hypnotizability. constructivist framework.International Journal of ClinInternational Journal of Clinical and Experimental ical and Experimental Hypnosis,(1), 6 6–27. Hypnosis, 45 (4), 433–446. Chaves, J.F., & Dworkin, S.F. (1997). Hypnotic control of pain: Faymonville, M.E., Mambourg, P.H., Joris, J., Vrijens, B., Fishistorical perspectives and future prospects. Internasette, J., Albert, A., & Lamy, M. (1997). Psychological tional Journal of Clinical and Experimental Hypnosis, approaches during conscious sedation. Hypnosis versus 45(4), 356–376. stress reducing strategies: A prospective randomized Chen, E., Joseph, M.H., & Zeltzer, L.K. (2000). Behavioral and study. Pain, 73(3), 361–367. cognitive interventions in the treatment of pain in children. Faymonville, M.E., Meurisse, M., & Fissette, J. (1999). HypnoPediatric Clinics of North America, 47 (3), 513–525. sedation: A valuable alternative to traditional anaesthetic Crawford, M.J., Knebel, T., Kaplan, L., Vendemia, J.M., Xie, techniques.Acta Chirurgica Belgica, 99 (4), 141–146. M., Jamison, S., & Pribram, K.H. (1998). Hypnotic analFaymonville, M.E., Laureys, S., Degueldre, C., DelFiore, G., gesia: 1. Somatosensory event related potential changes Luxen, A., Franck, G., Lamy, M., & Maguet, P. (2000). to noxious stimuli and 2. Transfer learning to reduce Neural mechanisms of antinociceptive effects of hypnochronic low back pain.International Journal of Clinical sis. Anesthesiology, 92 (5), 1257–1267. and Experimental Hypnosis, (1), 46 92–132. Danziger, N., Fournier, E., Bouhassira, D., Michaud, D.,Foderaro, L.W. (1996). Hypnosis gains credence as influence on the body.New York Times.February 24,p. 23. DeBroucher, T., Santarcangelo, E., Carli, G., Chertock, L., & Willer, J.C. (1998). Different strategies of modulation Foertsch, C.E., O’Hara, M.W., Stoddard, F.J., & Kealey, G.P. (1998). Treatment resistant pain and distress during can be operative during hypnotic analgesia, a neuro-physpediatric burn dressing changes. Journal of Burn Care iological study.Pain Management, 75 (1), 85–92. and Rehabilitation, 19 (3), 219–224. Defochereux, T., Meurisse, M., Hamoir, E., Gollogly, L., Joris, J., & Faymonville, M.E. (1999). Hypnoanesthesia for endo- Fordyce, W.E. (1976).Behavioral methods from chronic pain and illness. St. Louis: C.V. Mosby. crine cervical surgery: a statement of practice. Journal of Frankel, F.H., Apfel, R.J., Kelly, S.F., et al. (1979). The use of American Complementary Medicine, (6), 5 509–520. hypnotizability scales in the clinic: A review after six DePascalis, V., Maguarano, M.R., & Bellusci, A. (1999). Pain years.International Journal of Clinical and Experimenperception, somatosensory event related potentials and tal Hypnosis, 27 , 63–67. skin conductance responses to painful stimuli in high, mid, and low hypnotizable subjects: Effects of differen- Galovski, T.E., & Blanchard, E.B. (1998) The treatment of irritable bowel syndrome with hypnotherapy. Applied Psytial pain reduction strategies. Pain, 83(3), 499–508. chophysiologicalBiofeedback, 23 (4), 219–32. Dinges, D.F., Whitehouse, W.G., Onre, E.C., Bloom, P.B., Carlin, M.M., Bauer, N.K., Gillen, K.A., Shapiro, B.S., Gaynor, M. (1994).Healing E.S.S.E.N.C.E.: A cancer doctor’s practical program for hope and recovery . New York: Ohene-Frempong, K., Dampier, C., & Orne, M.T. Kodansha International. (1997). Self-hypnosis training as an adjunct treatment in the management of pain associated with sickle cellGhoneim, M.M., Block, R.I., Sarasin, D.S., Davis, C.S., & Marchman, J.N. (2000). Tape recorded hypnosis instructions as disease.International Journal of Clinical and Experiadjuvant in the care of patients scheduled for third molar mental Hypnosis, 45 (4), 417–432. surgery.Anesthesia and Analgesia,(1), 90 64–68. Eastwood, J.D., Gaskowski, P., & Bowers, K.S. (1998). The folly of effort: Ironic effects in the mental control of pain. Ginandes, C.S., & Rosenthal, D.I. (1999). Using hypnosis to accelerate the healing of bone fractures: A randomized International Journal of Clinical and Experimental controlled pilot study.Alternative Therapies Health and Hypnosis, 46 (1), 77–91. Medicine, 5(2), 67–75. Eimer, B.N. (2000). Clinical applications of hypnosis for brief Havens, R.A., & Walters, C. (1989). Hypnotherapy scripts: A and efficient pain management psychotherapy, Amerineo-Ericksonian approach to persuasive healing . New can Journal of Hypnosis, 43 (1), 17–40. York: Brunner/Mazel. Engvist, B., & Fischer, K. (1997). Preoperative hypnotic techHypnosis in the relief of niques reduce consumption of analgesics after surgicalHilgard, E.R., & Hilgard, J.R. (1975). pain. Los Altos, CA: William Kaufman. removal of third mandibular molars: A brief communication. International Journal of Clinical and Experi- Hilgard, J.R., & Hilgard, E.R. (1979). Assessing hypnotic mental Hypnosis, 45 (2), 102–108. responsiveness in a clinical setting: A multi-item clinical scale and the advantages over single item scales. InterErickson, M.H. (1966). The interspersal hypnotic technique for national Journal of Clinical and Experimental Hypnosymptoms correction and pain control. American Joursis, 27, 134–150. nal of Clinical Hypnosis, 8,198–209.

Hypnotherapeutic Advances in Pain Management

859

Hilgard, J.R., & LeBaron, S. (1984). Hypnotherapy of pain in chil- Meurisse, M., Hamoir, E., Defechereux, T., Gollogly, L., Derry, dren with cancer . Los Altos, CA. William Kaufman. O., Postal, O., Joris, J., & Faymonville, M.E. (1999). Hilgard, J.R., & LeBaron, S. (1982). Relief of anxiety and pain Bilateral neck exploration under hypnosedation: A new in children and adolescents with cancer: Quantitative standard of care in primary hyperparathyroidism. Annals measures and clinical observations. International Journal of Surgery, 229 (3), 401–408. of Clinical and Experimental Hypnosis, ,30 417–442. Milling, L.S., Kirsch, I., & Burgess, C.A. (1999). Brief modifiHitchcock, L. (1998). Myths and misconceptions about chronic cation of suggestibility and hypnotic analgesia: Too pain. In R. Weiner (Ed.), Pain management: A practical good to be true?International Journal of Clinical and guide (5th ed.). Boca Raton, FL: CRC Press. Experimental Hypnosis, 46 (1), 62–67. Holden, E.W., Deichman, M.M., & Levy, J.D. (1999). Empiri- Mills, J.C., & Crowley, R.J. (1986). Therapeutic metaphors for cally supported treatments in pediatric psychology: children and the child within . New York: Bruner/Mazel. Recurrent pediatric headache. Journal of Pediatric Psy- Montgomery, G.H., DuHamel, K.N., & Redd, W.H. (2000). A chology, 24(2), 91–109. meta-analysis of hypnotically induced analgesia: How Hrezo, R.J. (1998). Hypnosis, an alternative in pain management effective is hypnosis? International Journal of Clinical for nurse practitioners.Nurse Practical Forum, 9(4), and Experimental Hypnosis, (2), 48 138–153. 217–226. Muraoka, M., Komiyama, H., Hosoi, M., Mine, K., & Kubo, C. Iserson, K.V. (1999). Hypnosis for pediatric fracture reduction. (1996). Psychosomatic treatment of phantom limb pain Journal of Emergency Medicine, (1), 17 53–56. with post traumatic stress disorder: A case report. Pain Jackson, D.D. (1999). You will feel no pain. Smithsonian, 29 (12), 66(2–3), 385–388. 126–137. Johnson, M.E., & Hauck, C. (1999). Beliefs and opinions aboutNIT Technology Assessment Panel on Integration of Behavioral and Relaxation Approaches into the Treatment of hypnosis held by the general public: A systematic evaluaChronic Pain and Insomnia (1996). Integration of behavtion. American Journal of Clinical Hypnosis, (1), 42 10–20. ioral and relaxation approaches into the treatment of Kuhn, W. (1984). Chronic pain. Southern Medical Journal, 77, chronic pain and insomnia. Journal American Medical 1103–1106. Association, 276(4), 313–318. Lambert, S.A. (1996). The effects of hypnosis/guided imagery on the postoperative course of children. Journal of Develop- Ohrback, R., Patterson, D.R., Carroughen, G., & Gibram, N. (1998). Hypnosis after an adverse response to opioids mental and Behavioral Pediatrics, (5), 17 307–310. in an ICU burn patient.Clinical Journal of Pain, 14 (2), Lang, E.V., Benotsch, E.G., Fick, L.J., Lutgendorf, S., Berbaum, 167–175. M.L., Berbaum, K.S., Logan, H., & Spiegel, D. (2000). Hypnosis and hypnotherapy Adjunctive non-pharmacological analgesia for invasive Olness, K., & Kohen, D. P. (1996). with children. (3rd ed.). New York: Guilford Press. medical procedures: A randomized trial. Lancet, 29, 355 (9214), 1486–1490. Paige, G.G., & Ben-Eliyahu, S. (1997). The immune-suppressive Liossi, C., & Hatira, P. (1999). Clinical hypnosis versus cognitive nature of pain.Seminars in Oncology Nursing, (1), 13 behavioral training for pain management with pediatric 10–15. cancer patients undergoing bone marrow aspirations.Palsson, O. (1997). Hypnosis and IBS. Paper presented at the International Journal of Clinical and Experimental American Gastroenterological Association. Hypnosis, 47 (2), 104–116. Patterson, D.R., & Ptacek, J.T. (1997). Baseline pain as a modLynch, Jr. D.F. (1999). Empowering the Patient: Hypnosis in the erator of headache hypnotic analgesia for burn injury Management of Cancer, Surgical Disease and Chronic treatment.Journal of Consulting and Clinical PsycholPain. American Journal of Clinical Hypnosis, (2), 42 ogy, 65(1), 60–67. 122–130. Patterson, D.R., Adcock, R.J., & Bobardier, C.H. (1997). Factors Mauer, M.H., Burnett, K.F., Ouelette, E.A., Ironson, G.H., & predicting hypnotic analgesia in clinical burn pain. Dandes, H.M. (1999). Medical hypnosis and orthoInternational Journal of Clinical and Experimental paedic hand surgery: Pain perception, post-operative Hypnosis, 45 (4), 377–395. recovery and therapeutic comfort. International Journal Peebles-Klieger, M.J. (2000). The use of hypnosis in emergency of Clinical and Experimental Hypnosis,(2), 47 144–161. medicine.Emergency Medicine Clinics of North AmerMcGrath, M. (1998). Gimme a break! Prevention, 50 (6), 98–103. ica, 18(2), 327–338. Melzack, R. (1990). The tragedy of needless pain. Scientific Perry, C., Gelfand, R., & Marcovitch, P. (1979). The relevance American, 262 (2), 27–33. of hypnotic susceptibility in the clinical context. Journal Melzack, R., & Wall, P.D. (1965). Pain mechanisms: A new of Abnormal Psychology, 88, 592–603. theory. Science, 150 , 971–979. Rainville, P., Duncan, G.H., Price, D.D., Carrier, B., & Bushnell, Melzack, R., & Wall, P.D. (1983). The challenge of pain. New M.C. (1997). Pain affect encoded in human anterior York: Basic Books. cingulate but not somatosensory cortex. Science, Meurisse, M., Defechereux, T., Homoir, E., Maweja, S., Mar277(5328), 968–971. chettini, P., Gollogly, L., Degaugue, C., Joris, J., & Faymonville, M.E. (1999), Hypnosis with conscious Rainville, P., Hofbauer, R.K., Paus, T., Duncan, G.H., Bushnell, M.C., & Price, D.D. (1999a). Cerebral mechanisms of sedation instead of general anesthesia? Applications in hypnotic inductions and suggestions. Journal of Cognicervical endocrine surgery. Acta Chirurgica Belgica, tive Neuroscience, 11 (1), 110–125. 99(4), 151–158 .

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Rainville, P., Carrier, B., Hobauer, R.K., Bushnell, M.C., & Sternbach, R.A. (1978). Clinical aspects of pain. In R.A. Steinbach (Ed.),The psychology of pain . New York: Raven Duncan, G.H. (1999b). Dissociation of sensory and Press. affective dimensions of pain using hypnotic modulation. Pain, 82(2), 159–171. Stevensen, C. (1995). Non-pharmacological aspects of acute pain management. Complementary Therapy in Nursing Rusy, L.M. & Weisman, S.J. (2000). Complementary therapies and Midwifery, 1(3), 77–84. for acute pediatric pain management. Pediatric Clinics of North America, 47 (3), 589–599. Sthalekar, H. (1993). Hypnosis for relief of chronic phantom pain in a paralyzed limb.The Australian Journal of Sacerdote, P. (1966). The uses of hypnosis in cancer patients. Clinical Hypnotherapy and Hypnosis, (2), 14 75–80. Annals of the New York Academy of Science, 125, 1011–1019. Strassberg, D.S., Tilley, D., Bristone, S., & Oei, T.P.S. (1992). The MMPI and chronic pain: A cross-cultural view. Sandrini, G., Mianov, I., Malaguti, S., Nigrelli, M.P., Moglia, Psychiatric Assessment,(4), 4 493–497. A., & Nappi, G. (2000). Effects of hypnosis on diffuse noxious inhibitory controls.Physiological Behavior, Sutcher, H. (1997). Hypnosis as adjunctive therapy for multiple 69(3), 295–300. sclerosis: A progress report. American Journal of Clinical Hypnosis, 39 (4), 283–290. Schafer, D.W. (1996). Relieving pain: A basic hypnotherapeutic approach. Northvale, NJ: Jason Aronson Inc.. Vidavic-Vukic, M. (1999). Hypnotherapy in the treatment of irritable bowel syndrome: methods and results in Sellick, S.M., & Zaza, C. (1998). Critical review of five nonAmsterdam.Scandinavian Journal of Gastroenterology pharmacologic strategies for managing cancer pain. Supplement, 203, 49–51. Cancer Prevention and Control,(1), 2 7–14. Shor, R.E., & Orne, E.C. (1963). Norms on the Harvard groupWatkins, J.G. (1971). The affect bridge: A hypnoanalytic technique.International Journal of Clinical and Experimenscale of hypnotic susceptibility, Form A. International tal Hypnosis, 19,21–27. Journal of Clinical Hypnosis, 11, 47–49. Weitzenhoffer, M.M., & Hilgard, E.R. (1959). Stanford hypnotic Siegel, B. (1998).Love medicine and miracles . New York: susceptibility scale: Forms A and. BPalo Alto, CA: Harper & Row. Consulting Psychologist Press. Simon, E.P., & James, L.C. (1999). Clinical applications of hypWester, W.C., & O’Grady, D.J. (1991). Clinical hypnosis with notherapy in a medical setting. Hawaii Medical Journal, children. New York: Brunner/Mazel. 58(12), 344–347. Simon, E.P., & Lewis, D.M. (2000). Medical hypnosis for tem- Whorwell, P.J., Houghton, L.A., Taylor, E.E., & Maxton, D.G. (1992). Physiological effects of emotion assessment via poromandibular disorders: Treatmentficacy ef and medhypnosis.Lancet, 340 (8811), 69–72. ical utilization outcome.Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, Wright, B.R., & Drummond, P.D. (2000). Rapid induction anal90(1), 54–63. gesia for the alleviation of procedural pain during burn care.Burns, 26(3), 275–282. Smith, J., & Barabasz, A. (1996). Comparison of hypnosis and distraction in severely ill children. Journal of Counsel- Zachariae, R., Andersen, O.K., Bjerring, P., Jorgensen, M.M., & ing Psychology, 43 (2), 187–193. Arendt-Nielsen, L. (1998). Effects of opioid antagonist on pain intensity and withdrawal reflexes during inducSpiegel, D., & Moore, R. (1997). Imagery and hypnosis in the tion of hypnotic analgesia in high and low hypnotizable treatment of cancer patients. Oncology (Huntington), volunteers. European Journal of Pain,(1), 2 25–34. 11(8), 1179–1189 and 1189–1195. Spiegel, H., & Spiegel, D. (1978/1987). Trance and treatment: Zaza, C., Sellick, S.M., Willan, A., Reyno, L., & Browman, G.P. (1999). Health care professionals’ familiarity with nonClinical uses of hypnosis . Washington, D.C.: American pharmacological strategies for managing cancer pain. Psychiatric Press, Inc. Psychooncology , 8(2), 99–111. Staats, P., Hekmat, H., & Stats, A. (1998). Suggestion/placebo Zohaurek, R. (1985). Clinical hypnosis and therapeutic suggeseffects on pain: Negative as well as positive. Journal of tion in nursingNew York: Grune & Stratten. Pain and Symptom Management,(4), 15 235–243.

70 Drug Misuse and Detoxification John Claude Krusz, M.D., Ph.D. inherent ability exists to abuse what the drug does pharmacologically. The body that the drug is put into, however, is what is being abused, and in that sense, this author believes that the term drug abuse refers more to the abuse of the person, and when speaking about the drug itself, it is a case of misusing the drug. The other major point about A. Weil (1972) drug misuse is that it tends to portray the idea that the drug involved is one that generally is a nonprescription medication or one upon which social sanctions have been INTRODUCTION placed. Therefore, the terms drug abuse or drug misuse The use of drugs that produce powerful effects on mood, are confusing and derived mostly from social definitions, affect, and thinking and alter levels and states of con-as relating to people’ s behavior with pharmacologic subsciousness has been a part of our civilization sincestances. Different cultures consider various substances to recorded history. This refers to both illicit substances (e.g.,be included in what is deemed drug misuse patterns at opium, cocaine, cannabis, synthetic psychoactive subdifferent times. For instance, although no one would quesstances) as well as to licit and commonly available drugs tion the drug misuse concept of a person’ s use of 2 liters (e.g., alcohol, tobacco, caffeine-containing beverages). of blended spirits per day and the consumption of 80 Although the latter group of substances raises fewer emocigarettes in the same time on a chronic basis, one would tionally heated societal concerns than the former, use and hardly call the imbibing or consuming of the same submisuse of these substances are also discussed in this chapter. stances for a shorter time drug misuse (e.g., New sYear’ Eve party, a Mardi Gras celebration). Jaffe (1990) uses the terminology “nonmedical drug use” as a substitute for CONFUSING TERMINOLOGIES the older and more confusing term drug abuse, and the The term “drug abuse” has been used indiscriminately and author thoroughly agrees that changing the phraseology is confusing and inaccurate. It commonly refers to repet-would be helpful. Terms like drug abuse tend to connote itive usage of drugs that are productive of tolerance and the usage of societally disapproved substances, whereas physical dependence in a nonmedical or nontherapeutic drug misuse or nonmedical drug use includes a whole context. The author prefers the term “drug misuse” ratherspectrum of involvement and usage. This can include very than drug abuse for the following reason: On a pharmacasual or experimental use on a few occasions of even cologic level, one is not abusing the action of the drugcommonly available substances (e.g., nicotine, alcohol) to itself. It is merely a molecule with a set of pharmacologicthe use of certain substances for specific kinds of effects and biochemical activities relating to dosage and concen(e.g., consumption of large quantities of caffeine by students for the purposes of studying, the use of amphettration, as well as route of administration, but as such no … The use of drugs to alter consciousness is nothing new. It has been a feature of human life in all places on the earth and in all ages of history … the ubiquity of drug use is so striking that it must represent a basic human appetite…

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syndrome suggests that the drug is needed for social or amines and other central nervous system stimulants by truck drivers to circumvent occupational fatigue). Thepersonal well-being and that not using the drug has a most extreme example of drug misuse, of course, would greater cost to the individual’ s well-being and offers a include chronic daily usage of large amounts of sub-poorer quality of life. Drug dependence typically includes stances, licit or illicit, as originally conveyed in the more activities designed to procure the drug upon which the nonspecific term drug abuse. patient is dependent, and the seeking and obtaining of the drug will be given a higher priority in the individual’ s life than other ongoing behaviors or activities. Once again, the DRUG ADDICTION continuum of drug dependence is veryficult dif to sharply “Addiction” is another very confusing and, unfortunately, demarcate from recurrent drug use on an intermittent which does not have the characteristics of depenoften misused term. Many substances are considered basis, to or the behavioral syndrome of preoccupation with be addicting, and the usual connotation of an addict is dence a person who is hopelessly and irreconcilably rooted inattainment, securing of a supply, and repeated, often daily daily repetitive behaviors that are focused on obtaininguse of the substance. In that sense, drug dependence has the connotations of compulsivity and is behaviorally simand using large amounts of the same drug. In reality, the notion of addiction more properly should connote anilar to disorders that are chronic and relapsing in nature (Edwards, Arif, & Hodgson, 1981). extreme degree of drug dependence (see below). The degrees of drug dependence themselves form a large spec- The range of drug-dependent behavior is as extreme trum of usage from very casual to extremely habitual oras the concept of drug addiction (see above). On one end of the spectrum, it is as nontroubling in most people’ s addictive behaviors and are discussed in a succeeding minds as daily use of caffeine or tobacco, which certainly section in this chapter. Once again, the term addiction has become distorted, and the social definition or notion of anmeet the criteria for a drug-dependent behavioral synaddicted individual conveys a very severely impaired life-drome and yet do not have the social connotation of frank drug addiction. The other concept that creates a lot of style with a daily search for, and use of, the substance to which the individual is addicted. The other confusing ele-confusion is the idea that the drug-dependent behavior in ment for the term addiction relates to the mistaken notionsome way is disruptive, not only to the life of the person that addiction is synonymous with physical dependencewho engages in the drug-acquiring and drug-using behavior, but also that a societal cost exists as a result of that person’ s (see below). Physical dependence, as is discussed later, refers more to the occurrence of withdrawal symptomsrepeated search and usage of psychoactive substances. upon sudden cessation of drug use, whereas addiction does not have the same inference, although, once again, in the TOLERANCE minds of many people, the terms are often used interchangeably, and in that sense, imprecisely. It is particuThe concept of tolerance to a drug’ s effect is strictly a larly encouraging that major compendia on psychophar-pharmacologic issue and yet often also gets intermingled macologic mechanisms of drugs do not even mention the or exchanged with not only physical dependence, but also word addiction once in their very extensive reviews ofwith drug dependence, as discussed above. Tolerance, in numerous categories of psychoactive substances (e.g., its broadest pharmacologic sense, refers to a smaller effect Psychopharmacology: Third Generation of Progress , for any given dose of a medication or drug when given (Meltzer, 1987)). on a repeated basis. Therefore, in order to obtain the same pharmacologic effect, larger and larger doses of the medication or drug have to be administered. The classic examDRUG DEPENDENCE ple of tolerance to a psychoactive substance is the opiates. The term “drug dependence” is another confusing termIn this instance, tolerance includes shortened duration of with many different connotations. Unfortunately, it is also effect, a decreased intensity of effect (particularly for analgesic, euphoriant, and sedating activities of the drug), as well confused with physical dependence on drugs, and at the as an increase in the dose which would be considered lethal. outset, drug dependence fits many of the characteristics of a behavioral syndrome. This implies that an individual Two types of acquired pharmacologic tolerance are who is using a particular psychoactive substance willgenerally discussed. One is dispositional tolerance, which has to do with increasing the rate of metabolism of the devote a higher degree of effort to obtaining the substance drug over time so that the same dose is more rapidly and will presumably use the drug despite negative social metabolized and, therefore, the effective concentration on and medical sanctions. The term drug dependence once receptors or end organs is reduced, resulting in a smaller again refers to a spectrum of usages, although generally effect. Many examples can be cited. Among the more comit is taken to mean something more than strictly casual or intermittent use of a drug. The individual’ s behavioral mon are the liver enzyme-inducing properties of alcohol,

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drug dependence as a behavioral syndrome (see the folanticonvulsants (e.g., carbamazepine acid, valproic acid), lowing section). and barbiturates. Pharmacodynamic tolerance refers to adaptive The phenomenon of tolerance also can transcend multiple categories of drugs. This is known as cross responses within biologic systems that are affected by the tolerance, and chronic exposure to one drug can fredrug itself and result in a reduced response over time to quently produce a tolerant state to other categories of the same dose of a drug. Because many of the effects are biobehavioral in nature, tolerance of the pharmaco-drugs. Examples include cross tolerance of barbiturates dynamic type is often noted to develop rapidly. The classicto other sedative hypnotic compounds. In some cases, example is tolerance to the effects of opiates, particularlycross tolerance to amphetamines and cocaine and other stimulants is fairly easy to demonstrate, and perhaps with regard to the euphoriant and sedating properties of more rapid enzymatic metabolism of the drugs in comthe drug. Whereas tolerance to the respiratory depressant or miotic effects of opiates does not follow a similar mon may be a fundamental feature of the phenomenon of cross tolerance (Barrett, 1987). pattern, a marked pharmacodynamic tolerance exists when the drug is given repeatedly, and this is most obvious with effects such as euphoria. Unfortunately, the escalation of DRUGS AS BEHAVIORAL REINFORCERS a dose in a tolerant individual in order to produce a desired This section attempts to outline the underpinnings of degree of euphoria or sedation often carries the risk of allowing toxic effects of the drug to occur (e.g., fatal broader concepts already discussed, such as drug dependence, and some of the conditioning factors which may respiratory depression), because tolerance to this effect of promote continued drug-seeking behavior. The reinforcing opiates does not increase nearly as much as the more behavioral effects of the drug. The underpinning of phar-properties of drugs are well known, both in laboratory animals as well as in humans. Indeed, laboratory experimacodynamic tolerance is always on the basis that the ments have been designed to allow animals to perform neuronal populations the drug affects become altered in their activity in the presence of continued administrationrepetitive tasks, such as lever- or bar-pressing, the running of mazes, and other behavioral tasks. These learned behavof the drug. Tolerance to a multitude of substances can occur iniors are reinforced by the reward, a dose of a drug that presumably produces a pleasurable effect and, therefore, perhaps less dramatic ways, although the example of the promotes continued reinforcement and furthers behavior barbiturates and other sedative drugs also involves designed for obtaining more of the same drug. This is true pharmacodynamic tolerance. Additionally, dispositional for opioids, barbiturates, ethanol, and central nervous tolerance plays a larger role in permitting the use of escastimulants (e.g., cocaine, amphetamines, nicotine, caflating doses of these drugs to obtain a desired degree of feine). Many factors intervene in the effectiveness of a sedation or “high. ” Another factor in dispositional tolerdrug in promoting reinforced behavior, and most imporance may lead to a decreased dosing interval based on the tant are the properties of the drugs themselves, particularly more rapid metabolism of the drug and excretion from the if their actions are short and their euphoriant or stimulant body. It certainly is conceivable that when a drug is metabproperties are powerful in the central nervous system olized more rapidly, a tendency to administer the drug (CNS). The most dramatic example of reinforcement is more often exists, and in that sense the notion of the with cocaine and amphetamines. Laboratory animals will reinforcing ability of a drug comes into play. Drugs arecontinually bar-press, sometimes for thousands of repetinotorious reinforcers, particularly if their effects are verytions, to obtain a single dose of the drug, even in the profound and relatively short-lived or if their metabolism presence of toxic effects from the drug. Animals will is increased at a fairly appreciable rate with continued use. literally die in their attempts to obtain more of the preThe classic example of a powerfully reinforcing drug issumably pleasurable effects of cocaine. If placebo or cocaine and, to a lesser extent, amphetamines. The former saline is substituted for the drug, the furious activities will substance has a marked ability to act as a reinforcer, parcease after a time; however, they will return with an even ticularly in maintaining drug misuse behaviors, simply more rapid re-onset of behaviors if a single priming dose because the half-life of cocaine is exquisitely short. There-is given. A quite similar though less dramatic pattern is fore, the behaviorally reinforcing repeated administrationnoted with morphine and other opioids. The timing and of the substance tends to promote a pattern of use which intensity of behaviors needed to raise the dose occurs at results in a rapid establishment of drug-dependent behava slower rate than it does in the case of cocaine or amphetior. This is in the absence of any formal physical depen-amines. A lessened pattern of reinforcement is noted in dence on the substance, as might be encountered in the the case of barbiturates and other sedatives, and still less case of opiates, barbiturates, nicotine, or caffeine. This is seen with other drugs (e.g., nicotine), where the behavalso introduces the topic of drugs as reinforcers of behavior, ioral reinforcement is seen under a more restricted set of a powerful basic mechanism implicated in the generation ofexperimental conditions. Likewise, caffeine, despite being a

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relatively powerful CNS stimulant in large doses, is astate, and this often is in the absence of any effects on the relatively weak reinforcer. A common substance like eth-physical well-being of the individual. The perception of anol is one of the least reinforcing drugs in laboratorydysphoria and the threat of being left in a behaviorally experimental situations. In the laboratory setting, manyanxious state often are powerful negative reinforcers for factors determine whether or not an animal will self-continued use of a drug. Even a drug such as nicotine, which does not produce a strong state of physical depenadminister the drug (e.g., the CNS effects of the drug, the ficult to stop using amount of work required to obtain a dose, the time alloweddence, often will be extremely dif because of very subtle perceived threats to sone’ wellbetween the actual reinforcing behavior and the actual being in the absence of the drug. This, therefore, promotes drug administration). It should be noted that these behaviors are strikingly not in the presence of any physicalcontinued usage of the substance, presumably because there is an effect on psychological well-being with the dependence on the part of the animals (Johanson & nicotine present and a perception that all is not well if one Schuster, 1991; Young & Herling, 1986). The reinforcing properties may occur on both positivedoes not continually administer the nicotine in the form and negative bases. The former would be an example of cigarettes or tobacco. Modern approaches to withdrawal from nicotine include use of chewing gum or patches of behaviors that are reinforced because the drug induces pleasurable effects. The latter (negative reinforcement)nicotine in a graded dosage to slowly taper away from the usual blood levels of nicotine, which are self-administered would occur because the drug would terminate unpleasant during the day when one smokes (see section on nicotine). or anxiety-provoking states, such as pain. Examples of negative reinforcement in a clinical setting occur with These principles of positive and negative reinforcement are based on learning theory, and the issue of continued dependence on benzodiazepines and sedative hypnotics, drug usage can be viewed as behavior which is maintained as well as opiates, and many people continue to take the former two classes of drugs, not for their positive rein-by the consequences of the drug action on the individual forcing effects, but rather to circumvent the onset of anx-(Jaffe, 1989, 1990; Kaplan & Saddock, 1988). iety, panic, or other withdrawal symptoms (Busto, Sellers, Naranjo, Cappell, Sanchez-Craig, & Sykora, 1986; WickPHYSICAL DEPENDENCE ler, 1980; Woods, Katz, & Winger, 1987). The positive reinforcing effects of centrally acting The concept of physical dependence, mentioned previdrugs occur in spite of initially unpleasurable effects asso-ously, principally relates to repetitive use of a substance ciated with initial usage of certain drugs. This is mostthat establishes biochemical and pharmacodynamic tolclearly illustrated by morphine and other narcotic opiates.erance factors in biologic systems (neuroadaptation), The initial effects associated with the use of these drugs such that when drug use is stopped, a state of withdrawal can often produce severe nausea, vomiting, and other side occurs. This withdrawal state is the hallmark of physical effects that would appear to be not positively reinforcing.dependence and is based strictly on alterations in the In light of this, the euphoriant and other properties of theneuroadapted state of the organism consequent to drug are suf ficiently strong, and as tolerance for the repeated drug administration, usually of a drug that demunpleasurable effects develops, the predominant reonstrates principally pharmacodynamic tolerance but also inforcer remains the euphoriant effect of the drug thatmay exhibit dispositional and other tolerances. By fi- de promotes continued and escalating usage. Secondary renition, a strongly positive reinforcement has already inforcers are often social factors, such as sone’ peer group occurred, and the existence of a severe degree of drug or the perception that usage of the drug permits memberdependence, together with behaviors that in the past may ship in an elite club or circle of friends. Indeed, peerhave been termed addiction, is accompanied by a severely approval is often a very strong secondary reinforcer, and modified neuroadaptive state secondary to the drug use. this social reinforcement often will promote continued This neuro-adaptive state is a physiologically, biochemusage of a drug even though it initially causes unpleasurically, and pharmacodynamically changed system, which able effects. This is often seen in nicotine, marijuana, orhas been acted upon by the medication used, and these alcohol usage, at least in the initial stages. One also has systems have been modifi ed initially by the drug producto consider that as physical dependence develops (see ing the physical dependence. The sine qua non of physical below), the onset of any unpleasurable effects associated dependence is the expression of a state of withdrawal with discontinuation of regular drug use will automatically when the drug is abruptly terminated. It is implicit in the promote or reinforce continued administration of the drug.model of withdrawal that CNS functioning has been This would then act more as a negative reinforcer, as altered by continued administration of a drug. How rapoutlined above in the case of benzodiazepines, although idly the CNS returns to its baseline state after discontinuit is most dramatically encountered in the usage of mor-ance of the drug is different for various medications or drugs, and withdrawal symptoms can be quite severe. phine and other narcotics. Often, the cessation of repetitive usage of a drug will induce an anxiety-provoking aversiveBased on long-term usage of drugs like morphine or

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opium, withdrawal symptoms can be even more profoundof organic brain dysfunction. For example, the author has observed that patients with neurobehavioral seizures (e.g., and onset faster with pharmacologic antagonist medicaintermittent explosive disorder, temporal lobe syndromes, tions (e.g., naloxone), and one can demonstrate withdrawal symptoms after a single dose of morphine byother behaviorally aberrant states) often give a history of administering naloxone or nalorphine (Bickel, Stitzer, self-administering psychoactive substances for the purBigelow, Liebson, Jasinski, & Johnson, 1988; Heishman,pose of reducing internal anxiety and to produce a sense of calm and relative order insofar as their behavior and Stitzer, Bigelow, & Liebson, 1989). Diagnostic criteria for opioid withdrawal have been thought processes are concerned (unpublished observadeveloped and published in the DSM-III-R Diagnostic andtions). Furthermore, certain individuals will have docuStatistical Manual of Mental Disorders (American Psychi-mentable abnormalities on the electroencephalogram atric Association, 1987). Some of these criteria involve(EEG) and quantitative EEG (brain mapping). Some of these individuals, while they may require traditional psycessation of prolonged moderate or heavy use of an opioid chiatric diagnoses as they are treated in the medical sys(this is defined as several weeks or more) or, alternatively, tem, actually may have more of a fundamental organic reduction in the amount of opioid used, succeeded by at least three of the following: (1) craving for an opioid, derangement of their thought processes, emotions, and affect, as is often the case in temporal lobe disorders. (2) nausea and vomiting, (3) muscle aches, (4) lacrimation or rhinorrhea, (5) pupillary dilation, (6) piloerection or Some of these patients exhibit features behaviorally comsweating, (7) diarrhea, (8) yawning, (9) fever, andpatible with an organic brain disorder, such as a partial (10) insomnia. These diagnostic criteria, although by nocomplex seizure. This may manifest itself in purely behavmeans complete, at least give a list of withdrawal effectsioral terms and may be relieved or ameliorated by (selfmedicated) psychoactive drug use. Often, patients will that can be seen in the acute phase after discontinuance give a history of feeling calmer, thinking more clearly, of chronic or even acute opiate use. and other positive aspects related to ongoing and repetitive Abstinence syndromes create a spectrum of effects. use of amphetamines, cocaine, marijuana, or sedative hypThe immediate syndrome of abstinence is as exemplified in the case above. Less dramatically, withdrawal fromnotics. From a neurologic and neurobehavioral standpoint, s opinion, fundaalcohol, cocaine, nicotine, or sedative/hypnotics, thoughthis type of history is not, in the author’ mentally a psychiatric problem, but rather an organic state productive of many symptoms, is a fairly benign event. relievable by pharmacologic administration of psychoThe most life-threatening symptom for medical manageactive substances. This often predisposes an individual to ment is the occurrence of seizures. These are usually sinmany maladaptive patterns of behavior, and the issues of gle in occurrence and rarely require medication. Similarly, tolerance, physical dependence, and alteration of lifestyle even withdrawal from morphine rarely produces any lifebased on sustained drug-seeking and drug-using behavior threatening sequelae, although the person undergoing often become the primary focus of medical attention, withdrawal may be extremely uncomfortable until the whereas in reality one could postulate that these are secneuroadapted state returns to its biologic baseline. ondary spin-offs of an organically aberrant neurologic state. Nevertheless, various psychiatric criteria have been DRUG MISUSE AS PRIMARY developed for different kinds of drug misuse, and the history and evolution of psychiatric thinking in this area PSYCHIATRIC DISEASE are well summarized by Jaffe (1989). A very nicely sumThe misuse of psychoactive drugs raises some fundamenmarized and coherently presented chapter on these phetal questions about whether or not such use can be connomena is to be found in Dr. Steve Stahl’ s bookEssential sidered principally a behavioral disorder or principally aPsychopharmacology . psychiatric disorder. The author favors the former, and The evolution and refi nement of biologic and psychialthough a large body of data has been developed to catatric criteria regarding psychoactive drug use are very egorize dependence and substance abuse” “ (American much active processes and continue to progress. Indeed, Psychiatric Association, 1987), the author is by no means it will be interesting to see what new revisions are procertain that the vast majority of tolerant and dependentposed in upcoming DSM versions. One can certainly states consequent to repeated drug use are indeed based make a good case for the coexistence of primary psychion fundamentally psychiatric diseases. atric disorders and concurrent maladaptive drug use patWhile it is true that patterns of drug misuse can beterns as perhaps secondary biologic factors. Concurrent quite profound and can coexist with well-recognized psy-psychiatric treatment of both elements often comes under chiatric entities like bipolar and manic depressive illness,the rubric of dual diagnoses, wherein a primary psychischizophrenia, schizotypal, and the whole range of affecatric diagnosis is treated at the same time that one tive disorders, the author has noticed a strong pattern of attempts to detoxify or eliminate psychoactive substance drug misuse by patients who otherwise manifest evidence misuse patterns.

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This portion of the chapter outlines major issues relat-in idiopathic Parkinson’ s disease. A small epidemic of ing to usage of specific categories of psychoactive subyoung, opiate-misusing individuals surfaced in a fairly stances and includes a short synopsis of the scope of the short time in California in the early 1980s. Obviously, this problem. This was very well summarized by Mello andside effect was an unintended one, but is pharmacologiGriffiths (1987). The initial focus is on drugs with the cally treatable with dopaminergic agents normally used to largest societal impact (i.e., alcohol and tobacco), rather treat idiopathic Parkinson’ s disease. than focusing on the more traditional “hard core” items, Other “designer” opiates, such as alpha-methylfentasuch as narcotics and stimulants. From a psychiatric viewnyl, also surface from time to time and speak to the crepoint, the overuse of alcohol and alcohol dependence ativity of individuals attempting to use opiate derivatives ranks quite high in relationship to other psychiatric disor-on a chronic basis. These designer drugs are usually strucders. They outdistance other major psychiatric diseases, turally similar to the more regulated pharmaceuticals and such as depressive disorders, phobias, schizophrenias, and represent an attempt to evade regulatory control and legal phobic disorders, at least in terms of their lifetime preva-ramifications. Another so-called designer drug is MDMA lence rates. This translates into an enormous impact on (“Ecstasy,” “hug drug”) (Peroutka, 1987). This is only one public health issues, societal productivity, and the like. Itrepresentative of a whole family of phenyliso-propyhas been estimated that in excess of $100 billion per year lamines, which share CNS stimulant and hallucinogenic is lost in terms of productivity, actual and projected med-properties. Recreational drug use of derivatized substances ical costs, and the effects of crime related to the pursuit continued to be very prevalent in the 1990s. A number of of psychoactive drugs. This is probably a very conserva-items have been enjoyed, including gamma-hydroxybutive estimate, and the author suspects that the above figure, tyrate (GHB), flunitrazepam, and a host of amphetamine taken from a 1984 estimate, is probably a fifth of the actualanalogs, such as MDMA, MDEA, paramethylthioamphetcost to society. This is particularly true if one considersamine, DOET, DMA, TMA, and some of their derivatives, including overusage of legal intoxicants, such as alcoholand represent some 50 compounds with potential for wideand nicotine. spread illicit use. As noted above, they also bridge pharMajor forces and trends have developed in the med-macologically distinct categories of psychoactive subical world, and a much greater societal awareness of the stances (Glennon, 1987). These designer substances are impact of repeated use of alcohol and nicotine currentlycovered here in more detail. exists. The overall usage of hard liquor has decreased somewhat, although this may be offset by continued and MDMA (3,4-METHYLENEDIOXYMETHAMPHETAMINE) escalating nationwide usage of softer” “ forms of alcohol, “ECSTASY,” XTC, “ADAM,” “E” such as wine and beer. Generally, patterns of nicotine use have diminished somewhat, although this is still a veryThis substance has probably enjoyed more use or, more properly, has been more widely enjoyed in the last decade large problem in the adolescent or teenage population and continues to be a major problem in terms of lung cancerthan virtually all other designer drugs. MDMA was shown rates, particularly in women. A WHO report cites that 25to consistently produce, in humans, increases in systolic to 45% of women are smoking in wealthy nations world-and diastolic blood pressures, pupillary diameter, heart wide. This is thefirst international study of women and rate, and rises in plasma cortisol and prolactin (de la Torre et al., 2000). In rats, acute doses produced a hyperthermic tobacco use, and data suggest that female smokers will response. One week after acute dosing, about 50% of 5HT outnumber male smokers in the near future American ( and 5HIAA were lost in cortex and hippocampus, as were Medical News , 1982). binding sites to SSRI drugs, thus indicating degeneration The 1980s saw an explosion in cocaine usage, both in its usual hydrochloride form as well as in free-base orof 5HT neurons in the brain due to MDMA (Colado, Granados, O’Shea, Esteban, & Green, 1999). This remarkcrack cocaine form. The overall usage of cocaine seems able toxicity to the serotonergic system has been consisto have decreased somewhat, with an increasing trend seen tently observed and is a peculiar feature of MDMA and in the usage rate of addicting opiates, such as morphine related compounds like MDEA (“eve ”). One hypothesis and heroin. Indeed, designer-type drug use has been promrelates depletion of intraneuronal 5HT to activation of inent as clandestine chemists seek to modify or improve existing opiate molecules. One unfortunate spin-off ofpost-synaptic 5HT2a/c receptors located on GABA interneurons. This then leads to decreased GABA transmission such experimentation resulted in the appearance of a syndrome virtually indistinguishable from idiopathic Parkin- and consequent increased dopamine synthesis and release son’s disease based on the toxic effects of an impurity inthat then is taken up by the formerly depleted 5HT conthe synthesis of illicit meperidine (Langston, Ballard, taining neurons. The excessive dopamine in the 5HT nerve terminal is then deaminated by MAO-B, causing degenTetrud, & Irwin, 1983). The neurotoxin identifi ed eration of 5HT nerve terminals (Sprague, Everman, & destroyed the very same subnucleus in the substantia nigra which is etiologically and pathophysiologically involved Nichols, 1998). Chronic users of MDMA showed

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Medallo, Pujol, Vingut, Borondo, & Valverve, 1998) depressed serotonergic functions, including reduced proreported intentional overdose and death with MDEA. lactin and cortisol responses compared to controls, weeks after stopping the use of MDMA (Gerra, Zaimovic, Giucastro, Maestri, Monica, Sartori, Caccavari, and Delsig-2-CB (4-BROMO-2,5-DIMETHOXYPHENETHYLAMINE) nore, 1998). Cognitive problems have been documented ALSO KNOWN AS SYNERGY, HEROX, NEXUS, VENUS in MDMA users. They had dif ficulties with sustained This psychoactive substance is a hallucinogen enjoyed as attention tasks and verbal and visual memory. Poorer memory performance was associated with lower CSFa designer drug. It is one of a number of psychedelic 5HIAA levels (Bolla, McCann, & Ricaurte, 1998). Parrott substances initially created by the libertarian pharmacoland Lasky (1998) described the effects of MDMA ogist, Dr. Alexander Shulgin. It has been described as an (“Ecstasy”) on mood and cognition before, during, andexample of an empathogenic agent, as have MDMA, GHB, and other related substances (Velea, Hautefeuille, after a Saturday night dance. Several days after ingestion of MDMA, users felt more depressed, abnormal, unsocia-Vazeille, & Lantran-Davoux, 1999). These agents are overused at all-night parties called “raves, ” where obligble, and less well tempered than nonusers. They also peratory prolonged social contact is part of the environment. formed more poorly on memory tasks. Criteria for depen2-CB itself produces mild confusion, stupor, and a childdence were met in several cases of chronic and heavy like interest in visual phenomena; a typical dose is 20 to MDMA users (Jansen, 1999). Attempts have been made 40 mg; the effects last up to 6 hours. by PET scanning techniques to correlate the effects of MDMA on brain 5HT synthesis. In the dog, 5 hours after GHB (GAMMA-HYDROXYBUTYRATE) ALSO KNOWN AS “G” MDMA infusion, 5HT synthesis was about half of that at baseline and about one thirteenth of the synthesis seenThis 1 fatty acid derivative is structurally similar to GABA hour after infusion of MDMA, when a large increase wasand has pharmacologic properties as an inhibitory chemnoted. A decrease in 5HT transporter binding was also ical transmitter in the central nervous system. It has powseen in PET studies (Nishisawa, Mzengeza, & Diksic,erful CNS depressant effects and its actions may be medi1999). Recently, MR spectroscopy studies (Chang, Ernst, ated through specifi c receptors for this agent, or via Grob, & Poland, 1999) have shown that the brains ofactivity on GABA-B receptors. Some of its actions also MDMA users have larger myoinositol fractions in parietal may involve alterations in dopaminergic transmission in white matter, suggesting increased glial content and posthe basal ganglia. It has been used clinically as a general sibly inferring neuronal damage in these areas. Amphetanesthetic and to treat sleep disorders. It induces a state amine analogs can cause seizures as one consequenceofofeuphoria, and has been enjoyed recreationally during the last few years (Tunnicliff, 1997). Although initially overuse. The characteristics of stimulant-induced seizures thought to be safe, recent reports (Reuters Health, were studied by Hanson, Jensen, Johnson, & White (1990). Methamphetamine-related seizures were flu-in 10-27-2000) confirmed 71 cases of death due to ingestion of GHB or its precursor, 1,4–butanediol (also called BD enced only by diazepam and valproate whereas other antior “pro–G.”). BD can be obtained on the Internet and is convulsants were ineffective. rapidly metabolized to GHB in the body. BD has been sold as a dietary and body-building supplement and as a MDEA (3,4-METHYLENEDIOXYETHAMPHETAMINE) “EVE” sleep aid. It is also an industrial solvent. Fifteen of the This is another of the many substituted amphetamine anadeaths had no other intoxicants involved. Another case logs; it is not as popular or available as MDMA. However,report (Harrington, Woodward, Hooton, & Horn, 1999) it, too, has been shown to produce serotonergic deficits documented near-fatal or prolonged reactions to very and impair memory in rats (Barrionuevo, Aguirre, Del Rio, small doses of MDMA or GHB in a patient who is HIV& Lasheras, 2000). MDEA also produces dose-relatedpositive and being treated with protease inhibitors. These hyperthermia, and also affected 5HT transporter density drugs inhibit the cytochrome P-450 system in the liver and in the frontal cortex and in the hippocampus. The pathol-intestines and inhibit the metabolism of GHB and MDMA. ogy of fatal toxicity due to MDEA ingestion has been GHB is also commonly used at all-night dance parties. studied in seven males aged 20 to 25 (Milroy, Clark, & Of particular concern in the last decade is the escalatForrest, 1996). Marked changes were identified in the livering phenomenon of polydrug misuse. It is well known that with cell necrosis. Changes consistent with catechola-alcoholics often abuse tobacco, tranquilizers, antidepresmine-induced myocardial damage were seen in most of sants, and caffeine. Similarly, physically dependent narthe cases. In the brain, perivascular hemorrhagic changes cotic users often misuse other categories of drugs in an were noted in four cases. The changes were similar to attempt to stave off withdrawal symptoms (see above). A those seen in heat stroke, although only two cases had common substance like marijuana is often used with alcodocumented hyperthermia. An additional report (Arimany,hol and tobacco. Some of the history of legally prescribed

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protein complexes have been shown to be affected by co-intoxicants dates back to the era of laudanum, which was a mixture of wine and opium. The emergence ofethanol, including the GABA-benzodiazepine-barbitupolydrug use heightens the challenges for medical and rate-chloride ion receptor, the adenylate cyclase system, other practitioners in terms of successfully reducing orincluding the guanine-nucleotide-dependent coupling proeliminating simultaneous use of psychoactive substances. tein (G protein), sigma opiate receptor, Na+K+-ATPase, Also, the risk for medical complications consequent toas well as monoamine oxidase (Chen & Goldstein, 1976; multiple drug use escalates in parallel with the number ofLiljequist, Culp, & Tabakoff, 1986; Luthin & Tabakoff, substances used. This poses many new kinds of problems, 1984; Marks, Smolen, & Collins, 1984; Perlman & Goldparticularly where intravenous drug use is common. Thestein, 1984; Tabakoff & Hoffman, 1983, 1987). Therefore, widespread epidemic of AIDS, syphilis, bacterial although no specific receptor has been found for alcohol, endocarditis, and renal, hepatic, cardiac, and pulmonary the interactions of the substance with multiple neuromodcomplications of recurrent drug use add to the total cost ulating and neurotransmitter systems give additional to society (Jaffe, 1989, 1990; Mello & Grif fiths, 1987). depth, as well as confusion, to understanding of the basic pharmacology of alcohol. ALCOHOL Equally puzzling is the mechanism(s) that underlies the biochemical pharmacology of tolerance and physical The usage of ethanol is a worldwide phenomenon, somedependence to alcohol. Once again, numerous lines of what more prevalent in so-called technologically advanced evidence point to serotoninergic and peptidergic mechasocieties, such as North America and Europe. Alcohol is nisms in the development of ethanol tolerance. For undoubtedly the single most widely used substance on the instance, genetically distinct rodents that self-administer earth. It has been estimated that the total cost to society alcohol have been shown to have reduced serotonin for alcohol-related medical issues accounts for 10 to 13% of the nation’s total health expenditures. In 1975, the total(5-HT) concentrations in the brain. Drugs that inhibit 5-HT reuptake into axonal terminals have been shown to cost in terms of accidents, crime, health-related problems, and productivity exceeded $45 billion. Obviously, accu-decrease self-administration of alcohol by animal as well as human subjects. Turnover of norepinephrine in the CNS rate incidence and prevalence measures are extremely difficult to obtain, although population-based statistics showalso is altered consistently during chronic alcohol ingestion by animals and humans. An association of arginine that males age 18 to 64 have the highest lifetime prevavasopressin (antidiuretic hormone) with maintenance of lence rate. In women, age 18 to 24, alcohol-related probthe tolerant state to alcohol also has been shown in numerlems rank fourth in terms of prevalence among other psychiatric diseases (Myers, Weissman, Tischler, Holzer, &ous experiments. This naturally occurring brain peptide has multiple physiologic functions and is somehow Leaf, et al., 1984; Robins, Helzer, Weissman, Orvaschel, involved in learning and memory. The reverse is also true & Gruenberg, et al., 1984). in that antagonists to vasopressin can accentuate the loss Alcohol misuse has been separated in diagnostic criteria (American Psychiatric Association, 1987) from theof tolerance to alcohol. Genetically distinct rodents that older term “alcoholism. ” The latter term has been replaced lack this peptide were reported not to develop alcohol tolerance to prolonged administration of the substance by alcohol dependence, which implies prolonged exces1989; Jaffe, 1990; Tabakoff & Hoffman, 1987). sive use of alcohol such that sudden cessation results in(Bloom, a The pharmacology of tolerance to alcohol includes withdrawal syndrome. The enigma of how alcohol propharmacodynamic tolerance, together with eventual develduces its acute CNS depressant effects as well as the larger question of a specific locus of pharmacologic effect foropment of a state of physical dependence when alcohol is maintained in the bloodstream at high concentrations for the substance has been studied since the turn of the cenlong periods of time. Withdrawal phenomena begin to tury. Meyer (1901) first proposed a membrane hypothesis for alcohol’s intoxicating and sedating effects. He suggestedoccur within 10 to 96 hours after cessation of drinking, and so-called uncomplicated alcohol withdrawal may conthat alcohol affected neuronal membrane lipids, and over the years many scientists have sought to confi rm and extend his sist of mild tremors, anxiety, nausea, cramps, elevated blood pressure, hyperrefl exia, disturbed sleep, and theory. Indeed, alcohol has been shown by several lines of rebound of REM sleep, as well as hallucinations. Alcoholexperimental evidence to increase the uidity fl of lipids in offset seizures are also a relatively frequent complication neuronal membranes. These experiments have been perof the withdrawal state and can occur even with alcohol formed in vitro in membranes obtained from genetically present in the bloodstream. A reduction in blood level is sensitive mice that were predisposed to alcohol sensitivity or insensitivity. Gangliosides were found to be important ina sufficient trigger to onset of tonic-clonic seizures, which usually occur once or at most in brief flurries (“rum fits”). allowing alcohol’s effects on membrane uidity. fl A cross tolerance demonstrated between ethanol and other Membrane-bound proteins are affected by their surrounding lipids when alcohol is present. Numerous receptorsedative hypnotic drugs, including benzodiazepines, bar-

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biturates, and chloral hydrate, although none existfemales, and human fetal alcohol syndrome has been well between ethanol and opiate narcotics (Jaffe, 1990). described in alcohol-exposed fetuses (Mello, 1987). A more severe abstinence syndrome has been termed The treatment of alcoholism, both at the time of acute alcohol hallucinosis, with continued hallucinations, con-withdrawal as well as on a long-term basis, has taken many fusion, disorientation, weakness, and agitation. Hallucina-different approaches. Acute prevention of withdrawal tions are often persecutory and have extremely vivid charsymptoms can be accomplished readily via use of benzoacteristics. This state may last for 3 to 4 days and has been diazepines, as mentioned above. On a long-term basis, if termed delirium tremens or alcohol withdrawal delirium chronic anxiety is a predisposing factor to continued use (Jaffe, 1990). Although most alcohol abstinence syn-of alcoholism, then it makes sense that long-term admindromes are self-limiting, delirium tremens is a medicalistration of benzodiazepines and other anxiety-reducing emergency because of the instability of the cardiovascular agents may prove useful. Newer agents, such as buspirone system and also the potential for seizures. The larger long(BuSpar), which are serotonin agonists, also may play a term issue is that of a prolonged abstinent state, which role in the long-term treatment of alcohol-prone patients. can take many months or even years before normal bioSerotonin reuptake inhibitors, such as zemelidine and fluchemical equilibrium is established. oxetine, have been shown to reduce alcohol consumption Biological risk for alcoholism has been shown to havein alcohol-prone individuals (Jaffe, 1989; 1990). genetic underpinnings, and multiple factors have been elu- More traditional pharmacologic approaches that have cidated, including genetically determined differences andbeen used in the past to curb or eliminate alcohol conisoenzyme patterns for alcohol dehydrogenase, genetisumption include medications like disulfiram and, to a cally distinct brain proteins, differences in brainwave EEGlesser extent, carbamide. Both of these drugs inhibit the patterns, and in long-latency cognitive evoked potentialsalcohol-metabolizing enzyme, aldehyde oxidoreductase (P300). Two relatively distinct groups of alcoholics have(aldehyde dehydrogenase). This enzyme metabolizes a been characterized, namely, type I alcoholics, who exhibitbreakdown product of ethanol, namely, acetaldehyde, low novelty-seeking and high harm-avoidance behavior,which is normally converted to acetic acid. Therefore, by and who drink to alleviate anxiety, and type II alcoholics,inhibiting acetaldehyde’ s metabolism, levels of this interwho show high novelty-seeking and low harm-avoidancemediate build up and are associated with unpleasant side behavior and who mainly drink to experience alcohol’ s effects, such as tachycardia, flushing, vomiting, pounding euphoric properties (Cloninger, Dinwiddie, & Reich, in the chest, hypotension, sweating, and dizziness. These 1989; Schuckit, 1987). side effects are believed to act as deterrents and create a Although detoxification from alcohol is a complicated conditioned aversion to the usage of alcohol. Disulfiram matter, it can be accomplished rapidly with pharmacologicwas used for a long time, but its use currently has diminand medical measures instituted to prevent seizures and ished because of lack officacy ef and because of ethical acute cardiovascular collapse. Detoxi fication can be questions regarding its repeated administration. Other less accomplished using lorazepam or, more traditionally, thewidely used approaches from the past included the use of older benzodiazepines (e.g., chlordiazepoxide) adminisemetine and lithium, which produce protracted vomiting. tered daily. These compounds reduce the anxiety, tremuIt was felt that these agents could help induce conditioned lousness, and noradrenergic overactivity associated with aversion to alcohol. None of these techniques has been the acute withdrawal state. Curiously enough, conven-found to be useful routinely (Jaffe, 1989). Likewise, apotional anticonvulsants, such as phenytoin, are ineffectivemorphine, a dopaminergic agonist, also has been used as an in preventing alcohol-offset tonic-clonic seizures. Benzo-aversive conditioning agent and is a treatment for the recurdiazepines and perhaps sodium valproate and carbamrent craving and anxiety surrounding the cessation of drinkazepine may have a preferential ability to prevent alcoholing. Clonidine has been used to reduce some of the increased withdrawal seizures. As noted above, even after the acute central sympathetic tone in numerous drug cessation regiwithdrawal state to alcohol is finished, extended absti-mens, including alcohol, opiates, and CNS stimulants. nence features (the so-called prolonged alcohol abstinence In large measure, the mainstay of rehabilitation efforts syndrome) can occur for years, and persisting neuropsyfollowing the acute withdrawal of alcohol has centered on chological and electroencephalographic changes can be behavioral and cognitive therapies. The Alcoholics Anonseen (Grant, 1987; Mendelson & Mello, 1979). Permanentymous 12-Step Program remains a useful tool, although impairments in brain function also are known to exist,the efficacy rate for successful rehabilitation from chronic particularly in Wernicke’ s disease and Korsakoff ’s psy- alcohol use is quite low. Group and individual psychotherchosis, characterized by structural changes in mammilloapeutic efforts are important concomitants in an overall thalamic tracts with profound disruption of memory, approach to the rehabilitation from alcohol usage. In the deranged thinking processes, and confusion, often on last a decade, it has been increasingly recognized that alcopermanent basis. Other long-term effects of alcohol have hol use is a problem not only from the standpoint of the been seen in reproductive function, both in males and effects of that molecule on the central and peripheral

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nervous systems, but also as a worldwide problem with The pharmacologic mechanisms of nicotine affect respect to polydrug use of multiple CNS-active agentsthe cholinergic systems of the central and peripheral simultaneously. Indeed, alcohol, nicotine, and marijuananervous system with stimulation of nicotinic as well as muscarinic receptors. In addition, a large body of eviare the top three drugs used in a nonmedical setting according to National Institute on Drug Abuse statisticsdence imputes release of serotonin, dopamine, histamine, (National Institute on Drug Abuse, 1983). Since alcoholendorphins, and other neurotransmitters and neuromodis readily available, it is often used as a counter-drug toulators as additional central effects of nicotine (Jones, ed pharmacology of some “ smooth out” anxiety and dysphoria when other pre- 1987). A much more diversifi 4000 compounds has been identifi ed in tobacco (when ferred centrally active agents are not immediately availburned) and tremendously complicates the understandable. Heroin addicts in methadone programs and patients ing of not only nicotine effects, but also effects of other in other drug detoxifi cation systems for cocaine and potent substances contained in tobacco. Metallic ions, amphetamine abuse often use alcohol as a baseline tranradioactive compounds, alkaloids, tars, cyclic aromatic quilizing agent. This underscores the need to search for hydrocarbons, and other substances have been recovered better pharmacologic methods to treat underlying behavfrom tobacco that is burned. This makes tobacco the most ioral anxiety states. Perhaps newer central serotoninergic complex of all misused substances and engenders great agents (e.g., selective reuptake blockers) and the buspirone category of medications may prove useful in theconcern in terms of the epidemiology of cancers and other serious health complications, including cardiovasfuture. The author has observed that patients with an organically based predisposition to behavioral instabilitycular diseases and peripheral vascular disease. Chronic obstructive lung disease, effects on myocardial ischemia, and consequent dependence on multiple centrally active and acceleration of atherogenesis have also been demagents often respond to anticonvulsant therapy in ameliorating or abating drug use (unpublished observations).onstrated (Barry, Mead, Nabel, Rocco, Campbell, FenMore research is needed to defi ne the rate and prevalence ton, Mudge, & Selwyn, 1989). of CNS instabilities and usage of medications that sta- Despite the heightened national societal awareness of bilize organic brain dysfunction and their application in the ill effects of chronic tobacco use, increased usage has prevention of recurrent alcohol and other drug usebeen reported in the female population in the last 2 decades. National rates of the incidence of lung cancer in (Kreek, 1987). women are approaching that in men and may well surpass it in the near future. In general, the nicotine content of NICOTINE AND TOBACCO individual cigarettes has been reduced, and the average The practice of consuming nicotine in various forms isamount of nicotine per cigarette has decreased from 2.3 an example of a complex social behavior with multifac-to 1.2 mg, and the average yield of tars has similarly been torial inputs. The initiation and maintenance of this reduced from 38 mg to around 10 mg per cigarette. behavior have their roots in social and cultural bases. Although the tars are much more associated with serious The entire practice becomes a repeatedly reinforced, and even fatal medical complications, it is important to overlearned, and, in many cases, ex reflor automatic remember that so-called low-yield tar cigarettes do not behavior, re-inforced by repeated conditioning. Nicotinecontain less nicotine than the traditional high-tar preparain tobacco is a potent psychochemical, with central andtions (Benowitz, Hall, Herning, Jacob, & Jones, et al., peripheral nervous system effects as well as those on 1983; Jones, 1987). In addition, marked increases in national cardiovascular, gastrointestinal, skeletal, motor, andconsumption of other tobacco preparations, such as snuff endocrine systems (Jaffe, 1990). Nicotine has been demand chew, contribute to the problems on a national level. onstrated to produce tolerance as well as physical depen- Data accumulated from the literature show that the vast dence. Positive effects of nicotine have been demonmajority of people who have ceased using tobacco do so strated on various behavioral measures, such as on their own without any formal help. Therefore, most of facilitation of memory or attention, decrease in irritabil- the persons studied in the setting of tobacco cessation ity, appetite suppression, and euphoria when adminisreally represent a minority of tobacco users. Comparatered intravenously. Animals can be taught to self-admin-tively, only a very small percentage of chronic smokers ister nicotine, although the reinforcing effects are lessactually cease using tobacco each year, generally less than profound than cocaine or amphetamines. Nevertheless, 5% (Fielding, 1985; Orleans, 1985). The abrupt cessation the pharmacology of nicotine, together with the mode ofof nicotine use will reliably produce a withdrawal synadministration wherein each puff of a cigarette can bedrome that varies in intensity from person to person. Conconsidered a single dose of drug, make nicotine an tinued craving is a chronic problem akin to the prolonged almost ideal reinforcing agent, particularly with respectabstinence syndrome noted for alcohol and other centrally to its positive or pleasurable effects (as noted above), active drugs of misuse. Irritability, restlessness,ficulty dif including behavioral alerting. in concentration, headache, and increased appetite,

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together with insomnia, are frequent features of the nico-and stress management techniques, to teach patients to tine withdrawal syndrome. Indeed, EEG changes have been substitute other behaviors for repeated use of tobacco and documented for long periods of time after cessation ofnicotine (Jaffe, 1989). nicotine use, as are changes in physiologic parameters and performance on neuropsychological tests (Jaffe, 1990). CAFFEINE A host of treatment approaches have been tried, including behavioral counseling techniques and, moreAlthough far less productive of dependence than many of recently, the use of nicotine given in gradually reducedthe other substances discussed in this chapter, caffeine remains one of the most widely used substances in the dosages, either as a gum (nicotine polacrilex and Nicorworld. It is a CNS stimulant and a modulator of smooth ette) and most recently as a patch. Nicotine substitutes, muscle contraction with pleasurable effects, both physisuch as lobeline, have been tried in the past, but are not very useful due to the much weaker CNS effect of thiscally and psychologically. Caffeine has mood-elevating compound. Also, nicotine’ s inherent pharmacodynamic and antifatiguing properties. An average cup of coffee properties, together with the minute-by-minute regulationcontains about 100 mg of caffeine, and cola-based soft drinks contain about half that amount. Tea, chocolate, and of dosage obtained via the practice of smoking, make oral forms of nicotine, such as gum, a poor substitute. Thecertain other plants consumed by human beings contain behavioral reinforcing effects of the act of smoking, with caffeine and other xanthine derivatives (e.g., theophylline, all of its psychosocial implications, are powerful condi- theobromine), which also produce CNS excitation at tioning stimuli which perpetuate the habit in the first place.appropriate doses. It is not unusual to ingest 500 to 700 mg Patch forms of nicotine administration (e.g., Nico- of caffeine per day, and it has been estimated that 25% of derm™, Habitrol™) offer a continual release of nicotine the American population does so (Jaffe, 1989). into the system, such that dosage can be gradually reduced The establishment of dependence on caffeine is an over a matter of 6 to 10 weeks and hopefully withdrawaloverlearned social phenomenon and is inextricably woven into many cultural practices (e.g., afternoon tea, morning from nicotine accomplished in a gradual manner so as not coffee). From the standpoint of demonstrating withdrawal to induce negative behavioral phenomena associated with the nicotine withdrawal syndrome. Nicoderm and Habitroleffects upon cessation of caffeine intake, one of the most neurologic symptoms is that of headache, patches offer only one approach to accomplish cessation prevalent of together with increased fatigue. Headache, including vasnicotine use. Many other behavioral approaches, including cular migraine syndromes, can be precipitated or exacerhypnosis and acupuncture, aversive conditioning, and other bated by removing caffeine from the diet. Rarely, headmethods have met with partial success. Of prime importance aches will increase and persist for weeks after curtailment is the degree of motivation on the part of the smoker to end of caffeine intake. Complaints of fatigability and continued usage of tobacco and nicotine. Generally, higher decreased alertness also are common after stopping cafrates of cessation are noted in the setting of serious diseases. feine use. From a pharmacologic viewpoint, caffeine is a Physician advice often will go unheeded unless a concommuch weaker reinforcer of animal behavior in the laboraitant motivator exists for stopping the use of tobacco. Clonitory than other CNS stimulants, such as cocaine and dine also has been used in one study and was shown to be amphetamines. Chronic users of caffeine rarely report any promising as an adjunct in reducing use of tobacco and other euphoriant effects. After abstaining from the use of cafcentrally acting substances. Aversive conditioning techniques have also beenfeine, reintroduction of the substance will institute pleasurable effects in former chronic caffeine users. Thus, a tried, and one of the most effective methods is a so-called rapid smoking technique, wherein a skilled therapistlow level of neuroadaptation occurs with chronic caffeine works with the patient one on one. The patient inhalesuse. Once again, its short half-life lends itself to repeated administration and thus chronic repetitive dosing, which smoke from his or her own cigarette every 5 to 6 seconds, tends to escalate the daily dose of caffeine. In most cases, and this continues until the patient asks to stop administration of the nicotine. Presumably, the blood levels ofcaffeine can be withdrawn reasonably slowly without any adverse physiologic effects other than transient fatigue, nicotine create negative pharmacologic effects, such as irritability, and possibly headache. In fact, caffeine is nausea, and the author feels that this may be, in very found in many ergotamine preparations and has been used skilled hands, an appropriate method to create an aversive environment surrounding the use of tobacco. Commer-as an adjunctive medication for the treatment of migraine. cially available programs, which include many behavioralMany patients with chronic headaches can keep the headand aversive techniques, together with motivational tech-ache pattern at bay with caffeine dosed repeatedly throughout the day. niques, have been available and in some ways are more effective, at least in the short term, to produce a higher Extremely high doses of caffeine can theoretically produce suf ficient excitation to allow seizures to occur, cessation rate of tobacco use. Behavioral modifi cation particularly in patients with lowered seizure thresholds. techniques can easily be incorporated, as can biofeedback

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Societally, caffeine overusage tends to be part of pro-women, diminished prolactin levels are seen after smokgrammed behaviors, including concomitant use of nico-ing marijuana. Numerous lines of evidence point to some tine. The DSM-III-R (American Psychiatric Association, interaction of cannabinoids with humeral and cell-medi1987) diagnostic criteria for psychiatric disorders includeated immune system components. Of great concern is the that of caffeine intoxication, usually ingestion of more obligatory contamination of cannabis products with pesthan 250 mg of caffeine. In special situations, it mayticides, herbicides, and organic and inorganic metals, contribute to behavioral instability and thus may warrantwhich may add to the overall CNS toxicity (Jaffe, 1989, medical intervention to reduce unwanted side effects1990; Mendelson, 1987). Persistent levels of cannaboften seen with intake of large doses of caffeine. inoids and other extremely lipid-soluble substances have been demonstrated in tissues for months after cessation CANNABIS (MARIJUANA) of marijuana use, which raises concerns of long-lasting effects of chronic marijuana use on behavior, cognition, This CNS intoxicant has, from a world viewpoint, the and intellectual functioning. highest rates of usage, and it has multiple pharmacologic Statistical surveys of the incidence of marijuana usage properties, including euphoriant, mood-stimulating, show that a declining fraction of adolescents and young behavioral, and potent cardiovascular effects. References adults regularly use the substance, although it remains one to usage in Indian and Middle Eastern literature of the of the most commonly used psychoactive substances, and forms that are available reveal that cannabis and cannabis fully 50% of Americans have tried or used marijuana in products go by many names, from the euphemistic “grass, their lives. Like all behaviorally reinforcing drugs, a small weed, reefer, and pot” to ganja, bhang, dagga, hashish, segment of users will have unpleasant behavioral and carand sinsemilla. All cannabis is derived from the flowering diovascular effects or exacerbation or production of psytops of hemp plants, and the plant is indigenous to many chiatric abnormalities and on this basis will probably not parts of the world. The plant contains over 400 chemicals, use the substance repetitively. Anxiety, panic reactions, and about 50 of these are cannabinoids. The most abunand paranoid symptoms may be produced or aggravated dant psychoactive cannabinoids include cannabinol, cannabidiol, and isomers of tetrahydrocannabinol (THC). Thein susceptible individuals, and many users do not rate isomer responsible for most of the characteristic effectsthese as pleasant effects. In comparison, the anti-anxiety of ingested or smoked marijuana is D9-THC and it isand mild euphoriant properties of marijuana lend themresponsible for many of the psychostimulant, euphoricselves to repeated usage as mild intoxicants and relaxants. There is seemingly no tolerance for the pleasurable effects and, in higher dosages, hallucinogenic properties of the parent plant. Different cultures have extracted the activeof cannabis and, therefore, continued behavioral reinforcement would be expected to promote repetitive use of maringredients in various ways. In most cases, plants are ijuana. However, there is tolerance to some of its effects harvested and dried, and dried leaves and flowering tops are usually smoked, ensuring a rapid onset of effect.on mood, and it is likely that this is responsible for the Extraction of the cannabinoids into solvents also can pro-escalation of dosage needed to produce the same degree duce potent pharmacologic effects. The THC content ofof “high” with repetitive use. Paradoxically, a “reverse tolerance” to the effects of cannabis has been described, cultivated marijuana has steadily increased. In the 1960s, average THC content was 1 to 2% in domestically grownin that smaller and smaller doses are needed over time to marijuana, whereas today it is not uncommon for har-achieve certain desirable euphoriant effects. A wellvested material to contain 7 to 8% THC. Traditionally, described amotivational syndrome exists in cultures where more potent preparations, using only the flowering topsdaily usage of marijuana and hashish occurs. This has of the plant, often contain in excess of 10 to 15% of THCbeen described in the Caribbean (Jamaican) peoples, and there has been much debate as to whether or not marijuana and are known as hashish or hashish oil. The pharmacological effects of THC include seda-directly affects motivation or whether these are indirect effects of the drug (Cohen, 1982). Social usage of marition, decrease of aggressiveness, loss of ability to perform juana is often impossible to study in its own right because complex motor and psychologic tasks, perceptual and of concomitant usage of tobacco, alcohol, and other comsensory distortions or enhancements and, in larger doses, ataxia, incoordination, stupor, as well as hallucinations.monly used substances, often ingested in close proximity to marijuana itself. This complicates research protocols A great deal of energy has been extended in searching for marijuana receptors, and it is highly unlikely that theand epidemiologic studies of marijuana use. Attempts have been made to look for bona fide pharmamyriad effects of this substance will be explained by actions in a single particular kind of receptor in the CNS.cologic uses for marijuana. Trials of oral THC have been Effects of chronic marijuana usage include diminishedused successfully to reduce glaucoma in otherwise refractory gonadotropin-releasing hormone, luteinizing hormone,patients (Jaffe, 1990). Similarly, a synthetic cannabinoid and follicle-stimulating hormone levels in both sexes. Inderivative, nabilone, has been used as an antiemetic. This

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amines were, nonetheless, illicitly diverted. By 1980, substance also produces many of the psychoactive effects usage of amphetamines had declined rather dramatically, of natural D9-THC (Jaffe, 1990; Mendelson, 1987). Because of the production or exacerbation of psychi-in contradistinction to the escalating use of cocaine in our population. Clearly, the inverse relationships are atric symptoms and behavioral aberrations associated with s mind, based on the relative marijuana use, the DSM-III-R (American Psychiatric linked, at least in the author’ Association, 1987) has developed diagnostic criteria for aavailability of cocaine and relative nonavailability of amphetamines. In the 1980s, reports of clandestine mancannabis delusional order, as well as cannabis intoxication. These are generally utilized in conjunction with ufacturing operations for amphetamines and methamphetamines surfaced, and intranasal and intravenous use approaches to other chemical dependencies, and it is rare that prolonged psychotic or schizophreniform states willof “ crank” continues alongside that of cocaine. The population at highest risk for use and abuse of these subresult from acute misusage of marijuana or its derivatives. stances is the 18- to 25-year-old group. Cocaine is the The cannabis withdrawal syndrome has been described with impaired motor performance on discontinuation,only drug for which increasing risk of usage develops above this age group, although escalating usage of alcoassociated with insomnia, anxiety, and other symptoms reminiscent of withdrawal from sedative hypnotics. hol remains another major problem (Fischman, 1987; O’ Malley, Johnston, & Bachman, 1985). Whether this represents a mere return to the patient’ s baseline state of behavior is uncertain but remains a pos- Pharmacological mechanisms subserving repeated sibility. Once again, utilizing the principle that the anxi- self-administration of amphetamines and cocaine relate olytic and psychostimulant properties of marijuana maydirectly to the effect of these drugs on the dopamine system. In particular, their ability to block reuptake of dopamhelp correct a baseline state of agitation or internal dysine and also to act as dopamine agonists produces CNS phoria, one might, therefore, search for more appropriate pharmacologic management of individuals who repeat-excitation, and this is coupled with repeated dosing, which edly use marijuana and its derivatives, thereby circum-becomes a powerful behavioral reinforcer. On a practical venting the potential for engagement in illegal and soci-level, the effects of amphetamines are indistinguishable etally disapproved drug-seeking behaviors. Behavioral,from the effects of cocaine, even to seasoned users, with affective, and cognitive therapies certainly play a strong rolethe only major difference being the duration of the drug in the overall rehabilitation and management of individualseffect. The patterns of misuse for both substances tend to be similar, with a flurry of administration occurring in who have strong histories of chronic marijuana use. “runs” or binges, and that for cocaine generally lasting less than 1 or 2 days, whereas in the case of amphetamine CENTRAL NERVOUS SYSTEM STIMULANTS usage, a typical binge may last for several days. Generally, (COCAINE AND AMPHETAMINES) the intense repeated usage of these substances ends when The most powerful reinforcers in licit or illicit usage are the availability of the drug is curtailed or when the user the CNS stimulants, particularly cocaine. Reference has is exhausted, confused, or disorganized. Users will often been made (see above) to its powerful effects on reininject larger and larger amounts of a drug to obtain the forcement of self-stimulating behavior in animals and assame degree of rush or flash, and the free-base form of clinically observed by usage in people. In the last 10cocaine is said to be more profound in this respect. The years, cocaine has emerged as the statistical drug rush of is often described in orgasmic connotations and choice for recreational repeated self-administration.becomes the principal focus for repeated use during the Although traditionally snorted or used intravenously as abinge. Following such a binge, the user will often crash, soluble hydrochloride salt, free-base or crack cocaine has with profound lethargy and often will sleep for up to 24 enjoyed widespread misuse throughout many cultures in hours or longer to mitigate the severe CNS exhaustion the Western Hemisphere in the last decade. A similarattendant to prolonged stimulant use. The temporal pattern phenomenon has been described for misuse of amphetof binges consists of intense usage punctuated by short amines, which historically dates back to World War II periods of abstinence. A phenomenon called sensitization and to an epidemic of widespread amphetamine usage (Fischman, in 1987) exists which occurs with repeated psypost-war Japan in the 1950s. In the next 2 decades, chostimulant usage. This has been demonstrated in both amphetamine compounds were readily available pharmahumans and animals and consists of an increased effect ceutically, and many adolescents and young adults used of a specific dose of a stimulant with repeated adminisamphetamines, more so for their stimulant properties and tration. Thus, the repetitive patterns are akin to the stereoless apparently so for purely recreational purposes (Abeltypic behaviors elicited in animals with chronic adminisson & Fishburne, 1976). In 1970, the Harrison Act wastration of cocaine or amphetamines. Sensitization has been amended, and amphetamines were placed in Schedule described II, for numerous variables, namely, local motor with tight controls on distribution and dispensing of theactivity, stereotypic behaviors, increased seizures and starsubstances. Large quantities of manufactured amphettle responses, and other aspects of CNS stimulation. Post

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(1977) compared the effects of repeated usage of psychoand the greatest likelihood of relapsing to former cocaine stimulant drugs to animal models of “kindling” wherein use occurs during this phase. Whether or not this stage repeated low-level stimulation of hippocampal andmimics the natural cycle of binge use for amphetamines amygdala preparations resulted in prolonged after-dis-and cocaine is a point that has been debated (Jaffe, 1989). charges and seizure-like activity in brain preparations. The third and most prolonged phase of cocaine withAt the same time that the process of sensitization isdrawal may take up to a year and resembles the prolonged occurring, the process of tolerance also occurs with regard alcohol abstinence syndrome, with establishment of sucto the rush or flash obtained with a single dose of cocaine. cessful conditioned avoidance responses and behaviors Cross tolerance and cross sensitization occur among CNS based on a combination of behavioral retraining and posstimulants, and yet no tolerance occurs to the positive sibly medication. reinforcing effect of this group of substances on behavior. Various medications have been utilized to curb Thus, the ability of cocaine or amphetamines to act as cocaine craving, including clonidine and desipramine. reinforcers occurs consistently whether one has a short Very fragmentary data with Tegretol (unpublished results) history of repeated cocaine use or an intermittent historyalso indicate that this agent may be effective in curbing spanning many years. The effect of sensitization seems the to intense craving for cocaine and amphetamines. In the be consistently present, even with long periods of disconacute phases of withdrawal, haloperidol or other dopamine tinuance of drug use (Post, 1977). blockers may very well be useful. In some cocaine users, Treatment of dependence on cocaine and amphetparticularly with underlying cyclothymic disorders, lithamines is extremely difficult, as one can imagine, because ium has been reported to be helpful in reducing relapse of the extremely powerful behavioral and reinforcing to continued use of cocaine. It has been suggested that effects of these drugs. Nevertheless, the list of severe and chronic blockade of dopamine receptors may alter craving potentially fatal medical problems associated with unre-for psychostimulants. However, the opposite effect has strained use of cocaine mandates very vigorous efforts in also been demonstrated, wherein neuroleptics given to detoxification and rehabilitation of individuals who are recent cocaine users resulted in increased craving for the severely dependent on these substances. In addition, a mixdrug. Studies are in progress to determine which category ture of cocaine with heroin (so-called “speedballing”) addsof medicines may have long-term utility in curbing the additional measures of medical risk, and certainly cocaine nationwide epidemic of cocaine use. Similar treatments users are very well known to misuse multiple other sub-for amphetamine dependence have been developed, and stances, such as alcohol, sedative hypnotics, marijuana, and tricyclic antidepressants are currently being used, along opiates. Long-term serious psychiatric complications ofwith dopaminergic blockers to block craving and some of cocaine and amphetamine use include paranoid states and the euphoriant actions of amphetamine. Alpha-methyla syndrome virtually indistinguishable from paranoid paratyrosine (AMPT) was tried in older studies but is not schizophrenia with extreme hypervigilance. Persistentclinically available. AMPT blocks the formation of toxic psychoses, together with hallucinations, have been dopamine and ultimately norepinephrine and had been well described following prolonged amphetamine or found to block amphetamine-induced euphoria. However, cocaine use. More commonly, a briefer state of drug-it does not have any ability to block the effects of cocaine induced delirium with suspiciousness, paranoia, and visual or methyl-phenidate (Ellinwood, 1979). and tactile hallucinations (formication) occurs following Rehabilitative treatment for chronic users of stimubinges or runs of stimulant use. Of great concern are more lants is rudimentary at this point. Numerous psychologfatal medical complications (e.g., accelerated hyperten-ical approaches have been attempted, including behavsion, cerebrovascular infarction, intracerebral hemor-ioral, psychodynamic, and supportive psychotherapeutic rhages, myocardial infarctions, coronary artery spasms, techniques. In some cases, a contractual agreement by fatal cardiac arrhythmias, seizures, respiratory depression, the person in treatment has been beneficial. In this type gastrointestinal and peripheral vascular necrosis) from the of arrangement, the person undergoing treatment agrees prolonged vasoconstrictor effects of CNS stimulants. that the treating professional may inform his or her Withdrawal from cocaine reliably produces a syn- employer or professional societies if relapse into use of drome that is longer lasting and more pervasive than the cocaine or amphetamine occurs within a certain time typical crash following acute discontinuance of stimulantperiod. Within the boundaries of such an agreement, it use. The entire abstinence syndrome occurs over a long has been shown that a significant portion of patients period of time in stages. The first stage is rather brief,treated do abstain from a relapse into stimulant use. Howlasting 3 to 5 days, with anorexia and agitation beingever, much higher relapse rates were noted after expirareplaced by profound exhaustion, depression, hypersomtion of the contractual time period. Combining psychopnia, and hyperphagia. A second phase develops over the harmacologic approaches with behavioral and ensuing 6 to 12 weeks, with improved mood and a better psychotherapeutic techniques gives the best results, normalization of sleep; however, cocaine craving returns,because chronic stimulant use is felt to create a relative

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state of dopamine defi ciency by downregulating post- The pharmacologic actions of opioids that have predominant effects at µ or κ receptors are subclassified into direct synaptic receptors. This is by no means the only neurotransmitter system involved. Effects on the serotonin-effects, dependence-producing effects, discriminative effects, and reinforcing effects. Many of these studies have ergic system also have been described, and at this time tricyclic antidepressants still remain useful in helping tobeen donein vitro and in animals and have less relevance to the pharmacology of these substances in humans. Much attenuate relapse rates. By blocking the uptake of dopamine, serotonin, and norepinephrine, it is felt that the anti-of the pharmacologic subcategorization has been done with agents that are antagonists to various kinds of recepdepressant effects would help ameliorate the post-crash fatigue and lassitude that are parts of the second stage tors, of such as nalorphine. This was the first substance noted to cocaine withdrawal syndrome. At best, success rates are reverse the effects of morphine acutely, particularly currently limited, and better psychopharmacologic agentsanalgesic and euphoriant effects. Although nalorphine have to be developed, although desipramine is nowantagonized morphine-induced euphoria and precipitated withdrawal symptoms, it, too, could produce analgesia in favored among the tricyclic anti-depressants. humans. Unlike the euphoriant-producing morphine, nalorphine generally produces dysphoria in humans. An OPIOIDS even more selective opioid antagonist, naloxone, is curThe history of opiate use dates back to the 1st century rently in clinical use to acutely reverse some of the lethal A.D. and most likely even earlier. The prototypical opiate,effects of morphine or heroin, namely, those of respiratory morphine, is found in the opium plant. The advent of pipedepression and some of the effects on the cholinergic smoking ushered in the practice of ingestion by smoking,system peripherally. Naloxone (Narcan) can rapidly particularly in the Far East. Morphine and its syntheticreverse agonist actions of morphine and heroin and can derivative, heroin, remain very popular drugs of misusebe dramatic in reversing acute life-threatening effects of and are among the most severe tolerance- and physicaloverdoses in emergency room settings. A concerted effort dependence-producing substances known in modern pharhas been made pharmacologically to elucidate and premacology. There seems to have been a return to more serve analgesic properties of opioids with a minimum of heroin misuse nationally in the last 5 years, and this, ineuphoriant and physical dependence-producing properpart, reflects availability of natural materials and prevail-ties. No ideal molecule exists, although some success with ing market and social forces that wax and wane regarding a combination of analgesic effects (by virtueκ of -receptor different drugs of misuse. During the height of the 1980sstimulation) with a minimum of physical dependencecocaine era, misuse of opiates had waned somewhat. Howproducing properties has been achieved with mixed agoever, there seems to be a return to the levels of usage seen nist-antagonist molecules (e.g., nalbuphine, butorphanol, in the 1970s. pentazocine) (Woods & Winger, 1987). The pharmacology of morphine and other opioids has With respect to the withdrawal syndrome from opioids been progressing steadily since the identification of mul-and the practical management of detoxification from this tiple kinds of opiate receptors in the CNS. These devel-category of medication, volumes of literature have been opments in turn sprang forward from the identification ofwritten on opioid maintenance using methadone, and this naturally occurring endorphins and enkephalins in the cendrug enjoys a prime position in one of the major tral and peripheral nervous system. The µ receptor subtype approaches to treatment of heroin and morphine use in the is the site of action of the classic opiates, namely, mor-United States and other countries. The use of methadone phine, heroin, and codeine. These drugs are preferentially was pioneered by Dole and Nyswander in the mid-1960s. agonists at this receptor subtype. A second κ receptor is Methadone is an opioid with relatively pure µ-receptor the site of action of numerous other clinically useful drugs,agonist properties and has a longer half-life than heroin namely, butorphanol and nalbuphine. ∆A receptor has or morphine. It has proved to be relatively safe in terms been identified and seems to be the binding site for endogdaily use and to block the euphoriant effects of subsequent enous met-enkephalin. Aσ receptor also has been doses of heroin. Other opioid maintenance drugs have described, and stimulation of this receptor has hallucino-been investigated, although none is clinically available. genic and excitatory effects with very little analgesia.One such medication, l-a-acetylmethadole (L-AAM), is Most of the analgesic effects of opiates are mediated under investigational use. It is similar to methadone in its through the µ receptor. The pharmacology of the tolerance action but has long-lived metabolites and can be given and physical dependence to various effects of opiates every is other day. In any case, it is now more than 15 years quite complicated, and some of the newer agents (e.g., since L-AAM was introduced, and it still remains a conpentazocine, cyclazocine) have agonist effects at one troversial and investigational drug. Another investigational receptor subtype and antagonistic effects at other receptor drug, buprenorphine, blocks the subjective effects of subtypes. The pharmacology of these receptor subtypesparenterally is administered morphine or heroin (Mello & very well described (Jaffe, 1989; Woods & Winger, 1987).Mendelson, 1980). Apparently, when given to patients

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who are self-administering low doses of heroin, buprenor-to 6 months, and the cost of such programs is quite high. phine suppresses some of the withdrawal symptoms, There is no evidence to suggest that rapid detoxifi cation has whereas when given to patients using high doses of opiany greater relapse rate than more traditional techniques ates, it seems to precipitate abstinence, more like tradi(Jaffe, 1989). Furthermore, approximately 85% of heroin tional opioid antagonists. addicts meet criteria for at least one psychiatric diagnosis, The controversy surrounding use of methadone as and a it is often the more psychiatrically impaired patients replacement for heroin or morphine has been debated for who have the lowest rates of success in formal detoxifinearly 30 years. Proponents of methadone maintenance cation programs. feel that a slowly tapered oral dosing of methadone can successfully achieve detoxifi cation from heroin use. In SEDATIVE-HYPNOTICS AND BENZODIAZEPINES addition, the methadone can block some of the euphoriant “ rush” effects of injected heroin or morphine. Further- Among the most available substances in our society are more, one of the objectives of treatment is to preventbenzodiazepine anxiolytics and sedatives, and use and severe withdrawal which is associated with far highermisuse of this category of drugs have taken on dramatic proportions in the last 10 to 15 years. In past years, the relapse rates in return to use of injected opioids. Patients are often initially stabilized on 80 to 100 mg of oral same kind of problem occurred with use of older hypnotic/sedatives, such as barbiturates, which are much more methadone, and a tapering regimen which reduces the tightly regulated since implementation of the Controlled methadone dosage by 10% per week has often been employed. A more gradual taper (3% per week) is utilizedSubstances Act of 1970. Other nonbarbiturate sedatives, including glutethimide, methyprylon, chloral hydrate, and when the methadone dose falls below 20 mg/day. Oppomeprobamate, enjoyed widespread misuse in small segnents of the methadone system cite widespread diversion ments of the population. An excellent overview of the of methadone itself and the sale of the substance by heroin scope of benzodiazepine usage in the United States is addicts who are enrolled in oral methadone programs. Attempts have been made to institute oral naltrexonepresented in a Task Force Report of the American Psychiatric Association (1990) on benzodiazepine dependence, (Trexan) therapy when the methadone taper is nearly toxicity, and abuse. finished in order to have an oral opioid antagonist present There has been an increasing awareness over the last in the former user’ s system on a daily basis. The aim of decade that short half-life benzodiazepines can be probthis therapy is hopefully to block euphoriant effects of lematic, in terms of potential for both dependence and any subsequently injected opiate should the person return misuse. Withdrawal from benzodiazepines is commonly to former usage patterns. believed to represent a return of the original anxiety sympBecause the acute opioid withdrawal syndrome is toms for which the medication was prescribed (Grif fiths believed to be a state wherein the adrenergic nervous & Sannerud, 1987). Benzodiazepines and other sedative system is hyperactive, centrally acting α2 agonists (e.g., hypnotics are known to be fairly strong reinforcers, and clonidine) have been utilized to suppress some of the acute much experimental data in humans have provided abunwithdrawal reactions. Lacrimation, rhinorrhea, jitteriness, dant evidence that a true physical dependence, as well as and sweating can be attenuated by the oral administration of clonidine. Clonidine is far less effective against othertolerance, can occur with virtually every benzodiazepine. Those benzodiazepines that are more lipid-soluble tend to withdrawal phenomena, such as insomnia, craving, lethbe more problematic. Older benzodiazepines, such as argy, and muscle aches, but has been utilized successfully in tapering off oral methadone dosage and institution ofdiazepam (Valium), together with newer lipid-soluble short half-life preparations, such as alprazolam (Xanax) oral naltrexone, as discussed above. Blood pressure has to be monitored with clonidine, as it is a centrally actingand triazolam (Halcion), are much more problematic in terms of tolerance- and dependence-producing properties antihypertensive agent. Sedation also can be a problem, although with regard to the restlessness involved in opioidwith chronic usage. Withdrawal phenomena, including withdrawal, this side effect may indeed be quite useful. seizures, have been reported in patients who have misused Other techniques utilized for accomplishing opioid high doses of benzodiazepines, barbiturates, and other nonbarbiturate sedative-hypnotics. Agitation and restlesswithdrawal seem “hard-nosed” but take advantage of the ness generally occur in a predictable fashion, and the unpleasant nature of withdrawal as an aversive conditioning technique. Abrupt withdrawal without any pharmaco-length of time of the withdrawal process can range between several days to several weeks. logic supports has been advocated by some as a reasonable The magnitude of the problem of benzodiazepine misway of accomplishing rapid detoxification from opioid dependence. Since clinical withdrawal is rarely life-threat-use certainly far exceeds numerically that seen for opiates. It is estimated that 11 to 12% of the population has used ening, it at least has the advantage of accomplishing what can be a lengthy detoxification program in a matter ofbenzodiazepines at least intermittently, whereas about 3 days. Most oral methadone programs can continue for or 3 4% of the population uses benzodiazepines on a chronic

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basis. Upward of a 100 million prescriptions per year havewas believed that benzodiazepines most strongly reinforced their use in patients who have a predisposition been written for these substances, and iatrogenic depento misusing other categories of drugs such as alcohol, dence is a very real issue on a national level. Treatment modalities for benzodiazepine withdrawalother sedative-hypnotics, and opiates. Thus, benzodiazhave been devised using slow tapers and changes to longepine misuse continues to be a national phenomenon, acting, low-potency compounds. In general, avoidance ofand iatrogenic factors clearly contribute to the problem. long half-life compounds for use as nighttime hypnotics, A much more recent problem in the United States and together with avoidance of ultrashort-acting compoundsin the world in the last few years is the use of flunitrazepam, commonly marketed as Rohypnol. Street names for the same purpose, would be a wise choice in preventing for this drug abound: Rophies, Ropies, Roofies, Ropes, iatrogenic tolerance and dependence on benzodiazepines. Use of drug holidays is another technique that might favorRoches, Rochas, Rochas Dos, Rophs, Ropers, Ribs, R-25s, Roach-2s, Trip and Fall, Remember All, Mind a more rational use of this class of compounds. Beta blockers (propanolol), clonidine, carbam- Erasers, Forget Pills, and Date Rape Drug. This benzodiazepine, and buspirone have been used in the treatment azepine has been implicated in sexual assault (date rape) of withdrawal symptoms from benzodiazepines. Because cases especially when mixed with alcohol and is a cheap withdrawal effects are related to the uncovering of inhib-form of intoxicant (Saum and Inciardi, 1997). An estiitory GABA receptor sites in the CNS, drugs such asmated one in four women will be raped in their lifetimes carbamazepine may prove useful, not only to controland approximately 75% of these incidents will be acquainbenzodiazepine withdrawal seizures, but also to quiet the tance rapes. Flunitrazepam is odorless, colorless, and arousal state often seen in withdrawal (Klein, Uhde, &tasteless and produces drowsiness, impaired motor skills, Post, 1986; Ries, Roy-Burne, & Ward, et al., 1989). Bus-and profound anterograde amnesia. Ultrasensitive techpirone has been utilized in treating benzodiazepine with-niques are available to detect this drug in urine and blood drawal symptoms, and unfortunately does not preventsamples in suspected rape victims (Anglin, Spears, & emergence of such symptoms although clinically it mayHutson, 1997). Flunitrazepam and GHB have become the be useful on its own merit to treat underlying anxietydrugs of choice for date rape situations, as they cause while benzodiazepine dosage is tapered. Use of shortdisinhibition and relaxation of voluntary muscles and term phenobarbital also has been advocated in the treatcause lasting anterograde amnesia for events that occur ment of benzodiazepine withdrawal symptoms. It is pre-under the influence of the drug. Alcohol potentiates these ferred to pentobarbital, which has its own spectrum ofeffects (Schwartz, Milteer, & LeBeau, 2000). One study dependence-producing effects (Martin, Kapur, Whiteside,in Sweden looked at male juvenile offenders who had used Rohypnol frequently and described its effects in producing & Sellers, 1979). Of equal concern in selected populations of drug-feelings of increased power and self-esteem, in reducing using individuals is the combined usage of benzodiaz-fear and and insecurity, and in providing a sense that all epines with alcohol or opiates. In both cases, additivewas possible. It was also associated with loss of episodic and synergistic respiratory depression is a constant memory and with impulsive violence, especially when threat, and tolerance to respiratory depression does not used with alcohol (Daderman and Lidberg,1999a). The develop for any of these substances (Jaffe, 1990). Recauthors felt that the drug should be classified as a Schedule ommendations from the American Psychiatric Associa-1 drug in Sweden and they also pointed out in a second tion’s Task Force Report (1990) on benzodiazepine prepaper (Daderman and Lidberg,1999b) that flunitrazepam scribing include avoidance of short half-life abusers became cold-bloded, ruthless, and violent and did preparations; discontinuance symptoms can appear even not remember their violent actions. They discussed how at ordinary therapeutic doses; the immediate discontinuflunitrazepam could exert profound effects on GABAance symptoms are felt to be a rebound presentation of ergic systems and thus lower serotonin levels, a state the original anxiety symptoms with more severe with-where impulsive execution of violent crimes, including drawal symptoms, including seizures, being manifesta-suicides have been well associated. A retrospective study tions of bona fide physical dependence; the onset ofin Prague of intoxicated poisonings over 4 years revealed withdrawal symptoms occurs sooner and is more pro-that Rohypnol was the second most common intoxicant nounced with short half-life preparations; tapering forutilized, after alcohol (Rath and Vever, 1998). A survey high-potency short half-life preparations should be per-(between 1995 and 1997) in Dade County, Florida, of formed very gradually with additional use of other sup-benzodiazepines detected in biological samples from drivportive medication as mentioned above. The task force ers arrested while driving under the uence infl (DUI) guidelines also noted interaction of benzodiazepinesshowed that 10% of the samples were flunitrazepam, but with alcohol, particularly in terms of daily tasks, such that these numbers fell dramatically after it became a as driving and effects on memory consolidation, and itSchedule 1 drug in 1997 (Raymon, Steele, & Walls, 1999).

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HALLUCINOGENS: LSD, MESCALINE, PSILOCYBIN,

Pain Management: A Practical Guide for Clinicians, Sixth Edition

because these are easier to manufacture illicitly than LSD itself. PCP goes by a wide range of street names, including AND PHENCYCLIDINE “angel dust, ” “crystal,” or “hog.” Pharmacologically, PCP Perhaps no other psychotropic substance has generated affects multiple transmitter systems, but in particular, more research and theoretical interest into the mecharesearch has shown that it may antagonize CNS actions nisms of mental dysfunction than lysergic acid diethyla-of N-methyl-d-aspartate (NMDA), and the receptor for mide (LSD). This and other substances produce psychePCP may actually be a part of an NMDA receptor complex delic effects with perceptual and sensory distortions as controlling calcium and other ionic channels as well as well as hallucinations. The discovery in 1943 of LSD’ s sodium and potassium voltage-regulated channels. This is psychedelic effects by Hoffman stimulated a wave ofakin to the GABA-benzodiazepine-chloride ion channel excitement regarding potential use of LSD as a modelreceptor on which benzodiazepines and other drugs are for schizophrenia and other mental disorders. In thethought to exert their effects (Jaffe, 1989). 1960s and early 1970s, the use of LSD-like substances, One particularly relevant pharmacologic effect of including psilocybin (extracted from mushrooms) andphencyclidine is its agonist effect at the σ opiate receptor mescaline (found in the peyote cactus), escalated tremensite. Why the actions of PCP at the σ receptor site overlap dously in U.S. society. The experimental use of thesewith its effects on NMDA receptors is uncertain. Multiple substances to heighten self-introspection and self-fulfi lllines of data suggest the possibility that activation of the ment created a strong scientifi c interest scientifi cally in σ receptor and NMDA receptor has differential effects on unlocking the mechanisms for the effects of these drugs sodium or potassium conductance, which may explain on CNS functioning. Resurgence of the pharmacologic some of the excitatory effects of NMDA itself (Jaffe, mechanisms of these substances yielded abundant evi1989). dence that LSD and other psychedelic substances interact LSD and PCP are generally used in short runs or with serotonin (5-HT) receptors as well as other neubinges, with profound exhaustion and lethargy following rotransmitter systems in the brain. Actions of psychemultiple doses of these drugs. In the case of PCP, it is delic substances were demonstrated in many brain areas, often smoked with marijuana or misused along with alcobut in particular, the 5-HT2 receptor was felt to be a hol and other drugs. Toxic psychoses and flashbacks can fundamental site of action of LSD. Other hallucinogens occur with all hallucinogens, and “bad trips” have been (e.g., mescaline) were found to have more profound seen in a small percentage of hallucinogen users. These effects on the locus ceruleus in the brainstem, and subcan include states of paranoid ideation and can occur stances that block norepinephrine and serotonin receptors were found to be useful in preventing the psyche-randomly despite repeated “good trips” in past usage of the drug. PCP, in particular, has been likened to a mild delic effects of hallucinogens (Jaffe, 1990). Use of phencyclidine (PCP) and other similar sub-psychosis resembling schizophrenia, and although globally chronic misuse of hallucinogens and PCP was less stances has supplanted older hallucinogens. It and some of the newer designer drugs, such as MDMA, DOET, andprevalent in our society in the 1990s than it was in the 1960s and 1970s, there does remain a small percentage of the like (see above), have a plethora of pharmacologic actions in the CNS. Phencyclidine was first developed inpeople who prefer to misuse these substances on a repeated basis. the 1950s as an anesthetic for animals, and related substances, such as ketamine (Ketalar), are still used occa- Acute treatment of hallucinogen and PCP toxic effects includes use of phenothiazines and dopamine- and norepisionally as anesthetics. Originally, about 10% of patients anesthetized withnephrine-blocking drugs. Treatment with a dopamine phencyclidine would exhibit a state of delirium and blocker may be necessary for a week or longer, as protracted disorientation and toxic psychosis can occur, in particular, aggressive behavior on emergence from the medication. after phencyclidine. One unusual property of phencyclidine Phencyclidine and some of its related substances have is its enterohepatic recycling, which can delay excretion of hallucinogenic, analgesic, CNS stimulant, and depressant ers have been used in the past actions simultaneously. They are bona fide intoxicants,the compound. Urinary acidifi to hasten renal excretion of the substance. producing slurred speech, nystagmus, and gait ataxia, MDMA (ecstasy) has been mentioned already (see together with numbness of extremities. Sweating, cataabove) and remains a current hallucinogen used by a small tonic postures, rigidity, and a blank stare are often fraction of mostly adolescent and college-age individuals. responses to larger doses of the drug. Bizarre behavior, It has mixed pharmacologic actions with CNS stimulant aggressive outbursts, and amnesia can occur. Distortion and psychedelic and hallucinogenic properties. The conof sensory input to the CNS occurs, and evidence of CNS stimulation with sweating, fever, salivation, and muscletinued wave of popularity of so-called designer hallucinogens continues unabated and will likely remain a problem rigidity are seen. On the street, most of what is passed off as LSD is actually phencyclidine or similar derivatives,in a small segment of the drug-misusing population.

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879

SOLVENTS

on proper pain control management techniques, and unfortunately, most pain is approached as if it were acute pain. Drugs of misuse in this category involve a bewilderingThus, practitioners prescribe opiates and other depenarray of anesthetic gases and organic solvents, including dence-producing medications for conditions that are in xylene, toluene, benzene, kerosene, and gasoline, together themselves chronic and not likely to benefit from repeated with pressurized propellants like freon and other fluoro-administration of drugs. This problem is seen by every carbons. Hexane and some its derivatives are known to chronic pain practitioner, regardless of the population of produce peripheral neuropathies as well as an agitated, patients he or she treats, and a great deal of effort, redidisordered, encephalopathic state. Profound visual hallurection, and patient retraining is mandatory in getting most cinations, feelings of derealization, “spaciness, ” and dischronic patients to undo the effects of iatrogenic depentortions in the sense of time all occur. Chronic glue sniff-dence on opiates for chronic pain or headache problems. ing, in particular, is fraught with long-term effects, It is equally curious to the author that terminally ill including an encephalopathy secondary to widespread patients who deserve pharmacologic support in relief of brain damage from chronic administration of the volatiletheir pain often are, paradoxically, undertreated with painsubstance. Often, inhalant users are extremely young in relieving medications, with the vain hope of sparing the age, generally come from low income populations, and doterminally ill cancer-ridden patient the additional burden not have easy an access to other CNS-active agents. Sniffof addiction to an opiate. This seems trivial at best and ing of glue or a solvent from a closed container, such as further underscores the general lack of familiarity with a paper bag, or “huf fing” of inhalants is performed gen- proper use of highly addictive substances in the setting of erally as a group activity, and often other substances, such pain control, particularly in terminal diseases. as alcohol, marijuana, and nicotine, are used concurrently. Treatment approaches to detoxification of codeine, There is no specific treatment for acute CNS effects ofmeperidine, and oxycodone preparations are generally these substances other than removal of the offending solaccomplished fairly rapidly, and rarely is severe opioid vent. Typically, chronic users of inhalants tend to be dullwithdrawal a protracted problem. Most detoxifi cation in their affect, exhibiting some of the long-term sequelaemeasures utilize progressively smaller dosages of either of subtle, but widespread, encephalopathic process. the same or less addicting opiates, and therapy is often Neuropsychological testing often confirms problems withsupplemented with anti-infl ammatories, antianxiety memory and problems with motor speed performance on agents, clonidine, and adequate attention to establishment subcategories of neuropsychological testing. of a structured sleeping regimen. Substitution of agents A recent study (Young, Longstaffe, & Tenenbein, like carbamazepine for chronically painful syndromes that 1999) looked at the relationship of inhalant misuse to theinvolve sharp and burning pain (e.g., reflex sympathetic use of other substances. This was a survey done in the dystrophy, sympathetically mediated pain syndromes, setting of a juvenile detention facility with 209 children causalgias, and sharp components of peripheral and other incarcerated over a 3-month period. The study obtained neuropathies) often allows adequate pain management epidemiologic data about mean ages of substance misuse without resorting to dependence-producing medications. of a number of drugs, including inhalants. Mean age ofThe greatest challenge for the pain practitioner is in reedinitial experimentation for inhalants was 9.7 years, asucating the patient not to reach for the next dose of analcompared to 11.9 years for marijuana, 12.0 years for alcogesic, and this particularly rings true in the treatment of hol inebriation, 11.2 years for cigarette use, and 13.2 to chronic headache sufferers. Behavioral reorientation, 14.7 years for the remaining substances (opiates, CNS training in biofeedbacking and stress management, and stimulants, and psychedelics). Thus, the implication isnonpharmacologic approaches to pain (e.g., cranial elecmade that inhalant misuse in early life may be associated trotherapy stimulation and transcutaneous electrical nerve with misuse of other substances. stimulation therapy) offer the potential for adequate pain treatment for chronic conditions. AND

IATROGENIC DEPENDENCE ERGOTAMINE DEPENDENCE

One of the many tasks of physicians who routinely treat chronic pain patients is the detoxification and redirectionOne relatively rare, but nonetheless important, source of of medication usage patterns for chronic pain or headache iatrogenic dependence occurs in the use of ergotamine to patients who have been allowed free access to opiatecontrol recurrent headaches. Daily use of ergotamine in containing preparations for relief of their symptoms. It isas low a dosage as 2 mg can lead to a cycle of dependence truly regrettable that more emphasis on proper pain manon the medication, and often escalating doses are needed agement techniques is not offered during the routine medto achieve the same headache-free state. In fact, Saper and ical school or house ficer of training phases of practitio- Jones (1986) found that ergotamine used more than three ners. In the author’ s opinion, too little emphasis is placed times per week may also predispose patients to the phe-

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nomenon of ergotamine dependency. The use of daily In closing, the author would like to quote a passage from Aldous Huxley (1970): ergotamine can create a situation whereby headaches rebound if ergotamine is not continually administered. Over time, dosage of ergotamine increases, and any …That humanity at large will ever be able to dispense attempts to lower the daily dosage result in prompt exac- with Artificial Paradises seems very unlikely. Most men erbation of the headache. After a time, only minimal or and women lead lives at the worst so painful, at the best transient improvement in the headache pattern is noted, so monotonous, poor, and limited that the urge to escape, the longing to transcend themselves if only for despite escalation of ergotamine dosage. In addition, treata few moments, is and has always been one of the ment of the headache using other medication approaches principal appetites of the soul. And for private, for often fails in the setting of ergotamine dependency. For- everyday use there have always been chemical intoxitunately, detoxification from ergotamine can be accom- cants. All the vegetable sedatives and narcotics, all the plished with the use of repetitive intravenous dihydroer- euphorics that grow on trees, the hallucinogens that gotamine (DHE-45), together with intravenous opiates ripen in berries or can be squeezed from roots — all, and sedative anxiolytics (e.g., lorazepam), and detoxifica- without exception, have been known and systematically tion management of the ergotamine withdrawal headache used by human beings from time immemorial. And to these natural modifiers of consciousness, modern sciwill usually occur in 4 to 7 days (Raskin, 1988). After a successful withdrawal from ergotamine, headaches cease ence has added its quota of synthetics (p. 62). to be a problem for some time, but the patient is at risk for return of headaches and, therefore, effective pharmaREFERENCES cologic measures must be instituted to prevent relapse into another cycle of ergotamine dependence. Abelson, H., & Fishburne, P. (1976). National survey — main findings: Nonmedical use of psychoactive substances. Springfield, VA: National Technical Information SerCONCLUSION vice. Anglin, D., Spears, K.L., & Hutson, H.R. (1997). Flunitrazepam This chapter has discussed basic pharmacologic princiand its involvement in date or acquaintance rape. Acadples, such as tolerance and physical dependence, provided emy Emergency Medicine, 4, 323–326. an overview of the many different categories of misused Arimany, J., Medallo, J., Pujol., A., Vingut, A., Borondo, J.C., drugs and their patterns of misusage, and outlined ele& Valverve, J.L. (1998) Intentional overdose and death ments of detoxification of patients from these drugs. More with 3,4-methylenedioxyethamphetamine (MDEA; likely than not, there always will exist personalities who “Eve”): Case report.American Journal of Forensic Medwill seek to misuse mind-altering substances, whether for icine and Pathology, 19, 148–151. purely recreational purposes or to attain internal states of Barrett, J.E. (1987). Nonpharmacologic factors determining the peace or euphoria, or to counter, likewise, inner states of behavioral effects of drugs. In H.Y. Meltzer (Ed.), Psydisquietude, anxiety, restlessness, and ennui. Whatever the chopharmacology: The third generation of progress (pp. 1493–1510). New York: Raven Press. specific reason for misusing a psychochemical, hopefully either substitution of licit medication or replacement of Barrionuevos, M., Aguirre, S., Del Rio, J., & Lasheras, B. (2000). Serotonergic deficits and impaired passive-avoidance drug use by other self-activating behaviors would, in large learning in rats by MDEA: A comparison with MDMA. measure, result in diminished misuse. A better understandPharmacology, Biochemistry, and Behavior,65, ing of basic pharmacologic mechanisms also would result 233–240. hopefully in availability of medications with a minimal Barry, J., Mead, K., Nabel, E.G., Rocco, M.B., Campbell, S., potential for production of tolerance and physical depenFenton, T., Mudge, Jr., G.H., & Selwyn, A. (1989). dence. Exciting new prospects in the neurobiology and Effect of smoking on the activity of ischemic heart disneuropharmacology of peptides in the CNS are emerging ease.Journal of the American Medical Association, 3, rapidly. Undoubtedly, mind-altering properties of neu398–401. ropeptides, too, will come to light and be exploited byBenowitz, N.L., Hall, S.M., Herning, R.I., Jacob, III, P., Jones, R.T., et al. (1983).New England Journal of Medicine, drug-using experimentalists, as has occurred with drugs 309, 139–142. discussed in this chapter. It may very well be part of human nature to want to change or alter sone’ sensorium, Bickel, W.K., Stitzer, M.L., Bigelow, G.E., Liebson, I.A., Jasinski, D.R., & Johnson, R.E. (1988). Buprenorphine: hopefully to a place that is more peaceful and less trouDose-related blockade of opioid challenge effects in bled, and thereby achieve a state of relative inner peace. opioid-dependent subjects. Journal of Pharmacology That so many diverse chemicals producing so many difand Experimental Therapeutics, 247, 47–53. ferent kinds of effects are all capable of achieving whatBolla, K.I., McCann, U.D., & Ricaurte, G.A. (1998). Memory is perceived as inner harmony speaks for the myriad impairment in abstinent MDMA (“Ecstasy”) users. Neuunderlying emotional needs of humankind. rology, 51, 1532–1537.

Drug Misuse and Detoxification

881

Busto, U., Sellers, E.M., Naranjo, C.A., Cappell, H., Sanchez-Hanson, G.R., Jensen, M., Johnson, M., & White, H.S., Distinct features of seizures induced by cocaine and amphetCraig, M., & Sykora, K. (1986). Withdrawal reaction amine analogs.European Journal of Pharmacology, after long-term therapeutic use of benzodiazepines. New 377, 167–173. England Journal of Medicine, 313, 854–859. Chang, L., Ernst, T., Grob, C.S., & Poland, R.E. (1999). CerebralHarrington, R.D., Woodward, J.A., Hooton, T.M., & Horn, J.R. (1999). Life-threatening interactions between HIV-1 (1)H MRS alterations in recreational 3,4-methyleneprotease inhibitors and the illicit drugs MDMA and dioxymethamphetamine (MDMA, “ecstasy”) users. gamma-hydroxybutyrate. Archives of Internal Medicine, Journal of Magnetic Resonance, 10, 521–526. 159, 2221–2224. Chen, J.H., & Goldstein, D.B. (1976). Science, 196,684–685. Cloninger, C.R., Dinwiddie, S.H., & Reich, T. (1989). Epidemi- Heishman, S.J., Stitzer, M.L., Bigelow, G.E., & Liebson, I.A. (1989). Acute opioid physical dependence in post-addict ology and genetics of alcoholism. Annual Review of humans: Naloxone dose effects after brief morphine Psychiatry, 8,331–346. exposure.Journal of Pharmacology and Experimental Cohen, S. (1982). Marijuana and youth: Clinical observations Therapeutics,248, 127–134. on motivation and learning, ages 2–11. Washington, Huxley, A. (1970).The doors of perception . New York: Perennial D.C.: U.S. Government Printing fice. Of Library. Colado, M.I., Granados, R., O’Shea, C., Esteban, B., & Green, A.R. (1999). The acute effect in rats of 3,4-methylene-Jaffe, J.H. (1989). Psychoactive substance use disorders. In H.D. Kaplan & B.J. Saddock (Eds.). The comprehensive textdioxyethamphetamine (MDEA, “Eve”) on body temperbook of psychiatry,5th ed. (pp. 642–686). New York: ature and long-term degeneration of 5HT neurones in McMillan. brain: A comparison with MDMA (“Ecstasy”).PharJaffe, J.H. (1990). Drug addiction and drug abuse. In A.G. Gilmacology and Toxicology, 84, 261–266. man, E. Goodman, T.W. Rall, & F. Murad (Eds.), The Daderman, A.M., & Lidberg, L. (1999a). Flunitrazepam (Rohyppharmacological basis of therapeutics, 8th ed. (pp. nol) abuse in combination with alcohol causes premed522–573). New York: MacMillan. itated grevious violence in male juvenile offenders. J. Jansen, K.L.R. (1999). Ecstasy (MDMA) dependence, Drug and Am. Acad. Psychiatry Law, 27, 83–99. Alcohol Dependency, 53 , 121–124. Daderman, A., & Lidberg, L. (1999b) Rohypnol should be clasJohanson, C.E., & Schuster, C.R. (1991). Animal models of drug sified as a narcotic. Lakartidningen, 96,1005–1007. self-administration. In N.K. Mello (Ed.),Advances in de la Torre, R., Farre, M., Roset, P.N., Hernandez Lopez, C., substance abuse: Behavioral and biological research Mas, M., Ortuno, J., Menoyo, E., Pizarro, N., Segura, (pp. 219–297). Greenwich, CT: JAI Press. J., & Cami, J. (2000). Pharmacology of MDMA in humans.Annals New York Academy of Sciences, 914,Jones, R.T. (1987). Tobacco dependence. In H.Y. Meltzer (Ed.), Psychopharmacology: The third generation of progress 225–237. (pp. 1589–1595). New York: Raven Press. Edwards, G., Arif, A., & Hodgson, R. (1981). Nomenclature and classification of drug and alcohol-related problems: A Klein, E., Uhde, T.W., & Post, R.M. (1986). Preliminary evidence for the utility of carbamazepine in alprazolam withdrawal. WHO memorandum.Bulletin WHO, 59,225–242. American Journal of Psychiatry, 143, 235–236. Ellinwood, E.H. (1979). In R.I. Dupont, A. Goldstein, & J.DonO’ Kreek, M.J. (1987). Multiple drug abuse patterns and medical nell (Eds.), Handbook on drug abuse (pp. 221– 231). consequences. In H.Y. Meltzer (Ed.), PsychopharmacolWashington, D.C.: U.S. Government Printingfice. Of Fielding, J.E. (1985).New England Journal of Medicine, 313, ogy: The third generation of progress (pp. 1597–1604). 555–561. New York: Raven Press. Fischman, M.W. (1987). Cocaine and the amphetamines. In H.Y. Langston, J.W., Ballard, P., Tetrud, J.W., & Irwin, I. (1983). Meltzer (Ed.),Psychopharmacology: The third generaChronic Parkinsonism in humans due to a product of meption of progress.New York: Raven Press. eridine-analog synthesis. Science, 219 (4587), 979– 980. Gerra, G., Zaimovic, A., Giucastro, G., Maestri, D., Monica, C.,Liljequist, S., Culp, S., & Tabakoff, B. (1986). Life Sciences, 38, Sartori, R., Caccavari, R., & Delsignore, R. (1998). 1931–1939. Journal of Pharmacology Serotonergic function after (+/-) 3,4-methylene- Luthin, G.R., & Tabakoff, B. (1984). and Experimental Therapeutics, 228, 579–587. dioxymethamphetamine (“Ecstasy”) in humans. InterMarks, M.J., Smolen, A., & Collins, A.C. (1984). Alcoholism national Clinical Psychopharmacology, 13, 1–9. Clinical and Experimental Research, 390–396. 8, Glennon, R.A. (1987). Psychoactive phenylisopropylamines. In H.Y. Meltzer (Ed.), Psychopharmacology: The third Martin, P.R., Kapur, B.M., Whiteside, E.A., & Sellers, E.M. (1979). Clinical Pharmacology and Therapeutics, 26, generation of progress(pp. 1627–1634). New York: 256–264. Raven Press. Grant, I. (1987). Alcohol in the brain: Neuropsychological cor- Mello, N.K. (1987). Alcohol abuse and alcoholism: 1978–1987. In H.Y. Meltzer (Ed.),Psychopharmacology: The third relates.Journal of Consulting and Clinical Psychology, generation of progress(pp. 1515–1520). New York: 55, 310–324. Griffiths, R.R., & Sannerud, C.A. (1987). Abuse of and depenRaven Press. Mello, N.K., & Griffiths, R.R. (1987). Alcoholism and drug dence on benzodiazepines and other anxiolytic-sedative abuse: An overview. In H.Y. Meltzer (Ed.), Psychophardrugs. In H.Y. Meltzer (Ed.). Psychopharmacology: The macology: The third generation of progress (pp. third generation of progress(pp. 1535–1541). New 1511–1514). New York: Raven Press. York: Raven Press.

882

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Mello, N.K., & Mendelson, J.H. (1980). Science, 207, 657–659. Saper, J.R., & Jones, J.M. (1986). Ergotamine tartrate depenMeltzer, H.Y. (Ed.) (1987).Psychopharmacology: The third gendency: Features and possible mechanisms. Clinical eration of progress . New York: Raven Press. Pharmacology,9, 244–256. Mendelson, J.H. (1987). Marijuana. In H.Y. Meltzer (Ed.), PsySaum, C.A., & Inciardi, J.A. (1997). Rohypnol misuse in the United States.Substance Use and Misuse, 32, 723–731. chopharmacology: The third generation of progress (pp. Schuckit, M.A. (1987). Biology of risk for alcoholism. In H.Y. 1565–1571). New York: Raven Press. Meltzer (Ed.),Psychopharmacology: The third generation Mendelson, J.H., & Mello, N.K. (1979). Biologic concomitants of progress(pp. 1527–1533). New York: Raven Press. of alcoholism.New England Journal of Medicine, 301, Sprague, J.E., Everman, S.L., & Nichols, D.E. (1998). An inte912–921. grated hypothesis for the serotonergic axonal loss Meyer, H.H. (1901).Archives of Experimental Pathology and induced by 3,4-methylenedioxymethamphetamine. NeuPharmacology, 46,338–346. rotoxicology,19, 427–442. Milroy, C.M., Clark, J.C., & Forrest, A.R.W. (1996). Pathology Schwartz, R.H., Milteer, R., & LeBeau, M.A. (2000). Drugof deaths associated with “ecstasy” and “eve ” misuse. facilitated sexual assault (“date rape”). Southern MediJournal of Clinical Pathology, 49,149–153. cal Journal, 93,558–561. Myers, J.K., Weissman, M.M., Tischler, G.L., Holzer, C.E., Leaf, Tabakoff, B., & Hoffman, P.L. (1983).Life Sciences, 32, P.J., et al. (1984).Archives of General Psychiatry, pp. 192–204. 959–967. Nishisawa, S., Mzengeza, S., & Diksic, M. (1999). Acute Tabakoff, B., & Hoffman, P.L. (1987). Biochemical pharmacology of alcohol. In H.Y. Meltzer (Ed.), Psychopharmaeffects of 3,4-methylenedioxymethamphetamine on cology: The third generation of progress (pp. 1521– brain serotonin synthesis in the dog studies by positron 1526). New York: Raven Press. emission tomography.Neurochemistry International, Tunnicliff, G. (1997). Sites of action of gamma-hydroxybutyrate 34, 33–40. (GHB) — A neuroactive drug with abuse potential. ClinO’Malley, P.N., Johnston, L.D., & Bachman, J.G. (1985). In N.J. ical Toxicology, 35,581–590. Kozel & E.H. Adams (Eds.).Cocaine use in America: Velea, D., Hautefeuille, M., & Vazeille, G. (1999). LantranEpidemiologic and clinical perspectives(NIDA Davoux, C., New synthesis empathogenic agents. Research Monograph, 1961). Washington, D.C.: U.S. Encephale,25, 508–514. Government Printing Of fice. Orleans, C.T. (1985). Annual reviews. In W.P. Creger (Ed.),Weil, A. (1972). The natural mind: A new way of looking at drugs and the higher consciousness . Boston: Houghton Annual Review of Medicine (pp. 51–61). Palo Alto, CA: Mif flin. Parrott, A.C. & Lasky, J. (1998). Ecstasy (MDMA) effects upon mood and cognition: Before, during and after a SaturdayWickler, A. (1980).Opioid dependence: Mechanisms and treatment. New York: Plenum Press. night dance. Psychopharmacology(Berlin), 139, Woods, J.H., & Winger, G. (1987). Opioids, receptors, and abuse 261–268. liability. In H.Y. Meltzer (Ed.), Psychopharmacology: Perlman, B.J., & Goldstein, D.B. (1984). Molecular PharmacolThe third generation of progress (pp. 1555–1564). New ogy, 26, 547–552. York: Raven Press. Peroutka, S.J. (1987). Incidence of recreational use of 3,4-methylenedimethoxymethamphetamine (MDMA, “Ecstasy”) Woods, J.H., Katz, J.L., & Winger, G. (1987). Abuse liability of benzodiazepines. Pharmacological Reviews, 39, on an undergraduate campus (Letter). New England 251–419. Journal of Medicine, 317 (24), 1542–1543. Post, R.M. (1977). In E.H. Elloinwood & M.N. Kilbey (Eds.), Young, A., & Herling, S. (1986). Drugs as reinforcers: Studies in laboratory animals. In S.R. Goldberg & I.P. Stolerman Cocaine and other stimulants (pp. 353–372). New York: (Eds.), Behavioral analysis of drug dependence (pp. Plenum Press. 9–67). New York: Academic Press. Rath, D., & Vever, J. (1998). Poisoning in patients treated during 4 years at the Metabolic Unit of the Second InternalYoung, G.S.J., Longstaffe, S., & Tenenbein, M. (1999). Inhalant abuse and the abuse of other drugs, American Journal Medicine Clinic of the Charles University Medical of Drug and Alcohol Abuse, ,25371–375. School in Prague, Vnitr Lek, 44,654–657. Raymon, L.P., Steele, B.W., & Walls, H.C. (1999). Benzodiazepines in Miami-Dade County, Florida driving under the influence (DUI) cases (1995–8) with emphasis on MONOGRAPHS AND GENERAL REFERENCES Rohypnol: GC-MS confirmation, patterns of use, psychomotor impairment, and results of Florida legislation. American Medical News , April 1982, p. 22. Journal of Analytical Toxicology, 23, 490–499. American Psychiatric Association. (1987). Diagnostic and staRies, R.K., Roy-Burne, P.P., Ward, N.G., et al. (1989). Carbamtistical manual of mental disorders (3rd ed.). Washingazepine treatment for benzodiazepine withdrawal. ton, D.C.: American Psychiatric Association. American Journal of Psychiatry, 146, 536–537. American Psychiatric Association Publications (1990). BenzoRobins, L.N., Helzer, J.E., Weissman, M.M., Orvaschel, H., diazepine dependence, toxicity, and abuse: A task force report of the American Psychiatric Association. WashGruenberg, E., et al. (1984). Archives of General Psyington, D.C.: American Psychiatric Association. chiatry, 41, 949–958. Bloom, F.E. (1989). Neurobiology of alcohol action in alcoholReuters Health Information Services, 10-27-2000, Deaths linked ism. Annual Review of Psychiatry, 8, 347–360. to 1,4-butanediol, a precursor to rave party drug GHB

Drug Misuse and Detoxification

883

Gilman, A.G., Goodman, E., Rall, T.W., & Murad, F. (Eds.). National Institute on Drug Abuse (1983). Highlights from the national survey on drug abuse: 1982. U.S. Department (1990).Pharmacological basis of therapeutics (8th ed.). of HHS-DHS-ADAMHA (DHHS Publ. [ADM] New York: MacMillan. 83-1277). Washington, D.C.: U.S. Government Printing Kaplan, H.D., & Saddock, B.J. (Eds.). (1988). Synopsis of psyOffice. chiatry, behavioral sciences, and clinical psychiatry: Psychoactive substance disorders (5th ed.). Baltimore: Raskin, N.H. (1988).Headache(2nd ed.). Edinburgh: Churchill Livingstone. Williams & Wilkins. Kaplan, H.D., & Saddock, B.J. (Eds.) (1989). Comprehensive Stahl, S.M. (2000).Essential psychopharmacology — Neuroscientific basis and practical applications (2nd ed.). Camtextbook of psychiatry (5th ed.). Baltimore: Williams & bridge: Cambridge University Press. Wilkins.

71 A Multi-Systems Approach to Behavioral Health and Pain Management Richard H. Cox, M.D., Ph.D., D.Min. whole systems within a holistic context that allows the This chapter approaches behavioral health from a systems point of view rather than the more traditional behavioralteam to transcend the skills of the individual’s discipline medical designation, because it is important to identifyand reach into the depths of who each is as a healing with a larger body of information and practice than simplyperson and who the patient is who wishes to be healed. The purpose of this chapter is not to be definitive in that of medicine. Further, the usual connotation of “multidisciplinary” is not used because that labeling implies theany area, but rather to further the holistic gestalt of the utilization of skills of more than one professional disci- healing enterprise. Healing is both an art and a science, pline. Each discipline is more than a body of knowledgewith no one discipline capable of claiming ownership to and an accumulation of skills. We live in a world of sys-any larger part than any other discipline. In the most precise definition of healing, all disciplines and techniques tems. Sociologists recognize at least six such systems: the are only adjunctive to the person who has the pain. Healing social system, the political system, the economic system, comes from within the organism, not from the technique the educational system, the religious system, and the domestic system. In addition and in permutations, otheror system providing the knowledge. All modalities, disciplines, and specialties assist in the process. More often systems obviously exist as well. A multi-systems approach to behavioral health allowsthan not, therapies speed the healing process, help the the essence of many systems to impact the immediate body’s systems to sort out their own mechanisms for situation. In this discussion we are concerned with therepair, and stop any further progress of inflammation, problem of pain management. Any one system offers parinfection, and degeneration. Rarely, if ever, is it possible tial answers; however, in many, perhaps most instances, to designate the specific therapy that single-handedly proeven several systems offer less than complete answers.duced It the results. is only in the understanding of multiple systems that we When the outcome of a diagnosis and treatment is positive, all disciplines stand in line to accept the credit; can even begin to understand the complex and vexing problems of pain. However, only the multi-system when the outcome is less than desirable, it is difficult to find a discipline that will accept responsibility. The conapproach offers the patient and the practitioner a method for dealing with what will frequently be less than what cept of “turf ownership” by professional disciplines has either had hoped would eventuate. It is not only thebeen a serious detriment to finding methods for the maninvolvement of several different disciplines working agement of pain. Turf ownership has meant economic and together on a healing team; it is the inherent philosophy,power brokerage; hence, the needs of human suffering have been sacrificed because of the unwillingness of the attitude, expectations, modeling, spiritual depth, and many more contributions of each participant. It is the value ofhealing disciplines to share their knowledge, admit that 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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they have a limited area of knowledge, and work withhas emphasized techniques to the near dismissal of philosophy. Only several thousands of years later and in the other professionals in a collegial fashion. The concept of “systems” is crucial in that every heal-light of increased technology and failed healing have ing philosophy builds upon a system that supports bothWestern healers (particularly allopathic physicians) been the ideation and the practice of that particular approach. willing to incorporate the behavioral aspects of healing For instance, Western medicine works within a system that into their practices. has become highly technical, political, and costly. As in In truth, the majority of medical practitioners still do not incorporate the psychological, environmental, socioall such healing-art systems, it is not possible to change only one part without disrupting the entire system. Some-logical, spiritual, and behavioral components of life into times it is easier and more effective to introduce a thirdtheir practices. The name of the game in current Western ” thus further segmenting the body player to integrate, sort out, and use parts of multiplemedicine is “referral, and the mind from the spirit. The patient is left to integrate systems as needed to arrive at a desired end. Alternative what differing specialists have prescribed, but ostensibly approaches to healthcare are the third party in human suffering at this time. The combination of many systems for-none of them practices. It is not uncommon for a patient merly not admitted into the healing-art circle have forcedto be tangled in a web of many specialists and suffering from polypharmacy and tremendous confusion, as well as Western medicine to examine its system. Further, and probably more importantly, medical practice in the United Stateshis or her basic illness. Although each specialist is highly trained, each operates within the same system; thus, the has been forced to listen to patients who are no longer willing patient does not escape the single-system approach even to trust and pay for the one-system approach. Eastern as well as Western, and all other healing syswhen seeking a second opinion or changing physicians. tems, are steeped in cultural determinants that are not Many methods and disciplines that deal with pain exist easily changed. Folk medicine systems are bound in but a are not always administered within the medical system history all their own. The behavioral health systemand do not necessarily follow the medical model. Behavapproach allows for picking and choosing from manyioral medicine was originated by L. Birk in 1973 in relation to biofeedback. In 1977 the term was further canonsystems rather than ascribing to any one system in its entirety. However, in order for this to happen, the teamized at the Yale Conference on Behavioral Medicine. The seminal work of Wilbert Fordyce (cf. Fordyce, 1976), leader and all participants must allow themselves a proutilizing operant conditioning and building on the historfessional degree of freedom and have a healthy enough personal ego to withstand the criticism that can beical work of Pavlov and Skinner, led the way for understanding the psychological underpinnings and emotional expected from their more system-bound colleagues. There is no intent in this writing to deny or diminish interactions of pain. Behavioral health is used in this disthe valuable contributions of all disciplines to the processcussion to emphasize an even larger concept, namely, that of attaining and maintaining health. However, all health,behavior is the key to any and all pain management proboth the attaining and retaining of such, is in the finalgrams. Understanding the interdisciplinary approach to analysis“behavioral.” The patient who will not think pos- pain means integrating all management around the firm itively, eat responsibly, exercise adequately, comply withacceptance that behavior is the major principle regardless health provider prescriptions, and at least to a minimalof the technique or theoretical approach. Three major extent take charge of his/her own life, cannot hope to attain innovations sparked the beginning of modern pain theory: health. By the same token, disciplines that by overt orbehavior modification, neuromodulation, and psychocovert action limit patients to one practice of healing mayneuroimmunology. The Western world is now ready and requesting be potentially harmful. Disciplines that do not recognize another innovation. Healing as practiced in this generation the behavioral aspects of health and healing sacrifice their patients’health to the ego of their profession. The simplehas proven that even with the remarkable advancements fact that all disciplines rely upon their patients to be com-of medical technology and scientific interventions, the of the population cannot avail themselves of these pliant demonstrates the foundation and essential nature majority of benefits. Cost factors, bureaucracy, mismanaged care, and behavior as the primary basis for healing. Western healing arts have been very slow to recognize inattention to the inner person have made modern healing the behavioral aspects of health and healing. Eastern sysa vocational trade rather than a professional practice. tems recognized them and built behavioral components Increasingly we have machines, laboratories, and techniinto their healing systems thousands of years ago. The cians to do what professional practitioners formerly did. difference lies within the focus of the art. Western healingNo one can say that medical science has not advanced. has focused upon the techniques and abilities of the healer. One can, and must say, that medical practice has become The patient has been an object that was given pills, operless face-to-face patient oriented. Thus, the behavioral ated on, treated, etc. Eastern healing has always beencomponent a of practice has suffered tremendously. Patients philosophy first and techniques second. Western healingno longer benefit from the wisdom of an experienced

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practitioner, but are subjected to the statistical, actuarial, • Marriage/family therapists • Clergy third-party pay organizations, whose basic interest is not in health but in profit. The behavioral component of healing builds upon the Although there are many practitioners of varied sorts within these groups, and some that do not easily fit into concept that healing is much more extensive and deeper than solving the immediate problem of pain or dysfunc-any group, for the most part, the mainline professions tion. Most ailments and complaints are not the health/ill-dealing with human pain of a nonphysical sort are those listed. ness issue itself but rather the results of that issue. Therefore, relieving symptoms doubtless decreases suffering but Likewise, there are more kinds of intervention than may not in truth bring about actual healing. In a multi- could be listed in a reasonable chapter; however, most modalities dealing with nonphysical pain (and systems approach symptoms are seen as the results treatment of dysfunction, not the dysfunction. Therefore, healing isoften physical pain) are much more than the alleviation of symptoms. • Pharmacology To unite the behavioral elements of healing would • Psychotherapy/counseling require a transformation of the Western mind, and a will• Biofeedback ingness to subrogate financial gain to the betterment of • Hypnosis/relaxation/guided imagery the individual. Social systems, philosophical ideation, • Desensitization teaching methods, curriculum renovations, administrative approaches, and far more than can be discussed in this • Group process • Psychodrama short chapter will be needed to allow behavioral systems • Psychoeducation to bring together what they could and should do. The art • Bibliotherapy and science of medicine in Western thought do not allow • Marriage/family therapy for the broadest holistic approach to healing. Larry Dossey, M.D. has helped us to see that healing at its deepest • Pastoral care • Social work interventions level is primarily behavioral and secondarily technique • Alternative approaches (see the Encyclopedia based (see Dossey, 1993). of Alternative Medicine ) We now await a marriage of the marvelous technology of healing to our knowledge of human persons as spiritual beings. Such a union could indeed bring the By far the most prevalent current method for controlscience and art of healing together. Actually, some smallling human behavior and any resultant pain (both physical signs of this happening exist in isolated instances. Inand emotional) is medication. Although the profession best trained to manage psychopharmacology is psychiatry, some places teams of healers are working together within the overwhelming preponderance of psychotropic media much more egalitarian system rather than in a pyramidal system with a physician at the top giving orders tocations are prescribed by nonpsychiatrist physicians. Clinical psychologists (trained in recent years) are very well the subordinates on the staff. Where systems exist with one profession on “ the top, ” the obvious and practiced equipped to manage psychotropic medication. However, even though the literature is replete regarding the superior approach is that one part of the human is more important efficacy of combined psychotherapy with psychopharmathan others. It is true that in an emergency situation the cology, few psychiatrists continue to practice psychotherhemorrhage must be stopped to save the patient’ s life; however, if the patient has no will to live, it may all be apy today. In the not-too-distant past psychiatrists practiced both prescriptive medicine and psychotherapy. to no avail. Relieving pain and building, maintaining, and restor-Psychologists, who are doubtless the broadest-trained proing health belong to many different disciplines. Likewise,fessionals in the area of human emotions, and who do continue to practice psychotherapy, are as yet unable to dealing with the pain that accompanies human existence is the bailiwick of many professions. Human pain can beprescribe. Doubtless this fact will change as public knowlclassified as physical, emotional/behavioral, and spiri-edge and demand reveal the benefits of the psychologist tual/existential. This chapter primarily addresses only theas a single behavioral practitioner, who can provide both psychotherapy and medication as well as have the skills emotional/behavioral and the spiritual/existential. Some of the major professions that most directlyto work within many healing systems. Now that psychiatry has moved into other areas, largely medicating the assume care for these areas are severely mentally ill, the masses of persons needing assistance with the emotional problems of normal living are • Psychologists left without a single service source. • Psychiatrists This leaves the management of human emotional pain • Social workers split among numerous professionals to deal with a single • Counselors

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emotional problem. Depression, probably the most prev-soon have prescription privileges. The American Psychoalent of all mental illnesses, is illustrative of this point. logical Association at the 1996 Convention in Toronto, Canada endorsed moving toward prescription privileges The psychiatrist prescribes an antidepressant medication and may or may not refer for psychotherapy, and thefor psychologists, and five states are currently entertaining potential legislation. psychologist provides psychotherapy and may or may not All healing professions are evolving and only the refer for medication. future will tell us which professions will practice cerPsychiatry is best described divided into three areas. Behavioral psychiatry attempts to deal with emotionaltain specific methods. Most of the helping professions pain by combining psychotherapy with medication, with are branching out into areas previously practiced by other disciplines, and more and more there is doubt the emphasis on psychotherapy and medication as an adjunctive support. Organic psychiatry manages primarilyabout the essential training needed for the practice of with psychotropic medications, usually without psycho-specific modalities. It seems that turf-building and turfmaintenance have been more important than the actual therapy, while placing the emphasis upon neurochemistry. A third area of modern psychiatry, cosmetic psychiatry,professional expertise required for the application of a actively attempts to modify the personality and the behav-specific modality. iors resultant therefrom entirely by psychoactive agents For instance, social workers and counselors are including methods of treatment, such as hypnosis, and the (see Hedaya, 1996). A well-rounded, holistic, human-attentive discipline use of psychological tests into their practices that were does not exist. The well-trained clinical psychologist isonce believed to be the domain of psychology and psychiatry. Optometrists now prescribe medications, optidoubtless the closest to such a model. The clinical psychologist who has been trained in a practitioner-orientedcians are vying for the right to do refractions and, in some instances, are performing opthalmological functions not model program is knowledgeable of social systems, learning systems, family systems, biological/physiological sys-previously allowed. Nurses routinely prescribe pharmacologic agents with physician supervision that is sometimes tems, psychopharmacological systems, a wide variety of very minimal. Pharmacists are moving toward prescription diagnostic systems, and a broad spectrum of treatment authority, opticians are gearing up for doing vision examsystems. Such a well-trained professional still needs to be incorporated within the team rather than attempting to beinations, psychologists are now training for psychotropic prescriptive practice, and use of nurse midwives is no “all things to all people. ” We need to clarify the difference between health andlonger debated in many communities. In many settings, registered nurse practitioners are for all practical purposes healing. Behavioral approaches have value in attaining today’s family doctors. Physical therapists do spinal and maintaining health. They also have a valuable place in the role of healing. Most health professionals are, inadjustments and joint manipulation, once the turf of the truth, mostly practicing symptom relief, i.e., a part of chiropractor. Most of these, and many more changes did not take place because of training, but rather grew out of the healing process. Behavioral practitioners, of course, need, economics, and political desires. In some instances, at times also practice only small parts of the process. mainline medical practitioners were unwilling to provide However, the literature shows that they are much more prone to refer their patients for the benefi ts of other services to underprivileged and rural populations. In most instances, the practice began before the fordisciplines than vice versa. Although patients dealing with physical pain fre- malized education and training. Educational programs and certification followed the establishment of the practice. quently expect to need the services of more than one health service provider, in the realm of emotional pain, relativelySuch was the history of midwives. In a similar instance, patients were shown to benefit from manipulation; howfew patients expect that they will need the services of more than one provider. Further, relatively few patients receiveever, chiropractors were not allowed on hospital staffs. Physical therapists were already on the staff and respected the services they need in the treatment of mental illness. Physicians under-utilize psychologists for psychotherapypractitioners in their field. Manipulation was a “natural” and psychologists under-utilize physicians for medicaland with training (sometimes quite minimal) manipulative/adjustment techniques were introduced. Many more management. Recent changes in insurance-based medical practice have prohibited many of the referral benefits pre-illustrations of how patient need has permitted and even viously practiced and which practitioners of all kinds mandated changes in the health service system exist. The purpose of noting these changes, and the many not menwould like to continue to afford their patients. The changing field of training and practice, combinedtioned, is that the pain management not only does not with the evolving landscape of healthcare, is producingbelong to one profession, but also nearly every profession dramatic and traumatic changes. As has been noted, psyis currently undergoing a tremendous metamorphosis in chiatry has virtually abandoned psychotherapy. Psychol-order to encompass more and more of the problem of ogists are now trained in psychopharmacology and may human pain.

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We must recognize that in the final analysis, it ispatient to continue to report its presence. At differing times in our history, we have identified psychosomatic, somatobehavior that counts in society. Humans have illnesses all of the time, but society is usually concerned only whenpsychic, allodynic, histrionic, and other forms of pain that behavior is impacted by pain and/or suffering. Differentmedical science could not diagnose by laboratory or physages held forth different expectations for what was con-ical examination. Finally, most practitioners now recognize that the single most valuable measurement of pain is sidered normal health. Furthermore, cultures, ethnicities, and even gender demand and allow differences in what that is reported by the patient, regardless of what the tests considered normal. Behavior is the key. It is the key tomay show. Thus, the labels ascribed to various pain experiences are not important. Behavior intervention is, what is considered acceptable and when the patient s experience and ends changes geographic location, religious beliefs, or evenbecause it starts with the patient’ with the patient’s experience. jobs, what is acceptable may change. Although we as individuals may care how others feel, in truth, we as Behavioral health systems offer the most effective methods for “entering the patient’ s experience” and helpsociety really only care about how people act, and more ing the patient to move out of it. Further, it is rarely specifically, how that action affects us as individuals. In the final analysis, behavioral health is exactly that:possible to determine what aspect of treatment actually the result. Many practitioners have found that behavioral health. Changing behavior can be done in produced a the techniques psychotherapists believe were helpful and variety of ways. Sometimes behavioral changes come what patients report were actually helpful are often very about due to internal thought process reorganizations. different. Although this type of dilemma makes statistiOther times the changes are due only to social demand cally controlled research dif ficult, patient benefi ts are and we behave in a given way to avoid the unpleasantness of society’s reaction to us. At other times, changes inwithout doubt. behavior come about due to physical and/or mental Behavioral health systems work best within a team setting. The reason they are spoken of as “systems” is that changes of a structural nature, e.g., the loss of a limb or the result of brain (or other) surgery. The most effectiveeach professional entity recognizes that the combination of several disciplines is greater than the sum of the parts. behavioral change occurs when the individual has reaPain management when left to disciplines that practice in soned through his/her actions and by cognitive choice has isolation leaves the patient as the coach of the team and determined to act differently regardless of how he or she often as the untrained captain of his or her pain. The might feel or think. patient is certainly primary and must be central to the Personality type and parameters of known past behavplanning and implementation of any pain management ior are important indices to the adaptation, use/misuse, program; however, pain management given to a team pracand eventual outcome of illness. Although the astute interviewing clinician may have excellent clues and insighttice combines the best of several disciplines, includes the into these factors, even with short- or long-term observa-patient, and equally important, provides a constant quality tion, psychological assessment utilizing validated psycho-control check on the total treatment. logical tests is the best single method to obtain documen- Whether the treatment method is problem-solving tation for diagnosis and intervention in the behavioralcounseling, insight-producing psychotherapy, or psychoneuroimmunology, the behaviorally oriented practitioner aspects of pain management. It was Hippocrates himself who said, “It is more important to know what sort of will insist upon: person has a disease than to know what sort of disease a 1. A thorough and complete history of the patient, person has” (quoted from Alternative Medicine,1995). including, but not limited to, the pain syndrome. Human behavior, including the management of This encompasses religious and spiritual pain, is best infl uenced by cognitive choices. The comaspects, developmental landmarks and ficuldif pliant, cooperative, consciously participating patient is ties, emotional problems, family concerns, certainly the best patient for helpingndfi solutions. All social history, medical history, occupational professions have recognized the value of cognitive history, family systems, and at times a genointervention in behavior. gram, as well as numerous other informational Thus, one common thread prevails throughout almost items that arise in the course of taking a comall the professions, and that is counseling of some sort. plete history. (Few practitioners obtain a careThe difference is whether the counseling is incidental (as ful, complete history, particularly in the in the case of most medical management) or primary (as patient’s own words rather only than from a prein the case of psychotherapy). printed form.) In most instances, pain cannot be effectively managed s pre-morbid and morbid personality. apart from patient cooperation. As we do not have accurate 2. The patient’ Frequently, psychological testing combined with methods to measure pain objectively, it is possible for the the social history and a careful initial interview physical cause of the pain to be removed and for the

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provide these data. Psychological testing is the most cost-effective method for obtaining information of this nature. The Beck Depression Scale, The Hardiness Scale, the 16PF, The Minnesota Multiphasic Personality Inventory, The California Personality Inventory, the Edwards Personal Preference Schedule, and many more tests can be utilized to assess the personality. Those mentioned are considered “pencil and paper” type. Other specific tests are known as “projective techniques, ” such as the Rorschach Psychodiagnostic Test, the Thematic Apperception Test, Kinetic Drawing tests, and others. Tests in trained hands show how personality factors may be of value in understanding the etiology, process, and treatment of pain. Psychologists are helpful in understanding the meaning of pain, the secondary gains of pain, and the perceived purpose of the pain in a patient. The patient’ s perception is imperative. Pain, after all, is measured by the patient’ s perception. Without understanding how the patient perceives his or her world, the treatment of pain may only be a laboratory experiment. The reader is encouraged to review the discussion by Materson in this book. 3. The medical/physical/laboratory examination and diagnosis. Care needs to be given to other than routine blood, urine, and fecal tests. Routine tests frequently provide routine results. Physicians tend to be skeptical of some of the newer alternative-type diagnostic procedures. Further, an old axiom in medicine is still true: “We will not find it, if we don’t remember to look for it.” Persons with chronic pain usually have been through every routine test known and every common disease entity has been explored. The alternative practitioner often is successful when the traditional one is not because other avenues are being explored and tests considered by the general medical community as out-in-left-field are being pursued. A patient was recently referred to one practitioner who was two years post-CVA with residual hemiparesis and significant depression. Prozac and other SSRI mediations were part of her polypharmacological management by a variety of physicians of different specialties, but her condition was worsening. The use of her right arm and leg was only slightly better after two years of physical therapy, and her depression was severe and sometimes suicidal. Psychotherapy combined with auricular acupuncture produced dramatic results very quickly as two

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practitioners worked together. Medications were brought into reasonable control, and her mood was stabilized, with only minor episodic depressions. She is now opening doors with her previously paralyzed hand, utilizing prehensile grasp, and remarkably improved in overall social functioning. She, as well as her primary care physicians, were afraid of trying alternative approaches. Dr. Norman Shealy’ s book, Miracles Do Happen(1995), testifies to the effectiveness of alternative approaches to pain management. Collaborative interviews and networking for diagnostic and treatment information and patient support. No individual practitioner can offer suffi cient help in the limited time available. The family (and at times other networking persons) needs to be seen as a primary resource for support. This means family education, inclusion in the treatment plans, in the actual in-home treatment, and follow-up. Pawlicki discusses the role of the family elsewhere is this book. In primitive societies, the patient’s family actually assisted the nursing, dietary, and housekeeping staff in hospitals. The emotional, hence healing, support given to the patient is clearly benefi cial, to say nothing of the cost factor. The willingness to experiment with different approaches. No one method of treatment suffices for all patients. Practitioners who are unwilling to entertain new ideas and new methods become disappointed in results. Patients who are unfortunately stuck with such practitioners suffer from stagnation and closedminded thinking. The emotional/existential aspects of human pain frequently require a deeply spiritual intervention. Although it does not require a clergyperson, frequently a clergyperson trusted by the patient can make early interventions very effectively. Rituals, symbols, and highly personal spiritual actions often produce healing. Further, every person has his or her own interpretation of the meaning of pain and why it is being endured. When a patient believes that pain is inflicted by God and must be endured for heavenly reward, it is very dif ficult to allow anyone to take away the pain and hence take away the reward for faithful endurance! Last, but far from least, listen to the patient. Early labeling does not help. Considering a patient psychosomatic is of no value. Early correct diagnosis is obviously of major importance;

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The more one studies psychoneuroimmunology, the more one is forced to recognize the spiritual aspects of healing, including the value and art of touch, attitude, transfer of energy, prayer, meditation, and truly wishing another well. Such aspects of healing are not possible within negative relationships. Researchers who have studied healing in other cultures have documented both the positive and negative effects of psychoneuroimmology as well as the effects of cultural expectation. Voodoo, shaThis is particularly true in regard to emotional pain. manism, and other psychic manifestations of culture, reliThe concept of behavioral health systems includes the gion, and ethnicity are not unreal because they are psychic. They are all the more real because they emphasize the concept of the person as part of a system which includes the family, neighborhood, school, church, club, commu-underlying behavioral systems that produce and alleviate nity organizations, and all other aspects of occupation,human suffering. When behavioral health systems are encouraged to society, and the world with which they are closely linked. One cannot overemphasize that to treat the person is work to in harmony, the outcome is always greater. To argue treat the system. To attempt to treat the patient withoutwhether the physical pain produces the emotional or vice versa, as is sometimes discussed, is immaterial. It is only reference to the system is to assume an overly powerful role and to think that the infl uence of a few minutes in when the practitioners of all parts of the human dilemma the practitioner’s office can overcome the infl uence of join the same team that answers to the problem of human the many hours during the week with family, friends, pain are found. Behavioral health systems are crucial in understanding, not necessarily explaining, the causes of and the community. Sometimes patients must be allowed to live with theirpain. As part of these systems, the behavioral health scipain until they are ready to give it up. The practitionerentist utilizes a vast array of techniques and is often the best-equipped professional to be the team leader. should not feel discouraged or that he or she has failed when patients do not overcome pain. The reward is real Suffering and pain are not synonymous. We may be for both the patient and practitioner when pain is relieved;better able to assist with suffering than with pain. Persons however, if the practitioner is successful in truly enteringat peace with themselves and those around them clearly the patient’s world, and if the patient establishes a healthysuffer less when in pain than those who are not. Pain is reduced or increased by one’ s perception of suffering. The relationship with the practitioner, healing has begun. narcotics used for pain control are linked to physiology. The meaning of the relationship must be underscored. Pain and suffering may or may not be linked at the same Patients learn to trust when there is genuine caring. time and/or in the same way to physiology. Suffering may Patients know if they are being treated as a person. Transnot be reduced simply by the alleviation of pain. Why ference and counter-transference cannot be avoided; they can only be controlled and utilized productively. Positivehumans suffer is an age-old question epitomized in the biblical book of Job and doubtless discussed long before transference is to be encouraged. The misuse of the transference phenomenon, which produces a transgression that of time. We do not hope for understanding of the philoboundaries, has unfortunately led to “throwing out thesophical, theological, existential, and other esoteric baby with the bath. ” The behavioral health system includes aspects of pain. We do, however, believe that although we the practitioner as an integral part of the system. Themay not know why we suffer, we can learn to suffer less and assist others in relieving at least some of their sufferpractitioner who wishes to be a technician cannot extend his or her own healing qualities. The patient will responding. Suffering, as distinguished from pain, is a learned to a relationship with trust and will respond to a technicianresponse, as is the lack of suffering. Suffering occurs both in the presence and the absence of pain. Behavioral as to any machine. Some therapists take pride in avoiding relationships.responses are not always explainable; however, they may To think that one does so is only a figment of the imagi-be understandable. We do need to remember that pain is nation. Whenever two persons meet, let alone workmany times a friend, in that without pain we could die together on pain, an automatic, unavoidable relationship without knowing we were even ill. Suffering has its values. is established. The question does not have to do with The lack of suffering for some, and in some cultures, is whether there will be a relationship; the question only hasin and of itself painful. To relieve one of suffering does to do with whether it will be a positive, healing one or anot guarantee the relief of pain, nor does the relief of pain negative, damaging one. Many practitioners employ theguarantee the relief of suffering. healing tools of their trade only to cancel out those benefits Pain must also be seen as a disease entity in and of with their poor interpersonal relationship ability. itself not simply the result of injury or illness. It is possible however, we must not lose sight of the many times that the early diagnosis is wrong, but a plan of treatment is in place and not easily interrupted to look for another diagnosis. Because pain is perceived, and perception is reality to the patient, only the patient can tell the practitioner what hurts, what is wrong, and frequently what needs to be done to correct it.

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that at times pain is the illness. Pain disrupts, brings about REFERENCES dysfunction, produces further illness, and is far more thanAnderson, U. (2000).Immunology of the soul. Winter Park, FL: a combination of symptoms that could be classified as a Synchronicity Press. Birk, L. (1973).Biofeedback: Behavioral medicine (p. 362). New syndrome. Pain, when diagnosed as a distinct illness, York: Grune & Stratton. requires a full and complete behavioral and medical team Burton, Goldberg Group. (Compiled by). (1995). Alternative medto intervene. Frequently, until pain is seen as the illness icine. Fife, WA: Future Medicine Publishing. rather than the results of an illness, permanent relief is not Dossey, L. (1993).Healing words.New York: Harper. possible. When pain is recognized as the illness, behavFordyce, W.E. (1976). Behavioral methods for chronic pain and ioral approaches are mandatory in unraveling the mystery illness. St. Louis: Mosby. of pain and suffering. Hedaya, R. (1996).Understanding biological psychiatry. New York: Norton. Shealy, C.N. (1995). Miracles do happen. Australia: Element Books.

Section X Legal Considerations

72 Promoting Ethics and Objectivity in the Medicolegal Arena: Recommendations for Experts Michael F. Martelli, Ph.D. and Nathan D. Zasler, M.D., F.A.A.P.M.&R., F.A.A.D.E.P., C.I.M.E., D.A.A.P.M. INTRODUCTION

flicts. Some are easily avoidable and tend to be associated with the unscrupulous practices of a few. Many others, howThe skills required for conducting medicolegal evaluationsever, relate directly to the medicolegal context itself, where too often exceed the expertise of the professional performthe adversarial nature of the legal process conflicts with the ing them. This certainly appears true in the personal injury scientific and therapeutic ethics of clinical treatment. arena, where promises of large financial settlements and This chapter explicates the professional standards and higher forensic reimbursement rates have resulted in a proethical responsibilities of forensic experts who conduct liferation of practitioners choosing this specialization. Too medicolegal evaluations, with an emphasis on the role of often, this occurs without having procured sufficient spethe expert in facilitiating objective evaluations that assist cific training in medicolegal evaluations and/or having demthe court in its decision-making process. onstrated expertise in a clinical specialty independent of forensic practice. It is perhaps more so the case for chronic pain treatment providers who are frequently called intoPROMOTING OBJECTIVITY AND medicolegal proceedings as an incidental and sometimes GUARDING AGAINST BIAS undesirable consequence of routine clinical treatment. Importantly, identifying and mitigating ethical conflicts Without exception, the guiding principle in forensic ethics is the expectancy that the scope and content of an IE, that arise within the medicolegal arena present a formidable challenge for even the most skilled of forensic experts. Clin-subsequent reports, and testimony offered in depositions and court proceedings would be the same regardless of ical training in medical and graduate schools has a customary who retained the professional in question (American and usually exclusive focus on training related to advocating for the patient’s well-being. In independent examinations (IE)Academy of Physical Medicine and Rehabilitation, 1992; conducted within medicolegal contexts, the distinguishingAmerican Medical Association, 1997; Committee on Ethfeature is a requirement for objectivity that requires dissolu-ical Guidelines for Forensic Psychologists, 1991). Howtion of the patient–doctor relationship in favor of a dispas-ever, frequent observations of significant disagreement among professionals, supported by preliminary survey sionate examinee–examiner relationship. Collaborative rapdata collected by the authors, indicate that lack of objecport and expectancies of trust and assistance are eschewed. tivity, or bias, is an all-too-frequent occurrence. The resulting disparity produces many inherent ethical con0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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an anonymous survey of brain injury service providers There are several common sources of bias, most of from two southeastern cities, degrees of medicolegal which can be addressed in terms of general professional involvement and degree and type of nonobjectivity among ethics. fellow professionals were estimated, along with requests for personality descriptors. Bias ratings showed strong COMMUNICATIONS IN THE FORENSIC EVALUATION positive association with the estimated degree of medicoClear communications of ethical standards (e.g., informed legal involvement. Further, bias was fairly evenly distribconsent) with both the attorney and examinee prior touted and discretely categorized into the three bias category commencement of the evaluation are prerequisites for options included on the survey: (a) plaintiff slant; (b) establishing ethical interactions that facilitate objectivity.defense slant; and (c) retaining attorney slant. Further, Examinations from treating clinician vs. the unique intentthere was some association between skeptical or suspiof the independent examiner, which produce wide discrepcious behavioral traits and compulsive tendencies with ancies in terms of the type, scope, and time requirements practitioners perceived to have diagnostic biases more of the evaluation, should be clarified with the examinee.compatible with defense attorney interests/medicolegal Explaining that opinions regarding diagnoses, prognoses, involvements (i.e., defense expert). Histrionic or hypoand/or recommendations will not be shared directly shouldchondriacal and sympathetic personality traits were more be included. The policy of asking the examinee to sign an associated with practitioners perceived to have diagnostic informed consent form, with a witness present, is anbiases more favorable to plaintiffs (i.e., plaintiff ’s expert). increasingly adopted policy to be considered. Full apprisalDescriptions relating social finesse and flexible morals, in of the retaining attorney should also define the scope and contrast, were associated with practitioners perceived by extent of the services rendered. These issues will be disreputation as attorney’ s experts (i.e., agree with the retaincussed in greater detail below. ing side, whether defense or plaintiff). Importantly, a particular medicolegal specialization THE “PROFESSIONAL” EXPERT WITNESS can be presumed to result in continued reinforcement of Experts who derive a large part of their income (i.e., 50%)the same traits that served as a predisposition to the spefrom medicolegal evaluations may be at special risk forcializations, further reinforcing bias. Notably, the only compromised objectivity. Medicolegal work incurs fees protection against bias concerning pressures relating to that are substantially higher than regular clinical fees, withhigh reimbursement rates and personal biases is the insistence on striving toward a local reputation for being fair generally much greater reimbursement. Significant pressures to maintain continued highly lucrative medicolegaland objective (i.e., a “straight shooter”). referrals exert pressure to offer opinions consistent with Bias also can be associated with exclusive attorney the views of retaining attorneys, whose primary motiva-referral patterns. Many attorneys will avoid situations where there is consistent use of the same experts because tion is client advocacy. Importantly, courts and attorneys usually preferof the appearance of bias. Nonetheless, the medicolegal black/white opinions and eschew practitioners with lesscommunity is not without examples of professionals who simplistic diagnostic and conceptual viewpoints. Practi-have been the sole forensic experts for the entire caseload tioners can be subtly reinforced while garnering muchof an attorney over the course of several years. Probitive higher reimbursements (vs. standard clinical fees) byquestions during voir dire (i.e., questioning of an expert to establish the scope and depth of his or her expertise employing a more dichotomous and simplistic (and easier) adversarial ethic vs. a scientific (more laborious) ethic inprior to being accepted as an expert) frequently address their opinions that are solicited (and paid for) by attorneys.such questions, along with financial arrangements associated with forensic practice, etc. As is often the case, experts who are strongly invested in medicolegal practice will have an unequal weighting of referrals from defense or plaintiff attorneys, and inETHICS IN CONDUCTING extreme cases experts may completely exclude one of MEDICOLEGAL EVALUATIONS these two groups. Further, professionals, like others, only As a group, physicians pledge to uphold the Hippocratic have not biases, but also personal styles better suited for oath, which directs that first and foremost, they do no some settings than others. Based on results of previous ethics surveys (Pope &harm. Licensed psychologists, although they take no oath, Vetter, 1992; discussed below), observations of local pracby virtue of privilege of license, adhere to professional titioners, informal surveys and subsequent formal surveys ethics mandating that they promote the welfare of their conducted as part of an ethics review project, some prepatients, according to formal, professional, ethical guideliminary inferences were offered by the first two authorslines published by the American Psychological Associa(Martelli, Zasler, & LeFever, 2000a). Based on results oftion (APA) and any regulatory state statutes (American

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Psychological Association, 1995). The common threadEXPERTISE AND QUALIFICATIONS IN MEDICINE implicit in all professional interactions is doing no harm AND PSYCHOLOGY to patients and others to whom the expert has responsibility. This ideal extends to professional work in the medi-It has been previously noted that formal guidelines describing the qualifications to serve as an expert witness colegal community. In a membership survey of the American Psycholog-are only recently being developed. General Principle A of s Ethical Code ical Association (APA), randomly sampled psychologiststhe American Psychological Association’ were queried regarding ethical concerns in clinical psy-for Psychologists (1995) implicitly addresses this issue: chological practice (Pope & Vetter, 1992). Forensic psyPsychologists strive to maintain high standards of comchology ranked as fth fi among the 23 categories of reported incidents of ethical dilemmas behind confidenti- petence in their work. They recognize the boundaries ality, dual relationships, payment concerns, and teach- of their particular competencies and the limitations of ing/training concerns. Major concerns included presenta- their expertise. They provide only those services and use only those techniques for which they are qualified tion of false testimony, the attorney’ s role in procuring by education, training, or experience. desirable (potentially false) testimony, rendering of conclusions not grounded in objective data or scientific prinThis principle is especially relevant to guidelines ciples, and harm from reporting inaccurate data in forensic developed by Binder and Thompson (1995), which cover cases. Truly bitter language (e.g., “whore”), however, was issues related to maintaining awareness of the relevant reserved for descriptions of psychologists perceived as neuropsychological literature, seeking rigorous peer willing to present false testimony in court and/or who review to ensure competence, limiting practice to boundsuccumb to alleged attorney pressures or inducements for aries of competence, and seeking consultation as approthis kind of testimony. priate. Parallels certainly can be applied to physicians A more recent membership of the National Academy involved in the same process. of Neuropsychology (Brittain, Francis, McSweeney, In 1996, the American Medical Association published Fisher, and Barth, 1997) revealed concerns from the its Code of Medical Ethics through its Council on Ethical majority of 456 respondents regarding examiner compeand Judicial Affairs (AMA, 1997). Although this docutence (64%), inappropriate use of tests (61%), and conment is relatively general, it does stipulate that “medical flict between the law and ethics (55%). Further, 50% experts should have recent and substantive experience in opined that the APA ethics code was insuf ficient to address ethical problems in neuropsychology, while 57%the area in which they testify and should limit testimony ” The code also notes expressed dissatisfaction with the ability of ethics boardsto their sphere of medical expertise. that the “medical witness must not become an advocate to enforce guidelines. or a partisan in the legal proceeding. ” Additionally, it Clearly, such issues concern professionals practicing encourages witnesses to inform attorneys of “…all favorin the forensic and medicolegal arenas, the legal system, able and unfavorable information developed by the phyand those entities that make policy concerning training sician’ s evaluation of the case. ” and certification for professional competency. Unfortunately, most physicians and psychologists acknowledge There have been numerous other specialty organizathat they receive insuf ficient formal training or education tion publications dealing with recommendations for expert with regard to ethics in medicolegal/forensic situationswitness testimony. The American Academy of Physical s Board of Governors and that guidelines for ethical medicolegal practice haveMedicine and Rehabilitation’ approved a “white paper” on expert witness testimony in been lacking (Martelli, Zasler, & Grayson, 2000). April 1992. Central to these guidelines is the concept that Problematic situations are inevitable when medical the expert witness functions to educate the court as a and psychological ethics are brought into the courtroom, whole, as opposed to “representing either of the parties where adversarial client advocacy is the rule. Appreciation involved, even though the expert witness may have been and sensitivity to the potential disparities between concontacted primarily by one party. ” The guidelines note that flicting interests and ethics seem the most logical approach the ultimate test for accuracy and impartiality is a willto protecting the ethics and objectivity of medical and psychological examiners while affording the courts andingness to prepare testimony that could be presented unchanged for use by either the plaintiff or defendant. its representatives benefit of their expertise. In the current Further review of this document reveals several recomchapter, relevant ethical issues are reviewed in order to mendations which warrant attention: (1) the physician illustrate ethical behaviors as they relate to many common aspects of medicolegal situations. Although some of theshould identify opinions which are personal and not necessarily held by other physicians; (2) a distinction should current dilemmas described are unique to the interaction be made between medical malpractice and medical malof the American legal and healthcare systems, most have international relevance. occurrence when analyzing any case; and (3) there should

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be a willingness to submit transcripts of depositions and/orwould seem to promote standardized practice of neuropsychology while also providing a measure of quality courtroom testimony for peer review. Especially relevant are guidelines that have beencontrol for those who conduct neuropsychological assessadopted by the American Academy of Neurology andments for forensic cases. developed by the American Board of Medical Specialties The second standard regarding subject matter compefor the physician expert witness, which include the fol-tency proscribes the offering of opinions outside areas of a professional’ s competence. In addition, it requires conlowing two standards: tinuing active clinical practice in the area relevant to expert 1. The physician expert witness should be fully testimony, for 3 of the previous 5 years from the date of trained in a specialty or a diplomate of a spe- testimony. The failure to define level of “active clinical cialty board recognized by the American Board practice” might seem somewhat problematic, although by of Medical Specialties, and qualified by expe- implication, greater vs. lesser levels of active practice rience or demonstrated competence in the sub- would be more consistent with this principle. Consistent ject of the case. The specialty of that physician with APA Standard 1.05, which states that “psychologists should be appropriate to the subject matter in … maintain a reasonable level of awareness of current scientific and professional information, ” Binder and the case. Thompson (1995) offer that psychologists should remain 2. The physician expert witness should be familiar with the clinical practice of the specialty or the aware of general trends in the relevant neuropsychological subject matter of the case at the time of the literature, use up-to-date neuropsychological tests and occurrence, and should be actively involved in norms, rely on current knowledge, consider important the clinical practice of the specialty or the sub- demographic characteristics of individuals in making ject matter of the case for three of the previous interpretations, and acknowledge limitations in current knowledge. An ability to discuss relevant research literafive years at the time of the testimony. ture, accurately, and without notes, would be an obvious The preceding guidelines are frequently cited as ameasure of this ability. An additional issue with regard to identification of useful model for guiding expert witness qualification in clinical neuropsychology (Lees-Haley & Cohen, 1999).good expert witnesses in the area of evaluating persons With regard to the first standard, however, it should bewith neurologic disability relates to credibility. Aside from noted that standards of training in neurology are consid-the issues discussed above, it should be noted that many practitionersflaunt multiple certificates hanging on their erably easier to demonstrate than in neuropsychology. walls. However, for many organizations, these certificates Standardized medical school curricula, standardized residencies approved by the American Board of Medical Spe-represent little more that “vanity” boards, where eligibility cialties to insure common standard compliance, writtenrequirements are hardly stringent. The integrity of the examinations of basic medical information for individuals individual should, in part, of course, be measured by the with degrees from foreign medical schools, and eligibilityquality of the organizations they belong to, and the thorto sit for board specialty certification examinations all oughness of the inclusionary process for each organization. Relevant questions include whether the certifying exist as clearly demonstrable criteria. Clinical neuropsychology, as a profession, has been organizations required the individual to take some type of making greater efforts toward standardization of training,oral and/or written test, what other inclusionary criteria but given greater variability, has tended to rely even morewere employed, whether attendance is required at a certain strongly on board eligibility as an independent criterionnumber of approved courses per year, whether the orgawith which to evaluate education, training, and experience.nization is the primary certifying organization, and so on. The APA Division 40 definition of a clinical neuropsy- Inquiries about manner of receipt of board certifications chologist describes prerequisite training while suggestingand diplomates are important, given that certifying orgathat the attainment of the American Board of Professionalnizations and clinical specialty boards may have, in their Psychology (ABPP)/American Board of Clinical Neurop- earlier years, allowed “grandfathering” in of persons who sychology (ABCN) diploma is the clearest evidence ofwere not required to meet current inclusion requirements. s publication record, as competence as a Clinical Neuropsychologist (Division 40 Examination of the individual’ Executive Committee (1989). More recently, training well as the types of publications should be assessed. Relevant questions would include whether the articles were guidelines have been defined and accepted by professional organizations in neuropsychology (Hannay, Bieliauskas,published in peer-reviewed publications, and their recognized quality. In addition, lectures in one’ s claimed area Crosson, Hammeke, Hamsher, & Kof fler, 1998). Based on these training guidelines and definitions,of expertise should be reviewed, as should the organizaLoring (1995) proposed board eligibility as the training tions for whom they have lectured, with an emphasis on standard for expert witness consultations. This requirement looking for those that are nationally or internationally

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recognized. It is also important to critically examine anrequired by an expert witnesses. As such, the presence expert’s qualifications based in part on clinical, scientific, of a preexisting relationship should usually eliminate consideration of serving as an expert witness in the case academic, and administrative positions held, and the manner in which they gained appointment (e.g., the individ-where any other expert is available. It should be noted that this mandate is often at odds with the conceptualual’s historic performance, a voting process, or some less ization of experts in the legal community, where treating “ selective process). Martelli, Zasler, and Grayson (1999) have attemptedclinicians” are often considered to be more credible to summarize the relevant criteria by which professionalexperts from the standpoint that they have more familiarity with the patient. expert competence can be evaluated. These have been adapted for psychologist and physician specialists in Perhaps the only exception might occur when no other is or can be made available, or where declining to chronic pain assessment and treatment are included expert in serve as an expert witness might produce resultant harm Table 72.1. As can be seen, they are heavily borrowed to the patient from deprivation of needed service that from ethics in psychology. A qualifications checklist is included for the general knowledge/competency (again,outweighs threats to objectivity. In such cases, prudence borrowed primarily from psychology). In addition, a would mandate documentation in the report of both the selected qualifications checklist is included for Chronicpreexisting relationship and procedures and safeguards Pain Specialists. Finally, an Expert Opinion Compe-employed in order to facilitate the highest possible levels tency/Credibility Weighting summary list is offered, of objectivity. This should, of course, be balanced against which represents a preliminary framework for evaluatingpotential compromise of the therapeutic relationship if the patient did not receive the desired expert testimony and/or relative credibility of expert witnesses. opinions supportive of the patient’ s legal claim. In an effort to elucidate ethical confl icts due to DUAL/MULTIPLE RELATIONSHIP CONSIDERATIONS potential multiple relationships of medical professionals Multiple relationships potentially constitute an ethical engaged in standard medicolegal practice, Blau (1984; dilemma in the medicolegal context. For example, as indi-1992) differentiated the following professional roles: (1) cated in APA Ethics Code, Section 1.17 (1995): “ Treating Doctor, ” who has a special (usually empathic) bond with his/her patient, and whose role is to describe Psychologists must always be sensitive to the potential the everyday treatment procedures that were employed, harmful effects of other contacts on their work and on and not offer opinions beyond those contained in their those persons with whom they deal. A psychologist reports, or perform evaluations on the basis of anything refrains from entering into or promising another perother than medical necessity; (2) Expert “ Witness, ” who sonal, scientific, professional, financial, or other relawithout prior knowledge of the examinee obtains special tionship with such persons if it appears likely that such and extraordinarily complete information and for whom, a relationship reasonably might impair the psycholoin order to promote objectivity, no bond with the examgist’s objectivity or otherwise interfere with the psyinee is permitted; (3) Trial “ Consultant, ” whose funcchologist effectively performing his or her functions as a psychologist, or might harm or exploit the other party. tion, consistent with the adversarial process, is to assist with critical scrutiny and impeachment of experts and There is a strong tradition in clinical psychological opinions from the opposing side. As Blau notes, these practice relating to proscription of both developing per-roles represent different interests and obligations. Failsonal relationships with persons who are current or former ure to set limits and avoid mixing of the confl icting clients, or providing psychotherapeutic services to persons interests inherent in these contrasting roles would with whom a prior personal relationship exists. Clearly,undoubtedly reduce objectivity and compromise the this prohibition is intended, in the former situation, to opposing welfares of the different parties to whom obliprotect a patient from potential exploitation in a relation-gations are maintained. ship predicated on equal status by someone who main- Unfortunately, in a frequently observed occurrence by tains, or previously maintained, a relationship based on the authors, treating clinicians accept invitations to serve as higher power or skills and dependency. In the latter case, “ expert” witnesses when other professionals are available. the purpose is guarding against problems stemming from Although understandable, this practice is nonetheless probthe preexisting relationship obligations and biases con-lematic. This practice is appealing to attorneys for several flicting with the prerequisite objectivity required by a psy- reasons, including ease, as the professional is already chologist for effective diagnosis and treatment. involved; inherent time and/or cost savings to the patient The latter protection is most relevant in medicolegaland his or her legal representative; and the advantage of work. Consistent deliberate opinion exists that a preex-natural advocacy inherent in clinician– patient relationships. isting professional relationship would represent a poten-The problems include mixing of usually incompatible roles. tial conflict of interest that interferes with the objectivity The fact that this frequently occurs may be explained by

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TABLE 72.1 Summary Guidelines for Evaluating Professional Expert Qualifications Professional Expert Qualifications Checklist: General • Knowledge Competence Base (derived from APA Ethics and P.M. &R. White Paper): ❑ Remains aware of general trends in the relevant neuropsychological literature and incorporates current knowledge into ractice. regular p ❑ Uses up-to-date neuropsychological tests and norms and considers important demographic characteristics of individuals in making interpretations. ❑ Appropriately acknowledges limitations in current knowledge. ❑ Seeks rigorous peer review to ensure competence. ❑ Can discuss relevant research literature accurately, without notes. ❑ Limits practice to boundaries of competence, seeking consultation as appropriate. ❑ Is fully trained in a specialty or has earned a diplomate of a specialty board in spacialty area (i.e., Pain Management), and is qualified by experience or demonstrated competence in the subject of the case. ❑ Is familiar with the clinical practice of the specialty or the subject matter of the case at the time of the occurrence, and has been actively involved in the clinical practice of the specialty or the subject matter of the case for three of the previous five years at the time of testimony. Professional Expert Qualifications Checklist: Chronic Pain • Professional Organizations: • (A) Current Memberships • (B) Current Committee Memberships ❑ American Academy of Pain Management ❑ American Pain Society ❑ American Academy of Pain Medicine ❑ International Association for the Study of Pain ❑ Canadian Pain Society ❑ World Institute of Pain ❑ State or regional chronic pain associations ❑ Special national associations with significant pain management components (e.g., American Chiropractic Association, Assoc. for Applied Psychophysiology and Biofeedback) ❑ Am. Psychological Assoc: Division 22 (1/2 point) ❑ American Academy of Physical Medicine and Rehabilitiation (1/2 point) • Specialty Conference Attendances: • (A) # Attendances at Last Three Meetings of…? • (B) # Presentations at Last Three Meetings of…? ❑ American Academy of Pain Management ❑ American Pain Society ❑ American Academy of Pain Medicine ❑ International Association for the Study of Pain ❑ Canadian Pain Society ❑ World Institute of Pain ❑ State or regional dedicated Chronic Pain Conferences ❑ Conferences of specialty national associations with significant pain management components (e.g., American Chiropractic Association, Assoc. for Applied Psychophysiology and Biofeedback) ❑ Am. Psychogolical Assoc.: Division 22 — Rehab. Psychology (1/2 point) ❑ American Academy of Physical Medicine and Rehabilitation (1/2 point) • Professional Journal Familiarity: • (A) Do You Currently Subscribe to…? • (B) Have You Read ”“.(Latest Issue Article in)…? ❑ American Journal ofPain Management ❑ Clinical Journal of Pain ❑ American Journal of Pain ❑ Pain ❑ Cephalgia and/or Headache ❑ Current Review of Pain ❑ Cranio: The Journal of Craniomandibular Practice ❑ Archives of Physical Medicine and Rehabilitation (1/2 point) ❑ The Pain Clinic (1/2 point) ❑ The Pain Practitioner (1/2 point) ❑ Any Specific Pain related newsletter (1/2 credit per) ❑ What specialty dedicated chronic pain assessment and treatment books do you own? (author, pub. date) • Specialty Area Clinical Treatment Experience (last 2 years/lifetime): ❑# Clinical Patients Personally Treated (excluding assessment; ≥ 5 h total time) ❑# Clinical Patients Personally Assessed (not technician; ≥ 4 h total time)

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TABLE 72.1 (CONTINUED) Summary Guidelines for Evaluating Professional Expert Qualifications • Publication Record (last 3 years/lifetime): ❑# Publications in Recognized Specialty Journals ❑# Publications in Books in Specialty Area ❑# of Editorial Positions with Specialty Journals or Organizations ❑Recognized quality of the work • Presentations and Talks in Area of Expertise (last 3 years/lifetime): ❑# Lectures in Specialty Area ❑# Lectures at Relevant National or International Specialty Organization Meetings ❑# of Clinical, Scientific, Academic, and Administrative positions held ❑Manner of gaining appointments in positions held Additional Disability Evaluator Qualifications Checklist may be Relevant EXPERT OPINION: COMPETENCY/CREDIBILITY WEIGHTING (Last 3 Years Total Score and/or Last Year Total Score) _____ Professional Organization Memberships _____ Professional Meeting Attendances _____ Professional Meeting Presentations (Total #) _____ Professional Journal Subscriptions, Reading (Total #) _____ Specialty Direct Clinical Treatment Experience _____ Publication Record _____ Talks and Presentations in Relevant Area of Expertise _____ Relative Competence/Credibility Score

examiners. At a time when insurance reimbursement the typically greater emphasis in professional ethical codes to proscription of confl icts between professional and non- severely restricts payments, it would seem naive to think fi is an professional roles and activities than between differing pro-that attorney satisfaction with examinerndings irrelevant factor in the development of referral decifessional roles. Strasburger, Gutheil, and Brodsky (1997) argue that these confl icting professional roles should be sions, formal referral relationships, and/or social relainfl and adopavoided by offering the patient’ s treatment record in lieu of tionships. Subtle test-interpretation uences tion of adversarial and dualistic tendencies (e.g., testimony. That is, they recommend that treating doctors either–or, black–white) in interpretation of ndings fi may maintain strict role boundaries as fact witnesses and decline to perform the functions of an expert witness. In otherbe operative both above and below the level of expert words, treating clinicians ideally should provide testimonyexaminer or witness awareness. Such subtle threats to objectivity would seem especially likely in cases of only as fact witnesses, and decline expert witness actvities such as reviewing the reports or depositions of other wit-greater ambiguity in either test results, behavioral observations, and/or responses on measures of motivation and nesses. In situations where testifying as an expert witness response bias. cannot be avoided, they should acknowledge the inherent Importantly, the process of a consulting call to the conflicts in both testimony and reports. examiner from the referring plaintiff or defense attorney With regard to the relationships between attorneys and health practitioners, contrasting professional motivationsto discuss initial findings and favorability to the case often and standards produce frequently confl icting interests. represents an invitation to join the client–attorney team. fi additional paid Financial incentives, which are well-recognized threats toDepending on favorability of ndings, may be scheduled with the expert regarding objective patient reports, deserve equal consideration asconsultations a threat to to medical practitioners. Given the discrepancymethods of presenting findings and invariably, juxtaposing the findings against opposing counsel arguments. This between the adversarial client advocacy of attorneys, and the dispassionate, objective scientific ethics required ofpractice represents a subtle but incremental team invitation. This veiled invitation to join the client–attorney team physicians and psychologists, concern must necessarily be seems much less subtle when the issues of validity of raised when one considers that attorneys are the usual findings become equated with winning in court by a favorreferral source, payers, and consumers of examination able jury or judge ruling. findings and reports from experts. Moreover, medicolegal evaluations tend to be con- Another important influence of an adversarial legal ducted by a limited number of professionals in the com-process is the reinforcement of dichotomous opinions. munity, which fosters the development of social rela-Uncertainties, shades of gray, and reservations are usually tionships between referring attorneys and medicolegalnot conducive to an adversarial process and are often

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eschewed in the legal process. Our experience confirms ETHICAL ISSUES IN CONDUCTING AND the expectancy that the initial selection of an expert isINDEPENDENT EXAMINATION influenced by reputation and history with regard to the expert’s tendencies to think in “black and white” vs. Informed Consent “shades of gray” and/or to find single causes vs. multipleWithin the context of the actual examination, full disclodeterminants of behavior. Much less obvious are the tensure regarding the purpose of examination, as well as the dencies for social reinforcement and subtle increases and tests and procedures being utilized, is required to optimize decreases of interest or ego approval to potentially influ-examinee compliance. Examiners must be careful about ence opinions in borderline situations. such disclosure in order to promote a balance between For example, in the case of ambiguous clinical find-accurately representing the purpose of the testing to the ings where an opinion of either malingered or valid testexaminee, without increasing distrust in a process that is, results is rendered in an attorney consultation, an initiallyby its legal nature, adversarial. tenuous endorsement could inappreciably become As previously noted, many evaluations conducted strengthened by confirmatory bias. That is, the tendency from more traditional clinical referral sources and not to selectively considered evidence in accordance withoriginally performed as medicolegal evaluations become existing bias could be fueled by the clinician’s underlyingpart of subsequent litigation proceedings. This is espediscomfort with expressing opinions that appear uncertaincially true in cases of injury and impairment. The medicoor displeasing to the retaining attorney. legal context clearly imposes special obligations and With regard to the current healthcare environment,responsibilities for the medical professional. With regard Martelli, Zasler, and Grayson (1999) noted that currentto psychologists, relevant professional ethical principles managed healthcare organizations and practices leave have been elaborated. many physicians, psychologists, and other healthcare Section 1.21 of the APA Principles (1995) states: professionals feeling diminished. Their expertise, opinions, and recommendations are questioned, while their When a psychologist agrees to provide services to a services are constrained. Medical necessity has been person or entity at the request of a third party, the redefined by bottom-line business accounting that pays psychologist clarifies to the extent feasible, at the outset greater attention to cost-effectiveness demands, of the service, the nature of the relationship with each increased accountability, and a low-leniency, cost-cut- party. This clarification includes the role of the psycholting atmosphere. At the same time, reduced insurance ogist (such as therapist, organizational consultant, diagnostician, or expert witness), the probable uses of the coverage and reimbursement create pressures to maintain service provided or the information obtained, and the accustomed standards of living by identifying new fact that there may be limits to confidentiality. income sources for healthcare providers. Clearly, medicolegal work represents one of the last unregulated fron- Informed consent guidelines have been provided by tiers. The lucrative attorney referral-driven medicolegalJohnson-Greene, Hardy-Morais, Adams, Hardy, and arena clearly poses a real economic opportunity that not Bergloff (1997) for neuropsychological evaluations. only offers financial incentives, but also ego expertiseThey recommend that neuropsychologists explain fully enhancements, which signify pressures for bias that to all patients in language that can be easily understood ranges from subtle reinforcement of adversarial- andthe purpose of the examination, the reason for referral, dualistic-oriented opinions to shaping of perspective. Asand any limitations of confi dentiality. In medicolegal such, the typical healthcare professional should assume evaluations it is also important to indicate who will that the maintenance of scientific objectivity will neces-provide feedback about results, or explain that the cirsarily be difficult. cumstances of the independent evaluation dicate that no In a proposed remedy, Brodsky (1991) offers an inter-feedback is provided. esting recommendation for protecting medical profession- These ethical principles and related guidelines are als from mixing the disparate responsibilities of scienceprobably more easily observed for evaluations conducted and adversarialism. Brodsky offers objectivity an quotient at the request of the plaintiff ’s attorney, who functions as that equals the number of cases in which there is agreepatient advocate and usually has communicated the purment with the referring attorney, divided by the total num-pose and potential benefit of the evaluation. In addition, ber of cases. He suggests that base rate and referral difthe manner in which feedback will be provided is ference be acknowledged and offers a preliminary cut-offexplained. Requests for independent evaluations from point of 0.8 or greater for suggesting preexisting bias. The defense counsel, however, may be more challenging, given present authors consider this a somewhat liberal cut off, that the referral from the opposing attorney promotes and suggest a maximum of 0.75. greater distrust, especially when the examinee is informed

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regarding the nature of the assessment, the examiner’ s to fear of adversarial or biased procedures from the examrelationship to the opposing attorney or insurance com-iner, with or without reason, or attempts to collect as much pany, and information that feedback will not be providedinformation as possible to build stronger adversarial arguments to impeach opposite opinions. directly to the examinee. Available Guidelines and Assessment Procedures It has been observed previously that court orders sometimes have permitted attorneys and/or legal representaIn the medicolegal examination, documentation regarding tives to sit in on independent evaluations. In such cases, the evaluation and all procedures administered is usually the independent evaluation process is potentially cor-closely scrutinized by opposing counsel and his/her team rupted as an additional and uncontrolled factor is added of experts. Consequently, tests and assessment procedures that may influence examinee behavior and performance.selected for medicolegal circumstances usually represent Less invasive, but possibly still disruptive, is videotap-measures with a stronger research database, greater acceping of the independent examination. Probably least dis-tance within the profession, and more established history ruptive, although still possibly a threat to the integrity of use in the courts. With regard to psychology, selection of of the process, is the practice of audio taping of inde-such tests refl ects, in part, anticipation of attacks on the pendent evaluations. scientific validity of psychological instruments. Section 2.07 An additional ethical threat is posed when test materialof the APA Ethics Code (1995) states: and examination procedures are revealed. Unprotected disclosure of assessment instruments and examination (a) Psychologists do not base their assessment or intervention decisions or recommendations on data or test procedures potentially reduces the validity of such proceresults that are dated for the current purpose, and dures in future assessment situations with other persons (b) Similarly, psychologists do not base such decisions and, hence, potentially compromises the greater welfare or recommendations on tests and measures that are of the public at large. obsolete and not useful for the current purpose. With regard to psychological and neuropsychological tests instruments and procedures, task force committees Examiners are expected to use up-to-date tests and of the APA have issued reports with specific guidelines norms, rely on current knowledge, consider important intended to limit the disclosure of tests, in order to protect demographic characteristics of individuals in making the integrity and security of test materials, and to avoid interpretations, and acknowledge limitations in current misuse of assessment techniques and data (American Psyknowledge. Examiners are cautioned to interpret test chological Association, 1996). Notably, one of the tenets results carefully if experimental procedures are utilized or of the independent examination is that the examiner contests are used with individuals for whom normative data veys only information that was garnered within the context are not available. of the exam, does not alter exam findings in any way, and does not document things that did not occur. At a less Report Content and Related Issues tangible level, the independent examiner’ s role is to make objective clinical interpretations and inferences based on Necessary and usual parts of a comprehensive assessment dispassionate logic that is devoid of personal interest or physician examiners should use for any examinee include interests of others. In contrast to the attorney, who explic-the following: examinee demographic details; referral itly advocates as an adversary for his or her client, the source and party responsible for payment; basis of report; examiner should function only as an advocate for the truth. documents requested and reviewed, including those not Too often, however, the adversarial nature of courts, legal received; history of present illness; past medical history; proceedings, and attorneyscreeps” “ into the scientific family medical history; psychosocial history; educational arena and introduces a significant and powerful threat to history; vocational history; military history, if applicable; objectivity that can produce bias in persons purportedlylegal history, if applicable; review of systems; comprehenfunctioning as scientists. When creeping adversarialismsive exam findings, including pertinent negative findings; (Martelli, Zasler, & Grayson, 2000b) inflitrates the exam-diagnostic impressions; opinions regarding maximal medinations and opinions of scientists, distrust generated by ical improvement (MMI); causality and apportionment systems adhering to adversarial principles only increases. opinions; recommendations and relevant appendices. Of course, the nature of these systems dictates that they Specific information relevant to opinions should idemust attempt to discredit even the most objective scientifically be delineated when reviewing documents that procedures and ndings. fi Demands to be present andserved as the basis of the report. This provides documentation that not only were the records reviewed, but observe independent examinations may be either reactive Third-Party Observers

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also demonstrates a more deliberate analysis of the Ethical Considerations when Submitting Reports information, temporal relationship of complaints to any Ethical considerations clearly proscribe altering exam injury in question, analysis of symptom profi le in correlation with the type of injury or impairment being findings, or documenting things that did not occur. They also proscribe leaving out, or altering, potentially salient claimed, consistency of reporting over time, ndings fi suggestive of neurologic recovery pattern over time (orinformation from forensic or other reports. Further, the failure to address, and logically explain, inconsistent lack thereof), and clear delineation of inferential reainformation or findings, reduces credibility and invites soning, among other purposes. suspicion of bias. It should also be considered important to acknowlThe matter of issuing draft reports prior to the final edge potentially relevant information that was unavailreports poses an interesting dilemma that represents a able or not provided. For example, as is more often the potentially great danger to objectivity and ethical concase for defense-related evaluations, examiners may not duct. By introducing an opportunity for review and be given an opportunity (or make an effort) to interview comment, attorneys or other interested parties may corroboratory witnesses; this can be frustrating to legitissue requests for changes. Requests issued from attorimate examiners trying to do a thorough and objective neys or referring parties for changes to reports, often evaluation. for “ legal purposes”(e.g., to clarify technical points As part of the analysis of information and examinafor the court) or to clarify grammar, may represent a tion findings, an examiner’ s report should ideally slippery slope that leads to nonobjective input and posinclude (a) an evaluation of the appropriateness of the sible influence regarding other aspects of the examinadiagnostic testing procedures and process; (b) an estition findings and report. Recommendations that seem mate of the reliability and validity of thendings fi that prudent include avoiding draft reports under all circumserved as a basis for impairment claims; (c) an estimastances, and in order to avoid temptation or suspicion tion of degree to which the measures used were specifi c of impropriety, adopting a policy of refusal of any and sensitive to the condition being examined; as wellrequested report changes, except for correction of notaas (d) the degree of confi dence in interpretations and ble grammar or information errors. In the case of true opinions offered. Inherent in such testing should beand significant errors occurring in the context of the evaluations, both from a physical, as well as mentalreport, or where important clarifi cation of information standpoint, of response bias. is clearly relevant, three options can be advised: (1) Notably, many examiners feel uncomfortable com-attach an amended page to the report; (2) simply mark menting on the testing procedures and/or conclusions through (with a line) the incorrect portion of the report, of other clinicians. Objective assessment requires glo-without deleting or whiting out, and insert the correct bal analysis of opinions. This type of commentary isinformation; (3) produce a corrected version and docinherent in performing an adequate and comprehensive ument that it is an updated version and the rationale evaluation of any case. Meticulous evaluation of pre-for its production, while maintaining the original verinjury problems, including prior treatment, medical, sion with all other examinee records to produce upon psychiatric, and otherwise, developmentalficulties dif request. (e.g., attention defi cit disorder, or hyperactivity in As previously noted, sharing examination results school), psychoemotional problems during childhood,with the examinee are clearly proscribed by existing and learning disabilities, among other variables, mustethical guidelines and recommendations, as well as legal all be evaluated within the context of the clinical pre- statues in most states. Signing of an informed consent, sentation. Prior injuries, surgeries, and past use of mednoting the potential dangers associated with sharing the ication should be assessed, as should the frequency and information and/or report directly with the examinee, is severity, as well as functional signifi cance, of any com- increasingly recommended as standard procedure. It is plaint that is being claimed post-injury that also wasalso recommended that examiners have a disclaimer at present pre-injury. the end of a report which generally reiterates the basis The individual’s legal history, including police of the report and the opinions as germane to the expert’ s records, should be requested and reviewed, as this may qualifications and training, and the fact that all opinions have an impact on understanding current behavior. A hisare given with m “ edical probability, ” unless otherwise tory of certain types of legal problems may make an examstipulated. Finally, it is also advised that examiners iner more suspicious of some reported symptoms; noneinclude a statement that their conclusions are based, in theless, ethical imperatives require that the examiner part, on the assumption that the materials provided for remain unbiased, complete an objective assessment, and review are true, correct, and complete, and that if more not assume that individuals with certain types of back-information becomes available at a later date, opinions ground do not incur legitimate injuries. may be subject to change.

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Arrive at opinions only after reviewing all of the evidence from both sides of the adversarial RECOMMENDATIONS FOR EXPERTS fence, employing multiple data sources, completing an unbiased evaluation, and interpreting Providers of medical information and testimony have ultidata within the full context of comprehensive mate responsibility for ethical conduct as it relates to this historical, behavioral observation, and contexinformation. The authors offer the following recommentual information. Being otherwise favorable to dations for purposes of enhancing ethical relationships the retaining attorney’ s interests suggests between expert clinicians and the courts. endorsement of “opinion prostitute, ” “scientific perjurer,” or “hired gun” status (Martelli, Avoid or resist attorney efforts at enticement to Zasler, & Grayson, 2000b). The only way a join the attorney– client team. Such compropractitioner can reduce the likelihood of facing mises of scientifi c boundaries and ethical prinan “opinion prostitute” on the opposing side in ciples exist on a continuum ranging from stanfuture cases is to insist on establishing and dard attorney– client advocacy at the beginning maintaining a reputation for scientifi c objectivity. of the expert consultation phase (e.g., promoBalance cases from plaintiff and defense attorneys. tional information when rst fi retaining an Predilection for one side or the other suggests expert, with either provision of selective or bias and sets up predisposition to nonobjectivincomplete records or less than enthusiastic ity. For example, a preponderance of plaintiff efforts to produce all records) and extending work suggests a bias toward overdiagnosis to completion of the evaluation, when requests and/or uncritical sympathy, while a ratio that for changes in reports and/or documentation favors hiring by the defense suggests an undermight be made. diagnosis or skepticism bias. Perhaps Brodsky’ s Respect role boundaries and do not mix conflicting (1991) suggested cutoff ratio of 0.80 for roles. Remember that the treating doctor posfavorability findings (or our recommended ratio sesses a bond with the patient, but does not as of 0.75) would represent an initial cutoff for a rule obtain complete pre- and post-injury defense vs. plaintiff ratio. That is, experts information in the context of assessing causality should do at least 25% of their work for the oppoand apportionment. In contrast, the expert witsite side of the current case being represented. ness must conduct a thorough and multifaceted Further, it might be a reasonable expectation that case analysis sans the physician–patient reladata on these ratios be collected as an important tionship in order to facilitate objectivity and method for considering the objectivity of opinallow optimum diagnostic formulations. ions. Finally, the trial consultant’ s function in this Ensure against excessive favorability to the side of adversarial process is to assist with critically the retaining attorney or rm. fi Objectivity scrutinizing and attacking positions of experts demands that scientific opinions not be influfor the opposing side. These roles all represent enced by the position of the legal advocate. inherently different interests, and mixing them Importantly, Brodsky (1991) recommends can only reduce objectivity. using a ratio of 0.8 as a cutoff for detecting Insist on adequate time for thorough record review, excessive bias. That is, practitioners should posevaluation and report generation, and preparasess prerequisite objectivity to disagree with the tion for deposition and court appearances. referring attorney at least 20% of the time. We Work at building a reputation for general objectivity suggest that a more useful cutoff would be 0.75, and fairness, as well as reliance on multiple data where experts are expected to generate ndings fi sources, reaching opinions only after reviewing that do not support the referring attorney’ s posicomplete information from both sides and comtion at least 25% of the time (Martelli, et al., pleting an unbiased evaluation. 2000b). Spend a good part of your time actually treating the Never arrive at opinions that are inconsistent with patient population being examined or about plaintiff records, exam data, test data, behavwhom you are offering testimony. This treatioral presentation, etc., especially when such ment should be current, and with a comparable opinions are favorable to the side of the retainfrequency to that of treating practitioner speing attorney firm. Instead, always: cialists. Maintain the ability to discuss relevant Consider or mention, in reports and discussion, research and scientifi c methodology issues information not supportive of expressed opinions, including historical or behavioral obsercompetently and without notes.

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vation information; exam and test findings; discrepancies between plaintiff’s complaints and observed behavior and/or history; discrepancies between the severity of the injury and the severity of the reported symptoms; discrepancies between opinions and known occurrence rates (or base rates) in the general population; opinions and logical arguments of experts from the other side of the case, presented fully and in an objective manner. Strive to demonstrate objectivity by disputing the opinion of other experts only through a complete and deliberate logical dispute of a full and complete representation of the other expert’s findings, inferential reasoning, and conclusions. Always assess response bias and make efforts to guard against motivational threats to valid assessment. Avoid cutting corners, be thorough, and rely on standardized, validated, normed, and well-accepted procedures and tests. Limit use of technicians and non-M.D.s or nonPh.D.s for evaluation and testing. Intensively assess the client being evaluated, use only appropriate normative data for comparisons (e.g., persons of similar education or age; comparisons to medical patients vs. psychiatric patients), take into account the symptoms’ base rates (i.e., how frequently the symptoms occur in the general population and in the absence of the injury being evaluated), consider the many other explanatory factors for symptoms (e.g., medications, sleep disturbance, depression, etc.), and adjust the interpretations according to medical conditions (e.g., inherent somatic complaints of progressive disorders like M.S. and Parkinson’s and chronic pain), relevant situational variables (e.g., attention and other deficits correlated with chronic pain conditions, fatigue, insomnia/sleep deprivation), cultural factors (e.g., rural impoverished backgrounds) etc. Attempt to devise and employ a formalized quality assurance system that allows for monitoring and assessing (and improving) the validity and reliability of diagnostic and prognostic statements against real world findings. A formalized peer review system or similar mechanism that routinely allows for feedback from peers should be pursued. Always prepare examinees by emphasizing the importance of accurate/honest performance with full effort on all interview questions, exam-

ination procedures, and tests (e.g., to produce valid and reliable profiles that permit comparison with known symptom patterns). Further emphasize the liabilities associated with exaggerating impairments (e.g., producing invalid profiles, lower the credibility, suspicion of malingering of all symptoms). Recognize the limitations of medical and psychological data and opinions, and how, in science and medicine, few findings and symptoms are black and white, clean, or attributable to a single event (e.g., Occam’ s Razor). Increase attention to issues relating to scientifi c methodology, objectivity, maintenance of scientific rigor. Consider promoting increased awareness within the forensic professions of relevant issues relating to ethics and scientific objectivity. Promote utilization of objective data, such as Brodsky’ s (1991) ratio, in regular clinical practice, and recommend adoption of similar standards by local, state, and national professional organizations. Reinforce those who collate such data. Provide relevant information, including opinions and observations from known experts, as well as copies of relevant information such as this chapter, to colleagues. Promote issues relevant to legal use of medical and scientific evidence and testimony by encouraging courses in law school and programs offered by state bar associations and at annual trial lawyer and other association meetings.

REFERENCES American Academy of Physical Medicine and Rehabilitation (1992). Expert witness testimony. White Paper. American Medical Association, Council on Ethical and Judicial Affairs (1996–1997 edition).Code of medical ethics: Current opinions with annotations. Washington, D.C.: American Medical Association. American Psychological Association (1995). Ethical principles of psychologists and code of conduct. Washington, D.C.: American Psychological Association. American Psychological Association, Committee on Legal Issues (1996). Strategies for private practitioners coping with subpoenas or compelled testimony for client records or test data.Professional Psychology, 27, 245–251. Binder, L.M., & Thompson, L.L. (1995). The ethics code and neuropsychological assessment practices. Archives of Clinical Neuropsychology,10(1) 27–46. Blau, T. (1984).The psychologist as expert witness. New York: John Wiley & Sons.

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Loring, D.W. (1995). Psychometric detection of malingering. Blau, T. (1992). The psychologist as expert witness. Presented Paper presented at the annual meeting of the American at the National Academy of Neuropsychology annual Academy of Neurology, Seattle, WA. meeting, Reno, NV. Brittain, J.L., Francis, J.P., McSweeney, A.J., Fisher, J.M., &Martelli, M.F., Zasler, N.D., & Grayson, R. (1999). Ethical considerations in medicolegal evaluation of neurologic Barth, J.T. (1997). Ethics in neuropsychology: Where injury and impairment.NeuroRehabilitation: An Interare we now? Workshop presented at the annual meeting disciplinary Journal,13(1), 45–66. of the National Academy of Neuropsychology, Las Martelli, M.F., Zasler, N.D. & Grayson, R. (2000a). Ethics and Vegas, NV. medicolegal evaluation of impairment after brain injury. Brodsky, S.L. (1991). Testifying in court: Guidelines and maxIn M. Schiffman (Ed.),Attorney’s guide to ethics in ims for the expert witness. Washington, D.C.: American forensic science and medicine.Springfield, IL: Psychological Association. Charles C Thomas. Committee on Ethical Guidelines for Forensic Psychologists (1991). Specialty guidelines for forensic psychologists.Martelli, M.F., Zasler, N.D., & Grayson, R. (2000b). Ethics and medicolegal evaluation of impairment after brain injury. Law and Human Behavior, 15(6), 655–665. In M. Schiffman (Ed.),Attorney’s guide to ethics in Division 40 Executive Committee (1989). Definition of a clinical forensic science and medicine , Springfield, IL: neuropsychologist.The Clinical Neuropsychologist, 3, Charles C Thomas. 22. Hannay, H.J., Bieliauskas, L.A., Crosson, B.A., Hammeke, T.A.,Martelli, M.F., Zasler, N.D., & LeFever, F.F. (2000). Preliminary consumer guidelines for choosing a well-suited neuropHamsher, K. DeS., & Kof fler, S.P. (1998). Proceedings sychologist for evaluation and treatment of acquired of the Houston Conference on Specialty Education and brain injury (ABI). Brain Injury Source, (44), 36–39. Training in Clinical Neuropsychology. Archives of ClinPope, K.S., & Vetter, V.A. (1992). Ethical dilemmas encountered ical Neuropsychology, 13 . by members of the American Psychological Association: Johnson-Greene, D., Hardy-Morais, C., Adams, K.M., Hardy, A national survey. American Psychologist,47(3), C., & Bergloff, P. (1997). Informed consent and neuro397–411. psychological assessment: Ethical considerations and proposed guidelines.The Ethical Neuropsychologist, Strasburger, H., Gutheil, T.G., and Brodsky, B.A. (1997). On wearing two hats: Role conflict in serving as both psy11(4), 454–460. chotherapist and expert witness. American Journal of Lees-Haley, P.R., & Cohen, L.J. (1999). The neuropsychologist Psychiatry, 154 ( 4), 448–456. as expert witness: Toward credible science in the courtroom. In J.J. Sweet (Ed.), Forensic Neuropsychology. Lisse: Swets & Zeitlinger.

73 Business Side of Pain Management Devona Slater, C.M.C.P. The clinical side of pain management is only half the When trying to fill a position in the clinic it is best to battle. In today’s environment being paid for the profes-define the position and set a salary scale before considersional services you perform can be as complicated as ing any one person for a position. Many practices make treating your most complex pain patient. There is athe mistake of knowing “Sally” is the perfect employee wealth of information you must know that really should because she is a friend or used to work for a competitor. be classified as nonclinical but is just as important as the No one sits down and objectively looks at whether clinical information. Business expertise related to pain“Sally’s” skills match what is needed to accomplish the management is a necessity for every practice. You must job in the clinic. Choose staff wisely and avoid filling a recognize that if you do not run the business, the business position with “just a warm body. ” Finding the correct will run you. This chapter is a place to start building personnel will make your job easier down the line and your basic business skills. patience is important in making the selection. After finding that perfect employee it always amazes me how little training physicians give to staff on how they PERSONNEL, STAFFING, AND want the practice to run. Employees will generally live up MANAGEMENT STYLES to expectations set for them, but rarely succeed when no The first step in determining your staf fing is to look real- expectations are communicated. Orientation and training istically at the needs for your practice. A general rule offor each employee are very important steps to make the thumb for pain practitioners would be three or four staffclinic operate smoothly. Personnel files are an essential per physician, depending on your mode of practice. Theelement of any business and should be treated as confifirst two individuals would cover administrative duties dential information. Documentation in employee files is s medical chart. including, but not limited to, scheduling, answering as important as documentation in a patient’ phones, booking appointments, medical records, billing,The file should contain a current résumé, an emergency contact, specifi c tax forms (i.e., W-4 & I-9 and state insurance collections, credentialing, personnel administration, and accounting functions. If billing, accounting, or employment), signature sheet from compliance and policy payroll is outsourced, personnel will be reduced. You maymanuals, a current job description that lists expectations, need one clinical individual to start with, expanding to performance evaluations, salary history, incident reports, two or three as your practice grows. Clinical personneland any other personal information gathered regarding the employee. Please be aware that incident reports and pershould be an extension of you and used to handle back formance evaluations should be detailed and contain both office duties such as patient phone calls, prescription refills, lab reports, and initial charting for patient visits. A positive and negative notes. Accurate documentation may good pain nurse is worth his or her weight in gold, andbe your only defense if you have to defend unemployment will truly make or break the profitability of the clinic. claims or wrongful termination suits.

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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you spend the money brought in. In reality, nancial fi management starts with when the patient is scheduled for TABLE 73.1 the appointment. It is important for all of the staff to Sample Table of Contents realize that this is the first step to a successful practice. Administrative Manual Clinical Manual Explaining financial policies on the phone when the appointment is made sets the tone of the entire process Office hours and schedule Patient work-ups for the patient. The expectation is that the patient underTelephone management Triage stands his or her responsibility for payment, what the Appointment scheduling Charting Medical records management Patient education office will and will not do regarding insurance, and this Emergency procedures Standing orders allows the patient to be prepared for that first visit. This Front desk check-out Procedure set-ups is not something that should be viewed as greed but Patient billing and collections Narcotics policy instead as a service to inform. The approach is to capitalize Refund processing Sterilization guidelines on every patient contact to communicate expectations. You Accounting and bookkeeping Inventory control inform them to bring in any prescriptions they are taking; why not remind them that you need a copy of the insurance card, precertification, or checkbook for the co-pay. OPERATIONS MANAGEMENT Registration or the “check-in” process is something Every practice needs a bible of how and why the clinicthat is neglected in many practices and has a huge impact runs the way it does. In the fice of setting you will need on financial management. I cannot stress enough how several. First, you will want an employee manual, whichimportant complete and accurate information is from this will communicate what you expect from employees, out-very point forward. If the registration process breaks line benefits, and give some basic but essential information down, the entire financial process is in jeopardy. With all about your office. Some practices may choose to incorpo-the forms and tools in today’ s society, you would think rate compliance information in this manual or segregatethis step would be easy, but it is the one that needs the it into a separate manual. The goal of the manual is to set most attention in physician fices. of Remember how imporlines of authority, communicate basic business practices, tant selecting the right person is for the job. Invariably, I and define the benefit structure offered. It is necessary that will go into a physician’s office and find the least intellia written acknowledgment be retained in the personnel gent and lowest paid person in the front desk position. file of each employee stating that the manual was received, Not to belittle the point, but you get what you pay for and read, and understood by the employee. running the front desk is a critical process in the financial The second sets of manuals you will want to completehealth of your practice. are policy and procedure manuals. To accommodate per- It is recommended that you develop a form that capsonnel and for ease of understanding, I recommend breaktures not only the patient’ s information but also informaing the policy and procedure manual into two separatetion of a close relative or friend. This might be the only manuals, one for administrative staff and one for clinicalway to locate a collection problem, so keep in mind what staff. It is even helpful to break them into sections thatinformation is necessary in the process of skip tracing a mirror the tasks assigned to employees. Remember, these patient. The registration form should include an assignmanuals are to be very detailed concerning how you want ment of benefits form as well as a financial policy statetasks to be accomplished. Table 73.1 is a sample table ment. of Do not accept registration forms that are not filled contents for each manual. Stop and jot down a brief note out completely. The patient is telling you something by if you have strong feelings about how you want areasnot completing the information, i.e., “I don’ t care whether handled in your practice. you get paid or not. ” Stop right there and do not allow Many practices do not create a set of manuals untilthat patient into your practice. There are no shortages of something goes wrong. This is a huge mistake. Commupain patients; you might as well only see the ones who nication and documentation in the medicalfice of are as are interested in paying for your services. important as keeping medical records on patients. Writing The financial policy for your practice should specifthings down with specific instructions is a good way forically instruct patients on what administrative procedures you to establish expectations and goals for your practice. will be followed to help them obtain benefi ts for their Do not skip this step of creating a road map for thehealthcare. It should state clearly that patients are direction of your practice. expected to pay for medical services regardless of insurance coverage. Payment arrangements or payment options such as credit cards or bank loans may be outlined FINANCIAL MANAGEMENT in the policy. It also should inform the guarantor as to Many physicians make the mistake of believing that finan-when an account will be referred to a professional colcial management is solely the process of recording how lection agency. It is recommended that this be a two-part

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carbon form signed by the patient. One copy is given to the patient and the other is retained in the chart or billingTABLE 73.2 file for future reference. Charting Guides Many practices also need to include an ABN, 1. The medical record must be legible and complete. Advanced Beneficiary Notice. This is a form required by 2. Each visit should include the following: Medicare, which tells the patient that Medicare may not a. Date pay for the treatment they are requesting. In pain practices b. Reason for the visit this is common, and communicating this message right at c. Appropriate history and physical exam the beginning to the patient will help him or her under- d. Review of ancillary data, lab or X-ray, as indicated stand what the financial responsibility might be when e. Physician assessment f. Plan of care incurring this treatment option. This process of registration, precertification, and ben- 3. Past and present diagnosis should be accessible to the treating and/or efit structure has become so complicated that many prac- consulting physician. tices have hired what I would term as financial counselors.4. Rationale for ordering and the results of diagnostic tests, X-ray or If your practice chooses to hire such a specialist, you must lab, should be documented in the medical record. 5. Patient health risk factors noted. plan for this in your of fice layout. This individual will 6. Patient’s progress, including the response to treatment, change in need a private place to speak with patients about confi- treatment plan, revision of diagnosis, and patient noncompliance to dential matters. Again, personnel selection is extremely the plan should be documented. important. 7. The plan of care should outline specific treatments and medications, specifying frequency and dosage, any referrals or consultations to outside specialists, education given to patient or family, and specific THE MEDICAL RECORD instructions for follow-up with physician. s The chart has become so important that a chapter should8. Written support of the complexity of the visit and the physician’ medical decision-making process to create the plan for treatment. be devoted solely to its contents and organizational struc9. Medical documentation should not be limited to physician ture. I will summarize what should be a review for phy- documentation; nursing and other non-physician staff should be sicians regarding documentation. You must realize that dated and signed by the person making the chart entry. documentation is not only a communication tool for your 10. CPT/ICD-9 codes reported on the HCFA 1500 form must be own office but also will help you in medical-legal issues reflected in the documentation of the medical record.

as well as provide for a defense in billing. Each visit, yes, every encounter with the patient no matter how brief, The majority of third-party payors also subscribe to should follow the charting guidelines in Table 73.2. this methodology, making coding the industry billing stanA well-organized chart is like gold, precious, and to dard. CPT-4 codes tell the payor what services were probe guarded. Do not underestimate the importance of orgavided and billed, and ICD-9 CM codes provide reason the nization. Simple tools will help keep everyone current onmedical services were rendered. Documentation in the the status of the patient if the rules are followed. Painpatient’s medical record to substantiate codes listed on the charts should begin with the left side reflecting a medica-HCFA-1500 insurance claim form may be reviewed by a tion and patient visit summary. Separate sections for vispayor, pre- or post-payment of benefi ts. Payors may deny its/procedures, radiology findings, and previous medicalpayment or request a refund if documentation does not prorecords are suggested. The chart needs to work for you vide enough information to demonstrate that billed services and be organized so that all clinical staff can quicklywere performed or that services were medically necessary. identify risk areas for the patient. A complete revision of current diagnosis coding systems is underway with a target implementation date of CPT/ICD-9 CODING October 2001 in the United States. ICD-10-CM represents The Center for Medicare and Medicaid Services (CMS)the most significant revision of ICD (International Classification of Disease) since its inception. There are thouhas adopted a single diagnostic coding system, the International Classification of Diseases, Ninth Revision, Clin-sands more diagnosis codes (more than 50%), with more ical Modification (ICD-9-CM). This coding system is used characters; codes are alphanumeric and the organization has changed. The goal is granularity, i.e., to provide regardless of the setting in which the services are rendered in accordance with the coding guidelines and reportinggreater detail that will be useful in healthcare policy and outcomes research. requirements. Procedures/services are coded using the To code accurately, it is necessary to have a working Health Care Financing Administration’ s Common Procedure Coding System (HCPCS), of which the Americanknowledge of medical terminology and to understand the Medical Association’ s Physicians’Current Procedural characteristics, terminology, and conventions of the ICDTerminology, Fourth Edition (CPT-4) system is a part. 9-CM. Transforming verbal descriptions of diseases,

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injuries, conditions, and procedures into numerical desig-vided during a single encounter or on a single date of nations (coding) is a complex activity and should not beservice. undertaken without proper training. Physicians and coders often have a dilemma when attempting to code “pain” to the highest degree of speciOriginally, coding was accomplished to provide ficity. Standard coding requirements are to code to the access to medical records by diagnosis and operations highest degree of specificity and code the “disease, ” not through retrieval for medical research, education, and the symptom. In a pain management practice, it is often administration. Medical codes today are utilized to facilnecessary to code the “pain symptom” until the physician itate payment of health services, to evaluate utilization is able to make a more specific diagnosis; this may take patterns, and to study the appropriateness of healthcare several visits and diagnostic tests. costs. Coding provides the basis for studies and research Documentation should be reviewed and the patient’ s into the quality of healthcare. Coding must be performed correctly and consistentlycurrent pain diagnosis coded for each visit, independent to produce meaningful statistics to aid in the planning forof prior visits and treatment. Diagnoses change based on the health needs of the nation. At the physician/patienttreatment outcomes and diagnostic tests; the physician should provide a diagnosis for every encounter and/or encounter, the physician ascertains what is wrong with the procedure performed. patient through evaluation, diagnostic tests, and various forms of treatment. This information is then translated into Most Medicare carriers have implemented local medical review policies that list specific medical necessity the language of codes to send to the insurance carrier coverage guidelines determined by the diagnosis code requesting reimbursement for services and procedures perassigned. Policies vary from state to state so it is necessary formed based on medical necessity and diagnosis for each practice to review its own carrier’ s local medical involved. review policies. This can be done via the Internet. The The government’ s definition of medical necessity isa “ Web site is www.lmrp.net. service that is reasonable and necessary for the diagnosis or If a remittance advice lists “not medically necessary” treatment of illness or injury, or to improve the functioning as a reason for nonpayment, the patient’ s medical record of a malformed body member” (Medicare Carrier’ s Manand the carrier policy should be carefully reviewed to ual). In other words: determine if a different diagnosis would have been more appropriate. Billing personnel may need asistance from • Services must be consistent with the symptoms physicians to select a more appropriate code. A diagnosis or diagnoses of the illness or injury under treatshould not be altered unless documentation in the patient’ s ment; medical record substantiates the change. • Necessary and consistent with generally Third-party payors differ on coverage and benefits as accepted professional medical standards, i.e., well as reporting requirements. For example, carriers exist not experimental or investigational; that do not accept CPT-4 codes designated as “unlisted • Not furnished primarily for the convenience of procedure, ” which makes it very dif ficult to bill a procethe patient, the attending physician, or another dure that does not have a designated CPT-4 code. Carrier physician or supplier; and representatives should be queried for billing instructions • The service must be furnished at the most in such instances. appropriate level, which can be provided safely Another approach for carriers that do not accept and effectively to the patient. unlisted codes is to carefully choose a CPT-4 code that is very similar in description and objective and with a relaEstablishing medical necessity is the first step in third-tive value unit (RVU) (from the Medicare schedule) that party reimbursement. Justify the care provided by presentis also similar. Write to your major payors. Your letter ing the appropriate facts. These facts must be substantiated should contain information about the procedure (attach a by the patient’s medical record, which may be requestedprocedure report), what procedure code is thought to be by the insurance carrier for pre- or post-payment reviewappropriate, and additional explanation of the procedure. at any time. Explain that there is no CPT-4 code and that you will The first diagnostic code referenced on the HCFA-submit your changes under xxxxx procedure, and ask them fice if this is not acceptable or if 1500 claim form describes the most important reason forto please notify your of the care provided. Often a single ICD-9-CM code ade-the company would prefer that you use a different CPT-4 quately identifies the need for care. If additional facts arecode or its own specifically assigned HCPCS code. required to substantiate the care provided that day, list the Included with procedure descriptions are common ICD-9-CM codes in the order of their importance. Be diagnosis codes. This listing of diagnoses is not intended careful to link your diagnosis codes to the proper CPT-4to be exclusive of the indications for a specific procedure code, especially when more than one procedure is proor treatment. Diagnoses are a composite of some of the

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Medicare carrier policy statements and are intended as A copy of this quarterly publication can be obtained guidelines only. from: HCFA Correct Coding Initiative, AdminiStar Federal, P.O. Box 50469, Indianapolis, IN, 46250-0469.

CORRECT CODING INITIATIVE CHARGE TICKETS

On December 19, 1989, the Omnibus Budget Reconciliation Act of 1989 (P.L. 101-239) was enacted.Charge tickets should be designed as a communication Section 6102 of P.L. 101-239 amended Title XVIII of the tool for your billing staff. It should cover 90 to 95% of Social Security Act by adding a new Section 1848, Pay-the services you perform. Each year the charge ticket ment for Physicians’Services. This section of the Act should be updated for changes in CPT-4, procedure coding provided for replacing the previous reasonable charge or ICD-9, diagnosis coding. It should always include all mechanism of actual, customary, and prevailing charges levels of evaluation and management services with some with a resource-based relative value scale (RBRVS) fee type of guideline to remind physicians of the appropriate schedule, which began in 1992. medical situations that constitute each level. Accurate coding and reporting of services by physicians Most physicians do not have a system for establishing are major concerns of HCFA. Medicare carriers haveprices for the services they perform. While it is true that included in their claims processing system various computmany managed care fees are set, you must know your erized edits to detect improper coding of procedures. Many costs and individual statistics in order to evaluate whether of these edits are designed to detect fragmentation, or separate you are being paid fairly for your services. It is good to coding of the component parts of a procedure, instead of start with some outside resources. Gather the Medicare reporting a single code which includes the entire procedure. RBRVS fee schedule, the ASA Relative Value Guide, and any other professional society recommendations regarding The purpose of the National Correct Coding Council’ s (AdminiStar Federal) contract was to develop Correctfees and put them into a worksheet that identifies the Coding Methodologies for HCFA ’s Bureau of Program different schedules by CPT code. This will give you a Operations. This manual, termed the Correct Coding Ini-side-by-side comparison so that you can begin to analyze tiative (CCI), is used by all Medicare carrier intermediar-and draft your own fee schedule. ies and some commercial payors as well. Commercial The next critical step is to analyze your individual payors may have their own version of “CCI, ” sometimes practice data. Evaluate the demand for pain services in referred to as “black box edits, ” that are not published. your area and assess your competition. Gather some outEach CCI chapter consists of the Manual divided intoside resources from your region’ s business journal or the two sections: Chamber of Commerce regarding the payors in your area and the number of lives that each represents. Finally, look 1. Mutually exclusive procedures are those which at your utilization of the procedures you perform. cannot be performed during the same operative There are publications available for national averages or patient session; per year on physician charges. The important thing to 2. Comprehensive and Compound procedure code realize is that the information is on charges submitted, not combinations, which are divided into Column 1 on payments made. The information is available by region and Column 2 procedures. The Component pro- or by specific zip code. Normally, the information shows the cedure (column 2) will not be reimbursed when average allowable reimbursement paid by commercial paythe same provider renders the procedure on the ors and 50 to 75% and 95% of what most physicians charge. same date; this is referred to as unbundling. “ ” The most important element in setting fees is to identify how much it actually costs you to perform a procedure. Unbundling is essentially the billing of multiple procedure This can be done in several ways. Activity-based costing at the cost of each activity needed while performing codes for a group of procedures that are covered by looks a single comprehensive code. Attempting to bill separatelya procedure. Because most physician groups do not have ef do this, I recommend for these already bundled charges will constitute a claimaccounting expertise to ficiently estimating the direct costs by procedure, allocating a for unbundled codes. There are two types of unbundling: the first is unin-charge per procedure for overhead, and then adding an tentional and results from a misunderstanding of coding,acceptable mark-up for profit. and the second is intentional, when the technique is used Now go back to your spreadsheet and add the column by providers to manipulate coding in order to maximizeof cost. You have all the information you need to decide payment. It is important to refer to a current copy of thehow to set your fees. Profit cannot be realized if costs CCI to avoid billing unbundled codes. This practice of exceed income. Performing more services does not guarbilling unbundled codes is fraud and will be prosecutedantee profit. You must constantly monitor your payors with regard to the fee schedule that they pay. as such by the U.S. Attorney General.

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• Checks and balances must exist in your system to assure that you capture all charges into the billing system, that the insurance claims are generated, and that the money will come back to the practice within a reasonable time period. Thefirst check and balance should be the schedule to the charge tickets. This should be done every day with no exceptions. Balancing controls by either dollar amount or hash totals of CPTs should be implemented to verify the charge tickets to the computer system. When insurance claims are generated, some verification system as well periodic monitoring of the accuracy of the claims should be done. Payment could come as soon as 14 days if filing electronically or take up to 45 days. If no payment is received by the 45th day, immediate collection follow-up should be started. • Negotiate contracts that allow at least 90-day timely filing deadlines. • File electronically. • Keep track of internal turnaround time. • Keep track of claims turnaround time. • Work the mail to discover your problems.

collection calling. It is important to take the following approach: • • • •

Call the person by proper name. Have your facts ready. Be pleasant but matter of fact. Most importantly, Follow-up… Follow-up…Follow-up.

Many times collections is nothing more than teaching patients about responsibility for their portion of the bill. Continually reminding patients of their payment promises and staying in contact with accounts that have slow payment are necessary for your nancial fi health. Make sure your statements are easy to read and clearly tell the patient what you want them to do. Many times patients believe statements are only informational and have no call to action. Being in private practice means accepting that a few patients never intend to pay. Identification and early placement of those accounts with a professional collection agency are in the best financial interest of your practice. Staff need to concentrate on those accounts under 90 days in order to have effective collections. Finally, just a word to the wise: It is important for The most important fact you must face is that you arephysicians to recognize and admit when they need help not a bank. Accounts receivables on the books is not cash with business issues. Physicians are busy individuals and in the bank. Establishing and adhering to a financial policytrusting by nature. They must develop business skills in will benefit everyone in your practice. You must establishorder to survive. It is never wrong to ask for help or admit a system to collect co-pays and small balances at the time that something is not quite right, just do not wait too long services are rendered. Your best possible time for collecbefore inquiring. Seek advice from well-qualified profestion is when you see the patient for follow-up visits. sionals who have the reputation of being brutally honest. Remind patients of their balances and that you will help them collect benefits that they have paid for from their insurance carrier. You are entitled to be paid for the services you have performed. Today is a plastic society;REFERENCES accept MasterCard and Visa in your practice. Probably the best action for your practice is to makeAmerican Medical Association. (2000). Current Procedural Terit everyone’s responsibility to collect money. Knowing minology, Chicago: AMA Press. how to figure a bill, understanding co-pays and deduct-Medicode. (2000).International Classification of Diseases, Ninth Revision, Clinical Modification(6th ed.). Salt ibles, and filing secondary insurance immediately all help Lake City: Medicode. reduce the practice’ s accounts receivable. When it comes to patient statements, put a due date on the statement. All individuals pay bills by the day they are due. Physicians make the mistake of not having due dates on statements, which sends the message that it is OK for the patient to pay whenever they can. Many times office staff avoid collection calls. Collection calls are necessary to keep accounts receivable under control. Many times using a matter-of-fact attitude helps with making staff more comfortable in the process of

74 Pain Management: Medical and Legal Issues of Undertreatment James S. Lapcevic, D.O., Ph.D., J.D., F.C.L.M. The American physician is currently faced with a practiceevaluation, and management. Yet much pain remains underreported as well as undertreated (Anon., 1998; Dahlparadox (Parran, 1997), demanding a new balance in the prescribing of controlled medications for the treatment ofman, Dykes, & Elander, 1999). Varying patient populapain. This newly developed clinical dilemma comprisestions have been found to receive less than quality treatunderprescribing narcotic analgesics to a majority of painment of their pain if indeed any treatment at all (Bernabei, patients, while, on the other hand, overprescribing to aGambassi, Lapane, et al., 1998; Cleeland, Gonin, Baez, minority of patients. To stay the course of quality clinical Loehrer, & Pandya, 1997; Foley, 1997). practice requires physicians to understand both the med- In a survey of physicians, 82% responded that they ical and legal strategies undergirding the forces forging ahad not been adequately educated in pain management (Lavies, Hart, Rounsefell, & Runciman, 1992); patient new paradigm of medical care. Several thematic key issues surveys found more than half wanted decision capacity on are considered in this structure. when more analgesia should be given them. Pain, an important and serious symptom, is one of the most common reasons for seeking medical care (Weiner, 1993). Nine of ten Americans age 18 years or older report EDUCATIONAL INTERVENTIONS TARGET suffering pain at least once a month, and 42% of adults EFFECTIVE MANAGEMENT PAIN report experiencing pain every day (Gallup, Inc., 1999). Chronic pain is experienced daily by an estimated 75Pain is defined as an unpleasant sensory or emotional million people in the United States (Bostrom, Ramberg,experience associated with actual or potential tissue damDavis, & Fridlund (1997). In the last decade interest inage and described in terms of such damage (Merskey, pain management (Rorarius & Baer, 1994; Tittle & 1986). Classification of pain is either acute or chronic (see McMillan, 1994) has risen largely due to surveys revealingTable 74.1), although acute pain can evolve into chronic that inadequate pain control is a norm under traditionalpain if not treated fully, promptly, and adequately (Marclinical management, with as many as 75% of postopercus, 2000) to avoid such conversion (Katz, 1996). Effecative patients unnecessarily suffering unrelieved paintive management requires multifactorial assessment of (Shapiro, 1996). In recent years, we have gained a new components that differ only in magnitude from one awareness of pain, its effects on quality of life, and theaffected person to the next (Goldstein, 1999). Pain is a evaluation and issues involved in its treatment. Thedynamic process with a clinical significance (Carr, Jacox, increasing number of those experiencing pain and other Chapman, et al., 1992) affecting sympathetic nervous syschronic medical conditions urges physicians to stay abreast tem activity, neuroendocrine activity (Kehlet, 1989; Lutz of the most current and effective options for pain assessment, & Lamer, 1990), and it has adverse effects on the immune 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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TABLE 74.1 Classification of Pain Acute Pain Duration Pathophysiology Prognosis Treatment

0

1

No pain

2

3

4

5

6

7

Chronic Pain

Hours to week Identifiable Predictable Analgesics

8

9

Nonmalignant Malignant Months; years Unpredictable Not always identifiable Identifiable Unpredictable Multidisciplinary Multidisciplinary

10

TABLE 74.2 Major Recommendations to Include in a Program Designed to Enhance Relief of Pain

Worst pain

• Make sure that a report of unrelieved pain will raise a red flag ficient suf to attract the attention of clinicians. FIGURE 74.1 Visual analog scale for assessment of acute pain. • Make information about analgesics readily available, especially in the area where orders are written. system (Terman & Liebeskind, 1991). The control of pain• Promise patients that they will recieve responsive analgesic care, and can influence clinical outcome (Whipple, Lewis, urge them to facilitate this process by communicating their pain. Quebbman, et al., 1995) while unrelieved pain can impair• Define and implement policies (and safeguards) for use of advanced recovery (Brown & Carpenter, 1990; Carr, Jacox, Chap- techniques for pain control (such as intraspinal patient-controlled man, et al., 1992) as well as result in anxiety, depression,opioid infusion). sleep deprivation, or any combination of these. Pain itself• Assess on a continual basis both the process of pain control and can be clinically assessed by subjective direct and indirectprocedures used to achieve this clinical outcome.

methods utilizing pain scales to chart the pain intensity. Common measures of pain intensity are 1. Categorical scale of pain intensity. A simple descriptive scale representing the oldest approach to pain assessment. Most often, this scale consists of four categories: 0 = no pain, 1 = slight or mild pain, 2 = moderate pain, and 3 = severe pain. 2. Visual analog scale (VAS) (Figure 74.1). The patient is asked to draw a mark somewhere along the line between no pain = 1 and worst pain = 10. Good agreement between descriptive and visual analog ratings has been found (Litman, Walker, & Schneier, 1985). To ensure proper management of pain, healthcare professionals should chart pain as formalized in a report prepared by the American Pain Society (APS) Quality Care Committee (American Pain Society, 1995) (see Table 74.2). Pain assessment should be charted as the “fifth” vital sign (Oncology Nursing Society, 1998) in patient evaluation. The Veterans Administration has made a decision to implement in all its facilities the process of charting pain as a fifth vital sign. Continued assessment of pain should involve evaluating and charting at several critical times in the pain management process (see Table 74.3) (Jacox, Carr, Payne, Berde, Biebart,

TABLE 74.3 Instances When Pain Should Be Evaluated and Charted • Whenever there is a new report of pain • At regular intervals after initiation of therapy • At an interval commensurate with the therapy (such as 15 to 30 minutes after administration of parenteral drug therapy; 60 minutes after oral therapy)

Cain, et al., 1994). Distinguishing characteristics of acute and chronic pain (see Table 74.4) are summarized. Basic tenets (McCarberg, 2000) of pain management are 1. Do not assume a patient’ s pain is being adequately treated because the patient does not complain. 2. “Pain” should always be considered the fifth vital sign. Ask the patient about pain, prescribe what is needed to relieve that pain (including opioids, if necessary), and follow up with frequent evaluations of the ficacy ef of the treatment regimen.

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TABLE 74.4 Distinguishing Characteristics of Acute and Chronic Pain Acute Pain

Chronic Pain

A symptom of disease Is itself the disease Self-limiting Persists beyond the usual course of acute disease Provoked by Provoked by • Noxious stimulation • Chronic pathologic process • Tissue injury • Dysfunction of PNS or CNS • Abnormal function of somatice or visceral structures • Psychological and learned (environmental) factors Followed by emotional, psychological, and autonomic responses May not be followed by autonomic and neuroendocrine responses; vegetative state may emerge Has a biological function (alerting, warning, resting, healing) Never has a biological function

3. Modify treatment according to patient response. 4. Make use of both pharmacologic and nonpharmacologic methods for pain relief. 5. Involve the patient as much as possible in pain control strategies, explain options available, and foster a positive attitude in the patient toward dealing with pain. 6. Ensure continuity of pain management once the patient leaves the hospital; pain can and should be controlled in the outpatient setting to the same extent as when the patient is hospitalized.

pain originates in the nerves. Neuropathic pain can be defined as pain resulting from noninfl ammatory dysfunction of the peripheral or central nervous system without trauma or peripheral nociceptor stimulation, usually described by pain patients asburning, “ ” “shooting,” or “lancinating.” To make good pain management decisions, physiology, anatomy, and referred-pain pathways must be considered. There is no substitute for touching the patient. It has been said that the best cheap test for evaluating physiologic change and understanding the origin of a patient’ s pain is a good neurological physical examination (Saberski, 2000). The weak point in patient evaluation is the patient’s complaint; the strong must be the physician’ s knowledge that pain is complex, and may not be what is Over the past decade concerted efforts have been made expressed (Saberski, 2000). to educate healthcare providers regarding the need to aggressively treat pain. Reliance on the primary care phy- While it is important to stay abreast of new technologies sician, who is quite capable of treating routine chronicdespite dramatic technological breakthroughs, there can be pain conditions, continues due to the relatively small num-no replacement for a thorough and complete history and bers of pain specialists. The American Academy of Painphysical examination. Physicians may need assistance in Management, the American Academy of Pain Medicine,identifying chronic pain patients who are not adequately and the American Pain Society, professional organizations coping with the experience of pain while making their qualfor the study of the scientific and clinical aspects of pain,ity of life independent of the perception of pain. By asking have available membership directories that can help the three questions, clinicians can identify patients who are in primary care physician find help through a specialist inall probability not coping well and might bene fit from psyhis or her area. chological intervention that addresses self-ef ficacy. Pain is classified as acute or chronic. Acute pain is The self-efficacy screen (Kores, Murphy, Rosenthal, sometimes defined as pain that persists for less than Elias, 3 & North, 1990) comprises three questions (see months and can be understood when associated with an Table 74.5) with graded response. While this verbal screen acute injury as cause and effect. Chronic pain, on the other is not sufficiently sensitive to identify all pain patients in hand, is pain that persists for more than 3 months beyond need of psychological intervention, it will identify a subset the normal time of healing (e.g., pain related to chronicfor whom treatment can be expanded to address their back problems or sickle-cell disease). Diseases such as psychological and physiological pain management needs. AIDS can cause chronic noncancer pain and demand the Patients with pain may have an exaggerated response if same attention to pain relief as given to terminal cancer an underlying depression is also present. In patients using patients. Cancer pain is either resolved after the cancer long-term is opioids for treatment of chronic pain, some resolved or may continue indefinitely as a complicationuseful questions may be used to screen for signs of addicof otherwise curative therapy. tion (Ewing, 1984) (see Table 74.6). Portenoy (1996a) has Pain may also be classifi ed as neuropathic, or nocicep- classified aberrant drug-related behaviors into those probtive and visceral. Nociceptive and visceral pain originates inably more or probably less predictive of addiction (see Table 74.7). muscle, bone, or visceral structures, whereas neuropathic

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TABLE 74.5 Self-Efficacy Screen 1. Do you feel that by taking care of yourself you can limit your pain? 2. Do you feel that doctors/therapists will control your pain? 3. Despite your best efforts, does your pain prevent you from getting a good ’s night sleep?

Yes Yes Y es

No No No

Note: A negative response to questions 1 and 2 and a positive response to question 3 indicate poor coping and need for psychological intervention. Note that question 2 is keyed paradoxically. While one might expect the pathologic answer to question 2 to be a positive response, it is a negative response that is actually interpreted as significant.

TABLE 74.6 CAGE Test C A G E

Have you ever felt you should cut down on your substance use? Have peopleannoyedyou by criticizing or complaining about your substance use? Have you ever felt bad or guilty about your substance use? Have you ever needed an eye openerin the morning to steady your nerves or get rid of a hangover?

Yes No es YNo esY No esY No

Note: Any patient responding yes to two or more of the questions in this simple screening test should be subject to more intense scrutiny for the signs of addiction (Kores, Murphy, Rosenthal, Elias, & North, 1990).

abuse or addiction. Fear of addiction in the terminally ill patient is exaggerated as is the likelihood of inducing respiratory depression. Pain at the end of life can be adequately managed with Probably More Predictive clearly defined management strategies. The World Health • Selling prescription drugs Organization has proposed a three-step analgesic ladder • Forging prescription approach to pain management in which nonopioid, opioid, • Stealing or “borrowing” and adjuvant analgesics are used based on the type and • Frequent prescription “loss” intensity of pain (see Table 74.8). The steps are coupled • Injection oral/topical formulations • Obtaining prescription drugs form nonmedical sources to the Visual Analog Pain Scale assessment (see • Concurrent abuse of related illicit drugs Figure 74.1). The categories of analgesics and dosages are succinctly noted (see Table 74.9), while comparison of Probably Less Predictive opioids in oral and parenteral dosage conversion (see • Aggressive demand for more drug Table 74.10) shows clearly that dosage adjustments (Edu• Drug hoarding cation for Physicians, 1999) are necessary when routes of • Unsanctioned dose escalation administration or conversion from one opioid to another • Unapproved use of the drug are considered. Opioids are the mainstays and clearly the • Unkempt appearance agents of choice for treatment of moderate to severe pain. * Empirically divided into those that are assumed to be relatively more Through appropriate knowledge of opioid dosing intervals predictive and those that are assumed to be relatively less predictive of addiction. (Adapted from Portenoy, R. Journal K. of Pain and Symptom and titration of dose, severe pain even at end of life can be managed. Healthcare providers must remain diligent in Management, 11,203–217, 1996.) management of end-of-life pain because unrelieved pain for the terminally ill patient is an ethical issue (Ferrel & For pain of terminal disease, pain relief should beRhiner, 1994) as much as it is dehumanizing. The ethical principle of “double effect” allows for the administration provided because easing pain and improving functions are of opioids to control pain even though the dying process the goals when treating acute and chronic pain patients whether or not there exists a history of addiction. By usingmay be hastened (Cavanaugh, 1996). Physicians can and should enhance the dying patient’ s quality of life by questions geared to level of function and behavior, healthenabling the patient to avoid pain (Cavalieri, 1999). care providers can adequately assess probability of drug TABLE 74.7 Representative Aberrant Drug-Related Behaviors*

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TABLE 74.8 World Health Organization’s Three-Step Ladder of Analgesics Step 3: Severe pain (7 through 10 on pain scale) • Morphine • Hydromorphone • Methadone • Oxycodone • Transdermal fentanyl • With or without nonopioid analgesics • With or without adjuvant analgesics Step 2: Moderate pain (5 through 6 on pain scale) • Codeine • Hydrocodone • Dihydrocodeine • Oxycodone • Tramadol • With or without nonopioid analgesics • With or without adjuvant analgesics Step 1: Mild pain (1 through 4 on pain scale) • Aspirin • Other nonsteroidal anti-inflammatory drugs • Acetaminophen • With or without adjuvant analgesics

TABLE 74.9 Categories of Analgesic Dosages Analgesics Nonopioids

Opioids

Adjuvant Analgesics

Antidepressants Nonsteroidal Anti-Inflammatory Step 2 Opioids • Amitriptyline (25 to 150 mg at bedtime) • Aspirin (650 mg every 4 hours) • Codeine (100 mg every 4 hours) • Ibuprofen (400 to 600 mg every 6 hours) • Dihydrocodeine (50 to 75 mg every 4 hours)• Notriptyline (25 to 150 mg at bedtime) • Diflunisal (500 mg every 12 hours) • Hydrocodone (15 mg every 4 hours) • Sulindac (150 to 200 mg every 12 hours) • Oxycodone (7.5 to 10 mg every 4 hours) Anticonvulsants • Naproxen (250 to 500 mg every 12 hours)• Propoxyphene (180 mg every every 4 hours)• Carbamazepine (100 mg to 200 mg twice or four times daily) • Diclofenac (50 to 75 mg every 12 hours) • Valproic acid (200 to 400 mg twice or four times • Salsalate (750 to 1500 mg every 12 hours)Step 3 Opioids • Morphine (15 mg every 4 hours) daily) • Oxycodone (7.5 to 10 mg every 4 hours) • Gabapentin (300 to 1800 mg three times daily) Acetaminophen (60 mg every 4 hours) • Hydromorphone (50–150 mg every 4 hours) Tramadol (50 to 75 mg every 8 hours) • Transdermal fentanyl (50 mg/hour) Local Anesthetics • Lidocaine (1.5 mg/kg IV) • Mexiletine hydrochloride (400 to 600 mg/d) Capsaicin (topically three times daily) Steriods • Prednisone (20 mg/d to 80 mg/d) • Dexamethasone (4 mg/d to 16 mg/d) a All dosages are oral unless specified otherwise. From Education for Physicians on End-of-Life Care . Participants handbook, American Medical Association, Chicago, IL, 1999. With permission.

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Allegations of prescribing too much, too little, or not prescribing a controlled substance that was needed accordTABLE 74.10 ing to the definition outlined in federal or state guidelines Comparison of Opioids in Oral and may be open to court interpretation through expert witParenteral Dosage Conversions nesses brought in by medical boards, plaintiffs, or the Oral Dosage Opiod Parenteral Dosage Drug Enforcement Agency (DEA). Claims that prescribing behavior was not in good faith or not reasonably 15 mg Morphine 5 mg necessary, requirements designed to establish medical 10 mg Oxycodone — necessity which may be redefined ad hoc, can make it 4 mg Hydromorphone 1.5 mg difficult for physicians to justify their treatment decisions. 15 mg Hydrocodone — 100 mg Codeine 60 mg To avoid unwittingly running a collision course with these 150 mg Meperidine 50 mg complex issues, better training in proper pain management hydrochloride procedures is necessary for physicians (Carr, 1998). Generally, physicians who prescribe scheduled or nonschedAdapted fromEducation for Physicians on End-of-Life uled analgesic medications believe their patients need Care. Participants handbook. American Medical Associathem. Physicians must be aware of the immediate medition, Chicago, IL, 1999. With permission. colegal ramification, including the burden of proof, that must be considered when analgesic medications are preGUIDELINE DEVELOPMENT scribed (Clark, 1998). Ideally, treatment guidelines should be based on data Many Americans are now over the age of 60. That segment from the medical literature, case law, and clinical expeof the population of the United States over 65 will double rience, although the boards that administer and interpret in the next 33 years, with the oldest of the old, those over healthcare practice acts are comprised of state governage 85, the fastest growing segment of the entire populament offi cials’ appointees whose members’ biases may tion. The elderly represent 12.7% of the population or one be reflected in the guidelines (Hill, 1996b). While not in every eight Americans (James, 2000). By the year 2030, all state medical boards hit the mark, many experts favor 20% of our population will be over 65. As the population state medical policy, issuing from the medical boards ages, more conditions causing pain, from arthritis to maligrather than from elected ficials, of directly addressing nancy, will emerge. A signifi cant proportion of all pharma- physicians concerns through medical guidelines. In ceuticals will be analgesic agents (Hill, 1996). 1999, The Ohio State Medical Association, in cooperaIn the past decade, societal and government needs tion with the state legislature, distributed a new clinical have molded medical practice into a less variable and more handbook titledPain: The Fifth Vital Sign.Distributed standardized activity (Hill, 1996a). Guidelines for pain to all physicians, but directed at primary care physicians, management have been issued by such diverse groupsthe as booklet encouraged better pain management includthe World Health Organization, the American Pain Soci-ing a step-by-step guide to documentation requirement ety, the American Society of Anesthesiologists, the Amer-compliance. ican Academy of Pediatrics, the International Association In 40 states, a variety of efforts have been underfor the Study of Pain, and the United States Agency fortaken to improve pain management: lawmakers through Health Care Policy and Research (AHCPR) (Hill, 1995).specific legislation, regulators through new regulations, Federal oversight of controlled substances extends and state medical boards through revised or newly into community standards of care. According to theadopted guidelines and policy statements on pain treatAHCPR guidelines (1992), opioids may be prescribed toment as state governments and medical boards focus treat acute and chronic pain, but the prescribing physi-on pain (see Table 74.11). Good documentation (the cian assumes the burden of proving that the prescription virtual flack jacket), despite its hassles, is one way to falls within normal clinical procedures for pain manage-reduce the likelihood of a routine inquiry mushrooming ment. A physician prescriber of a controlled substanceinto a full-blown investigation, although nothing — not is obligated to demonstrate both the medical necessity the best documentation, the best guidelines, or the most and adherence to law of such a choice. Many healthcare enlightened regulatory attitudes — will reduce physipractice acts do not provide for the interpretation ofcian risk to zero, but that seems the inherent nature of phrases such aspracticing “ medicine in a manner incon- the occupation. The kind of medical documentation sistent with public health and welfare” (Hill, 1996b). It adequate for most medical problems is often seen as is often the legal process that later nes defi these concepts inadequate in the treatment of pain (Hoover, 1996). The of “ reasonably necessary” and “good faith” that are American Medical Association (AMA) and the Amercritical to the justification, and even legal defense, of ican Hospital Association (AHA) have formulated cricontrolled substance prescribing in an individual case.teria, in the development of an increasing number of

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aggregate, and reduce unexplained variations in medical practice (Carr, Jacox, Chapman, et al., 1995). TABLE 74.11 AHCPR guidelines for effective pain relief promise State Governments and Medical Boards Focus on Pain patients attentive and effective analgesic care as well as Medical Board quantification in the medical chart of pain assessment Pain Pain Guidelines and Policy and pain relief. AHCPR has issued recommendations State Laws Regulations Statements regarding use of medications for management of pain in Alabama X adults after extensive literature review and evaluation of Alaska X data. The AHCPR guidelines establish basic principles Arizona X with which analgesic drug treatment should comply (see Arkansas X Table 74.12) and integrate specialized technology and California X X nonpharamacologic approaches. A systematic review of Colorado X X the literature is used to compile evidence for each mode Florida X X of pain relief. Type I evidence comes from large trials; Georgia X Idaho X Type Ia evidence is derived from multiple, randomized, Iowa X controlled trials that may be consolidated as meta-analKansas X ysis. Type Ib data originate from at least one large, ranLouisiana X domized, controlled study with statistically signifi cant Maine X results. Type II studies involve well-designed but nonMaryland X randomized comparisons. Type III evidence is from Massachusetts X descriptive studies. Type IV evidence is expert consenMichigan X X sus, based on the opinions of prominent practitioners Minnesota X X (Carr, Jacox, Chapman, et al., 1992). Balanced Analgesia Mississippi X X combines an opioid and a nonopioid to reduce the opioid Missouri X Montana X requirement and has now become standard practice Nebraska X X (Joshi, 1994). Certain opioids should be avoided when Nevada X X possible. Meperidine hydrochloride is not recommended New Jersey X for long-term use because of the potential for accumulaNew Mexico X X tion of normeperidine, a toxic metabolite, that can cause North Carolina X confusion or seizures. Propoxyphene, for example, is an North Dakota X opiate with a 13-hour half-life. It is metabolized by a Ohio X X X mechanism of n-demethylation through a saturable Oklahoma X X X mechanism, forming the metabolite norpropoxyphene. In Oregon X X X the elderly, susceptibility to the accumulation of this Pennsylvania X X Rhode Island X X potential toxic metabolite exists. Additionally, partial and Tennessee X X mixed opioid agonists such as buprenophine hydrochloTexas X X X ride, pentazocine hydrochloride, butorphanol tartrate, Utah X and nalbuphine hydrochloride, because of their limited Vermont X efficacy and possible toxicity, should be avoided (Cherny Virginia X X & Portenoy, 1994). Washington X X X The newly found appreciation calling for aggressive West Virginia X X action against acute pain resulted in the Federation of State Wisconsin X Medical Boards of the United States, Inc. promulgating Wyoming X model guidelines in 1998 for pain management strategies Note: These laws and regulations give physicians immunity when pre-and objectives (Model Guidelines, 1998). Clinicians will scribing opioids for intractable pain. be held to those guidelines, and the quality of medical Sources:Health Policy Tracking Service of the National Conferences ofpractice will be judged in part by the ability to meet those criteria. Some states have adopted even more stringent State Legislatures, September 1999; and the Pain and Policy Studies guidelines for pain treatment: at present, certain barriers Group, University of Wisconsin-Madison, January 2000. to delivery of adequate analgesia and pain management treatment guidelines, to guide policy makers in thisexist. Members of the healthcare team, patients, and the area. Primary criteria include the potential to improvehealthcare system continue impeding the delivery of individual patient outcome, affect a large patient pop-proper analgesia (see Table 74.13) (Jacox, Carr, Payne, ulation, reduce cost either for the individual or in the et al., 1994).

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TABLE 74.12 Pain Management Guidelines Medications for Management of Pain in Adults Medication

Evidence*

Oral NSAIDs

lb, IV

Oral NSAIDs in conjunction with opioids Parenteral NSAIDs Oral opioids

la, IV

Intramuscular Subcutaneous

lb, IV IV lb, IV lb, IV

Intravenous

lb, IV

PCA (systemic)

la, IV

Epidural and intrathecal opioids

la, IV

Comments

Precautions

Effective for mild-to-moderate pain. Begin pre-operatively.

Relatively contraindicated in patients with renal disease and risk of or actual coagulopathy. May mask fever. Potentiating effect resulting in opioid sparing. Begin pre-operatively. As above.

Effective for moderate-to severe pain. Expensive. Useful if opioids As above. contraindicated, especially to avoid respiratory depression and sedation. Route of choice. As effective as parenteral in appropriate doses. Use as oral medication tolerated. The standard parenteral route, but injections painful and absorption unreliable. Hence, avoid this route when possible. Preferable to intramuscular route when low-volume continuous infusion Avoid this route for long-term is needed and intravenous access ifficult dif to maintain. Injections repetitive treatment. painful and absorption unreliable. Parenteral route of choice after major surgery. Suitable for titrated bolus Significant risk of respiratory or continuous administration but requires special monitoring. depression with inappropriate dosing. Intravenous or subcutaneous routes recommended. Good steady level Significant of risk of respiratory analgesia. Popular with patients but requires special infusion pumps and depression with inappropriate dosing. staff education. When suitable, provides good analgesia. Use of infusion pumps requires Significant risk of respiratory additional equipment and staff education. Expensive if infusion pumpsdepression sometimes delayed in are used. onset. Requires careful monitoring.

* la = evidence obtained from meta-analysis of randomized controlled trials. lb = evidence obtained from at least one randomized controlled trial. IV = expert consensus based on the opinions and/or clinical experiences of respected authorities. NSAID = nonsteroidal anti-inflammatory drug. PCA = patient-controlled analgesia.

TABLE 74.13 Barriers to Delivery of Adequate Analgesia Healthcare Professionals

Reasons for Patient Reluctance to Report Pain

Healthcare System

• Inadequate knowledge of pain management (especially clinical pharmacology) • Poor assessment of pain • Concern about: • Regulation of controlled substances • Side effects of pain medication • Development of tolerance • Fear of patient addiction

• Fear that pain means progression of disease • • Want to be a “good” patient • • Do not want to distract physicians from treating underlying• disease • • Reluctant to take pain medication • • Fear of addiction or of being classified as an addict • Concerned about adverse reactions and development of tolerance

Low priority given to pain management Inadequate reimbursement Limits availability of treatment Limits access to treatment Restrictive regulation of controlled substances

Modified from Jacox, A., et al. (March 1994). Management of Cancer Pain. Clinical Guideline. Rockville, MD: U.S. Department of Health and Human Services.

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FOCUS ON PAIN

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recommended at should “ know” levels. State medical boards or medical societies are good resources. Caveat: A In 40 states (see Table 74.11), a variety of efforts have potent reminder finds that knowledge alone is insuf ficient been made to improve pain management. Some of these to promote behavioral change (King, Bungard, McAlister, have been undertaken by lawmakers through specific leget al., 2000); in the absence of other actions such steps as islation, or by regulators through new regulations. Othersdisseminating a medical guideline or providing continuing are results of revised or newly adopted guidelines and medical education are unlikely to significantly, or even policy statements on pain treatment from state medical measurably, improve the effectiveness of an intervention boards. Aimed at making standards uniform across the (Goff, Canely, & Gu, 2000). nation and encouraging better pain management, physi- For decades, improving the quality of healthcare delivcians who prescribe a controlled substance “for a legiti-ery relied on changing physician behavior. Experience has mate medical purpose” are reassured not to worry about shown that quality improvement is better achieved through board action or that of a state regulatory or enforcement system solutions that support clinicians in providing qualagency. The Federation initiative was endorsed by the ity care (Calonge, 2000). The imperative to measure, proDrug Enforcement Administration and by advocates formote, and improve the quality of medical care continues better pain management. The medical use of controlled to be an essential, if not daunting, endeavor. The quality substances has gained a new legitimacy, but physician of healthcare is, in the opinion of many, a serious problem fears of regulatory scrutiny linger. (Chassin, & Galvin, 1998). Research demonstrates that Historically, from the advent of the Victorian era until physicians overuse healthcare services by ordering unnecafter World War I, doctors were held largely responsibleessary interventions (Leape, 1992; Nyquist, Gonzales, for the heroin, morphine, opiate, and cocaine problem that Steiner, & Sande, 1998), underuse services by failing to swept the United States. The Harrison Narcotic Act ofprovide a standard of care that would produce favorable 1914 began the heavy-handed crackdown on narcotics that outcomes (Chasin, 1997), and devise the wrong treatment narrowed the scope of medical practice and interfered with plan or improperly execute the correct plan (Leape, 1994). their legitimate medical use, especially in pain manage-Quality assurance in the healthcare system is an important ment (Guglielmo, 2000). A short decade ago, conventionalpublic health objective (Lohr, 1990). The lessons of hiswisdom in the medical establishment was that physicians tory confirm that the medical factors that have prompted treating chronic pain with opioids were at substantial riskmedical malpractice litigation still continue but are in the of being sanctioned by state medical regulatory boards for public interest: scientific innovation, uniform standards, overprescribing (Hill, 1993; Joranson, 1992; Portenoy,and liability insurance (Gostin, 2000). From a legal per1996b). A review of state medical board actions from 1990spective, government directly and indirectly (the tort systo 1996 reveals that the perception of regulatory risk fartem) regulates the healthcare system. exceeds the reality (Martino, 1998). A California study Medical malpractice litigation ostensibly seeks higher (Morrison & Wickersham, 1998) concluded that most quality care. Tort law, on the other hand, functions to deter offenses of disciplined physicians involved some aspectsubstandard medical conduct, to avoid unnecessary injury, of patient care (e.g., inappropriate prescribing) and in the and as a fair method of compensation. Several reform face of increasing consumer complaints, medical regulamethods are currently under public debate, the most promtory boards may have increased dealings with physicians inent among these proposals being capitation on damages, who commit disciplinary offenses. Regulatory risks asso-which has been enacted in some states. Although this ciated with overprescribing are still perceived as real andapproach does not eliminate liability, it is proposed that such far greater (Glanelli, 1999) than those associated withaction would decrease fear of inordinate damage awards. underprescribing despite regulatory relief efforts. The premise of the regulatory relief efforts was that the undertreatment of pain is a public health problem. Ann M. EMERGING STANDARD OF CARE IN PAIN Martino, Ph.D., executive director of Iowa’ s Board of Med- MANAGEMENT AND LEGAL IMPLICATIONS ical Examiners, recommends new laws be written to discipline physicians who prescribe too little pain medication.The rapidity of change in the clinical practice of medicine Ironically, she writes, the most immediate means [of achiev-has brought frustration because of decreased autonomy, increased oversight, pressures on reimbursement, and alleing good pain management] may not be regulatory relief but gations of fraud and abuse. Malpractice and legal complimore regulation (Martino, 1998). cations of care have increased. It has been recommended that physician education is ts key to better pain management. Knowledge of the best Despite the widespread promulgation of the benefi drug and nondrug methods for controlling pain and of theof opioid analgesics in all types of pain statesacute, — federal and state laws that apply to medical practice is chronic, and cancer — fear and trepidation remain on

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opioid analgesics, and reluctant to be viewed as too demanding of more in the way of care than has been TABLE 74.14 proffered. Laypersons can hardly be more sophisticated Key Points Included in the Controlled Substances Act and knowledgeable about an emerging aspect of clinical • Opioids are necessary to public health. medical practice than healthcare professionals (Cleeland, • A mechanism is devised for external medical input. 1992). In 1996, an international panel of distinguished • Drug availability is guaranteed. healthcare professionals assembled by the Hastings Center • The federal definition of an addict does not include the chronic pain (International Project, 1996) identified the goals of medpatient. • Regulations specifically recognize the treatment of intractable pain icine as with opioids • Prescription size is not restricted. • Without a special license granted by the DEA, physicians may not provide methadone maintenance for patients with known addiction to controlled substances.

The prevention of disease and injury and promotion and maintenance of health; The relief of pain and suffering caused by maladies; The care and cure of those with a malady, and the care of those who cannot be cured; and The avoidance of premature death and the pursuit of a peaceful death.

TABLE 74.15 Liability Issues in Pain Management

The stated goals strike a remarkable balance between the curative and the palliative approaches to patient care, Liability to Patients strongly suggesting that the hegemony of the curative For cost-containment practices that affect pain management (Townsend, model that is the hallmark of modern medical education 1983) and practice reflects a medical ethos inconsistent with the For inappropriate pain management core values of medicine (Rich, 2000). Liability to Third Parties For injury caused by patients treated for pain (Heller, 1992; Vainio, 1995; EMERGING Wilchinsky, 1989) Liability to Patients, Healthcare Providers, and Third Parties For risks and side effects of drugs and pain management devices

LIABILITY ISSUES IN THE MANAGEMENT OF PAIN

It is argued that there are three essential duties of a healthcare professional (Edwards, 1984) regarding pain management: the part of physicians prescribing opioids. The Uniform Controlled Substance Act of 1970 provides for the reg- 1. The first duty is to minimize iatrogenic (physiistration of those handling controlled substances, as well cian-induced) pain; no further pain and sufferas for the labeling, order forms, record keeping, and ing are to be inflicted upon a patient beyond the reporting of substances or their use. Key points included unavoidable consequence of a reasonable effort in the Controlled Substances Act are listed in to effect a cure. Table 74.14. 2. The second duty is to be a competent practition-er in pain management. Effective appliThe issues of safety, ficacy, ef and compliance assocication of state-of-the-art pain relief ated with the use of controlled substances invite problems techniques is required to relieve as much pain of liability (see Table 74.15). States exercise parallel proas possible without imposition of patient burhibition on the nonmedical use of controlled substances den that exceeds benefi ts. This is a duty that with most statutes based on the 1970 Model Uniform can reasonably be placed on all physicians Controlled Substances Act. It is the intricacies and interwho care for pain patients and not one relationships between federal and state laws regulating the reserved for pain or palliative care specialists prescribing of opioid analgesics that have been repeatedly only. It is time for those physicians who are identified as one of the more significant barriers to the most likely to see chronically ill patients in provision of effective pain management and palliative care the first line of duty (general practitioners, (Rich, 2000). The barriers to pain management provide oncologists) to make pain control and palliaplausible reasons for so many patients to experience tive care a part of routine clinical practice undertreated pain. Collectively, these barriers have either (Stjernsward, et al., 1996). contributed to or caused an enduring epidemic of pain and suffering trailing in the wake of untreated pain (Rich, 3. The third duty is to adequately inform the 2000). Patient-related barriers to good pain management patient of the risks and benefits of alternative also exist. The general public is ignorant and fearful of pain management strategies, including that of

Pain Management: Medical and Legal Issues of Undertreatment

not pursuing pain relief (Emanuel, 1996). Physicians have a duty to continue their education throughout their professional lives to maintain their practices consistent with advances in science and technology.

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TOWARD A NEWER MEDICAL MODEL

Inadequate pain control appears to be the spur for increased interest in physician-assisted suicide, but one reason for inadequate pain management is an unfounded concern of both patients and healthcare providers that pain control is a form of euthanasia. Euthanasia refers to the The issue of whether physicians should be insulated intentional act of painlessly putting to death persons with from ethical or legal responsibility for undertreating pain incurable and distressing disease as an act of mercy due to deficiency in this area of medical education (Amer(Black’s Law Dictionary , 1979). Appropriate pain manican Medical Association, 1996) was in seemingly direct agement aims to reduce suffering, not cause death. contradiction with the AMA ’ s Principles of Medical Ethics In January 1998, Kirk Robinson, president, and Kathand the current opinion of the AMA on Professional ryn Tucker, director of legal affairs, for the Oregon-based Rights and Responsibilities (1996). organization Compassion in Dying Federation (CIDF), There is a developing healthcare professional consensent a memorandum to every medical board in the United sus that failure either to effectively manage pain that can States arguing that dying patients have a right to adequate be managed or to refer the patient to a professional who pain medications. Although the focus of the memorandum can bring state-of-the-art techniques to bear on the probwas end-of-life care, it outlined a series of steps for each lem, constitutes a breach of professional ethics and state a board to follow in addressing the perceived risks departure from an emerging standard of care (Oherney & for overprescribing controlled substances and the Catane, 1995). The concept of the patient’ s legal right to absence of any risk real or imagined for underprescribing effective pain management and the correlative duty on the medications to any patient experiencing pain. The idea part of physicians because of their virtual monopoly onthat state medical boards should take on the responsibilthe authority to prescribe narcotics to provide effectiveity of scrutinizing licensees for inadequate pain care was pain management to patients has begun to emerge in the urged, as well as the adoption of underprescribing as a last decade. One of the first serious discussions on poor ground for discipline. Additionally, the Compassion in pain management as an example of medical malpractice Dying Federation (CIDF) put all boards on public notice was conducted by Margaret Sommerville, a Canadianthat it was willing to assist chronic pain patients and legal scholar and bioethicist (1986). With the prevailingtheir families in making complaints and/or inling fi suits standard of care, it is argued that because it is abundantly against practitioners who fail to provide adequate pain clear that physicians traditionally fail to alleviate pain, arelief through underprescribing. patient would find it difficult to establish undertreatment In July of 1994, the California Medical Board issued of pain as a departure from the applicable standard of care. a formal statement on “Prescribing Controlled Substances The failure of the medical profession to adopt and consisfor Pain Management. ” The Board stated that “principles tently apply readily available therapeutic modalities thatof quality medical practice dictate that citizens of California who suffer from pain should be able to obtain the relief would improve patient care presents precisely a situational scenario ripe for judicial standard setting. With deficien-that is currently available” and that “pain management ” Concomitantly, cies in prevailing custom and practice so clearly inconsis-should be a high priority in California. tent with the traditionally attributable goal of the medical the Board issued “Guidelines for Prescribing Controlled Substances for Intractable Pain” Webster’ ( s Third New profession, courts appear likely to revert to a past irresistible impulse to find the entire profession negligent International Dictionary, 1993) which included the following admonition: (Hooper, 1932). A primary impetus for the promulgation of clinical practice guidelines for pain assessment and management The Board strongly urges physicians to view pain manhas been the demonstration, through recent studies, that agement as a priority in all patients… . Pain should be assessed and treated promptly, effectively and for as many healthcare professionals lack, or fail to apply, long as the pain persists. The medical management of basic knowledge and skills in this area. A declaration pain should be based on up-to-date knowledge about that “ not relieving pain brushes dangerously close to the pain, pain assessment and pain treatment (Medical act of willfully infl icting it” has become one of the Board of California, 1994). strongest statements recorded from an objective, nonclinician perspective (Morris, 1991). The willful infl icThe legal theory of negligence in medication error tion of pain is torture, which is foreclosed to the gov- lawsuits can be applied to cases claiming inappropriate ernment by the Eighth Amendment to the U.S.management of pain (Frank-Stromborg & Christiansen, Constitution, as cruel “ and unusual”even in punishment 2000). In any allegation of inappropriate pain manageof convicted criminals. ment, the patient (plaintiff) must prove:

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1. that a duty of care was owed to the patient by the defendant (healthcare professional); 2. the duty owed was breached with conduct that violated a standard of care recognized in the profession; 3. that breach of the duty owed was the cause of injury or the suffering; and 4. the patient (plaintiff) suffered damages as a result (Keeton, Dobbs, Keeton, & Owen, 1984).

a breach of accepted medical practice resulting in injury and legally recognized damage to the patient. Courts are now willing to hold physicians liable for allowing a patient to suffer because of a failure to provide appropriate pain relief under the recognition of improper pain management as a breach of good and acceptable practice. A medical malpractice judgment exceeding $1 million against the Veterans Administration included an award of $125,000 for pain and suffering predicated largely upon the defendants’ failure to provide suf ficient pain medication in the final days of the patient’ s life (Gaddis v. United States , In cases involving pain control, the professional will be 1997). The primary claim and bulk of the total award for judged according to the expectation of what a reasonable damages in a South Carolina case was based on a failure practitioner would have done in similar circumstances to timely and properly diagnose and treat the patient’ s (Willis, 1998). In general, the standard of medical care a throat cancer. physician may with reason and fairness be expected to possess is that commonly possessed or reasonably avail- In California, William Bergman, a man in his early 80s, wrenched his back pulling a battery out of a car. Over able to minimally competent physicians in the same speciality or general field of practice throughout the Unitedthe next few days he developed more and more back pain, which was originally thought to be a strain–sprain until States. A physician should have a realistic understanding of the limitations of his or her knowledge or competencethe patient became immobilized due to the pain (Tucker, and, in general, exercise minimally adequate medical2000). He was taken to the emergency room of a northern judgment Hall ( v. Hilbun, 1985). In litigation, the appro- California hospital whereupon he was hospitalized for priate specialty is located to provide information throughsevere pain in his back with a diagnostic finding of metastatic lung cancer. The patient indicated he wished no testimony about the standard of care and any deviation treatment for his cancer but wished only to receive pain from such standard. In most cases involving questionable medication that would allow him to return to his home pain treatment, the standard of care usually is defined and represented by the AHCPR guidelines. A minority of juris-and functionality for what time he had left. Dr. Wing Chin became Mr. Bergman’ s assigned physician for his hospidictions take the position that adherence to customary talization. The patient was reported by nursing to have practice should not insulate a physician from malpractice increasing Visual Analog Pain Scale (VAS) ratings despite liability if the patient (plaintiff) can provide persuasive receiving Demerol on a prn order for pain relief based on evidence that the physician failed or refused to apply patient request. Bergman was subsequently discharged to readily available measures that would have prevented his home with the oral pain medication Vicodin. Demerol harm to the patient. The Wisconsin Supreme Court is inadequate for cancer pain relief and is inappropriate (Nowatske v. Osterlok , 1996) stated that should customary for use in the aged due to nervous system toxicity that medical practice fail to keep pace with developments and may develop as a side effect of metabolite formation. advances in medical science, adherence to custom might Morphine agents are appropriate for cancer pain relief. constitute a failure to exercise reasonable care. Evidence Oral Vicodin is indicated for moderate to moderately that a defendant followed customary practice is not the sole test of professional malpractice Toth ( v. Community severe pain. Pain medications for cancer pain relief should Hospital, 1968). The notion that an entire medical spe-be given at specific times, not on a prn basis. Dr. Chin s pain and when asked cialty (Helling v. Carey, 1974), or at least all the members was called regarding Mr. Bergman’ about morphine agents for pain relief, the family was told of a particular locale, would never be guilty of negligence that he (Dr. Chin) did not possess the required multiple by adhering to a substandard standard of care fell to a prescription form pad to order these pharamaceuticals for Louisiana appellate court statement: patient use. After 2 days at home in what was described as “agonizing pain, ” a hospice nurse succeeded in conWe are firm in the opinion that it is patently absurd, tacting William Berman’ s regular physician, who immeunreasonable, and arbitrary to hold that immunity from diately administered Roxanol achieving pain relief. Mr. tort liability may be predicated upon a degree of care Bergman died the next day. or procedure amounting to negligence not withstanding Mr. Bergman’s daughter (Beverly Bergman) was so such procedure is generally followed by other members of the profession in good standing in the same commu- disturbed by her father’ s suffering that she made formal nity (Favalora v. Aetna , 1962). complaint, supported by independent expert opinion, to the Medical Board of California (MBC), that the pain Most lawsuits brought by patients against healthcarecare provided to an elderly, terminally ill cancer patient providers are for medical malpractice, which is defined aswas inadequate.

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California is among the most progressive states in refuse medical treatment. The record shows that Mr. McAfee has attempted, in the past, to disconnect his venattempting to improve pain care. In 1994, the MBC adopted an official guideline on pain management, which tilator, but has been unable to do so due to the severe pain specifically identifies failure to adequately manage pain he suffers when deprived of oxygen. His right to have a sedative (a medication that in no way causes or accelerates as “inappropriate prescribing.” The MBC expressly recdeath) administered before the ventilator is disconnected ognized that this is a form of professional misconduct, is a part of his right to control his medical treatment. subject to the full range of sanctions. The MBC agreed with Beverly Bergman that the phyThe implication of this ruling is that providers may sician had failed to provide adequate pain care but be held accountable for not providing such measures (Shadeclined to take any action against the physician (Letter piro, 1996). from MBC, 1998). It was not until after the MBC concluded that inadequate pain relief had been provided but In a North Carolina negligence law suit, a healthcare declined to take any disciplinary action that a formal com-provider was held liable for the first time for failure to treat serious pain appropriately Estate ( of Henry James v. plaint was filed. Hillhaven Corp., 1990). In February 1999 what appears to be the first malpracHenry James, 74 years of age, a retired house painter, tice suit against a physicianBergman ( v. Chin , 1999) was diagnosed with cancer of the prostate for which he grounded primarily on failure to properly manage a was subjected to removal of his testicles. The cancer, patient’s pain, was led fi in Superior Court of California however, was metastatic in nature, having spread to his (Gaddis v. United States , 1997; Bergman v. Eden Medical leg and spine. His pain was severe and excruciating. He Center, 1999). Cases of inadequate pain treatment may was placed in a nursing home in February 1987. Almost result in civil liability in tort cases with signi ficantfinancial at once, nursing began cutting his prescription pain medimplications. The unusual aspect of the Bergman case is ications by giving him on some days mild headache medthat a cause of action under the California Elder Abuse icines, placebo substituted for morphine, or nothing at all. Statute is included, which provides heightened remedies to The nursing supervisor explained to the family he was in what would be available under a medical malpractice claim, danger of becoming a drug addict and because James and including punitive damages, no cap on damages, and attorhis family were Medicare and Medicaid recipients she did ney’s fees. The defendant physician and hospital agreed that not like her tax dollars supporting his drug habit. Eventuthe family was only entitled to the limited remedies availally, Mr. James became irritable, withdrawn, and bedfast, able in a malpractice claim, repeatedly disputed the elder where he lay sweating and moaning in pain dying 4 abuse claim, and petitioned for it to be dismissed. In January months later. His family eventually filed a complaint with 2000 the court ruled against dismissal of the elder abuse a state regulatory agency and went to court. On November claims, recognizing that inadequate pain care can constitute ½ 3days of elder abuse. Kathryn Tucker, Esq., director of legal affairs20, 1990, trial began in North Carolina. After testimony, the jury took less than 1 hour to render the for the Compassion in Dying Federation, explained that a verdict that the nursing home had been negligent in failing successful trial means the Bergman family will be able to to provide Mr. James adequate pain relief. At the trial, recover significant damages and as exposure for inadequate Catherine Faison, James’ great niece, explained that as far pain care becomes more signifi cant, providers will be more as the nursing home was concerned, when he died, it was motivated to attend and treat pain properly under exposure a closed issue; it was over. “It’ s not over for me, ” Faison to significantly greater nancial fi risk (Partners Against Pain, 2000). Dying patients clearly have the right to adequatetold the jury. “ I can’t sleep at night when I think about pain medication; this was recently recognized by thethe fact that he had to lay over there and suffer… I think Supreme CourtVacco ( v. Quill, 1997;Washington v. Glucks- about him laying there hurting, saying I want my medication, and not being able to get it. I don’ t want to suffer berg, 1997; Burt, 1997). like that… I don’ t think anybody would. Somebody needs Illustrative of the law’s recognition that assurance of to say you can’ t do it. ” comfort and appropriate pain control are integral compoSafe harbor provisions in intractable pain legislation nents of appropriate medical care State ( v. McAfee , 1989) is, in this instance, a quadriplegic who was incapable ofenacted in many states grant immunity from discipline to physicians who treat intractable pain. These enactments spontaneous respiration and sought court approval for discontinuation of his respirator. The Georgia Supreme Courtclarify the position that physicians shall not be disciplined affirmed the patient’ s right to refuse medical treatment and for treating intractable pain with large doses of medication, even if such prescriptions hasten the moment of the held that he was also entitled to have a sedative adminispatient’s death, as long as the intent is simply to alleviate tered at the time: pain. Such provisions are designed to clear the confusion that may occur because of the similarity with prescribing Mr. McAfee’s right to be free from pain at the time the medications to end a patient’ s life. ventilator is disconnected is inseparable from his right to

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In 1999, the Oregon Board of Medical Examinersdirectives. Where questions or concerns arise about complying with such pain management instruction, ethics disciplined a physician for the undertreatment of a patient’ s committees should be consulted (Shapiro, 1994). intractable pain. Dr. Paul Bilder, an Oregon monary pul specialist, was disciplined for a pattern of failing to treat Appropriate pain management aims to reduce sufferpain adequately (Goodman, 1999). The physician was ing, not cause death. When physicians deliberately adminreported to have undertreated patients as followsister lethal doses of medications — even for reasons of (Mascheri, 1999). compassion — they risk prosecution for homicide, and when lethal doses of medications are prescribed, they risk 1. Tylenol (Loeb, 1996) was used for an elderly prosecution for assisting suicide. male cancer patient’ s musculoskeletal pain, To avoid exposure to criminal prosecution, physicians denying requests for stronger medications when should (a) prescribe medications in doses in accordance pain increased. He also denied a nurse’ s request with what is necessary to manage pain with good medical for catheterization, citing a risk of infection. judgment; (b) clearly communicate their rationale for pain The patient died the next day. medication prescriptions with patients, their families, and 2. He removed a catheter from an 84-year-old man other caregivers; and (c) clearly document the intent against the patient’ s and family’s request, behind and need for the medication prescribed. directing that he instead use diapers. He further Investigations of physicians for perceived excessive reduced a hospice nurse’ s requested dose of 5 prescribing of pain medication reduces physician willingto 20 mg of Roxanol every 4 hours to 0.25 cc ness to treat pain with strong pain medications. This is and gave Tylenol (Loeb, 1996) to treat the one factor contributing to the problem of undertreatment patient’s 102° temperature. The patient died of pain. During the past few years, aggressive educational that evening. efforts have begun to correct the undertreatment of pain 3. He refused a request for sedatives and pain con- and other physical suffering in dying patients — a major trol for a 35-year-old intubated, mechanically failing in medical care (Noble, 1999). ventilated woman who became increasingly A pending federal bill would have significant adverse restless, had increased wheezing, and was fight- impact on progress in this area. The Pain Relief Promotion ing the ventilator. After the patient extubated Act of 1999 (PRPA, 2000), should Congress decide to herself, the doctor ordered a paralytic agent but enact it, would increase physician exposure to investigano sedative following reintubation. tions for prescribing aggressive pain treatment at the end 4. He used physical restraint to intubate a 33-year- of life. It is the public fear of intolerable suffering that is old man without using anxiolytics or narcotics. a major reason for public support of assisted suicide (BlenThe patient had been admitted with severe don, Szalay, & Knox, 1992). In 1994, Oregon became the pneumonia associated with hypoxemia. The first state in the nation to pass a law permitting physicianphysician, it is claimed by the board, engaged assisted suicide. By November, 1997, all barriers (e.g., legal in “ unprofessional or dishonorable conduct” challenges and ballot measures to rescind the law leading to and “gross negligence or repeated negligence, ” delays in implementation) were put aside and Oregon’ s according to a stipulated order released by the Death with Dignity Act became fully operative. board. While the physician will not lose his The legal effect of PRPA is at odds with its appealing license, this is the first time a state board has title because the act, introduced by Rep. Henry Hyde taken this type of actions. (R, IL) and Sen. Don Nickles (R, OK), is designed to override Oregon’ s physician-assisted suicide law (BNA Thus, in addition to potential liability to patients for Health Law Reporter, 1999). The primary goal of PRPA inappropriate pain management, professional discipline ofis to prevent physicians in Oregon from continuing to healthcare professionals also may ensue. As a result implement of the Death with Dignity Act (Orentlicher & development and growing acceptance of pain management Caplan, 2000). Title I of the PRPA amends the Controlled guidelines, medical boards may be more inclined in theSubstances Act to nullify Oregon’ s physician-assisted suifuture to undertake disciplinary action for inadequate paincide law. Section 101 of PRPA states opiates, drugs, and management. other controlled substances may not be intentionally used Increased use of advanced directives resulting from“for the purpose of causing death or assisting another passage of the federal Patient Self-Determination Actperson in causing death. ” While rejecting assisted suicide, (effective December 1, 1991) also may increase physi-Title I of PRPA makes a strong statement favoring palliacians’ exposure to professional discipline for inappropri- tive care as a part of a legitimate medical practice to use ate pain management. In the interests of sustaining proa controlled substance with the intent to alleviate patients’ tection, physicians are advised to honor appropriate pain pain — “even if the use of such a substance may increase management instructions set forth in patients’ advanced the risk of death” (PRPA, 1999 S102). Educational and

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training programs for local, state, and federal law enforce-patient who dies of natural causes, the death may be misment personnel on the legitimate use of controlled sub-takenly ascribed to the medication. The PRPA would manstances in pain management and palliative care (PRPA, date that those dif ficult, and subjective, questions be 1999). In deciding what uses of controlled substances are resolved by the criminal process, after the fact. Physicians consistent with the public interest, the U.S. Attorney Gen-are left exposed to the general criminal penalties associeral “shall give no force and effect to state law authorizingated with Section 841(a) if they potentially should have or permitting assisted suicide or euthanasia” (PRPA, known that the dosage they prescribed would result in 1999). death, even if their subjective intent in fact was to provide Title II of PRPA provides for “programs to provide palliative care. If the physician uses aggressive doses of opiate drugs to provide palliative care and is charged under education and training to healthcare professionals in palliative care.” The PRPA would potentially expose to crim- the PRPA, a conviction would result in draconian conseinal prosecution physicians in every state who providequences. The intent to cause death can be inferred from pain management drugs that they knew would or couldthe drug or dose ordered, the potential therefore exists for increase the likelihood of a patient’ s death. Under physician incarceration if the local authorities view, in retrospect, the dosage received by the patient as excessive. Section 101 of PRPA, the line between acceptable palliative care and unacceptable assisted suicide fined is de A physician convicted under PRPA for using a Schedule II drug and causing a patient’ s death faces a minimum solely by the physician’ s intents. sentence of 20 years in prison and a maximum sentence Section 401 of the Controlled Substances Act (CSA) of life in prison. contains a broad prohibition on the distribution and dispensing of federally controlled substances, and violation The Controlled Substances Act is an anti-drug abuse of Section 401 carries criminal penalties. Section 303,law enforcement statute administered by the Attorney General (Testimony before Senate, 1998). The Departhowever, provides a so-called safe harbor from the broad prohibition (of Section 401) for the medical profession,ment of Justice was given the authority to prevent and allowing physicians to use such federally controlled sub-prosecute illicit drug use, a power that has been exercised stances, including the drugs necessary to ease the paininoflarge part by the DEA. Under the Pain Relief Promotion Act (PRPA) instead of looking to medical experts and the patients, in the course of their practices. When Congress passed the Controlled Substances Act to address ficktraf FDA for guidance on the appropriate use of opioids, baring in illicit drugs, it employed language that incidentally biturates, and other palliative drugs in end-of-life care, physicians also would have to consider the views of ’s DEA covers physicians who use controlled substances to assist agents (Testimony before House, 1999). a patient in suicide or perform euthanasia. As currently drafted, PRPA adds to the end of that safe-harbor section By using a federal statue to override an Oregon health(Section 803) two new elements of law that when read incare law, PRPA contravenes the principle of federalism, a the context of the CSA, radically affect the ability of fundamental tenet of American law. The regulation of physicians to practice medicine. The amendment rst fi medical practice traditionally has been the province of includes a deceptively physician friendly support for states and their medical boards, not that of the federal government and its law enforcement agencies. The preaggressive pain management that “may increase the risk of death” and next adds a provision removing from amble to the Medicare law expressly prohibits any federal Section 823 the use of such federally controlled sub-“supervision or control over the practice of medicine or stances to intentionally cause or assist in the causing ofthe a manner in which medical services are provided” (Iglehart, 1992). patient’s death. Without this safe-harbor provision, physiIn the past decade, physicians have become more cians in Oregon who comply with their patients’ wishes likely to face civil lawsuits as well as criminal prosecupursuant to that state’ s Death with Dignity Law will be tions when charged with substandard medical care. It is subject to the CSA criminal sanctions. The notion of intent likely that the PRPA would induce physicians to avoid the and the unclear manner in which it is used in S.1272 threat of legal liability and again exacerbate the undercreates trouble for physicians in all states whether or not treatment of pain causing increased suffering in the they plan to engage in physician-assisted suicide. Legally, patients with pain. Pressure on physicians to undertreat intent is considered to be established where there is knowlpain will increase under PRPA, yet the risk for so doing edge that the death is substantially certain to occur as a is an increasingly punitive reality — truly placing physiresult of the conduct; however, intent also can be found cians between the rock and the hard place. where death should have been reasonably expected to occur as a result of the conduct. When intent is the critical issue, physicians must be concerned that law enforcement CONCLUSION officers will see a criminal intent where none existed. The Pain is one of the most common reasons for seeking medrisk of prosecution is exacerbated by the fact that when high doses of medication are utilized in a terminally ill ical care, yet it is often inadequately treated. Untreated,

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American Pain Society, 4700 W. Lake Avenue, Glen View, Illithe pain accompanying illnesses slows recovery, severely nois 60025-1485; (847)375-4715, Fax (847) 375-4777. impairs an individual’ s quality of life, and adds signifi cantly , No. H205732-1 (Cal. App. Dep’ t. Super. Ct. to the healthcare system’ s financial burden. The Joint Com- Bergman v. Chin Feb. 16, 1999). mission on Accreditation of Healthcare Organizations Bergman v. Eden Med. Ctr ., No. H205732-1 Cal. Sup. Ct., (JCAHO) standards (the new evidence-based pain manAlameda Cty. (Medical negligence and elder abuse for agement standards introduced by JCAHO) (Phillips, 2000) failure to adequately treat ain in elderly patient dying of asserts that individuals seeking care at accredited hospilung cancer) (pending). tals, behavioral health facilities, and healthcare networks, Bernabei, R., Gambassi, G., Lapane, K., et al. (1998). Managehave the right to appropriate assessment and management ment of pain in elderly patients with cancer. SAGE of pain. All patients are to be screened for the presence Study Group. systematic assessment of geriatric drug of pain. For those reporting pain, a complete assessment use via epidemiology. Journal of the American Medical must be conducted to characterize a patient’ s pain by Association, 279,1877–1882. location, intensity, and cause, including a detailed history,Black’s Law Dictionary.(1979). (5th ed., p. 497). St. Paul, MN: physical examination, psychosocial assessment, and diagWest Publishing. nostic evaluation. Blendon, R.J., Szalay, U.S., & Knox, R.S. (1992). Should phyThe most reliable indicator of pain existence and sicians aid their patients in dying? The public perspecintensity is the patient’ s self-report because it is more tive. Journal of the American Medical Association, 267, accurate than others’ observations. These standards do not 2658–2662. dictate specific pain management procedures nor advocate Bostrom, B.M., Ramberg, T., Davis, B.D., & Fridlund, B. (1997). in any way the use of certain drugs (e.g., opioids). Survey of post-operative patients’ pain management. Journal of Nursing Management, 341–349. 5, A discussion of the emerging standards and guidelines (Jacox, Carr, & Payne, 1994) coupled with developingBrown, D.L., & Carpenter, R.L. (1990). Perioperative analgesia: A review of risks and benefits. Journal of Cardiothodisciplinary and legal consequences to remold physician racic Anesthesia, 4,368–383. action and delivery of medical care utilizing the fulcrum Burt, R.A. (1997). The Supreme Court speaks: Not assisted of inadequate pain management as inappropriate medical suicide but a constitutional right to palliative care. New care appears designed to move physicians into fungible England Journal of Medicine, 337, 1234–1236. units in need of surveillance to assure compliance with all controlling legal authority. The House version of the PainCalonge, N. (2000). Processes and targets for improving the quality of healthcare. Preventive Medicine and Managed Relief Promotions Act was passed in October of 1999, Care, 1(3), 149–152. although a filibuster is expected when the bill is introduced Carr, D.B. (1998). Clinical pain management guidelines. Emerin the Senate.

gency Medicine, 30 (45), S2–S6. Carr, D.B., Jacox, A.K., Chapman, C.R., et al. (1992). Acute pain management: Operative or medical procedures and trauma. Clinical Practice Guideline. AHCPR Pub. No. REFERENCES 92-0032. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department 21 USCA § 841(b)(1)(c) (1999). of Health & Human Services. Agency for Health Care Policy and Research. (1992). Acute Pain Carr, D.B., Jacox, A.K., Chapman, C.R., et al. (1995). Acute Management Guideline Panel. Acute Pain Management: Pain Management. Guideline Technical Report, No. 1. Operative or Medical Procedures and Trauma. Pub. No. AHCPR Pub. No. 95-0034. Rockville, MD: Agency for 92-0032. Washington, D.C.: U.S. Department of Health Health Care Policy and Research Public Health Care & Human Services. Policy and Research, Public Health Service, U.S. American Academy of Pain Management, 13947 Mono Way #A, Department of Health and Human Services. Sonora, California 95370; (209) 533-9744, Fax (209) Cavalieri, T.A. (1999). Pain management at the end of life. 533-9750. Journal American Osteopathic Association, (6), 99 American Academy of Pain Medicine, 4700 W. Lake Avenue, S16–S21. Glenview, Illinois 60025-1485; (847) 375-4731, Fax — Hastening or (847) 375-4777. The AMA-recognized speciality soci- Cavanaugh, T.A. (1996). The ethics of death death-causing palliative analgesic administration to the ety of physicians who practice pain medicine. terminally ill. Journal of Pain and Symptom ManageAmerican Medical Association. (1996). Code of Medical Ethics. ment, 12,248–254. American Medical Association. (1999). Education for Physicians on End-of-Life Care. Participants handbook. Chicago,Chasin, M.R. (1997). Assessing strategies for quality improvement. Health Affairs (Millwood, VA). 16, 151–161. IL: American Medical Association. American Pain Society Quality of Care Committee. (1995).Chassin, M.F., & Galvin, R.W. (1998). The National Roundtable on Health Care Quality: The urgent need to improve Quality improvement guidelines for the treatment of healthcare quality.Journal of the American Medical acute pain and cancer pain. Journal of the American Association, 280,1000–1005. Medical Association, 274, 1874–1880.

Pain Management: Medical and Legal Issues of Undertreatment

931

Cherny, N.J., & Portenoy, R.K. (1994). The management ofGostin, L. (2000). A public approach to reducing error, medical malpractice as a barrier. Journal of the American Medcancer pain. CA.A Cancer Journal for Clinicians, 44, ical Association, 283,1742–1743. 263–303. Clark, H.W. (1998). Legal implications of prescribing opioid Guglielmo, W.J. (2000). Can doctors put their fears to rest? controlled substances. Emergency Medicine, 30 (45), Medical Economics,(February 21), 47–59 from David E. Joranson, director of the Pain and Policy Studies S29–S33. Group at the University of Wisconsin — Madison. Cleeland, C.S. (1992). Documenting barriers to cancer pain management.Current and Emerging Issues in Cancer Pain: Hall v. Hilbun, 466 So.2d 856,871 (Miss. 1985). Research and Practice, 321, 325–327. Heller, M.B. (1992). Emergency management of acute pain: New Cleeland, C.S., Gonin, R., Baez, L., Loehrer, P., & Pandya, K.J. options and strategies. Postgraduate Medicine, 39–47. (1997). Pain and treatment of pain in minority patientsHelling v. Carey, 519 P.2d 981 (Washington, 1974). The most with cancer. The Eastern Cooperative Oncology Group often-cited case in which a court essentially condemned Minority Outpatient Study.Annals of Internal Medicine, an entire medical speciality. 127, 813–816. Hill, C.S. (1993). The Negative Influence of Licensing and DisDahlman, G.-B., Dykes, A.-K., & Elander, G. (1999). Patients’ ciplinary Boards and Drug Enforcement Agencies in evaluation of pain and nurses’ management of analgePain with Opioid Analgesics. Journal of Pharmacology sics after surgery. The effect of a study day on the subject Care and Pain Symptom Control, 43–62. 1, of pain for nurses working at the thorax surgery depart-Hill, Jr., C.S. (1995). When will adequate pain treatment be the ment. Journal of Advanced Nursing, 30, 866–874. norm? Journal of the American Medical Association, Edwards, R.B. (1984). Pain and the ethics of pain management. 274, 1881–1882. Society of Science and Medicine, 18, 515–517. Hill, Jr., C.S. (1996a). Adequate pain treatment: a challenge for Emanuel, E.J. (1996). Pain and symptom control: patient rights medical regulatory boards. Journal of the Florida Medand physician responsibilities. Hematology and Oncolical Association, 83,677–678. Editorial. ogy Clinics of North America, 10, 41–47. Hill, Jr., C.S. (1996b). Government regulatory influences on Estate of Henry James v. Hillhaven Corp. (N.C. Super. Ct., opioid prescribing and their impact on the treatment of Hertford Cty. 1990).Faison v. The Hillhaven Corp ., No. pain of nonmalignant origin. Journal of Pain and Symp89 CVS 65 (Hertford Cty. Super. Ct. N.C. Dec. 1990) tom Management, 11, 287–298. ($15 million jury award, half of which was punitive, Hoover, v. Agency for Health Care Administration , 676 So.2d against nursing home nurse’ s conduct in failing to pro1380 (Fla. Dist. Ct. App. 1996) (Florida medical discivide prescribed pain medications to terminally ill plinary board penalized and restricted physician for perpatient, settled on appeal for undisclosed amount). ceived excessive prescribing of pain medication; action Ewing, J.A. (1984). Detecting alcoholism: The CAGE questionof board reversed by court); Hollabaugh v. Arkansas naire: A critical review.Journal of the American Medical State Med. Bd., 861 S.W.2d 317 (Ark. Ct. App. Association, 252,1905–1907. 1993)(similar case in Arkansas). Favalora v. Aetna Cs. & Sur. Co. , 144 So.2d 544, 551 (La. Ct. Iglehart, J.K. (1992). The American healthcare system: IntroducApp. 1962). tion. New England Journal of Medicine, 326, 962–967 Ferrel, B.R., & Rhiner, M. (1994). High-tech comfort: Ethical (citing 42 USC § 1395). issues in cancer pain management for the 1990s. Journal International Project of Hastings Center. (1996). The Goals of of Clinical Ethics, 2,108–112. Medicine: Setting New Priorities.Hastings Center Foley, K.M. (1997). Management of cancer pain. In V.T. De Vita, Report (Nov.-Dec.), S1. S. Hellman, & S. Rosenberg (Eds.), Cancer: Principles Jacox, A., Carr, D.B., & Payne, R. (1994). New clinical practice and practice of oncology (5th ed., pp. 2807–2841). Philguidelines for the management of pain in patients with adelphia: Lippincott-Raven Press. cancer. New England Journal of Medicine, 330, Frank-Stromborg, M., & Christiansen, A. (2000). The untreat651–655. ment of pain: A liability risk for nurses. Clinical Journal Jacox, A., Carr, D.B., Payne, R., Berde, C.B., Biebart, W., Cain, of Oncology Nursing, (1), 4 41–44. J.M., et al. (1994). Guideline Panel. Management of Gaddis v. United States , 7 F. Supp. 2d (D.S.C. 1997). Cancer Pain. Clinical Practice Guideline Number 9. Rockville, MD: Agency for Health Care Policy and Gallup, Inc. (June 9, 1999). Pain in America: Highlights from a Research, U.S. Department of Health and Human SerGallup survey. vices, Public Health Service; AHCPR Publication No. Glanelli, D.M. (1999). Opioid prescriptions rarely lead to rebuke, 94-0592. study finds. AMA News (Professional Issues) February James, G. (2000). Addressing barriers to healthcare for our eld8. erly. Family PhysicianJournal of American College of Goff, D.C., Canely, L.K., & Gu, L. (2000). Increasing the approOsteopathic Family Practice,(9), 4 9–13. priate use of reductase inhibitors among patients with coronary heart disease enrolled in a network — model Joranson, D.E. (1992). Opioids for chronic cancer and nonmanaged care organization. Preventive Medicine and cancer pain: A survey of state medical board members. Managed Care, 1,141–148. federation bulletin.Journal of Medical Licensure and Discipline, 9, 15. Goldstein, F.J. (1999). Management of acute pain. Journal American Osteopathic Association, 99(6), S1–S5. Joshi, G.P. (1994). Postoperative pain management. International Anesthesiology Clinics, 113–126. Goodman, E. ( 1999). Charlotte Observer . September 11.

932

Pain Management: A Practical Guide for Clinicians, Sixth Edition

Katz, W.A. (1996). Approach to management of non-malignantMerskey, H. (1986). Classification of chronic pain, descriptions of chronic pain syndromes and definitions of pain terms. pain. American Journal of Medicine, 101, 54S–63S. Pain, Suppl. 3, S1–S226. Keeton, W., Dobbs, D.B., Keeton, R.E., & Owen, D.G. (1984). Model Guidelines for the Use of Controlled Substances for the Prosser and Keeton on the law of torts. St. Paul, MN: Treatment of Pain. (1998). Euless, TX: Federation of West Publishing. State Medical Boards of the United States, Inc. Kehlet, H. (1989). Surgical stress: The role of pain and analgesia. Morris, D.B. (1991).The culture of pain , 134. British Journal of Anaesthesia, 63, 189–195. King, K.M., Bungard, T.J., McAlister, F.A., et al. (2000). for the Morrison, J.M, & Wickersham, M.S. (1998). Physicians disciplined by a state medical board. Journal of the American CQIN Investigators. Quality Improvement for CQI. PreMedical Association, 279 (23), 1889–1893. ventive Medicine and Managed Care,129–137. 1, Kores, R., Murphy, W.D., Rosenthal, T.L., Elias, D., & North, Nickles proposal opposes legalized assisted suicide. BNA Health Law Reporter June 24, 1999; 8, 1027 W.C. (1990). Predicting outcome of chronic pain treatment via a modified self-ef ficacy scale. Behavior Noble, H.B. A shift in the treatment of chronic pain. New York Research and Therapy, 24. Times,August 9, 1999, A13. Lavies, N., Hart, L., Rounsefell, B., & Runciman, W. (1992). Nowatske v. Osterlok , 543 N.W.2d 265,2710272 (Wis. 1996). Identification of patient, medical and nursing staff atti- Nyquist, A.-C., Gonzales, R., Steiner, J.R., & Sande, M.E. tudes to postoperative opioid analgesia: Stage I of a (1998). Antibiotic prescribing for children with colds, longitudinal study of postoperative analgesia. Pain, 48, upper respiratory tract infections, and bronchitis. Jour313–319. nal of the American Medical Association, 279, 875–877. Leape, L.L. (1992). Unnecessary surgery. Annual Review of Pub- Oherney, N.I., & Catane, R. (1995). Professional negligence in lic Health, 13,363–383. the management of cancer pain. Cancer, 76,2181. Leape, L.L. Error in Medicine. (1994). Journal of the American Oncology Nursing Society. (1998). Oncology Nursing Society Medical Association, 272, 1851–1857. position: Cancer pain management. Oncology Nursing Forum, 25, 817–818. Letter from Medical Board of California to Beverly Bergman dated August 19, 1998 states in pertinent part: “OurOrentlicher, D., & Caplan, A. (2000). The Pain Relief Promotion medical consultant did agree with you that pain manAct of 1999, A serious threat to palliative care. Journal agement for your father was indeed inadequate. ” of the American Medical Association, 283 (2), 255–258. Litman, G.S., Walker, B.R., & Schneier, B.E. (1985). Reassess-Pain Relief Promotion Act of 1999, HR2260, § 101. ment of verbal and visual analog ratings in analgesicParran, T. (1997). Prescription drug abuse — A question of balstudies.Clinical Pharmacology and Therapeutics, 38, ance.Medical Clinics of North America, 81, 967–978. 16–23. Patient Self-Determination Act, 42 U.S.C. sect. 395 et seq. Loeb, J.L. (1996). Pain management in long-term care. American (1991). Journal of Nursing, 99 (2), 48–52. (Recent studies have Phillips, D. (2000). JCAHO pain management standards are found that acetamenophen is the most commonly preunveiled.Journal of the American Medical Association, scribed and appropriate pain relief medication for mild 284, 428–429. to moderate pain.) Policy and Practice. (2000, November 1). Pain act provides no Lohr, K.N. (Ed.) (1990). Medicare: A strategy of quality assurrelief. Family Practice News . ance. Washington, D.C.: National Academy Press. Portenoy, R.K. (1996a). Opioid therapy for chronic nonmaligLutz, L.J., & Lamer, T.J. (1990). Management of postoperative nant pain: Clinicians’perspective.Journal of Law and pain: Review of current techniques and methods. Mayo Medical Ethics, 24,296–309. Clinic Proceedings, 65,584–596. Portenoy, R.K. (1996b). Opioid therapy for chronic nonmaligMarcus, D.A. (2000). Treatment of non-malignant chronic pain. nant pain: Medication history review of the critical American Family Physician, 61, 1331–1338. issues. Journal of Pain Symptom Management, 11, Martelli, M.F., Zasler, N.D., & Grayson, R. (1999). Ethical con203–217. siderations in medicolegal evaluation of neurologic Purdue Pharma Limited Partnership. (2000). Undertreatment of injury and impairment.NeuroRehabilitation: An Interpain goes to court as elder abuse. Partners against Pain, disciplinary Journal,13(1), 45–66. 3(1), 4. Martino, A.M. (1998). In search of a new ethic for treating Rich, B.A. (2000). A prescription for the pain: The emerging patients with chronic pain: What can medical boards do? standard of care for pain management. Wm. Mitchell Journal of Law and Medical Ethics, 26, 332–349. Law Review, .1 Mascheri, L.L. Associate Director, State Government Affairs.Rorarius, M.G.F., & Baer, G.A. (1994). Non-steroidal antiIntractable Pain Legislation. AOA Division of State inflammatory drugs for postoperative pain relief. CurGovernment Affairs: September, 1999. rent Opinion in Anesthesiology, 358–362. 7, McCarberg, B. (2000). Managing the acute pain patient: Allevi-Saberski, L.R. (2000, August). Frailty: My name is physician. ating the pain . Family Practice Research Journal, 22(9), The weak, the strong link, and the pain evaluation: Not S4–S7. all pain is the same. The Pain Clinic,7–8. Medical Board of California (July 29, 1994). Guideline for pre- Shapiro, R.S. (1994). Legal bases for the control of analgesic scribing controlled substances for intractable pain. drugs. Journal of Pain and Symptom Management, 9, 153–159. Medical Board of California Action Report 4 (Oct. 1994).

Pain Management: Medical and Legal Issues of Undertreatment

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Tittle, M., & McMillan, S.C. (1994). Pain and pain-related side Shapiro, R.S. (1996). Healthcare providers’ liability exposure effects in an ICU and on a surgical unit: Nurses’ manfor inappropriate pain management. Journal of Law and agement.American Journal of Critical, 3,25–30. Medical Ethics, 24,360–364. , 239 N. E. 2d 368, 373 Sommerville, M.A. (1986). Pain and suffering at the interfacesToth v. Community Hosp. at Glen Cove (N.Y. 1968). of medicine and law. University of Toronto Law Journal, Townsend, R.J., Spartz, M.E., Fahrenbruch, R.W., et al. (1983). 36, 286. Hospital labor cost savings in dispensing analgesics: State v. McAfee , 259 Ga. 579, 385 S.E. 2d 651 (Ga. 1989). Controlled vs. non-controlled. Hospital Formulary, 18, Stjernsward, J., et al. (1996). The World Health Organization 716–720. cancer pain and palliative care program: Past, present, and future.Journal of Pain and Symptom Management, Tucker, K.L. (2000). Lecture notes. On Inadequate Treatment of Pain: Accountability, American Academy of Pain Man12, 65–68. agement 11th Annual Clinical Meeting. T.J. Hooper, 60 F.2d 737,740(2d Cir. 1932). Judge Learned Vacco v. Quill, 117 S. Ct. 2293 (1997). Hand’s words: … a whole calling may have lagged in Vainio, A., Ollila, J., Matikainen, E., et al. (1995). Driving ability the adoption of new and available devices. Courts must in cancer patients receiving long-term morphine analgein the end say what is required; there are precautions so sia. Lancet, 346,667–670. imperative that even their universal disregard will not View cancer pain as a “pathogenic agent” to treated, expert says. excuse their omission. (1998). Oncology News International, 7(10), 36, 43. Terman, G., & Liebeskind, J. (1991). Pain can kill. Pain, 44, Washington v. Glucksberg , 117 S. Ct. 2258 (1997). 3–4. Editorial. Webster’s Third New International Dictionary . (1993). “IntracTestimony before the House Subcommittee on the Constitution table” is a term used to describe any situation or condiof the Committee on the Judiciary, Hearings on HR220 tion that is unmanageable or untreatable. on the Pain Relief Promotion Act of 1999, 106th Cong. Weiner, S.L. (1993).Differential diagnosis of acute pain by body 1st Sess (June 24, 1999) (testimony of David E. Joranregion (pp. 1–2). New York: McGraw-Hill. son). Whipple, J.K., Lewis, K.S., Quebbman, E.J., et al. (1995). AnalTestimony before the Senate Committee on the Judiciary, The ysis of pain management in critically ill patients. PharLethal Drug Abuse Prevention Act of 1998, ” 105th macotherapy, 15,592–599. Cong. 2nd Sess. (July 31, 1998) (testimony of PrincipalWillis, J. (1998). Should nurses start running from patients ’ Deputy Associate Attorney General Joseph N. Onek). complaints?Nursing Times,94(15), 7–12. The board’s letter stated: “There is insuf ficient evidence Wilschinsky v. Medina,775 P.2d 713 (NM 1989). The New at this time to warrant pursuing further action in this Mexico Supreme Court ruled that a physician could be case. Yourfile shall be maintained with the Medical held liable to a man who was injured by an automobile Board for future reference in the event we receive addidriven by his patient to whom he had administered drugs tional complaints in the future which, along with your that caused drowsiness. It further held that a physician complaint, could constitute suf ficient evidence for disdoes have a legal duty to use reasonable care in treating ciplinary action.” patients, and that this duty extends to the driving public when the physician administers drugs known to cause The Oregon Death with Dignity Act, Oregon Rev. Stat. § 127.800 drowsiness and impairment of judgment. (1996).

75 Provider Accountability for Inadequate Pain Management Kathryn L. Tucker, J.D. Patients in the United States are routinely undertreated for It is not uncommon for physicians to be investigated for prescribing controlled substances in amounts that regpain. This problem has been widely recognized and doc’s conumented in the medical literature. In a seminal medicalulators perceive as excessive. Even if the physician study of end-of-life care, researchers found that 50% ofduct meets relevant guidelines for pain management, such all patients who died during hospitalization “experiencedinvestigations may result in physician discipline, including suspension or revocation of prescribing authority, other moderate or severe pain at least half of the time during limitations on medical practice, and other penalties their last 3 days of life” (SUPPORT, 1995). Elderly patients are particularly vulnerable to insuffi- (Hoover v. Agency for Health Care Administration, 1996). cient pain treatment. A recent study in the Journal of the It has become widely recognized that the multiple copy American Medical Association found that up to 40% of prescription laws deter physicians from writing prescriptions for controlled substances, and thus, create barriers cancer patients in nursing homes are not appropriately treated for pain. In addition, 26% of those experiencingto access to adequate pain medication. In response, some pain did not receive any pain medication, and 16% werestates have, in recent years, eliminated traditional multiple given over-the-counter pain relievers like aspirin or ace-copy laws (N.Y. Public Health Law, 2000). This is a step taminophen for their pain (Bernabei, et al., 1998). At thein the right direction; yet, it is unlikely to correct the serious problem of inadequate treatment of pain on its own. same time, it is well established that only perhaps 10% of dying patients have conditions in which alleviation of pain The American Society of Law, Medicine, and Ethics is truly difficult or impossible (Jacox, et al., 2000). (ASLME) recently undertook a reform effort, the Project One repeatedly identified cause of this problem ison Legal Constraints on Access to Effective Pain Managephysician concern that prescribing controlled substances ment. The Project developed a model Pain Relief Act that will invite regulatory agency oversight (Breaking Down creates a “safe harbor” for physicians who prescribe pain the Barriers, 1998). Other factors inhibiting adequate painmedication as long as the physician substantially complied treatment described in the medical literature include thewith accepted practice and care guidelines for pain manfear that strong pain treatment will hasten death (Schneiagement (The Pain Relief Act, 1996). This safe harbor derman, 1997), and the concern that the patient willshelters physicians from both disciplinary and criminal become addicted to the pain medication (Stavish, 1997).action if the physician can “demonstrate by reference to Oversight is triggered in some states by laws thatan accepted guideline that his or her practice substantially require duplicate or triplicate prescription forms, with complied with that guideline. ” The physician also must copies going to reviewing authorities. These laws werehave kept appropriate records, written no false prescripintended to deter illegitimate drug use. Unfortunately, theytions, obeyed the CSA, and not diverted medications to have had an enormous impact on legitimate use, as well. personal use (The Pain Relief Act, 1996). 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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The safe-harbor concept is also encompassed in state physician had failed to provide adequate pain care (MBC laws known as Intractable Pain Treatment Acts (IPTA).Letter, 1998). Yet the MBCdeclined to take any action The existing state statutes generally provide shelter from against the physician (MBC Letter, 1998). At least one disciplinary action, but make no mention of criminal expo-other case of inadequate pain care presented to the MBC, sure. The California IPTA, for example, provides that “noalso supported by an expert opinion that the pain care was physician or surgeon shall be subject to disciplinary actioninadequate, was also closed without any corrective action. by the board for prescribing or administering controlled substances in the course of treatment of a person for intractable pain” (California Business and ProfessionalSIGNS OF CHANGE: ACCOUNTABILITY IN Code,§ 2241.5(c)). To be immune from board discipline THE MEDICAL DISCIPLINARY AND TORT this IPTA requires that the patient not be known to haveCONTEXTS EMERGE chemical dependency or to be using drugs for nontheraThere are signs, however, that the laissez-faire attitude peutic purposes. The physician must prescribe medicaregarding inadequate treatment of pain is beginning to tions for therapeutic purposes, keep appropriate records, change. In 1999, a state medical disciplinary board took not write false prescriptions, and prescribe in a manner consistent with the state and federal CSA (California Busi-corrective action against an Oregon physician who failed to treat his patients adequately for pain (Goodman, 1999). ness and Professional Code, § 2241.5(c)). Unfortunately, IPTAs have proven to be largely inefCases of inadequate pain treatment are beginning to fectual (Rich, 2000). Reports continue to document thatresult in civil liability in tort cases, with significant finanundertreatment of pain is pervasive (Rich, 2000). Thecial implications Estate ( of Henry James v. Hillhaven situation in California exemplifies this failure. Corp., 1990; Gaddis v. United States, 1997; Bergman v. California is among the most progressive states inEden Med. Ctr. , 2001). The recent emergence of guideattempting to improve pain care. The state legislaturelines and standards governing appropriate pain care perpassed its IPTA in 1990 (Rich, 2000). In 1994 the Medicalmits establishing that, in a specific case, the pain care Board of California (MBC) provided all California phy- provided was inadequate and should result in professional sicians with a copy of the clinical guidelines for pain discipline. Medical organizations establishing standards management issued by the U.S. Agency for Health Care or guidelines for pain treatment include the World Health Policy and Research (AHCPR), and adopted a policyOrganization (1986), the American Pain Society (1995), statement in May 1994 encouraging aggressive pain care. the American Medical Association (McGivney, et al., Subsequently, the MBC (1994) adopted an ficial of guide1984), AHCPR (1992), the Federation of State Medical line regarding pain management, which specifically iden-Boards (1998), and the Joint Commission on Accreditatifies failure to adequately manage pain as “inappropriate tion of Healthcare Organizations (JCAHO) (2000). These prescribing.” In explicitly making undertreatment of pain guidelines all indicate the importance of pain management a type of inappropriate prescribing, the MBC has xpressly e as an essential element of medical treatment. recognized that this is a form of professional misconduct There are new requirements for mandatory assessment and, thus, subject to the full range of sanctions. and routine charting of pain, imposed by the VA system, In 1997, the California legislature passed the Pain state law, and JCAHO accreditation provisions (California Patient’s Bill of Rights (California Health and Safety Code Health and Safety Code § 1254.7). These provisions will § 124960). This law provides, in pertinent part, that “a increase patient awareness of their right to good pain care, patient suffering from severe chronic intractable pain has increasing the likelihood that patients will seek accountthe option to request or reject the use of any or all modalities to relieve his or her severe chronic intractable ”pain.ability for inadequate pain care, and will enable patients and their advocates to establish with a clear documentary (California Health and Safety Code § 12496(h). This law explicitly confers a specific right on Califor- record that the pain care provided in a particular case was nia citizens to request any and all modalities to relieveinadequate and should result in professional discipline. pain. Yet, notwithstanding California’ s official posture of The record developed by the new assessment and charting rules will for the same reasons also make civil liability on a commitment to ensuring that patients receive adequate various theories, including professional negligence and pain care, including specifically adequate access to opioid elder abuse, easier to establish. analgesics, we cannot assume that physicians are providing adequate pain care or being held accountable when This is entirely appropriate and necessary because they do not. A recent specific case demonstrates this. knowledge of how to treat pain is available. The problem In 1998, the MBC was presented with a formal com-is that without outside motivation, physicians fail to acquire and apply available knowledge. Physicians must plaint, supported by an independent expert opinion, that the pain care provided to an elderly, terminally ill cancerbe motivated to acquire and apply this available knowlpatient was inadequate. The MBC itself agreed that the edge (Rich, 2000).

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American Pain Society. Quality improvement guidelines for the As these types of cases become more common, risk treatment of acute pain and cancer pain, Journal 274 of managers can be expected to undertake efforts to minimize American Medical Association, 1874 (1995). risk, leading to more attentive and aggressive provision of Assembly Bill 487 California State Legislature, 2001 Session. pain care. Bergman v. Eden Med. Ctr., No. H205732-1 Cal. Sup. Ct., Alameda Cty. (physician’ s failure to adequately treat pain in elderly patient dying of lung cancer) found to CHANGES IN LAW ON THE HORIZON be reckless conduct violating elder abuse statute. Jury Laws such as Intractable Pain Treatment Acts and Pain awarded $1.5M to survivors. Relief Acts, which currently provide a safe harbor for Bernabei, R., et al. (1998)Management of pain in elderly physicians who follow guidelines in prescribing medicapatients with cancer , Journal of American Medical Association,279, 1877, 1879. tions to relieve pain, may be revised to explicitly create t, Recrough waters for physicians who fail to do so. Such revi-Breaking down the barriers to effective pain managemen ommendations to improve the assessment and treatment sions would require disciplinary action, or provide an of pain in New York State, Report to the Commissioner explicit tort cause of action, when there is failure to adeof Health, (Jan. 1998) hereinafter “NY Report”; Institute quately prescribe, order, administer, or dispense pain manof Medicine, (1997); see also, Approaching Death, agement therapies, including controlled substances such Improving Care at the End of Life , at 191, 197 (National as opioid analgesics, for pain relief or modulation in accorAcademy Press) (1997) (laws designed to prevent diverdance with prevailing clinical practice guidelines. sion of drugs such as triplicate prescriptions and limits In the wake of the cases involving inadequate pain care on the number of medication dosages prescribed are presented to the Medical Board of California, discussed burdensome and deter legitimate prescribing of opioids above, which resulted in no action by the Board, such legto patients at the end of life); David Joranson, State islation has been introduced in the California State LegisMedical Board Guidelines for Treatment of Intractable Pain, 5, American Pain Society Bulletin , 2 (May/June lature. In its original form, the proposed California legisla1995) (citing California study reflecting that physicians tion would mandate the MBC to, at a minimum, compel avoid prescribing controlled substances including “tripphysicians shown to have failed to treat pain adequately to licate” drugs for patients with intractable pain for fear receive continuing education in pain management (Assemof discipline by the medical board); Robyn S. Shapiro, bly Bill 487, 2001). AB487 has been amended and is Health Care Providers’ Liability Exposure for Inapproexpected to pass in a form that requiresCalifornia all phypriate Pain Management, 24; Journal of Law, Medicine, sicians to obtain continued education in pain management. and Ethics, 360, 363 (Winter 1996) (identifying fear of By amending state law relating to pain in this way, legal penalties, especially disciplinary action, as one of essential steps in encouraging and motivating physicians the most important reasons health professionals underto treat pain appropriately will be accomplished. Such treat pain. Citing California survey revealing that 69% of physicians stated that the potential for disciplinary amendments would create rough waters for physicians action made them more conservative in their use of who fail to treat pain adequately. This is essential opioids in pain management). because a safe harbor is not enough; the seas outside California Business & Professional Code § 2241.5(c). must be rough. Physicians who presently fail to adeCalifornia Health & Safety Code § 124960. quately treat pain are already in a safe harbor, in the California Health & Safety Code 1254.7; § See CAMH Standard sense that there is rarely professional accountability for RI.1.2.8; CAMLTC Standard RI.2.6; CAMAC Standard such conduct. There must be a reason to seek the safe RI.1.2.7; CAMHC Standard RI.1.1.8; CAMBHC Standard harbor. Until physicians are aware that professional conRI.1.2.7. http://www.jcaho.org/standard/pm_hap.html. sequences and accountability attach if they fail to treat CIDF Letter. (1998). The idea that state medical boards should pain adequately, necessary improvement in the provision take on the responsibility of scrutinizing licensees for of pain care will not occur. inadequate pain care was presented to all 50 state medical boards by Compassion in Dying Federation (CIDF) in a letter sent in January 1998. Letter on le at fi CIDF offi ces. REFERENCES AND Estate of Henry James v. Hillhaven Corp . (N.C. Super. Ct., Hertford Cty. 1990) ($15 million jury award, half of ANNOTATED BIBLIOGRAPHY which was punitive, against nursing home for nurse’ s conduct in failing to provide prescribed pain medicaAcute pain management: operative or medical procedures and tions to terminally ill patient, settled on appeal for undistrauma clinical practice guideline (Clinical Practice closed amount). Guideline No. 1, Publ. No. 92-0032 (Feb. 1992) (visited Gaddis v.United States , 7 F. Supp. 2d 709 (D.S.C. 1997) (dam5/31/00) ages awarded to deceased patient’ s estate and to family ; for failure to treat pain of terminally ill cancer patient AHCPR, Clinical guideline no. 9: Management of canadequately).Guideline for Prescribing Controlled Subcer pain, Pub. No. 94-0592 (Mar. 1994).

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ination of the need for a duplicate or triplicate pad will stances for Intractable Pain , Guideline adopted by the facilitate prescribing. Others are skeptical, asserting the MBC July 29, 1994. concern that scrutiny would be applied to prescribing Goodman, E. (1999). Reporting that Dr. Paul Bilder, an Oregon pulmonary specialist, was disciplined by the Oregon controlled substances is in no way mitigated by a proMedical Board for a pattern of failing to treat pain adegram that enables electronic data sorting and review. quately.Charlotte Observer.Sept. 11. Prescribing Controlled Substances for Intractable Pain , policy Hoover v. Agency for Health Care Admin. , 676 So. 2d 1380 (Fla. statement of the MBC adopted May 6, 1994. Dist. Ct. App. 1996) (Florida medical disciplinary board Rich, B. (2000).A prescription for the pain: The emerging stanpenalized and restricted physician for perceived excesdard of care for pain management , Wm. Mitchell L. sive prescribing of pain medication; action of board Rev. 1. reversed by court); see also, Hollabaugh v. Arkansas Scheiderman, L.J. (1997). The Family Physician and End-of-Life State Med. Bd. , 861 S.W.2d 317 (Ark. Ct. App. 1993) Care, Journal of Family Practice, 45, 259 (citing Sidney (similar case in Arkansas). See generally, J. Sullum, No H. Wanzer et al. (1989). The physician’s responsibility Relief in Sight, 28 Reason 22 (Jan. 1997). toward hopelessly ill patients: A second look, New Jacox, A., et al. (1994). (Cancer pain can be relieved for up to England Journal of Medicine, 320, 844–849). 90% of patients); American Pain Society, Treatment of Stavish, S. (1997). HCFA ’s palliative care study: Is payment pain at the end of life: A position statement from the incentive enough? Ann. In. M., 126,I-55, I-56. American Pain Society(visited May 30, 2000) SUPPORT (Study to Understand Prognoses and Preferences for

Outcomes and Risks of Treatments) Principal Investiga(“Well-trained clinicians can provide adequate pain tors (1995). A Controlled Trial to Improve Care for Serirelief for more than 90% of dying cancer patients. ”) ously Ill Hospitalized Patients,Journal of American JCAHO, Comprehensive accreditation manual for hospitals: The Medical Association, 274,1591, 1594.See alsoJacox, official handbook (CAMH) (visited 5/31/00) A., et al. (1994). New clinical-practice guidelines for the . management of pain in patients with cancer, New England MBC Letter to Beverly Bergman dated August 19, 1998. This Journal of Medicine, 330, 651 (pain associated with canletter states in pertinent part: “Our medical consultant cer is frequently undertreated); Joranson, D., et Opioal. did agree with you that pain management for your father ids for chronic cancer and non-cancer pain: A survey of was indeed inadequate. ” The board’s letter stated: state medical board members , 79 Fed. Bull.:Journal of “There is insufficient evidence at this time to warrant Medical Licensure & Discipline , (4), 15–49 (1992) pursuing further action in this case. Your file shall be (reporting on studies that refl ect “ that adequate pain conmaintained with the Medical Board for future reference trol is not being achieved in a signifi cant portion of in the event we receive additional complaints in the patients, and that patients often do not receive analgesics future which, along with your complaint, could constito match the severity of their pain, ” notwithstanding that tute sufficient evidence for disciplinary action. ” pain can be well controlled for more than 85% of all McGivney, W.T., et al., The care of patients with severe chronic cancer patients). The systematic undertreatment of pain pain in terminal illness, 251 Journal of American Medhas been of ficially recognized by the Agency for Health ical Association,1182 (1984). Care Policy and Research (AHCPR), AHCPR, Acute pain Model guidelines for the use of controlled substances for the management: Operative or medical procedures and treatment of pain,85 Fed. Bull:Journal of Medical Licentrauma, clinical practice guideline(“ Half of all patients sure & Discipline84 (1998) (“[P]rinciples of quality medgiven conventional therapy for their pain — most of the ical practice dictate that …people …have access to 23 million surgical cases each year — do not get adequate appropriate and effective pain relief… The Board encourrelief.”

ages physicians to view effective pain management as a See alsoVon Roenn, J.H., Physician attitudes and practice part of quality medical practice for all patients with pain, in cancer pain management, 119 Annals of Internal Medacute or chronic, and it is especially important for patients icine, 121, (1993) (A survey of doctors treating patients who experience pain as a result of terminal illness. ”) with cancer found that 86% of the respondents felt “that New York Public Law. (2000). Some states have phased out the majority of patients with pain were undermedicated. ”) multiple copy prescription programs, substituting elecThe Pain Relief Act. (1996). Journal of Law, Medicine, & Ethics, tronic data programs, e.g., N.Y. Pub. Health Law 24, 317 (1996). §§ 3332-3333 (Consol. 2000) ; 710 Ill. Comp. Stat. 570 World Health Organization,Cancer pain relief(1986). (West 2000) (amended in 1999). It remains to be seen if this substitution will mitigate the problems caused by the multiple copy programs. Proponents assert that elim-

76 Law Enforcement and Regulatory View about Prescribing Controlled Substances for Pain Dale A. Ferranto, M.S. A BRIEF HISTORY OF DRUG ABUSE, ENFORCEMENT, AND REGULATION

would thus find America with 400,000 morphine addicts (O’Brien & Cohen, 1984, p. XV). Ignorance among medical professionals combined In order to fully appreciate the law enforcement andwith popularization of hypodermic therapy (Weston, regulatory view about prescribing controlled substances1952) gave birth to an American drug dependence that has for pain, it is valuable to study the history of drug abuseyet to be cured. At the time, opium was perceived as a and the resultant parallel development of governmentalvice but not a menace, so governmental regulation merely policy and control. This history is, in fact, the story of took the form of taxation. pharmaceuticals. Aldous Huxley, the famous British Amidst the dark cloud of drug abuse naívete that soon author, succinctly noted that “pharmacology antedatedengulfed America, two healing arts organizations were agriculture” (O’Brien & Cohen, 1984, p. IX). Drugs have founded. The American Medical Association (A.M.A.) been used and abused for centuries in medicinal, relibegan in 1847, and the American Pharmaceutical Associgious, and recreational settings. One of the earliest menation (A.P.A.) was founded in 1852. Though weak and tions of herbal medicines occurs in the Old Testamentunsupported until 1900, each association would play vital book The Song of Solomon. In Chapter 4, verses 13 and roles in awakening the United States government and the 14, Solomon sings of “spikenard” and “aloes”. The earlypeople to the evils of drug abuse. Through legislative Chippewa Native Americans used spikenard as a cough influence and sponsorship of model prescribing and pharmedicine, and aloe is still used today as a disinfectant macy laws, the medical professionals assumed a major and burn remedy. portion of the responsibility to detoxify the nation. Various world events and scientific advances contrib- As the twentieth century began, attention toward another uted to America’s attitude toward drugs and the abuse of drug, alcohol, so consumed the early era prohibitionists that drugs through the centuries. The isolation of morphinein 1881, to some people, opiate abuse was the favored alterfrom opium in 1804, coupled with opium’s commercial native. TheCatholic World Magazineof that year reported, value demonstrated by two intense Opium Wars between “The gentleman who would not be seen in a barroom… proEngland and China, and the subsequent development cures of his supply of morphia and has it in his pocket ready the hypodermic syringe in 1853 were medical break-for instantaneous use. It is odorless and occupies but little throughs of a double-edged nature. Most physiciansspace”(O’Brien & Cohen, 1984, p. XV). Also, patent medbelieved that relieving pain with needle-administered mor-ications containing opiates and cocaine deluged America as phine was harmless because the injected drug bypassed cure-alls for “misery, general aches, pains, headaches, and the digestive tract. The immediate post-Civil War erathat tired feeling”(Weston, 1952, p. 16).

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Physicians, though now organized in a medical assoNarcotic Law (1914), the Drug Abuse Act (1970), and the ciation, continued on courses of misguided treatments. Anti-Drug Abuse Act of 1988. Opiate abusers were medicated to keep them comfort- The nexus between drug abuse and prescriptions also led James H. Beal, an outspoken pharmacist/lawyer of the able, not clean. Narcotic- and cocaine-based elixirs and cocktails enjoyed thriving “medicinal” markets. Drug A.P.A., to propose a model state pharmacy law for habitforming drugs. Though not enthusiastically embraced by abuse had a firm, yet unrecognized, foothold on America. s model But from all embryonic indicators of this terrible disease,his medical and pharmacist colleagues, Beal’ government failed to react and develop policy to confrontbecame a turning point in endorsing further narcoticthe problem early, particularly when the commercial pro-related healing arts legislation. duction of heroin as diacetylmorphine (1898) emerged The diverse and heterogeneous growth of America during the new twentieth century fragmented our society on the market. The evolution of regulatory and enforcement activi- resulting in more formal sanctions and controls by government on pharmaceutical substances of abuse (Richties started with mere taxation (1864) and research ardson, 1974, p. 86). While the subject of drug abuse (1886) when Congress announced an act to “Provide for the study of the nature of alcoholic drinks and narcotics,temporarily disappeared from government scrutiny during the World Wars, Great Depression, and Korean War, and their effects upon the human system” (Weston, 1952, ict. p. 17). Exercising national intervention in matters pre-it reemerged with vengeance after the Vietnam confl viously reserved for the individual states, the FederalAmerica’s appetite for drugs exploded and, simultaGovernment embarked on a course of codification ofneously, drugs were being developed at a tremendous s pharmaceuticals narcotic laws (Johnson, 1988). And, while not entirelyrate: approximately 75% of today’ were formulated within the last 40 years. The suptaboo, “recreational” drug use was coming under greater ply–demand equation of this phenomenon has remained suspicion, and unless one obtained drugs by prescription, a great deal of negative stereotyping of addicts wasso unbalanced that full, complete, and effective enforcement of drug policies could now only be achieved in a attached to opiate consumption. Americans, though, continued to cherish and readilypolice state. seek physician prescribed drugs. This patent medicine The diversion of pharmaceutical controlled substances presented a unique regulatory and enforcement problem craze of high opiate content medications and the delayed to authorities trying to prevent drug abuse. The Drug realization that “dangerously addicting substances were distributed with little worry for their effect” (Musto, 1973, Abuse Warning Network (D.A.W.N.) reports that highp. 7) caused two major events. The first was a revival oflight hospital overdose admissions and coroner death an old form of professional criminality, drug diversion, reports in over 800 hospitals nationwide consistently indicated that pharmaceutical drugs were involved in approxand the second was a reaction by state and federal agencies imately 50% of the deaths and, of the top 20 drugs of to control the first. The criminal physician and pharmacist seized theabuse, 15 were pharmaceuticals. Three sources of these opportunity to cash in on the highly lucrative pharmaceu-drugs primarily appeared in criminal casework. The first tical drug business. Their enterprise, though, was nothing was identified as “doctor shoppers” or patients who sucreally new. In 1604, Miguel de CervantesMan in of Glass cessfully scammed prescribers for medications. The secoffered his view of the unscrupulous doctor, writing, “Phy- ond was prescribers themselves who had lost the ability sicians may and do kill without fear or running away andor desire to practice medicine, and consequently decided ” The third without unsheathing any other sword than that of a pre-to merely make a living by writing “script. scription” (Cervantes, p. 78). Additionally, Sir Arthur source was prescription forgers Intermingled among the enforcement and regulatory Conan Doyle, himself a physician, allowed Sherlock Holmes to conclude, “When a doctor goes wrong he isthrusts to halt drug diversion by unscrupulous patients the first of criminals. He has nerve and he has knowledge”and prescribers was the increasing concern about phar(Doyle, 1977). So doctors thus inclined and known asmaceuticals and pain management. Because many of the “croakers” or gentlemen of high rank who like their basedrugs of choice being diverted and scammed were opiand comfort without earning it (Keegan, 1987, p. 129)oids, synthetics, and other acute and chronic pain medications, the legitimate medical practice prescribing of emerged as drug diverters and suppliers for drug abusers. The government’ s reaction and policy response to the these drugs came under the same umbrella of enforcement and regulatory suspicion. Many states enacted mulrising epidemic of pharmaceutical drug abuse quickened tiple copy prescription programs hoping to monitor and in the early 1900s. Prescription requirements increased for control pharmaceutical drug diversion and abuse. In opiate substances, and curing addiction became a true legal and medical challenge. Federal laws, originallymany cases, however, prescribers felt impeded in otherwise legitimate prescribing practices by the increased argued as unconstitutional, were then enacted, and they included the Pure Food and Drug Act (1906), The Harrisongovernment oversight. The result was that many patients

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as measures to comply with the state and federal prescribwho truly needed the opiate-strength medications did not receive them. More professionally palatable and patient-ing laws, and they are the same foundation from which friendly prescription drug law and regulation options, administrative disciplinary actions, criminal prosecutions, particularly in the emerging medical discipline of pain and civil litigations are launched. management, would therefore be required as America Enforcement and regulatory agencies generally establish priorities for investigative case management. Attenentered the next millennium. tion toward prescribers has traditionally focused on the “Four Ds”: dishonest, duped, dated, and disabled. NonliTHE MISSION OF ENFORCEMENT AND censed individuals (particularly medical clinic ownREGULATION ers/operators) involved in pharmaceutical drug diversion and abuse usually manipulate prescribers to achieve illeThere is a great deal of misinformation and misconception gal, profit-driven goals, and they may also be involved in about the intended role of law enforcement and regulation prescription forgery, pharmaceutical drug smuggling, and in the prescribing, administering, and dispensing of pharbilling fraud. maceutical drugs. Some of the misunderstanding stems High on the food chain of enforcement and regulatory from weak investigative casework that resulted in poor personnel is the “dishonest” prescriber. This licentiate may administrative decisions and prosecutions. Horror stories have lost the ability or desire to practice within accepted are passed from prescriber to prescriber, and the facts are legitimate medical needs. Commonly driven by a get richmany times distorted. As a result, newly licensed and quick greed, the dishonest prescriber makes a good living authorized prescribers begin their careers suspicious and merely by “writing script” and sale of their signature. Both somewhat paranoid about the role of government in the the public safety and the integrity of the medical profesbusiness of medicine. sion demand immediate and intense efforts to stop the The enforcement and regulatory mission is not activities of the dishonest prescriber. intended to meddle in the practice of medicine. Overzeal- The “duped” prescriber is really a victim of a drugous and inexperienced investigators occasionally display seeking patient. In most states, a patient who “scams” a an interfering, authoritative attitude that regrettably sup-prescriber for a controlled substance has committed a ports allegations of meddling but they are not encouraged crime. Specifically, the patient withholds material facts by their employers to do so. from the prescriber, i.e., the patient is receiving controlled Similarly, enforcement and regulatory authorities substances from other prescribers. This obtaining by fraud have no desire to deny patient care and pain relief. Howand deceit is most pronounced by clever patients who are ever, initial complaints and information received by theterrific actors, knowledgeable about prescribing practices investigators, medical consultants, and prosecutors often and thePhysician’s Desk Reference, and present physical raise questions as to the type, quality, and quantity ofailments that are dif ficult to confirm, and strike at the most medication treatment the patient is alleged to be receivopportune times and vulnerable targets such as weekend ing or being denied by the prescriber. This concern ofemergency departments (Burke, 2000), clinic lunch hours, authorities may erroneously translate into interferingand on-call medical group partners. with specific drug needs of the patient and prescribing The third of the F “ our Ds” is the dated prescriber. actions of the prescriber. This prescriber has simply not kept abreast of current The interest and obligation of enforcement and regu-medical prescribing practices and, consequently, either latory authorities, though, are to prevent the diversion ofprescribes incorrectly or refuses to prescribe as necessary pharmaceutical drugs from legitimate medical practice toor becomes an easy drug source to be duped. Continuing illegal uses. Pharmaceutical controlled substances, particmedical education is the key to salvaging this prescriber ularly pain medications, command a very high value onand maintaining contemporary standards of legitimate the “street.” While the vast majority of prescribers never medical care. intentionally divert drugs to illegitimate use, hosts of interThe“disabled” prescriber is a person who has personal ested“patients” and other nonlicentiates actively mingle dependency problems that interfere with the professional and network in the pharmaceutical drug environment withpractice of good healthcare for his or her patients. Drug the sole goal of separating the drugs from the prescriber abuse is one of the most common disabling causes for and pharmacist. prescribers. Many regulatory boards and bureaus provide It is also in the public and consumer safety interestsrehabilitation to disabled prescribers through impaired for enforcement and regulatory personnel to ensure the practice programs that limit the prescriber’ s authority highest medical standards of prescribing. Many states while being paired with another prescriber who has legal have specific guidelines issued by their licensing boards oversight and reporting responsibility. Successful compleand bureaus to prescribers detailing the criteria used to tion of the impaired practice program can lead to full restoration of prescribing privileges. evaluate prescribing practices. These standards are used

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Enforcement and regulatory attention toward painchilling effect and overcoming an opia phobia. Both management prescribers could likely be generated by communities must communicate internally as well as conduct of any one of theFour “ Ds.” It should be clear, together to discover the middle ground that will allow though, that the dishonest prescriber, particularly in theeach to accomplish the prescriber, the police, and, most specialty of pain management, would be a very highimportantly, the patient’ s best interests. Dr. Daniel A. casework priority. At the same time, educating theDotson sums up this needed approach writing, Exacer“ police and the prescriber about legitimate and acceptbating the fundamental misinformation and peer pressure able standards of prescribing for pain would help to(about prescribing for pain) is the effect of the regulation better focus limited healthcare, enforcement, and reg-by various state and federal agencies which have — been ulatory resources where they will do the most good forhistorically and, in some cases, still are — unable to the patient. distinguish between the self-destructive drug-seeking lifestyle of the addict and the productive and responsible life of the legitimate pain patient consuming the same OPIA PHOBIA AND MULTIPLE COPY or greater doses of narcotics” (Dotosn, 2000). PRESCRIPTION PROGRAMS Many states are now in the process of modifying or While the mission of enforcement and regulatory author-eliminating the real or perceived barriers to legitimate controlled substance prescribing for pain. In California, ities as previously described seems clear and well intenmodel legislation exists regarding the treatment of intractioned, prescribing paranoia, whether real or perceived, table pain, prescribing for the terminally ill, and a bill of has emerged particularly among pain management prerights for pain patients. Nationally, electronic and paperscribers. Described as a “chilling effect” or “opia phobia, ” form multiple copy prescription systems are being a serious, sometimes overly cautious reluctance to treat pain patients with appropriately prescribed controlled sub-reviewed, revised, and in some cases, abandoned. Progress stances exists throughout this community of prescribers. is slowly being made on the monitoring and medical fronts Affected prescribers maintain that excess governmental to affect better pain patient care. oversight and regulation coupled with multiple copy and electronic prescription systems for pharmaceutical drugs drives their inaction. Dr. Russel Portenoy may haveLEGITIMATE PRESCRIBING IN GOOD described it best, “Laws and regulations intended to curtailMEDICAL PRACTICE illicit opioid use may be an unintended impediment toThrough their enforcement and regulatory agencies and legitimate prescribing. ” in concert with federal prescribing codes a variety of states No empirical studies have demonstrated this theory ofhave published guidelines for prescribers who treat prescribing paranoia but it clearly ranks as an important patients for intractable pain. The Medical Board of Calielement in the discussion of pain management. Possibly fornia guidelines which follow are one example, and they the closest measure of this chilling effect was observed are predicated upon the “position that the public is best when the state of New York placed benzodiazepines into served by a healthcare environment where physicians are its prescription monitoring system. The prescribing of free to exert their own best medical judgment consistent benzodiazepines dramatically decreased. The disturbing with accepted community standards of care” (Medical effect of this response was quite possibly the undertreatBoard of California, 1996): ment of conditions requiring sedative, tranquilizing, and hypnotic medications. In the specialty of pain management, the relationalHISTORY/PHYSICAL EXAMINATION cause and effect of opia phobia may manifest itself more A thorough medical history and physical examination dramatically and tragically. Dr. Brad Stuart, speaking frommust be accomplished. Prescribing controlled substances a hospice perspective, illustrates one such outcome stating, for intractable pain in California also requires evaluation “Even though we know how to treat pain effectively, manyby one or more specialists. physicians consistently undertreat it for a variety of reasons. No wonder sick people are looking for a way out”TREATMENT PLAN/OBJECTIVES (Stuart, 1999). Managing legitimate pain by prescribing controlled substances in legitimate medical practiceThe treatment plan should state objectives by which treatment success can be evaluated, such as pain relief and/or should be immune to any perception of enforcement and improved physical and psychosocial function, and indicate regulatory barriers. if any further diagnostic evaluations or other treatments Once again, understanding the problem and educating to the communities of regulators as well as the reg-are planned. Several treatment modalities or a rehabilitaulated about the solution are key steps in warming thetion program may be necessary.

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INFORMED CONSENT

of pain medications to patients. The fear was based upon the addiction of patients and subsequent treatment of The physician should discuss the risks and benefits of the addicts that resulted in criminal prosecutions, administrause of controlled substances with the patient or guardian. tive discipline, and lawsuits. Now the courts and administrative law judges are entertaining actions regarding the PERIODIC REVIEW undertreatment of pain. In at least one such case, the The physician should periodically review the course ofalleged failure to treat pain has been charged as elder abuse opioid treatment of the patient and any new information(Lazarus & Stanton, 2000). The outcome of such cases about the etiology of the pain. Continuation or modifica-may chart new approaches to pain management prescribtion of opioid therapy depends on the physician’ s evalua- ing and should, therefore, be closely monitored by pain treatment specialists. tion of progress toward treatment objectives.

CONSULTATION

THE FIFTH VITAL SIGN: The physician should be willing to refer the patient asPRESCRIBING FOR PAIN necessary for additional evaluation and treatment to The medical discipline of pain management has been achieve treatment objectives. Physicians should give spematuring for decades. Effective procedures and therapies cial attention to those pain patients who are at risk for to treat pain are growing in number every year. Pain is misusing their medications. The management of pain in now considered a critical vital sign in the medical workup. patients with a history of substance abuse requires extra Yet, discussion and dilemma about the correct balance care, monitoring, documentation, and consultation withbetween treatment and regulation exist. Perhaps this addiction specialists, and may entail the use of agreements needed balance can be achieved in an integrated approach between the provider and the patient to specify rules forby the prescribers, the police, and the public through edumedication use. cation, expertise, and teamwork. It is imperative that the medical community, the enforcement and regulatory authorities, and the patients have open dialog about their missions, responsibilities, The physician should keep accurate and complete records, including the medical history and physical examination,and needs. The myths about prescribing practices held by the police and the myths about enforcement practices other evaluations and consultations, treatment plan objecheld by the prescribers need to be eliminated in order tives, informed consent, treatments, medications, agreethat patients can better understand and reap the ts benefi ments with the patient, and periodic reviews. of their true treatment options and limitations. At the same time, all parties to the pain treatment issues need COMPLIANCE WITH CONTROLLED SUBSTANCES LAWS to stay informed and educated with contemporary knowlAND REGULATIONS edge about available care within regulatory boundaries To prescribe substances, the physician must be appropriand community standards. And, when such care and/or ately licensed in California and comply with federal andconditions become obsolete, the same interested parties state regulations for issuing controlled substances preshould collectively see that they are legally discontinued scriptions. Documented adherence to these guidelines will or changed. Prescribers as well as government regulators also substantially establish the physician’ s responsible treatment of patients with intractable pain and will serve toshould be experts in their respective fields. Pain managedefend that treatment practice in the face of complaintsment prescribers should be well versed in available treatments, controlled substances, alternative healing (Shanwhich may be brought. The identification and acknowledgment of pain-pre- non, 2000) including nutrition (Fox, 2000), and multidisciplinary approaches to integrated therapies. scribing issues by enforcement and regulatory agencies have Enforcement and regulatory personnel should understand been huge steps forward in improving patient care. Legislation and published prescribing guidelines for prescribingthe limits of legal and administrative standards, acknowledge and appreciate the complexities of pain management, controlled substances to pain patients also have contributed to better understanding the responsibilities and limitationsand exercise their authority in fairness and under the spirit of the prescriber, the patient, and the police. Circling thisof the law to seek justice. structure of pain management healthcare and regulation, The shared education and expertise of each interest however, is an evolving body of criminal and civil litigation. group (prescribers, police, and public) in a teamwork Historically, the concern of most enforcement agencies,approach will enhance the likelihood of better communication and cooperation in solving pain management regulatory boards, and prescribers has been overprescribing

RECORDS

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issues. Achieving necessary compromises in draft legisREFERENCES lation and proposed treatment regimens can speed up bureaucratic processes and advance patient care without Burke, J. (2000). Emergency room shoppers. Partners In against pain: E.D. physician, beware the opioid shopper (5th undue delay. This common interest approach for ed., p. 4). H. Lazarus & M. Stanton (Eds.). Stanford, improved treatment of the patient will also help to disCT: Purdue Pharma Limited Partnership. courage the damaging us vs. them philosophy between Cervantes, M.D. (1604/1983). Man of glass . Franklin Center: prescriber and regulator. The Franklin Library, As we begin the new millennium, healthcare providDotson, D.A. (2000). Why not relief?, Pain Physician, 3,65. ers are on the leading edge of patient driven treatment Doyle, A.C. (1977).The adventure of the speckled band . Franklin of pain. The patient’ s voice supported by new legislation Center: The Franklin Library, is now an integral component of the decision-makingFox, M.C. (2000, Sept./Oct.). Eat this, ache less, Fitness Swimmer, treatment process. While the options available are mul20. tidisciplinary ranging from traditional medicine to trans- Johnson, H.A. (1988).History of criminal justice. Anderson dermal magnets, one of the most basic courses of care, Publishing Company, Cincinnati, 209. Keegan, J. (1987). The mask of command . Viking Penguin, Inc., prescribing strong controlled substances, remains an New York. action fraught with paranoia of government regulatory oversight and penalty coupled with a perceived addictionLazarus, H. and Stanton, M., Eds. (2000). Undertreatment of pain goes to court as elder abuse.Partners In against consequence for the patient. As a result, the patient sufPain (5th ed., p. 1) . Stanford, CT:Purdue Pharma Limfers needlessly; and, studies have shown that pain can ited Partnership. kill (Liebeskind, 1991). Liebeskind, J.C. (1991). Pain can kill, Pain, 44,3. Good prescribing is based upon the practice of goodMedical Board of California. (1996). Treatment of intractable medicine. The prescriber who embraces established treatpain: A guideline, Action Report, Sacramento, 57, 1. ment guidelines during the initial and all subsequentMusto, D.F. (1973).The American disease: Origins of narcotic adjustments to prescribing, dispensing, and administering control. New Haven, CT: Yale University Press. controlled substances to pain patients will unlikely haveO’Brien, R. & Cohen, S. (1984). The encyclopedia of drug abuse , New York: Facts on File, Inc. any problems with enforcement and regulatory authorities. Urban police in the United States. Port Legitimate medical indication is the guiding principle for Richardson, J.F. (1974). Washington:Kenikat Press. the prescriber. The laws and regulations that exist to curtail dishonestShannon, S. (2000, July). Alternative healing: What really works? Readers Digest,45. and dangerous prescribing practices of unscrupulous preStuart, B. (1999, May). Assisted suicide: The illusion of free scribers are not intended to deny the treatment of legitichoice,San Jose Mercury News, San Jose. mate pain. They should not impede legitimate prescribingWeston, P.B. (Ed.). (1952). Narcotics U.S.A. , New York: Greenor allow government authorities to meddle in the practice burg. of medicine. The enforcement and regulatory authorities, with support from the medical community, should be used to their full extent to protect the patient and the public healthcare trust.

77 Ethics of Care: Pain Management and Spirituality Myrna C. Tashner, Ed.D. For an effective discussion of the ethics of care and pain uted theories of cognitive and social development, includmanagement and spirituality, we must reexamine how we ing environment and relationships studies. But in the last 25 years, according to the American Psychological Assoview ourselves: body, mind, and spirit. Since the time of René Descartes, humankind has ciation, society’s concerns about adolescence, aging, and gradually learned to focus on itself as body (matter) andlife span have become the focus of psychology. At the end mind (brain). In general, this is due to a “deal” workedof the 19th century, psychology was concerned with the out between Descartes and the Pope. In order to get perstudy of mind and consciousness through introspection, mission to study the body, Descartes appealed to the Pope thus describing experience. Now at the end of the 20th for permission to dissect a human corpse. In their agreeand beginning of the 21st, the focus of psychology has ment, Descartes agreed that he would have nothing to do broadened to a science and practice concerned with human with the spirit/soul, the mind, or the emotions if he shouldbehavior, as well as the mental process that underlies find them in the body. The soul, mind, and emotions wereexperiences and behavior. the exclusive jurisdiction of the church at that time. Des- Maybe it is time to put us back together; after all, we are body, mind, and spirit/soul, a whole being. This chapcartes claimed the physical body as his realm of study, ter shows that when we manage our pain, and/or heal, we thus separating the body from the mind. This bargain set seem to do it as a whole being using our minds, emotions, the tone and direction of science for the next 200 years. and spirits within the body physical. It divided the human into two distinct and separate spheres The establishment of the study of ethics may be conthat could not overlap. sidered the result of humankind’s movement away from This agreement gave us the Cartesian era with its reductionist methodology, which attempts to understandand/or forgetting of the natural laws, or the Laws of the life by examining the tiniest pieces of it and then extrap-Universe with the primary law: We are all one. Ethics is designed to protect and ensure that we do not harm those olates from those pieces to generalities about the whole. Human development has been studied formally sincewho choose to place themselves in our care. We must the time of St. Augustine, but its beginnings date to theremember to do no harm to ourselves as well. In primitive moral principles of conduct and proper actions days of Jesus, and even back to the ancients. However,cultures, it were part of the expected behavior of a member of the has only been in the last 100 years or so that psychologists applied scientific methods to the examination of humantribe. Only in particular situations, when the member chose to invalidate someone else’s personal space, or development. Sigmund Freud was the first. He is credited with the beginning of psychoanalytic theory, a significantneglected to respect the rights of his or her fellow tribe members, did the chief or medicine person get involved study of human development. Later, Jean Piaget contrib0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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to resolve the matter. For example, in the Mayan culturethe body without necessarily recognizing the energy of a tribesman would be expelled from the tribe and sent to the soul/spirit that lies behind illness and, therefore, canlive alone in the jungle for lying. not heal the body or the soul/spirit. To put it simply, how In our complex society, made up of members of manyoften do we not pay attention to our inner knowing and different cultures and backgrounds, we have evolved a excuse it by saying something like, “Oh, well, I just missed specific professional discipline called ethics, or laws ofit.” Then we relieve our guilt and responsibility by telling professional conduct for our professional disciplines, suchourselves that everything will work out okay. And that is as medicine, psychology, ministry, and law. These aretrue, everything will work out, with or without your coopstandards of expected behaviors to be considered a memeration. However, it can be more fun and fulfilling to learn ber of that group, or professional tribe. about the beauty of breathing from meditation rather than The Dalai Lama, (1999) a respected religious leader,from emphysema. Medicines aim to relieve the symptoms, has written a book on the subject of ethics for our newbut they may or may not heal the body, and medicine millennium in which he describes ethics as a “universalprobably will not heal the pain of the soul/spirit. I have responsibility” the individual needs to be a responsiblegiven up counting the number of patients who have told person. Responsibility is a word derived from “respond-me, “If only I had stopped smoking or stopped being ere,” the Latin word for the ability to answer. It is the sexually promiscuous, this would not have happened.” The ability to answer the urgings of our intuition and our heart,fact is, if we are not responsible, respectful, and compasas well as respond with intelligence in the discipline wesionate, and if we do not listen to our intuition, eventually have chosen to practice. For example, we need to follow we have a good chance of contributing to a body illness. our awareness of what is needed to function as a healthy The science of psychology is in a situation similar whole person, as well as how to maintain our body–to that of the science of medicine. Over time and under mind–spirit’s wellness. the influence of Cartesian philosophy of thought, psyRespect is also paramount. It is so important to respect chology has come to mean the science of the study of what our bodies tell us, we need to look again at what our the personality, emotions, and cognitions without recogpatients/clients are really telling us are their problems, and nizing the force and energy of the soul that lie behind respect what they say. Although managed care does not the configurations and experiences of the personality. like to reimburse for it, nor consider listening a part of Therefore, psychology cannot heal the soul/spirit either, care, or consider it appropriate to pay for it, the art ofbecause the current science is focused on that which is listening and questioning is important before diagnosingvisible to others. and prescribing treatment and medications. To be a good listener, we need to begin by practicing on ourselves. How often do we listen to ourselves, seri-FROM TREATING SYMPTOMS TO TREATING ously listen, and then respect what our intuition tells usTHE WHOLE PERSON FOR WELLNESS about our body, mind, and spirit? This is an area of fertile ground for self-study, growth, and development, and pos-Now we are experiencing a shift in attitude toward the sibly for forgiveness of self and/or others. Paying attentiontreatment of illness from the Descartes reductionism to holism, considering the body, but also the mind, emoand appreciating what we learn about ourselves can only tions, soul/spirit. In some medical practices (e.g., Dossey, deepen our appreciation for and commitment to ourselves. Chopra, Sheely) healthcare professionals are working with Experience is a very good teacher. the patient’s body and spirit. Dossey’ s Reinventing MedCompassion is the word used to describe the feeling icine (1999) describes the coming era of medicine as of empathy (including love, affection, kindness, gentleincluding a focus on and use of spiritual energy for healing ness, generosity of spirit, and warm-heartedness) toward intervention in hospitals. others, while honoring our limitations to remove their problems or pain from them. Before we can have true There is scientific evidence to support the importance of emotions in pain management and healing. Research compassion for others, we need to be compassionate by Candice Pert (1997) on the molecular energy of emotoward ourselves. To have compassion means to undergo or suffer with a patient or loved one the painful experiencetions and how these emotions connect and influence the Molecules of Emotions . As a graduate in his or her life. Again this study begins with self, being body is described in with and going within ourselves, and then learning to livestudent, Pert laid the foundations for the discovery of s pain suppressors and ecstasy well and in harmony with self. It starts with responsibility endorphins, the body’ for our needs and well-being through respecting what weinducers. Her later discovery of the opiate receptors extended to every field of medicine and contributed to the learn about the self, and living in compassion and harmony synthesis of behavior, psychology, and biology. She went with self. We are involved in and dedicated to the science ofon to show that neurotransmitters secreted by the brain medicine and pain management. Currently, it seeks to heal change physical activity, including behavior, mood, and

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emotion. She described stress as information overload, gests a that illness possibly may be the means through which condition in which the body system is taxed with emo-God leads us to discover more about ourselves. This could tional unprocessed information to the degree that the body be true of the challenge of disease, or aging.Seat In of shuts down with what we call disease. Stress prevents the the Soul(1989), Zukav describes spirituality as the immormolecules of emotion from flowing freely. She discoveredtal process itself, that pertains to that which is immortal for herself the value of meditation practice and the powerwithin you, the individual. of visualization. I like to think that spirituality gives power back to you The scientist and philosopher, Gary Zukav, addressed as a person and makes you responsible for your life force. the issues of the spirit and soul in his book Seat of the Spirituality empowers you as a person. Spirituality places Soul (1989). He defined the soul as an energy system and the power where it belongs, in and with you. You are described humans as multisensory beings, as opposed responsible to as a person, but by listening to your “inner five-sensory beings, capable of perceiving and appreciatvoice,” you can learn much about yourself, your attitudes, ing beyond the human five-sensory personality. He stated and behaviors including your pain. This knowledge can that compassion, clarity, and boundless love are natural to lead to pain management and healing. the soul, and life is the opportunity of the soul to learn This self-awareness reframes you in the world. In lessons about the laws of physics and the Universe.sLife’the Cartesian concept of you as body, which has many experiences are for the purpose of soul growth, power, and systems that function for living, pain and illness are signs energy. The soul has a reverence for all of life. To beof malfunction in a system of the physical body. But if reverent is to be spiritual. Reverence creates compassion, you consider yourself a spiritual being and the center of kindness, and patience. the dynamic of living, not your body, then your world In a sense we have come full circle, from the Popelooks like this: You are a spiritual being, living in a and the Catholic Church maintaining their priority over spiritual world, governed by spiritual laws, having a the whole human, to medicine and science, which were human experience. The effects and consequences of this able to study the body, to physicians like Freud and Jung change in the order of things are awesome, for each effect who focus on the “untouchable” psyche or soul, to psy-follows the Laws of the Universe, which are really simchologists taking the soul and studying behavior and perple. For example, as you intend, so it shall be. Or, as sonality, to medicine now realizing it needs to consideryou think, so you are. the person as a whole vs. pieces or parts — body, mind and spirit— in holistic medicine.

NATURE OF SPIRITUALITY

Spirituality can be a deep search for the meaning of life. Much of our knowledge of spirituality has come from For some time religions have focused on the practice of Eastern traditions (Hindu, Buddhist, etc.), Jesus and belief and ritual for the purpose of honoring the divine,Paul, Native Americans, mystics including Ralph Waldo or God, or Yahweh, or Allah. It can lead to and/or be aEmerson and Henry David Thoreau, and contemporary spiritual experience, but not necessarily. Religion is a set ones, such as C. Myss, D. Chopra, N. Walsch, and the of doctrines, dogmas, beliefs held by a group of believers Dalai Lama. who may form a church. That brings to mind the image Spirituality has an unseen dimension, beyond the fiveof people gathering in a building. sense component of energy. Healing of illness and pain Spirituality is not religion. It conjures up a sense of has a historical involvement with spirituality. Some sugthe sacred and the soul. Our patients evolve into exploring gest that this is what the master teacher Jesus Christ was what spirituality means for them. Deepak Chopra, M.D.,attuned with his many miracles. Humankind’ s fascination in How to Know God(2000) describes spirituality as learn- with this energy was evident in 18th-century Europe in ing to cooperate with God, learning that there is one realmedical societies that were challenged by some of their ity, the spiritual, that nothing lies outside the mind of Godmembers to explain the healing process. In 1900 in Vienna or awareness. the physician Franz Mesmer formulated a theory of healC. Myss, inWhy People Don’t Heal and How They ing using the energy of magnets and gravity. His ideas Can (1997), describes spirituality as accepting divinetook hold in the United States, and influenced, among direction, which is an ongoing process of self-discovery.others, a New England watchmaker P.P. Quimby. Through It starts with a quiet, growing dissatisfaction with institu- his study of mesmerism Quimby produced changes in the tional religion, and an inner sense that there must be more mind by use of the mind. Quimby renamed the work to spirituality, the need to seek it out using meditation and“hypnosis,” but later came to believe that a Higher Intela new path to inner power. It is a journey in self-discoveryligence can work through us to correct thought errors that and an approach to God from a point of view that is notcooperated to create illness. Belief patterns of patients had tied to a specific religion, but is more general. Myss sug-to change. Quimby said he thought that was how Jesus

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Christ healed and he proceeded to heal using this prin- and continued my schedule. I don’ t remember exactly ciple. Quimby attracted students and followers, including how long it took, but within a few days, I was aware Mary Baker Eddy, who experienced her healing through of a lot of pain in that arm which now had many more his work, and who later founded Christian Science. She blisters. To make a long story short, I went to my believed that prayer and the power of the mind could physician who diagnosed shingles and prescribed bring about healing. It is interesting to note that some medication for pain. insurance companies pay for the services of Christian Of course, the prescribed medication was strong, Science practitioners. and I experienced side effects. The pain didn’ t go Eddy’s student and fellow mystic, Emma Curtis Hop- away, but got worse. I had a choice: go into the kins, founded the Metaphysical School in Chicago. A New hospital for a morphine drip, or just live with the side York physician, Dr. H. Emily Cady, and Charles and Myr- effects of the prescription drugs. tle Fillmore, co-founders of Unity School of Christianity, Instead, I chose to take aspirin and practice the studied in Hopkins’school. Dr. Cady wrote a classic work relaxation technique I had learned in yoga. And I had for Unity School on the power of the mind entitled Lessons the bright idea to add the image of white light flowing in Truth (1892), in which she detailed her understanding into my body going to the site of each hurting nerve of the teachings of the master Jesus as practical and appli-ending and surrounding it, relieving it of the inflamcable for healing, as well as pain management. She mation. I asked that it relieve me of the pain. explained a relationship with the Almighty One that was I knew about breathing and relaxation from yoga. personal, practical, and the essential responsibility of the My doctor had told me aspirin was the strongest nonindividual. She emphasized discipline of the mind and prescription painkiller. But the image was something responsible management of thought. Remembered from that came from within me. I quickly became aware these 19th-century metaphysicians are sayings based onthat when I was in the relaxed state with that image, the Law of Mind Action theme, i.e., change your thinking I was pain free. It was natural to be grateful and I and change your life; or, thoughts held in mind produce giggled with delight. after their kind.

SPIRITUALITY AND PAIN MANAGEMENT

The following story was told to the author by a Native American friend. When we talk about spirituality, pain management, and In the late 1960s, I developed severe pain in my the power of the mind to heal, we are talking about con- left hand. The fingers were swollen with red speckcepts that have a historic base in our culture. Keep in mind les. I thought I had been bitten by something. Within that when we talk about spirituality and pain management, days the pain and swelling had gone to my left knee, we are not necessarily talking about healing of the phys- and my ankle and foot were painful and swollen. ical body, although that is what people in pain want. After 2 weeks of aspirin and Tylenol, ice and heat, Pain is a word that describes the experience of physI saw my family doctor. He examined me and ical pain caused by cancer, surgery, burn; emotional/menordered blood tests. Several days later I received tal pain that can be situational or chronic; or spiritual pain his diagnosis: rheumatoid arthritis. He told me to as in a dark night of the soul or loss of the sense of self. expect continued pain and deterioration to the level We learn and grow, because pain can be a teacher. It can of being wheelchair bound. I was devastated. I had set up an addiction, not only to medications but also to three small children, a husband, a life. I couldn’ t the experience of pain for the benefits it can give us. be a cripple. In the following true illustrations, we discuss four I called my mother in tears. She listened and told pain-filled experiences and the use of the mind and the me she would study and pray about it. My mother inner spiritual power to manage the physical pain. was Native American, of the Choctaw nation. She was raised with both white and Native traditions. My grandfather was English. My sisters and I were raised with a mixture of both cultures. I refer to my mother The author’s experience with this concept was as a graduate student. I was working three part-time jobs as Native American, but never referred to myself as to meet expenses. I also was studying for my licensing such. My father was very white Irish. The pain continued. I called my mother again. boards and doing my dissertation research. I also was She said she was praying. Nothing happened. very conscious of what I ate as I was just beginning Several days later I went to my mother’ s house. my study of yoga, and learning to breathe correctly My dad was out back in his garden. Mother met me and to relax my body. One day I noticed small blisters at the door. She said she was expecting me. I limped on my right forearm, but I thought nothing of them

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inside. She placed a kitchen chair in the middle of the room, pointed and said,Sit.” “ I sat. Mother began by placing her hands on my shoulders, then my head. She began speaking with gut spouch. After a few minutes she began doing a slow native two-step dance around my chair. I had seen the dance many times in my lifetime and I accepted it as “ right.” I began to relax. My mother’ s tempo increased. Then she began speaking in another language. Her voice rose and fell. Her feet beat a tempo, and I felt my whole being slip into her chant; although I didn’t understand the words, the tempo of her feet beat a chant into my heart. Time passed, maybe hours, I don’t know. She finished by placing her hands to my head and shoulders and ordering the spirit of illness to leave my body, never to return. Was the pain gone at that time? No. But the next morning I awoke to less discomfort. By noon I could open and close my left hand. Within 3 days I was working — pain free. The medical community may say I went into spontaneous remission. I say I was healed. Some 30 years later, I fell up the stairs at work. (Most people fall downstairs; I took a different route.) I hit my right knee on the stair’ s edge. That evening, it was very sore. Two days later I rose from the dining table but couldn’ t walk. The pain increased to the point that I couldn’t ambulate without excruciating pain. Tears came to my eyes as I started up the stairs. I tried to ignore the pain and the symptoms. I tried to ignore the swelling. Finally, my uneven gait was noticed by my co-workers. I was sent to the doctor. He took X-rays. “Lucky, ” he said, “nothing is broken. All you have,” he told me, “is degenerative arthritis. Bone on bone. It can only get worse. ” I just looked at him, “How can that be, there wasn’t any pain before I fell. ” He offered pain medications and an anti-inflammatory, and told me to go home and live with At it. “ your age you can only expect these problems to occur,” he said. And that’s what pissed me off. I refused the steroids but took over-the-counter medications. Days, weeks passed, the pain continued. Finally, one day when I was alone, I screamed out to my mother, who had been gone for 10 years, “Why did you leave me! I need you!” I needed her to heal me. I want her to heal my pain. Couldn’ t she hear me crying? Couldn’ t she hear my heart begging for relief? Nothing happened. Silence. I wanted to feel her presence. I wanted to feel her touch. I asked the Great Spirit to help. Once again silence. Or perhaps I just didn’ t hear. We constantly hear that we make our own reality, so I started to try to direct healing toward myself. I asked others to pray. Nothing seemed to change.

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And then one night I dreamed. I saw my mother as a young woman of 17 dancing in eld a fi of wildflowers, laughing in a carefree manner. I tried to run to her, to stop her, just so she could touch me, and I touch her. I knew that if I could touch her I would be healed. She kept dancing just out of my reach. When I woke up, I woke up to pain. Days passed. I constantly asked and prayed for help. I asked for the Great Spirit to intervene. And I asked that if my mother had any influence on her current plane of existence, to please help me. I dreamed of my mother again. As previously, she was just beyond my touch. The next day while driving down the highway, I had to stop quickly, and tromped with my right leg on the brake. The pain ripped from my knee to my right hip. I had to pull over to the side of the road. I sat there for a few minutes. I said, “Great Spirit, Mother, help me!” In my head, or out of the air, I heard, “You don’t need me. I taught you what you need to know. ” The truths she had taught me began to enter my awareness:“No one can teach you the ways of the spirits/God. These things are only learned in your own silence. Look to your own spirituality. ” This is not what I wanted to hear. I wanted my mother to give me the magic formula that she had used 30 years ago. “What is my spirituality?” I asked. Spirituality is a way of looking at and understanding this earth and yourself, a way of knowing what it is all about. “I’m not looking for spirituality, Mother, ” I hollered out. “I ’ m looking for healing. ” Mother had always taught us that the spirit is everywhere: in the water, rocks, trees, birds. “How is this supposed to help now? I’m in a car. I can’ t go out into the woods, the forest. ” I sat there fighting with her voice in my head, because that’ s where it was. I finally was able to drive home. I’ m a nurse. But you cannot learn to work with Indian spirituality by going to medical school. An old holy person, a medicine person can teach you about herbs, and that everything must be in its proper place. They can teach you about using smoke, sweet grass, sage, and cedar for cleansing the environment and the air. They can teach you all of these things, but if the human spirit is not ready, the soul will not accept the teachings. The native peoples believe that we were put on this earth with animals, plants, trees, and water. (I was taught this as a child, but I forgot this as an adult.) Native peoples believe that power comes from these things. Indian healers receive the power from spirit. Spirit is everywhere. You hear of animal helpers, but they don’t give power; they are messengers that bring instructions from the spirit.

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I continued to fight what Mother had said. How could my mother speak to me, a grown woman in a car going down the highway? And why did I keep calling to her? Because, deep in my heart, I knew that the spirituality my mother had taught me was still there. After several days of fussing in my mind with how and why this was happening to me, I realized that I had to take control. I could almost sense my mother smirking in the corner: “So, finally you are going to do something about this. You have the qualities and abilities. You can heal yourself. ” How could I take control? My body was controlling my every move, because of the pain. How could I take control? I couldn’ t even lean over to pick up a rock, smell the flowers. I could just see her saying, “You’ ll do it. You’ll figure it out.” So I did. I began by taking an inventory of my being. I realized that I was overweight. My eating habits left a lot to be desired, and I always felt that exercise was self-abuse. So what could I do? Once again I asked Great Spirit to help me. I realized that the task before me was more than I could handle alone. How could I change what had occurred over decades of life? Then I had another dream. Mother always taught me that dreams are powerful things, almost like visions. In the dream I saw myself as I had seen my mother in a previous dream: not in a field of wildflowers, but as a young Indian girl running through the wooded hills of my childhood, barefoot, with the hair streaming down my back. In the dream the young girl turned and smiled at me, and I knew she was myself. What struck me most about my younger self was my smile and pain-free demeanor. That weekend a dear friend came to visit. We stood back by the pond. I began telling her about the pain in my leg and my inability to walk and function. I told her about how I had been this way before, and how my mother had danced around my chair when I had received my healing 30 years earlier. Her face was puzzled,“How did she dance? Show me. ” I began to do the two-step, slowly, as mother had done those years ago. I danced as she had danced the two-step to the spirit for my healing. My feet slipped naturally into the rhythm, my knees bent without pain, and I began the dance in the spirit of thanksgiving. My healing had begun. We went into the house and announced that I was able to dance without pain. I now knew without reservation that I was in charge of my healing. My healing was and is spiritual. One must be ready to be healed. If our spirit is not ready, we will continue to live the role of sickness and pain. Sickness may be comforting to some. Many find their needs

fulfilled in this way. I chose not to be sick or in pain. My spirit was willing to accept the healing. My spirit recognized that the time was right in a few traditional ritual dance steps. I know with the help of the Great Spirit, the loss of well over 50 pounds, the dietary changes to feed my soul, not just to satisfy my body, daily thanks to the Creator, and occasional thanks to my mother, I am now able to live as the spiritual being my mother taught and raised me to be with a much thinner body and lighter soul.

Bill’ s story. “It happened so fast! Fire exploded out of the carburetor! My hands, head, chest, arms, my whole upper body was torched (50% of his body had thirddegree burns) in the direct line of the flames, and I couldn’t help but inhale the flames. ” This began a life experience for Bill. Jeanne, his wife, was a nurse and rushed to his side with blankets to smother the flames that were frying her love. (She received second-degree burns on her hands and arms. Her hair was burned on the front of her head.) The ambulance arrived and Bill was care-flown to the closest burn center, a 3-hour trip. The inhalation of the fire caused his throat to close, so he required intubation to survive the flight. Jeanne did not fly, but her nursing supervisor gave her a blanket and told her to go with Bill in the air ambulance, and sent her off to the plane. Burns have to be the most painful experience, and third-degree burn, which is what Bill had experienced, the worst. If you have had the experience of burning your finger on a hot pan, you may remember what that feels like. Now multiply that feeling exponentially and begin to get a sense of what Bill was feeling. Two sets of skin grafts failed, due to infections and complications, and medical staff was concerned if the third graft would take. Jeanne stayed by Bill’ s side. She is a woman of prayer and faith. Weeks passed, and with two failed skin grafts and concern that the third might not take, she prayed. That night when she had just gone to bed, she began to pray, “Oh God, I can’ t do this, I can’t lose him, I can’t face this. It is in your hands. I give up control.” Almost immediately, the darkened room lit up with a bright blue light. The wall to her left opened up, and she could see into the burn unit. Bill was sitting in a recliner chair swathed in bandages: his arms, his chest, and his face. She saw a hand up to an elbow with thumb and index finger extended. The forefinger touched the ngers fi on Bill’s right hand. Jeanne became frightened by what she saw. She

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thought, “I can’t be seeing this, I must be crazy, I must be having a dream, I can’ t be seeing this, ” and the vision faded. Jeanne fell into a deep sleep that night. Prior to the vision she had slept very poorly since the day of the accident. The next morning Jeanne was at the burn center as early as they allowed visitors. As she walked through the door, Bill was sitting in the recliner as in her vision, swathed in bandages, but the tips of his right hand were pink, whereas the day before they were black. She told him of her vision. Bill looked at her and said he had had a dream, her vision. Did they share a vision, a dream? They didn’ t question it. Jeanne took Bill home 2 weeks later. “Does he have scarring? Yes. Does he have residuals? Yes. Daily he lives with the scarring, the external perceptions. Do we see the scars? No. What we see is a whole person, able to function with all the human deformities, at a high level. ” From that day forward, Bill felt he was healed. He even told his nurses he was going to get well. Bill had accepted his healing and his healing process had begun. When I asked Bill what he did to cooperate with the healing, all he would answer was, “I don’ t know.” What Jeanne tells is that the nurses in the burn unit told him to breathe deeply like a woman in childbirth. Breathe deeply, relax, and don’ t focus on the pain. He went into an altered state of consciousness. Bill did say that he had to go within and not focus on anything. In his words, he had to “clean his mind. ” A psychologist would say that he disassociated and detached from the pain. Jeanne said that when she changed the bandages at home, she, too, would go into an altered state, and disassociate from her perception of pain. After the experience with the bright blue light, Bill was able to function on less medication than expected. When Bill was released from the hospital, he went home on ibuprofen. To this day, he only takes ibuprofen for pain. “ We always thought there was a greater power; now we know,” were the couple ’s final words on the experience.

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painful, to the degree that he needed a cane and couldn’t climb stairs. Surgery was his only alternative. In that surgery, they would fuse three vertebrae in his spine, making a paste of bone graft from his hip. Randy was the head chaplain at the hospital, and always was there for anyone in need of prayer support. In his time of need and in preparation for his surgery, he asked the persons of prayer he trusted to pray with him for a successful outcome. In addition to Christians, his prayer team included those of Native American belief and Jewish, Buddhist, and Muslim traditions. This was his prayer team, and he related that he went into his surgery without fear. Even though this was a delicate surgery requiring the most skilled of surgeons, he had no fear. Randy was no stranger to surgery. Previous postsurgical experiences of migraine and nausea could have presented a fear factor. He awoke out of the anesthesia with only a flash of nausea, which immediately dissipated. Randy’s wife, Joan, and one of his chaplain staff were waiting in his room as he was wheeled from recovery. He reported that he was so pain free and so hyped that he was unable to sleep until well past midnight. Nurses became concerned as he laid awake channel surfing and watching TV. Surgery was on Tuesday. Wednesday morning Randy was standing, and that afternoon he walked with assistance. It did hurt and he did feel it, but there was no pain. He took an occasional pain shot the first couple of days. Joan took Randy home on Saturday, and he walked up the stairs to the bedroom. He walked down those stairs Sunday and back up. He took hydrocodine every few hours for the first 10 days, as a prophylactic measure. But he just never had pain. It was all pretty amazing. And Randy learned about the power of prayer over pain.

These four stories have four things in common. First, a power of the mind and heart existed to co-create the healing process. Second, each individual had medical involvement in his or her process. Third, each didn’ t hesitate to ask others to pray with and for his or her healing Randy’s story. Randy was born with a deformity, mild spinal and highest good. These were persons who they knew bifida. He had lived with it all of his life. But with could be objective and hold for the highest good without age the deformity grew more pronounced and visible. attachment to the outcome. And fourth, each was actively For example, you could tell if Randy was tired or had involved in his or her process. And unspoken, all learned a bad day, because he would walk through the hospital to love themselves, forgive themselves for their parts in the corridors leaning to the right, and that leaning became health challenge (illness), accept that healing is possible, more pronounced with time. It also became more and trust the Universe for their learning and highest good.

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What do these stories tell us as healthcare professionpatients tell us what they want for healing. Professionals who have had their own challenges may know what is being als committed to the healing arts and process? At some said. Not that I advocate experiencing pain, but the experipoint, each patient makes a decision, consciously or unconsciously, what his or her healing process will be. Asence of pain is a powerful teaching experience, emotionally, spiritually, and physically. The experience of in the stories above, at some point the patients decided mentally, at pain makes us conscious of how powerful the the deep soul level that they wanted to experience healing. body/mind/spirit is when it is in pain. It signals us to wake Each stated with feeling, he or she desired physical healup and pay attention. And with help, it makes us grow. It ing, and as that experience evolved, each healing meant teaches us how important our healthcare skill is in pain alignment with the inner spirit. It wasn’ t instantaneous, management. But it also teaches us that what is done on although it could have been. Rather it was across time, the outside to us is not the whole story in pain managepossibly for the purpose of learning more about soul, ment. An inner quality to pain management exists that is spirit, and inner strength and power. Note, too, that the “illness-challenged” ones asked friends for prayer support.the responsibility of patients, and they hold the key to the effectiveness of pain management and healing in whatever They chose persons who would be detached emotionally, and would hold for the highest good of the Universal plan.form it takes. We are to perform our skill, then step back, While friends held for the highest good, the chal- be aware, and listen, refraining from other than supportive comments. It is well documented that patients give power lenged person worked at what was his or her task for the healing. This included not only taking prescribed medi-to the words we say about their process, which can be cations, but also practicing relaxation, losing weight,more potent than the medicines dispensed, or adjustments and manipulations made. To illustrate, while writing this changing diet, using images to cooperate and facilitate chapter, my friend Joan telephoned. She had asked me to with the process. Also note that healing had to be accepted before itpray with her during a foot surgery. It was not an unusual could occur. This brings up an interesting point: thesurgery, but she knew the power of prayer. On the day she phoned, it was 3 months post-surgery and I inquired as to challenged ones at some level came to terms, consciously or unconsciously, with what their contributions to the how she was doing. She replied that she had been to the doctor for a check-up and he had commented that her foot creation of the challenge was. They accepted responsiwas healing nicely. He told her that she was actually 3 bility and in that acceptance were able to take the next weeks ahead of schedule, and he was surprised. She action step. ” This brings us to the discussion of forgiveness. Thechuckled as she responded, “I’m not. Pain management and healing aren’ t new as we noted author recalls asking the physician who diagnosed the at the beginning of the chapter. Descartes began the scishingles how this could have happened, as she was leadentific study of the body, which paved the way for learning ing a wholesome lifestyle with good nutrition, exercise, how the body physical works. Pert provided us with the etc. She had to come to terms with and forgive herself molecular level of understanding energy in the body. From for not honoring the body’ s limitations before the pain the spiritual perspective, Jesus and the ancients were able could be managed. Until she could forgive herself for to do healings, and with the help of Mesmer and the failing to recognize the body’ s needs and limitations, it metaphysicians we learned the power of words and prayer would continue to give signals in the form of pain. Carfor healing. These insights help us humbly acknowledge olyn Myss’ 1997 book on the power of forgiveness to our limitations as healthcare professionals, encourage our heal indicates that forgiveness is the key to healing. Canrespect, and recognize our patients and their power, immadice Pert’s (1997) research suggests that the act and feelnent and transcendent, for pain management and healing. ing of forgiveness send peptides along the neurotransmitIt reminds us that the management of pain is a cooperative ters to the hurt part of the body, which helps create the process between patient and all levels of caregiving. Each healing. Forgiveness is a powerful energy experience, an of us is reminded that we are powerful beings, not by act of self-love and self-responsibility with tremendousmight or muscle, but by the power of our word and healing power. thought. Forgiveness is a powerful tool of pain management, as are healing and love. Forgiveness creates wholeness, and nonforgiveness keeps us separated. When someWHAT IS THE HEALTHCARE PROFESSIONAL’S thing is separated or broken from the whole, there is pain. POSITION IN THIS PROCESS? Forgiveness brings healing because there is wholeness and If we have done our own personal listening and learning,oneness again. we will see more of these healing experiences in our Finally, pain is the tool for teaching each of us to practices. Awareness of our process helps us be more function as a whole person, and eventually a whole gentle and quiet, as well as better able to listen and hear people — body, mind, and spirit. In the process we learn what our patients are telling us. In the best way they can, about and discover our whole selves. We learn the power

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Dossey, L. (1999).Reinventing medicine. New York: Harper. of our thoughts and words to shape our life experiences. This is the ethics of care.

REFERENCES Anon. (1999). A century of psychology. APA Monitor, 30, 11. Cady, H.E. (1892).Lessons in truth.Unity Village, MO: Unity Books. Chopra, D. (2000).How to know God.New York: Harmony Books. Dalai Lama. (1999).Ethics for the new millennium . New York: Riverhead Books.

Myss, C. (1997).Why people don’ t heal and how they can. New York: Three Rivers Press. Pert, C. (1997).Molecules of emotion. New York: Touchstone. Shepherd, T. (1985). Friends in high places.Unity Village, MO: Unity Books. Walsch, N. (1999).Friendship with God.New York: G.P. Putman’s Sons. Zukav, G. (1989).Seat of the soul.New York: Fireside.

78 Documenting Pain Barbara L. Kornblau, J.D., O.T.R./L., F.A.O.T.A., D.A.A.P.M. and Lori T. Andersen, Ed.D., O.T.R./L. INTRODUCTION

practitioners. Obtaining payment from insurance companies seems to take more work and for less money. Workers’ Documenting pain presents unique challenges for pain compensation seems to constantly reduce services it will practitioners. Because one cannot actually see pain as one cover and the amount it will pay for those services. Payers can see a broken leg or a rib on X-ray, for example,want second opinions and pain practitioners face more and documentation of the signs and symptoms plays a critical more regulations from numerous government programs. role in effective treatments. Though documentation presents challenges to pain pracMany stereotypes about individuals suffering from titioners, it also records our successes and presents them to pain exist in the world of payers, insurance adjusters, the world. If done carefully, it helps grease the reimbursedefense attorneys, workers’ compensation administrators, ment wheel. The medical record almost always constitutes family members, and others. For example, often, when the the only evidence payers, case managers, and others see to patient in pain enters the world of litigation, the individual justify pain management treatment and payment. faces a world of nonbelievers. Pain patients often are dismissed as having psychiatric problems rather than On the other hand, the pain practitioner’s documentaphysical problems. For example, some still argue thattion also can tout failures and/or lend credence to the conditions such as fibromyalgia are not physical syn-failures of others. For example, when something goes wrong with a patient, the medical record serves as the key dromes at all. Sometimes patients face accusations of malingering by nonbelievers rather than the reality of suf-evidence the jury or judge sees to prove that the clinician met the standard of care. fering from pain syndromes. Some think an absence of objective evidence makes it Accurate documentation of pain in medical records can make a significant difference in the lives of patients. impossible to diagnose pain. Others claim medical and rehabilitation providers cannot measure pain to prove its exist-Often the contents of the medical record play a significant ence. The mistaken belief that patients with chronic painrole in determining whether or not a pain patient receives workers’ compensation, social security disability, or other cannot progress gives payers an excuse to deny reimburseimportant benefitsSmollen ( v. Chater , 1996) ment to therapists. Further, some payers accept the erroneous notion that occupational and physical therapy intervention One can define medical record documentation as a s condition and the with patients suffering from chronic pain falls short of the serial and legal record of the patient’ course of the medical or therapeutic intervention from necessary skilled care required for reimbursement. admission to discharge (Aquaviva, 1998). This record In addition to these stressors faced by the pain practitioner, in the 21st century, pain practitioners face increas-describes how the patient functioned and the behaviors the patient displayed at the time of initial evaluation, during threats of malpractice, and managed care. Case maning the course of treatment, and at discharge. Essentially, agers and panel membership often limit access to pain 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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the medical record should “tell the story” or “paint a other organizations all require monitoring of documentapicture” of the patient and the medical care provided. tion to determine continuity of care and quality of services (Joint Commission on Accreditation of Healthcare Organizations, 2001a). REASONS FOR DOCUMENTATION Documentation prevents clinicians and facilities from Documentation serves several purposes. First and foreunsubstantiated claims of wrongdoing — in other words, most, accrediting bodies require it (Joint Commission on“CYA.” For this reason, hospitals usually include requireAccreditation of Healthcare Organizations, 2001a). Toments for documentation in their policies and procedures. maintain accreditation status, hospitals, rehabilitation pro-Physicians who fail to follow a hospital’ s documentation grams, outpatient programs, and others must maintain policy can lose their hospital privileges. Board ( of Trustees documentation according to the requirements of theirof Memorial Hospital of Sheridan County v. Pratt , 1953). accrediting bodies so they can maintain accreditation staAccurate documentation can protect clinicians from errotus. Accreditation is often required to qualify for reim- neous charges of malpractice, or criminal charges of bursement. Self-audits are performed as required by improper use of narcotics. Proper documentation can proaccreditation standards between surveys performed by the tect clinicians from civil and criminal penalties resulting accreditation bodies themselves. from charges of Medicare and Medicaid fraud and abuse Documentation in the medical record provides a com-or other civil or criminal charges (McKessy, 1998). munication method for the members of the healthcare Fiscal reviewers, auditors, intermediaries, and payers team. Healthcare clinicians may find themselves with lit-often review documentation to determine if services billed tle-to-no face-to-face contact. Other means of communi-were, in fact, provided. These reviewers and auditors may cation, such as telephone contact, prove ficult dif because also review documentation to determine if services were of diverse schedules and the varied places where patients medically necessary. The Medicare program requires that receive care. All healthcare clinicians have access to and services must be reasonable and medically necessary in should access the medical record. This access enables order for coverage and reimbursement for the care of the clinicians to read the documentation of other team mempatient under the Medicare Guidelines. As the saying goes, bers and thus keep apprised of the course of treatment, “In God We Trust, All Others Must Document. ” patient status, and progress from other viewpoints. This helps team members make appropriate decisions about Private insurance companies have similar requirepatient course of treatment and facilitates coordination ofments. Triggers that may start an audit or claims denial include overprescription of controlled substances; providpatient care. Looking ahead, documentation provides data for treat-ing the wrong medication; providing treatment without pre-authorization, referral, or prescription; absence of a ment innovations, research, and education. For example, a new type of pain treatment is administered to alleviatetreatment plan; lack of patient compliance; using too many patients’ pain. Documentation of the type of treatment modalities; and continuing treatment without improvement or results. Proper and complete documentation can rendered, the amount of treatment, the timing of treatment, protect the practitioner from potential problems. and patient status and behaviors after treatment will demFinally, most licensure laws require that healthcare onstrate the ef ficacy and effectiveness of treatment. Data collected from all of those treated will provide researchersprofessionals keep written medical records justifying the with outcomes data that clinicians also can use to justifycourse of treatment. Failure to do so can result in disciplinary action against the licensee. (See Table 78.1.) the treatment to payers. Outcomes data collected from documentation can be used for promoting or marketing one’ s program. For 78.1 example, if an outpatient pain program has designed TABLE a specific program for returning injured workers to the Reasons for Documentation workplace and the program succeeds in helping these 1. To comply with accreditation requirements. injured workers return to work, the data available from2. To communicate with other members of the healthcare team. the documentation will demonstrate the ficacy ef and effec- 3. To provide data for treatment innovations, research, and education. tiveness of the program. These data can be used to promote 4. To collect outcomes data to market programs. the program to case managers and others. 5. To provide data for quality assurance, continuous quality improvement and/or total quality management, peer review, and Documentation can be used for quality assurance and continued competency. continuous quality improvement efforts to determine the effectiveness of specific treatment interventions or pro-6. To prevent unsubstantiated claims of wrongdoing (CYA). grams. The Joint Commission on Accreditation of Hospi-7. Payers review documentation to ensure treatment was performed as billed and medically necessary. tal Organizations (JCAHO), the Commission on Accred8. Most licensure laws require documentation. itation of Rehabilitation Facilities (CARF), and various

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physician to disciplinary actionState ( Board of Medical Examiners v. McCroskey , 1994). The medical record serves as a legal document. State and In some jurisdictions, the jury can assume that missing federal laws and regulations establish minimum standards evidence, if produced, would have been unfavorable to the for record keeping. These record-keeping standards serve spoiler. Other jurisdictions simply will exclude altered as prerequisites to state licensure, receipt of federal fundevidence while some courts will impose sanctions against ing, and participation in federal programs such as Medi-the spoiler. Spoilers can also face criminal charges or care. As a legal document, medical records document the dismissal of their case (Seigfreid, undated). nature of the care provided, including the quantity and In addition to spoliation, clinicians must also watch quality of care, and protocols used for treatment. The out for falsification of documents. As a legal document, medical record also documents the charges for the care clinicians must never falsify anything in the medical given. Above all, the medical record carries the signature record or face civil as well as criminal charges lest they of the clinician. do. In People vs. Smithtown General Hospital, a surgeon State and federal laws prescribe the contents of the and a nurse falsified the medical record by omitting any medical records, and the ownership, access, and confidenreference to a prosthetic device salesman who assisted tiality requirements of medical records. Various laws alsowith hip replacement surgery. The surgeon and superviscontrol how long clinicians must keep medical recordsing nurse were criminally indicted for falsifying business following discharge. The length of time often is based records in the first degree, which was upheld by the court upon the statute of limitations for various administrative, when the defended appealed to have the indictments discivil, and criminal laws. For example, participation in missed P ( eople v. Smithtown General Hospital , 1978). Medicare requires providers to keep medical records for a length of time to enable the government to conduct investigations for fraud and other matters. CHARACTERISTICS Medical records that play a role as a “legal document”OF GOOD DOCUMENTATION often come under scrutiny in administrative, civil, and criminal actions. For example, attorneys involved inDocumentation must be clear, concise, objective, logically organized, legible, and contemporaneous. To communiadministrative and civil cases such as divorce/custody, insurance fraud, medical malpractice, personal injury,cate effectively, the documentation must be clear. To be workers’ compensation, disability benefits, and licensureclear, the healthcare professional must use terminology common to the people who will read the documentation. board discipline may subpoena medical records to present Know thy audience. Clinicians must assume someone else as evidence. As a recognized legal document, pain practitionerswill read their records. s documentation often finds its should never destroy or alter records after the fact to The pain practitioner’ way before the eyes of adjusters, attorneys, jurors, or conceal a mistake or error. Chances overwhelmingly point others with little to no working knowledge of pain jargon. to the reality that someone already has a copy of the Medical records with pain jargon or other medical jargon original records as they appeared before the clinician lack clarity for a lay audience and lose much in translation. altered them. Further, these types of alterations are illegal Clear, jargon-free, understandable documents can save cliand subject clinicians to disciplinary action and, in some nicians a trip to court. In some jurisdictions, attorneys can cases, criminal action. We call this conduct “spoliation. ” subpoena medical records alone. If the attorney can underBlack’s Law Dictionarydefines spoliation as “(t)he destruction of evidence” or “the destruction of, or thestand the records, it ends there. If the records are not clear, a duces tecum , which significant and meaningful alteration of a document orthe attorney may send subpoena requires the clinician to bring the documents to a deposiinstrument” (Nolan, 1979). In Bondu v. Gurvich , the Flortion to read and explain them. ida Court of Appeals allowed a family member to proceed with an independent action for spoliation when the hos- The use of abbreviations also renders medical records unclear. Facilities and agencies often develop an approved pital was unable to produce the medical records needed as proof in a malpractice action. The patient died duringlist of abbreviations for use in medical records. It is important that healthcare practitioners use the appropriate terthe administration of anesthesia in a triple by-pass operminology or abbreviations, otherwise it will be like readation. Without the medical records as evidence, the maling a foreign language for another healthcare practitioner. practice action could not proceed Bondu ( v. Gurvich , 1995). In another case involving spoliation, State Board Even worse, miscommunication can occur with devastatof Medical Examiners v. McCroskey , the Court found that ing results. The story of a physician who ordered ear drops for a patient is an example of miscommunication. The changing and backdating a note about a patient who bled to death cast doubt on the integrity of the medical record, physician wrote in the medical record that the medication violated the standard of care, and correctly subjected the was to be administered t.i.d. in the patient’ s R ear. As there

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tion: “If I can’t read it, I am not going to pay you. ” Like was no circle around the R, the recognized abbreviation for “right,” the medication was administered elsewhere — late entries, illegible documentation attracts suspicion: not in the “ear. ” “What are they trying to hide?” Concise documentation presents the most important Illegible documentation does not provide protection information about the patient without unnecessary distrac-(or CYA value) should the clinician face charges of maltors. It is much easier for one to read a concise record that practice, fraud, or disciplinary action. In fact, illegible gets to the point, as opposed to a lengthy note that one documentation can lead to serious harm to the patient, and has to search for the relevant information. Most impor-charges of malpractice, if other members of the healthcare tantly, payers do not want to search for the informationteam cannot read information. The classic problem arises they need for payment. Those records will likely end upwhen the pharmacist is unable to read the physician’ s at the bottom of the payment pile in favor of anotherillegible handwriting. In Texas, this problem led a jury to practitioner’s concise records. award almost a half million dollars to the family of a man Avoid extraneous notes in the medical record that canwho received the drug Plendil, used to treat high blood confuse the reader or add unintended information. A notapressure, instead of the drug written on the prescription, tion in a chart referring to what another clinician reportedIsordil, used to treat severe chest pain or angina (WebMD with a handwritten “B.S. ” in the margin proved rather National News Center, 1999). embarrassing for the clinician who, during her deposition While the damage caused by illegible or sloppy docwas asked to explain the abbreviation. umentation may not always lead to death of a patient, it Pain practitioners must use objective terms in theircan seriously damage one’ s reputation. Sloppy documendocumentation. Pain behaviors and status should be tation can lead a jury, case manager, or insurance adjuster described using measurable terms. Phrases such as “tolto believe the patient received sloppy care from the pain erated treatment well” or “patient doing well” provide no practitioner, which may lead to problems in the legal arena objective data. Payers and others in the medical record or a decrease in one’ s referral base. audience concern themselves with objective, functional The rules of documentation recognize that clinicians changes the patient makes in response to treatment intersometimes do make legitimate errors in writing their docvention. Clinicians should quantify pain measures andumentation. When clinicians make errors, they should record objective changes in pain. Clinicians shoulddraw a single line through the error, and write their initials describe the principles and methodologies used to reach and the date beside the error. Alternatively, clinicians may their conclusionsDaubert ( v. Merrell Dow Pharmaceuti- append the record with an explanation of the error. Eracals, 1993). Objective records omit any pejorative com-sures and correction fluid play no role in the medical ments about patients. record. Should clinicians not correct their errors, they live Clinicians must organize their records in a logical by the adage, “If it’s in the chart, you did ”it. manner. No one wants to hunt through documentation to find specific information. Further, the time delay during TYPE AND FREQUENCY the hunt may cause the patient harm. Categorizing information into sections and subsections easily identified by OF DOCUMENTATION headings will assist readers in finding the information they The type and frequency of documentation vary from facilseek. Clinicians should present data in an organized manity to facility and are also affected by regulatory agencies ner. In all cases, documentation should include a date and such as JCAHO and CARF, state laws and regulations, time of entry. Clinicians should record their documentation contem-and third-party payers. Agencies and facilities often have poraneously and in a timely manner. Some clinicians finda procedure by which documentation forms are reviewed for possible inclusion in the medical record. personal digital assistants (PDA) such as palm pilots helps initial evaluation upon ful to write their documentation contemporaneously, while Clinicians perform the patient’ they examine their patients. By documenting when anthe patient’s admission to a service. Information documented in initial evaluations should include at a minimum event occurs, the clinician ensures a more accurate picture of what occurred. The more removed in time one writesmedical history, current medications, allergies, drug sensitivities, presenting complaint, and assessment informathe medical documentation, the more the medical record begins to look like a work of fiction. Furthermore, a latetion. Initial evaluations may be written in longhand using a specific format, in a checklist format, dictated, written entry in the medical record attracts suspicion. Finally, the documentation must be legible. Informa-on a personal digital assistant (PDA), or some combination tion written illegibly is considered to be undocumented orof methods. Oftentimes, regulations dictate the amount of time a healthcare practitioner has to complete and enter not written: “If I can’t read it, you didn’t write it.” Illegible documentation will find its way to the bottom of the the initial evaluation into the medical record. In addition, payer’s payment pile in favor of easy-to-read documenta-in circumstances where a patient is transferred to another

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service, regulations or policies may require that clinicianspolicy (for inpatient records), accreditation bodies, state complete a new initial evaluation on the patient and doc-licensing regulations, federal regulations for various proument it in the medical record. grams such as Medicare, and professional standards of Progress notes for each visit, daily or weekly, also arepractice. often required as part of the medical record documenta- Because many pain patients are involved in the court tion. The provider of pain management services deter-system in some way, pain practitioners need to prepare mines the overall style of progress notes. Progress notes themselves for encounters they and their documentation may also be written longhand, or in checklist format,may have with the legal system. Regardless of what the dictated or written on a PDA, or combination again,applicable law or regulation states, in practice, if subpoedepending on the department, type of service, practice, etc. naed for a deposition, everything becomes part of the Many clinicians use S.O.A.P. note format for their medical record. Attorneys will send requests listing every progress notes. One should use care when using S.O.A.P. possible item that might relate to the patient. This could notes so to avoid writing “soapy” S.O.A.P. notes. Soapyencompass, for example, all items on your computer hard S.O.A.P. notes skimp on the information provided so thedrive pertaining to the patient, including, but not limited reader loses the picture quality of treatment. These soapy to, emails, draft reports, etc.; handwritten notes pertaining notes include phases such as “Patient doing ”well, “Conto the patient; copies of telephone messages; appointment tinue treatment, ” “Tolerated treatment well, ” “No Combook entries for all of the patient’ s scheduled appointplaints,” and the symbol∅, instead of descriptive, func- ments; and any other documents pertaining to the patient. tional information about the patient. The pain practitioner should include certain items in Some healthcare professionals such as physicians docthe medical record that will obviate the need to rely on ument a separate entry for every contact they have with memory 2 years down the road when the patient’ s case the patient. In contrast, other healthcare professionals such comes up before a judge. By preparing in advance with as occupational therapists and physical therapists may not proper documentation, the pain practitioner can look thordocument a separate entry for each contact. Rather, the ough and professional when questioned about treatment frequency of documentation may be determined by thethat occurred in the distant past. Time spent answering frequency of change of status of a patient and/or treatment questions regarding the patient or former patient’ s work provided. For example, an acute-care facility would prob-status, disability status, and impairment rating is reduced ably require more frequent documentation than a skilledif documentation is complete. Table 78.2 lists and nursing facility because status of patient may change more describes minimal content of the pain practitioner’ s medfrequently. In another example, a rehabilitation therapistical record. Statutory requirements, conditions of particiwho consistently provides the same treatment each visit pation in federal or state programs and accreditation bodmight only summarize the type of treatment provided andies will probably require additional items. progress in a note documented each week. A contact note may be entered in the medical record to document phone DOCUMENTATION OF PAIN contacts with other healthcare practitioners, the patient, and the patient’ s family members. In the 1980s and early to mid-1990s, as a result of fear of Discharge notes or summaries state what treatment addiction, public policy steered physicians away from prehas been rendered, improvement made, instructions given scribing narcotics for patients suffering from chronic pain. to the patient and/or significant others, and recommendaPhysicians were disciplined or threatened with disciplintions for further or future care. Copies or records of allary action for overprescribing narcotics especially to should be kept and/or placed in the medical record. Dis-patients with chronic pain (Angarola, 1994). Comprehencharge documentation should include the condition of thesive documentation of the need for pain medication propatient at discharge, and the reason for discharge. Reasons vided one of the tools for defending oneself from charges for discharge may include goals met, no further progress of overprescribing narcotics. However, documentation of anticipated, or patient’ s care transferred to another agencythe prescription of narcotics, if against state laws and reguor healthcare practitioner. lations, also could work squarely against the physician. Thus, the looming threat of discipline and the fear of addiction led to underprescribing of narcotics by many CONTENT OF MEDICAL RECORDS physicians (Angarola, 1994). With studies showing as The medical record consists of items dealing with themany as one half of all patients in pain not provided with overall care of the patient. It may include correspondence, appropriate pain medication, public policy shifted away phone call transcripts, copies of prescriptions, billingfrom the fear-based, underprescribing of pain narcotics to records, personal digital assistant (PDA) records, emaila realistic approach based upon the needs of the patient records, results of lab tests, X-rays, and others. The con(Oregon Board of Medical Examiners, 1999; U.S. Agency tents of the medical record may be determined by hospital for Health Care Policy and Research, 1994).

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TABLE 78.2 Minimal Content of Pain Practice Medical Record* Informed consent History and physical examination • Including history of drug substance abuse Drug sensitivities or allergies Document the pain with symptoms: • Location • Duration • Frequency • Intensity • Precipitating or aggravating factors Restrictions, limitations, and activity level • Correlate pain to function • How does the pain limit the ability to work or dress, etc.? • How does the pain affect mental status? • Is the patient depressed? • Can the patient drive safely? Evidence of impairment • Pain itself is not an impairment Subjective and objective measures of pain Copies of prescriptions legibly written Use of narcotics** • Record dose, amount, and number of refills • Document/contract, signed by the patient acknowledging • Use of controlled substances • Side effects and material risks • Method for dealing with • Exacerbations • Lost presciptions • Noncompliance with treatment • Misuse of medications • Substance abuse Referrals to other professionals Notation of reading consults and lab results Compliance with treatment Monitoring or other devices Follow-up required? Follow-up appointments scheduled and dated? Signature and date on every entry Discharge documentation • Reason for discharge • Referral upon discharge • Condition upon discharge • Conclusions • Instructions given Handouts given to patients — copies in charts Time saving information (in case a request comes later) • What information will workers’compensation want from you as a provider? • What information will social security want from you as a provider? • Is the person working now? If not, why not? • What kind of impairment does the patient have?

The acceptable contemporary approach to pain treatment emphasizes an assessment of the patient’ s pain, documentation of pain and management of the pain (Angarola, 1993; Oregon Board of Medical Examiners, 1999; U.S. Agency for Health Care Policy and Research, 1994). The key methodology to prove one’ s compliance with these basic elements lies in proactive comprehensive documentation using, at a minimum, the elements listed in Table 78.2. Recognizing the controversy in prescribing pain medication that led to underprescribing of pain medications and the resulting unnecessary suffering of patients in pain, the JCAHO developed standards for pain management, enforceable through its accreditation process. These standards, effective for JCAHO surveys that occurred after January 1, 2001, state that all “patients have the right to appropriate assessment and management of pain” (Joint Commission on Accreditation of Healthcare Organizations, 2001b). Pursuant to the standards, the healthcare organization must take steps to ensure the pain of “all patients is recognized and addressed appropriately” (Joint Commission on Accreditation of Healthcare Organizations, 2001b). JCAHO standards require initial and regular reassessment of pain in patients. Proper documentation will demonstrate compliance with these standards. According to the JCAHO standards, when documenting pain symptoms, the pain practitioner should include location, duration, frequency, intensity, quality, patterns, and precipitating, alleviating, or aggravating factors, and pain management history (Joint Commission on Accreditation of Healthcare Organizations, 2001b). However, the practitioner must realize that pain itself is not a disability. It is important to document how the pain restricts a patient’s activity and his or her participation in life roles. The pain symptoms must be correlated to function. To document a pain patient’ s function, the pain practitioner may ask the following: Is the patient depressed? How has the pain affected his or her relationship with others? How is the pain affecting his or her mental status? Can the patient concentrate well enough to perform activities? Does the patient comply with the treatment regime? How does the pain limit the patient’ s ability to dress or care for him or herself? Can the patient drive safely?

The JCAHO standards delegate to each organization the * Check their state licensure laws to add state-mandated requirements responsibility to develop follow-up criteria for evalus documenand relevant accreditation bodies for their requirements. (From Jointation of patients in pain. The pain practitioner’ s Commission on Accreditation of Healthcare Organizations, Pain Stan-tation will be key to showing compliance with JCAHO’ standards. Among the suggested criteria, the standards dards for 2001, 2001a.) ** Recommended for physicians. look at the need for information on the impact of pain on

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daily life, function, sleep, appetite, relationships with oth-practitioners a simplified process upon which to base treatment, policies, protocols, and checklists. ers, concentration, and others emotions. JCAHO surveyors will rely on the clinician’ s documentation to measure Avoiding the use of similar looking or sounding medcompliance with the standard. Therefore, documentation ications also lowers the likelihood of error. If physicians should reflect these areas. Clinicians who develop systems prefer to use certain specific medications on a regular for documentation will assure they cover all of the bases.basis, using preprinted prescription pads in a checklist format also can help eliminate errors. Pain practitioners can eliminate other documentaTHE SYSTEMS APPROACH tion errors by putting systems in place to document TO DOCUMENTATION telephone calls with patients and consulting physicians. Systems for justifying and monitoring narcotics such as Agency for Healthcare Research and Quality (AHRQ) the contract listed in Table 78.2 provide one simplifi ed (2001b) research shows that most medical errors are sysmethod to document a potential problem on a consistent tems errors. For example, when a surgeon amputated basis. Finally, pain practitioners should have systems to Willie King’ s healthy leg, the system designed to track monitor the effectiveness of the systems they have put the proper body part through surgery failed (Institute of in place. Medicine, 2000). Errors such as this are not the result of individual negligence or misconduct. The system failed and resulted in harm (Institute of Medicine, 2000). SUMMARY Documentation plays a signifi cant role in systems Three rules of thumb to remember: within healthcare. Peer reviewers and others can trace errors through documentation and documentation done properly can show an absence of errors, compliance with • If you charged for it, you did it. • If the reader can’ t read it, you may not have accreditation standards, or proof the system is properly done it. working, resulting in error-free quality care. • If you changed it after the case was filed in The Institute of Medicine report (2000), “To Err is court or after you submitted a copy to the payer, Human: Building a Safer System, ” suggests that the you have a big problem. healthcare system look to ergonomic principles used in other industries but up to now ignored by the healthcare Good medical record documentation can ensure qualindustry to improve ef ficiency and lower the error rate. ity care and protect the patient and practitioner. Some of these methods that are successful in reducing errors in the medication process can be used to reduce errors and omission in documentation. These successful methods of prevention based on ergonomic principlesREFERENCES include reducing reliance on memory which can be fallible Agency for Healthcare Research and Quality. (2001a). Medical and cause errors, simplifying of procedures, standardizing errors: The scope of the problem [On-line]. Available: treatment processes, using standardized protocols and http://www.ahcpr.gov/qual/errback.htm checklists, and decreasing reliance on multiple data entry Agency for Healthcare Research and Quality. (2001b). Reducing (Institute of Medicine, 2000). errors in healthcare [On-line]. Available: Pain practitioners can incorporate several of the ergohttp://www.ahcpr.gov/research/errors.htm nomic principles into their documentation systems toAngarola, T. J., & Joranson, D.E. (1993). Wins and losses in improve efficiency and decrease documentation errors, in pain control.APS Bulletin, 4 (3), 8–9. Angarola, T. J., and Joranson, D.E. (1994). Recent developments other words, to streamline the process. To reduce reliance in pain management and regulation. APS Bulletin, 4 (1), on memory, pain practitioners can use personal digital 9–11. assistance (PDA) or handheld computers to write the documentation as the patient reports it to the clinician. ThisAquaviva, J. (1998). Effective documentation for occupational therapy. Bethesda, MD: American Occupational Thermethod also eliminates reliance on handwriting for orderapy Association. ing medication and other treatments, thereby eliminating Board of Trustees of Memorial Hospital of Sheridan County v. potential errors (Agency for Healthcare Research and Pratt. 262 P.2d 682 (Wyoming Supreme Court 1953). Quality, 2001a). Bondu v. Gurvich , 473 So.2d 1307 (Fla App. 3 Dist. 1995). Standardizing and simplifying treatment policies andDaubert v. Merrell Dow Pharmaceuticals , 509, 579 U.S. protocols and implementing checklists help the pain pracSupreme 1993). titioner avoid confusion and reliance on memory. InInstitute of Medicine. (2001).To err is human: Building a safer essence, JCAHO’ s pain management standards spell out health system[On-line]. Available: http://books.nap. a standardized protocol for pain management, which gives edu/books/0309068371/html/51.html#pagetop

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. 402 N.Y.S.2d 318 Joint Commission on Accreditation of Healthcare Organizations.People v. Smithtown General Hospital Supreme Court, Suffolk County 1978. (2001a, February 4). 2001 Medical Record Review SumSeigfreid, J. (Unknown). Spoliation of evidence. Baker, Sterchi, mary Sheet[On-line]. Available: Cowden, & Rice LLC. Available: http://www.bscrhttp://jcprdw1.jcaho.org/accred/medrecs/im3211.html law.com/Seminars/Spoliation_of_Evidence/spoliation_ Joint Commission on Accreditation of Healthcare Organizations. of_evidence.html [2001, February 6,]. (2001b, February 6). Pain Standards for 2001 [On-line]. Smollen v. Chater . 80 F.3d 11273 (9th Cir. 1996.) Available: http://www.jcaho.org/standard/pm.html. State Board of Medical Examiners v. McCroskey . 880 P.2d 1888 McKessy, A.S.I., & Sanner, R.J. (1998, July/August). Protecting Colorado Supreme Court 1994. your practice with a Medicare and Medicaid compliance program [On-line]. American Academy of Family Phy- U.S. Agency for Health Care Policy and Research. (1994). Management of cancer pain (clinical guide) [On-line]. Available: sicians. Available: http://hstat.nlm.nih.gov/ftrs/default.browse? http://www.aafp.org/fpm/980700fm/mckessy.html dbK=4&tocK=5&ftrsK=64273&tocm=00&lineK=0&t=9 Nolan, J. C., & Connolly, M.J. (1979). Black’s law dictionary. 81321719&collect=ahcpr St. Paul: West Publishing Co. Oregon Board of Medical Examiners. (1999). BME statement of WebMD National News Center. (1999). Bad handwriting led to man’s death [World Wide Web]. Available: http:// philosophy on pain management [On-line]. Available: onhealth.webmd.com/conditions/briefs/item,52258.asp http://www.bme.state.or.us/topics.html#Pain_Management

79 Motor Vehicle Accidents Christopher R. Brown, D.D.S., M.P.S In the last 30 years, there have been more than 10 million to fully appreciate and estimate the resulting forces that “moderate to severe” injuries and over 1.5 million deaths inmay contribute to human injury potential. the United States from motor vehicle accidents (MVAs). The National Safety Council reported in 1996 that 11.2 million LOW SPEED VS. HIGH SPEED traffic collisions occurred. Of those, 9.6 million were a combination of property damage only and/or nondisabling injury For practical purposes, the working definition of a lowcollisions. The economic cost to the United States was estispeed impact is a collision in which the change in velocity mated to be $176.1 billion — a staggering amount of money. of the vehicles (usually the one that contains an occupant In terms of the dollar costs involved, Evans (1991) in claiming an injury) is less than 10 mph. It must be emphaTraffic Safety and the Driver indicates property damage sized that this defi nition of low speed is subjective. to top the list at 37%, with medical costs in fifth place at Clearly, no general consensus among experts exists. 6% of the total. Data from the National Highway Traf fic Although it is commonly accepted to describe impact Safety Administration (1987) estimate the following: severity and injury potential as functions of change in velocity, caution should be used when considering impacts of $ (Billions) % (Total Expenses) grossly dissimilar durations. Comparison of impacts based Property 27.0 37.0 solely on their respective changes in velocity inherently Insurance 21.0 28.0 assumes the impacts occurred over a similar duration, typiProductivity 16.0 22.0 cally 90 to 140 msec for low speed impacts. For the majority Legal and court 4.0 6.0 of accidents this is a reasonable assumption. However, in Medical 4.0 6.0 some collisions, such as underride or sideswipe collisions, Emergency (transportation, 0.7 0.9 the impact duration may be in excess of 300 msec. Given diagnosis, and support) an equal change in velocity, a vehicle that undergoes a longer Miscellaneous 0.45 0.6 duration impact will be exposed to lower peak forces. For Understanding what happens to humans in MVAsthis reason, underride and override collisions, although sometimes involving very high dollar amounts of property takes more than statistics, graphs, and charts. It requires noadamage” “ collision. a combination of learning tools, investigative procedures,damage, can be less severe than As an example of the effects of impact duration, conand a thorough understanding of human anatomy and sider skidding a vehicle to a stop. In theory, decelerating a physiology. vehicle from 30 mph to a stop by applying the brakes From an engineering perspective, we need to know involves an impact between the tires and the roadway with certain factors about the automobile such as weight, speed, and its vector (direction of motion). Other factors that maya change in velocity of 30 mph, but with an impact duration of approximately 2.0 sec. The skidding vehicle is decelercontribute to overall force need to be understood as well

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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ated at approximately 0.7 gs. Although braking a vehicle toanything based on a population smaller than what is statisa stop involves a 30-mph change in velocity, this is a quitetically significant in the measured population is erroneous. a REMVA. Most different event than a 30-mph front-to-barrier impact. The There is no such thing as typical REMVAs are offset collisions producing torsion, tension, barrier impact occurs over a much shorter duration and compression, and shear forces to the human body as a typically involves decelerations of 30 to 50 gs. A factor to consider in low-speed rear-end motor vehi-whole and to the individual parts. cle accidents (LSREMVAs) is impact forces concentrated In reality, actual numbers regarding REMVAs are impossible to track (fatal vs. nonfatal). over very small areas. As an everyday event, this may occur while backing into a small diameter pole in a parking lot or contacting a corner or small area of a bumper. REAR-END MOTOR VEHICLE ACCIDENTS Vehicle structures typically deform in proportion to the amount of force applied. In impacts with narrow objectsWhile statistics on fatalities are easy to track, the statistics or to the corners of vehicles, the contact forces are dison injuries are not. This especially holds true when it tributed over a very small area producing large localcomes to REMVAs. Take, for instance, the port of statistical stresses (force per unit area). These large local stresses entry for comparing the two. With a fatality, police are can damage bumper and vehicle components at changes involved, certificates are signed — a definite traceable sysin velocity below the strength of that area. Testing by thetem exists. A defi nite path which societies have determined Insurance Institute for Highway Safety indicates that thealso needs to be followed. amount of damage and costs of repair will vary dramatically With injuries, however, this is not the case. Take into from car to car and will even vary greatly for the sameconsideration the possible portal of entry into the medical vehicle depending upon the type and angle of low speed system of the United States. A victim of a MVA may very collision (Kaufman, et al., 1993). These factors have to be well start out at the emergency room with a description taken into consideration to determine forces transferred. of minor injuries that do not need immediate attention. At In reality, though, the definition changes situationallythat point, there may or may not be any type of follow according to needs. Low speed infers that the occupants through. The victim may be referred back to a family can’t be hurt. High speed infers they can. As a rule ofphysician if he or she has one, or the victim may be left thumb, engineering studies will routinely define low speedto find his or her own way. as less than 10 mph closing speed. The choices people have for treatment of pain are Can you draw the same conclusions? Are the colli-varied. For instance, for the treatment of headaches folsion biomechanics the same? Are the injury mechanisms lowing a REMVA, the person may choose to visit a the same? physician, a chiropractor, a dentist, a massage therapist, In professions that deal with MVAs and human injury, an acupuncturist, an optometrist, an ophthalmologist, an erroneous assumption often exists that “one size fits and so on. all.” In other words, there is a mechanism of injury that Statistics, as a result, are not accurate and there is no either happens or does not happen — people get hurt or predetermined course of action as in fatalities. In fact, they don’t. In the dental profession regarding TMJ inju- even the accepted terminology varies from source to ries, it was assumed that for TMJs to become injured insource on how to even describe injuries as a result of a rear-end motor vehicle accident (REMVA), the mandibleREMVAs. They may be described as STI (Soft Tissue had to go through a full range of motion. Videos of Injuries), MIST (Minimal Impact Soft Tissue), CAD (cerLSREMVAs clearly indicate that in low speed collisions vical acceleration deceleration) — all these descriptions it is often not the case. A few authors, therefore, erroneare used to describe a pattern or type of injury as a result ously assume that because this particular mechanism of “whiplash.” Even with the difficulty of tracking these injury is not present the TMJs cannot be injured. That, oftypes of injuries, it has been estimated that 1 to 2 million course, is false logic. All parts of the body no matter whatCAD injuries occur per year from REMVAs (Evans, the location can receive injuries from many sources. Cli-1992). The 2 million per year estimates occur at rates nicians need to be aware of these mechanisms to clearly roughly 5480/d, 1827/8 h, 228/h, 114/half h, and 4/min. understand, diagnose, and treat the injuries they see. Not only are REMVA injuries substantial in number, they also can produce long-term residual effects. In fact, Understanding leads to a more definitive diagnosis and the rate of recovery in whiplash injuries is poor; 20 to more effective treatment. Statistics themselves are not particularly significant40% of whiplash injuries have debilitating symptoms that when trying to predict individual occurrences. Statisticspersist for years (Carette, 1994). Patients destined to may be used as an academic yardstick butt can’ be used recover will do so in the first 3 to 4 months after initial to predict how an individual or small group of occupantsinjury (Barnsley, et al., 1994). The consequences are both will respond in any given situation. Predicting or judging long term and far reaching, resulting in extended sick leave

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and increases in disability (Per-Olof, et al., 1998). Beyondlation between live human response and other factors that time period the probability of permanency increases.increases. This is because all other testing measures purely While statistics vary greatly, it is safely assumed thatmechanical response but no material response. Pain and up to 50% of all REMVAs will result in some type of neck dysfunction often result from the material response of injury. The risk of occupant disability is approximately 3 viscoelastic human tissue. In other words, the quicker the impact, the higher the forces received, the more mechanto 6%, a staggering number when one considers the numical a human will respond and, therefore, mechaniber of motor vehicle accidents per year (Ono, et al., 1993). cal/cadaver/computer modeling becomes more relevant. There is no truth to the assumption that injured people get In low-impact REMVAs a few good studies with humans better after some type of settlement or what is known as exist but virtually none with surrogates that correlate with “green back poultice. ” human motion. As a result, while all crash test studies among living, nonliving, and nonhuman subjects yield TESTING METHODS FOR PREDICTING good statistics for study and provide cost-effective ways HUMAN INJURY to measure mechanical output, at best they provide unconfirmed approximate vague guidelines for human injury. Testing methods used to determine the kinds and types of What crash and test studies won’ t do will give subinjuries received in MVAs fall into five categories: jective information such as: 1. 2. 3. 4. 5.

Humans (live) Animals Cadavers Computer modeling Anthropomorphic test dummies

1. 2. 3. 4. 5. 6.

Pain Central Nervous System (CNS) information Biological information Physiologic information Kinetic dysfunction following impacts Latent reaction

The only totally accurate way to predict human response in REMVAs is to actually use living, breathing All information gathered from crash test studies is humans. Obviously, some restrictions apply for thesestatistical in nature and can never be applied to an inditypes of situations. vidual in a given situation. First of all, humans get injured. A review of studies using live, human testing reveals that humans are brought to the bare minimum level of injuries and thenBIOMECHANICS no more. There are obviously good reasons for that! Biomechanics is a very inexact science when it comes to Therefore, the threshold of human injury is not totally human beings. While mathematical predictions are accustatistically accurate. rate and easily obtainable, human reactions under different Another drawback to the use of humans in crash tests stresses are not. How can one explain when a person’ s is that although all test situations have very specific paramparachute fails to open, and he or she beats the odds and eters small variables will cause a great change in human survives a multi-thousand foot fall while another person response to input forces. Variables such as occupant seatwill trip coming down some stairs, fall several feet and ing, anticipation of impact, the weight of apparatusdie? Examples of human response to energy input quickly strapped to the patient, helmet vs. no helmet, etc. greatly lead one to the conclusion that the predictability of indimodify the parameters of human response, making each vidual response is based strictly upon the individual’ s individual crash in truth anecdotal. response; nothing more, nothing less. It is important, howIt also should be noted that crash tests are not designed ever, to understand generalities so that a practicing clinito hurt human beings — they are designed to note human cian can approach human injury with logical sense. motion and/or response to energy input. All other testing There are four basis response modes for a body subsources, while providing great statistical information, pro-jected to external forces: vide no actual correlation to human injury. If one carefully reads published reports through the Society of Automobile 1. Elasticity. Elasticity is defined as deformation Engineers (SAE), it will be obvious with a few biased induced during forced application, which is exceptions that human motion studies do not predict injucompletely recovered when the load is recovries or lack thereof, but carefully note that they are indiered. An example of this is the perfect spring. vidually dependent. This type of reaction is rarely found in the All other types of testing including cadavers are not human body. accurate for the human response in low-impact REMVAs. 2. Plasticity. Plasticity results from deformation of the initial geometry when the load is released. In high speed crashes as the Delta V increases, the corre-

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In other words, the loading and unloading path normal circumstances, the initial axis of rotation and are different. The absorbed energy is the prod- resulting translation can very well be different from one TMJ to another within one person, resulting in axes of uct of force× motion in the direction of motion. Plastic deformation in essence equals the per- rotations that are not coupled symmetrically with one manently stored (absorbed) energy. A good another. The surface of the TMJs can be nongeometric for example of plastic deformation is the human earlobe’s response to weighted earrings or many reasons, including degenerative joint disease, inserts. When pressure is applied over time, the remodeling, growth, angles of eminentia, scar tissue, etc. soft tissue of the ear will bend and be perma- The condition and surface of the articulating surfaces and supporting structures and the resulting musculature funcnently changed. tion determine the potential motions of the TMJs resulting 3. Viscoelasticity. Viscoelasticity is body deformation under a load such that it recovers its in a very complex motion system. For the ICR of the TMJs to be accurately detergeometry upon load release, but it does so by mined, they would have to be rotating cylinders that following a different loading path. The initial geometry is recovered but the body absorbs remain stationary throughout the motion, which of some of the applied energy. In a mechanical course they do not. The mandible changes its position sense, shock absorbers and tires are good exam- as it moves throughout the range of motion. The result ples. Human soft tissue responds in a viscoelas- is not just a change of the head of the mandible, but the tic manner unless force is applied to the point mandible itself. As it translates, rotates, moves in a 3-dimensional position, the ICR changes as well. Studof actual tissue rupture. ies also indicate that the trajectory of the condylar heads 4. Brittleness. A brittle body ruptures with neglialong the surfaces can be affected by velocity (disgent plastic flow. Up to the point of rupture, however, response is purely elastic. The best tance/time) and is a multiplane vector that can be example of this is glass. While each part of the affected by muscle soreness, speed of forced opening, human body under various conditions can rotational forces, compressive forces, and shear forces. exhibit some of these properties, in the true The ICR of the TMJ will change dramatically in a very sense of the word, the human soft tissues slight, fractional opening. When the ICRs of the TMJs are not perfectly matched, the articulating surfaces of respond in a viscoelastic manner. the joints can be either distracted or compressed, depending upon which moment in time is measured. INSTANTANEOUS CENTER OF ROTATION Rapid acceleration, such as that experienced in an (ICR) REMVA, can affect the standardization of motion of the TMJs, creating nonhabitual moment arms resulting in ICR of a joint is the mathematical determination of a excessive forces not physiologically compatible with the theoretical point on which all motions rotate. The concept human anatomy involved. These changing patterns from of ICR in a kinematic and biomechanical sense is an moment to moment will result in gross motor dysfuncimportant one. It can be considered under healthy condition, which will produce differing articular motions. The tions to be the physiological center upon which human result is that the ICR of the TMJs is a mathematical motions of a given joint will move. Various ICRs have theory only and not an accurate representation of reality. been measured and determined for different body parts. TMJs and their supporting structures can become excesHowever, in an REMVA, the ICR may change within sively damaged from indirect trauma such as that microseconds, causing a great change in load distribution received by whiplash. The following is a list of potential of the human body. In a landmark study by Kaneoka, et al. TMJ injury mechanisms: (1999), the ICR of the spinal column was measured and found to change in as little as a sub-4-mph Delta V resultMechanisms Contributing to TMJ Injuries without Direct Impact to ing in a pathological motion. the Mandible as a Result of LSREMVAs The term ICR has been misapplied and misunderstood in some instances of human motion. This is especially true1. Coefficient of friction — change in fluid viscosity— fluid is in the TMJs. First of all, the motions of TMJs are not different, rough, yielding more drag. skull purely rotational and do not move around the fixed axis 2. Blunt trauma due to linear condyle distalization compared to — bruising and tearing of soft tissues. of rotation. The axis rotation of TMJs will vary in ana3. Slowness of muscles to react (seen in electromyographic studies) — tomical planes. When subsequent motion of the head and Muscles and joints don’ t have to go through full range of motion neck apparatus exists, or compressed tissue in the retro- (ROM) for injury to occur. discal area, the TMJs translate from the first moment. In4. Morphology of articulating surfaces may not be smooth, especially this instance, virtually no pure rotation occurs. Under under compression.

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Mechanisms Contributing to TMJ Injuries without Direct Impact to the Mandible as a Result of LSREMVAs (continued)

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OCCUPANT

TO

AUTOMOBILE

The second collision, occupant to automobile interior, can

5. Cellular ability to repair is altered. also be generalized into four separate phases: 6. ICR is altered and changes through ROM. 7. Fast and slow wave motion from headrest and condylar distalization 1. 0 to 100 msec. The initial phase occurs at 0 to resulting in tearing of soft tissues at hard tissue junctions. 100 ms. When the vehicle moves forward out 8. Hydraulic differential between upper, lower joint space, and disc under the test subject, initial forward and verapparatus. tical motion of the hips and low back occurs. 9. Set up for repetitive strain syndrome — change in posture of neck Simultaneously, the upper part of the seat and mandible/upper jaw/skull. Occlusion doesn’ t change. begins to flex rearward under the load of the 10. Sympathetically maintained pain syndrome may contribute to degenerative joint disease over time. torso which remains stationary during this time 11. Tearing of pre-existing adhesions, fibrotic tissue. period. 12. Bleeding in the TMJs (hemarthrosis). 2. 100 to 200 msec. During the first 100 msec, the 13. Referred pain patterns from other peripheral injuries. seatback reaches maximum rearward move14. Most TMJ diagnoses are inaccurate and/or misdiagnosed in the first ment. The subject moves upward and forward place. Common Soft Tissue Acceleration/Deceleration (STAD) MIST Injuries of the Head and Neck Resulting from LSREMVAs 1. 2. 3. 4. 5. 6. 7. 8.

Temporal tendinitis Myofascial trigger points (MFTP) Ernest syndrome Occipital neuralgia (GON, LON) Cervical facet joint inflammation TMJ posterior capsulitis TMJ lateral capsulitis Myalgia

Note: These clinical injuries can occur as a result of the previously mentioned mechanisms.

COLLISION DYNAMICS There are three different types of collisions in every REMVA: 1. Automobile to automobile 2. Occupant to automobile interior 3. Occupant body part to body part

resulting in neck compression, cervical spine straightening, and movement upward and rearward. The head is in a chin-up type of position and begins to rotate rearward. By 160 msec, the vertical motion of the torso begins to pull the neck forward as the head continues into the extension. During this phase, significant shearing forces and ramping may start (vertical rotation). 3. 200 to 300 msec. At 200 msec, maximum vertical motion has taken place. At 250 msec, the head starts a forward motion. The seatback returns to its original position while the torso extends back down the seatback. 4. 300 to 400 msec. At 300 msec, the descent of the torso is now complete and is moving at the same velocity as the vehicle. At 400 msec, active deceleration of the neck occurs. At 400 msec, all impact-related motions are virtually completed and the human body is moving at the vehicle’s velocity.

The total time for human movement in REMVAs is between 0.1 to 0.2 sec. Whether the impact results from AUTOMOBILE TO AUTOMOBILE low or high velocity, the time of energy exchanged is The easiest type of collision to understand is automobilevirtually the same. This is due to the biomechanical propto automobile. The motion is commonly divided into four erties of the elements involved and may vary only by a few fractions of a second. different phases: 1. 2. 3. 4.

Contact Vehicle at the peak of acceleration Vehicle starting to slow down Vehicle slowing to a stop

OCCUPANT BODY PART

TO

BODY PART

Human injury comes not from therst fi collision, but from the second and third collisions. Obviously, contact from the human being to parts of the automobile can All such factors as bumper height, weight of the vehicle,produce great amounts of soft tissue injury. These can angle of impact, and environmental factors may change come from movement of the body into the seat, the the function of time and velocity resulting in an overlap headrest, a seatbelt, steering wheel, dashboard, automoof each phase. bile pillars, windshield, etc. All are potential injury mechanisms for human beings. However, the third col-

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lision (body part to body part) has a great effect, espe- Impacted Body Side Side Away from Impact → cially in low impact situations. As the automobile goes Force Generated Zero Force through the motions, keeping in mind Newton’ s laws of motion, the occupants remain stationary relative to the The result is a net force that produces differential automobile but seem to move toward the impact. Thedeceleration between body segments. The resulting biooccupant lags behind the car, the torso lags behind the mechanical stresses (shear, compression, torque, etc.) acthips, the neck lags behind the torso, the head lags behind ing simultaneously, and in opposite directions, often yield the neck, the vertebrae lag behind one another, the mansoft tissue damage. dible lags behind the cranium, etc. As a result, the motion of the human during this time period is a nonphysiological motion resulting in points of injury, which WAVE MOTION will almost always be at the connective tissue junctionsStress waves travel at the speed of sound (square root of between hard and soft tissues (as commonly seen in the the ratio of the Young’ s modulus to the material density). TMJs and cervical vertebrae). The result is injuries to muscles, ligaments, and tendons. In an offset collision 1. Travel through the body (which most are), a great amount of rotational forces 2. Subject portions to local stresses and forces will be placed on the body. The occupants will experi3. Localized compressions ence compression and shear forces, which cause great 4. Localized tensions injury to the soft tissue. The differences in load variations to the human body during cycles of motion result Wave speeds for car material are approximately 9843 in multiple stress and strain points. Each REMVA is to 16,404 ft/sec (10 times the speed of sound). Time of unique and, accordingly, no such thing as pure forwardenergy transfer is 0.1 to 0.2 sec which means the energy and backward motion exists. Biomechanical forcestravels the length of the car (15 ft) in 1.5 msec. applied in REMVAs are always multidimensional. As a Elastic waves travel 67 times the car length (approxresult, there is no Delta V or closing speed under whichimately 33 reverberations) in the energy transfer time of a person cannot get hurt, nor is there a Delta V or closing 0.1 to 0.2 sec. speed over which all people will get hurt. The injuries Although viscoelastic for the most part at low forces, are a result of individual response at a moment in time.human soft tissue responds in an elastic manner. At high These principles and conditions apply to soft tissueforces and as a function of time in which the force is injuries and all body parts. The rate of acceleration ofapplied, soft tissue may respond in a plastic manner resulting in permanent injury. Plastic waves travel much slower any given body part is of utmost importance (Newton’ s second law). The forces increase dramatically with an(slightly faster than the collapsing of impact surfaces) in increase in acceleration. Soft tissue properties differautomobiles and in human tissue as well. In MVAs, both waves are present due to crushed and uncrushed vehicle when applied with time variables. Crushing of soft tissues can occur in blunt impactcomponents. Not surprisingly, then, injuries often occur at locations remote from the impact site. The velocity when body surface deforms and soft tissues get com(Newton’s second law) of deformation is the predominant pressed between impact site and other hard tissues. Examfactor in determining the magnitude of wave created. ples of these are 1. Tissues at the nuchal line and headrest (skull HIGH VELOCITY and headrest) 2. Tissues between spinal column and seatback Stress waves from impact site travel at the speed of sound 3. Tissues between vertebrae during ramping and in the surrounding tissues. Injuries occur at submarining 4. Tissues between the condyles and skull (TMJ 1. Interfaces of unlike tissues (menenges, TMJs, injuries) muscle to bone attachments, facial linings, etc.). 5. Attachments of muscles (i.e., trapezius) during 2. Tissue/air interfaces (intestinal wall/gas, sinus ramping and contact with friction of the seat, cavities/linings). headrest, and body supports built into seats 6. Etc. A differentiation of tissue movement is contributed by the following mechanisms of injury: Because a moving body has inertia, when it collides a force is immediately produced on the impacted surface 1. Compression and expansion of the stressed tisthat starts to slow the body as a whole. sues.

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2. Production of pressure differential across a MUSCLE SPLINTING (PRE-TENSED) boundary. 3. “Spalling” energy is released as an energy wave Pre-tensing of the muscles can have an effect on injury in attempts to go from a dense to less dense medium. LSREMVAs in the following manners: (The wave is tensile, most human soft tissues can 1. Increase injury potential withstand more compression than tension.) 2. Decrease injury potential 3. Have no effect on injury potential

LOW VELOCITY (MOST COMMONLY EXPERIENCED IN MVAS)

Contradictory? It is, but any or all of these can apply to each individual on any occasion or all at once and can Stress waves travel at less than 15 m/sec. Transverse waves apply to various body parts. For example: of lower velocity and long duration (shear waves) are produced by displacements of body surfaces. The results 1. Tighten neck are differentials created at 2. Lock knees anticipating impact a. Sites of attachments b. Sites of body part collisions

3. Pushing on the brake 4. Bracing with arms on the steering wheel anticipating impact

These forces will vary more when considering not only Any number of human responses can affect injury a difference in tissue viscosity but structural/architecturalpotential. The principles of movement are all the same. differences as well on both micro and macro levels. All of the above can also relate directly or indirectly to cellular damage. Cell injury can occur when mechanical trauma damages the cell membrane, impairing its ability to act as a barrier to extra cellular calcium. Too Tremendous amounts of pressure exerted within closed much intra-cellular free calcium can overwhelm the systems cause tearing at micro and macro levels. Fluid mechanisms that normally maintain a relatively constant systems (i.e., shock absorbers) exhibit various mechancalcium concentration. The cell’ s inability to dispel the ical characteristics under different rates of loading. Dif-calcium can lead to an increase in osmotic pressure causferent types react in a dissimilar manner. The contain“ ing swelling, cell membrane damage, metabolic depleers” burst when loaded quickly. In other words, tissuetion, and cell death. This can occur in skeletal muscles, reaction is time sensitive. The forces generated will besmooth muscles (blood vessel muscle lining), and nerve released through the path of least resistance. In humans, tissues. Mechanical cellular damage (from stretching) this path is often the point of connection between softalso can alter nerve tissue conduction. This cellular damand hard tissues. age can result in muscle spasm, alteration of localized blood flow, hyperirritability, dysfunction, breakdown, and pain. All the aforementioned principles can apply to × ENERGY INPUT AND FORCE COMPRESSION: soft tissue injury on all levels simultaneously. ×C F

HYDRAULIC PRESSURES

MAX

MAX

This formula relates to how much energy is placed onCommon Soft Tissue Injuries Resulting from REMVAs a subject (or body part) during impact and how much is “ lost” during the transfer. Tissues and organs can1. Cervical strain/sprain 2. Cervical facet joint inflammation disrupt and dissipate energy transference. The larger the 3. Occipital neuralgia Fmax × Cmax the more energy loss will be experienced in4. Myospasm the soft tissues and, therefore, more potential for5. MFTPs destruction. 6. Temporal tendonitis This relates back to Newton’ s first law (bodies at 7. Stylomandibular ligament insertion tendinosis (Ernest Syndrome) rest…). How much energy it takes to move tissues will8. Injuries to the TMJs determine injury potential. Tissues that slide over each • Lateral capsulitis other and don’ t resist won’t absorb as much energy as • Posterior capsulitis • Hemarthrosis those which cannot get “ up and go”as fast as others. The lag time between body part motion due to differ- • Disc displacement ences in location, density, and reaction to forces plays a • Reducing • Nonreducing part in this phenomenon. • Adhesions in the superior and inferior joint spaces

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threshold. The Biomechanical Assessment Profile (BAP), a position assessment questionnaire developed by the author, allows the clinician and the occupant to help deterIn The Real World (ITRW) mine the true position at the time of impact. The slightest • There are no set thresholds for injuries to soft tissue. occupant position variation will greatly affect injury • There are no set thresholds for injuries to hard tissues. potential resulting in large increases of impact forces • Biomechanical trauma is unpredictable and anecdotal. • Tissue strengths and tolerance will vary under different conditions. (SAE # 91294; SAE # 930211). A normal position, such as that assumed by a crash • Body parts accelerate at different rates. • Body parts move at rates different from the car and from one another. test dummy, is not a normal position for most occupants (SAE # 700361). Being out of position is actually more normal for occupants than being in position, if normal ABBREVIATED INJURY SCALE (AIS) is defined by the posture of crash test dummies at the The AIS was developed in 1971 by the Association fortime of impact. Positioning varies by occupants ’ driving the Advancement of Automobile Medicine and the Soci-habits, anatomy, seat comfort, and anticipation of a ety of Automobile Engineers to statistically track injury collision. categories. Injuries for each body region area are placed There are three common actions of bullet vehicle drivinto seven levels (0 to 6). The AIS level is based on theers prior to impact: level of injury revealed by an examination shortly after the crash by doctors trained in its application (Gennarel- 1. Braking lii, et al., 1998). 2. Swerving 3. Spinning/yawing 0 No injury. 1 Minor (may not require professional treatment). These motions will change the following: 2 Moderate (nearly always requires professional treatment, but is not ordinarily life threatening 1. Impact angles of vehicles or permanently disabling). 2. Closing speed 3 Serious (potential for major hospitalization and 3. Vehicle contact long-term disability, but normally not life 4. Will potentially negate built-in safety systems threatening). 5. Will potentially affect vehicle damage 4 Severe (life-threatening and often permanently disabling, but survival is probable). These factors also greatly affect the passenger position 5 Critical (usually requires intensive medical at the time of impact. Virtually all rear impact testing with care, survival uncertain). dummy and cadaver subjects has been conducted with 6 Maximum (untreatable, virtually unsurvivable). properly positioned occupants (erect, backs firmly placed against the seat back) (SAE # 912914). Being out of As the AIS increases, the cost of medical supportposition can dramatically change the occupant’ s reactions greatly increases. However, the purpose of the AIS is forto forces and resulting kinematics. Humans react quite statistics only. differently than crash test dummies especially in low No level is supposed to be used as a predictor ofspeed accidents. Variations in occupant positioning may final outcome nor to estimate the cost of treatment. Itcontribute little to injury potential in high-speed crashes is possible for injuries at any AIS level to subsequentlybut can greatly increase or decrease injury potential in prove fatal, although the threat to life potential of thelow-speed collisions. injury increases steeply with increasing AIS level (Evans, 1992). PRE-EXISTING CONDITIONS Principles Affecting Soft Tissue Injuries (How People Get Hurt): Thresholds for Soft Tissue Injuries

“Pre-existing” is a term that is often misunderstood and abused. Susceptibility to injury does not negate the fact that damage can occur. In fact, a pre-existing condition can radically lower the amount of energy required to cause OCCUPANT POSITION AT THE TIME OF IMPACT soft tissue damage. While there may be evidence of a Occupant position at the time of impact, one of the mostcondition radiographically, such as in localized bone important variables, is commonly overlooked andbreakdown of the cervical spine or the condylar head of assumed in REMVAs. Occupant position will greatly the TMJs, the person may have been asymptomatic and reduce the Delta V required to surpass the soft tissue injury remained so throughout his or her life if not for the large

INDIVIDUAL TOLERANCES AND RISK OF INJURY

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amount of energy transferred in such a short period ofAGE (> 65 YEARS): time as in a motor vehicle accident. In fact, pre-existing conditions can make a person Older drivers: more susceptible to injury when forced to move faster or Are more prone to injury more than is habitually required. These conditions may Have decreased capacity for recovery include, but are not limited to: Have poorer recovery Arthritis Cervical disc disease Fibromyalgia TMD of many varieties Myofascial disorders Emotional disorders Drug use Chronic subluxation Poor spinal alignment Cranial lesions Reaction time. The time span of energy input is rapid; total time is 0.1 to 0.2 sec. In contrast, human response time is slow (even healthy people’s muscular reactions don’ t begin until .08 to .14 sec). Total personal response time has been estimated at 2.5 sec but will vary according to each individual and the circumstance at the time of impact.

OCCUPANT SIZE In general: The larger the occupant’s mass, the less likely an injury will occur. Taller occupants have been shown to be at risk for higher neck injury (tall and thin vs. short and fat). Size may correlate with age (child vs. adult; adult vs. old). Size of body parts can influence injury potential.

DIRECT

VS. INDIRECT

TRAUMA

What is the difference between direct and indirect trauma? Can you separate the two when it comes to MVAs? Can you tell the difference clinically and with diagnostic testing? Actually, under the examination of an MRI or cliniCan an acute problem be superimposed over a cian’s diagnostic exam, tissue reaction and dysfunction chronic condition? Of course, this possibility can andare the same. should be taken into consideration when arriving at a differential diagnosis. It is crucial that the clinician Examples of direct trauma have a thorough understanding of the patient ’s condi1. Penetrating — puncture tion. A thorough health history is essential and may 2. Penetrating — laceration include contacting previous treating clinicians. Good 3. Crush mechanisms (Yes and No) diagnostic equipment and excellent diagnostic skills are also necessary. Examples of indirect trauma

GENDER (WOMEN COMPARED STATISTICAL GENERALIZATIONS

TO

MEN):

Woman have: Approximately two times more minor soft tissue injuries than men Smaller neck diameters and longer necks Higher frequency of spinal stenosis Greater involvement in crashes/million miles driven (National Safety Council) Higher frequency of injury claims More severe injuries More treatment Higher healthcare bills Slower recovery Greater disability Worse prognosis More overall joint injuries (including TMJ)

1. Coup–contra-coup brain injury 2. Concussion (football helmet blow, boxer sustaining blow to the mandible) 3. Fracturing a bone — direct or indirect? 4. Spraining a knee, elbow, wrist by abnormal/repetitive movement (tennis elbow) 5. Repetitive strain syndromes of all types (carpal tunnel) 5. TMJ injuries As previously mentioned injuries commonly occur at the interfaces between unlike tissues due to the 1. Differential of speed of body parts (lagging behind) 2. Differential of tissue makeup yielding variance of wave transfer 3. Differential of hydraulic pressure 4. Hard tissue rebounding

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5. Crush mechanism of hard tissues approximating each other 6. Cellular damage

ing a rear-end motor vehicle collision direct impact to the head, neck, and torso of the target vehicle occupants by the seatbacks/headrests occurs that can result in soft tissue injury. Each connective tissue junction has potential for sufThat Affect Headrest Protection of Occupants fering stress/strain. These types of mechanisms rarely, Factors if ever, occur by themselves. Biomechanical forces in the 1. Positioning real world occur in multiple directions and confl icting 2. Ramping of the body degrees simultaneously. The delineation between direct 3. Flexion of the seatback and indirect trauma is not one of physiological origin 4. Head rides above and below but rather medicolegal only. Human tissues are limited5. Distance the occupant’ s head travels to make initial contact in their ability to respond and are governed by the same (longer = more force) laws of physics as the rest of the universe. To say that, 6. Occupant positioning for instance, the soft tissues of the TMJs or their sup-7. Occupant’s length of neck, arms, torso 8. Awareness of impact (bracing) porting structures cannot be injured unless the mandible is directly struck indicates a lack of understanding, edu-9. Virtually nonfunctional at best and detrimental at worse cation, truthfulness, or all three. In fact, most injuries to the human body except at the exact point of impact are Headrest design and position may contribute greatly indirect in nature. to potential cervical/head injury. Due to occupant motion

AUTOMOBILE COMPONENTS THAT CONTRIBUTE TO HUMAN INJURY POTENTIAL

or pre-impact positioning, the headrest may even increase occupant injury.

SEAT CONSTRUCTION

Federal Standard FMVSS 207 advocates strength requirements of 20 times the weight of the seatback. Most seats weigh about 40 lb. The resulting strength would be 800 Next to the position of the occupants at the precise time lb — not enough in a significant impact. In fact, impacts of impact, headrests are the most commonly overlooked s designed ability to contributors to head/neck injuries in REMVAs. They aremay produce forces beyond the seat’ often the silent contributors to occupant cervical injury.rebound, resulting in seatback collapse that greatly affects Federal law (FMVSS) requires that “head restraints mustthe amount and direction of force to the occupant (SAE # 670919). be at least 27.5 in. above the seating reference point in the highest position and not deflect more than 4 in. under Seat construction is not uniform from one car to the a 120-lb load. ” Or, they must not allow the relative angle next. It varies in: of the head and torso of a 95th percentile dummy to exceed 45° when exposed to an acceleration of 8 gs. 1. Angle Vans and light trucks from 1991 have had to comply 2. Stiffness with standards. Studies show a 85-cm seatback height 3. Elasticity necessary to account for 95% of male occupants and 4. Materials 100% of female occupants. However, the generalization 5. Coefficient of friction of headrest design does not allow for individual height differences and resulting cervical strain. The distance an Seat design helps determine relative impact of each occupant’s head has to travel before impacting the head-body part: rest in a rear-end collision can greatly increase the forces applied to the head and neck (SAE # 670919). This 1. Can lead to large differential between head, distance can vary not only from structural design but also spine, shoulders, pelvis, and supporting soft because of the occupant’ s build and seating preference. tissues. American consumers as a rule prefer adjustable head- 2. Change angle of force vectors. rests, but rarely have them adjusted to achieve maximum 3. Compression of the spine in association with effectiveness. They are often set too low to protect the bending forces of the rotating pelvis. head/neck complex. 4. Relativeflexibility of the seat can help deterTransfer of energy (0.1 to 0.2 sec) and the slowness mine relative flexibility of the spine. of human cervical muscles to respond (0.08 to 0.14 sec) 5. Can greatly affect shear, and rotational forces result in almost no one being able to avoid direct contact on the occupant. with the headrest. Therefore, in almost every case involv-

HEADRESTS

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6. Occupant rebound motion after the input of AIRBAGS energy is greatly influenced by the seat design, AIRBAG STATISTICS and can increase these forces. The seatback’ s rebound velocity at up to 150% of the initial • Over 103 million (50.3%) of the more than 206 velocity. million cars and light trucks on U.S. roads have 7. If the torso rebounds before the head has driver airbags. Over 77 million (37.5%) of these reached its rearmost position, the relative velocalso have passenger airbags. Another 1 million ity between the head and torso will produce new vehicles with airbags are being sold each unequal rebound speeds (SAE # 930211). month. 8. In LSREMVAs, the rebound of the occupants • Through September 2000, driver airbags have in the front seat may be due more to the elasinflated in over 3.3 million vehicles in crashes. ticity of the seat back than to vehicle decelerMore than 560,000 passenger airbags inflated ation. when a passenger was occupying the right front Lack of seat uniformity makes LSREMVA cervical studseat. ies difficult to standardize. As previously stated, any given • The National Highway Traf fic Safety Adminisstudy cannot be used to generalize or apply to a given tration estimates that more than 5899 people individual. are alive today because of airbags. • Of the 62 drivers killed by airbags (48 females, RAMPING 14 males), 40 are believed to have been unbelted, 21 are believed to have been using The angle of the seat produces forces that may direct lap/shoulder belts (5 of these may have misused the occupant up the seatback. The target vehicle ’s rear their belts; 2 of these were unconscious and may be deflected upward or downward depending upon slumped over their steering wheels so they were the relative center of gravity between the target and on top of their airbags; 2 used the shoulder belt bullet vehicles, resulting in the occupant traveling up only; 1 used the lap belt only). Belt use is the seat in a rearward position (relative to the car but unknown for the remaining driver. stationary to the earth). The extent of ramping depends upon: By 1995, 100% of passenger cars have driver systems, and 87% have passenger systems. A total of 85% of trucks 1. Angle of seatback deflection. Occupant ramphave driver systems, and 23% have passenger systems ing increases as seatback angle increases. (SAE # 960665). 2. Slack of lap portion of the seatbelt — rearward deflection of the seat causes slack in the seatbelt. Use of a belt or no belt may affect occupant AIRBAGS ARE DESIGNED TO SAVE LIVES motion. Overall, airbags have decreased belted fatalities overall by 12 and 27% of deaths in frontal crashes. It is estimated that 70% of frontal crash fatalities can be prevented by Four Important Factors of Body Motion Leading to Occupant Injury Related to Seat Construction properly wearing safety belts and airbags (SAE # 922523). Airbags save lives and decrease severity major of inju1. Head displacement, translation, rotation ries in exchange for increasing the number of minor inju2. Differential motion of head, neck, torso ries. There is an increase in abrasions, contusions, and 3. Occupant ramping up seatback lacerations. The body regions most frequently injured are 4. Occupant rebound the head and neck, upper extremities, trunk, and lower No fully instrumented rear impact tests are required byextremities. Of injuries received 90% are AIS I (SAE # 960658). Airbags actually increase the total number of law for seat design. In high impacts seatbacks cushion the occupants from great accelerations. In low impactsinjuries from vehicle collisions, especially in the Delta V of 16 to 32 km/hr (10 to 20 mph) (SAE # 960658). the same qualities account for greater occupant accelerOccupant groups at risk from airbag deployment ation in the rebound phase. The seatback design and include resulting ramping may increase injury potential to the struck automobile occupants during low-speed collisions. There is a design trade- off between comfort and 1. Unrestrained 2. Elderly function/occupant protection. 3. Small stature 4. Disabled

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5. Children 6. Out of position 7. Compromised health status of occupants Significant factors that may infl uence injuries in MVAs with airbag inflation: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

distributed forces. The driver’ s side is smaller and circularly shaped. It has less time and distance in which to inflate due to the steering wheel. Passenger-side airbags are rectangular, and three to vefitimes larger than those on the driver’s side. Airbag tethers limit intrusion of the airbag into the driver’s space and allow for more lateral expansion (untethered bags extend 250 to 300 mm toward the driver and untethered bags extend 380 to 510 mm). Airbags deflate in about 80 to 100 msec through vent holes in the back of the bag.

Severity of crash Interior compartment intrusion Age of restrained occupant Health status including medications, drug, and alcohol use Occupant height, weight, and proportions Diagnostic Circuitry Occupant position at time of impact/inflation Safety belt wearing including proper position- The circuitry has three main functions: ing 1. Entire system is evaluated every time the vehiOther occupants in the vehicle affecting the cle is turned on. restrained driver 2. Continuous monitoring. Loose objects in the vehicle 3. Operates a backup power source for inflation Pre-crash factors including pre-crash cardiac should there be system power failure. arrest, drowning, fire, and suicide

AIRBAG SYSTEMS

COMMON SOFT TISSUE INJURIES RESULTING FROM AIRBAG INFLATION

Airbag inflation is an explosion (200 mph) capable of killing a person in which the force is stopped in time by a nylon bag. It has four elements:

1. Abrasions, contusions to the head, neck and chest 2. Abrasions on the hands 1. Crash sensors and controls 3. Burns on the hands 2. Inflator 4. Transient/permanent parasthesia of the chin 3. Air bag itself 5. Injuries to the TMJs— external and internal 4. Diagnostic circuitry a. Posterior capsulitis (damage to posterior lamina) Sensors b. Disc displacement 1. Reducing A ball in a tube or spring mass sensors are mounted in 2. Nonreducing the front of the vehicle, and are designed to activate airbag c. Lateral capsulitis deployment when a sudden deceleration occurs in the d. Adhesions in superior and inferior joint vehicle’s forward motion of approximately 16 to 19 km/h space (9 to 11 mph). Deployment starts 15 to 20 msec after e. Synovitis initial impact. f. Hemarthrosis 6. Supporting structures Inflator a. Temporal tendons b. SM ligaments (Ernest syndrome) A pyrotechnic device infl ates a gas generant (sodium c. Teeth fractures and avulsions azide) in 18 to 23 msec; 21 to 27 msec after impact the burning sodium azide produces nitrogen gas that expands 7. Cervical strain/sprain the nylon airbag. The actual inflation takes 20 to 40 msec. 8. Cervical facet joint inflammation The force exits and inflates the airbag at approximately 9. Occipital neuralgia 10. Myospasm 200 mph. 11. MFTPs 12. Sphenopalatine ganglion neuralgia Nylon Airbag 13. Paresthesia at impact site Nylon provides a high strength/weight ratio, and is abra- 14. Compression neuropathies sion resistant with good elongation properties allowing 15. Closed head injuries for uniform stress distribution along seams with equally

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FROM

BOTH DIRECT

1. 2. 3. 4.

Increase Increase Increase Increase

in in in in

sternum fractures neck sprains thoracolumbar spine injuries serious cervical spine injuries

“Smart” airbags that adjust their performance characteristics based upon the environment present at the time of the collision are in development. They are designed toAll “ increases” noted after mandatory seatbelt laws “sense” the following: (Evans, 1992). In addition, lap belts: 1. Occupant seat position 2. Size of occupant 1. Can cause internal injuries upon frontal crashes 3. Child or infant or rebound from REMVA if the belt is positioned 4. Severity of crash (closing speed) superior to the superior iliac crest of the pelvis. 2. Can cause severe strain on the lower back due There is a tremendous need for clinical case studies to external forces. of injuries resulting from airbag deployment. Observa3. Do not stop occupants from still striking the tions need to be documented and published by treating dashboard, steering wheel, or windshield with clinicians so engineers can have accurate information their heads. from the field. 4. Can cause “flailing” injuries of the lower extremities. 5. Can increase acceleration of the head/neck SAFETY BELTS upon rebound in a REMVA. Seatbelts are not perfect but nevertheless are among the most effective and simplest devices that help save lives. A three-point shoulder harness (essential for airbag safety): Although 49 states have seatbelt laws yet it is estimated that only 69% of U.S. citizens use seatbelts even when 1. Can cause increased forces to the neck in a mandated. Seatbelts are designed to comfortably t 80% fi MVA even if properly positioned. of the U.S. population. 2. Can add rotational forces to the head/neck upon

HOW SEATBELTS HELP PROTECT

THE

OCCUPANTS

Seatbelts help in the following ways: 1. Controls ramping up the seat back. 2. May reduce the velocity of the occupant relative to the vehicle interior and thus reduce injuries resulting from occupant contacts. 3. Usage may minimize the potential of occupants to be out of position at the time of impact. 4. Allows the driver to be in position to remain in control of the vehicle after the impact. 5. May be effective in controlling forward rebound of the occupant. 6. Keeps occupant within the vehicle. 7. In frontal impacts, extends the time of “ride down,” thus, effectively reducing the force on the occupant. This is accomplished by both structural design and stretching of the fabric. 8. Reduces the frequency and severity of occupant impact with the vehicle’ s interior (second collision). Occupants can still strike the vehicle’ s interior including dashboard, steering wheel, and windshield.

rebound (occupant rotates toward the door). 3. May actually increase likelihood of cervical injury in low speed collisions. 4. Reduce the incidence of serious injury by >57% (SAE # 912913). Shoulder belts while very effective in saving lives can directly affect injury patterns and, in fact, cause injuries in low-speed accidents. Some common injuries include 1. Bruising and abrasions of shoulder, chest, neck, and abdomen 2. Cervical/head rotational and acceleration soft tissue damage Even with seatbelts occupants can still directly contact the car’s interior with their heads. This can vary according to the severity of the impact, location of the impact, and occupant body proportions.

VEHICLE DAMAGE AS A PREDICTION OF HUMAN INJURY

One of the most contentious areas of motor vehicle acciMost injuries from lap belts fall into the category of dent injuries is comparing the severity of injury to the AIS I but can still cause permanent injury or death. cost of automobile repair. Although this argument rst at fi

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seems logical, upon further examination it is revealed to be fallacious. Facts about MVAs and the resulting biomechanics and kinematics: 1. Biomechanics is an unpredictable science. Mathematically, scenarios can be predicted via computer modeling, etc. and information can be gathered following an accident by extensively monitored crash test dummies or other surrogates, but one little change in an almost endless supply of variables can result in dramatically different resulting forces and injury potential. In fact, measurements may differ between individual test subjects in the same carefully monitored crash test rendering predictions of outcome totally inaccurate. Applying the measured outcomes from crash test studies to predict an individual’ s chance of physical harm in a completely different accident is impossible. In fact, valid scientific papers are all quick to point out that the gathered data cannot and should not be used in this manner (SAE # 930211). 2. If there is truly a cost/injury ratio, then the higher the cost of repair, the more extensive the injuries to the occupants. In fact, often the opposite is true. Whenever a non-bumper impact to a vehicle occurs, large amounts of upper body damage occur to the vehicles involved. Vehicular panels are meant to crush, dispersing energy transfer over a longer period of time, and thus reducing the forces applied to the occupants. In today’ s vehicles with computerized components the cost of repair can be quite high with very little energy transfer to the vehicle itself. In fact, a recent crash test demonstrated the cost of repair to the same vehicle at the same impact speed varied by over $1000, depending on the angle of impact. In bumper impacts a great amount of force can be transferred to the occupants with little or no vehicular damage. As has been previously discussed, bumpers are not designed to reduce impact to the occupants — they are meant to reduce the costs of repair in a collision (Kaufman, et al., 1993). 3. In no instances do the amount of energy transfer and resulting injury involving humans directly correlate with the cost of repair to plastic, metal, etc. This is easily demonstrated by watching a football game. When a player gets hit in the head, do the managers look at the helmet and determine if an injury has truly occurred based on the amount of damage to the plastic helmet?

On the other hand, when a person has an internal injury from a fall, is it correct to examine the floor upon which he or she landed and determine if an injury has occurred by the amount of damage to the floor? Of course not, yet this is attempted routinely in injuries resulting from MVAs. 4. Each accident must be analyzed as its own separate entity. The dollar amount to repair the involved automobiles cannot be correlated with injury potential.

When attempts are made to understand injuries that result from motor vehicle accidents many factors have to be included. The more the treating clinician understands about the forces involved, the more accurately treatment can be rendered. The cost of repair to the vehicles involved, however, is one factor that may be of interest for academic and epidemiological reasons but cannot be used as a yardstick for measuring the extent of injuries or the length of treatment time, or estimating the cost of service provided.

SUMMARY Understanding the biomechanics and occupant kinematics in MVAs is essential for the clinician who treats soft tissue injuries. New car safety has dramatically decreased car accident fatalities in the United States. The result, however, is a new challenge to our healthcare system. People who would have died in the past are now living, but with extensive injuries. Soft tissue injuries are often dismissed as an annoyance or something that “you have to learn to live with.” The truth is that they often can be debilitating and greatly affect the quality of life of victims and their families. “Learning to live with it” is not the answer. The answer lies in partnerships among victims, their families, treating clinicians, and third-party payers, partnerships based upon education and understanding. Too often a battleground is formed with experts representing vested interests lining up on each side. The result is a “double victim”: one who was a victim of trauma from the automobile accident and also of the trauma of enduring medicolegal confrontations. Treating clinicians can also become victims of sorts. It is commonly reported that carefully and thoroughly treating MVA victims is looked upon with distrust by third-party payers. Suggestions are being made that the practitioner cannot solely govern the formulation of a treatment plan (Farnham, 2001). Treating clinicians can become discouraged by the constant conflict of trying to help the patient heal and being castigated for trying to do so at the same time. As automobiles become more ficient ef in reducing deaths, the complexity of the injuries of the survivors will increase. Clinicians must strive continually

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Evans, R.W. (1992). Some observations on whiplash injuries. to increase their diagnostic and treatment skills, keeping Neurology Clinics, 10,975–979. the best interests of the patient first and foremost. It is one of the most beautiful compensations in life that no person can sincerely try to help another without helping themselves. Ralph Waldo Emerson

REFERENCES Barnsley, L., et al. (1994). Clinical review: Whiplash. Pain, 283–307. Carette, S. (1994). Whiplash injury and chronic neck pain. New England Journal of Medicine, 330 , 1083–1084. Evans, L. (1991).Traffic safety and the driver (p. 8). New York: Van Nostrand Reinhold.

Farnham, E. (2001, April). Workers’ comp abuse: Can we ever tip the scales?Claims, 56. Gennarellii, T., et al. (1998).The abbreviated injury scale. Sonora, CA: AAPM. Kaneoka, K., et al. (1999). Motion analysis of cervical vertebrae during whiplash loading.Spine, 24,8, 763–770. Kauffman, M., et al. (1993). Status report. (Vol. 3, pp. 2–7). Arlington, VA: Insurance Institute for Highway Safety. Ono, K., et al. (1993). Influence of the physical parameters on the risk to neck injuries in low impact rear-end collisions. Presented at the International Conference on the Biomechanics of Impacts, Eindhoven, The Netherlands, Sept. 8–10. Per-Olof, B., et al. (1998). Sick leave and disability pension among passenger car occupants injured in urban fic.traf Spine, 23, 9, 1023, 1028.

Section XI Future Trends

80 Achieving Insurance Independence in the Age of Managed Care Christopher R. Brown, D.D.S., M.P.S. INTRODUCTION

1. Individual decisions. You have to develop the courage to take control of your future. This means in body, soul, mind, concept, and most importantly, actions. Without that commitment, you are doomed to stand in the breadline of healthcare delivery waiting for the crumbs that are left, especially in the area of managed care. 2. Working together. Each of us desires to become successful. Contrary to popular myth, there is no such thing as a “self-made” person. Highly successful people are always striving to establish relationships with their peers. One of the buzzwords of modern times is “networking.” Networking is an essential aspect of success to the healthcare practitioner. The days of a solitary person isolating him- or herself within the confines of a practice without other professional contact are gone. We have to literally join hands to help each other or our ability to provide individual care tailored to each patient’s needs will be gone.

There has never been a better time to practice pain management in all of history!!!How many of you reading this book feel this in your heart and mind? Unfortunately, probably very few. The statement is absolutely true, however, and this chapter will help you start finding your path toward success in pain management. In the history of the most common affliction, pain, there has never been greater opportunity for successful healing. The technology and knowledge are there for predictable individual success. Opportunities that did not exist even a few short years ago are commonplace today. Yet in the midst of these opportunities lies a dark specter hovering over every field in the healing arts: Managed Care. The very name brings depression into the hearts of many practitioners no matter what their degrees. It seems the powers that be in our different professions have already given up and handed the mantle of control of patient care over to accountants and actuaries. The following concepts can be the first steps in dealing with your life, your success, and healing the pain of • How many of you who once loved to practice your career. now wish you had not chosen your profession? These guidelines are not for everyone. In fact, only • How many of you have given up on the idea of about 5% of those reading this will actually grasp and success and are just hanging on? accept the concepts presented. It has been said that about • How many of you feel alone and vulnerable? 5% of the U.S. population make the decisions that dictate • How many of you are tired of being scared? the other 95% of the population’s lifestyles. The same percentage probably holds true in the healing arts as well. If this sounds like you and you want things to change, To those 5%ers the future lies in two main avenues: then perhaps you are one of the 5% who will become the

0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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warriors of our professions. Our patients need our help. As a result of new technology, longer lives, new disThe rule of the day, however, is “physician heal thyself. ” eases, higher demand, etc., the costs and, more imporIn Micah 6:8, the author asks what God requires of Histantly, the risks involved dramatically changed the face of people. Is it the normal customs of the day? Is it rivers ofproviding insurance coverage. As a result, the risk of predicting outgoing expenditures for the companies grew oil or thousands of sheep? The answer, as is always the case, lies in simplicity: Seek justice, love kindness, walkunpredictable. Insurance companies make money by accurate predictions balancing future risks with future income. humbly with your God. All the techniques contained in this chapter are justThat’s the nature of the industry. Something in the formula had to change. means to help implement these ancient guidelines. Without these basic truths, all knowledge will be for nothing. Make no mistake about it, capitalism is at the heart of our system. If insurance companies didn’ t make large These concepts are designed to lift those 5%ers to a level sums of money with limited risk, then there would be no of practice few can imagine. The few who dare to take back their destiny. Success is a choice — so is failure. insurance. The days of any of us thinking insurance comWhich will you choose? There is no doubt in my mind panies are altruistic in nature have fallen by the wayside, and really that’ s OK. that every person is a living, breathing, self-ful filling prophecy. We become that upon which we dwell. In as For a while, the formula changed by dumping huge sums of money into the funnel and adding some restricmuch lie the attitude and fate of your practice. Each day we redefine ourfice of and create the envi- tions such as demanding out-patient surgery instead of the traditional in-hospital. The result? On paper it looked ronment in which we live. Each day holds the same potential as the next— no more, no less. Each day we choosegood, but in the good old American tradition, the marketplace responded. Out-patient surgery clinics sprang up all to be happy, sad, mad, fulfilled, or empty. Each day has over the place. The costs? — Of course, they escalated. the potential of holding great achievement. We have the choice of processing the events of the day and deciding Now the real culprit became predicting the future. In other words, if the future risks could be controlled along how to react. Events should not dictate our moods unless with costs, then true savings and control could be realized. we make a choice to do so. In II Timothy 2, Paul uses an illustration to demon- That, in essence, is managed care: risk control. Instead of strate teamwork: In a house are many vessels: those the of insurance companies taking on the risk, they are now gold, silver, and pottery. All are different but all are usedsharing the risks with the providers and the patients. to enhance the household. Just like each vessel, each of Actually, a pretty smart and pretty fair deal, in a way; us is different. We all feel, act, and react differently underthat is, in concept. The problem is that there are other entanglements as well. At first glance, it would seem that any given circumstance. Also like each vessel, we are the hardest thing for us as private practitioners is an appardistinctly created and trained to serve a purpose. Each ent drop in income. While obviously that doesn’ t make vessel uniquely made is designed to serve a purpose only it can fulfill; yet all work together for the common good. one jump for joy, it is not really the problem. The true problem is taking the decision process out of the hands The purpose of this chapter is for each doctor and staff to find his or her unique position in the team to work for theof the practitioners and patients and placing it in the arena common good of helping the patients whom we serve. of a third party in some far-off land. It also robs doctors of their most precious assets: freedom of choice and the When I’ve been successful,ve I’ been in control. resulting happiness. Money comes and goes. Money not spent can be saved, invested, and ultimately multiplied. Katherine Hepburn Happiness not spent today does not lead to happiness tomorrow. Happiness is a fleeting commodity with no shelf life. It is important for the doctors, their staff, and WHAT IS MANAGED CARE? patients served that the provider and the whole personal The concept of managed care has been around for quite delivery system be happy and customized. some time. Historically, the industrial revolution is perPain patients are unique and have to be approached haps the best example of an actual “starting” point. Com-that way. Many of these problems don’ t fit into actuary panies, along with the company store, had the company tables with the means now used. Currently one way of “doc” long before insurance was a concept in healthcare. dealing with patients in a managed situation is to ignore If you were sick or injured, the company doctor took carethem, shift cost to someone else, and hope they go away, of you. Costs were cheap and so were the results. In those or better yet, deny them treatment because a certain procedure or ailment does not fit into their coverage. This limited days, that was the best that could be done. Howpolicy is expensive and absurd. It is costing everyone ever, along the way, insurance companies decided they untold millions of dollars, and lives are being destroyed. could make a large profit from illness, hence the concept These new plans have been carefully marketed as the of health insurance was born.

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picture of a dental chair with cobwebs on it saying, “this savior of our private system and for now, Congress and the American people for the most part are buying into it.will be you in the near future. ” No joke, it really was that Most practitioners are resigned to this story as their future, blunt. For a moment, please try to get rid of the emotion but if you want a different future, keep on reading. Thisjoined with this issue and take a cold hard look at the is not the true story for our patients and us. A silver liningprograms in which you are involved or have been tempted to this cloud exists and together we will find and live it. to join. This chapter is not about insurance bashing, but rather In the healing arts, the marketing truism is that a taking control of our destiny. healthy practice needs to reinvest 5% of its gross back into the practice in the form of marketing to attract new WHAT DOES MANAGED CARE DO FOR PATIENTS? patients. Five percent! Does anyone out there belong to any plans that only drop your fees 5%? If you do, then Managed care provides a safety net of bottom line care it is probably a plan that is cost effective, if there is an for patients. It is, in essence, catastrophic coverage equal drop in marketing costs to offset the decrease in wrapped in the delusion of comprehensive care. It is the earnings. If your fees are dropped more than 5%, then epitome of marketing. Promising something that cannot how much more? Most of the managed care plans reduce be delivered all the while convincing the recipients s it’ fees about 35%! the best that can be done. If these principles were applied Many practitioners have an overhead of around 60%. to you or me, it would be considered malpractice. Our If an office only has an estimated profi t margin of 5%, society, however, has decided to grant special dispensahow can the practitioner make any money? By volume? tion allowing for this misbehavior. The main drawback, Come on. It’ll never happen. Let’ s play a game. A new to reiterate, is it leaves the patients out of the decision marketing firm comes along and says, Doctor, “ have I loop. Are people truly so stupid or misinformed that they got a deal for you. I have a group of patients who may should not be allowed to make their own healthcare or may not come to you, butmI’ willing to market them decisions? In my opinion, the average individual is quite with no upfront costs for you at all. However,mI’going capable. I’m sure the people who devise these plans to ask you to pay me 35% of the gross charges (before would whole-heartedly agree. In fact, they feel so overhead) for every patient who walks in the door!!!” strongly in that direction that they limit the patients’ How long will those marketing rms fi last? Oh, they’ d do choices up front. As a result, the risk is reduced. If quite well. In fact, they’ re called managed care organiinstead of three choices, the patient now only has two, zations (MCO) and they areourishing. fl The main probthen the risks are cut 33% right from the start. Now this lem is not the patients, their employers, or even the fact is all well and good for someone with a runny nose or that insurance companies want to make money, it is the other predictable medical problems, but what about the fact that doctors are willing to fall back on their heels pain patient who needs a multidisciplinary approach? It and pay exorbitant rates for marketing. Let go of your is hard to establish risk exposure so they are swept under s all MCOs do for you— nothing more the rug. Their choices are limited to the point of oftenfear, docs. That’ and nothing less. Why do thousands of doctors work for not being able to get better within the system. This is reduced fees? Strictly out of fear and lack of self-respect where the 95%ers give up and throw in the towel. Guess and self-confi dence. Those are the only reasons I can what, though? Pain is one of the best motivators and come up with. It isn’ t for the lack of income. Heck, I people will continue to seek care from those who can was losing money on every patient as it was, nanso fi heal them. Most patients who understand their problems cially I was gaining nothing. and have hope are willing to own their health concerns There are all sorts of formulas on how to determine and stop looking for abig “ brother” to pay the bill. This if you can afford to be involved in an MCO. The invasion is the area we will open your eyes to later. Don’ t give of Normandy on D-Day could not have been as compliup — keep on reading; … people will continue to seek cated as some people try to make it. All it takes to arrive care from those who can heal them. at an answer for you personally is to do the following: Ask yourself, your wife/husband, and your staff this simWHAT DOES MANAGED CARE DO ple question: Are you willing to spend up to 35% of your FOR THE PRACTITIONER? gross income to market new patients into your practice? Managed care when you boil it down is nothing more thanIn real overhead terms, that means if all things remain the same, you could lose almost half your patients at an MCO a marketing scheme to assure you of patients in the future; nothing more and nothing less. It is a system built on thereimbursement of 65%, keep the other half at full pay and premise of “if you don’t join our plan, someone else will remain relatively the same in terms of net income. Think about it! If the answer to the above question is ”“no, then and you’ll be left out in the cold with no patients. ” In fact, one of the early marketing fliers sent to myfice of was a you need to consider your role in managed care.

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YOUR WORST ENEMY — CREATING AND ACCEPTING FAILURE Quick, without thinking, who is your practice ’s worst enemy? Make a list: 1. 2. 3. 4. 5. 6.

MCOs Your front-desk person The IRS The ADA/AMA/ACA, etc. Your patients Anyone else but you…

The first step starts with a desire for some internal modifications. You’re the captain and you need to start making changes in your fice of to ensure your success. Only when you understand the problems within and without can you develop a strategy for practice that will properly reward your efforts. It’ s been said that if you keep on doing what you’ve been doing, you’ ll keep on getting what you’ve been getting. In the past, that was a true statement. In this day and age of information overload and increasingly rapid changes, if you keep on doing what you’ ve been doing, you’ ll get less and less. The “less” ’mI referring to is not just money, but less of life including

Wrong! • Less time with your family and friends Without question, the worst enemy with whom you • Less time in meditation and worship have to deal is you, and your attitude. The first step toward • Less peace in your heart and mind getting your practice life together is confronting the true • Less enjoyment of your profession enemy. To quote the wise sage Pogo: “I have met the enemy and he is us. ” We have blamed everyone but the In other words, you lose your balance of life. You only one responsible for our failures. Managed care? sIt’ not have so much time and energy to give to all your projects. the fault of the insurance companies. They are out to make If one area of your life pulls away all your attention, then a profit and are doing so at record rates. They have paid another aspect suffers. Energy can be neither created or the price of millions of advertising dollars and are reapingdestroyed — it can only be changed into other kinds of the rewards. energy. Our lives are the same way. Every ounce of energy We have no one to blame for our circle of fear andwe use takes away from something else. Your time and failure but ourselves by allowing negative thinking andenergy are limited. It’ s always easier to talk about what poor planning to enslave us. The first step in any type ofwe ought to do and harder to do it. The first step to recovery program is to admit there’ s a problem and own achieving success is allowing yourself the right to succeed. up to it. You have a choice for the kind of future you desireThis is a very important step that is often missed. Walter and deserve. You no longer have to fear the future. Success Hailey of Planned Marketing Associates refers to this as or Failure— Which Do You Choose? Life is a choice; the “Permission Statement. ” Allowing yourself and your success is a choice. The first thing you have to do is choose office to succeed above your previous expectations is an where you want to be. Are you happy with your life? Areimportant psychological barrier that you must break. you happy with your circumstances? Are you happy with Breaking the 4-minute mile was thought to be imposyour income, level of patient care, etc.? If the answers to sible and was not accomplished until Roger Bannister these questions are “no” then you need to make a decision did in 1954. But did you realize that the impossible about change. Don’ t wait for the next MCO contact to barrier was broken seven times that same year by other come down the road and hope it don’ t take anything else runners after Bannister succeeded? The impossible away from you and your patients. became commonplace. If you continue to practice the way you do now, then Don’t expect permission for success to come from don’t be amazed when you get the same results? Rememanyone but you and those who care about you. Do you ber, “What you sow so shall you reap. ” Don’t plant weeds think other practitioners (your loving colleagues) who are and expect roses. Things will only get worse. If yourunhappy want to see you succeed? If you discuss this practice is losing ground, then what are you doing aboutwith them, they will be glorious naysayers and try to keep it? Sitting around and complaining, drinking too much you from changing. After all, one defi nition of someone alcohol, running away to the golf course and pretendingelse’s success issomeone “ who is slightly less advanced the problems aren’ t there, blaming others, getting an ulcer, than I am.” Don’t rely on your colleagues to applaud your self-destructing…what? desire to change. If you and your staff agree that it is OK There are answers to all the problems you have into succeed, then you will have taken the rst fistep to your practice. Most are easy, some are hard. Up until now, success. Most professional practices never get this far outside forces were calling the shots. You need to make along a the road to freedom. Modernfices of have been the decision to dispel the circle of fear surrounding your prac-victims of brilliant marketing. The doctor in our society, tice and control your own destiny. Do you want things towhile still respected, used to be looked upon as the answer to our health problems. Through careful marketing and change? Not back to the way things used to be but rather strategic positioning by third-party payers, the doctor ’s better than they used to be.

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role has been perceptually altered to part of our healthcare Individuals with great self-esteem will accomplish t get this confused with the doctor who system’s problems. Healthcare deliverers charge “ too great things. Don’ always argues with the speaker at meetings and always much, test too much, pad expenses,” etc. So begin at the drives the most expensive car. Self-esteem allows for quiet beginning and let it be OK within you to achieve success. control; one of the most self-destructive mechanisms is You can’t fool the person in the mirror. If you feel good lack of control. Don’ t try to fool yourself. Self-esteem is enough about yourself to allow success, then success can something you must feel inside that you deserve. Develfollow. Before you achieve, you must believe. Deserving oping a good work ethic and team effort will help fuel success, however, is more than a slogan. All the motivational posters and cliches won’ t do you any good if it that inner engine that allows for success. Learning a selfesteem motto to be repeated over and over will not make isn’t in your heart. success become a reality. If we keep telling ourselves ll we’ The best way for you to be successful is to deserve be successful, but not do the necessary mechanics, all success. Those who are willing to pay the price of success we’re doing is fantasizing. While positive verbal firmaaf in blood, sweat, and tears over a long period of time will be successful. Hard work, in other words, is the foremosttions are important, unless they are linked with the mechanics necessary to bring success, we are only deceivkey to success. On the other hand, aimless hard work will serve no purpose. You must work hard in the right direc-ing ourselves. Our words will be hollow and our selfesteem will never rise. tion. Success in any profession is not achieved by winning the lottery or luck, but rather by working incredibly hard over a long period of time. Allowing yourfice of to succeed GOALS means developing a work ethic that is second to none in Most successful people are dreamers: basically ordinary your area of expertise. This means a no-compromise attitude toward working hard and doing the right things allpeople who are not afraid to think big and dare to be different. Our dreams are our master plan, a direction in the time. When your of fice affirms success, it alsofirms af a work ethic that will put others in second place. Managedwhich we want to head. Yet dreams are often something so vague that they are nothing more than nebulous concare takes away the drive to succeed. Shedding that cloak nition. Goals, however, are our master and affirming your own destiny brings back the desire tocepts with no defi plan, our step-by-step on how to live our dreams. Study work hard. Your practice once again becomes fun. Everyany business success no matter what the eld, fiand you’ll body wants to succeed but few people (5%ers) are willing find a common thread is having written, defi ned goals, to pay the price in terms of hard work. This step alone and a plan on how to achieve them. What are your ficeof will help propel your office to the next level. dreams? Neither I nor anyone else can articulate them for you. SELF-ESTEEM The first step is to have a clear vision of what you want: what you want to accomplish. For many people, this Self-esteem is the value we place on the face in the is the hardest step. Too many times our goals are built mirror — ourselves. We all know people who would beupon advice from others, what society thinks we should willing to put in a job application as a speed bump anddo, or plain old greed. None of the above will work for still feel inadequate. Feeling good about yourself is essenthe long haul. At this point of your decision process, the tial to your office’s success. Constantly having a third details are not important. For those readers who love party dictate your treatment of pain patients will wear youdetails, this concept will be dif ficult. The object is to down over a period of time. The degradation of yourdetermine where you want your life to go, not how to get clinical judgments by someone probably below your clin-there. It’s often best at this point not to seek outside ical skill level won’t make him/her any smarter and will counsel unless your goals directly affect your family. eventually bring you mentally down: the old “one bad Especially don’t seek counsel from your professional apple…” scenario. peers. They often can be the worst naysayers in your life. People who have low self-esteem are often unfocused, Why would they want you to change? That may make confused individuals who are easily frustrated. This is anthem feel uncomfortable. almost fatal flaw in your position as a healthcare practice There’s a line from an Amy Grant song “when the leader. People with low self-esteem create alibis for theirworld around you sees you’ ve changed, don’ t expect them failures. They also constantly blame others for their mis-to applaud…. ” Believe me, advice will come out of the takes. People in this situation often think there’ s a “secret” woodwork at this stage and very little will be supportive. out there somewhere that others know that theyt.don’ It’s When the Wright brothers decided they wanted to make difficult to work with these kinds of people in yourfice. of a flying machine, do you suppose the general consensus It’ s even harder to deal with such a person over the phone of their peers was supportive? I’m sure there would have dictating your clinical decision. been fellow bicycle makers lined up around the block with

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t really something advice about how their plan would never work, how fool-worth working at, then it probably isn’ ish they were, and how the bicycle industry would notyour heart desires and your prophecy is true. Itt isn’ accept a flying machine. History is rife with countlessworth your effort. So, in the process, be sure and match examples of people who set goals who were laughed at, your goals to your gifts. That way each success builds cursed at, and discouraged in every way. Leave your toward the next. Disappointment in one area can actually trusted colleagues out of the decision loop entirely untilmotivate you to excel in another. you know your desired direction. Even with your friends and spouse, the danger is the instinctive reaction of many people to start discouraging you, even with the best ofESTABLISHING GOOD intentions. This is a private matter: what you want, whatCOMMUNICATION SKILLS you need. The time for sharing comes later in the process. Communication is one of the toughest, most demanding, You need to think, articulate, and write down the yet most rewarding skills you can acquire. Everyone needs goals. If you do this, you are ahead of 98% of all practito communicate better. The ability to communicate clearly tioners. As previously stated, this step can be very ficult dif is fundamental to success. Many people think good comfor some. For others, it may take 30 seconds. tDon’ aim municators are born, not made; that you either have it or toward an illusion. A goal is often confused with a wish. you don’t. Not true. Communication, both good and bad, To “qualify” as a goal the accomplishment must be meais a habit that can be learned and mastered. Communicasurable. Wishes are not. Examples of wishes that have tion is interaction outside yourself with other people in a been presented to me as goals are way that the right information is conveyed at the right time. It is, therefore, important not only to learn how to 1. Having peace and harmony in thefice of communicate, but when to do so. Content and time go 2. Be the best I can be hand in hand. Both aspects are essential. Communication 3. Achieving financial independence involves much more than the practitioner lecturing to staff While these are ne fi thoughts, they are totally lacking and patients. It also involves asking the right questions in measurability. How will you know if and when they and patientlylistening to the responses. The first place to start with proper patient communiare achieved? For instance, being “ the best that you can be” is a fine slogan for Army recruiters, but what does cation is where many practitioners make a fundamental it mean? Can we all not bebetter” “ every day of our error: asking patients what they expect as a result of seeklives? How about achieving nancial fi independence? I ing your care. In other words, what are their treatment goals? Sometimes you have to initially ignore your own recently read a survey asking people what that meant. For those with net worths less than 1 million dollars,preconceived notions of what the patient wants to achieve. financial independence meant hitting the million-dollarDon’t assume — don’t guess…Ask!! The object is not to cram your philosophy down mark. For those with net worths greater than 1 million patients’ throats, but rather to make your goals and their dollars, the figure jumped to 5 million. For those with goals the same. Asking, followed by listening, begins the net worths of 5 million, the defi nition jumped to 15 building of a relationship with people that will overcome million!!! The moral of the story is, don’ t aim toward an many barriers. By listening, you gain trust and make your illusion. Make sure the goals you set are yardsticks that patients more comfortable with you and your program. As can be held up to the light of scrutiny so you can see a provider for an MCO, the relationship between you and instantly whether or not you have hit your mark. your patient is initially based on the fact that you are As a bonus, those around you will catch the passion willing to work more cheaply than the next guy. Patients as well and your team will remain focused. Will you fail are drawn to you because you are on a “preferred” list. occasionally? Of course you will. There will be days, Your communication with the patient is continually broeven weeks, where you seem to be going in reverse. ken by the intervention of a third party. Communication Some people who read motivational books get pumped is fundamentally flawed from the beginning. up until the first adversity comes along and pop” “ goes the balloon and they fall back to where they started. In If you fulfill patients’ desires rather than dictate treatfact, they may fall back even farther becoming bitter inment, then everyone has the same agenda from the start. the process. We all know those who live their lives inToo many times doctors try to dictate what pain patients should do rather than lead them in the direction that they defeat. Success and goal achievement always progress in fits and starts. That’ s normal. The difference between already desire. This only propagates ingrained resistance from the word “go. ” It is a blueprint for failure. winners and losers is that the losers quit when adversity One of the basic truths of any successful program is strikes. That’s why it’s important to establish goals you ” his or her problem. Until care about enough that you are willing to overcome theallowing the patient to “own rough spots and keep moving forward. If a goal is notyou and the patient are on the same side, how can you

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expect success? Also, how can you define success with a The fact that we successfully graduated and are in patient until you know what he/she even wants? practice proves we all basically have what it takes to be We all know that some patients want 100% success successful, yet what has happened to our professions and all the time or they are not satisfied — unrealistical to beus? For many, it has been a slow process of giving up a sure, but it is what they expect. That behavior needs to be little of our practice at a time and persevering in the determined up front. We’ ve all had the bad experience of wrong areas, which have resulted in the erosion of private finding out after the fact that a patient’ s expectations were practice. impossible to achieve in the first place. Unfortunately, this Many of us have just become sidetracked from all the is often discovered after treatment has been initiated. It is distractions of modern practice life. Don’ t look to all of much better to tell patients what can and tcan’ be achieved the excuses others use for their failures and for not achievbased on their desires before therapy has begun. Most ing their dreams. Look within, forgetting excuses, and start patients have a more realistic approach and have reasonlooking instead for answers. Without dogged pursuit of able expectations. Knowing this up front greatly reducesyour goals and dreams, you and your practice will never the stress of practice and allows for true healing to occur. reach its full potential. How do you achieve a successful The point is, how will you know what the patient wants practice in the long run? How do you turn your practice unless you ask the patient? around? How do you become the clinician you always Fulfilling a patient’s desires will allow him or her to dreamed you could be? You do the right things every day, be a partner in the healing process and assures you day of after day. Consistency and persistence will make all clinical success as defined by the patient, not you. Gone your plans fit together and reestablish your practice on are the days of the doctor/dictator. They are replaced by your terms. the doctor/partner. When you replace your dictator role with that of a partner, you will without question experience ESTABLISHING GOOD SYSTEMS the following: Without good systems, you will be like a car out of align1. Increase in case acceptance ment. When you’ re going 15 mph, it seems to run pretty 2. Increase in case success well, but when you’re up to 80 mph the vehicle almost 3. Increase in your income jumps off the road and you fight for control the whole 4. Increase in your practice satisfaction time. With good systems come good habits. The old adage 5. Increase in your enjoyment of life “ practice makes perfect”is not true. Perfect practice 6. Increase in self-esteem makes perfect. Simply repeating the same mistakes over 7. Decrease in your stress and over will not get you anywhere. Your systems need to be analyzed in light of your dreams and goals. Make your systems work for you and what you want to achieve, PERSISTENCE not vice versa. This is often a key to slavery in modern We are in a society built on drive-through windows, elec-practices. Unless you have accomplished step one (asking tronic access, and instant gratification. Persistence and permission to succeed with your staff), you will meet with hard work are not fashionable. They are, however, the major staff opposition. Don’ t let that happen or you will fabric from which success is woven. This is the part thatbe taking a U-turn on the road to freedom. Watch out for determines if your of fice will be successful in the age of a scary word— change. managed care. Persistence will make your ficeofgreat. Utilizing systems often conjures up thoughts of Persistence allows you to fulfill your dreams. assembly-line healthcare delivery. In fact, however, develIt is easy to read any book on success, get all pumped oping good systems allows you to be more creative in your up, and start the next day to achieve your dreams. It is daily relationships with people. Good systems allow you something else, however, to do things right a month, amore time to spend with your patients in an unhurried year, 5 years from now. Many people dream of the hom-manner. Good systems allow you to utilize your time in erun ball, winning the lottery, waiting for their ship to a proper, effective manner, resulting in a more relaxed come, in, etc. You can compile all the get-rich-quick cli- delivery of care. Your ability to properly serve your chés you can think of, when, in actuality, financially suc-patients will increase while your stress will decrease. cessful people are the ones who make a plan and stick to it. That means, not only when it feels good, but also whenPOSITIONING YOURSELF FOR SUCCESS: there’s major opposition. Persistence is what got us allTHE ROAD NOT TAKEN through those long days of school. Dogged determination Positioning your practice for successful growth may go prevailed even when the days of practice seemed far away. We all remember waiting tables, driving cabs, or whateveragainst conventional wisdom. It seems that nearly all the experts claim the future of healthcare delivery is a manhelped make ends meet.

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aged care model. Whether this will be true for society orand the patients. Everybody ends up stressed from the not, no one can answer. Whether it is true for your indi-whole process. However, when established financial plans vidual practice only you can answer. When you and yourare in place and followed with persistence, the system will staff can develop the ability to make patients feel betterwork and produce satisfied patients who are willing to pay about themselves when they visit you than they do anyfor your services. where else, then you will have practice success no matter You can never provide healthcare for every person in what direction society takes. The healing and loyalty ofyour community. It physically can’ t be done. You have to pain patients are more often directed by how you treatmake a choice. Which patient would you rather position them rather than by strict methodology. your office to provide care for? We live in a consumer age. People, regardless of how Most practitioners daily set themselves up to provide much they complain about costs, still want quality and arecare for the patients with the least invested in their generally willing to pay for it. Notice, I said “quality”. health — patients who tax you and your staff emotionally You can’t charge for what you can’ t deliver. So don ’ t ever and financially. Why not choose to serve those who are be tempted not to do what’ s right for your patients. willing to invest in their care and provide you with opporUnscrupulous behavior will always negate success in the tunities to provide treatment options that will give them a long run. The best practice position is to make co-deci-chance for true healing and a pain-free life? We as pracsions with your patients without outside interference fromtitioners are faced with two basic choices: third parties. Looking at the buying habits of people indicates an 1. Follow the crowd. Drop treatment goals so low interesting trend. Often, price is not the main obstacle that we give the cheapest form of care and fool when it comes to purchases. The main concern is how to our patients into thinking they are getting all pay for it! Fitting a purchase of any kind into the monthly our professional and personal skills can offer. budget is usually the deciding factor when making buying The scenario will fill the model for managed decisions for something that a person wants. Planning care cost containment. The risk is placed on your office’s successful nancial fi future must include your shoulders and off those of third parties accommodating your patients’ financial obligations and while letting someone else make your decisions creating avenues for payment. for you and your patients. This is the road most There are two ends of the spectrum, both of which are healthcare practitioners are traveling. Is this disasters for practice growth when it comes to financial what you want? Will this satisfy your life’ s planning for patient payment. They are opposite in nature dreams? yet identical in results. 2. The road not taken. Develop high standards for The first is denying all patients’personal financial your program, learn to properly communicate, obligations and relying solely on third parties for financial carefully monitor its successes with outcome’ s responsibilities. Without that personal commitment, there measurement, skillfully market the type of is no pressure to get well. We all have examples of that patients you wish to treat, and provide reasonin our office; two categories are welfare and cap programs. able avenues of payment for your patients. All Across the nation in all disciplines of healthcare, these are decisions for your patient’ s treatment will be generally the two groups of patients who don’ t show for between you and your patient. Is this what you their appointments, don’ t do what you ask, and generally want? Will this satisfy your life’ s dreams? feel no responsibility for their actions. The result is financial and case failure. Financial commitment often begets Two roads diverged in the woods and, healing. It is just human nature. I took the one less traveled by The other end of the spectrum is putting all the obliAnd that has made all the difference. gations on the patients upfront. In a utopian society, that would be wonderful. I have heard of practitioners — perRobert Frost haps you’re one of them — who always demand payment in full, upfront from everyone all the time. I wish it could Most people (95%) will not take this road. That leaves be that way, but realistically if you want to build a solid endless opportunities for those of us who choose to place volume, you must make some accommodations. ourselves in the top 5% of our fields. There are lots of The most predictable strategy is to provide reasonable patients who want to get well and demand the best. In avenues for payment on your terms. Let me repeat, on essence, there is very little competition when it comes to your terms. You can’ t let patients say, “just bill me, doc, ” or your practice will be swallowed up. sIt’amazing how excellence. There is much competition for mediocrity. But in one billing cycle you go from being the patient’ s savior how are patients to know the difference? Can we assume to the villain. It builds resentment from you, your staff, because we know ourselves that our patients should auto-

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matically be aware of our skills? In reality, what if our computerized telephone screenings and statistics, people clinical skills are just mediocre? What if we are just crave attention. It’ s sad to say but in today’ s world of another office? Let’s face it, if patients perceive all prac- practice, spending time with your patients is indeed a USP. titioners as being equal, then why not choose the cheapest? It also touches one of the most basic of human needs: the If you want a shirt and see the exact one you want in two need to be loved and paid attention to. Have you ever places, why not choose the cheaper of the two? heard of patients complaining that a healthcare deliverer To free your professional life, you must be able tospent too much time with them? Of course not. But how make it obvious to patients that yourfice of is different. many times have you heard just the opposite? No matter Different is good. People like different. The first step in what your USP, the element of spending time with your becoming a different and uniquefice of is to do the things patients is the most valued trait of all. you love. You have to develop uniqueness about your You must not only find your USP, but also develop it practice — a position that allows your talents and thoseto the best of your ability. That will mean staff support in of your staff to stand out in the crowd. the growth process. It also will probably mean furthering your education. An important aspect of change and growth is making technology a strategic resource. Learning the USP importance of strategic technology is an important step In the business world, this is known as a USP (Uniquebecause it affects every aspect of your practice. You need Service Position). In the healthcare sense of the term, to it ask the right questions and be sure you are getting the right answers. can be thought of as a type of speciality determined and defined by your talents, desires, and state practice laws. It means your practice will become a work in progress. In other words, what makes you different from any otherMake sure your USP aligns directly with your goals and office so that people are willing to become your patients.that of your staff so your life will grow in the process. It Setting your goals also involves identifying your gifts. will also help you achieve the all-important balance Make your job your love, your hobby. Ask yourself and needed between your professional and personal life. Balt come easy. Most successful, happy people your staff, “What does our fice of do better than any other ance doesn’ office?” Sifting through all the different procedures canlead a well-rounded life. In the long run, this provides more reserves of energy, depth of character, and a stressbe difficult and you can expect some false starts. That’ s fine. It’s part of the process. Don’ t become obsessed with free perspective on life. your failures, but rather focus on your strengths. It may help to actually list the procedures that you consider more It don’t come easy. fun than work and determine which ones you do better Ringo Starr than anyone else you know. When you find that area, then that can become your USP — the aspect of your fice of that makes you so unique that people are willing to bypass PATIENT PROFILE other clinicians to come to you; aspects of your practice that people are willing to gladly pay for even if their After you have determined your USP, you need to define what type of patient you want to serve and are able to insurance companies fail to do so. Some examples of USP in different disciplines are: serve best. This is the next logical step in your journey toward freedom of choice in today’ s healthcare environ1. Dentistry: pain management, cosmetics, time ment. It is also one of the most important elements of a successful, happy career. You can’ t please everyone. You spent with the individual 2. Medicine: work-related injuries, pain manage- can’t serve everyone. When first starting to practice, most clinicians try to be all things to everyone.sIt’impossible ment, time spent with the individual 3. Chiropractic: myofascial therapy, corrective but it’s also natural to try. After all, most people who go into healthcare fields sincerely want to help others. therapy, time spent with the individual That’s the way it should be. However, those who are 4. Massage: sports injuries, therapeutic touch, wise learn early in their careers that you can’ t be all things time spent with the individual to everybody. Those who try end up exhausted, burned 5. All disciplines: nutritional counseling, vitamin out, and bitter. Most providers learn this lesson slowly and botanical complementary care over a long period of time, eventually finding a niche from As you may have noticed, one theme is listed consis-which to practice. Any healthcare provider by accident or tently: time spent with the individual. Managed care isby design will develop a patient profile. We are constantly forcing clinicians to become more cost effective. One ofreminded of situations that we often take for granted. the most obvious ways to do that is to spend less time Let’s look at a few examples in the business world. with each patient. In this world of being a number, andDid you know that McDonald’ s target market is only 15%

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of the entire population in the United States? In other 9. Walk-ins words, around 85% of American citizens don’ t go to 10. Emergency service McDonald’s. Rather than be discouraged about the numDefining a patient population is as diverse as the wants bers, McDonald’ s markets to the people who will go to McDonald’s. When you enter under those golden arches, of the practitioners. It may take some creative thinking you know what you will get. It’ s all the same wherever and time to find out just what type of patient fits your you go. So what do you get at McDonald’ s? You get practice’s needs. Discuss this with your staff. Their input predictable food (not necessarily good), fast, at a cheap is of the utmost importance and is crucial to your fice of price. You know what you’ ll get, how fast you’ll get it, growth. and how much it’ll cost in a clean, well-lit environment. Cloth napkins and candlelight? Forget it. A clown, maybe,THE 80/20 PRINCIPLE and a toy in a Happy Meal™, but that’ s about it. Don’t When beginning to define your patient population, keep expect a sirloin steak or a private chef. You won’ t find in mind the 80/20 principle. In fact, this principle is a great them there. There are those people who want steaks and private chefs. There’ s nothing wrong with that. However, yardstick with which to measure all procedures and activhow much success would McDonald’ s achieve if they, ities. Train your office to think in terms of 80/20. Thinking in terms of 80/20 allows you to compare along with their Big Mac™ and fries, offered filet mignon, relationships, time, and productivity. Because 80% of your baked Alaska, and a sushi bar? More than likely, it would income will come from 20% of your patient load, the first spend a lot of money and actually lose hamburger sales place to begin modifying your practice is to define who in the process. Yet with focused marketing, McDonald’ s those patients are. Concentrating on those patients will has consistently been one of the fastest growing compabring the most effective results. What does concentrating nies in the world, all the while relinquishing 85% of the mean? It can mean marketing, continuing education, or market. It can’t please everyone but is determined to just scheduling extra time with them to help establish please the customer who wants its products. better relationships. As a result, if those same 20% give Most healthcare providers carry the mental image that you 80% of your practice pleasure, then your personal they have to serve everyone all the time. No matter how satisfaction and that of your staff will increase as well. hard you try, you just can’ t do it. You have to define your The line between work and pleasure will begin to blur and population. If you choose to accept a managed care propracticing will become fun again. gram, you are already defining your patient population based upon price. In fact, your target market is chosen for The second step is to do something about the weaker 80% of your practice that only accounts for 20% of your you. You may compete somewhat with other fices of within the provider network, but the defining paradigm is priceproduction and satisfaction. Eliminating your biggest source of irritation may be the best place to start. For based. You have to decide if that is the arena in which you want to compete. If you’ ve made the decision not to go instance, one of the biggest aggravations and revenue for many practices are last-minute cancellations and the managed care road, then you and your staff need losses to “no shows. ” The lost time literally adds days to your work define what type of patient you want to serve. schedule and can be the biggest overhead costs that you There are many ways to define your patient populaare forced to bear. Instead of the doctor storming up to tion. Many practitioners opt to define their patient poputhe front desk and yelling at his receptionist, why not start lation by procedure. If a person needs a certain procea “no cancellation policy” for your patients? Might you dure(s), then he or she fits the profile. There are other lose some patients in the process? Yes, but guess what? ways, though, that may help define your patient base. The They will now be messing up someone else’ s schedule possibilities include: and not yours. Not only will you drop the aggravation, 1. People without insurance who pay with cash, but you will also become much more productive and regain control of your schedule. Now you guide the schedcredit card, or check ule. Before it was left up to the weakest part of the team, 2. People with only certain types of insurance. the patients who saw very little value in your services. In 3. People with indemnity insurance 4. People who pay cash upfront regardless of other words, utilizing this technique instead of being controlled, you are able to take control and guide your practice insurance coverage in the direction you choose. As a result, one of your patient 5. Patients in a certain age bracket 6. Patients who can come in at certain times of profile attributes may be people who value your services enough to keep their appointments. the day Some patients will really challenge your staff. After 7. Patients who always show up on time all, they have no control over their lives — why should 8. Patients who don’ t cancel their appointments at you? That’s why it’s important to have defined goals with the last moment

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team members who back up one another. This especially Another wonderful by-product is being able to take includes the doctor. Nothing will break the morale of themore time off. Instead of having your time stolen one staff more quickly than a doctor undercutting a staff mem-appointment at a time, those hours turn into days, which you and your staff can utilize for continuing education, ber after he or she has gone through the trouble of enforccommunity service, or just rest. The result is a happy, ing a rule upon which you have all agreed. It takes courage ficient time away from the of fice to at first to hold fast to the rules but it pays off rapidly. Your stable staff with suf remain excited and cultivate a positive mental attitude. office collectively makes up its mind and collectively The 80/20 Principle by Richard Koch lists several enforces it. ways to implement this rule into your every day life: Unless you decide to change the direction of your office entirely, chances are 80% of your patients do not • Celebrate productivity rather than raise average fit your desired profile and 20% cause you most (80%) of efforts. your aggravation. Changes must be made on purpose. Your • Look for the short cut rather than run the full office will not improve by accident. Your fice of must course. develop an 80/20 mentality to grow and regain your prac• Exercise control over our lives with the least tice freedom. You must constantly ask yourself, “What is possible effort. the 20% that is leading to the 80% and which 80% is it • Be selective, not exhaustive. leading to?” You must never assume that your ficeofis on • Strive for excellence in a few things, rather than automatic pilot and your problems are solved. 80/20 thinkgood performances in many things. ing is not linear but rather part logical and part intuitive. • Delegate as much as possible. Your practice situation cannot be analyzed strictly by the • Choose employees with extraordinary care. numbers. Allow your creativity to bloom. You will be • Only do the things we enjoy the most and do amazed at how rapidly and effectively implementation of the best. shared changes will positively affect thefice. of You will • Look beyond the obvious to uncover the ironies certainly get more from less. More personal time, more and oddities. fun, more income, more satisfaction, and more happiness. • In every circumstance work out where 20% of The less? Less stress, fewer patients to see every day with the effort can lead to 80% of the positive results. better results, less conflict, and less frustration. There are • Calm down, work less. Rather than pursue really no boundaries to your success. As you grow, the every possible opportunity, target a limited boundaries grow as well. number of very valuable goals where the 80/20 The first reaction of many clinicians is that there is principle will work. little chance of escaping from the low yield activities. • Make the most of those few “lucky” streaks in They feel these time wasters are an essential part of their life when we are at our creative peaks. service to others. “I have to do XYZ, ” or put another way, “my patients would leave if I don’ t….” If you catch yourRemember the quote from Arnold Palmer, “Golf is a self thinking this way, think again. There is a great dealgame of luck. The more I practice, the luckier I ”get. more leeway in your practice than you are accustomed to The greatest part about utilizing the 80/20 principle believing. The point of successful utilization of the 80/20in your life is that you do not need to wait for someone principle begins when you begin to think unconvention-else to do it for you. You have the ability to turn your life ally. Following the crowd will get you just what the crowd into the one dreams are made of. You remember the dream gets. Don’t expect anything more. But even if dropping for which you worked all those hours in school? The one low-value activities does require a radical change in yourthat somehow got lost in the daily struggle to survive? practice, you can deal with it. The other alternative is to You have the ability within you to multiply all your watch your practice diminish a little at a time. Successhighs and subtract all your lows. Your life can take on and happiness will never be achieved. more and more relevance and shed the energy-draining Can you entirely eliminate problem areas? More thantime wasters. You can isolate all the great aspects that likely not unless you somehow decide to not treat or hiremake you unique both personally and professionally and human beings. You can minimize those most troublesome climb out of your daily rut. As an even greater plus, you areas, however, maximizing your happiness and productivity can help your staff and patients achieve more than they in the process. When you have identifi ed the activities that had expected. People will appreciate you more because take 20% of your time and yield 80% of the desired results,you appreciate them more. If you want to get the most make plans to turn the 80/20 around. A short-term goal that from 80/20 thinking, you have to integrate it into your is achievable is to nudge the 20% of the time spent on life. Will it take some effort? Of course it will! Let’ s face productive activities up to 40% within a year. This oneit — like it or not, changes are coming down the road for change can have a profound effect on your practice. healthcare providers. The choice is not if your practice

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will change but rather how it will change. The choice of disciplines couldn’t understand their problems “because ” how you will change and adapt for your benefit and thosethey’re not like me. A problem that is unique to any given profession does of your staff and patients is still up to you. not exist. The same challenges occur in chiropractic, dentistry, medicine, massage therapy, automobile repair, selling MASTERMIND ALLIANCES shoes, etc. As long as you are dealing with people and A mastermind alliance is a relationship built when two ortheir money, the basic problems are all the same; only the more minds work together toward common goals. Theindividual circumstances and procedures change. Allow mastermind principle lets you utilize the full strength, yourself the privilege of tapping into the minds of people experience, knowledge, and training of other people withwith a common purpose but different perspectives. It is similar desires. You can overcome any challenge oran exhilarating experience. achieve any goal in your practice if you use the mastermind principle effectively. No one has ever achieved out-MARKETING standing success in any field without applying the mastermind principle. All great minds are stimulated to Once your USP and your 80/20 patient profile are defined, creativity through contact with others of like desires. ith-W then the next step is to let others know about it, in other out this contact, you will run out of creative energy and getwords, marketing. As you know, marketing carries many off track. The steps of forming a mastermind group are connotations, from sincere helper to used car salesman. Marketing should be a natural extension of your personal 1. Determine your purpose. A group cannot deter- self. A multitude of excellent marketing courses, books, mine a purpose if the individuals have not done and tapes are available. The most important aspects of any so first. You must be sure the purpose of the marketing program for your USP are group is the same as yours. This doesn’ t have to be down to the detail, but very close. Once you have decided what purpose a group will fulfill for you, then move on to step two. 2. Select members of your alliance who will help you attain your goals. Don’ t select members because you know and like them. Save those relationships for social settings, if desired. Make sure each member has the ability to work in harmony with others. A person who totally dominates meetings will adversely affect the group. Discord will destroy your alliance. There must be a complete meeting of the minds without hesitation from any member. In the mastermind setting, personal ambitions must be subordinate to the success of the goals and purposes of alliance. The harmony of your alliance is built upon mutual respect and honesty. 3. Determine your rewards for being involved with a mastermind group. They can be whatever you find is needed. These will vary according to each individual member’ s personal needs. 4. Set a time and place for regular meetings. Your alliance must be a priority or other commitments will get in the way.

1. 2. 3. 4.

It fits with your desires (goals/focus). It’s easy to implement. It’s cost effective. It has measurable results (it works and you can prove it).

Note that one of the aspects not listed is “expensive. ” Some practitioners think if you throw a lot of money at a marketing program, it will be effective. Not so. Some of the most effective marketing programs are inexpensive. While it may be a good ego boost to see your smiling face plastered all over town, it may do nothing for your practice. Remember one true fact: people want to feel special. Despite all the problems in the modern healthcare delivery system, people still generally respect caregivers and want their personal attention. Which is better: working in five extra patients a day to pay for a super expensive marketing program so you can see even more patients or perhaps seeingfive fewer patients and spending more time with each one individually so your overhead is less and your patients are happy with your care? Expensive and effective don’t always go hand in hand. When making paradigm shifts within yourfice, of start with the simple marketing programs first before you get into expensive, extensive ones. Include your staff in marketing decisions. They will appreciate it and be able to Your professional mastermind alliance does not haveprovide creative ideas that can be tailored to your individto consist solely of others in the same profession. The ual needs. Marketing should be fun and productive. If it beauty of these relationships is that most creative solutions is not, then your goals and desires are not in alignment. to obstacles often come from outside your given area. Our main obstacle is not managed care or third-party Individual healthcare providers are often guilty of thinking payers and other various programs, but rather our lack of they have the market cornered on problems, thinking other self-esteem, lack of determination, and lack of desire to

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succeed. Positioning yourfice of for success is a matter of knowledge with total comprehension and apply doing the right things, at the right time, all the time, and that knowledge to your individual circumdeveloping a plan and sticking to it. There is no doubt stances. about it. There has been no better time to practice in the 3. Discretion. The ability to break down informahistory of mankind. Opportunities for greatness are all tion into specialized parts. To be able to digest around you. The choice is yours. information, categorize, and sort data so decisions can be made simpler in lieu of distinct circumstances and desired results. FINAL THOUGHTS 4. Insight. Perception of the truth and hidden nature of things. Insight is developed as a result One of the main problems as practitioners is that we feel of the culmination of all achievements. It is the we are facing the future alone. Make no mistake about ultimate strength from which you may operate. it, private practice and clinicians being the decisionInsight is the beginning and result of wisdom. makers are under attack by well-fi nanced organizations. Still, every crisis creates great opportunity. The fact that Surround all these gifts with vigilance. Be attentive. so many practitioners are willing to follow the winds that blow them in any direction leaves those who wishAlways watch, work, and hone your skills. Be disciplined. to develop happy productive lives almost unlimited Your practice life is like that of an athlete who must constantly work out to keep his/her physical attributes opportunities. By nature of the trends, niche markets are ready when opportunity for success presents itself. If being created for creative thinkers at a greater rate than you’re attentive, then your insight will allow you to recever before. The avenues for healthcare practitioners to be successful are virtually unlimited and growing moreognize opportunities and give you the skills to achieve them. It will take care of you far beyond measurable so every day. Don’t expect to do things the way you used to and getachievements. You will be successful even when logic says t good results. It won’ t work. Don’t expect our overseeing you can’t. Like the old maxim, “Those who say it can’ be done often get in the way of those doing ” Success it. governing organizations to help us. Just as our patients doesn’t happen by accident. fall into the cracks of the healthcare system, we, the creDeveloping wisdom, understanding, discretion, and ative thinking practitioners, fall in the cracks of our representative organizations.sIt’important to associate with insight takes hours, months, and years. Success is the point people of like minds to recharge your batteries and allowat which preparedness meets opportunity. If you wait for the creative juices to flow. There’ s an old saying, “We things to happen and only then get ready, you will meet grow too soon old and too late smart. ” If you wish to be with frustration and a sense of loss. Opportunity knocks all the time. The trick isn’ t being there to open the door successful, then make the choice to do so. tDon’ follow the crowd. It will take courage to take those first steps butat the precise moment but rather living in a state of preparedness with the ability to react. Success often comes the results as defined by your goals that lead to your dreams will be worth the effort. Proverbsthrough 1 5 disguised as a problem rather than being perceived at first as “golden.” Surround yourself with people who are posexplain how to achieve happiness, the ultimate goal of everyitive and believe in your mission. Apply these truths to one who is reading this book. The following are the essential your life and you will always be happy. Seek and develop keys to happiness: these skills and, no matter what, your success will never be in question. You already have the tools to develop all 1. Wisdom. The ability to know what is right, true, and enduring; good judgment; knowledge; to the opportunities you will ever need. Your talents in conaccept counsel, criticism, and instructions with- junction with proven applied principles will assure your success. You have a choice for the kind of future you desire out anger; and to always keep learning. 2. Understanding. Being able to perceive with and deserve. You no longer have to fear the future. Success your senses. To be able to internalize your or failure — which do you choose?

81 A Practical Approach to Outcomes Measurement Michael E. Clark, Ph.D. and Ronald J. Gironda, Ph.D. INTRODUCTION

This void in outcomes assessment guidance is remedied in the ensuing pages. We offer clinicians a practical Outcomes assessment has become one of the “catchmeans of selecting and using outcomes measures in an words” of the 21st century among healthcare systems. efficient and rational manner. In this regard, we first briefly With the advent of the Joint Commission for Accreditationreview the recent history of healthcare outcomes assessof Healthcare Organizations (JCAHO) pain standardsment and the factors that contribute to its importance in (2000), insurance company practice parameters, and state today’s pain practices. Next, we discuss issues that need and/or federal practice guidelines (Agency for Health Careto be considered in the selection of outcomes measures, Policy Reform, 92-0032; 94-0592) outcomes assessment and briefly review the most useful pain outcomes instruhas become a necessary component of pain practice irrements. Finally, we outline a method for developing an spective of practice setting. A multitude of pain outcomesappropriate outcomes methodology based on specific instruments or outcomes systems exist, yet little guidance practice needs and outcomes interest. Note that our intent is offered as to how to choose an appropriate instrument is not to promote any specific outcomes methodology or or set of instruments. Indeed, a literature search on the outcomes instrument. Instead, we hope to provide a topic of “pain treatment outcomes” yielded numerous arti-method whereby any clinician can determine what availcles reporting pain treatment results using a variety ofable instruments best meet the needs of his or her practice outcome measures, but no articles focusing on how to and the limits of the setting. select an appropriate outcomes method. In the absence of specific selection criteria, practition-DEFINITION OF OUTCOMES MEASUREMENT ers’ choices of outcomes methods may be determined Outcomes measurement refers to the systematic collection more by happenstance than need. Often, instrument availability, economics, and marketing serve as the primaryand analysis of information that is used to evaluate the efficacy of an intervention.Systematic collection requires determinants of instrument selection rather than outcomes objectives or empirical findings. The end result may bethat data are collected in a consistent, repetitive manner using the same outcomes measures or instruments. Analythe selection of an outcomes measurement system that has limited reliability or validity, fails to meet the needs of sis refers to the process of summarizing and reviewing the data to identify any meaningful trends. Often this second the practice setting, requires extensive financial or temporal investments, or, on occasion, overwhelms the practi-stage of outcomes measurement is underutilized. Data tioner with mountains of irrelevant or even inaccurate data.may be collected but are either filed away and not used,

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or data summaries are prepared but never reviewed by the Other national and local bodies also have begun to recognize the necessity of monitoring the effects of pain most appropriate individual or body. treatment. Pain treatment guidelines, which include stanOutcomes measures usually are collected prior to and following an intervention. In healthcare systems, usuallydards for pain outcomes monitoring, have been developed or adopted by the Agency for Health Care Policy and we assume that the changes in health status we observe are the results of our intervention efforts. However,Research (1992, 1996) and the American Pain Society (1995). These guidelines incorporate recommendations although outcomes measurement may involve very sophisfor pain outcomes monitoring, as does the National Pain ticated procedures that are grounded strongly in science, in most cases it lacks the rigor of more formal researchManagement Strategy implemented by the Department of endeavors. Thus, it is important to remember that withoutVeterans Affairs (2000). additional data gathered in more controlled settings we With the increasing emphasis on medical care cost containment, healthcare insurers have become more intercannot be certain that the observed changes result directly ested in the cost effectiveness of pain treatment (Kulich from our treatment efforts. & Lande, 1997). As a result, outcomes data may be required to justify charges for selected pain interventions. HISTORICAL PERSPECTIVE Marketing efforts also may benefit from developing an The first systematic use of outcomes measurement in outcomes measurement system in that competition for the healthcare dates to the early 1900s when Ernest Codman, healthcare dollar is rampant and evidence of enhanced a surgeon at Massachusetts General Hospital, introduced outcomes and treatment ficacy ef may increase patient a method of monitoring surgical outcomes (Campassi &referrals. Additionally, professional responsibilities and Lee, 1995; Tarlov, 1995). Subsequently, in 1950 health-ethics may imply the necessity of monitoring outcomes. care outcomes were included as one of three medical For example, many professions require that we not implequality management tiers (Tarlov, 1995; Iezzoni, 1997).ment treatments that we know are harmful or ineffective. However, not until the late 1980s and early 1990s didYet, if we do not monitor outcomes we have no way to healthcare outcomes monitoring became commonplace. determine whether our efforts are effective. And finally, In 1988 Ellwood proposed that an outcomes management outcomes data, although they are not generally as reliable technology be implemented to monitor the quality of as data from laboratory studies, provide us with an empirhealthcare service delivery (Ellwood, 1988). With the pro-ical basis for treatment decisions where before we had liferation of managed care organizations, the focus ononly opinion based on anecdotal observations of the effecenhanced service delivery quality inherent in the earlytiveness of treatments. outcomes management approaches has expanded to include cost containment, improved patient satisfaction,BARRIERS TO PAIN OUTCOMES MONITORING and increased quality of life as additional goals. Although regulatory, accreditation, professional, consumer, and payor interest in pain outcomes has stimulated RATIONALE FOR OUTCOMES MEASUREMENT a rapid growth in the development of pain outcomes manThere are numerous reasons why pain treatment outcomes agement systems, it is important to remember that the monitoring has become an integral part of today’ s health- initial and primary purpose of outcomes management in care delivery systems. In some treatment settings outgeneral, and pain outcomes assessment fically, speci is comes management is mandated by regulatory bodies. For quality improvement . Unfortunately, numerous examples example, outcomes assessment is part of the State exist of where pain outcomes data have been used in a puniMaine’s Department of Public Health’ s standards for pain tive (e.g., denial of claims, denial of services) rather than management (Dreyer, 1998). Similarly, major healthcarea quality improvement fashion, particularly when cost accreditation organizations now require that the compo-containment is the ultimate goal. As a result, some pronents and results of pain treatment efforts of memberviders are reluctant to adopt rigorous outcomes methfacilities are monitored. The Rehabilitation Accreditation odologies. Yet it is our opinion that implementation of an Commission (CARF) has been at the forefront of theseappropriate pain outcomes management system provides efforts by developing elaborate outcomes standards for the best defense to the misuse of data cited above. For pain treatment programs (1999). JCAHO (2000) adopted example, the data cited to deny claims or services typically standards for pain management in Acute Care and Behavoriginate from local, regional, or national practitioner ioral Health settings that were implemented beginningdatabases. These data reflect considerable variability in January 2001. In addition, the American Academy of Paintreatment approach, practitioner experience, and effectiveManagement (AAPM) pain treatment accreditationness and rarely include pain-specifi c outcomes. In fact, they requirements mandate that an outcomes management sysare not true outcomes data at all, but ratherect refl patterns of professional practice. The collection of practice-based, tem be in place (1997).

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pain-specific outcomes data using reliable and validated instruments provides an excellent means of challenging denial practices, particularly if the outcomes information also demonstrates reductions in medical utilization (i.e., cost savings) following pain treatment. Of course, numerous other barriers to adoption of a pain outcomes methodology exist (Rudy & Kubinski, 1999). Staff time to collect, summarize, and review data is necessary, and training in instrument administration and scoring may be required. Administrative approval and support must be obtained, along with funds to cover related FIGURE 81.1 Effects of pain blockades. external costs (e.g., instrument purchase, trainer or consultant’s time). Patient and staff resistance and burden (e.g., time to complete the measures) should be anticipated Pain intensity is the most common patient-oriented measure, and typically is the outcome of greatest imporand minimized prior to implementation. tance to the patient. Other key domains of patient functioning may include medication use, physical status FACTORS AFFECTING THE SELECTION (strength, flexibility), functional impairment, and emotional dysfunction, among others. Note, however, that the OF OUTCOMES MEASURES patients’ primary interest will be pain relief. Numerous Several factors influence the selection of appropriate pain reliable and validated instruments are available to assess outcomes measures. They include the objectives of outthese other domains of pain outcomes (see “Pain Outcomes measurement, the type of pain treated, and the comes Instruments” for a limited review). characteristics of the pain service setting. Patient-focused outcomes may be used in a number of ways. Information about average changes in pain measOBJECTIVES OF OUTCOMES MEASUREMENT ures following different treatment alternatives may assist the patient and the clinician in choosing which pain interPain outcomes methodologies differ in their objectives. vention best addresses the individual’ s pain problems and Patient-focused outcomes approaches are concerned priexpectations. They also are a necessary component of marily with evaluating and improving patient treatment program evaluationefforts that validate treatment effecoutcomes. Service delivery outcomes approaches focus on tiveness. The latter often are useful for marketing pain monitoring and enhancing pain service delivery systems. services or for increasing the likelihood of an insurer’ s Professional association outcomes guidelines or standards payment for the services. (International Association for the Study of Pain, 1991) often address the former, while standards for service deliv- As an example, consider the hypothetical situation ery outcomes tend to originate with accreditation organi-where providers at a university-based anesthesiology pain zations (e.g., JCAHO). It is important to note that theseclinic decide to evaluate the effectiveness of their pain two approaches are not mutually exclusive. More elabo-blockades. To accomplish this, they administer a multidimensional pain outcomes instrument to all patients with rate outcomes systems may include aspects of each. Indeed, some pain accreditation bodies (AAPM andchronic nonmalignant pain undergoing the procedure prior CARF) require that both types of pain-related outcomesto the first nerve block and again following the last nerve block. They also readminister the instrument 6 months be addressed. after treatment to assess the short-term stability of any obtained changes. After 1 year of data collection Patient-Focused Outcomes (6 months of follow-up assessment) they graph their results, which are presented in Figure 81.1. Outcomes methods that are patient focused primarily are Based on these results, the providers conclude that the concerned with treatment-related changes in patients’ pain pain blockades appeared to provide some short-term pain experience. These are the outcomes most familiar to pain relief and functional status improvement. However, they practitioners. To assess treatment-related change, at least two administrations (pretreatment and posttreatment) ofalso conclude that the average benefits of the treatment were temporary, because after the 6 months following the relevant outcome measures are required. Often a series treatment the improvements had dissipated. As a result of of measures collected at intervals during the individual’ s thesefindings they decide to restrict their use of the protreatment provides the best picture of progress and may give more information regarding theficacy ef of changes cedure for the time being to individuals with severe acute pain or cancer pain, and to adopt other strategies for treatin treatment (e.g., altering the type or dosage of pain medications) occurring within the overall treatment episode. ing chronic nonmalignant pain.

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Service Delivery-Focused Outcomes Service delivery outcomes approaches are those that focus on the thoroughness andficiency ef of the pain service delivery system rather than on patient outcomes per se. Service delivery outcomes measures are used to evaluate the performance of the service delivery system as it applies to the provision of pain treatment services. Performance measures may be compared to goals established by the service delivery organization, regulatory bodies, or to standards developed by accrediting bodies. Often this type FIGURE 81.2 Mean pain ratings during burn debridement. of outcomes measurement approach is linked closely to quality improvement (QI) programs, where the ultimate goal is to improve the delivery of health services. Based on these service delivery outcomes data, a QI The recent dissemination of JCAHO pain standards has plan is developed. Components of the plan include training stimulated healthcare systems to develop measures staff to to better assess and treat pain, educating patients address service delivery outcomes. Unlike patient-oriented regarding their pain treatment rights and the range of pain outcomes approaches where numerous reliable and validated interventions that may be implemented, improving outcomes instruments are available, data regarding service patient-controlled analgesia options, and reviewing Team delivery outcomes generally are derived from compliance4’s practices in detail to identify what factors (including reviews of patient care documentation. Most often these chance effects) account for their lower levels of pain relief. reviews are conducted by randomly selecting and manually During the QI process, pain ratings data will continue to reviewing records to determine whether pain-related docube collected, and the interventions identified above will mentation is present, and if so, whether it meets the applibe implemented in steps to allow estimates of the relative cable standards. Standards may be those established byimpact an of each. external body (e.g., JCAHO) or those developed within the Other examples of possible service delivery outcomes healthcare organization and adopted as policy. derived from the recent JCAHO standards include Because the provision of pain services first requires the identification of individuals with a “pain problem, ” • Percent of patients with significant pain who methods for differentiating between those with and withhave a plan of pain care in their medical records. out significant pain must be developed. Given that the • Percent of patients with significant pain where JCAHO pain standards require that all patients be pain education was provided to the patient and screened for pain (Joint Commission for the Accreditation family. of Healthcare Organizations, 2000), one way to identify • Percent of patients with significant pain where those requiring further pain assessment and treatment is evidence exists that pain interventions were to define a pain intensity “trigger value. ” When a patient provided. reports a pain intensity equaling or exceeding this value, • Patient satisfaction ratings of the service delivthe need for additional pain services is established. Service ery system and service environment. delivery outcomes measures then may be used to determine how well these pain services were delivered. Deter- All of the above examples include a patient-focused mining which specific outcomes measures to include pain measure (i.e., pain intensity) as the basis for identidepends on the objectives associated with the overall outfying the patient population of interest. However, the pricomes management program. Often selection of at least mary intent of each is to evaluate theficiency ef of the some of the measures will be determined by relevant outdelivery of pain services rather than the effectiveness of comes standards or service delivery policies. pain treatments. Consider the following example. A large tertiary care medical center that serves as a regional trauma center has TYPE OF PAIN identified reduction of debridement pain in its burn unit as a primary facility goal, motivated in part by concern overDetermining which patient outcomes domains to measure an upcoming JCAHO survey. An initial QI plan has beenalso depends on the type of pain typically treated in the setting of interest. For example, in a post-surgical unit, developed to monitor changes in debridement pain ratings acute pain is likely to be the primary focus. Goals of pain as the first step in the process. Pain scores are collected treatment typically are limited to pain reduction. In this every 15 minutes from all patients undergoing the procedure on each of four burn unit teams. Data are collected for 1situation, pain intensity measures, collected over time (e.g., 1-hour periods), may be the only pain outcomes month. Results are presented in Figure 81.2.

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TABLE 81.1 Recommended Outcomes Domains by Type of Pain Acute Pain

Cancer Pain

Pain intensity

Pain intensity Pain intensity Physical impairment Physical impairment Interpersonal impairment Interpersonal impairment Emotional dysfunction Emotional dysfunction Activity level Activity level Sleep difficulties Pain-related fears Sexual impairment Recreational impairment Sleep difficulties Vocational impairment Sexual impairment

FIGURE 81.3 Pain scores over time on a postsurgical recovery unit.

Chronic Pain

PRACTICE SETTING Practice settingrefers to characteristics of the pain service delivery environment. Primary among these are the type and complexity of pain treatment services provided and the degree of administrative support. Nature of Pain Services Pain treatment encompasses a wide variety of interventions delivered in a multitude of settings. Some may measure of importance. An example of the results of thisinvolve minimal healthcare resources (medication mantype of outcomes evaluation is presented in Figure 81.3, agement) while others may be highly technical (dorsal and could be used to support the effectiveness of the pain column stimulator implants) or lengthy (comprehensive treatment methods used in this setting. multidisciplinary treatment). In general, the complexity Contrast this with a setting where chronic nonmalig-of the outcomes system utilized should parallel that of nant pain is the most frequent presenting problem.the corresponding practice setting. That is, settings utilizing minimal treatment resources (total staff time and Chronic pain treatment goals generally encompass equipment) do not require, nor do they justify, elaborate changes in many domains of function beyond pain reducoutcomes measurement. In contrast, treatment settings tion. Therefore, an appropriate outcomes measurement system should include multidimensional measures ofwith high resource demands (i.e., higher treatment pain-related functioning (International Association for costs) should utilize a broader spectrum of outcomes the Study of Pain, 1991). Figure 81.4 illustrates some ofmeasures to detect change (or lack of change) in multiple outcomes domains. the changes in these measures that might be expected following treatment. Note that the chronic pain outcomes A brief example may clarify this point. In an outinclude pretreatment, posttreatment, and follow-up mea-patient, single-provider pain clinic where the primary sures of functioning. Changes in measures from pretreatmode of pain treatment is pharmacological and resource ment to posttreatment support the short-term ficacy ef of demand is low, the associated patient-focused measures the interventions. However, the overarching goal ofmight be limited to pain intensity ratings and some brief chronic pain treatment is to modify patients’ long-term measure of pain interference. A service delivery-focused measure, such as patient waiting times, also might be behaviors and adjustment. Therefore, readministration of the multidimensional measures at a point following treat-added. In contrast, an inpatient or outpatient pain surgical intervention practice, where resource demand is high, ment cessation is one way to assess the stability of treatmight be expected to monitor multiple patient-focused ment-related changes, and is required by some pain program accreditation bodies (American Academy of Pain(pain intensity, functional impairment, changes in emoManagement, 1997; CARF, 1999). Table 81.1 summa-tional status, return to work, etc.) and service deliveryfocused (complication rates, surgical time, costs) over a rizes suggested domains of outcomes relevant to specifi c longer timeframe. types of pain.

FIGURE 81.4 Changes in pain outcomes.

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Administrative Support

be used in multidisciplinary settings, they also should conform to the Measurement Standards for InterdiscipliIn the ideal practice setting, there would be no relationshipnary Medical Rehabilitation established by the American between the type of outcomes system adopted and the Congress of Rehabilitation Medicine (Johnston, Keith, & degree of administrative support available. Unfortunately,Hinderer, 1992). in most cases, the degree of administrative support has a It is important to note that adequate test or measure large impact on selection of an outcomes approach. Given validity and reliability do not ensure that a measure is the costs involved (i.e., supplies, contracts, and staff time), appropriate for the outcomes context of interest. Although administrators may be reluctant to approve outlays for the determination of the appropriateness of a measure programs with no direct financial returns. usually is a simple task (e.g., evaluating whether the eduThere are several steps a provider can take to maxication or knowledge requirements for completing the meamize administrative support for pain outcomes measuresure are consistent with the target population’ s abilities), ment. First, identify all regulatory (state or federal), prooccasions when the inappropriateness of a pain measure fessional, and accreditation standards or guidelines that may not be immediately apparent do exist. For example, apply. Next, identify any local pain standards of practice consider the situation where an outpatient, hospital-based that include pain outcomes requirements. Third, gather pain treatment clinic wants to evaluate the effectiveness any available pain outcomes materials from local competof its pain treatments. The clinic is in an urban area, with ing providers. Refer to these standards, regulations, and limited parking facilities, and caters mostly to elderly, local outcomes data in the body of the pain outcomes inactive patients with multiple pain complaints. Clinic proposal. It may be helpful to include some examples of providers decide to use an 11-point (0 to 10) pain rating consequences experienced by providers or settings that scale (a reliable and well-validated measure of pain intendid not abide by the appropriate outcomes requirements sity) as the primary effectiveness measure, administered as an additional means of persuasion. Last, meet with the prior to every visit. Patients are asked to report their curadministrative representative and present the basis and rent levels of pain using the 11-point scale. Data are colanticipated costs for the pain outcomes measurement prolected and reported for a 6-month period. Results reveal gram. Compromise may be necessary, but if the proposal no change in pain scores over time, and clinic staff memis complete, well documented, and involves reasonable bers conclude that their efforts are not effective. costs, the likelihood of approval will be maximized. Are these conclusions justifi ed? Probably not, as the question asked (current pain intensity) likely was not the PAIN OUTCOMES INSTRUMENTS best measure of pain intensity in this situation. Consider the difficulty this group of patients experiences in reportSelection of appropriate instruments to use in a pain outing for their appointments. They must prepare themselves comes program requires some familiarity with basic meafor travel, arrange travel to the appointment, transport surement principals. Test reliability refers to the constancy themselves to the clinic area, and sit in uncomfortable of measurement; that is, the extent that the instrument “ current pain” yields similar results when administered under identicalchairs waiting to be seen. As a result, their rating may be closer to a worst “ pain” rating, and may or very similar circumstances (Johnston, Keith, & Hinnot accurately refl ect the effectiveness of treatment. A derer, 1992). If an instrument is unreliable, it is likely to better pain measure might instead be their usual “ pain” generate inconsistent results that reflect the random effects which is less affected by the transient uences infl of the of error rather than any systematic change attributable to situation. Figure 81.5 presents hypothetical differences treatment factors. Reliability is a necessary condition for validity, but adequate reliability does not ensure validity (Green, 1992). Validity generally refers to the degree to which the instrument measures what it was designed to measure (Johnston, Keither, & Hinderer, 1992). There are several types of validity which are assessed by different methods. In this review, we have chosen to emphasize concurrent validity, or how well the instrument or measure compares to other established (“gold standard”) measures of the construct or variable. Measures with good concurrent validity exhibit relatively high and clinically significant correlations with established measures of the pain domain under study. Measures adopted for use as part of a patient-focused outcomes system should exhibit adequate reliability and validity (CARF, 1999). If they are to FIGURE 81.5 Pain scores over time.

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TABLE 81.2 Domains of Outcome Assessed by Unidimensional Measures Measure (Items)

Pain Intensity

NRS/VAS (1) MPQ (20) PDI (7) SIP (136)

Current, average, best, worst— — Pain Rating Index — — — Pain interference in role functioning — — Pain interference in physical, — psychosocial, and overall functioning — — Depression — — Depression — — Anxiety — — — — — —

BDI (21) CES-D (20) STAI (40) PASS (40) TS (17)

Pain Interference

Emotional Distress

Pain-Related Fear — — — —

— — — Pain-related fear and avoidance Pain-related fear and avoidance

Note: NRS/VAS = Numeric Rating Scale/Visual Analog Scale; MPQ = McGill Pain Questionnaire; PDI = Pain Disability Index; SIP =s Sicknes Impact Profile; BDI = Beck Depression Inventory; CES-D = Center for Epidemiologic Studies-Depression Scale; STAI = State-Trait Anxiety ntory; Inve PASS = Pain Anxiety Symptoms Scale; TS = Tampa Scale.

between current and usual pain ratings gathered under includes the assessment of pain intensity, pain interference, these conditions, and clearly illustrates the desirability ofemotional distress, vocational functioning, patient satisfaccarefully considering all aspects of a meas-ure when evaltion, and medical resource utilization. The most common uating appropriateness. approach to assessing multiple outcomes domains is to assemble a battery of unidimensional instruments, each of There are several pain-specific self-report instruments which measures a single pain outcomes domain. In the folthat may be used to assess treatment outcome. The following review of selected pain treatment outcomeslowing sections, we attempt to provide readers with several choices of acceptable unidimensional outcomes instruments measures is limited to measures that have been validated within each outcomes domain. A summary of key unidimenwith pain patient samples and were judged by the authors sional instrument characteristics is presented in Table 81.2. to have some utility for outcomes assessment. Absent from this review are several well-validated measures, such as the Coping Strategies Questionnaire (CSQ) (Rosensteil & Pain Intensity Keefe, 1983), which tap important aspects of the pain Pain intensity measures form the basis of all pain treatexperience and have been widely used in pain research, but lack significant evidence of utility for general pain ment outcomes measurement approaches and are essential outcomes assessment. For the reader who is interestedfor in most pain service delivery outcomes measures as well. Luckily, the measurement of pain intensity is perhaps the a wider range of pain measures, more comprehensive reviews may be found elsewhere (Bradely, Haile, & Jawor-simplest component of outcomes assessment, and there are several easy-to-administer, psychometrically sound ski, 1992; Jensen & Karoly, 1992; Tait, et al., 1987). Both unidimensional and multidimensional pain out- scales available. The three broad categories of commonly used pain intensity measures include the Visual Analog comes measures are reviewed in the following pages. Criteria for inclusion in this review were (1) evidence of Scale (VAS), Numeric Rating Scale (NRS), and Verbal acceptable reliability; (2) data supporting instrumentRating Scale (VRS). The VAS and NRS typically consist validity (particularly concurrent validity); (3) prior use as of a single item requiring the patient to quantify the inten” “usual,” “least,” or “worst” a pain outcomes instrument; and (4) high utility for painsity of his or her “current, pain. Empirical evidence suggests that the combination of outcomes assessment, as judged by the authors. “least” and “usual” pain ratings provide the best estimate of actual pain intensity, while “least” may be the single UNIDIMENSIONAL MEASURES most accurate predictor (Jensen, et al., 1996). However, for practical purposes clinicians can have confidence in In contrast to standards for acute pain treatment, current the choice of a single VAS or NRS rating of “usual” pain, chronic pain treatment standards necessitate the assessment of outcomes across multiple dimensions of functioningwhich appears to provide a reasonably valid estimate of (CARF, 1999). Although specifi c standards vary by type of actual pain. Interestingly, “current” and “worst” pain ratings were found to have a weaker relationship with actual pain, treatment modality, and practice standards, comprepain intensity (Jensen, et al., 1996). hensive pain treatment outcomes measurement generally

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Pain Management: A Practical Guide for Clinicians, Sixth Edition

A reliable and well-validated form of the VAS is a Pain Interference 10-cm line anchored with the phrases no “ pain” and “worst possible pain” or “excruciating pain. ” Patients are A central goal of pain intervention is to reduce the extent to which pain impairs physical activity, emotional functioning, instructed to bisect the line at the point that best represents their level of pain, and the score is simply the length ofand psychosocial role fulfillment. Several unidimensional measures of pain interference are available to assess the the segment to that point. The VAS has been found to be degree and nature of pain-related limitations in one or valid and sensitive to changes in acute, cancer, and chronic pain (Breivik, Bjornsson, & Skovlund, 2000; DeConno, more domains of functioning. It should be noted that et al., 1994; Ogon, et al., 1996), and it yields ratio levelalthough some of these measures, such as the Sickness Impact Profile (SIP), tap pain interference across multiple data (Jensen, et al., 1992). Although comparisons of horizontal and vertical line orientations yield mixed results,domains of functioning, the primary construct assessed is using the VAS horizontally may provide slightly higher the single dimension of pain-related impairment. These measures of pain interference should not be confused with sensitivity (Ogon, et al., 1996; Jensen, et al., 1999). The NRS consists of a numeric range from 0 to 10 orinstruments that simply quantify functional status and do 100 with anchors similar to those of the VAS, and can benot attempt to account for the role of pain in an individadministered in oral or written form. Individuals are askedual’s level of impairment. This difference is illustrated by to quantify their pain levels by choosing a single numberthe contrast between the SIP psychosocial scale, which measures the extent of emotional and social ficulties dif from the 11- or 101-point scale. The NRS has been found that are attributed to the pain condition, and the Beck to have good psychometric characteristics (Jensen, et al., Depression Inventory (BDI) (Beck, 1987), which assesses 1999) and to be sensitive to changes in acute, cancer, and depressive symptomatology without concern for etiology. chronic pain (DeConno, et al., 1994; Paice & Cohen, The Pain Disability Index (PDI) (Pollard, 1984) is a 1997). The data provided by the NRS can be treated as seven-item measure of pain interference in physical and ratio level (Jensen & Karoly, 1992). psychosocial role performance. The PDI has good internal Verbal rating scales typically consist of a list or lists consistency α( = 0.87) (Tait, et al., 1987) and 1-week of pain descriptors that are rank ordered along a contintest–retest reliability (intraclass r = 0.91) (Gronblad, et al., uum of severity. Patients are asked to select the most and it has been shown to effectively discriminate appropriate descriptor or set of descriptors, and a score 1993), is groups of pain patients with varying levels of disability assigned based on the rank(s) of the chosen word(s) (Tait, Chibnall, & Krause, 1990). The measure appears to (Jensen & Karoly, 1992). The McGill Pain Questionnaire be sensitive to change (Strong, Ashton, & Large, 1994), (MPQ) (Melzack, 1975a) is a well-validated, widely used and it is valid for use with chronic and post-operative pain VRS that consists of 20 lists of descriptors of the sensory, patients (Pollard, 1984). Factor analysis supports the clasaffective, and evaluative dimensions of pain (Melzack, sification of the PDI as a unidimensional measure of pain 1975b). Support for the tripartite structure of the MPQ is interference (Tait, Chibnall, & Krause, 1990). The PDI mixed, and factor analyses generally reveal significant has practical appeal as a brief, easy-to-use, and overlap among factors (Donaldson, 1995; Holroyd, et al., psychometrically sound measure of general pain interfer1992; Turk, Rudy, & Saolovey, 1985). The standard scorence when less comprehensive assessment of pain-related ing procedure yields a Pain Rating Index (PRI) for each disability is adequate. of the three subscales, although in practice these subscales are often summed to create a single PRI. The PRI has The SIP is a widely used, 136-item measure of perceived impairment (Brown, 1995; Williams, 1988) with been shown to be sensitive to change and valid for use high test–retest reliability (0.92) and internal consistency among acute, cancer, and chronic populations (Davis, 1989; Lowe, Walker, & MacCallum, 1991; Sist, et al., (0.94) (Bergner, et al., 1981). The SIP administration 1998). However, as is true of other verbal scales, it onlyinstructions were altered by Turner and Clancy (Turner & yields ordinal level data because questions have been Clancy, 1988) to reflect pain-related impairment rather raised about the assumption of equidistance between than general physical impairment. The 14 SIP subscales ranked descriptors (Choiniere & Amsel, 1996). assess pain interference across a wide range of functionPractical considerations suggest that the VAS or theing, and they are combined to form the Physical, Psychosocial, and Total scales. The SIP scales have been found NRS may be preferred to the MPQ or other verbal scales to possess good concurrent validity in chronic pain and for the clinical assessment of pain intensity as they provide psychometrically superior data that are relatively easy tocancer pain patients (Beckham, et al., 1997; Watson & Graydon, 1989), and they are sensitive to change resulting collect and score. When ease of administration and scoring from multidisciplinary inpatient treatment for chronic pain are of greatest concern, the 11-point NRS may be the best (Jensen, et al., 1992). From a practical standpoint, the choice. In contrast, when greater measurement precision main weaknesses of the SIP are its length and the relative is desirable, the advantage goes to the VAS or to the 101-point NRS. difficulty of scoring the inventory. In addition, individuals

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with pain may find many SIP items to be less face validpositives among chronic and cancer pain patients. However, like the BDI, the CES-D has been shown to disand relevant to their conditions than those of measures developed specifi cally to tap pain-related disability. criminate between chronic pain patients with and without depression, and removal of somatic items did not Nevertheless, the SIP remains the gold standard for detailed assessment of self-reported pain interference. appreciably improve accuracy (Geisser, Roth, & Robinson, 1997; Turk & Okifuji, 1994). Nonetheless, higher cutoffs should be used in pain populations. Emotional Distress The impact of anxiety on pain treatment outcome Although the measures of emotional distress presented has not been studied as extensively as that of depression. here are not pain specific, they are widely used in pain However, the existing evidence suggests a high concorintervention outcomes assessment. This reflects the condance between pain and anxiety (Polantin, et al., 1993), siderable association between emotional distress and pain, and the need to address these symptoms in comprehenthe importance of treating concurrent depression and anxsive pain intervention is well recognized. The iety, and the recognition that psychological variables canState–Trait Anxiety Inventory (STAI) is a 40-item selfhave a significant impact on treatment outcome. The fol-report inventory of state and trait anxiety that possesses lowing emotional distress measures were selected based adequate psychometric properties (Spielberger, et al., upon their brevity, convenience, and general acceptance 1983), and is widely used for pain outcomes measureamong pain researchers for outcomes assessment. ment. The STAI is sensitive to change (Mongini, Defi lThe BDI is a 21-item measure of depressive symp-ippi, & Negro, 1997) and is an adequate choice for the tomatology (Beck, 1987). This widely used instrument hasclinician wishing to quantify levels of both acute anxiety been shown to have adequate psychometric properties and the more stable tendency to perceive sone’ environ(Beck, Steer, & Garbin, 1988), and it is sensitive to change ment as threatening. resulting from multidisciplinary pain clinic treatment (Kleinke, 1991). The BDI discriminates well between Pain-Related Fear chronic pain patients with and without depression (GeisRecently, researchers have begun to focus on the role of ser, Roth, & Robinson, 1997). However, researchers have pain-specific emotional distress in the experience of pain. raised questions about the appropriateness of using the BDI to detect depression among pain patients (de C. Wil-Emerging data indicate that pain-specific emotional disliams & Richardson, 1993). Several BDI items containtress, particularly pain-related fear, may play a more important role than general levels of affective disturbance somatic content (e.g., sleep disturbance, fatigability, and somatic preoccupation) that is confounded with com-in the development and maintenance of pain-related physmonly observed symptoms of chronic pain syndromes,ical disability (McCracken, Faber, & Janeck, 1998). The construct of pain-related fear may be defined broadly as and several studies have suggested that pain patients may the fear of pain and the avoidance of behaviors that are produce higher scores on these items as a function of their pain-related physical symptomatology (Plumb & Holland,anticipated to produce painful sensation or injury. 1977; Wesley, et al., 1999). While this may limit total Although no evidence currently exists linking levels of score comparisons with nonpain populations, removal ofpain-related fear to treatment outcome, the available data suggest that pain-related fear may seriously compromise the somatic items has not been found to improve the an individual’s willingness to initiate and persist in the accuracy of the measure for discriminating depressed from degree of physical reactivation and restoration that is nondepressed chronic pain patients (Geisser, Roth, & Robessential to reversing the progression of pain-related disinson, 1997). Consequently, clinicians may choose to use ability. Accordingly, clinicians and researchers are beginthe BDI for treatment outcomes, although accurate classification of depressive symptomatology may requirening to pay more attention to the role of pain-related fear in pain treatment outcome. higher cutoffs. An alternative measure of depression favored by Of the few available unidimensional measures of painrelated fear, the Pain Anxiety Symptoms Scale (PASS) some researchers for pain outcomes is the 20-item Center for Epidemiologic Studies-Depression Scale (CES-(McCracken, Zayfert, & Gross, 1992) and the Tampa Scale D) (Radloff, 1977). The CES-D has high internal reli- (TS) (Kori, Miller, & Todd, 1990) are the most promising. ability (α = 0.85) in normal populations and good con- The PASS is the longer of the two measures, with 40 items current validity in chronic and cancer pain populationsassessing cognitive and pain-related physiological anxiety (Beckham, et al., 1997; Radloff, 1977). The CES-D maysymptoms, escape and avoidance responses, and fearful appraisal of pain (McCracken, Zayfert, & Gross, 1992). The be somewhat more sensitive to change than the BDI (Turk & Okifuji, 1994). Normed on a normal population, four PASS subscales have good internal consistency the CES-D suffers from many of the same limitations(McCracken, Zayfert, & Gross, 1993), and the total score as the BDI, potentially producing a high number of falsehas good predictive validity and appears to be adequate for

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TABLE 81.3 Domains of Outcome Assessed by Multidimensional Measures Outcome Dimensions Pain intensity Pain interference

BPI (32)

MPI (52)

Right now, average, least, worst Pain severity subscale Pain interference in physical Pain interference in physical functioning functioning; activity level Emotional distress Pain interference in mood and Emotional distress; interpersonal relations support/response from others Pain–related fear — — Vocational functioning — — Medical resource utilization — — Patient satisfaction — —

NPDB–VA v.2 (74) Usual (0–10 NRS) Pain interference in physical functioning; activity level Emotional distress; pain interference in interpersonal activities Pain-related fear Employment status; pain work interference Inpatient and outpatient visits; surgeries Satisfaction with various treatment components

Note: BPI = Brief Pain Inventory; MPI = Multidimensional Pain Inventory; NPDB-VA v.2 = National Pain Data Bank-VA Version 2, NRS, Numeric Rating Scale.

outcomes assessment (McCracken, Faber, & Janeck, 1998). Advantages and Disadvantages Scores on the PASS have been found to predict self-reported of Unidimensional Instruments pain severity, disability, pain behavior, and range of motion on straight leg raise (McCracken, et al., 1993; McCracken,Unidimensional pain outcomes instruments generally are easily available, inexpensive, and necessitate minimal et al., 1996). In addition, pain patients classifi ed as d “ ysfi-ef functional” by the Multidimensional Pain Inventory (MPI) administration training time. Additionally, they are an cient means of collecting data when only a single or a few (Kerns, Turk, & Rudy, 1985) were more likely to produce selected outcomes domains are to be assessed. Unfortuhigh scores on the PASS than those classifi ed as i“nterpersonally distressed”or as “adaptive copers”(Asmundson, nately, using unidimensional measures to assess multidimensional pain treatment outcomes requires assembling Norton, & Allerdings, 1997). a battery of individual instruments. The idiosyncratic Perhaps a better measure of the pain-related anxiety nature of these batteries often restricts or prevents comparis the TS, a 17-item instrument developed to assess kinesiophobia, or the fear of movement and activity dueisons between local outcomes data and community benchto concerns about injury or reinjury (Kori, Miller, & marked data. In addition, some of these instruments are Todd, 1990). Although limited, recent evidence suggestsquite lengthy and may include items that are not directly relevant to pain. Thus, while unidimensional measures may that the TS may possess greater predictive validity than be the most ef ficient means of collecting pain data for one the PASS and other measures of pain-related fear. The or two selected pain outcomes domains, the use of many TS has been found to be a superior predictor of a range unidimensional measures to cover all key chronic pain of pain symptoms and behaviors, even after controlling outcomes domains may decrease the utility of the obtained for known confounding factors such as pain intensity data while increasing staff and patient burden. and duration, gender, and negative emotionality. For example, the TS was an incrementally valid predictor MULTIDIMENSIONAL MEASURES of self-reported disability and behavioral performance during a lifting task after controlling for pain onset, In response to the limitations associated with batteries of lower extremity radicular pain, and pain intensity, while unidimensional instruments, a few multidimensional pain the PASS was not (Crombez, et al., 1999). In addition,outcomes tools have been developed. Three of these are the TS has been found to be a superior predictor ofdiscussed below. Perhaps due to differences in the nature disability as compared to pain intensity, biomedicaland extent of acute, cancer, and chronic pain conditions, signs and symptoms, and negative emotionality (Crom-two of these three instruments were developed to assess a bez, et al., 1999; Vlaeyen, et al., 1999). Although nospecific type of pain. Validation of each of these three measures has been restricted largely to the types of pain for data on the ability of either the TS or the PASS to capture which the instrument was originally developed. Table 81.3 treatment-related change exist, either measure may be appropriate. However, given its superior predictivepresents a comparison of the key features of these instruvalidity and shorter length, the TS appears to be thements, while Table 81.4 summarizes the strength of coninstrument of choice for assessing treatment-inducedcurrent validity support for the instruments across acute, cancer, and chronic nonmalignant pain populations. changes in pain-related fear.

A Practical Approach to Outcomes Measurement

TABLE 81.4 Concurrent Validation Support for Multidimensional Measures Measure

Acute

BPI MPI NPDB-VA

Moderate None None

Cancer Strong Weak None

Chronic Nonmalignant None Strong Moderate

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patients consisting of dysfunctional, interpersonally distressed, and adaptive copers or minimizers categories (Turk & Rudy, 1990). Clinicians may find this typology useful for purposes such as planning pain treatment or testing the effectiveness of different interventions or intervention components across MPI groups of patients. National Pain Data Bank

The National Pain Data Bank (NPDB) is a softwaredriven, outcomes package consisting of intake, posttreatBrief Pain Inventory ment, and follow-up questionnaires. The NPDB was The Brief Pain Inventory (BPI) (Cleeland & Ryan, 1994) developed specifically to assess treatment outcomes, and it is the only measure that encompasses all of the domains is a 32-item instrument developed to assess pain history, pain intensity, perceived recent response to med-of functioning typically considered to be essential to comication/treatment, and pain interference. The BPI is wellprehensive outcomes measurement. The outcomes package allows the clinician to track changes in pain intensity, validated among cancer and chronic disease pain patients, pain interference, emotional distress, pain-related fear, and it has been translated into several languages. Factor vocational functioning, patient satisfaction, perceived analytic studies consistently have revealed the two factors improvement, and medical resource utilization from of pain severity and interference across samples and lanintake through follow-up, obviating the need to use more guage versions (Caraceni, et al., 1996; Radbruch, et al., than one measure. In addition, a large database of bench1999; Saxena, Mendoza, & Cleeland, 1999; Wang, et al., 1996). However, empirical data are limited mostly to can-mark data is available to allow comparisons with the outcomes of similar modalities across the nation, a requirecer and chronic disease samples, and little is known about the sensitivity to change or psychometric properties of thement of many pain treatment standards (e.g., CARF). instrument when used with chronic pain populations. Selected subsets of NPDB items have been found to have moderate (0.73) to high (0.94) internal reliability (American Academy of Pain Management, 1997). A preliminary Multidimensional Pain Inventory investigation of the psychometric properties of the instruThe MPI, formerly the West Haven–Yale Multidimen- ment among a chronic pain impatient sample revealed that sional Pain Inventory, is a popular pain measure that was the NPDB demonstrated good concurrent validity in reladeveloped to facilitate the comprehensive assessment tion of to a number of widely accepted gold standard meachronic pain patients (Kerns, Turk, & Rudy, 1985). sures of pain-related impairment (Clark & Gironda, 2000). Designed to be used in conjunction with behavioral andAnalysis of the final data set has confirmed the preliminary psychophysiological measures, the 52 items comprise 12 findings, and investigations of test–retest reliability, consubscales that are dispersed across three sections: (1) pain current validity, and sensitivity to change are currently intensity, pain interference, dissatisfaction with currentbeing conducted. functioning, appraisal of support from others, perceived life control, and affective distress; (2) punishing, solici- Advantages and Disadvantages tous, and distracting responses from significant others to of Multidimensional Measures displays of pain behaviors; and (3) frequency of the performance of household chores, outdoor work, activities away Multidimensional pain outcomes measures have several from home, and social activities (Kerns, Turk, & Rudy, advantages relative to unidimensional measures. Because 1985). The 12 subscales possess good internal consistency these instruments were specifically designed for pain pop(α = 0.70 to 0.90) and acceptable 2-week test–retest reliulations, they often contain fewer total items than combiability (r = 0.62 to 0.91). Adequate levels of unique vari-nations of corresponding unidimensional measures and ance and concurrent validity have been demonstrated for tend to be better integrated. Additionally, as the instrumost scales (Kerns, Turk, & Rudy, 1985). The MPI ments are uniform, results can be compared across treatappears to be sensitive to change, but the utility of specific ment settings or geographic regions, which may assist in subscales may vary across levels of adaptation and functhe eventual development of universal pain outcomes tioning (Strategier, et al., 1997). benchmarks. Disadvantages of the multidimensional measures are that they may be moreficult dif to obtain, In addition to the measurement of treatment outcomes, the MPI has been used to classify chronic pain patients in require additional administration or scoring training as order to identify major treatment needs. Cluster analyses well as more data entry and management time, are more have yielded a three-group typology of chronic paincostly in some cases and, with the exception of the NPDB,

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ommendations) will enhance administrative interest in the do not cover all of the key chronic pain outcomes domains. effort. Nevertheless, when assessing multiple domains of outcomes in clinical settings, multidimensional measures • Meet with the appropriate administrative generally are more practical. representative to discuss anticipated costs and needed resources, citing any relevant local polA PRACTICAL APPROACH icies, local or national regulations, professional TO OUTCOMES MEASUREMENT practice guidelines, or local competitors’ outcomes practices and marketing data. The process of designing a pain outcomes methodology • Define the administrative limits (funds, posiconsists of a series of discrete steps and requires that tions) that are operative. factors relevant to the outcomes system development pro• Negotiate an agreement regarding support for cess, such as those described above, be considered carethe necessary resources. fully. In the following pages we provide an outline of our suggested approach to this endeavor in the hope that it SELECT THE RELEVANT OUTCOMES DOMAINS will assist the reader through this process. Decisions regarding which pain outcomes domains to include often involve compromises between available IDENTIFY OUTCOMES OBJECTIVES resources and outcomes objectives. Yet outcomes efforts The first step in developing a pain outcomes measurement can be too ambitious as well. Collecting data for outcomes system consists of identifying goals, objectives, and scope domains that are not central to the outcomes program of the outcomes program. objectives is a waste of staff resources and patient time. • Identify the basis for establishing the pain outcomes strategy. It may be a new hospital policy, legal opinion, or accreditation standard. Familiarity with the underlying rationale may make it easier to enlist administrative and staff support. • Determine whether the outcomes objectives primarily focus on pain treatment issues or on the efficiency of pain service delivery. This distinction will have important implications for the eventual selection of outcomes measures. • Define the scope of the outcomes plan. Are all available pain treatments to be included, or will only selected treatments be monitored? Does the plan cover every type of pain (acute, cancer, and chronic), or is it limited to only one or two? • Choose which types of service settings will be included. Is it limited to outpatient areas, inpatient units, or specialty pain clinics? Are all providers working in the defined areas participating, or only some? • Decide whether the outcomes data collection will be ongoing or limited to a preselected time interval.

IDENTIFY ADMINISTRATIVE SUPPORTS

AND

• Select the relevant outcomes domains according to the focus of the outcomes program (treatment effects or service delivery), type of pain population involved (acute, cancer, or chronic), and setting. • Avoid adding outcomes domains that are not directly relevant to the outcomes objectives. Additional domains may be added later if objectives change. • Review any applicable guidelines, standards, or policies to ensure that all needed domains are included.

SELECT

OR

DESIGN

THE

NEEDED OUTCOMES MEASURES

Selecting Patient Outcomes Measures If the objectives of the outcomes program involve evaluating the effects of pain treatment, it is likely that suitable pain outcomes instruments will be available for use. This will avoid the difficulties associated with designing and validating a new instrument and will minimize delays in implementing the outcomes programs.

LIMITATIONS

Without sufficient administrative support, efforts to develop a pain outcomes system will fail. Staff will resent the added responsibilities in the absence of increased staff or concrete rewards. Presumably the basis for developing the pain outcomes system (JCAHO standards, insurer rec-

• Identify potential instruments that assess the outcomes domains of interest (Tables 81.2 and 81.3 may be helpful when matching outcomes instruments to outcomes domains). • Investigate the reported reliabilities and review the validation data available for the identified instruments. • Review any available data concerning readinglevel requirements, and determine whether

A Practical Approach to Outcomes Measurement

those requirements are consistent with the target population’s reading abilities. • Attend to instrument length, administration and scoring requirements, and costs so as to maximize value and minimize resource demands. • Determine whether the instruments are available in other languages if this is desirable given the characteristics of the target population. • Choose the instrument or battery of instruments to use based on the above information. Designing Service Delivery Outcomes Measures

1007

DESIGN

AND

PREPARE

THE

OUTCOMES DATABASE

Preparation of the outcomes database prior to implementation of data collection requires reviewing every outcomes item or measure as well as all data entry and organization issues. Often this process yields valuable information that may streamline data collection and data management procedures. • Decide what database and data analysis tools will be used. • Design the necessary records storage and retrieval tools and conduct a “dry run” of data entry to identify any data collection problems. • Make certain that the confidentiality of any patient information is maintained by discarding identifying information or by utilizing elaborate coding or encryption strategies. • Develop a data analysis plan in advance of data collection efforts.

As indicated previously, service delivery outcomes measures generally are not available in the form of validated outcomes instruments. In fact, with the exception of generic customer satisfaction measures, pain service delivery measures typically need to be designed locally. Fortunately, these measures are relatively simplistic. Usually, they involve tracking whether required pain documentation is present or whether designated pain services were provided in an ficient ef and timely fashion. COLLECT THE OUTCOMES Thus, designing appropriate service measures may involve • Provide training in outcomes measure adminisno more than developing pain-specific chart review forms tration and data collection routines to relevant or simple customer feedback tools. staff. • Test the data collection procedures using only • Identify the specific service delivery outcomes a few patients (treatment outcomes project) or questions of interest. records (service delivery project) prior to full• Design the necessary outcomes tools (e.g., chart scale implementation. review forms, customer satisfaction surveys). • Arrange for backup coverage for the individuals • If patient surveys or questionnaires are collecting the data in the event of unexpected involved, evaluate item wording, specifi city, absences. and reading level to meet the target population’ s • Periodically review the workflow and data colabilities. lection procedures to identify and troubleshoot any problem areas.

DEVELOP PROCEDURES NEEDED

FOR IMPLEMENTATION

ANALYZE, TREND, AND REPORT THE DATA Once the scope of the outcomes project has been defined and the outcomes measures have been selected, specific Unfortunately, it is common to find that elaborate outprocedures for implementing the outcomes system must comes data have been collected at significant expense but be developed. then are virtually ignored! Outcomes data analysis and trending are the cornerstones of an effective outcomes • Determine how the pain patients targeted for program. Analysis involves more than “eyeballing” the study will be identified. data. Although the level of statistical analysis will vary • Identify the roles, responsibilities, and training depending on the objectives of the outcomes plan and the needs of all involved staff. psychometric sophistication of the staff involved, at the • Develop a timeframe for implementing all very least, it will be necessary to statistically summarize aspects of the outcomes system. the data in a way that directly addresses the outcomes • Decide on a sampling strategy (i.e., randomly questions of interest. Ongoing review of the results by key sample from among all possible data sources personnel is critical and is mandated by some regulatory or attempt to collect data from every source or accrediting bodies. during the data collection phase) depending on the sample size desired and the projected time• For an ongoing outcomes program, establish a frame. timeframe for systematically reviewing and

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•

•

•

•

•

•

•

reporting on the obtained data (monthly, quarterly, semiannually, or annually). Develop a report template that provides summary data regarding the outcomes questions and use that same template for each reporting period in order to allow comparisons over time. If performance improvement actions are instituted prior to or during a data collection period, note the nature of the changes implemented, along with the date, in the database so that the effects of the changes can be evaluated. After each reporting period, review data from all prior periods in concert with the current results in order to identify trends of change in the data. Provide each staff person involved in the project with copies of the analysis report and schedule a meeting after each data collection period for review and discussion of the data and any identified trends. Design and complete a brief version of the analysis report for distribution to key administrators to help maintain their support for the project. Use the obtained data to explore any additional outcomes questions or to investigate observed trends in the data. Implement treatment protocol changes based on the identified trends. Changes should be introduced sequentially in order to allow the effects of each change to be evaluated separately. Review the outcomes data following each change in treatment protocol and decide whether to accept or reject the change.

practice of pain treatment, and perhaps reconsider some of our treatment biases. It is an opportunity in that it provides us with the motivation and the means to empirically justify that which we do, and to improve what we do or how we do it in order to increase our treatment effectiveness and efficiency. In the preceding pages we attempted to summarize and briefly explore some of the key issues related to pain outcomes measurement endeavors. We also presented a general framework for designing and implementing outcomes measurement in pain treatment settings. In recognition of the wide variety of pain practitioner settings and outcomes objectives, we tried to maintain a generalist’ s approach to the topic. In this regard, we may have sacrificed precision to enhance utility. It is our hope that the information we provided will be of value to clinicians seeking to better understand and improve the effectiveness of their pain treatment interventions.

ACKNOWLEDGMENT This material is the result of work supported in part by the Rehbilitation Research and Development Service, Office of Research and Development, Department of Veterans Affairs.

REFERENCES

Agency for Health Care Policy Reform. (1992). Acute pain management: Operative or medical procedures and trauma, Pub. No. 92-0032. Washington, D.C.: U.S. Department • of Health and Human Services. Agency for Health Care Policy Reform. (1996). Management of cancer pain, Pub. No. 94-0592. Washington, D.C.: U.S. Department of Health and Human Services. SUMMARY American Academy of Pain Management. (1997). National Pain Data Bank reliability study.Pain Program Standards , Interest in outcomes monitoring in healthcare systems will Spring, 4–6. only increase in the immediate future. Within the field ofAmerican Academy of Pain Management. (1997). Pain program pain treatment, we will see growing demands for data accreditation manual(p. 21). Sonora, CA: American supporting the effectiveness of our interventions. RegulaAcademy of Pain Management. tory and accreditation bodies increasingly will emphasizeAmerican Pain Society. (1995). Quality improvement guidelines for the treatment of acute pain and cancer. Journal of the importance of pain outcomes programs for providers the American Medical Association, 274, 1874–1880. across all treatment settings. Indeed, the recent development of JCAHO pain standards and the growing nationalAsmundson, G.J.G., Norton, G.R., & Allerdings, M.D. (1997). Fear and avoidance in dysfunctional chronic back pain interest in pain issues already have had a profound effect patients.Pain, 69, 231–236. on the pain management field. Given these trends, it is Beck, A.T. (1987).Beck Depression Inventory . San Antonio, TX: only prudent that we anticipate these changes and enter The Psychological Corporation. the 21st century prepared to incorporate outcomes measBeck, A.T., Steer, R.A., & Garbin, M.G. (1988). Psychometric ures as a standard part of pain treatment efforts. properties of the Beck Depression Inventory: TwentySome practitioners might portray the ever-increasing five years of evaluation. Clinical Psychology Review, 8, demands for pain documentation and treatment outcome 77–100. data as a punitive, nonproductive exercise. We see it as Beckham, J.C., et al. (1997). Self-ef ficacy and adjustment in both a challenge and an opportunity. It is a challenge in cancer patients: A preliminary report. Behavioral Medthat it will require us to evaluate more closely our clinical icine, 23,138–142.

A Practical Approach to Outcomes Measurement

1009

Bergner, M., et al. (1981). The Sickness Impact Profile: Devel-Geisser, M.E., Roth, R.S., & Robinson, M.E. (1997). Assessing depression among persons with chronic pain using the opment and final revision of a health status measure. Center for Epidemiological Studies-Depression Scale Medical Care, 19,787–805. and the Beck Depression Inventory: A comparative Bradely, L.A., Haile, J.M., & Jaworski, T.M. (1992). Assessment analysis.Clinical Journal of Pain, 13,163–170. of psychological status using interview and self-interview instruments. (chap. 12). In D. C. Turk & R. Green, B. (1992). A primer of testing. In A.E. Kazdin (Ed.), Methodological issues & strategies in clinical research Melzack (Eds.),Handbook of pain assessment . New (chap. 10). Washington, D.C.: American Psychological York: Guilford Press. Association. Breivik, E.K. & Skoglund, L.A. (1998). Comparison of present Gronblad, M., et al. (1993). Intercorrelation and test–retest relipain intensity assessments on horizontally and vertically ability of the Pain Disability Index (PDI) and the Oswesoriented visual analogue scales. Methods and Findings try Disability Questionnaire (ODQ) and their correlation in Experimental Clinical Pharmacology, 20, 719–724. with pain intensity in low back pain patients. Clinical Breivik, E.K., Bjornsson, G.A., & Skovlund, E. (2000). A comJournal of Pain, 9,189–195. parison of pain rating scales by sampling from clinical Holroyd, K.A., et al. (1992). A multi-center evaluation of the trial data.Clinical Journal of Pain, 16,22–28. McGill Pain Questionnaire: Results from more than Brown, D. (1995). Quality assessment and improvement activi1700 chronic pain patients. Pain, 48, 301–311. ties should be incorporated into our pain practices. Pain Iezzoni, L. I. (1997). Assessing quality using administrative data. Forum, 4, 48–56. Annals of Internal Medicine , 127, 666–673. Campazzi, E.J., & Lee, D.A. (1995). Quality is in the eye of the International Association for the Study of Pain. (1991). Core beholder: Patient satisfaction and outcomes mancurriculum for professional education in pain (2nd ed.). agement in physician practices. American Health ConSeattle: International Association for the Study of Pain. sultants, 1, 3336. Jensen, M.P. & Karoly, P. (1992). Self-report scales and proceCaraceni, A., et al. (1996). A validation study of an Italian verdures for assessing pain in adults. In Turk, D.C. and sion of the Brief Pain Inventory (Breve Questionario per Melzack, R., Eds.,Handbook of pain assessment (chap. la Valutazione del Dolore). Pain, 65, 87–92. 9). New York: Guilford Press. CARF … (1999). The Rehabilitation Accreditation Commission, Jensen, M.P., et al. (1992). Validity of the Sickness Impact Profile 2000 medical rehabilitation standards manual (pp. Roland scale as a measure of dysfunction in chronic 46–66). Tucson, AZ: CARF...The Rehabilitation Compain patients.Pain, 50, 157–162. mission. Jensen, M.P., et al. (1996). The use of multiple-item scales for Choiniere, M., & Amsel, R. (1996). A visual analogue thermompain intensity measurement in chronic pain patients. eter for measuring pain intensity. Journal of Pain and Pain, 67, 35–40. Symptom Management, 11, 299–311. Jensen, M.P., et al. (1999). Comparative reliability and validity Clark, M.E., & Gironda, R.J. (2000). Concurrent validity of the of chronic pain intensity measures. Pain, 83, 157–162. National Pain Data Bank: Preliminary results. American Johnston, M.V., Keith, R.A., & Hinderer, S.R. (1992). MeasureJournal of Pain Management, 10, 25–33. ment standards for interdisciplinary medical rehaCleeland, C.S. & Ryan, K.M. (1994). Pain assessment: Global bilitation. Archives of Physical Medicine and use of the Brief Pain Inventory. Annals Academy of Rehabilitation, 73(Suppl.), S3–S23. Medicine (Singapore), 23, 129–138. Joint Commission for the Accreditation of Healthcare OrganizaCrombez, G., et al. (1999). Pain-related fear is more disabling tions. (2000). Pain assessment and management stanthan pain itself: Evidence on the role of pain-related fear dards. http://www.jcaho.org/standard/pm_frm.html. in chronic back pain disability. Pain, 80, 329–339. Kerns, R.D., Turk,D. C., & Rudy, T.E. (1985). The West HavenDavis, G.C. (1989). The clinical assessment of chronic pain in Yale Multidimensional Pain inventory (WHYMPI). rheumatic disease: Evaluating the use of two instruPain, 23, 345–356. ments.Journal of Advanced Nursing, 14, 397–402. Kleinke, C.L. (1991). How chronic pain patients cope with depresDe Conno, F., et al. (1994). Pain measurement in cancer patients: sion: Relation to treatment outcome in a multidisciplinary A comparison of six methods. Pain, 57, 161–166. pain clinic. Rehabilitation Psychology, 36, 207–218. de C. Williams, A.C., & Richardson, P.H. (1993). What does theKori, S.H., Miller, R.P., & Todd, D.D. (1990). Kinisophobia: A BDI measure in chronic pain? Pain, 55, 259–266. new view of chronic pain behavior. Pain Management, Donaldson, G.W. (1995). The factorial structure and stability of 3, 35–43. the McGill Pain Questionnaire in patients experiencing Kulich, R. & Lande, S.D. (1997). Managed care: The past and oral mucositis following bone marrow transplantation. future of pain treatment. APS Bulletin, 7, 4–5. Pain, 62, 101–109. Lowe, N.K., Walker, S.N., & MacCallum, R.C. (1991). ConfirmDreyer, P. (1998). Adoption of standards of the American Pain ing the theoretical structure of the McGill Pain QuesSociety, Circular Letter #2–9–379. Augusta, ME: tionnaire in acute clinical pain. Pain, 46, 53–60. Department of Public Health, State of Maine. McCracken, L.M., et al. (1993). Prediction of pain in patients Ellwood, P.M. (1988). Outcomes management: A technology of with chronic low back pain: Effects of inaccurate prepatient experience. New England Journal of Medicine, diction and pain-related anxiety. Behavior Research and Therapy, 31,647–652. 318, 1549–1556.

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McCracken, L.M., et al. (1996). The assessment of anxiety and Saxena, A., Mendoza, T., & Cleeland, C.S. (1999). The assessment of cancer pain in north India: The validation of the fear in persons with chronic pain: A comparison of Hindi Brief Pain Inventory— BPI-H. Journal of Pain instruments. Behavior Research and Therapy, 34, and Symptom Management, 17, 27–41. 927–933. Sist, T.C., et al. (1998). The relationship between depression and McCracken, L.M., Faber, S.D., & Janeck, A.S. (1998). Painpain language in cancer and chronic non-cancer pain related anxiety predicts non-specific physical compatients.Journal of Pain and Symptom Management, 15, plaints in persons with chronic pain. Behavior Research 350–358. and Therapy, 36,621–630. Spielberger, C.D., et al. (1983). Manual of the State-Trait Anxiety McCracken, L.M., Zayfert, C., & Gross, R.T. (1992). The Pain Inventory (Form Y) (pp. 9–17). Palo Alto, CA: ConsultAnxiety Symptoms Scale: Development and validation ing Psychologists Press. of a scale to measure fear of pain. Pain, 50, 67–73. McCracken, L.M., Zayfert, C., & Gross, R.T. (1993). The Pain Strategier, L.D., et al. (1997). Multidimensional assessment of chronic low back pain: Predicting treatment outcomes. Anxiety Symptom Scale (PASS): A multimodal measure Journal of Clinical Psychology in Medical Settings, 4, for pain specific anxiety symptoms. Behavior Therapist, 91–110. 16, 183–184. Strong, J., Ashton, R., & Large, R.G. (1994). Function and the Melzack, R. (1975a). The McGill Pain Questionnaire. In patient with chronic low back pain. Clinical Journal of Melzack, R. (Ed.)Pain measurement and assessment Pain, 10, 191–196. (pp. 41–47). New York: Raven Press. Tait, R.C., Chibnall, J.T., & Krause, S. (1990). The Pain Disability Melzack, R. (1975b). The McGill Pain Questionnaire: Major Index: Psychometric properties. Pain, 40, 171– 182. properties and scoring methods. Pain, 1, 277–299. Tait, R.C., et al. (1987). The pain disability index: Psychometric Mongini, F., Defilippi, N., & Negro, C. (1997). Chronic daily and validity data.Archives of Physical Medicine and headache, a clinical and psychological profile before and Rehabilitation, 68,438–441. after treatment.Headache, 37,83–87. Tarlov, A.R. (1995). Multiple influences propel outcomes field. Ogon, M., et al. (1996). Chronic low back pain measurement Medical Outcomes Trust Bulletin , 3, 1–3. with visual analogue scales in different settings. Pain, Turk, D.C., & Okifuji, A. (1994). Detecting depression in chronic 64, 425–428. pain patients: Adequacy of self-reports. Behavior Paice, J.A., & Cohen, F.L. (1997). Validity of a verbally adminResearch and Therapy, 32, 9–16. istered numeric rating scale to measure cancer painTurk, D.C., & Rudy, T.E. (1990). The robustness of an empirically derived taxonomy of chronic pain patients. Pain, intensity. Cancer Nursing, 20,88–93. 43, 27–35. Plumb, M., & Holland, J. (1977). Comparative studies of psychological function in patients with advanced cancer. I: Turk, D.C., Rudy, T.E., & Salovey, P. (1985). The McGill Questionnaire reconsidered: Confi rming the factor structures Self-reported depressive symptoms. Psychosomatic and examining appropriate uses. Pain, 21, 385–397. Medicine, 39, 264–276. Polantin, P.B., et al. (1993). Psychiatric illness and chronic lowTurner, J. A., & Clancy, S. (1988). Comparison of operant behavioral and cognitive-behavioral group treatment for back pain.Spine, 18, 66–71. chronic low back pain.Journal of Clinical and ConsultPollard, C.A. (1984). Preliminary validity study of Pain Disabiling Psychology, 56,261–266. ity Index. Perceptual and Motor Skills, 59, 974. Veterans Health Administration. (2000). VHA national pain Radbruch, L., et al. (1999). Validation of the German version of management strategy, Pain assessment: The 5th vital the Brief Pain Inventory.Journal of Pain and Symptom sign (pp. 27–29). Washington, D.C.: Veterans Health Management, 18,180–187. Administration. Radloff, L. (1977). The CES-D scale: A self-report depression Vlaeyen, J., et al. (1999). Fear of movement/(re)injury and musscale for research in the general population. Journal of cular reactivity in chronic low back pain patients: An Applied Psychology Measures, 385–401. 1, experimental investigation. Pain, 82, 297–304. Rosensteil, A.K., & Keefe, F.J. (1983). The use of coping strat-Wang, X.S., et al. (1996). The Chinese version of the Brief Pain egies in chronic low back pain patients: Relationship to Inventory (BPI-C): Its development and use in a study patient characteristics and current adjustment. Pain, 17, of cancer pain [see comments]. Pain, 67, 407–416. 33–44. Watson, J.H. & Graydon, J.E. (1989). Sickness Impact Profile: Rudy, T.E., & Kubinski, J.A. (1999). Program evaluation methA measure of dysfunction with chronic pain patients. ods for documenting pain management effectiveness. In Journal of Pain and Symptom Management, 152–156. 4, J. Gatchel and D. Turk (Eds.), Psychological approaches Wesley, A.L., et al. (1999). Toward more accurate use of the to pain management: A practitioner’s handbook (chap. Beck Depression Inventory with chronic back pain 18). New York: Guilford Press. patients.Clinical Journal of Pain, 15,117–121. Santor, D.A., et al. (1995). Examining scale discriminability in Williams, R.C. (1988). Toward a set of reliable and valid measthe BDI and CES-D as a function of depressive severity. ures for chronic pain assessment and outcome research. Pain, 35, 239–251. Psychology Assessment,131–139. 7,

82 Enhancing Adrenal Function Arnold Sandlow, D.C. and Afshin Shargani, D.C. INTRODUCTION

of gross pathology should any thought at all be placed on subtle, seemingly ubiquitous symptomatology? One of the most overlooked issues faced by the healthcare “As the signs and symptoms of adrenal dysfunction pain practitioner on a day-to-day basis is realizing andare often relatively non-specific, adrenal disorders must addressing the role of the adrenal gland and its dysfunction be considered in the differential diagnosis of many comas related to the pain and nonpain patient alike. Thismon complaints” (Miller & Tyrell, 1996). chapter enables the practitioner to recognize, diagnose, This chapter focuses on a continuum that exists someand treat this common and underdiagnosed condition. where between the likes of Addison’s disease and CushIn our modern-day society we are barraged with var-ing’s disease and is secondary to chronic maladaption. ious forms of stress on a daily basis. Some stressors are This chronic maladaption to stress leads to adrenal exhauseasy to adapt to, others can become seemingly insurtion and has been referred to by many different names. mountable. Stress and stress-related disorders have been Dilman and Dean (1992) called it the Adrenal Maladapconsidered a significant cause of disease and may contribtation Syndrome, or hyperadaptosis. David Walther ute to perhaps 75% of all illnesses. Pain subjects the (1988), in Applied Kinesiology-Synopsis, calls it funcpatient to additional stress, which can potentially lead totional or relative hypoadrenia. Others call it adrenal stress-related disorders. insufficiency, exhaustion, or burnout (Table 82.1). Thoughts about the adrenal gland automatically In contemporary society, long-term, never-ending relate to thoughts of stress. They are inseparable. For the emotional stress creates a tired or worn-out adrenal gland, most part the lay public is familiar with the adrenal glandprincipally because the adrenal gland does not have a and its role in handling stress. From the perspective ofchance to rebuild. Because stress is cumulative, stresses the pain management practitioner the adrenal gland plays to which the body must react over time can cause mild to a major role, often unnoticed, and wholly underesti-moderate adrenal insuf ficiency, the most common clinimated. Understanding the relationship between the adrecally observed entity. In this condition the individual can nal gland and the patient in pain can increase the ability still react to stress; however, it will be done less ficiently ef of the practitioner to treat and manage the patient as and a will take more time. whole, addressing the underlying causes as well as the The goal of health is to maintain homeostasis. When main causative factors. the hypothalamic–pituitary–adrenal (HPAA) axis is disMuch of the healthcare in the United States is directedturbed, homeostasis is lost. A DHEA/cortisol balance (two toward crisis care. Should we just wait until our patienthormones secreted by the adrenals) is considered to be a has a full-blown organic dysfunction, or should we realizecritical marker of overall hormonal health. and be concerned with an adrenal gland that would allow Also highlighted are diagnosis, laboratory testing, us a higher level of health and well-being but is not func-homeostasis, hormonal regulation, and feedback mechanisms, i.e., HPAA, and natural methods of controlling and tioning to meet the demands of the body? In the absence 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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TABLE 82.1 Common Causes of Adrenal Stress • • • • • • • • • • • •

Anger Fear Worry/anxiety Depression Guilt Physical or mental strain Excessive exercise Sleep deprivation Light-cycle disruption Going to sleep late Surgery Trauma/injury

• • • • • • • • • • •

Chronic inflammation Chronic infection Chronic pain Temperature extremes Toxic exposure Malabsorption Maldigestion Chronic illness Chronic/severe allergies Hypoglycemia Nutritional deficiencies

medulla, or independently. Cortisol’ s main action is catabolism of fats and amino acids from their stores in adipose tissue, muscle, lymphatics, and bone, making them available for producing energy and the synthesis of other compounds including glucose and proteins. Cortisol promotes gluconeogenesis and protein synthesis by the liver, enhances the effects of glucagon and growth hormone and decreases glucose uptake by the peripheral tissues. This results in increasing blood sugar levels for use by brain and heart tissues. Cortisol is also a well-known and potent anti-inflammatory agent exerting its effects by decreasing the permeability of capillary endothelium, stabilizing the liposomal membrane, and promoting production of arachadonic acid, a precursor of prostoglandins.

SEX HORMONES enhancing the function of the glands and the important hormones they produce. Adrenal sex hormones are produced by the cells of the zona reticularis, the innermost layer of the adrenal cortex. The majority of these hormones are androgens, in the form ADRENAL GLANDS AND THEIR HORMONES of dehydroepiandrosterone (DHEA), which has one fifth The adrenal glands (or suprarenal glands) are the major of testosterone’ s potency. Other adrenal sex hormones, organs that deal with life’ s minor and major ups and including estrogen and progesterone, are manufactured in downs. They are pyramidal-shaped structures located on very small amounts. Although they make up the main top of each kidney. The adrenal glands are made of two source of androgens in women, under normal conditions distinct sections: the outer cortex and the inner medulla. these hormones have a minor role in men mainly due to They are essentially two different endocrine organs. Thethe presence of testosterone. adrenal cortex is made of three distinct layers or zones, After the age of 25 a gradual decrease in DHT prowhich produce different types of hormones. The zonaduction is noted and at 75, it is 15 to 25% of its peak. glomerulosa is the outermost layer, which produces the DHEA levels have an indirect relationship with cortisol mineralocorticoids (aldosterone). The zona fasiculata isproduction. Therefore, a comparison of DHEA-S vs. corthe middle layer, which produces glucocorticoids (cortisol)tisol levels can be used as an indicator of the patient’ s and the zona reticularis is the innermost layer involved inresponse to stress. DHEA also has been shown to act as the production of sex hormones, mainly androgens. a protective guard against stress in laboratory animals (Hornsby, 1997). ALDOSTERONE EPINEPHRINE

AND

NOREPINEPHRINE

Aldosterone plays a vital role in the body, and its total absence, if untreated, can lead to death. Aldosterone stimThe inner part of the adrenal gland, the medulla, is made ulates the kidneys to excrete K and recapture Na, decreasof chromaffin cells and is essentially a part of the autoing the blood K levels and increasing the Na levels.nomic nervous system. It produces the catecholamines Increased levels of sodium, in turn, increase blood volume epinephrine (adrenaline) and norepinephrine (noradrenaand pressure. Release of aldosterone is stimulated by line), as well as endorphins. These hormones play a major increased blood K levels, decreased Na levels, loss of role in exciting the sympathetic nervous system for what blood, and decreased blood pressure and volume. Control is commonly known as the fight-and-flight response. The of blood pressure is in part achieved through the renin-endorphins are natural painkillers and are secreted alongangiotensin system with angiotensin II stimulating theside epinephrine and norepinephrine. release of aldosterone.

HYPOTHALAMIC–PITUITARY–ADRENAL (HPA) AXIS AND BIOSYNTHESIS Cortisol is the main hormone produced by the adrenalOF ADRENAL HORMONES

CORTISOL

glands in response to various short- or long-term physical, psychological, and physiological stressful stimuli Stimulation and control of the hormonal production by the in conjunction with catecholamines from the adrenaladrenal gland are orchestrated by a feedback mechanism

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immune system that regulates the HPA axis (Marx, Ehrhart-Bornstein, Scherbaum, & Bornstein, 1998). The control of cortisol production is achieved by a negative feedback mechanism exerted by ACTH and cortisol. ACTH acts on the hypothalamus and decreases CRF production. Cortisol acts on both the hypothalamus and pituitary and decreases CRF and ACTH production. In the absence of stressful stimuli, cortisol production follows a normal circadian rhythm associated with sleep and wake cycles. Cortisol secretion is at its highest around 8 a.m. and gradually decreases, reaching its lowest point at midnight. Under prolonged stressful stimuli the brain overrides the normal negative feedback loop, constantly stimulating the adrenal cortex to produce cortisol. This disrupts the normal circadian rhythm of cortisol and results in a whole host of cortisol-related physiologic disorders, as well as hypertrophy of the adrenal glands. Increased cortisol levels are associated with accelerated aging, depression, schizophrenia, chronic fatigue syndrome, immune dysfunction, decreased REM sleep, obesity, hypertension, heart disease, and suppressed thyroid function. Figure 82.2 shows the pathway of cortisol synthesis in the adrenal cortex. This synthesis begins with the FIGURE 82.1 HPA axis and feedback loops. (Reprinted with conversion of cholesterol to pregnenolone, by the enzyme 20 α-hydroxylase, 22 hydroxylase, and 20,22 desmolase. permission of Great Smokies Diagnostic Laboratories.) In turn, pregnenolone (the mother of all hormones) may between the hypothalamus, pituitary, and adrenal glands. be converted into either sex hormones (androgens and This is known as the HPA axis. estrogens) or mineral and glucocorticoids, more likely A healthy HPA axis (Figure 82.1) is one that involvesproduced in the presence of chronic stress. an intricate interplay of positive and negative feedback Pregnenolone’ s conversion to cortisol involves a series loops that make up this marvelous homeostatic mechaof enzymatic reactions, which are, in turn, controlled by nism. The major players in this orchestra of hormonesACTH and other stimulants of the adrenal gland as disinclude cortisol, which is produced by the adrenal gland,cussed earlier. A genetic defi ciency of any of these adrenocorticotropic hormone (ACTH) produced by theenzymes can result in overproduction and underproducpituitary, and the corticotropin-releasing factor (CRF) pro-tion of the dependent hormones. duced by the hypothalamus. In addition to its regulation by the pituitary, ACTH is synchronized by counterregulation of CRF. A short-loopADRENAL GLAND DISORDERS negative feedback on CRF by ACTH also emanates from Adrenal gland disorders can be categorized into adrenothe hypothalamic–pituitary region. corticol hyper- or hypoactivity, resulting in severe excess The process starts with the release of the CRF from or deficiency of adrenal cortex hormones, respectively. the hypothalamus in response to physical, psychological, These conditions can be the result of pathological condiand physiologic stressors. CRF induces release of ACTH tions within the gland itself, pituitary gland, supporting or corticotropin from the anterior pituitary directly into glands, or can be iatrogenic in nature. the blood. ACTH acts on the cells of the zona fasiculata, stimulating cortisol production and release. ADRENOCORTICOL DEFICIENCY Activation of the HPA axis due to a given stimulus leads to a stress response, which modulates the immune Adrenocorticol deficiency is highlighted by a signifi response. The interactions between the HPA and the cant decrease in production of one or all adrenal horimmune system are characterized by a circuit, whichmones. This can be due to pathological conditions includes activation of the HPA-axis and initiation of the involving the adrenal gland itself or other causes. The stress response that, in turn, has immune-modulating patient’s presentation varies, depending on the affected properties, and a feedback mechanism derived from the hormones.

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FIGURE 82.2 The steroidogenic pathway.

Addison’s Disease

known as congenital adrenal hypertrophy. In this group of conditions the enzymes responsible for production of corPrimary adrenocorticol defi ciency involves inherent dis- tisol and aldosterone are deficient genetically, and dependease of the adrenal cortex and is also known as Addiing on the severity of their defi ciency can result in son’s disease. In Addison’ s disease all adrenal hormones decreased production of cortisol and aldosterone that can are affected but most pronounced are the effects of be chronic or life threatening. The enzymatic deficiency decreased cortisol and aldosterone. Clinical ndings fi also results in a buildup of aldosterone and cortisol preinclude decreased weight, malaise, and gastrointestinal cursors, which are converted to sex hormones, primarily upset. Cortisol defi ciency results in hypoglycemia and androgens. This results in premature puberty in male childecreased ability to handle stress, while decreased dren and virilism in female children. The decreased adrealdosterone results in decreased blood pressure and elecnal hormone production results in an overproduction of trolyte imbalance. Other ndings fi include increased ACTH by the pituitary gland, which causes hypertrophy ACTH production by the pituitary; decreased blood lev-of the adrenal gland. els of cortisol, aldosterone, and T4; and increased TSH. Increased pigmentation is another physical nding fi of Secondary Adrenocorticol Deficiency adrenocorticol defi ciency, which is due to increased production of ACTH and accompanying melatonin by theSecondary adrenocorticol deficiency is the group of dispituitary gland. orders wherein the adrenal gland’ s function is intact but While Addison’s disease is insidious, eventually it will does not receive appropriate stimulation for production result in severe deficiency of the adrenal hormones. This and release of its hormones. The most common cause of is known as Addison’ s crisis, a serious life-threatening this type of condition is decreased function of the pituitary emergency requiring immediate medical intervention. gland due to various causes, which results in decreased Autoimmune and iatrogenic factors are the leadingproduction of ACTH and, in turn, cortisol, while aldostercauses of Addison’ s disease in the Western countries,one’s production remains intact. whereas tuberculosis is the leading causative factor world- Disorders of the renin and angiotensin system due to wide. Other causes include metastases, adrenal hemorkidney disease and other causes are another rare type of rhage, hemochromatosis, adrenomyeloneuropathy, and secondary adrenocorticol defi ciency, which results in iatrogenic drug use. decreased production of aldosterone while cortisol production remains intact. Drug-induced adrenocorticol deficiency can occur as Inherent Errors of Metabolism a result of treatment with pharmaceuticals including Another cause of adrenocorticol deficiency is inherentMetyrapone, opDDD (Metiotane), Aminoglutethemide, errors of metabolism of the adrenal gland itself. It is alsoKetocoazole, and Etomidate.

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of “just being sick.” A triad was always present in this syndrome. After exposing rats to various types of stress This group of disorders is characterized by excess producthey were sacrificed. Dissection revealed (1) adrenal cortion of the adrenal hormones aldosterone and cortisol. tex enlargement; (2) atrophy of the thymus, spleen, lymph nodes, and all other lymphatic structures; and (3) deep Cushing’s Syndrome bleeding ulcers in the stomach and duodenum. Cushing’s syndrome is characterized by excess cortisol in Selye classified the progression of stress on the body the circulation due to cortisol-producing adrenal tumors,and its influence on the adrenal glands. The classification “ eneral Adaptation Syndrome” (GAS) ACTH-producing pituitary gland tumors, or iatrogenic is called the G (Selye, 1956). Three stages exist including alarm, resiscauses. When the excess in cortisol production is due to tance, and finally exhaustion. adrenal tumors, excess androgens will also be present. When excess cortisol is due to ACTH-producing pituitary Alarm Reaction : The alarm reaction is characterized tumors the condition is known as Cushing’ s disease. Iatroby surprise and anxiety and is considered to be genic Cushing’ s is the most common type and is the result a general call to arms. The adrenal glands will of treatment by glucocorticoids for their immunosuppressecrete hormones, i.e., epinephrine, norepisive or anti-inflammatory benefits. nephrine, and hydrocortisone. This phase is Cushing’s syndrome is characterized by a round or extremely rapid and the mechanism by which moon face, Buffalo hump, central obesity, thin arms and a seemingly petite mother lifts a car to get her legs with muscle wasting, testicular atrophy and menstrual child out from under it. disturbances, high blood pressure, osteoporosis with increased risk of fractures, and immunosuppression result- Resistance : With continuation of stress the body ing in increased susceptibility to infections. Mental moves into this second phase, in which the body changes may include depression, insecurity, uncertainty, prepares to continue and adapt to the prolonged and possible psychosis. fight ahead. Adrenal hypertrophy and other factors of the stress triad are found in this stage. Conn’s Syndrome An individual can respond and meet the demands of the stress as long as this stage conConn’s syndrome is characterized by elevated levels of tinues. If the adaptive stress is resolved, a rapid aldosterone and is almost always the result of aldosteronereturn to the resting state can be achieved. producing adrenal tumors, but on rare occasions it can Exhaustion: When the adrenal glands can no longer also be due to renin-producing tumors. Elevated levels of meet the demands placed on them due to proaldosterone result in increased blood pressure and longed stress, this stage is evident. This is then hypokalemia, which can lead to other clinical manifestareferred to as adrenal maladaptation, or hypertions (Cotran, Jumar, & Robbins, 1989; Jeffcoate, 1993; adaptosis, a term credited to Dilman and Dean Berkhow & Fletcher, 1987). (1992) (Dilman, you may recall, is responsible for the neuroendocrine theory of aging). HyperPheochromocytoma adaptosis is considered by some to be a precursor to Cushing’s syndrome. It is characterized by Pheochromocytoma is the only disease of the adrenal medulla that is caused by a tumor, which produces an prolonged exposure to excess cortisol levels and excess of catecholamines. Symptoms of this disease is caused by the loss of hypothalamic sensitivity include periodic high blood pressure, nausea, excessive to the inhibitory effects of cortisol (Dilman, sweats, pounding-type headache, anxiety, vomiting, and 1981). It is the chronically hyperactive HPA axis palpitations. that causes these symptoms. These same high levels of stress have been shown by Selye (1976) to lead to many of the diseases of aging. Robert THE SCIENCE OF STRESS Sapolsky, the author of Why Zebras Don’t Get Ulcers also recognizes the role of these hormones A Canadian professor, Hans Selye, M.D., is responsible in disease (http://www-med.stanford.for pioneering the field of stress research. For this reason edu/school/Neurosciences/faculty/sapolhe was given the title “the father of stress. ” His writings on the subject date back to the 1930s, and he is credited sky.html, 2000; Sapolsky, et al., 1987). Additionally, chronic health problems, long-term with writing over 1700 papers and 39 books on the subject. nutritional deficiencies, and long-term emotional As the undisputed expert on the subject, he observed as early as 1925 that common symptoms are present in problems can all lead to the state of adrenal many diseases. He came to classify this as the syndrome exhaustion.

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Researchers have identified eight physical indicatorscortisol and the concentration of DHEA is 1/20th that of of an individual’s stress load (McGwen, 1998). Stressful cortisol. DHEA and its sulfate have been shown to be life events such as divorce, job loss, family arguments,interconvertable. Testosterone is purported to be five times and even traf fic jams, in addition to daily maladaptation, more potent than androgens. DHEA-S is primarily proall add to stress. Among the stress indicators are duced from DHEA in the adrenal gland and liver. Several organs that are targets of androgenic and estrogenic sex hormones convert DHEAS back to DHEA. 1. Increased blood pressure The plasma half-life of DHEA is relatively short, at 2. Suppressed immunity to disease just under 30 minutes. It is for this reason that over 95% 3. Increased fat around the abdomen of circulating DHEA is in the form of sulfate (Berdanier, 4. Weak muscles Parenta, & McIntosh, 1993; Rosenfeld, Rosenberg, Fuku5. Bone loss shima, & Hellman, 1975). 6. Increases in blood sugar In females, androgens are the main source of male sex 7. Increases in cholesterol levels steroids. In sexually mature humans, ACTH stimulates the 8. Increases in steroid hormones, i.e., cortisol secretion of adrenal sex steroids. How our bodies react by manufacturing stress hor- DHEA-S is the major source of androgens for the fetus mones is ostensibly even more significant than how webefore birth. DHEA-S is detectable by age 7 and serum of both DHEA and its sulfate appear to be feel about the events. When an episode of acute stressconcentrations is highest in the third decade of life (Bonney, et al., 1984). experienced, cortisol is secreted to protect us by activating, through a complex chain of events, the body’ s defenses. Levels then begin to gradually decrease and continue to Acute stress (in the sense of “fight” or “flight” or major drop. By the age of 70 or 80 years, values have plummeted life events) and chronic stress (the cumulative load ofto approximately 20% of peak values in men and 30% in woman (Bonney, et al., 1984; Rotter, Wong, Lifrak, & minor day-to-day stresses) can both have long-term conParker, 1985). sequences. DHEA has a very short half-life (less than 30 minOne of Selye’ s first observations of the general adaputes); therefore, it is stored as its sulfated form, DHEAtation syndrome was that animals under extended stress S, which makes up to 95% of its circulating levels. DHEAdeveloped sexual derangements. Intense stress causes S can be readily converted to testosterone, estrione, and young animals to cease to grow and lactating females to produce no milk. Prolonged stress may be partially orestradiol and plays a role in a variety of physiologic processes including protein synthesis and thyroid hormone totally responsible for amenorrhea in female athletes who are under intense training (Brooks-Gunn, Warren, &function (Fitzgerald, 1992). Hamilton, 1987). Recent research reports that wounds heal Adrenal insufficiency leads to a deficiency of DHEA. In a study published in the New England Journal of Medmore slowly when patients are under psychological stress (Kiecolt-Glaser & Glaser, 2000). With constant sympa-icine oral doses of 50 mg per day of DHEA or placebo thetic activation the immune system becomeswere administered over a period of 4 months to women who were adrenal insuf ficient. They were evaluated for depressed.Years of scrutiny have revealed that never-ending stressors unfavorably influence brain development. effects on well-being and sexuality, as well as on serum hormone and other biochemical values (Arlt, Callies, Current research finds that those women who have et al., 1999; Oelkers, 1999). When it came to scores of higher levels of cortisol (the stress hormone) tend to have more abdominal fat. Dr. Elissa Epel (2000) of UCLA depression, anxiety, general well-being, and the physical stated,“Psychological stress may increase abdominal fatand psychological aspects of sexuality, these adrenally in healthy people who have normal resting levels of cor-deficient women were shown to have significant positive effects from DHEA supplementation (Oelkers, 1999). tisol and are of average weight. ” DHEA (12.5 to 50 mg/day taken in the a.m.) and pregnenolone (10 to 100 mg/day taken in the a.m.) have been NEUROENDOCRINE THEORY OF AGING recently propelled to the forefront by their over-thecounter availability and more is being published daily DHEA (Hornsby, 1997). DHEA has been touted as being effective Dehydroepiandrosterone (DHEA), a 17 keto-steroid andfor immune dysfunction, longevity, obesity, and depresDHEA-S, its more powerful sulfate, are the major adrenalsion. The verdict is not conclusive on all these possible androgens. Secreted by the adrenal cortex in the innermost usages, but they clearly are showing promise. The stronlayer, the zona reticulosa, this steroid, which is largelygest evidence exists for its use with hormone replacement produced from the precursor pregnenalone, has been and for anti-aging. One marker of aging is a decrease in implicated as a possible anti-aging hormone. SerumGnRH (gonadotrophin-releasing hormone) that may result concentrations of DHEA-S are 20 times that of serumin loss of reproductive function. This loss of function can

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FIGURE 82.3 Lab report of salivary cortisol and DHEA. (Reprinted by permission of Great Smokies Diagnostic Laboratory.)

be reversed with a short administration of DHEA (Li, In a related study done by the National Cancer InstiGivalois, & Pelletier, 1997). tute (Sephton, Sapolsky, Kraemer, & Spiegel, 2000), salDHEA is distinctive to primates. It is found in high ivary cortisol levels were checked four times daily in 104 patients with metastatic breast cancer for a period of 3 levels only in humans, chimpanzees, and gorillas, and less consecutive days. Patients with “flat” rhythms, an indicaso in monkeys. Several articles talk about the anti-obesity effects oftion of a lack of normal variation, were found to have DHEA. “The anti-obesity function of DHEA is not simply earlier mortality along with lower levels of natural killer one of inhibiting fat synthesis and deposition but is one(NK) cells and suppressed activity of those cells. of affecting a number of pathways that contribute to the A nine-fold increased risk of recurrent breast cancer maintenance of the isoenergetic state rather than the prohas been associated previously with extreme or severe motion of positive energy balance” (Berdanier, Parente,stress (Ramirez, 1989). & McIntosh, 1993).

LABORATORY TESTING THE STRESS-IMMUNITY CONNECTION

SALIVARY TESTING

It has long been proposed that the more stress on the body, irrespective of source, the more likely the immune systemA simple test to determine hormonal deficiency and imbalance is gaining widespread popularity. Saliva testing is will be depressed. Elevated corticosteroids are known to unique in that it measures the unbound hormone, which have a significant effect in reducing immune defenses. In is that portion available to the cells of the body. About 1 a recent study (Creuss, et al., 2000), 34 women with stage I and II breast cancer were divided into one of two ran-to 10% of the steroids in the blood are in unbound, or free domized groups. One group received cognitive-behavioralform. Because only unbound steroids can freely diffuse into various target tissues in the body, they are the only stress management; the other group was placed on a waiting list. After 10 weeks of stress management, relaxationhormones considered biologically active. Because it is the training, and cognitive therapy, patients from the treatmentmost active part of the hormone, saliva testing is a good way to analyze how hormones affect your health. group noted significant changes that included a greater sense of purpose and meaning in their lives, better family One of its main advantages is in the ease of collection. relationships, and shifted priorities. Not surprisingly, theirIt is noninvasive, easy, convenient, painless, and can be done cortisol levels had dropped and were significantly lowerat home by the patient in the privacy of his or her own (p < 0.03) when compared with the waiting-list patientshome. When blood work is utilized to ascertain adrenal who did not receive this care. hormonal levels, those same levels could easily become

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During the Ceausescu regime in Romania thousands of children became orphaned as a by-product of his malevolence. Neglect that included being left alone in cribs or playpens, absent any stimulation and interaction, resulted in withdrawn, unpredictable children, who were prone to rocking in place and staring blankly at visitors. Harvard researchers have documented their later development, which included dif ficulty coping with normal human interaction and touch (Holden, 1996; DiPietro, 2000). Simply being touched and held throughout the first FIGURE 82.4 Linear correlation between salivary and serum few years of infancy may well set up constructive stresshormones. (Reprinted with permission of Great Smokies Diagresponse patterns that last a lifetime. nostic Laboratory.) elevated if the patient has any fear about injections, thus OFFICE TESTING giving elevated and inaccurate information. Results retrieved in a stress-free environment will likely be the mostRAGLAND’S SIGN sensitive. Figure 82.4 illustrates a comparison of hormone A simple test to help assess the status of the adrenal glands levels in saliva vs. serum, demonstrating a direct correlation. can be performed in an fice-based of setting as part of a When evaluating adrenal hormones, a 24-hour pattern thorough examination. Instead of simply taking a blood of cortisol is examined at four different times, while pressure reading while the patient is in the seated posture, DHEA is measured on two occasions in the same day. begin by taking a reading while the patient is supine on Saliva samples are not just being utilized for DHEA the table. After recording the reading, immediately repeat and cortisol; they are being employed for measuring many the blood pressure in the standing position. Under normal hormones including estradiol, progesterone, testosterone and melatonin. Our hormones control many importantcircumstances, the systolic blood pressure should rise at psychological and physiological roles including our resis-least 8 mmHg. An abnormal drop in the systolic pressure is considered positive for adrenal hypofunction and this tance, sleep patterns, and longevity. Thus, these tests prodrop is referred to as postural hypotension. vide physicians with accurate, dependable data that can be influential in prescribing hormones with confidence. Mark Flinn, of the University of Missouri, has been NUTRITIONAL CONSIDERATIONS studying the relationship that exists between health in In the context of this chapter it would be virtually imposchildren and stress. He maintains that the two best ways sible to enumerate and elucidate all the potentially beneto measure stress are by measuring the adrenal hormone ficial supplements that aid in restoring a more properly cortisol in saliva and by asking questions. This study has functioning adrenal gland. We endeavor to discuss merely amassed data over the course of 13 years. In that time those that appear to be most advantageous and have the Flinn has collected more than 25,000 saliva samples from 287 children who live in the same rural Caribbean islandheaviest weight of published literature. village. An average of 96 separate samples were collected from each child. In addition, Flinn has tracked their growth,ADAPTOGENS checked their health records, measured their levels of resisThis group of substances helps the body adapt to stress, tance, watched, listened, and asked questions in order to be and has been shown to reduce the damage of the stress very aware of what was happening in each of their lives. response, maintain homeostasis during chronic stress, He concludes that family matters more than anythingreduce most evidence of the alarm stage, and delay the else in a child’s life. Stress hormones course through aexhaustion phase. Royal Bee Jelly (one of the world’ s child’s system when a family has problems. “In the vil- richest sources of pantothenic acid needed for the adrenal lage, illness among children increases more than twofold glands) is an adaptogen; however, the most widely following significant stress, ” says Flinn (Small, 2000). researched are Siberian ginseng Eleutherococcus ( sentiCompilation of saliva subsequent to significant con-cosus) and licorice Glycyrrhiza ( ) (Ritchason, 1995). flict within a group of children consistently failed to show high levels of cortisol, whereas one of those same children, Licorice returning home late from shopping a couple weeks later, had salivary cortisol levels that rose 60% above normal.Licorice is a perennial herb native to the Mediterranean This study gives scientific confirmation to the importanceregion, central to southern Russia, and Asia Minor to Iran, of how emotional stress contributes to physical illness. now cultivated throughout Europe, Asia, and the Middle

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East (Bruneton, 1995; Karnick, 1994; Leung & Foster,element causing inhibition of peripheral metabolism of 1996). It is one of the most widely used medicinal herbscortisol that binds to mineralocorticoid receptors in like and is found in numerous traditional formulas (Leung &fashion to aldosterone. Foster, 1996). Licorice is one of the most extensively Two hypotheses for licorice’ s mechanism of action researched medicinal and food plants. Licorice root has have been suggested by research: been used therapeutically for several thousand years in both Western and Eastern systems of medicine (Leung & 1. The binding of glycyrrhetinic acid to mineraloFoster, 1996). corticoids receptors, and/or The Latin name for licorice isGlycyrrhiza glabra. 2. Blocking the action of 11-beta-hydroxysteroid Dioscorides, a 1st-century Greek physician is responsible dehydrogenase. for its genus name, Glycyrrhiza,which comes fromglukos (sweet) andriza (root) (Foster & Tyler, 1999). The pharRecent publications advocate that both hypotheses macopeial name for licorice is Liquiritiae radix and it is may be implicated, particularly with the substantiation known by other names including Liquorice, Gancao,that the blocking of 11-beta-hydroxysteroid dehydrogesweet root, Yasti-madhu and Glycyrrhiza. nase is short term and that subsequent to its occurrence, While the first recorded cultivation of the herb was in the pseudoaldosteronism is directly linked to increased the 13th century by Piero de Cresenzi from Bologna, itsplasma concentration of licorice metabolites and their use was first documented on Assyrian clay tablets ca. 2500 binding to mineralocorticoids receptors. 11-beta-hydroxB.C.E for the treatment of coughs and relief of the unwel-ysteroid dehydrogenase usually metabolizes glucocorticome effects of laxatives. The Greeks used it ca. 372 to coids into inactive compounds rapidly, thereby controlling 287 B.C.E. for asthma, dry coughs, and all pectoral dis-glucocorticoids’access to mineralocorticoids and glucoeases. In China, first mention of the herb was inShen the corticoids receptors. Increased glucocorticoid concentraNong Ben Cao Jing (ca. 25 C.E.). In addition to its advan- tion in mineralocorticoid responsive tissue results from tageous properties as an expectorant and antitussive, the the licorice thwarting inactivation of hydrocortisone. This Chinese pharmacopeia notes its antispasmodic relief on results in glucocorticoids occupying mineralocorticoid gastrointestinal smooth muscle and its desoxycorticosreceptors and producing a mineralocorticoid response that terone-like action (Tu, 1992). Further to its other benefi-is demonstrated by hypertension and increased sodium cial effects, the current ayurvedic pharmacopoeia reports retention (Chandler, 1997). it as an adrenal agent (Karnick, 1994). Licorice root and Extreme quantities of licorice consumption (more extracts as well as fluid and solid are in the U.S. National than 20 g per day) have elevated concerns about the potenFormulary (1985). Studies have investigated and docu- tial for glycyrrhizin in licorice producing pseudoalmented its favorable effects as an anxiolytic (Chen, Hsieh, dosteronism (excess levels of aldosterone), which may & Lai, 1985). The British Herbal Compendium reported cause symptoms of headache, hypertension, lethargy, its actions as an anti-inflammatory, expectorant, demul-potassium loss that upsets the balance of sodium and cent, and adrenocorticotropic (Bradley, 1992). potassium and possible cardiac arrest. The pseudoaldosHarvesting comes from cultivation of roots that are 3terone-like effects are generally attributed to the glycyrto 4 years old. The roots and stolons contain glycyrrhizin,rhizic acid. Of note, within several weeks of cessation any also called glycyrrhizic or glycyrrhizinic acid (5 to 9% by symptoms of hyperaldosteronism disappear (Mantero, weight), which is believed to be some 50 times sweeter1981). A deglycyrrhizinated licorice (DGL) preparation than sucrose. That same sweet taste is lost or reduced has been developed that provides most of the therapeutic when in an acidic medium (Leung & Foster, 1996). benefits while reducing risk. Licorice is a natural way to supplement the body’ s Usage should be limited to no more than 4 to 6 weeks endogenous cortisol production, giving the adrenals aat a time to prevent potentiation of glucocorticoids and well-needed rest. Dosage is 25 to 100 mg/day. Pharmamineralcorticoids. Prolonged use with high doses may copeial-grade licorice root must contain no less than 4%result in water and Na retention and K loss. This may be glycyrrhizic acid, calculated in the dried root. accompanied by edema, hypertension, and hypokalemia. Chemically speaking, licorice root contains triterpe- It is not recommended while pregnant and is contraindinoid saponins (4 to 24%), mostly glycyrrhizin, along with cated with liver cirrhosis, hypertonia, hypokalemia, severe a mixture of potassium and calcium salts, flavonoids (1%),kidney insufficiency, and cholestatic liver disorders. amines (1 to 2%), asparagines, choline, and betaine; amino acids; 3 to 15% glucose and sucrose; starch (2 to 30%); Ginseng polysaccharides; sterols; resin and volatile oils. Research done by Heikens, Fliers, Endert, Ackermans, and vanThe Latin name for ginseng Panax is ginseng.Its pharMontfrans (1995) proposes that the hydrolytic metabolite ofmacopeial name is Ginseng radix. Other names for it glycyrrhizic acid, glycyrrhetenic acid, is the major dynamicinclude Chinese ginseng, Korean ginseng, true ginseng

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The Commission E monographs from Germany noted and Asian ginseng. The genus name Panaxis derived from the Greekpan (all) andakos(cure), meaning cure-all. Like that the resistance of rodents was enhanced when various licorice, ginseng’ s therapeutic uses were recorded overstress models such as coldness and immobilization tests were performed. 2000 years ago in the oldest comprehensive material medSiberian ginsengEleutherococcus ( senticosus ) is in ica, Shen Nong Ben Cao Jing . Ginseng is a slow-growing perennial herb native tothe same family but contains eleutheros instead of ginsenosides. It is also considered to be adaptogenic. the northeastern mountain forests of China, Korea, and British the far eastern portions of Russia. It is cultivated exten- Use is contraindicated in hypertension. The sively in these same countries. Flowering of the plantHerbal Compendiumcontraindicates use during pregnancy; however, the Commission E report fails to begins in the fourth year and its roots take 4 to 6 years until the plant reaches full maturity. Many types andcorroborate that. Ginseng is known to have estrogenic activity. It could negatively affect estrogen-dependent grades of the herb exist. diseases in woman, i.e., endometriosis, brocystic fi Pharmacopoeia grade ginseng from both China and breasts, or breast cancer. Japan should be collected from the dried matured root Dosage for the root is between 1 and 2 g/day for as in the autumn. The rootlets must be removed. Confi rmation of botanical identity is confi rmed by thin-layer chro- long as 3 months at a time. Tinctures, fluid extracts, stanmatography (TLC) in addition to micro- and macro- dardized extracts, and decoctions are also available and dosage is dependent upon the source. Ginseng needs to scopic examination. Asian medicine uses dried ginseng as a tonic tobe taken for at least 1 month before any positive effects revitalize and replenish vital energy (qi). Traditional are likely to be felt. uses include as a prophylactic aid to restore resistance, Ginseng along with another adaptogenic herb, ashwagandha, has been suggested to influence adrenal hormone reduce vulnerability to sickness, and encourage health activity by helping to support normal HPA function and longevity. The origins of its activity are based on whole body(Brown, 1996). Other herbs shown to be of benefit to the adrenal effects rather than specifi c organs and systems, which glands include astragalas, bayberry, borage, burdock, provides support to the time-honored view that ginseng kava, kelp, parsley, and rose hips (Leung & Foster, 1996). is a tonic that can invigorate the functioning of the organism as a whole. Ginseng is in the national pharmacopoeVITAMINS AND NUTRIENTS ias of several European countries, Russia, and China. In the United States, it has been used as a stand-alone herb Vitamin C reduces the effects of chronic stress by decreasor as the main ingredient in a wide range of tonics, anding cortisol production (American Chemical Society, energy and immunostimulant supplements. Over the1999; Nathan, van Droux, & Feiss, 1991). A high dietary course of the last half-century, numerous scientifi c studintake of vitamin C may even help reduce the effects of ies of varying quality have been published on ginsengchronic stress by inhibiting the release of stress hormones. (Foster & Chongxi, 1992). Ten clinical trials have inves- Ascorbic acid when given orally (1 g twice daily) also tigated the ef ficacy of ginseng on physical stress andbuffered exogenous ACTH-induced increases in cortisol. psychomotor functions. An additional function of ascorbate in the adrenal glands One such study by Caso Marasco et al. reported on is as a protective compound for cytochrome (Hornsby, its ability to improve quality-of-life in persons subjected Harris, & Aldern, 1985). to high stress (Caso Marasco, Vargas Ruiz, Salas Villago- Evidence indicates adrenal cortex function is compromex, & Begona Infante, 1996). This same study foundmised in the event of a deficiency of vitamin B5 derivathat when ginseng was added to the base of a multivitamin tives and metabolites (Gregory & Kelly, 1999). Alternait improved subjective parameters in a population exposed tively, the administration of pantethine in several to high physical and mental stress. This suggests an adapexperimental animal models appears to enhance adrenal togenic effect to this combination. function (Kosaka, Okida, Kaneyuki, et al., 1973; Onuki & The biologically active constituents in P. ginseng Hoshino, 1970). are made up of a fusion of triterpene saponins known Lipoic acid, known as the universal antioxidant, as ginsenosides. Ginsenosides are found nowhere else appears to prevent the accretion of catecholamines in carin nature. The two main ginsenosides, Rb1 and Rg1,diac tissue secondary to stress. It also augments the abocorrespondingly suppress and stimulate the central nerlition of catecholamine degradation products (Fomichev & Pchelintsev, 1993). vous system. It is proposed that these contrasting actions may contribute to the adaptogenic portrayal of Other nutrients that demonstrate possible effects this herb and its ostensible capacity to balance corporal include tyrosine, phosphotidylserine (PS), and plant stefunctions. rols and sterolins.

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TABLE 82.2 Associated Symptoms and Consequences of Impaired Adrenals • • • • • • • • • • • • • • • • •

BIOFEEDBACK

Low body temperature Weakness Unexplained hair loss Nervousness Difficulty building muscle Irritability Mental depression Difficulty gaining weight Apprehension Hypoglycemia Inability to concentrate Excessive hunger Tendency toward inflammation Moments of confusion Indigestion Poor memory Feelings of frustration

• • • • • • • • • • • • • • • • •

Alternating diarrhea and constipation Osteoporosis Auto-immune hepatitis Auto-immune diseases Lightheadedness Palpitations (heartfluttering) Dizziness that occurs upon standing Poor resistance to infections Low blood pressure Insomnia Food and/or inhalant allergies PMS Craving for sweets Dry and thin skin Headaches Scanty perspiration Alcohol intolerance

In a recent study in the Journal of Behavioral Medicine, progressive relaxation was shown to be the most Biofeedback utilizes audiovisual input to teach patientseffective means of reducing the stress response when comto control their own reactions to pain, stress, and similarpared to music, attention control, and silence, which were noxious stimuli. Patients are able to visualize graphicfound to be effective, but less so (Scheufele, 2000). representations of the effects of noxious stimuli on var- Sleep is an often overlooked piece of the health ious physiologic responses such as blood pressure, heart puzzle that has recently been shown to be of major rate, skin temperature, and sweating on computer monsignificance. A new study in the Journal of the Ameritors or auditory input. Then through trial and error sub-ican Medical Association(JAMA) reports that sleepjects learn to control these physiological responses in related hormone imbalances often start to surface in the order to decrease the negative effects of the noxious mid-1930s (Cauter, Leproult, & Plat, 2000) 149 healthy stimuli on their bodies. men between the ages of 16 and 83 were involved in Biofeedback has had particular success when utilized this sleep study. By the time the men reached 36 to 50 in the treatment of chronic pain and stress management years of age the amount of sleep spent in the most (Kong, Lim, & Oon, 1989). Typically, a series of five to restful state (slow wave) had decreased by almost 80% ten treatments are given. from the late teens and early 20s. Sleep deprivation on any given night results in increased levels of cortisol and decreased growth hormone secretion the subseIMPROVING ADRENAL HEALTH quent night. The relationship between sleep quality and WITH LIFESTYLE hormone function may very well be a two-way street: lack of adequate sleep may interrupt hormonal equilibThe most common reason why the adrenals are impaired rium and at the same time hormonal imbalances can is unresolved emotional stress. Attend to this first. Recogtrigger sleep dif ficulties. nize concealed causes of stress. These could include toxins In a related editorial in the same JAMA issue, Blackfrom solvents, pesticides, yeast, dysbiosis, parasites, strucman (2000) notes that early intervention (with hormonal tural misalignments, etc. Optimize the diet. Also, get appropriate amounts oftesting) is the best method for screening. sleep. Because repair and rest occur between 11 p.m. and When it comes to dealing with stress, humor plays a significant role that should be acknowledged and encour1 a.m. these tools should be optimized. From an acupuncaged. Humor helps us make sense of, understand, and cope ture point of view, the gallbladder releases toxins between with reality and serves as nature’ s biofeedback, stressthese same 2 hours. If you are awake, they can back up control system (Woodhouse, 1993). into the liver.

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Massage, avoidance of food allergies and hypersensithings including cuddling, touching, and holding signal tivities, proper diet, and changed attitudes are just some the beginnings of a healthy adrenal gland. Experiments of the positive tools that can be utilized in an effort towith rat pups that had especially attentive mothers found improve lifestyle. Learning stress management is a quin-they have more of a certain type of receptor on the surface tessential tool in reducing adrenal tension. of the hippocampus than in the relatively neglected group of rats. These specific receptors responded to a cortisolEXERCISE like hormone. The fact that more of these corticosteronereceptors were present presages that the brain would be The positive effect exercise plays in reducing daily stressmore sensitive and ficient ef in utilizing this hormone to cannot be overemphasized (Carmack, et al., 1999). terminate the stress response. Among working adults, physical activity performed durThe conventional medical establishment has frowned ing leisure time was found to decrease perceived stress upon natural approaches to managing adrenal function, (Aldana, Sutton, Jacobson, & Quirk, 1996). generally because there has been no apparent relationship Exercise is a great stimulator of positive mental and established between many illnesses and waning adrenal physical well-being. It increases oxygen uptake by red function. More often than not, adrenal decline is perceived blood cells, lymphatic circulation, excretion of toxins, and as a side effect of the disease process instead of as the has a profound positive effect on one’ s self-image. Exerdirect cause. It may be borne out that the decline of the cise also increases endorphin production, which can indiadrenal gland is, in fact, both an indirect cause and a side rectly reduce stress and pain throughout the body. Caution effect of numerous persistent and acute infirmities. should always be exerted not to over exercise, which will overstress the body, thus reversing the beneficial effects. The sum of all the stresses during the course of a Clinical experience strongly suggests that exercise islifetime can contribute to the aging process. The neuroan effective way for stressed individuals to enhance theirendocrine theory of aging validates the paralleling decline sense of self-control and coping self-worth (ACSM). Theof the endocrine glands and the aging process. It further bears out that restoring more youthful hormonal levels to importance of regular aerobic activity as a means of dealing with stress is well documented. In addition to severalthese same organs can slow down, and in many instances reverse, some of the effects of that same aging process. positive effects already mentioned, it has been shown to reduce the cardiovascular impact of emotional stressors Profoundly potent herbs, along with certain vitamins including ascorbic acid, vitamins B1 and B6, the co(Sotile, 1996). Other forms of exercise that increase relaxation andenzyme forms of vitamin B5 (pantethine) and B12 mental focus include yoga and Tai Chi Chuan. The term(methylcobalamin), the amino acid tyrosine, and other “ relaxation training” has been used to describe thesenutrients such as lipoic acid, phosphotidylserine, and plant types of intervention. Other relaxation training tech- sterol/sterolin combinations (Kelly, 1999; Shelygina, Spivak, Zaretskii, et al., 1975). DHEA and pregnenalone niques are self-hypnosis, meditation, breathing exercises, supplementation, and a healthy lifestyle that includes regand biofeedback. Many believe that combining more than one type ofular exercise, proper rest, humor, de-stressing the nervous system and energy flows of the body through chiropractic relaxation training increases their effectiveness. and acupuncture, progressive relaxation, and biofeedbackmake up the foundation of a prescription for a strong and CONCLUSIONS vibrant adrenal gland. In the absence of serious disease, tumors, or other pathology, there exists a state of adrenal overuse that is brought on by difficulty dealing with the increasing stresses of life. REFERENCES Every human has a different adaptational capacity (i.e., 6/18/2000 http://www-med.stanford.edu/school/Neurosciences tolerance to stress). Irrespective of the stressor, the /faculty/sapolsky.html. response they elicit from the body is very similar, the most ACSM’s resource manual for guidelines for exercise testing and common being from emotional stimuli. prescription (3rd ed., p. 550). Philadelphia: Lippincott Recent advances in laboratory tests utilizing saliva Williams & Wilkens. that are both easy and convenient have been developedAdrenal to maladaptation syndrome. (1998). VRP Nutritional help with diagnosis. Early testing, as promulgated by News,12, 5. Blackman (Scheufele, 2000), is the first line of defense inAldana, S.G., Sutton, L.D., Jacobson, B.H., & Quirk, M.G. maintaining a stronger endocrine system. (1996). Relationships between leisure time physical A healthy endocrine system starts essentially at the activity and perceived stress. Perceptual Motor Skills, embryologic level. From the time of birth the simplest of 82(1), 315–321.

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Current mediArlt, W., et al. (1999). Dehydroepiandrosterone replacement inFitzgerald, P.A. (1992). Adrenal cortex physiology. cal diagnosis and treatment (p. 982).MA Lange Publishwomen with adrenal insuf ficiency.New England Journal ers. of Medicine,30, 341(14), 1013–1020. Berdanier, C.D., Parente, J.A., Jr., & McIntosh, M.K. (1993). IsFomichev, V.I., & Pchelintsev, V.P. (1993). The neurohumoral dehydroepiandrosterone an anti-obesity agent? Federasystems of patients with ischemic heart disease and tion of American Societies for Experimental Biology under emotional pain-stress: The means for their pharJournal, 7(5), 414–419. macological regulation.Kardiologiia, 33, 15–18. Berkhow, R., & Fletcher, A.J. (1987). The Merck manual(15th Foster, S., & Tyler, V.E. (1999). Tyler’s honest herbal: A sensible ed.). Whitehouse Station, NJ: Merck. guide to the use of herbs and related remedies . New Blackman, M.R. (2000). Age-related alterations in sleep quality York: Haworth Herbal Press. and neuroendocrine function: Interrelationship and Foster, S., & Chongxi, Y. (1992). Herbal emissaries: Bringing implications.Journal of the American Medical AssociChinese herbs to the West (pp. 102–112). Rochester, VT: ation, 284(7), 861–868. Healing Arts Press. Bonney, R.C., et al. (1984). The interrelationship betweenGregory, S., & Kelly, N.D. (1999). Nutritional and botanical plasma 5-ene adrenal androgens in normal women. interventions to assist with the adaptation to stress. Journal of Steroid Biochemistry, 20(6A), 1353–1355. Alternative Medicine Review, 4(4), 249–265. Bradley, P.R. (Ed.). (1992). British herbal compendium (Vol. 1.) Heikens, J., Fliers, E., Endert, E. Ackermans, M., & van MontBournemouth: British Herbal Medicine Association. frans, G. (1995). Liquorice-induced hypertension — a Brooks-Gunn, J., Warren, M.P., & Hamilton, L.H. The relation new understanding of an old disease: Case report and of eating problems and amenorrhea in ballet dancers. brief review. Netherlands Journal of Medicine, 47(5), Medicine and Science in Sports and Exercise, 19, 1. 230–234. Brown, D. (1996, Summer). Licorice root: Potential early inter- Holden, C. (1996). Child development: Small refugees suffer the vention for chronic fatigue syndrome. Quarterly Review effects of early neglect. Science,274, 1076–1077. Nature and Medicine,95–97. Hornsby, P.J. (1997). DHEA: A biological perspective. Journal Bruneton, J. (1995). Pharmacognosy, phytochemistry, medicinal of the American Geriatrics Society, ,45 1395–1401. plants. Paris: Lavoisier Publishing. Hornsby, P.J., Harris, S.E., & Aldern, K.A. (1985). The role of Carmack, C.L. (1999).Annals of Behavioral Medicine, 21(3), ascorbic acid in the function of the adrenal cortex: Stud251–257. ies in adrenocorticol cells in culture, Endocrinology, Caso Marasco, A., Vargas Ruiz, R., Salas Villagomez, A., & 117(3), 1264–1271. Begona Infante, C. (1996). Double-blind study of a Ipel, E. (2000, September).Psychological Medicine,62, multi-vitamin complex supplemented with ginseng 623–632. extract. Drugs under Experimental and Clinical Jeffcoate, W. (1993).Lecture notes on endocrinology , 5th ed. Research, 22 (6), 323–329. Blackwell Scientific Publications. Cauter, E., Leproult, R., & Plat, L. (2000). Age-related changes in slow wave sleep and REM sleep and relationship withKarnick, C.R. (1994).Pharmacopoeial standards of herbal plants (Vols. 1–2). Delhi: Sri Satguru Publications. growth hormone and cortisol levels in healthy men. Kelly, G.S. (1999). Nutritional and botanical interventions to Journal of the American Medical Association, 284(7), assist with the adaptation of stress. Alternative Medicine 861–868. Review, 4(4), 249–265. Chandler, R.F. (1997). Glycyrrhiza glabra. In P.A. De Smet, K. Keller, & R. Hansel,Adverse effects of herbal drugs Kiecolt-Glaser J., & Glaser, R. (2000, April 15). Presentation to the British Psychological Society. (Vol. 3). New York: Springer Verlag. Chen, H.C., Hsieh, M.T., & Lai, E. (1985). Studies on the suan-Kong, D.S., Lim, L.J., & Oon, C.H. (1989). Biofeedback and stress management strategies, Annals of the Academy of zaorentang in the treatment of anxiety. PsychopharmaMedicine, Singapore, 18(3), 261–265. cology (Berlin),85(4), 486–487. Cotran, R.S., Kumar, V., & Robbins, S.L. (1989). Robbins patho- Kosaka, C., Okida, M., Kaneyuki, T., et al. (1973). Action of pantethine on the adrenal cortex of hypophysectomized logic basis of disease (4th ed.). W.B. Saunders. rats. Horumon to Rinsho,21, 517–525. Creuss, D.G., et al. (2000). Cognitive-behavioral stress manageEncyclopedia of common natment reduces serum cortisol by enhancing positive con-Leung, A.Y., & Foster, S. (1996). ural ingredients used in food, drugs, and cosmetics (2nd tributions among women being treated for early stage ed.). New York: John Wiley & Sons, Inc. breast cancer. Psychosomatic Medicine, 62(3), 304–308. Dilman, V. (1981). The law of deviation of homeostasis in dis-Li, S., Givalois, L., & Pelletier, G. (1997). Dehydroepiandrosterone administration reverses the inhibitory influence eases of aging, John Wright. PSG. of aging on gonadotropin-releasing hormone expression Dilman, V., & Dean, W. (1992).The neuroendocrine theory of in the male and female rat brain. Endocrine, 6(3), aging and degenerative disease . Pensacola, FL: The 265–270. Center for Bio-Gerontology. DiPietro, J.A. (2000). Baby and the brain: Advances in childMantero, F. (1981). Exogenous mineralocorticoid-like disorders. Clinical Endocrinology and Metabolism,10(3), development.Annual Review of Public Health,21, 465–478. 455–471.

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Marx, C., Ehrhart-Bornstein, M., Scherbaum, W.A. & Bornstein, Sapolsky, R., et al. (1987). Stress and glucocorticoids in aging. Endocrinology and Metabolism Clinics of North AmerS.R. (1998). Regulation of adrenocorticol function by ica, 16(4), 965–980. cytokines relevance for immune-endocrine interaction. Scheufele, P.M. (2000). Effects of progressive relaxation and clasHormone and Metabolism Research, 6–7, 416–20. sical music on measurements of attention, relaxation, and McGwen, B.S. (1998). Protective and damaging effects of stress stress responses. Journal of Behavioral Medicine, 23(2), mediators. New England Journal of Medicine , 338, 3, 207–228. 171–179. Selye, H. (1956).The stress of life . New York: McGraw-Hill Miller, W.L., & Tyrell, J.B. (1996). The adrenal cortex.EndoIn Book Co. crinology and metabolism. New York: McGraw-Hill. (rev. ed.). New York: McGrawNathan, N., van Droux, J.C., & Feiss, P. (1991). American and Selye, H. (1976).The stress of life Hill Book Co. French Anesthesiologie et Reanimation, 10(4), 329–332. National Formulary (NF) (16th ed.) (1985). Washington, D.C.: Sephton, S.E., Sapolsky, R.M., Kraemer, H.C., & Spiegel, D. (2000). Diurnal cortisol rhythm as a predictor of breast American Pharmaceutical Association. cancer survival.Journal of the National Cancer InstiOelkers, W. (1999). Dehydroepiandrosterone for adrenal insuftute, 92(12), 994–1000. ficiency.New England Journal of Medicine, 30, 341(14), Shelygina, N.M., Spivak, Ria., Zaretskii, M.M., et al. (1975). 1073–1074. Influence of Vitamin C, B1 and B6 on the diurnal periOnuki, M., & Hoshino, H. (1970). Effects of pantethine on the odicity of the glucocorticoid function of the adrenal adrenocorticol function. Horumon to Rinsho, 18, 601–605. cortex in patients with atherosclerotic cardiosclerosis. Ramirez, A.J. (1989).British Medical Journal, 298(6669), Voprosy Pitaniya,2, 25–29. 291–293. Small, M. (2000, August),Discover, 66–71. Ritchason, N.D. (1995).The little herb encyclopedia . SacraSotile, W.M. (1996).Psychosocial interventions for cardiopulmento, CA: Woodland Health Books. monary patients: A guide for health professionals. Rosenfeld, R.S., Rosenberg, B.J., Fukushima, D.K., & Hellman, Champaign IL: Human Kinetics. L. (1975). 24-hour secretory pattern of dehydroepi- Tu, G. (Ed.). (1992).Pharmacopoeia of the People’ s Republic androsterone and dehydroepiandrosterone sulfate. Jourof China, 118–119. (English Ed., 1992). Beijing: nal of Clinical Endocrinology and Metabolism, 40(5), Guangdong Science and Technology Press. 850–855. Walther, D. (1988).Applied kinesiology , Colorado: Synopsis Rotter, J.I., Wong, F.L., Lifrak, E.T., & Parker, L.N. (1985). A Systems DC. genetic component to the variation of dehydroepiandros-Woodhouse, D.K. (1993). The aspects of humor in dealing with stress.Nursing Administration Quarterly, 18(1), 80–89. terone sulfate.Metabolism,34(8), 731–736.

83 Aromatherapy for Pain Relief A.R. Hirsch, M.D. In explaining the persuasive attraction of alternative med-synthesized compounds are not. However, in the treatment icine, Kaptchuk and Eisenberg (1998) note, “The funda-of neurologic and psychiatric diseases, literature does not mental premises are an advocacy of nature, vitalism, scidifferentiate between them (King, 1994). No distinction ence, and spirituality.” With this in mind, the science will be made herein between the use of synthesized as underpinning aromatherapy will be explored. opposed to naturally occurring oils.

DEFINITIONS

BACKGROUND

One of the difficulties in understanding aromatherapy is thatWhy is the concept of aromatherapy under consideration it means different things to different people. One part of itstoday? One reason is its history. Throughout history, odordefinition that is agreed upon is that aromatherapy uses odorants have been used to treat various diseases. More than ous compounds to promote health and healing (Kaptchuck 5000 years ago the Egyptians treated disease using odors & Eisenberg, 1998). Beyond this, opinions differ. Aroma-(Lindsay, Pitcaithly, & Geelen, 1997), and 3500 years ago chologists speak of using odors not to treat disease, but the to Babylonians used odors to exorcise demons of disease promote wellness. Aromatologists believe in ingestion of the(Roebuck, 1988). The ancient Aztecs also used odors to substance being used as well as its inhalation (Price & Price, treat disease. Aromatherapy has known no cultural or geo1995). Many aromatherapists believe in using massage cographic boundaries. Virtually all cultures have fumigated incident with inhalation (Tisserand, 1977). In this chapter, the sick (Buchbauer, 1993). aromatherapy is defi ned as the use of odorants as inhalants to treat underlying medical or psychiatric conditions. This definition excludes any effects of ingestion or percutaneous ANATOMY OF OLFACTION absorption, although they may be signifi cant depending upon the method of application (Weyers & Brodbeck, 1989).Neuroscience provides insight into the mechanisms by which odors may impact behavior and neurologic functioning. As defined, aromatherapy use is also independent of any effects of coincident, noninhalational therapy, such as mas- There is an anatomic basis for the belief that odors can affect the brain and behavior (Brodal, 1969). Once an sage, interpersonal interaction, or bathing. This definition is consistent with the literature indi- odor passes through the olfactory epithelium, it must stimcating that real aromatherapy involves the uptake of fra-ulate the olfactory nerve, which consists of unmyelinated grant compounds only through inhalation, not by otherolfactory fila. The olfactory nerve has the slowest conduction rate of any nerve in the body. The olfactory fila pass methods (Buchbauer, 1993). Many in the aromatherapy community believe thatthrough the cribiform plate of the ethmoid bone and enter natural or essential oils are effective and that artificialthe olfactory bulb. During trauma, much damage occurs

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in this bulb (Hirsch & Wyse, 1993). Different odors local- lateral amygdaloid nuclei, the lateral preoptic area of the hypothalamus, the nucleus of the diagonal band of Broca, ize in different areas of the olfactory bulb. Inside the olfactory bulb is a conglomeration of neu-the medial forebrain bundle, the dorsal medial nucleus and ropil called the glomeruli. Approximately 2000 glomeruli submedial nucleus of the thalamus, and the nucleus reside in the olfactory bulb. Four different cell types makeaccumbens. up the glomeruli: processes of receptor cell axons, mitral It should be noted that the entorhinal cortex is both a cells, tufted cells, and second-order neurons that give off primary and a secondary olfactory cortical area. Efferent collaterals to the granule cells and to cells in the periglom-fibers from the cortex project via the uncinate fasciculus to erular and external plexiform layers. The mitral and tuftedthe hippocampus, the anterior insular cortex (next to the cells form the lateral olfactory tract and establish a rever-gustatory cortical area), and the frontal cortex. (This may berating circuit with the granule cells. The mitral cells explain why temporal lobe epilepsy that involves the uncistimulatefiring of the granule cells, which, in turn, inhibit nate often produces parageusias of burning rubber, known firing of the mitral cells. as uncinate ts fi (Acharya, Acharya, & Luders, 1996). A reciprocal inhibition exists between the mitral and Some of the efferent projections of the mitral and tufted cells. This results in a sharpening of olfactory acu-tufted cells decussate in the anterior commissure and form ity. The olfactory bulb receives several efferent projec-the medial olfactory tract. They then synapse in the contions, including the primary olfactory fibers, the contralat-tralateral parolfactory area and contralateral subcallosal eral olfactory bulb and the anterior nucleus, thegyrus. The exact function of the medial olfactory stria and prepiriform cortex (inhibitory), the diagonal band of Broca tract is not clear. The accessory olfactory bulb receives (with neurotransmitters acetylcholine and GABA), the afferentfibers from the bed nucleus of the accessory olfaclocus coeruleus, the dorsal raphe, and the tuberomamillary tory tract and the medial and posterior corticoamygdaloid nucleus of the hypothalamus. nuclei. Efferent fibers from the accessory olfactory bulb The olfactory bulb’s efferent fibers project into the project through the accessory olfactory tract to the same olfactory tract, which divides at the olfactory trigona into afferent areas, for example, the bed nucleus of the accesthe medial and lateral olfactory stria. These project to thesory olfactory tract and the medial posterior cortianterior olfactory nucleus; the olfactory tubercle; thecoamygdaloid nuclei. It should be noted that the medial amygdaloid nucleus (which, in turn, projects to the ventraland posterior corticoamygdaloid nuclei project secondary fibers to the anterior and medial hypothalamus, the areas medial nucleus of the hypothalamus, a feeding center); the cortex of the piriform lobe; the septal nuclei; and theassociated with reproduction. Therefore, the accessory olfactory bulb in humans may be the mediator for human hypothalamus, in particular the anterolateral regions of the hypothalamus, which are involved in reproduction. Thepheromones (Hirsch, 1998a). neurotransmitters by which the olfactory bulb conducts its Some unique aspects of the anatomy of the olfactory information include glutamate, aspartate, NAAG, CCK, system are worth mentioning. Smell is the only sensation and GABA. to reach the cortex before reaching the thalamus. The only The anterior olfactory nucleus receives afferent fiberssensory system that is primary ipsilateral in its projection, from the olfactory tract and projects efferent fibers, whicholfaction does not depend upon the cortex, as has been demonstrated in decorticated cats. decussate in the anterior commissure and synapse in the contralateral olfactory bulb. Some of the efferent projec- Neurotransmitters of the olfactory cortex are multiple, tions from the anterior olfactory nucleus remain ipsilat-including glutamate, asparatate cholcystekinin, LHRH, eral, and synapse on internal granular cells of the ipsilatand somatastatin. eral olfactory bulb. Furthermore, perception of odors causes modulation The olfactory tubercle receives afferent fibers from theof olfactory neurotransmitters within the olfactory bulb olfactory bulb and the anterior olfactory nucleus. Efferentand the limbic system. Virtually all known neurotransmitfibers from the olfactory tubercle project to the nucleusters are present in the olfactory bulb. Thus, odorant modaccumbens as well as the striatum. Neurotransmitters of ulation of neurotransmitter levels in the olfactory bulb, the olfactory tubercle include acetylcholine and dopamine.tract, and limbic system intended for transmission of senThe area on the cortex where olfaction is localized,sory information may have unintended secondary effects that is, the primary olfactory cortex, includes the prepiri-on a variety of different behaviors and disease states that form area, the periamygdaloid area, and the entorhinal are regulated by the same neurotransmitters. For instance, area. Afferent projections to the primary olfactory cortexodorant modulation of dopamine in the olfactory bulb/liminclude the mitral cells, which enter the lateral olfactorybic system may affect manifestations of Parkinson’ s distract and synapse in the prepiriform cortex (lateral olfac-ease. Mesolimbic override to many of the components of tory gyrus) and the corticomedial part of the amygdala.Parkinson’s disease have been well documented, for examEfferent projections from the primary olfactory cortex ple, motoric activation associated with emotional distress extend to the entorhinal cortex (area 28), the basal and and fear of injury in a fire.

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EMOTIONAL AND BEHAVIORAL EFFECTS OF ODORS

tubercle, and from there to the prepiriform cortex, the amygdala, and numerous other limbic system structures support this (Brodal, 1969). Odors can affect behavior by acting as alternative sensory Smells are described differently from other sensory stimuli. The phenomena of visual system mediation of themodalities, adding credence to their connection to emomovements of Parkinsonian gait through the visual stimulition. Other sensory modalities are first described cogniof lines placed on the floor (Dietz, Goetz, & Steddings,tively; a picture, for instance, is identified as being of a 1990) is an example of alternative stimuli. Other sensoryship, a woman, or a house and only secondarily is it input, including pain, has been shown to inhibit the Jack-described affectively: “I like, ” or “I dislike it” (Ehrlichman sonian march in epilepsy (Gowers, 1881 in Efron, 1957).& Halpern, 1988). But odors arerst fi and foremost Similarly, odors may act as competing sensory stimulidescribed affectively: “I like, ” or “I dislike” it. during an uncinate seizure (Efron, 1957). It seems possible The olfactory/limbic/hippocampal connections help to that other sensory input, including odors, could modifyexplain olfactory-evoked nostalgia, the phenomena Parkinson’s disease as well as other neurologic conditionswhereby an odor induces a vivid recall of a scene from by acting as competing sensory stimuli. the distant past (Hirsch, 1992). In 86% of 989 subjects Using another mechanism of action, odors can affectqueried, certain odors triggered vivid associations analobehavior and mood by producing secondary effects on the gous to a flashbulb memory. Classically, an event must emotions of the individual. This is different from a direct induce strong emotions for deposition of such memories neurophysiologic effect of the limbic system. Rather, the to occur (Squire, 1987; Brown & Kulik, 1977). By directly odor can change the mood of the individual, which then stimulating the limbic system, odors likewise can act as has secondary neurologic effects. For instance, mood or the inducing agent. This phenomenon was vividly level of alertness can affect a variety of neurologic condescribed by Proust (1934), who wrote that the aroma of ditions, including the perception of pain. A soldier who is madeleine dipped in tea evoked a flood of memories and severely wounded in battle may continue to fight and not nostalgic feelings. Olfactory-evoked recall is usually a feel pain until the battle is over. Studies also suggest that positive experience, but it can be negative, as in the olfacpersons in a positive state of mind are less bothered by tory flashbacks of posttraumatic stress disorder (Kline & pain (Fields, 1967). Rausch, 1985). Hence, it seems possible that olfactorySubstantial evidence exists that odors can affect mood. evoked nostalgia may affect behavior because approxiAs early as 1908, Freud stressed the importance of olfacmately 90% of these memories are associated with strong tion on emotion in his description of a patient with an affective tones (Laird, 1988). obsessional neurosis. The facts brings to the forefront the question of how odors impact behavior or mood. The answer can be repBy his own account, when a child, he recognized everyresented by either of two constructs: the Lock and Key one by their smell, like a dog, and even when he was grown up he was more susceptible to sensations of smell Theory or the General Affective Theory of Odors. than other people … and I have come to recognize that a tendency towards osphresiolagnia which has become extinct since childhood may play a part in the genesis of neuroses.

THE LOCK

AND

KEY THEORY

OF

ODORS

The lock and key theory of odors (also called the systemic effect theory) (Buchbauer, 1993) suggests that odor acts In a general way I should like to raise the question very much like a specifi c neurotransmitter, a drug, or an whether the inevitable shunting of the sense of smell as enzyme. In this paradigm, an odorant has a fic speci effect a result of man’ s turning away from the earth and the on behavior or emotion — one odor for one emotion or one organic repression of smell pleasure produced by it does odor for, at most, a few emotions. Thus, an odor could be not largely share in his predisposition to nervous disviewed like a medication in the pharmacopeia. For instance, eases. It would thus furnish an explanation for the fact in the world of neurology, propranolol is used for modulathat with the advance of civilization it is precisely the tion of essential tremor, migraine headache, and anxiety. sexual life which must become the victim of repression. However, one would not use propranolol as a treatment for For we have long known what an intimate relation exists insomnia, dementia, or multiple sclerosis. The lock and key in the animal organization between the sexual impulse theory suggests that specifi c odors have specifi c effects. and the function of the olfactory organs. This theory has been proposed in virtually every book about c odors are recommended for Of all the sensations, olfaction is the one most inter-aromatherapy in which specifi twined with limbic system functioning (MacLean, 1973). specific health effects (Damien & Damien, 1995; CunningThe profuse anatomic and physiologic interconnectionsham, 1995; Feller, 1997; Price, 1991; Price & Price, 1995; through the olfactory bulb, stria, and nuclei to the olfactorySchnaubelt, 1995; Keville & Green, 1995).

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An argument supporting the Lock and Key Theory isones induced mainly disgust and anger (Alaoui-Ismaili, et al., 1997). that odorants exert central nervous system (CNS) effects outside a subject’ s conscious awareness. In test animals, Milter, et al. (1994) also showed that exposure to the more lipophilic an odor is, the greater its sedativeodors could change emotions in the same direction as the effect. In addition, steric differences in odors create dif-hedonic valence of the odor. Using the startle reflex ampliferent effects despite similarities in perceived odor andtude as a physiologic indicator of emotional valence, he volatility (Buchbauer, 1993; Buchbauer, et al., 1993). found that the odor of hydrogen sulfide2S) (H increased ex amplitude and the odor of vanillin According to the Lock and Key Theory, odors act asthe startle refl a drug (Buchbauer, 1993) with a potentially pharmaco-reduced it. logic mechanism of action. The odorants are integrated in Aromatherapists recognize the affective impact of odors as the mechanism of action. Buchbauer notes, A “ the membrane of the cells causing an increase in membrane volume due to disruption of the membrane lipids.pleasant odor has always been, and still is, an important factor for people to feel good, and feeling well is synonThis leads to electrical stabilization of the membrane, thus blocking the inflow of calcium ions and suppressing per-ymous with good health. Therefore, we can conclude that meability for sodium ions. As a result, action potentialall substances which are able to create a certain amount production is inhibited, which induces narcosis or localof well-being and well-feeling possess therapeutic properties and, therefore, can be called therapeutic agents” anesthesia. At higher concentrations of odorant, the conductivity of potassium ions is reduced. It also is possible(Buchbauer, 1990). The General Affective Theory of that the odorants act on protein kinase C, which couldOdors might be extended to include nonodorants in the pharmacologic arena such as valium. Valium may be useimpact upon the spontaneous rhythm of nerve cells (Buchful for virtually all medical conditions because reducing bauer, 1993). This mechanism of action is further supported byanxiety makes conditions such as chronic pain, movement established physiology for the action of an odor on thedisorders, or insomnia less bothersome. Hence, an entire branch of medicine could be built around Valium: “Valiotarget organ, in this case, the brain. Inhalation of an odortherapy.” If one ascribes aromatherapeutic results to the ant would have to produce measurable levels in the blood, sufficient to pass through the blood–brain barrier. StimpflGeneral Affective Theory as the mechanism of action, it follows that any odor that one likes induces a happier state et al. (1995) demonstrated that this does occur. One subject inhaled 1,8-cineol for 20 minutes, which produced aand, hence, would have a positive effect on any disease. linear increase of 1,8-cineol in the blood, up to 275 ng/ml,Again, the concept could be expanded beyond odors to a level high enough to allow penetration of the any environmental stimuli, for example, a bird singing or a pretty landscape. AStar Wars movie might induce blood–brain barrier (Stimpfl, et al., 1995). happiness in some observers and could be seen as inducing a positive mood state. The positive mood might lead to a THE GENERAL AFFECTIVE THEORY OF ODORS reduction in pain, anxiety, and negative feelings. One An alternative theory, the General Affective Theory of could then categorize this as a form of alternative therapy: Odors, also called the Reflectorial Effect Theory (Buch-“Lucastherapy. ” bauer, 1993), holds that an odor experienced as hedoni- Reliance on the General Affective Theory of Odors cally positive induces a positive, happy mood and whenimplies that virtually any sensory stimulus could be used in a happy mood, an individual does almost everythingas a therapeutic tool. This largely trivializes the definition better. For instance, when a person feels happy, it is easier of therapy. to learn and to sleep, and headaches are less frequent. Another problem with the General Affective Theory According to the General Affective Theory, a single odorof Odors is that the same odor, in different contexts, may could have a multitude of diverse effects, thus affectinginduce opposite emotional tones (Sugawara, Hino, & virtually all behaviors. Kawasaki, 1999). InThe Invalid’s Story , Mark Twain The major premise that hedonically positive odorscompares the disgust at the odor of a rotting corpse to the induce happier moods was demonstrated by Alaoui-delight at the smell of cheese. The odors were the same Ismaili, et al. (1997); 44 subjects inhaled five odorants,but perceived to be from different sources. This suggests namely, vanillin, menthol, eugenol, methyl methacrylate,that an odor that is contextually appropriate in one situaand propionic acid. Six autonomic nervous system paramtion might be considered totally inappropriate in another. eters were recorded: skin potential, skin resistance, skin Smelled in a positive context, it would be appreciated as temperature, skin blood flow, instantaneous respiratoryhedonically positive and would enhance a positive affecfrequency, and instantaneous heart rate. Evaluation of tive state; smelled in a negative context, it would be perthese parameters demonstrated a pattern consistent with ceived as hedonically negative and would, thus, induce a known emotional states. Hedonically pleasant odorsnegative affective state. Therefore, the same odor could evoked mainly happiness and surprise, and unpleasant produce opposite mood states and opposite effects.

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A variant of the General Affective Theory is that HEALTH EFFECTS OF MALODORS odors may induce a mood more congruent with the demands of the external environment. For instance, ifHealth effects of malodors can be divided into six catethe external environment requires that the individual begories: respiratory, chemosensory, cardiovascular, immune, neurologic, and psychologic. alert, the odor induces awareness of this; therefore, the individual responds by becoming more alert. Alternatively, if the external environment is such that it is more Respiratory. Asthmatics are especially affected by malodors. Any strong odor may induce an appropriate to be relaxed, the odor induces that awareattack in persons with unstable asthma and, ness and the individual responds by becoming more even in nonasthmatics, malodors have been relaxed. Evidence for the validity of this variant comes demonstrated to affect the cardiorespiratory from studies of muguet odor. Where the external demand system. Increased ambient oxidant levels coris for a greater degree of relaxation, individuals do relate with slower cross-country running times become more relaxed, and in an environment where they in high school students (Wayne, Wehrle, & Carare required to be more alert and vigilant, they become roll, 1967). more alert. Warm, Dember, and Parasuraman (1991) Chemosensory. Chronic exposure to malodors from demonstrated this effect of odorant-induced recognition pulp mills can cause permanent olfactory loss of affective demands. A total of 40 subjects underwent (Maruniak, 1995). vigilance tasks for 40 minutes during which they Cardiovascular. Certain malodors can induce an received periodic 30-second whiffs of air or one of two adrenocortic and adrenomedullary response hedonically positive fragrances: muguet (independently leading to elevated blood pressure and a subsejudged as relaxing) or peppermint (independently judged quent increase in stroke and heart disease as alerting). Those who received either the relaxing or (Evans, 1994). alerting fragrance detected more signals during the vigImmune. Immune function may be compromised ilance task than the unscented air controls p = (0.05). either directly, as a result of olfactory/neural This odorant-induced congruence of mood may also projections to lymphoid tissue (Evans, 1994), be applied to the pharmacologic agent, valium. Valium or indirectly, as a result of malodor-induced can induce opposite mood states in the same individual depression or other negative mood states at different times. It can reduce anxiety to enhance con(Weisse, 1992). centration on a test, or it can reduce concentration to act Neurologic. Chronic exposure to intermittent malas a soporifi c when the same individual is suffering with odors from a U.S. Navy dump site in Port insomnia. Orchard, Washington induced cortical and subA corollary to the General Affective Theory is that cortical dysfunction, which was manifested by hedonically negative odors or malodors have a negative encephalopathy: limbic encephalopathy and effect on mood. If this is true, the simple elimination or cephalgia (Hirsch, 1995d). Both ambient 2NO masking of malodors with neutral or hedonically positive and SO2 impair visual adaptation to darkness odors would induce positive effects. and sensitivity to brightness, and increase alpha Literature supports the negative effects of hedonically wave desynchronization on EEG (Izmerov, negative odors. Miner (1980) described some effects of 1971). exposure to the odor of livestock waste. They included Psychologic. Recognized for centuries and noted by annoyance, depression, nausea, vomiting, headache, shalFreud and others, psychologic effects of odors low breathing, coughing, insomnia, and impaired appetite. vary widely among individuals. Persons under One of the malodorous pollutants that has been studmajor stress are particularly vulnerable to the ied, trichloroethylene, a universally present air pollutant, psychologic effects of ambient malodors can cause cephalgia (Hirsch & Rankin, 1993). Acute expo(Evans, 1994). Persons with a distorted or sure to nitrogen tetroxide can cause cephalgia (Hirsch, impaired olfactory sense may be annoyed by 1995a) and chronic neurotoxicity (Hirsch, 1995b). Acute odors that other persons usually consider pleasexposure to chlorine gas can cause neurotoxicity (Hirsch, ant (Evans, 1994). 1995c). In 1991, Neutra, et al. (1991) reported that people Certain bad odors irritate nasal passages. Resultant living near hazardous waste sites suffer more physical trigeminal stimulation releases adrenaline, leading to a tense symptoms during times when they can detect malodors and angry state. Thus, bad odors can trigger aggression that than when they are unaware of them. Shusterman (1992) may then be covertly expressed. For example, in one experdemonstrated that even at levels considered nontoxic, iment college men were instructed to apply electric shocks chemical effluviums can cause physical symptoms. of varying intensity to their colleagues, supposedly for the

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purpose of training them. When bad odors were present, CONTRADICTORY THEORIES the subjects chose to inflict greater degrees of pain upon their colleagues (Rotton, et al., 1979). Another exampleIf the General Affective Theory of Odors is true, a single involves air pollution. On days when malodorous air pol-odor can induce a positive mood in one person and a lution is high, the number of motor vehicle accidentsnegative mood in another. This negates the Lock and Key Theory in which odors’effects are produced outside of increases, indicating that people drive more aggressively in a polluted environment (Ury, Perkins, & Goldsmith, conscious awareness. Robin, et al. (1999) demonstrated this using eugenol. Eugenol, which is often associated 1972). Various studies show how mood and well-being sufferwith the smell of dental cement, was rated pleasant by nonfearful dental subjects and unpleasant by fearful subin the presence of malodors. Residents exposed to the jects (p = 0.036). Changes in subjects’ autonomic nervous effluvium from nearby commercial swine operations system measurements were consistent with their emoreported that they suffered increased tension, fatigue, contional states; (Robin, et al., 1998; 1999) 19 subjects were fusion, depression, and anger, and that their vigor exposed to eugenol while recording six autonomic nerdecreased (Schiffman, et al., 1995). According to one vous system parameters, including two electrodermal, two study (Rotton, et al., 1978) ambient pollutants decreased thermovascular, and two cardiorespiratory. The results of personal attraction. In a German urban area, the moods of seven subjects with high dental fear were compared with young adults fluctuated in synchrony with the daily flucthose of 12 without such fear. Those with dental fear had tuations in quality of environmental air, a pattern espea stronger electrodermal response p = (0.006), suggesting cially marked among more emotionally unstable individthat eugenol triggered different emotional responses uals (Brandstatter, Fuhrwirth, & Kitchler, 1988). Further, depending upon the unpleasantness of the subject’ s past daily diary entries of women in Bavaria showed that varidental experiences. Thus, the same odor can have different ations in their psychologic well-being coincided with varieffects depending upon the past experience of the individations in ambient air quality. The correlation was particual (Robin, et al., 1998). ularly marked among women suffering from chronic On the other hand, if the Lock and Key Theory is true, diseases such as diabetes (Bullinger, 1989a; 1989b). In and an odor’ s behavioral effects are produced outside of Israel, negative health effects were significantly associated awareness and independent of affective reaction, this with levels of urban pollution (Zeidner & Schecter, 1988). negates the General Affective Theory of odors. Ludvigson The number of family disturbances and the numberand Rottman do just that, demonstrating that the scent of of 911 emergency psychiatric calls also were linked tolavender enhances mood state while impairing arithmetic malodors in the environment, as determined by ozone reasoning p( = 0.01) (Ludvigson & Rottman, 1989). levels (Rotton & Frey, 1985). In several cities, the number Given the previous information, several factors must of psychiatric admissions paralleled the quality of envibe taken into account in reviewing the literature regarding ronmental air (Briere, Downes, & Spensley, 1983). efficacy of aromatherapy in the treatment of neurologic In a study of the malodorous emanations from adisease. Can odors elevate mood as the general affective mulching site southeast of Chicago, it was found that ontheory maintains or do they act in lock and key fashion? days when the miasma wafted from the site to the school Were the odors tested considered hedonically positive by across the street, children at the school demonstrated each subject? This question is essential because what is increased behavioral problems (Hirsch, 1998b). hedonically positive for one person can be hedonically Malodorous ambient SO 2 levels correlate with psychi- negative for another, and an odor that is hedonically posatric admissions, child psychiatric emergencies (Valen-itive at one concentration may be hedonically negative at tine, et al., 1975), and behavioral ficulties dif with another (Distel, et al., 1999). Was an associated change in decreased cooperation (Cunningham, 1979). Ambientmood independent of the desired effect? Was there a conNO2 levels covary with psychiatric emergency room visitstrol group? Was it a single-blind or double-blind proce(Strahilevitz, Strahilevitz, & Miller, 1979). dure? Was the subject size ficient suf to obviate falsely In nonsmokers, the odor of cigarette smoke has been positive test results? Did the subjects of the experiment demonstrated to exacerbate aggressive behavior (Joneshave & a normal or near-normal sense of smell? Bogat, 1978). Could suggestion have an effect? This is particularly The fatigue and annoyance caused by ambient malrelevant because various studies suggest that, as in tradiodors undoubtedly reduce individuals ’ capacities to tional pharmacologic intervention (Flaten, Simonsen, & function normally. Their abilities to tolerate frustration, Olsen, 1999), odors have both placebo and nocebo effects to learn, and to cope with other stressors are impaired. as demonstrated by Knasko, Gilbert, and Sabini, (1990). In one laboratory study, subjects exposed to unpleasant Knasko subjected 90 people to water vapor sprayed in a odors experienced increased feelings of helplessness room; 30 subjects were told that the water vapor odor was pleasant, 30 that it was unpleasant, and 30 that it was (Rotton, 1983).

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using specific odorants. These claims do not indicate neutral. Those who had been told that the odorant was pleasant reported being in a better mood than did the other whether the mechanism of action is primarily analgesic, two groups p( = 0.05). Subjects who had been told thesoporific, or anxiolytic. Suggested odorants include cloves odor was unpleasant reported having more health sympfor dental pain (Price & Price, 1995); wintergreen for toms (p < 0.0003). muscle pain (Price & Price, 1995; Gobel, et al., 1995); Were the experiments controlled not only for the effectmenthol, ginger, lemon grass, rosewood, clary sage of suggestion, but also for the effect of expectation of(Damien & Damien, 1995), cajeput, tea tree, juniper, pepoutcome? It seems possible that persons with a positive per, and rose (Walji, 1996), for headaches (Price & Price, view of aromatherapy who believe that odors can have 1995); a lavender (Passant, 1990) lavandula angustifolia, positive effect will experience a positive effect because ofchamaemelum mobile , ocimum basilicum, origanum their bias. majorana, rosmarinus of ficinalis (Price & Price, 1995), The effect of expectation has been demonstrated neueucalyptus (Damien & Damien, 1995), and true melissa rophysiologically by Lorig and Roberts (1990) who meas-(Price, 1991) for migraine; mentha× piperita for “headured the contingent negative variation (CNV) of the EEGache caused by digestive disorder” (Price & Price, 1995); in 18 subjects presented with a mixed odor of lavender,peppermint and eucalyptus for tension headache (Saller, jasmine, and galbanium. They found CNV amplitude forHellstein, Hellenbrecht, 1988). the mixed odors varied depending on what the subjects Experimental studies of odors for pain management were told about it p( = 0.05). are few. Hirsch and Kang (1998) studied 50 chronic sufDid the experimenter consider the effect of socialferers whose headaches met International Headache Socidesirability whereby subjects try to please the examinerety criteria. Upon olfactory testing, only 31 demonstrated . by biasing their answers? (Visser, 1999) normal olfactory ability. Green apple odor was given in In light of such questions, one must be circumspectan aromatherapy inhaler. Only 15 subjects found the odor regarding articles touting aromatherapeutic ficacy ef in the hedonically pleasant. In this open label, nonblinded study, treatment of neurologic disease. Because the basic physsubjects served as their own controls. The control condiiologic mechanism of aromatherapy intervention has not tion consisted of resting in a dark, quiet room, and the been fully established, skepticism seems all the more experimental condition involved inhaling the green apple appropriate. odor while resting in the same dark, quiet room. Results indicated that green apple odor produced no statistically significant improvement over simple resting in a dark, AROMATHERAPY FOR VARIOUS quiet room. However, in the subgroup of 15 subjects who NEUROLOGIC DISEASES liked the odor, there was a statistically significant reducAs a general rule, neurologic diseases can be positively tion in the severity of the headache p 10% for the injured muscle but not the issue of consistency vs. functional overlay. Individuals for the unaffected muscles, the result is relevant with soft tissue injury may or may not have nerve damage. for treatment follow-up. When such nerve damage is of the sensory type and 2. The test/re-test repeatability of repeated Sinvolves the A, Aα, and Cδ fibers, the C.P.T. evaluation EMG dynamic protocol testing can be evaluis an excellent tool for exclusion of nervous lesion vs. ated if clinically necessary by at least three myofascial or other type of soft tissue pathology (Liu, repetitions during at least 1 month of testing or Kopacz, & Carpenter, 1995; Masson & Boulton, 1991). treatment. The repeatability validation may be For the clinician who cannot afford the effort and considered if the responses vary within 10%. luxury of repeated S-EMG dynamic protocol testing in This holds true for the S-EMG normal or pathoorder to satisfy all the objectivity criteria defined above, logical variables. it is advisable to use such S-EMG dynamic protocol test3. The reliability of the S-EMG dynamic protoing no less than three times in the course of the clinical col testing results may need to be evaluated relationship. for treatment adequacy in comparison with Thus, the patient/evaluee may have to be tested with known databases for the same kind of injury/ S-EMG dynamic protocol testing during (1) the diagnostic response. evaluation, at the (2) beginning of the treatment period 4. Because such results are available for most and (3) at the end of the treatment period. skeletal muscles, the S-EMG dynamic protocol Ideally, the responses should show a decrease or distesting may be considered in terms of specificappearance of the pathological curve variables described ity, sensitivity, and predictive values. above. The eventual responses should be quite similar on 5. As the treatment is initiated, repeated S-EMG the affected soft tissue injury site and on the contralateral dynamic protocol testing may show improve- site. ments in the overall pattern of change from pathological electric curves to normal curves Objective Treatment Outcome Measurement during activity and rest. Objective treatment refers to numerical modalities For the clinician who cannot afford the effort and involved in the pain rehabilitation process. Such modaliluxury of repeated S-EMG dynamic protocol testing toties may be analgesics, in which case one would have to satisfy all the objectivity criteria defi ned above, it is know the type of “pain killer” and the posology given in advisable to use such S-EMG dynamic protocol testingtime. The objective outcome could be a linear follow-up no less than three times in the course of the clinicalof the pain level at the beginning of the treatment, at each relationship. Thus, the patient/evaluee may have to be visit, and at the end of the treatment period. For instance, tested with S-EMG dynamic protocol testing during (1) the initial soft tissue injury pain level intensity may be the diagnostic evaluation, at the (2) beginning of the9/10; in time it may show a decrease pattern to 7/10, 5/10 treatment period, and (3) at the end of the treatment and eventually reach 1/10 at the end of the treatment period. Ideally, the responses should show a decrease period. or The example given above is pertinent to one pain disappearance of the pathological curve variablestreating modality or to a combination modalities. of The described above. The eventual responses should be quite main object is to demonstrate a framework of pain level similar on the affected soft tissue injury site and on themeasurement that is consistent, numerical, and spans the contralateral site. beginning to the end of the treatment period.

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Strengths and Limitations of Pain Investigation Methodologies

Pain Management: A Practical Guide for Clinicians, Sixth Edition

strength may be that of the pain recognition at rather similar micro-electrical stimulation intensities, if the test is done repeatedly. Every scientific methodology has inherent strengths and Its limitation is that recognition is a subjective perceplimitations. Therefore, it is incumbent upon the researcher,tion and expression. However, repeated C.P.T. testing and investigator or clinician to utilize multiple modalities or statistical analysis of the results can demonstrate consistency methodologies. The choice of combination(s) must beor rule out inconsistency. Performance of this test as part of such that the strength of one modality can overcome the the battery described above can validate the pain symplimitation of another modality. Furthermore, while theo- tom/perception, because the presence of pain should be parretically any result derived from any individual modality alleled by the consistent response pattern in all the tests. may have artifact properties, results deriving from a bat- Thus, one can investigate pain of soft tissue injury tery of modalities cannot be considered technical artifacts. with several modalities and counter the limitations of one In terms of pain investigation, pain questionnaireswith the strength of another. have the strength of consistency if they are given repeatedly. At the same time, responses are subjective because RELATIVE LOSS OF STRENGTH (L.O.S.) pain is a subjective phenomenon, thus the limitation of Acute soft tissue injury is often followed by loss of questionnaires. The same criteria apply to the pain picture strength of the injured muscle or myotatic unit (Anchor or visual analogue. The strength of the pain perception threshold meth-& Felicetti, 1999; Sella & Donaldson, 1998). The L.O.S. odology is that it helps to differentiate the perception ofmay involve direct or indirect trauma to the skin, subcutaneous tissue, blood vessels, nerves, fascia, and skeletal pressure from that of pain. Furthermore, it helps to assess individual perception of maximal tolerable pain thresholdmuscle as well as periosteum and bone. As stated, only at the point of pressure. The limitation of the modality isL.O.S. involving the muscles and fascia is discussed in this presentation. that the subject could state, without any check for consistency, that he or she has pain or maximal pain. This inher- Acute L.O.S. is reflected by the body’ s reflex of splintent limitation was modified with the test of consistencying. The injured part is “splinted, ” i.e., defended by the (Sella & Donaldson, 1998) that modifies the original pro-surrounding area in terms of muscles, joints, and fascia cedure which required testing of the injured or symptom-as well as the contralateral area and the appropriate myoatic site. The contralateral and other sites are tested at least tatic units of either side. The deconditioning maintained three to five times for consistency of the numerical valueby pain and tissue inflamation results in relative L.O.S. If of pain perception. If the responses are statistically conthe acute L.O.S. is not resolved properly through investisistent, especially with regard to pain perception of thegation and treatment, it may result in the development of symptomatic site, then the test can be considered valid.myofascitis and protective guarding L.O.S. The same considerations apply to the tissue compli- L.O.S. assessment of soft tissue injury is easy to ance measurement (T.C.M.). perform in terms of the statistical requirements The strength of the S-EMG modality in the investigativedescribed above. Loss of strength can be measured objectively with dynamometry. A variety of dynamommode is that it measures the consistency of effort of any muscular activity. If the amplitude of contraction pattern iseters are on the market. They may refer to several areas abnormal related to pain or other dysfunction, it will remainof the body. For consistency, dynamometric testing must be performed at least throughvefi repetitions and measo as an autonomous factor. The same applies to the parameter of spectral frequency. Specifi city and sensitivity studies sure the internal consistency of strength performance of have shown that the likelihood of amplitude curve abnor-the evaluee or patient. mality is high in myofascial pain, when tested with S-EMG For repeatability, the dynamometry or other method(Sella, 2000a). The limitation of the S-EMG modality is thatologies utilized to assess strength should show a good it cannot measure the intensity of the pain; to date no studies measure of repeatability for L.O.S. assessment and rehahave been done on the subject so far. bilitation of strength. When normative values or databases S-EMG can be utilized concomitantly with other of objective measurements are known, the results of the modalities. It can strengthen the reliability of the resultsL.O.S. investigation and/or treatment should be measured against those normative values for reliability. of the pain questionnaire, pain visual analogue, P.P.T., and T.C.M. by the demonstration of internal consistency, When the specificity, sensitivity and predictive values because S-EMG has been shown to demonstrate internal of any L.O.S. investigative methodology are known, the consistency well (Sella, 2000c). clinical results may be comparable to such data. The funcThe current perception threshold modality investigatestional utilization of any L.O.S. investigative methodology the perceptual threshold of electric stimulation of (closeis as good as the results obtained in relation to it. Thereto the surface) nerve endings of peripheral nerves. Its fore, the clinician may want to describe the validity of the

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application of the L.O.S. investigative tool in terms of thequestionnaire during (1) the diagnostic evaluation, at the results obtained from knowledge of the treatment. (2) beginning of the treatment period, and (3) at the end of the treatment period. Ideally, the responses should Because it is necessary to evaluate the treatment show in time a decrease or disappearance of L.O.S. results before, during, and post-treatment, any methodology for L.O.S. investigation/treatment needs to be objec-symptoms with treatment. tive and numerical for the overall outcome measurement. The L.O.S. Visual Analogue Methodologies for soft tissue L.O.S. measurement are considered below. This is a visual format that allows the patient/evaluee to describe on a line or graph the intensity of the L.O.S. The L.O.S. Questionnaires visual analogue is usually formatted on a “___/5” scale where 0/5 represents the highest functional degree of Questionnaires can be used to assess the event and L.O.S. perceived in intensity and 5/5 represents full presence of L.O.S. The evaluee/patient needs to be asked about the perception of L.O.S. before the injurystrength. as well as at the time of examination. L.O.S. question- The visual analogue is easy to perform and takes very little time to accomplish. In terms of the parameters naires also may assess strength rehabilitation through the treatment period. Any L.O.S. questionnaire utiliza-described above for the L.O.S. questionnaire, the application in soft tissue injury evaluation may have to betion is rather similar to the visual analogue testing for soft validated through the statistical and functional criteriatissue injury L.O.S. perception. described above. Thus, the following may need to be applied in order for the clinician or investigator to be 1. The L.O.S. visual analogue may be repeated at able to state that objective validity to the results of the least five times within 1 month of testing or L.O.S. questionnaire exists: beginning of treatment. The responses may be validated by showing internal consistency of coefficients of variation (CV < 10%) among the 1. The questionnaire may be repeated at least ve fi five or more repetitions for each test. times within 1 month of testing or beginning of treatment. The responses may be validated 2. The test/re-test repeatability of L.O.S. visual by showing internal consistency of coef ficients analogues can be evaluated by the response of variation (CV < 10%) among theve fi or consistency to the L.O.S. inquiry. The repeatmore repetitions for each question and ability validation may be considered if the response. responses vary within 10%. 2. The test/re-test repeatability of such repeated 3. The reliability of L.O.S. visual analogue results questionnaires can be evaluated for the response for adequacy of treatment may need to be evalconsistency to the L.O.S. inquiry. The repeatuated by comparison with known databases for ability validation may be considered if the the same kind of injury/response. responses vary within 10%. 4. If such results are available, the L.O.S. visual 3. The reliability of the questionnaire results may analogue may be considered in terms of specineed to be evaluated in comparison with known ficity, sensitivity, and predictive values. databases for the same kind of injury/response. 5. As the treatment progresses, repeated L.O.S. 4. If available, the L.O.S. questionnaire may be visual analogue testing may show improveconsidered in terms of specificity, sensitivity, ments in the overall numerical values representand predictive values. ing the L.O.S. parameter. 5. As the treatment is initiated, repeated L.O.S. questionnaires may show improvements in the For the clinician who cannot afford the effort and overall symptoms/signs, especially with regard luxury of repeated L.O.S. visual analogues to satisfy the to the overall intensity of the soft tissue injury objectivity criteria defined above, it is advisable to use L.O.S. such L.O.S. visual analogues no less than three times in the course of the clinical relationship. For the clinician who cannot afford the effort and Thus, the patient/evaluee may have to respond to an luxury of repeated L.O.S. inquiry questionnaires to sat-original L.O.S. inquiry or L.O.S. visual analogue during isfy the objectivity criteria defi ned above, it is advisable (1) the diagnostic evaluation, at the (2) beginning of the to use such questionnaires no less than three times in the treatment period, and (3) at the end of the treatment period. course of the clinical relationship. Thus, the patient/eval-Ideally, over time the responses should show a decrease uee may have to respond to an original L.O.S. inquiryor disappearance of the L.O.S. symptoms with treatment.

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DYNAMOMETRY

Pain Management: A Practical Guide for Clinicians, Sixth Edition

treatment the responses should show a decrease or disappearance of the L.O.S. symptoms i.e., an increase in the Dynamometry is the most useful methodology for meas-number of kilos or pounds. uring strength (Sella & Donaldson, 1998). It measures the sum total of myotatic unit strength rather than individualS-EMG muscle. Therefore, soft tissue injury to one muscle and probable L.O.S. in that muscle are reflected by L.O.S. on Surface electromyography is a valid methodology for the the dynamometric testing. However, the testing involvesinvestigation and treatment of soft tissue injury L.O.S. several groups of muscles and it is likely that all the otherwhere skeletal muscles are affected (Sella, 1993, 1995, muscles involved in the testing try to “protectively guard” 1998a, 1998b). S-EMG reflects the degree of muscular the injured muscle and put out more effort than they wouldelectrical activity and effort during rest and dynamic have done otherwise. action (Basmajian & DeLuca, 1985). The S-EMG methDynamometry involves mechanical or electronic odology has been described in terms of specificity, sensigauges. The numbers obtained for the various degrees tivity, and predictive values, laterality, internal consisof effort tested represent the overall strength of volun-tency, repeatability, and reliability. tary contractions of the muscular groups that are active S-EMG involves dynamic protocols of bilateral myoin the testing. tatic units, at least one of which is affected by a soft tissue In forensic terms, it may be relevant to identify any injury site. The S-EMG amplitude parameter is useful as degree of symptom magnification of L.O.S. perception byan indicator of muscular effort and ability to proceed with applying the dynamometric instrument to several musclea determined effort. The affected muscle will show a groups (homolateral and contralateral) and identify L.O.S.higher amplitude of activity potentials (V RMS) by comperception in areas which have not suffered from softparison with the nonsymptomatic contralateral muscle tissue injury. (Sella, 1995, 2000a). This may be because it needs to use and elicit utilization of an increased number of contractile 1. Dynamometry may be repeated at least five elements in order to obtain and achieve the same strength times on the affected and contralateral areas 1 requirement end result. month of testing or beginning of treatment. The However, injured muscle strength is usually lower responses may be validated by showing internal than that of the asymptomatic muscle and at a certain point consistency of coef ficients of variation (CV < of effort requirement, it can no longer sustain the effort 10%) among the five or more repetitions for and increase the amplitude of contraction. Clinically, that each test. occurs when the evaluee/patient gets rather severe mus2. The test/re-test repeatability of such dynamom- cular pain and states that he/she can no longer sustain the etry can be evaluated for response consistency. effort of contraction. Repeatability validation may be considered if As compared to dynamometry, S-EMG does not strength testing results vary within 10%. reflect exactly strength but rather effort and ability to elicit 3. The reliability of dynamometry results may effort (Kumar & Mital, 1996). On the other hand, it is need to be evaluated for adequacy of treatment specific to any given muscle in the myotatic unit, including through comparison with known databases for the injured muscle. As stated above, dynamometry is not the same kind of injury/response. specific to a given muscle but to the whole myotatic unit 4. If such results are available, the dynamometry or to the sum total of the myotatic units involved in the may be considered in terms of specificity, sen- effort of strength testing (Sella & Donaldson, 1998). sitivity, and predictive values. 1. The S-EMG dynamic protocol testing may be 5. As the treatment is initiated, repeated dynamorepeated at least five times for each ROM segmetric testing may show improvements (kilos ment on the affected area and on the contralator pounds) in the overall numerical values reperal area at any particular time. The responses resenting L.O.S. perception. may be validated by showing internal consistency of coefficients of variation (CV < 10%) For the clinician who cannot afford the effort and among the five or more repetitions for each test. luxury of repeated dynamometry to satisfy the objectivity If the CV > 10% for the injured muscle and its criteria defined above, it is advisable to use dynamometry loss of strength but not for the unaffected musno less than three times in the course of the clinical relacles, such a result is relevant of treatment foltionship. Thus, the patient/evaluee may have to be tested low-up. with dynamometry during (1) the diagnostic evaluation, at the (2) beginning of the treatment period, and (3) at the 2. The test/re-test repeatability of such S-EMG end of the treatment period. Ideally, in time and with dynamic protocol testing can be evaluated if

Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury

clinically necessary by at least three repetitions during at least 1 month of testing or treatment. The repeatability validation may be considered if the responses vary within 10%. This holds true for the S-EMG normal or pathological variables. 3. The reliability of S-EMG dynamic protocol testing results treatment adequacy may need to be evaluated in comparison with known databases for the same kind of injury/response. 4. Because results are available for most skeletal muscles, the S-EMG dynamic protocol testing may be considered in terms of specificity, sensitivity, and predictive values. 5. As the treatment is initiated, repeated S-EMG dynamic protocol testing of L.O.S. may show improvements in the overall pattern of change from pathological electric curves to normal curves during activity and rest.

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to one L.O.S. treating modality or to a combination of modalities. It is most relevant to demonstrate of measurement of strength regained through therapy which is consistent and numerical and spans from the beginning to the end of the treatment period. Strengths and Limitations of Loss of Strength (L.O.S.) Investigation Methodologies

In terms of L.O.S. investigation, the L.O.S. questionnaires are consistent if they are given repeatedly. At the same time, the responses are subjective because L.O.S. is a subjective phenomenon, thus the limitation of questionnaires. The same criteria apply to the L.O.S. picture or visual analogue. The strength of the S-EMG modality in the investigative mode is that it measures the consistency of effort for any muscular activity. If the amplitude of the contraction pattern is abnormal, it will remain so as an autonomous For the clinician who cannot afford the effort and factor. As described above, in general, the amplitude of luxury of repeated S-EMG dynamic protocol testing in muscular contraction (at the minimal voluntary contracorder to satisfy all the objectivity criteria defi ned above, tion level of effort) is higher in a muscle affected by loss it is advisable to use such S-EMG dynamic protocolof strength, probably because of the need to recruit more contractile elements for the activity (Sella, 1995). testing no less than three times in the course of the The limitation of the S-EMG modality is that it clinical relationship. cannot measure the intensity of the L.O.S. (Kumar & Thus, the patient/evaluee may have to be tested with S-EMG dynamic protocol testing during (1) the diagnosticMital, 1996). evaluation, at the (2) beginning of the treatment period, S-EMG can be utilized concomitantly with dynamomand (3) at the end of the treatment period. Ideally, theetry. Thus, it can demonstrate internal consistency in itself and also validate the statistical demonstration of the interL.O.S. responses should show a normalization of the Snal consistency of dynamometry (Sella & Donaldson, EMG amplitude curve described above. 1998; Sella, 2000c). The eventual responses should be quite similar on the affected soft tissue injury site and on the contralateral site. Thus, one can investigate L.O.S. of soft tissue injury with several modalities and counter the limitations of one The S-EMG spectral analysis parameter mirrors the element of fatigue. Muscles which have been injured andwith the strength of another. suffer from L.O.S. are easily fatigable in clinical terms. Improvement of strength and stamina may be mirrored byRELATIVE LOSS OF RANGE OF MOTION (L. ROM) the S-EMG spectral analysis results which show the decAcute soft tissue injury is often followed by L. ROM remental curve of the affected/treated muscle to parallel related to functional shortening of the injured muscle, that of the asymptomatic muscle. myotatic unit or joint components (Anchor & Felicetti, 1999; Sella & Donaldson, 1998). The L. ROM may Objective Treatment Outcome Measurement involve direct or indirect trauma to the skin, subcutaneous Objective treatment refers to numerical modalitiestissue, blood vessels, nerves, fascia and skeletal muscle, involved in the L.O.S. rehabilitation process. Such modal-articular components, as well as periosteum and bone. As ities may include physical therapy aimed at musclestated, only L. ROM involving the muscles and fascia are discussed in this chapter. Acute L. ROM is reflected by strengthening, agility, and increased endurance. The objective outcome could be a linear follow-up of the the body’s reflex of splinting. The injured part is “splinted,” i.e., defended, by the surrounding area in terms L.O.S. level at the beginning of the treatment, at each visit, of muscles, joints, and fascia as well as the contralateral and at the end of the treatment period. For instance, the initial soft tissue injury L.O.S. level may be 50% of the area and the appropriate myotatic units of either side. The contralateral strength. With therapy, the strength mayloss of range of motion maintained by pain and tissue inflamation results in relative L. ROM. If the acute L. increase and normalize in time to 95% of the expected level in terms of the contralateral strength. This is pertinentROM is not resolved properly by investigation and treat-

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ment, it may result in the development of myofascitis and 1. The questionnaire may be repeated at least five protective guarding of L. ROM-related features. times within 1 month of testing or beginning of treatment. The responses may be validated as L. ROM assessment of soft tissue injury is easy to showing internal consistency in terms of coefperform using the statistical requirements described ficients of variation (CV < 10%) among the five above. L. ROM can be measured with goniometry (inclior more repetitions for each question and nometry) objectively. A variety of goniometers and incliresponse. nometers are on the market (AMA, 1993; Gerhardt, 1992). They may be applicable to several areas of the body. It is 2. The test/re-test repeatability of such questionnaires can be evaluated for consistent response to very important to utilize the right instrument with the the L. ROM inquiry. Repeatability validation may appropriate consistency of methodology (Gerhardt, 1992). be considered if the responses vary within 10%. For consistency, goniometric testing should be performed at least through five repetitions measuring the 3. The reliability of questionnaire results may need to be evaluated in comparison with known internal consistency of joint motion performance of the databases for the same kind of injury/response. evaluee or patient. For repeatability, the goniometry or other methodologies utilized to assess joint motion should 4. If available, the L. ROM questionnaire may be show a good measure of repeatability for L. ROM assessconsidered in terms of specificity, sensitivity, ment and rehabilitation of joint motion. For reliability, and predictive values. when normative values or databases of objective measure- 5. As the treatment progresses, repeated L. ROM ments are known, the results of the L. ROM investigation questionnaires may show improvements in and/or treatment should be measured against those norjoint ROM overall symptoms/signs, especially mative values in terms of reliability. with regard to the overall intensity of the soft There are several consensus ROM speciality tables. tissue injury. However, the human joint ROM needs further studies in terms of normative data acquisition. For the clinician who cannot afford the effort and When the specificity, sensitivity and predictive valuesluxury of repeated L. ROM questionnaires to satisfy the of any L. ROM investigative methodology are known, objectivity criteria defined above, it is advisable to use clinical results may be comparable to such data. The funcsuch questionnaires no less than three times in the course tional utilization of any L. ROM investigative methodol- of the clinical relationship. Thus, the patient/evaluee may ogy is only as good as the results obtained in relation to have to respond to an original L. ROM questionnaire it. Therefore, the clinician may want to describe the valid-during (1) the diagnostic evaluation, at the (2) beginning ity of the application of the L. ROM investigative tool in of the treatment period, and (3) at the end of the treatment comparison to the results obtained from knowledge ofperiod. Ideally, with treatment and time the responses other treatment. should show a decrease or disappearance of the L. ROM symptoms. Because it is necessary to evaluate treatment results of joint motion rehabilitation before, during, and after treatment, any methodology for L. ROM investiga- The L. ROM Visual Analogue tion/treatment needs to be objective and numerical in This is a visual format which allows the patient/evaluee terms of the overall outcome measurement. The following methodologies for soft tissue L. ROM to describe on a line or graph the extent of joint ROM loss. The visual analogue may be formatted on a ___/Xº measurement are considered. scale where 0/0º represents the highest functional degree of L. ROM perceived (ankylosis) and Xº/Xº represents full L. ROM Questionnaires joint motion. Questionnaires can be used to assess the cause and pres-The visual analogue is easy to perform and takes very ence of loss of joint range of motion. The evaluee/patientlittle time to accomplish. In terms of the parameters described above for the L. ROM questionnaire, the applineeds to be asked about his or her perception of L. ROM before the injury as well as at the time of examination. L.cation is rather similar to visual analogue testing for soft tissue injury L. ROM perception. ROM questionnaires also may assess joint motion rehabilitation through the period of treatment. Any L. ROM questionnaire utilization in soft tissue injury evaluation 1. The L. ROM visual analogue may be repeated may have to be validated in terms of the statistical and at least five times within 1 month of testing or functional criteria described above. Thus, the following the beginning of treatment. The responses may may need to apply for the clinician or the investigator to be validated by showing internal consistency be able to state that the L. ROM questionnaire’ s results using coefficients of variation (CV < 10%) are objectively valid. among the five or more repetitions for each test.

Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury

2. The test/re-test repeatability of such L. ROM visual analogues can be evaluated for response consistency to the L. ROM inquiry. Repeatability validation may be considered if the responses vary within 10%. 3. Reliability of the L. ROM visual analogue results may need to be evaluated in comparison with known databases for adequacy of treatment for the same kind of injury/response. 4. If such results are available, the L. ROM visual analogue may be considered in terms of specificity, sensitivity, and predictive values. 5. As treatment is initiated, repeated L. ROM visual analogue testing may show improvements in the overall numerical values representing the L. ROM parameter.

2.

3.

4.

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area within 1 month of testing or the beginning of treatment. The responses may be validated by showing internal consistency with coef ficients of variation (CV < 10%) among the five or more repetitions for each test. The test/re-test repeatability of such goniometry can be evaluated through the consistency of the response. Repeatability validation may be considered if the joint motion testing results vary within 10%. Reliability of the goniometry results may need to be evaluated in comparison with known adequacy of treatment databases for the same kind of injury/response. If such results are available, the goniometry may be considered in terms of specificity, sensitivity and predictive values. As the treatment is initiated, repeated goniometric testing may show improvements in the overall numerical values representing L. ROM perception of degrees of motion.

For the clinician who cannot afford the effort and 5. luxury of repeated inquiry using L. ROM visual analogue to satisfy the objectivity criteria defined above, it is advisable to use the methodology no less than three times in the course of the clinical relationship. Thus, the patient/ evaluee may have to respond to an original L. ROM visual For the clinician who cannot afford the effort and analogue during (1) the diagnostic evaluation, at the (2)luxury of repeated goniometry in order to satisfy the beginning of the treatment period, and (3) at the end ofobjectivity criteria defined above, it is advisable to use the treatment period. Ideally, with time and treatment thesuch goniometry no less than three times in the course of responses should show a decrease or disappearance of the the clinical relationship. Thus, the patient/evaluee may L. ROM symptoms. have to be tested with goniometry during (1) the diagnostic evaluation, at the (2) beginning of the treatment period, Goniometry (Inclinometry) and (3) at the end of the treatment period. Ideally, responses should show a decrease or disappearance of the Goniometry is the most useful methodology for measuringL. ROM symptoms in time with treatment, i.e., normaljoint motion (Cailliet, 1994). It measures the sum total ofization of the degrees of joint motion. myotatic unit and joint motion rather than individual muscles or joint components. Therefore, soft tissue injury toS-EMG one muscle and probable L. ROM in that muscle are reflected by goniometric testing. However, the testingSurface electromyography is a valid methodology for the involves several groups of muscles and the joint. It is likelyinvestigation and treatment of soft tissue injury L. ROM that the other muscles involved in the testing try to pro-where skeletal muscles are affected. S-EMG reflects the tectively guard the injured muscle and suffer from func-degree of muscular electrical activity and effort during rest tional L. ROM as a consequence. Inflamation of the jointand dynamic action. The S-EMG amplitude curve of a may reduce the ability to achieve full motion. Goniometryjoint motion may be different if that motion is partial or complete. In other words, the amplitude curve of the involves mechanical or electronic gauges. The numbers biceps during 50% of full elbow flexion will be different obtained with various degrees of tested effort represent the overall joint motion of the muscular groups that arethan that of 100% of full elbow flexion. active in the testing. The S-EMG methodology has been described already In forensic terms, it may be relevant to find any degreein terms of specificity, sensitivity, predictive values, laterof symptom magnifi cation of L. ROM perception by ality, internal consistency, repeatability, and reliability. It applying the goniometric instrument to several muscleinvolves dynamic protocols of bilateral myotatic units, at least one of which is affected by a soft tissue injury site. groups and joints, homolateral and contralateral, and identify the L. ROM perception in areas that have not suffered The S-EMG amplitude parameter is useful as an indifrom soft tissue injury. cator of muscular effort and the ability to proceed with a determined effort through full joint ROM. As compared 1. Goniometry may be repeated at least five times to goniometry, S-EMG does not refl ect exactly joint on the affected area and on the contralateral motion but rather effort and ability to elicit effort. On the

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other hand, it is specific to any given muscle in the myo-modalities may include physical therapy aimed at muscle tatic unit, including the injured muscle. As stated above,stretching and lengthening as well as joint ROM. The goniometry is not specifi c to a given muscle but to the whole objective outcome could be a linear follow-up of the L. myotatic unit or to the sum total of the myotatic units andROM level at the beginning of the treatment, at each visit, joint(s) involved in the effort of joint motion testing. and at the end of the treatment period. For instance, the initial soft tissue injury L. ROM level may be 50% of the 1. S-EMG dynamic protocol testing may be contralateral joint motion. With therapy, the joint motion repeated at least five times for each segment of may increase and normalize in time to 95% of the expected ROM on the affected area and on the contralat- level of contralateral joint motion. eral area at any particular time. The responses The example given above is pertinent to one L. ROM may be validated by showing internal consis- treating modality or to a combination modalities. of It is tency of coefficients of variation (CV < 10%) relevant to demonstrate a framework of measurement of among the five or more repetitions for each test. joint motion normalization through therapy which is conIf the CV > 10% for the injured muscle and its sistent and numerical and spans the beginning to the end L. ROM but not for the unaffected muscles, of the treatment period. such a result is relevant treatment follow-up. 2. The test/re-test repeatability of such S-EMG Strengths and Limitations of Loss of Range of Motion dynamic protocol testing can be evaluated if clin- (L. ROM) Investigation Methodologies ically necessary by at least three repetitions during at least 1 month of testing or treatment. For L. ROM investigation, L. ROM questionnaires have the Repeatability validation may be considered if the strength of consistency if they are given repeatedly. At the responses vary within 10%. This holds true for same time, the responses are subjective because active L. ROM is a subjective phenomenon, thus the limitation of the S-EMG normal or pathological variables. questionnaires. The same criteria apply to the L. ROM 3. Reliability of the S-EMG dynamic protocol testing results may need to be evaluated in com- picture or visual analogue. The strength of the S-EMG modality in the investigaparison with known databases for the same kind tive mode is that it measures the consistency of effort of of injury/response for treatment adequacy of L. any muscular activity at any given point or curve of joint ROM. ROM. If the amplitude of the contraction pattern is abnor4. Since such results are available for most skelmal related to L. ROM, it will remain so as an autonomous etal muscles, the S-EMG dynamic protocol testfactor. The limitation of the S-EMG modality is that it ing may be considered in terms of specificity, cannot measure the extent of active L. ROM (Kumar & sensitivity, and predictive values. Mital, 1996; Sella, 2000b). 5. After treatment is initiated, repeated S-EMG S-EMG can be utilized concomitantly with goniometry. dynamic protocol testing of L. ROM may show Thus, it can demonstrate internal consistency and also valiimprovements in the overall pattern of change date the statistical demonstration of goniometry’ s internal from pathological electric curves to normal consistency (Sella, 2000c; Sella & Donaldson, 1998). curves during activity and rest. Thus, one can investigate L. ROM of soft tissue injury For the clinician who cannot afford the effort and with several modalities and counter the limitations of one luxury of repeated S-EMG dynamic protocol testing towith the strength of another. satisfy all the objectivity criteria defined above, it is advisRELATIVE LOSS OF ADEQUATE FUNCTION (L.A.F.) able to use such S-EMG dynamic protocol testing no less than three times in the course of the clinical relationship. Acute soft tissue injury is often followed by loss of adeThus, the patient/evaluee may have to be tested with Squate function of the injured muscle or myotatic unit EMG dynamic protocol testing during (1) the diagnostic (Sella, 1995; 1998a; 1998b). The L.A.F. may involve evaluation, at the (2) beginning of the treatment period, direct or indirect trauma to the skin, subcutaneous tissue, and (3) at the end of the treatment period. Ideally, the blood vessels, nerves, fascia, and skeletal muscle as well responses of L. ROM should show a normalization of the as periosteum and bone. Only L.A.F. involving the musS-EMG amplitude curve described above. The eventual cles and fascia are discussed in this chapter. responses should be quite similar on the affected soft Acute L.A.F. is reflected by the body’ s reflex of splinttissue injury site and on the contralateral site. ing. The injured part is splinted, i.e., defended by the surrounding area of muscles, joints, and fascia as well as Objective Treatment Outcome Measurement the contralateral area and the appropriate myotatic units Objective treatment refers to numerical modalitiesof either side. De-conditioning may be maintained by amation, and resulting relative loss of involved in the L. ROM rehabilitation process. Such pain, tissue infl

Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury

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strength and range of motion. If the acute L.A.F. is not variation (CV < 10%) among the five or more resolved properly through investigation and treatment, it repetitions for each question and response. may result in the development of myofascitis and protec- 2. The test/re-test repeatability of such questiontive guarding. naires can be evaluated for response consistency to the L.A.F. inquiry. The repeatability L.A.F. assessment of soft tissue injury can be pervalidation may be considered if the responses formed according to the components described above. vary within 10%. However, because function is very variable in different individuals, there may be a need for further testing for 3. The reliability of the questionnaire results may pain, loss of range of motion, or loss of strength. Funcneed to be evaluated in comparison with known tional testing needs to follow the same procedural and databases for the same kind of injury/response. statistical principles described above. 4. If available, the L.A.F. questionnaire may be For consistency, it is important to perform any test as considered in terms of specificity, sensitivity many times as possible and measure internal performance and predictive values. consistency of the evaluee or patient. Repeatability, any 5. The treatment progresses, repeated L.A.F. quesmethodology or diversity of methodologies utilized should tionnaires may show improvements in the overshow a good measure of repeatability for L.A.F. assessall symptoms/signs, especially with regard to ment or reduction. Normative values or databases of the overall intensity/frequency of the soft tissue objective measurements of loss of function related to soft injury L.A.F. tissue injury are not available because of the diversity of such losses. Nonetheless, the clinician needs to be on For the clinician who cannot afford the effort and guard for consistency of performance or lack of perfor-luxury of repeated L.A.F. inquiry questionnaires to satisfy mance of individual functional activities, e.g., typing on the objectivity criteria defined above, it is advisable to use a computer. such questionnaires no less than three times in the course When the specificity, sensitivity and predictive valuesof the clinical relationship. Thus, the patient/evaluee may of any L.A.F. investigative methodology are known, thehave to respond to an original L.A.F. inquiry questionnaire clinical results may be comparable to such data. The funcduring (1) the diagnostic evaluation, at the (2) beginning tional utilization of any L.A.F. investigative methodology of the treatment period, and (3) at the end of the treatment is only as good as the results obtained in relation to it.period. Ideally, with time and treatment the responses Therefore, the clinician may want to describe the validityshould show a decrease or disappearance of the L.A.F. of the application of the L.A.F. investigative tool in terms symptoms. of the results obtained from knowledge of the treatment. Because it is necessary to evaluate the treatment The L.A.F. Visual Analogue results before, during, and after treatment, any methodology for L.A.F. investigation/treatment needs to haveThis is a visual format which allows the patient/evaluee objective and numerical overall outcome measurement. to describe on a line or graph the intensity and/or freThe following methodologies for soft tissue L.A.F. quency of the L.A.F. It also may describe graphically the type of L.A.F. that one perceives. The visual analogue is measurement are considered. usually formatted on a ___/10 scale where 10/10 represents the highest degree of L.A.F. perceived in intenL.A.F. Questionnaires sity/frequency and 0/10 represents a complete lack of No soft tissue injury loss of function questionnaires exist.L.A.F. of any region before or after treatment. Therefore, the clinician needs to use models of question- The visual analogue is easy to perform and takes very naires utilized for L. ROM and L.O.S., and modify them little time to accomplish. In terms of the parameters for each individual loss of function case. Any L.A.F. ques-described above for the L.A.F. questionnaire, the applicationnaire utilization in soft tissue injury evaluation may tion is rather similar for the visual analogue testing of soft have to be validated using the statistical and functionaltissue injury L.A.F. perception. criteria described above. Thus, the following may need to apply for the clinician or the investigator to be able to 1. The L.A.F. visual analogue may be repeated at state that there is objective validity to the results of the least five times within 1 month of testing or the L.A.F. questionnaire: beginning of treatment. The responses may be validated by showing internal consistency of coefficients of variation (CV < 10%) among the 1. The questionnaire may be repeated at least five five or more repetitions for each test. times within 1 month of testing or beginning of treatment. The responses may be validated by 2. The test/re-test repeatability of such L.A.F. showing internal consistency of coef ficients of visual analogues can be evaluated for response

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consistency to the L.A.F. inquiry. The repeatability validation may be considered if the responses vary within 10%. This holds true for the variables of L.A.F. intensity, frequency, or quality. 3. The reliability of the L.A.F. visual analogue results may need to be evaluated in comparison with known databases of adequacy of for the same kind of injury/response treatment. 4. If such results are available, the L.A.F. visual analogue may be considered in terms of specificity, sensitivity and predictive values. 5. After treatment is initiated, repeated L.A.F. visual analogue testing may show improvements in the overall numerical values representing the L.A.F. parameters.

numerical and spans the beginning to the end of the treatment period.

STRENGTHS AND LIMITATIONS OF LOSS OF ADEQUATE FUNCTION (L.A.F.) INVESTIGATION METHODOLOGIES

In terms of L.A.F. investigation, the L.A.F. questionnaires have the strength of consistency if they are given repeatedly. At the same time, the responses are subjective because L.A.F. is a subjective phenomenon, thus the limitation of questionnaires. The same criteria apply to the L.A.F. picture or visual analogue. The strength of the S-EMG modality in the investigative mode is that it measures the consistency of effort of any muscular activity, be it normal or related to dysfunction. If the amplitude of the contraction pattern is abnormal related to L.A.F., it will remain so as an autonomous factor. The limitation of the S-EMG For the clinician who cannot afford the effort and modality is that it cannot measure the L.A.F. level luxury of repeated inquiry of L.A.F. visual analogue to (Kumar & Mital, 1996). S-EMG can be utilized consatisfy the objectivity criteria defined above, it is advisable comitantly with dynamometry, goniometry, or other to use such L.A.F. visual analogues no less than three modalities described above (Sella & Donaldson, 1998). times in the course of the clinical relationship. Thus, the Thus, one can investigate L.A.F. of soft tissue injury patient/evaluee may have to respond to an original L.A.F. with several modalities and counter the limitations of visual analogue inquiry during (1) the diagnostic evaluaone with the strength of another. tion, at the (2) beginning of the treatment period, and (3) at the end of the treatment period. Ideally, with time with RADIATION OF SYMPTOMS AND DYSFUNCTION treatment the responses should show a decrease or disapTO THE CONTRALATERAL SIDE OF THE INJURY SITE pearance of the L.A.F. symptoms. Acute soft tissue injury is often followed by loss of adequate function of the injured muscle or myotatic unit A number of objective tests such as dynamometry, goni-(Anchor & Felicetti, 1999). The contralateral and related sites are called into action. The general pattern and process ometry etc. may be applicable on a case-by-case basis loss ” It is important to note of functional activity. No example can be given since eachas known as “protective guarding. that the protective guarding has an immediate positive and loss of function may include different components. beneficial effect of sparing the injured site. A problem ensues if the injured site does not get S-EMG immediate investigative and rehabilitative attention. In the This technology is probably the only soft tissue injury latter case, protective guarding regresses from functional methodology applicable to most, if not all, losses of func-benefit to a dysfunctional process. Only symptoms and tional activity. The parameters of utilization during inves- dysfunctions involving the contralateral side of the injury site muscles and fascia are discussed in this chapter. tigation and treatment have been described above. The contralateral side is overworked, and muscular effort and imbalance are reflected shortly by the symptom OBJECTIVE TREATMENT OUTCOME MEASUREMENT of fatigue. Eventually, there may be functional loss of Objective treatment refers to numerical modalitiesstrength and even joint inflammation. The muscles and the involved in the L.A.F. rehabilitation process. Such modal-fascia may develop primary or secondary myofascitis ities are usually multiple. The objective outcome could be(Busquet, 1998; Cailliet, 1988a; 1992a; Travell & Sima linear follow-up of the L.A.F. level at the beginning of mons, 1983). the treatment, at each visit, and at the end of the treatment If the initial dysfunction related to protective guarding period. For instance, the initial soft tissue injury L.A.F. and indirect radiation of symptoms is not resolved propintensity level may be 9/10, in time it may show a decrease erly during investigation and treatment, it may result in pattern to 7/10, 5/10, and eventually reach 1/10 at the end the development of chronic pain and further dysfunction. of the treatment period. It is important to demonstrateIt is likely that for muscular function, an engram change measurement of the L.A.F. level which is consistent andexists, with the engram of the contralateral side becoming Multiple Modalities

Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury

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dysfunctional. Therefore, in addition to the investigationThe Contralateral Symptoms Radiation and treatment of the various symptoms such as described Visual Analogue above, there is need for S-EMG biofeedback (neuromuscular reeducation) to redress the chronic functional dis-This is a visual format which allows the patient/evaluee to describe on a line or graph the intensity and/or freequilibrium. The assessment of the symptom radiation to thequency of contralateral symptoms radiation. It also may contralateral side may be performed using the compo-describe graphically the type of symptoms of soft tissue nents described above. However, since function is veryinjury perceived. The visual analogue may be formatted variable in different individuals, there may be an addi-on a ___/10 scale where 10/10 represents the highest tional need for testing for pain, loss of range of motion,degree of contralateral dysfunction/radiation perceived in or loss of strength. Functional testing needs to followintensity/frequency and 0/10 represents a complete lack of such dysfunction before or after treatment. The visual the same procedural and statistical principles described analogue is easy to perform and takes very little time to above. For consistency, it is important to perform any testaccomplish. In terms of the parameters described above for other symptoms questionnaires, the application is as many times as possible and measure the internal consistency of the evaluee’ s or patient’s performance. rather similar for the visual analogue testing for soft tissue For repeatability, any methodology or diversity of injury radiation to the contralateral side. methodologies utilized should show a good measure of repeatability in terms of symptoms radiation assess-Objective Tests ment or reduction. A number of objective tests such as dynamometry, goniNormative values or databases of objective meaometry, etc. may be applicable from case to case of funcsurements of contralateral loss of function related to tional activity losses. No example can be given because soft tissue injury are not available because of the divereach loss of function may include different components. sity of such losses. Nonetheless, the clinician needs to be on guard for consistency of performance or lack of S-EMG performance of individual functional activities, e.g., typing at a computer. This technology is probably the only soft tissue injury When the specificity, sensitivity and predictive valuesmethodology applicable to most, if not all, losses of funcof any contralateral investigative methodology are known,tional activity related to symptom/signs radiation to the the clinical results may be comparable to such data. The contralateral side. The parameters of utilization during functional utilization of any contralateral investigative investigation and treatment have been described above. methodology is only as good as the results obtained in relation to it. Therefore, the clinician may want to describeObjective Treatment Outcome Measurement the validity of the application of the contralateral investigative tool in terms of the results obtained from the knowl-Objective treatment refers to numerical modalities edge of the treatment. involved in the rehabilitation process of radiation of symptoms to the contralateral side. Such modalities are usually Because it is necessary to evaluate treatment results before, during, and after treatment, any methodology formultiple. The objective outcome could be a linear followcontralateral radiation of symptoms/signs and investiga-up of the dysfunction level at the beginning of the treatment, at each visit, and at the end of the treatment period. tion/treatment needs to be an objective and numerical For instance, the initial soft tissue injury contralateral overall outcome measurement. The following methodologies for soft tissue contralat- dysfunction intensity level may be 9/10, in time it may show a decrease to 7/10, 5/10, and eventually reach 1/10 eral radiation measurement are considered: at the end of the treatment period. The main thing is to demonstrate a framework of measurement of the dysfuncQuestionnaires of Contralateral Symptom Radiation tional level which is consistent and numerical and spans No soft tissue injury symptoms radiation to the contralat-the beginning to the end of the treatment period. eral side questionnaires exists. Therefore, the clinician needs to use the model of questionnaires utilized for L.RELATIVE EARLY OR LATE DEVELOPMENT OF MYOFASCIAL ROM and L.O.S., and modify such a model for eachPAIN SYNDROME EXEMPLIFIED BY TRIGGER POINTS individual case of contralateral radiation/loss of function. Any such questionnaire utilization in soft tissue injury Myofascitis, exemplified by the presence of trigger points evaluation may have to be validated according to theand associated pain and dysfunction usually develops early in the chronology of soft tissue injury (Anchor & statistical and functional criteria described above.

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Felicetti, 1999). The symptoms are usually a combination Muscular hypotrophy can be investigated with circumof the following: ferential measurements (AMA, 1993). The limitation of this technique is that it measures the whole myotatic unit 1. The presence of exquisitely tender trigger of the muscle, i.e., for biceps brachii hypotrophy, the points with or without radiation circumferential measurement also assesses the other arm 2. The presence of tenderness on the involved muscles such as the triceps, brachialis, and brachioradialis. muscle Nonetheless, this is an objective technique. As such it 3. The presence of loss of strength, time depen- can be utilized within the statistical framework described dent on the same muscle above. Muscular shortening of functional origin may pro4. The eventual functional shortening of the duce pain with motion and functional loss of joint ROM. affected muscle and possibly of the primary These features can be investigated with the means dismyotatic unit followed by loss of strength of cussed earlier. the subtended joint(s) S-EMG testing of the hypotrophic/shortened muscle can 5. The presence of pain that may become chronic be done within the framework of the S-EMG ROM protoand dysfunctional in itself cols. A hypotrophic muscle usually shows loss of strength 6. The radiation to the contralateral side with posand increased amplitude of contraction (µV RMS). Theresible dysfunction in terms of secondary develfore, the S-EMG statistical techniques and the dynamometopment of trigger points and myofascitis to that ric statistical techniques are valid within this context. region In terms of treatment, physical therapy aimed at mus7. Development of symptoms in the radiation area cular agility, strengthening, and endurance in conjunction Radiation of myofascial dysfunction to the contralat- with S-EMG neuromuscular rehabilitation helps redress the hypotrophy/shortening of the dysfunctional muscles, even if eral side is usually referred to as a late development in the chronology of myofascitis. It is important for the cli- applied late in the history of the pathologic event. The same statistical criteria for objectively follow-up of the treatment nician to understand whether a muscle affected by trigger results described above apply within this context. points is a primary muscle or a secondary muscle. In terms of treatment, a muscle which has secondary myofascial involvement needs treatment not only for itself, but alsoSOFT TISSUE INJURY: for the contralateral muscle/myotatic unit that was origiIMPAIRMENT MEASUREMENT nally affected by the soft tissue injury. The questionnaires and investigative modalitiesIf there is a forensic or medicolegal issue with the etiology described above are valid within the framework of theand post-treatment results of soft tissue injury, the clinisymptoms/signs which develop and present themselves cian in may be asked to perform an impairment evaluation. primary or secondary myofascitis. The objective identifi-The clinician needs special training for this task. On the cation of a reduction of symptoms/signs needs to followassumption that one can perform such an evaluation, the the same numerical pattern described above for each major following parameters are paramount to the granting of any soft tissue injury. impairment-related percentage:

LATE DEVELOPMENT OF MUSCULAR HYPOTROPHY/ATROPHY AND RELATIVE SHORTENING

1. The affected part or system must have attained the state of “maximal medical improvement” (AMA, 1993; Sella & Donaldson, 1998). This Muscular hypotrophy has to be identifi ed as resulting means that the intensity/frequency/quality of from structural or functional etiologies (AMA, 1993; any present symptom/sign must have a rather Sella, 1995). The clinician needs to rule out neurological constant value within at least 6 months prior to pathology from myofascial dysfunction. This presentathe evaluation, and presumably stay within the tion does not involve muscular or fascial diseases such same range for the foreseeable 24 months. This as genetic, metabolic, endocrine or toxic myopathies, excludes, of course, terminal events such as and related conditions. amputations or other surgeries which preclude The hypotrophy related to untreated myofascial conreturn to thestatus quo ante function without ditions is a functional one, in the sense that the muscle the help of prostheses, etc. may regain its normal size as the rehabilitative treatment progresses (Bousquet, 1998; Calilliet, 1992a). A finding 2. The impairment needs to be considered within medical technology knowledge to be permanent of muscular hypotrophy and functional shortening is clinrather than temporary in nature (AMA, 1993). ically a sign of lack of appropriate treatment for at least 2 months after the original injury event. A temporary impairment cannot be granted the

Objective Evaluation and Treatment Outcome Measurements in Soft Tissue Injury

status of permanency as with a given degree of permanent disability. 3. The examinee needs to use approved impairment percentages granted according to legal criteria, which may apply differently from state to state. The degree of impairment may be granted according to the consensus process and utilization of the AMA Guidesor other criteria texts (AMA, 1993), as may be found in the Social Security, Workers’Compensation, or federal guidelines, legislative rules, etc. 4. All permanent percentages depend on an objective evaluation process with the statistical input described above.

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Cailliet, R. (1994).Hand pain and impairment . Rene Cailliet Pain Series, Edition 4. Philadelphia: Davis Co. Fischer, A.A. (1977a). New developments in diagnosis of myofascial pain and fibromyalgia. Physical Medicine and Rehabilitation Clinics of North America, 8, 1–21. Fischer, A.A. (1977b). New approaches in treatment of myofascial pain. Physical Medicin and Rehabilitation Clinics of North America, 8,153–169. Fischer, A.A. (1984). Diagnosis and management of chronic pain in physical medicine and rehabilitation. A.P. In Ruskin (Ed.). Current therapy in physiatry (pp. 123–145). Philadelphia: W.B. Saunders. Fischer, A.A. (1987a). Pressure algometry over normal muscles. Standard values, validity and reproducibility of pressure threshold.Pain, 30, 115–126. Fischer, A.A. (1987b). Pressure threshold measurement for diagnosis of myofascial pain and evaluation of treatment results.Clinical Journal of Pain, 2,207–214. SUMMARY Fischer, A.A. (1987c). Muscle tone in normal persons measured by tissue compliance.Journal of Neurological and This chapter described criteria for the objective evaluation Orthopaedic Medicine and Surgery, 227–233. 8, of parameters of dysfunction related to soft tissue injury Fischer, A.A. (1990). Application of pressure algometry in manand tissue response. The methodologies described may be ual medicine.Journal of Manual Medicine, 5, 145–150. utilized in a specific or focused manner as they pertain to Fischer, A.A. (Summer, 1994). Quantitative and objective docuspecific dysfunctions. For instance, dynamometry may be mentation of soft tissue abnormalities: Pressure algometry appropriate in strength testing. Utilizing the strengths of and tissue compliance recording. Spinal Manipulation, different methodologies to counter the limitations of oth1–4. ers is part of the arsenal of diagnostic investigation and Fischer, A.A. (1997). Clinical use of tissue compliance meter follow-up through rehabilitation. for documentation of soft tissue pathology. Clinical Journal of Pain, 3,23–30. Fischer, A.A., & Chang, C.H. (1985). Electromyographic evidence of paraspinal muscle spasm during sleep in REFERENCES patients with low back pain. Clinical Journal of Pain, 27, 203–210. AMA. (1993). AMA guides to evaluation of permanent impairment (4th ed.). Chicago: American Medical Association.Galen, R.S. (1979). Selection of appropriate laboratory tests. In D.S. Young, et al. (Eds.). Clinician and Chemist: The Anchor, K., & Felicetti, T.C. (Eds.) (1999). Disability analysis Relationship of the Laboratory to the Physician. Washin practice (chap. 15, pp. 279–314). Dubuque, Iowa: ington, D.C.: Association for Clinical Chemistry. Kendall/Hunt Publishing Co. Documentation of joint motion (rev. 3rd Basmajian, J.V. & DeLuca, C.J. (1985). Muscles alive, their Gerhardt, J.J. (1992). ed.). Portland, OR: Oregon Medical Association. functions revealed by electromyography (5th ed.). Baltimore: Williams & Wilkins. Kumar, S., & Mital, A. (1996).Electromyography in ergonomics. Toronto: Taylor & Francis. Busquet., L. (1998).Les chaines musculaires (Tomes I, II, III, IV). Paris: Frison Roche. Liu, S., Kopacz, D.J., & Carpenter, R.L. (1995). Quantitative assessment of differential sensory nerve block after Cailliet, R. (1988a).Low back pain syndrome . Rene Cailliet Pain lidocaine spinal anesthesia. Anesthesiology , 82(1), 60–63. Series, Edition 4, Philadelphia: Davis Co, Maigne, R. (1996).Diagnosis and treatment of pain of vertebral Cailliet, R. (1988b).Soft tissue pain and disability . Rene Cailliet origin. Baltimore: Williams & Wilkins. Pain Series, Edition 2. Philadelphia: Davis Co. Cailliet, R. (1991a).Neck and arm pain. Rene Cailliet Pain Masson, E.A., & Boulton, A.J.M. (1991). The neurometer: ValSeries, Edition 3. Philadelphia: Davis Co. idation and comparison with conventional tests for diabetic neuropathy.Diabetic Medicine, 8,S63–S66. Cailliet, R. (1991b).Shoulder pain . Rene Cailliet Pain Series, Edition 3. Philadelphia: Davis Co. Melzack, R. (1975). The McGill pain questionnaire: Major properties and scoring methods. Pain, 1, 277–299. Cailliet, R. (1992a).Head and face pain syndromes . Rene Cailliet Pain Series, Edition 1. Philadelphia: Davis Co. Melzack, R. (1987). The short form McGill pain questionnaire. Pain, 30, 191–197. Cailliet, R. (1992b).Knee pain and disability . Rene Cailliet Pain Series, Edition 3. Philadelphia: Davis Co. Pope, M., Anderson, G., Frymoyer, J., & Chaf fin, D. (Eds.). (1991).Occupational low back pain. Assessment, treatCailliet, R. (1993).Pain: Mechanism and management . Rene ment and prevention. St. Louis: Mosby Year Book. Cailliet Pain Series, Philadelphia: Davis Co.

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Sella, G.E. (1993).Muscles in motion: The S-EMG of the range Sella, G.E. (2000a).Muscular dynamics: Electromyographic assessment of energy and motion. Martins Ferry, OH: of motion of the human body. Martins Ferry, OH: GENMED Publishing, GENMED Publishing. Sella, G.E. (2000b). Graphics of motion: The electromyography Sella, G.E. (1995).Neuromuscular testing with S-EMG. Martins of muscular dynamics. Martins Ferry, OH: GENMED Ferry, OH: GENMED Publishing, Publishing. Sella, G.E. (1997). Daubert and new technologies: An indepenSella, G.E. (2000c). Internal consistency, reproducibility & relident medical examiner’ s view (Parts 1 & 2).Forensic ability of S-EMG testing.Europa Medicophysica, 36, 1, Examiner, The Official Journal of the American College 31–38. of Forensic Examiners,(8), 6 5–8. Guidelines for neuro-muscular reeducation: Sella, G.E. (1998a). The utilization of S-EMG in neuromuscularSella, G.E. (2000d). The electromyographic approach. Martins Ferry, OH: rehabilitation, Proceedings 9th European Congress of GENMED Publishing, Clinical Neurophysiology, Ljubljana, Slovenia, June Sella, G.E., & Donaldson, C.C.S. (1998). Soft tissue injury eval4–7, pp. 357–359. uation: Forensic criteria: A practical manual. Martins Sella, G.E. (1998b). S-EMG Utilization in low back pain invesFerry, OH: GENMED Publishing, tigation and rehabilitation.KinesitherapieScientifique, Travell, J., & Simons, D. (1983). Myofascial pain and dysfunc383, 35. tion: A trigger point manual(Vol. I & II). Baltimore: Williams & Wilkins.

85 From Psychics of the Body to Clinical Outcome via Neurochemistry Gary W. Jay, M.D., F.A.A.P.M., D.A.A.P.M. The title of this chapter was given to me. At first I didn’t When I began to practice pain management in 1980, like it: “Psychics of the body”? Then I realized that this interdisciplinary pain management programs were coming is, more times than we’d like to think and far more into their own. Patient outcomes were good. Over the last frequently than we would like to admit, an accurate2 decades, the business people controlling the application description of what may pass for medicine, particularlyof medicine, good or bad, realized that while these types pain management. of patient treatment programs did work, they were expenLooking at the way we were trained, anatomically sive. So, getting reimbursed for applying inter- or transbiased for the most part, we have become a group of disciplinary pain treatment was lost, because of monetary physicians who think we know what is going on wheninterests rather than patient care interests. seeing a patient purely on the basis of where the pain is Anatomical, mechanistic algorithms were developed located. The differential diagnosis then becomes a matter and placed into the practice setting. Physicians didn’t need of which nerves connect to which nerves and the spinal to be told what they could or couldn’t do. They were just cord, and then the brain, and how we can stop the pain stymied by their inability to receive payment for services from peripheral nervous system response to injury. that the insurers didn’t feel like reimbursing. Some insurWe have begun to develop a significant armamentarers went even further, independent of medical realities, ium in our treatment options. Almost always, it beginsdetermining which disorders were, to them, real, and with analgesics. Good primary care physicians recognize which ones were not. Those that insurers did not want to that they need to ameliorate a patient’s pain. That is what recognize as real were a priori not real and medical treatthey were trained to do. So, unless there are reasons for ment for them did not justify reimbursement. doing any tests, the vast majority of which look at anatomy Today business people who are involved in running (plain X-rays, CAT scans, MRI scans), analgesic medica-pain centers ask, “You tell me that psychological or psytions are utilized. chiatric input is necessary in the treatment of chronic pain Then there are the pain management specialists who patients. Well, how come I can’ t find any multidisciplinary are trained to do blocks. They do them very well. Unfor-pain centers that have psychologists in them?” tunately, some are satisfied in knowing that a patient’s Unfortunately, they are correct. pain is in his or her neck. Like any carpenter with a Some of these folk have looked at the nonmedical hammer, everything is a nail. The patient, therefore, willrealities and determined that a real interdisciplinary pain undergo a series of epidural blocks. If these don’t stop the center now consists of a physician and a physical therapist. patient’s pain, he or she is trundled off to another type ofWhy? Both can receive reimbursement, however poor it specialist, frequently a psychiatrist or psychologist. may be.

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reveal that his broken arm is healing well. His general A lot of psychologists are driving cabs, it seems. surgeon is happy with the way the abdominal wounds from So, where does that leave us? It seems to this author surgery have healed. His primary care physician gives him that it leaves us with four choices. First, pain management specialists should band together for the sake of theirmore medication, “mild” opiates, for his continued compatients and ght fi this administrative determination of plaints of headache. “appropriate care” of chronic pain patients. This needs to Six months later, Mr. Jones is complaining about conbe done locally, regionally, and nationally, at the varioustinued headache as well as pain in the abdomen around the scar tissue and continued pain in the arm. levels of the insurance companies, the HMOs, the PPOs, and, of course, in Washington. However, until three phy- Tests are done; CAT scans, MRI scans, blood work, all are normal. Mr. Jones is now a chronic pain patient, sicians in a room can come to a single consensus, this probably won’t happen. More importantly, if an insurance with no anatomical or mechanistic explanations of any of company doesn’ t want something to be done, it has the his pain complaints. The initial injuries were clear, “exact” problems with clout (read: Money) to not only assure that it doesn’ t get ramifications directly to the periphery. Pain from Mr. done, but also to destroy those physicians who care Jones’ injuries was transmitted via the peripheral nervous enough about their patients to persistently try to do it. system to the spinal cord and then to the central nervous Second, we can meekly continue to do things the way system via neuroanatomic pathways that are understood: they are now. Incredibly intelligent pain management phyPain, via Cand A-delta fibers, comes into the spinal cord sicians are losing their livelihoods as well as their selfrespect because they can’ t band together effectively to dorsal horns, some decussate and travel rostrally via the spinothalamic tract, among other pathways. The question, enable the best patient care to be used. The national phyarm is healed, sician organizations appear to be too mired in their own6 months later, is simply put: Mr. Jones’ he had no complications from surgery for his ruptured internal politics to help. spleen, and no anatomical lesions exist in the cervical Third, we can do our best to teach the patients, the folks who have lost their ability to receive the care theyspine. Yet, he still has pain. need and deserve, and enlist their help in trying to change The peripheral nervous system has no reason to be the way things are. Unfortunately, if the layperson t isn’ ringing the pain bell, no reasons for nociception to be continuing. sick, he or she seems to find no reason to fight for someMany physicians stop there in their analysis and begun thing not needed. At least not yet. Finally, we, as physicians, can make the best of whatto look for secondary gain issues or other motivations for we have left to use to help our pain patients. Anatomical,Mr. Jones to have pain. Does he like his narcotics too much? Does he want to stay home and not return to work? mechanistic treatments are going to have to take second place to a better understanding of neurochemistry: the The obvious fact is that peripheral mechanisms of pain physiology and the pathophysiology of the “software” of may affect central mechanisms. These central mechanisms both the peripheral and the central nervous systems. may essentially take on a nociceptive life of their own. At this point, treating the peripheral end organ does not help As the insurance companies, HMOs, and PPOs have the pain, as the pain is now central in nature, with contindetermined, it costs only 1.2 cents for a generic acetamiuous central nervous system input that is no longer a nophen and codeine tablet. Cheap enough to allow hundreds of the first initiating peripheral mechanisms. and thousands to be prescribed. This makes some sensefunction to belly them, as an hour of hands-on physical therapy costs far more. Most commonly, the surgeon looks at Mr. Jones’ In their minds, stopping the pain is ne, fi and drugs, especially and can’t find a reason for the pain. The orthopedist cannot find a reason for continued arm pain, which is now assoinexpensive ones, are good ways to do this. ciated with edema, hyperesthesia, and even allodynia. The As pain management physicians, we should be the most knowledgeable regarding the pathophysiology ofprimary care physician cannot find a reason for Mr. Jones’ headache, except possibly some minimal spasm in the neurotransmitter systems in the brain, and how to use this cervical paravertebral muscles and the bilateral trapezius information for the betterment of our patients. However, looking at the original premise of how we musculature. were taught, we tend to look at the anatomy first. Patient In general, physicians tend to look for the primary anatomical reasons for pain, acute or chronic. When they Jones is in a motor vehicle accident. His spleen is ruptured; this is verified by a CAT scan, so we surgicallyare not found, the ability to give further aid is uncertain. remove it. His arm is broken. Radiographic studies show The pain is a pathophysiological problem that cannot be found on examination. Windup phenomena, whereby us the break. Orthopedists are called in and the appropriate treatment is performed. Mr. Jones’ headaches secondary continuous C-fiber stimulation of the wide dynamic range to the acceleration/deceleration, or whiplash injury heneurons in the spinal cord, which turns these “on-off” cells received, are treated with NSAIDS. He is out of the hos-on, full time, cannot be anatomically located via any stanpital in a week. Medical rechecks with his orthopedistdard testing. Pain derived from the sympathetic nervous

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system secondary to such a physiological problem cannot The pathophysiology of chronic (posttraumatic) tension-type headache has been described in detail in another be seen with any anatomical test currently used. chapter in this volume. To summarize: initial myofascial There are no blood tests for pain, nor are any other nociception secondary to the acceleration/deceleration anatomic, mechanistic tests of chronic benign pain feasible at this time. Greater levels of information must beinjury will, if not treated appropriately in the first 2 to 6 weeks postinjury (via physical therapy, NSAIDS, and for obtained and used by the pain management specialist. some patients a muscle relaxant) will develop into a myoBefore one can utilize a test for selective tissue conducfascial pain syndrome, with continuous nociceptive infortance (sudomotor, or sweat testing), the physician must mation going to the cervical aspects of the trigeminal have determined a basis for looking. nucleus and then rostrally. Continued nociception will Pathological changes of the central nervous system do exist in patients with chronic pain if it is of neuropathic induce changes in the serotonergic system via loss of or sympathetic origin. Neuroma formation, deafferenta-metabolic ability to maintain homeostasis and the develtion, Wallerian degeneration do occur, with cell death inopment of “empty neurons” as well as serotonergic recepthe periphery as well as the spinal cord. Gliosis followingtor hypersensitivity. Affective disorders secondary to these neurochemical changes of the serotonergic, noradsuch neuronal cell death has been found on autopsy same to renergic, and endogenous opiate systems occur. The prioccur in the spinal cord, as well as in the thalamus. Howmary locus of pain from chronic tension-type headache ever, there are no tests available to the clinician that show then becomes central, secondary to dysmodulation of such this. neurotransmitter systems, while the initiating peripheral When pain becomes centralized, techniques must be mechanisms become secondary. used to deal with aberrant, dysmodulated neurotransmitter At this point, physical therapy will be palliative, as systems. Anticonvulsant medications which function by increasing inhibitory neurotransmitter functions (such asthe pain problem is central, not peripheral. gabapentin working to increase GABA, gamma amino- To treat this entity one must return the central neurobutyric acid, an inhibitory neurotransmitter; or clon- transmitter systems to a homeostatic norm. Treatment azepam, which increases GABA in the internuncial neu-should thus be geared to this goal. The use of neuropharmacological entities that can do this is mandatory. Serorons of the spinal cord) become very useful, despite the tonergics and GABAnergic medications, possibly with fact that no seizures are occurring. However, one must know the pathophysiology of theothers, are necessary. The use of other types of medicaproblem on a neurochemical level to knowing what med-tions such as the alpha-II agonist tizanidine, which acts as a muscle relaxant and also works to diminish muscle ications to use, and why. Unfortunately, again, some clinicians treat by rote.pain via noradrenergic system manipulation, also may be effective, but only if used by physicians who recognize They have read in a journal that gabapentin helped, anecdotally, several patients with reflex sympathetic dystro-the problem for what it is and utilize neuropharmacologphy/complex regional pain syndrome-I and so they use itical manipulations that can appropriately affect central neurotransmitter systems. at the dosages that they read were used. I think this is bad only insofar as the clinicians are doing something that All that stated, the clinician must remember that while they have read about to help a patient without fully under-trying to return the dysmodulated central neurotransmitter systems to normal pharmacologically, the associated sleep standing the pathophysiological problem they are attemptdisorder must be dealt with (again, serotonergically), ing to treat, or more importantly, why it may help. along with physical therapy to stop any further continuaOf course, with so much to read and so many specialties and subspecialties to read it for, I certainly would nottion of peripheral nociception, and psychological care, to prevent the affective problems of depression and/or anxiexpect all physicians who use gabapentin (again, only an ety (both with a neurochemical basis) from persisting and, example) to have such a deep understanding of its neurotherefore, preventing the return of central neurotransmitter pharmacology. But, this is an area that the pain specialist should be accountable for learning; in reality, any and allsystem(s) homeostasis. pain specialists who are responsible for the diagnosis and Then there is the issue of chronic analgesic usage. treatment of chronic pain should be highly conversant withThis problem creates a separate headache entity, analgesic rebound headache. The continuous use of analgesics, narthis information. This is an area of extreme import, a place where we,cotic or not, will further depress the innate, endogenous opiate system via a negative feedback loop. Until this as pain specialists, can and should excel. Turning to Mr. Jones’headaches, the applied treat- headache form, which is purely neurochemical/neurophysiological in nature, is dealt with by stopping all exogment has been analgesics, starting with simple analgesics and then climbing the WHO (World Health Organization) enous analgesics in a safe, physiological manner, no other form of treatment for any of the headache problems Mr. ladder to narcotics. This is a simplistic, knee jerk response to the complaint of pain, in this case, chronic headache.Jones is enduring will be effective.

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Finally, there is the continued abdominal pain that is We appear to be at some sort of crossroad. Pain is now the “fifth vital sign” in the VA hospital system. JCAHO bothering Mr. Jones. His pain is described as lancinating, with electrical-like jolts. These pain attributes speak for(Joint Commission on Accreditation of Hospital Organineuropathic pain, most commonly from the cutting of sen-zations) has decided to come out with specific guidelines for the treatment of pain. CARF (Commission on Accredsory nerves during the surgery. These nerves may develop itation of Rehabilitation Facilities) has been doing this for neuromas, with ectopic electrogenesis inducing continuous nociceptive information. This continuous afferent nocicep-years. What is most confusing is that the CARF guidelines tive stimulation can induce central changes, rst fiat the level stress and demand an interdisciplinary treatment team. of the spinal cord, and later in the brain. Once again, the clinician is forced to think about cen-What I have seen of the JCAHO guidelines echoes this. tral neurochemical changes as well as, at least initially,Some states even tie reimbursement to being CARF accredited. I would certainly think this reasonable, if not peripheral changes. The use of tricyclic antidepressant (TCA) medications to help with the nerve-generatedfor the fact that we clinicians who go the extra mile to (neuropathic) pain may work both centrally as well asachieve such accreditation lose money every time, as we peripherally, with the TCAs also acting as local anesthet-must (and wish to) bring in psychological care, biofeedback for stress reduction, and more, as the guidelines ics at the site of nerve injury/ectopic electrogenesis and/or via the peripheral sodium pumps. Anticonvulsant medica-indicate we must. tions also may work both centrally and possibly periph- Yet, the vast majority of insurance companies, HMOs, erally. Mexiletine Hcl, essentially an oral form of and PPOs, along with Medicare and Medicaid, will not — the same ones we lidocaine, has been used for its ability to diminish abnor-pay for (reimburse) these services must have to meet accreditation standards. mal nerve impulses. Again, the use of specific medications This all leaves us to do what we can, in spite of the for their specific abilities to deal with the specific pathophysiological problems associated with a particular formmoneyed forces arrayed against us. We should be gathering information regarding the varof pain is appropriate and of extreme import. The use of narcotics for central and neuropathic painious treatment modalities, single or multiple, that are used has been felt only recently to be useful. The logic, overeffectively, or not so effectively, for specific pain problems. Clinical outcomes measurement is important and all the last several years, is that all pain must be eradicated. This is surely a worthy goal. I have found that narcoticspain specialists should focus more on this. Evidence-based are useful, but only in combination with other appropriatemedicine is important, and will hopefully become more important as time passes. Money saved by pain specialists neuropharmacological treatments, specifi cally to maxiwho use proper treatments and who can document their mize function. The use of narcotics with N-methyl-D-aspartate outcomes, monetarily and from other aspects such as (NMDA) receptor antagonists is an area of burgeoningdegree of pain relief, degree of functional return, and research. To date, none are clinically helpful. Oral dosingreturn to work data, is important information to document. The data may eventually have some impact on the insurers. of dextromethorphan creates significant side effects. Ketamine, in several forms, is being investigated. These med- Nonfunding of treatment by insurers and employers appears to be bad judgment, as they do not save costs, just ications are being tested to see if their use will decrease problems with narcotic tolerance as well as possibly allowput them off into the future, where a patient may need several times the initial amount of capital for care than a lesser dosage of narcotic to be utilized, again, very would have been necessary had it been done appropriately worthy goals. s pain problem. Some clinicians are pushing the use of chronic nar-at the onset of the patient’ What we as clinicians also can do is work to undercotics for chronic benign headache. In my 2 decades of stand the pathophysiology of chronic pain in enough detail treating thousands of headache patients, I have never had to use the tools, the medications we do have, in the best to use this tactic to ameliorate or eradicate chronic headway possible. This may be, for now at least, the best we ache. However, I was able to utilize an interdisciplinary can do to help our chronic pain patients. We should be the treatment protocol to effectively treat headache patients. best at doing it, and have the greatest understanding of Now, with the inability to be reimbursed for appropriate the intrinsic reasons for using specific medications to deal interdisciplinary treatment of chronic headache patients, with specific CNS neuropharmacological abnormalities. this may become the surrogate treatment of choice because fewer and fewer of the appropriate modalities are being It is the least, or the most, we can do. reimbursed when used to treat these patients.

86 Musculoskeletal Ultrasound John Porter, M.D. and Michael S. Jablon, M.S.T. BRIEF HISTORY

centers, it is much less expensive than other imaging studies. Disadvantages, such as a learning curve, ease of interAccording to leading radiologist Barry Goldberg, in an arti-pretation, and variable image quality, seem to be dimincle published in the May 1998 issueDiagnostic of Imaging, ishing as technology and experience increase. “…in ten years ultrasound will account for more than half Ultrasound is the ideal modality for the examination of all soft-tissue imaging studies.” Ultrasound, which is theof soft tissue because of its multiplanar and real-time first study of choice in obstetrics and cardiology, will capabilities. Sonography yields anatomic information durbecome the primary imaging study for all soft-tissue abnor-ing active and passive mobilization that is unattainable malities, with CT, MR, nuclear medicine, and angiography with other modalities. In addition, synovial and cartilage relegated to a secondary position when, in rare instances, thickness can be accurately quantitated, providing an objecultrasound cannot provide adequate diagnostic information. tive means of following patients with infl ammatory arthritThe history of ultrasound dates back to 1912 when ides. Ultrasound examination of deep-seated joints such as Lewis Fry Richardson in England patented two schemes the hip and shoulder is especially valuable. Joint effusions, for obstacle avoidance as a response to the sinking of the loose bodies, tendonitis, and tendon and muscle ruptures can Titanic. The outbreak of World War I in 1914 and the all be demonstrated sonographically. The noninvasive nature menace of the submarine focused new attention on ultraof the examination and lack of ionizing radiation make it sound as a way to detect objects underwater. very well accepted by patients, especially children. Since ultrasound’ s potential value in clinical medicine was first realized in the late 1940s and early 1950s, a slow but steady advance in its use has occurred. This ULTRASOUND — THE NEW GOLD process has been spurred by improvements in technology STANDARD FOR SHOULDERS that have enabled ultrasound systems to obtain increasIn the April 2000 issue of the Journal of Bone and Joint ingly refined anatomical detail and to detectowfl in Surgery, Sharlene A. Teefey M.D., et al., in an article increasingly smaller vessels. ” conThe utilization of ultrasound has progressed to theentitled “ Ultrasonography of the Rotator Cuff, “ ltrasonography was highly accurate for point at which almost 25% of all imaging studies world- cluded that U wide are ultrasound exams. The World Health Organiza-detecting full-thickness rotator cuff tears, characterizing their extent, and visualizing dislocations of the biceps tion recommends the use of ultrasound after basic X-ray, and not CT or MR, due to wide availability of scanners. tendon.” The article also revealed the results…“Ultraed all sixty-five full thickThe merits of ultrasonography as a diagnostic studysonography correctly identifi are obvious. It is noninvasive and has no know risk. It canness rotator cuff tears (a sensitivity of 100 percent). be done quickly, with little discomfort to the patient, and There were seventeen true-negative and three false-poscity of 85 percent). The the capacity for bilateral imaging makes comparison withitive ultrasonograms (a specifi ” the asymptomatic, contralateral limb possible. In mostoverall accuracy was 96 percent.

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FIGURE 86.1 A normal biceps tendon in a transverse imagingFIGURE 86.2 A complete medial dislocation of the biceps tenplane. (s) skin surface; (ad) anterior deltoid; (tl) transversedon. The transverse humeral ligament (small arrows) appears humeral ligament; (b) biceps tendon. markedly distended.

MUSCULOSKELETAL ULTRASOUND VS. MRI BENEFITS

OF

MRI

MRI use in medicine dates back to the early 1970s, and it has several advantages over diagnostic ultrasound. First, MR images, because of the similarity to actual anatomy, are familiar to both radiologists and referring physicians. Second, MR images can be acquired at distant sites 24 hours a day and interpreted in a timely and cost-ef ficient manner. Third, MR images provide a comprehensive evaluation of an extremity, including abnormalities of bone, cartilage, and soft tissues. Finally, standard MRI protocols have been systematized to the point that they are mostly operator independent. FIGURE 86.3 A normal supraspinatus tendon. (s) skin; (d) deltoid; (c) coracoid process; (b) bursa; (st) supraspinatus tendon; (h) humerus. Sonography, which has been used in medicine for more

BENEFITS

OF

ULTRASOUND

than 30 years, has a different set of benefits. First, new and continuously improving high-frequency transducersallows for evaluation in the neutral position and during allow detailed visualization of superficial structures. Sec-external rotation. This view is important as transient ond, sonography is portable, more available, and less medial subluxation of the long head of the biceps brachii expensive. Third, because sonography works in real time, tendon may occur only in this position. Because MRI procedures such as joint aspiration can be guided with is utilizing static pictures, if transient biceps brachii sonography once an abnormality is detected. Fourth, tendon dislocation is not present in the neutral position because sonography measures motion, a dynamic examiit will remain undetected (Jacobson, 1998) (Figures 86.1 nation may detect abnormalities that are present only with and 86.2). joint positioning and not obtainable with MRI. Another abnormality that may be identified better by Sonography should be the modality of choice whensonography than by MRI is calcium hydorxyapatite crystal a tendon abnormality is clinically suspected. It is likely deposition or calcific tendonitis. Because calcifications, that because of the new high-resolution transducers diflike tendons, appear as low signal on MRI images, their ferentiation between full-thickness and partial-thicknessintratendonous presence may go unrecognized (Figures tendon tears can be identifi ed with greater ease than 86.3 and 86.4). with MRI. In addition, when evaluating the biceps The Achilles tendon can be quickly and accurately brachii long head tendon for subluxation, the sonogramevaluated. Sonography, like MRI, is useful in demon-

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FIGURE 86.4 The area of increased echo signal within the FIGURE 86.6 An enlarged gastrocnemius-semimembranosis interstitial fibers of the supraspinatus tendon is consistent withbursa, consistent with a Baker’ s cyst. calcification (arrow).

semimembraneous bursa, or Baker cyst. Sonography can confirm the presence of a cystic mass between the semimembraneous and the medial head of the gastrocnemius tendons. The diagnosis of Baker cyst, however, requires demonstration of a communicating neck between the posterior knee joint and the semimembraneous-medial gastrocnemius cyst. Other cystic masses can essentially be excluded once this communication is identi fi ed (Figures 86.5 and 86.6). For patients with contraindications for MRI sonography is recommended as an alternative imaging method. Potential contraindications for MRI include the presence of certain metal implants or metal foreign bodies, cardiac pacemakers or other implanted electronic devices, pregnancy, and claustrophobia. FIGURE 86.5 A normal posteriomedial aspect of the popliteal GENERAL APPLICATIONS fossa. (mg) medial head of the gastrocnemius muscle; (st) semiSONOGRAPHY OF MUSCLE membranosis tendon.

OF SONOGRAPHY

Fifteen years before the development of MRI, ultrasound strating full-thickness tendon tear, partial-thickness tear,was the first real time imaging modality available for the and tendonitis. High-resolution sonography allowsevaluation of muscle pathology. Sonography can provide detection of an intact plantaris tendon,ficult dif at best all of the information available with MRI and more with to identify with MRI imaging. When a full-thickness regard to muscle pathology. Its spatial resolution and defAchilles tendon tear is identifi ed by sonography, passive inition of muscle structure are usually superior to that plantar flexion is used to determine if the torn tendon provided by MRI. ends become approximated. Obtaining similar results Numerous muscular pathologies can be readily with MRI imaging would require patient repositioning detected with sonography. Small intramuscular lesions, and generally is not done. Accurate sonographic infor-localized inflammation and edema within the tissue (myomation regarding the plantaris tendon and the tornsitis), and detection of intramuscular lesions are readily Achilles tendon approximation can assist the surgeon indetected with sonography. Sonography provides the functional capability of evaluating an area in motion; therefore, deciding between surgical and conservative treatment. even the most obscure of intramuscular pathology can be Cost savings and patient convenience will become major detected. Overstretching (distraction) lesions, which most considerations in the near future. A palpable mass within the medial aspect of the pos-often occur in runners, ballet dancers, and gymnasts, are terior knee suggests the possibility of gastrocnemius-also routinely identified with sonography.

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TENDONS

These intrasubstance tears cannot be repaired surgically. Sonography demonstrates the full extent of the Prior to the application of ultrasound to the evaluation of thelesion. This allows the surgeon to prepare most accurately musculoskeletal system, clinicians relied on low-kilo voltagein a pre-operative setting. radiography and xeroradiography to aid in the diagnosis of Three other disease processes are included in the diftenomuscular injury (Bock, et al., 1981). These techniques ferential diagnosis of soft tissue lesions of the shoulder. provided little information beyond indicating the site of soft These are biceps tendonitis, biceps tendon dislocation, and tissue swelling. Ultrasound provides detailed informationedema of the rotator cuff (Jobe & Jobe, 1983). about the involved anatomy and nature of the pathology. Chronic tendonitis is easily diagnosed by an experiSONOGRAPHY OF LIGAMENTS enced musculoskeletal ultrasound sonographer. Frequently an increase in synovial fluid does not exist. The Traumatic injury of ligaments in the knee and ankle are most common finding is thickening of the tendon itself very common, usually involving athletes participating in (Middleton, et al., 1985; 1986). Ultrasonic comparisons contact sports. Clinical examination is usuallyficult dif to with the asymptomatic side are essential to make the diagperform immediately following an injury. Chronic liganosis of chronic tendonitis (Bruce et al., 1982; Crass et al., mentous injuries and cartilage defects associated with 1984, 1986; Demarais et al., 1984; Dillehay et al., 1984; either acute or chronic trauma areficult dif to evaluate Blei et al., 1986; Fornage, 1986). clinically. Arthroscopy is an excellent tool to evaluate the Tendonitis is almost always attributable to chronic cruciate ligaments and menisci, but extracapsular ligatrauma and a high level of athletic activity (Roels & Marments cannot be visualized. Computed tomography (CT) tens, 1978; Feretti, Puddu, & Mariani, et al., 1985). The lacks appropriate contrast resolution to delineate ligamensonographicfindings are identical in all locations. Focal tous structures. Ultrasound and magnetic resonance imagthickening of the tendon and increased distance between ing (MRI) are the best diagnostic modalities utilized today the longitudinal collagen bers fi are invariably present. for the examination of ligaments. Both of these imaging Focal hypoechoic areas within the tendon are also present. techniques provide multiplanar capability and demonThe longitudinal tendon fibers are seen to be intact. In strate ligamentous anatomy well (van Holsbeeck & Introsome patients, tendonitis continues for years with intercaso, 1991). mittent flare-ups. Calcification is most common at the The advantages of ultrasound over MRI are ambuladistal tendon insertion. tory diagnostic capabilities, along with dynamic examination, cost, and patient compliance. The test also can be TENDON RUPTURE performed in the locker room, bedside, or in a physician’ s office. Often, rapid diagnosis allows for prompt therapy Rotator cuff tears are a frequent finding in the elderly and may be entirely asymptomatic. Autopsy studies of indi-and rehabilitation, thus giving a better diagnosis. viduals more than 55 years old have discovered rotator cuff tears in 32% (Peterson & Gentz, 1983). However, aSONOGRAPHY OF BURSAE true traumatic tear is a rare finding. These lesions are most The word bursa is derived from the Greek, meaning a common in athletes, such as baseball pitchers, javelin wine skin. In modern usage, bursa refers to a variety of throwers, and football quarterbacks. The principal sonographic ndings fi (Bretzke, Crass, structures that have several features in common. They are Craig, 1985; Linnen et al., 1985) are uid-filled fl defects in all saclike structures with a lining similar to that found in the supraspinatus tendon and increased uid in fl the subac- diarthrodial joints. In addition, they are situated to faciliromial deltoid bursa. In some chronic cases of rotator cufftate movement of musculoskeletal structures (Canoso, tear, the supraspinatus muscle layer may be completely 1981). Bursae are found in areas where a ficant signi absent (Mack, Matsen, Kolcoyne, et al., 1985). The diam-amount of motion can be expected, yet not necessarily eter of the tear measured sonographically is always smaller isolated to synovial joints. The analogy of a wine skin is quite appropriate; both than that observed with arthroscopy, plain film arthrography, or CT arthrography (Beltran, Gray, Bools, et al., 1986).have their greatest dimensions in length and width. This In all of these invasive diagnostic modalities the joint isprovides a large surface area that occupy little volume distended with uid, fl air, or both. This leads to an exagger- under normal circumstances (Codman, 1931). When positioned between two structures, this alignment allows ation of the dimensions of the tear and the degree of muscle mobility and gliding of one structure on the other. retraction (Ahovuo, Poavolaine, & Slatis, 1984). Tendon tears can be isolated to the intrasubstance Some anatomists (Gray, Piersol) believe that bursae are fibers. Often, they will not communicate with the capsulesacsfilled with fluid. This is a misconception resulting from studies performed by injecting bursae with various materials. or subacromial deltoid bursa. OF

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Physicians who perform bursography and bursocopy often debated in literature (Depalma, 1983; Refior, Krodel, & Melzer, 1987). There is, as yet, no proof of the relationship share this misconception because they distend the bursae with contrast material or irrigationuid. fl In reality, bursae of these findings to certain types of shoulder disease, such contain only a thin lm fi of viscous fluid, which serves as a as hydroxyapatite deposition disease, impingement, and rotator cuff disease. More recently, finding ossification in lubricant. The walls are separated by uid a flfilm approximately 1 mm thick. There fore, bursae are really potentialthe coracoacromial ligament, acromioclavicular osteoarspaces, only becominguid-filled fl sacs under pathological thritis, and narrowing of the subacromial space have been cited as signs of rotator cuff disease (Peterson and Gentz, conditions (van Holsbeeck & Introcaso, 1989). Bursae are divided into two groups, communicating1983; Resnick & Niwayama, 1988; Gielen, van Holsand noncommunicating, depending on their relationshipbeeck, Hauglustaine, et al., 1990). to a joint space. Noncommunicating bursae are more com- Both arthrography and arthroscopy of the shoulder were introduced during the 1970s. Arthroscopy of the mon in humans. Further categorization of bursae may be shoulder is, without doubt, the most complete examination made based on their location: subcutaneous or deep of the rotator cuff (Ogilvie Harris & Wiley, 1986). The (Canoso, 1981). Subcutaneous bursae are located between orthopaedic surgeon examines the articular surface of the a bone and the overlying skin, such as the pre-patellar and rotator cuff through the joint. Then a new incision is made olecranon bursae. Bursae are located in many places deep to examine the bursal surface of the cuff through the in the fascia. They separate the joint capsule, tendons, subacromial deltoid bursa. Not only are rotator cuff tears ligaments, and fascial planes (iliotibial tract). Ultrasound provides the clinician with a noninvasive seen, but tears of the labrum also are visualized. The orthopaedic surgeon has a clear view of the synovial cavity means of examining the bursae. In acute traumatic bursitis and can, therefore, diagnose synovial disease at an early the primary value of sonography is to confirm that disease stage. Arthroscopic surgery may be performed during the is limited to the bursa. Associated tendons, ligaments and same session (Van Holsbeeck & Introcaso, 1989). joint space are easily examined to exclude bursitis secondary to pathology originating in these structures (Fig- A disadvantage of arthroscopy is the invasive character of the procedure. Numerous complications such as ures 86.7 and 86.8). neurovascular complications, damage to the labrum, considerable muscle injury, infection, and hemarthrosis have SONOGRAPHY OF THE SHOULDER been described (Jeffries, Gainor, & Allen, et al., 1987; Lindenbaum, 1981). Chronic draining fistulas and leaking In the 1960s, clinicians called the shoulder the “forgotten of synovial fluid are often cited as the most common joint” (Golding, 1962). There were no diagnostic modalcomplications (Henderson & Hoson, 1982). ities other than plain radiography for shoulder evaluation. Not all shoulder pathology is detectable with an arthroPlain films are normal in more than 90% of patients with scope (Jobe & Jobe, 1983). Rotator cuff lesions communichronic shoulder pain. Tendon calcifications are present cating with the joint or subacromial-subdeltoid bursa are in some of these patients; others have ossified tendon detected arthroscopically (Refi or, Krodel, & Melzer, et al., insertions or cystic lesions around the anatomical neck. 1987). Rotator cuff edema andbrosis, fi generally regarded The significance of all these plain film findings is still as the precursor of a rotator cuff tear, are not an arthroscopic

FIGURE 86.7 A normal supaspinatus tendon and overlying SA- FIGURE 86.8 Inflammation and thickening in the bursa consisSD bursa (arrows). tent with bursitis.

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diagnosis (Neer, 1983). Orthopedic surgeons refer to these abnormalities as impingement syndrome. Arthrography of the shoulder is less invasive than arthroscopy (Ahovuo, 1984). This procedure identi fies full-thickness tears of the rotator cuff and tears involving the articular surface of the supraspinatus tendon. Detection of incomplete tears to the superior surface of the rotator cuff requires injection of the subacromial deltoid bursa (Neer, 1983). This type of tear is less common, and represents less than 5% of all rotator cuff tears. Most of the interventional radiologists, therefore, rarely perform an injection of the subacromial deltoid bursa. Arthrography has not been found to be effective in the evaluation of edema and interstitial defects of the rotator cuff. Like FIGURE 86.9 The normal distal supraspinatus tendon along the arthroscopy, arthrography is costly, invasive, and usually greater tuberosity. uncomfortable for the patient. Impingement is the most common pathology causing chronic shoulder pain (Neer, 1983). It is caused by compression of the anterior cuff against the anterior acromial edge and coracoacromial ligament. The initial developments are edema and hemorrhage, which progress to tendonitis and fibrosis. Partial and full-thickness tears of the rotator cuff are the end stage of the disease spectrum referred to as “impingement syndrome. ” Unfortunately, no clinical tests exist that will differentiate impingement from rotator cuff disease. The persistence of symptoms may help the clinical diagnosis, depending on the patient’ s age and history. The majority of patients will experience 10 to 15 years of chronic shoulder pain before impingement progresses to rotator cuff tear. Treatment for the early stages of impingement syndrome is often drastically different from the treatment for rotator cuff tears. Tendonitis of the rotator cuff is generallyFIGURE 86.10 A grossly retracted supraspinatus tendon (st). A complete absence of the supraspinatus tendon is a reliable treated conservatively for as long as possible. This usually indicator of a full thickness tear. (d) = deltoid; (b) = bursa; (gt) entails avoidance of painful elevation of the arm, anti= greater tuberosity. inflammatory medication, and injections of anti-in flammatory drugs into the subacromial space. Rotator cuff tears are With such a large potential group of patients, ultrasound is treated differently. Surgery is usually recommended when preferred to more invasive, expensive, and time-consuming large full-thickness tears exist. Early intervention is importechniques, such as arthrography, arthroscopy, and magnetic tant before the tear becomes too large, grossly retracted and resonance imaging (MRI). The cost effectiveness of the techsubsequently nonrepairable (Figures 86.9 to 86.12). the fi In a patient with impingement syndrome and rotator cuffnique and its noninvasive capability make ultrasoundrst choice when evaluating soft tissue injuries. tendonitis, a conservative, noninvasive approach is optional. The ideal technique should be readily available for Every examination of the shoulder should begin with screening a large population with chronic shoulder paina plain radiograph. The most detailed examination of the bony anatomy is still the conventional radiograph. Suband be able to distinguish tears from edema of the cuff in the majority of cases. Ultrasound is the ideal technique.stantial narrowing of the subacromial space with an acroIt is noninvasive and widely available for screening on amiohumeral distance equal to or less than 5 mm is due to large rotator cuff tears. In these cases, no further investilarge scale (Crass, 1987; Mack et al., 1985). Reported gations are necessary (Cofield, 1985). Radiographs also sensitivity is more than 90% (Van Holsbeeck 1991). can exclude referred pain to the shoulder due to a lesion in the adjacent structures or a neurovascular syndrome WORKUP OF SHOULDER DISEASE secondary to a Pancoast tumor (Batemen, 1983). The estimated frequency of rotator cuff tears in people more When chronic shoulder symptoms persist and normal than 60 years old is approximately 30% (Cofi eld, 1985). plain films and positive clinical test results indicating cuff

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FIGURE 86.11 Coronal view of the AC joint. (a) = acromion; FIGURE 86.12 Degenerative changes involving the acromion process and distal clavicle (arrows). ≤ developing spur is iden(dc) = distal clavicle; (st) = supraspinatus tendon; (h) = humerus; tified (small arrowhead). Effusion is present within the joint (e). (s) = skin.

the effectiveness of treatment and the progression of disdisease exist, ultrasound is the tool of choice for estabease (Aisen, McCune, McGuire et al., 1984). lishing a diagnosis. Arthroscopy should be considered In summary, sonography is a valuable diagnostic tool when patients present with normal radiograph and a norfor both extra-articular and intra-articular pathologies. If mal sonogram of the shoulder, but with an unequivocalthe intra-articular examination is normal, no additional clinical examination (limited abduction). imaging studies are needed. Abnormal sonographic exam-

SONOGRAPHY OF LARGE SYNOVIAL JOINTS

ination is an indication for evaluation with MRI, arthrography, or arthroscopy.

Large synovial joints are dif ficult to evaluate clinically; SONOGRAPHY OF THE ELBOW, WRIST, therefore, ultrasound examinations are often requested. AND HAND Ultrasound is broadening our approach to the evaluation of joint disease. Even the smallest joints can be examined Clinical examination of the elbow, wrist, and hand is less sonographically, i.e., interphalyngeal joints in the hands complex than examination of the shoulder, knee, and hip. and feet. Arthroscopy is limited to the intra-articular strucThese joints are much more accessible due to their supertures. It allows the orthopaedic surgeon to evaluate the ficial nature. Ultrasound is valuable in the diagnosis of cartilage and perform corrective surgery in the same promuscle, tendon, and ligament pathology, as well as cortical cedure. However, arthroscopy is an invasive technique abnormalities, i.e., stress fractures, bone cysts, and arthriwith the possibility of risk to the patient. tis. When radiographic examination is normal, ultrasound The main advantage of ultrasound over arthroscopy is is indicated to evaluate persistent pain and swelling. its ability to examine the extra-articular soft tissues. Many pain syndromes do not originate in bone or articular cartiTHE ELBOW lage. Until now, these were strictly clinical diagnoses. Sonography can be used to diagnose disease of the extraThe most common soft tissue disorder of the elbow is articular tissues with high sensitivity and specifi city. Sonog- epicondylitis. Tendonitis of the common extensor tendons raphy can be tendonous, ligamentous, and muscular lesions. (tennis elbow) and commonexor fl tendons (golfer’ s It can differentiate scar, granulation tissue, and complete and elbow) are often mistaken for intra-articular pathology, incomplete tears. In addition, ultrasound is completely non-due to their close proximity. invasive and requires no anesthesia or pre-medication. Lateral epicondylitis is most frequent in elbow disIntra-articular pathology also can be accurately diag-orders. Biceps and triceps tendonitis also may be misnosed utilizing sonography. It can routinely identify intra- taken for joint pathology. These problems are best evalarticular effusion. In addition, ultrasound can locate syn-uated with ultrasound because calcifi cations are seen ovial inflammation, hemarthrosis, and loose bodies withinonly in chronic disease. At the same time, the examiner the joint. Cartilage and synovial thickness can be measalso can evaluate for intra-articular loose bodies or carured accurately, providing an excellent method to evaluate tilaginous defects. Joint effusion is a clear indicator of

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FIGURE 86.13 A normal common flexor tendon insertion (cft) FIGURE 86.14 Inflammation of the common flexor tendon and along the medial epicondyle (me). adjacent soft tissues. Note the large effusion (e).

Intra-articular and extra-articular pathologies are joint pathology. The most frequently observed joint pathology in the absence of radiographic ndings fi is car- equally common causes of knee pain. Pain and swelling tilaginous loose bodies. These loose bodies will be found of the knee accompanied by a normal radiographic examin the anterior joint recess (Figures 86.13 and 86.14). ination are a clear indication for an ultrasound examination. Arthrography and arthroscopy are invasive techTHE WRIST AND HAND niques that evaluate only the intra-articular pathology. Sonography has the capability of demonstrating noninvaThe initial indications for ultrasound examination of the sively both intra-articular and extra-articular pathologies. wrist and hand are evaluation of tendon disorders and Ultrasound can provide information about a joint during identification of the origin of swelling. Tendon ruptures a real-time examination. No other diagnostic imaging are easily detected with ultrasound. A motion evaluation modality has this capability. In addition, the risk, discomhelps to identify tendon dislocations and entrapment. fort, high cost, and delay that may be expected with other Tenosynovitis of the flexor tendons of the wrist and carpal diagnostic procedures do not exist. tunnel syndrome are diagnosed easily with ultrasound. Tendonitis is a common cause of knee pain. Most Identification of synovial cysts and specification of their frequently involved are the quadriceps, biceps, and patelorigin are easily diagnosed with ultrasound. A cyst arising lar tendons. Increased edema and decreased acoustic sigfrom a tendon sheath differs from that of a cyst originating nal within the involved tendon are visualized. Calcificafrom the joint. This can help in surgical management. tions often are seen in cases with chronic tendonitis. Often these cysts feel solid during clinical assessment and Bursitis also may be the cause of knee pain. Traumay be mistaken for boney hypertrophy. The triangular matic, septic, and hemorrhagic etiologies may cause burfibrocartilage of the wrist also may be examined. sitis. Rupture of Baker’ s cyst is almost always associated with pain and swelling of the knee, which may extend to SONOGRAPHY OF THE KNEE, HIP, involve the entire lower extremity. Ultrasound also is valuAND ANKLE able in evaluating ligamentous injuries, synovial cysts, ganglia, muscle tears, aneurysms, and venous thrombosis. KNEE Examination of intra-articular pathology can demonstrate synovial thickening, meniscal tears, articular cartiSonographic examination of the knee is a commonly lage defects, loose bodies, and cruciate ligament tears. requested study of the lower extremity. The knee is a Several limitations must be kept in mind. Tears of the bicondylar joint stabilized by soft tissue structures: ligaposterior horn of the meniscus are diagnosed more easily ments, tendons, menisci, and the joint capsule. These structures are all easily injured by trauma, particularlythan tears of the mid-body and anterior horn. The only sports-related trauma. Ultrasound is the only readily avail-absolute limitation of the intra-articular examination is able nonsurgical technique for the examination of softthat the cartilage surface of the patella and tibial plateau tissue injuries at the time the patient presents for clinicalcannot be examined due to the lack of an acoustic window. evaluation. Normal plain lm fi examination following Technical advances, such as new transducers and the furinjury is a definite indication for sonographic examination.ther development of transmission ultrasound, will reduce

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FIGURE 86.16 A torn meniscus with distention of the medial joint capsule along with herniation of the medial meniscus (arrowheads).

FIGURE 86.15 The normal triangular wedge” “ representing the medial meniscus. Note the deep layer of the MCL and joint capsule appears intact (MCL/JC). thickness of the fascia at this location may be indicative

for plantar fascitis. or eliminate these limitations. However, a normal sonographic examination demonstrating no effusion indicates that the source of pain lies outside of the joint (FiguresHEMATOMA 86.15 and 86.16). Hematoma formation is a hallmark of muscle rupture. The degree of the hematoma is an excellent indicator of the HIP extent of the underlying pathology. Intramuscular Trauma to the hip results in bony injury almost exclu-hematoma is characterized by blood dissecting within the sively. This is due to the protection and stabilizationfascial planes between muscles. More extensive injury will inherent in its ball-in-socket confi guration. Often, the result in formation of intramuscular fluid collections easily identified on ultrasound images. trauma is the result of a motor vehicle accident or sportsrelated injury. Plain radiograph and computed tomogra- The evolution and resolution of intramuscular phy (CT) are the best diagnostic modalities for evaluat-hematoma do not differ from hematoma anywhere in the ing these injuries. However, when radiographs and CTbody. Their initial sonographic appearance is that of a are normal, ultrasound examination is an excellent diag-homogenous hypoechoic fluid collection. nostic tool to consider. HEALING MUSCLE RUPTURE Ultrasound is highly sensitive in the identi fication of joint effusion. Joint effusions may be seen in infection, Ultrasound is an excellent diagnostic tool for the evaluainfl ammatory arthritis, osteonecrosis, trauma, and tion of the various stages of muscle healing which often tumoral diseases. can take between 3 to 16 weeks to complete. The role of sonography in the identifi cation of muscle ANKLE rupture healing lies in three areas. First is the identifi cation The most common ankle injury is a sprain/strain. Mostof the extent of injury and measurement of the separation of frequently, the lateral ligament complex is involved andwound margins. The larger the percentage of muscle tissue involved and the greater the distance of retraction, the larger the anterior talofibular ligament is damaged. The peroneal proportion of scar tissue. This information will help the tendons and medial flexor tendons are beautifully imaged clinician in determining what steps are necessary, and if any sonographically. These structures usually are completely exposed for sonographic examination. A motion evalua-are indicated. Ultrasound-guided aspiration of a hematoma may be desirable at the time of examination to reduce the tion is recommended to assess integrity and function. Cordistraction gap (van Holsbeeck & Intracosa, 1991). tical irregularities also can be detected in the ankle, i.e., stress fractures, bone chips, and osteochondral defects. In The availability, ease of examination, no contraindiaddition, joint effusions are easily identified. The plantarcations to its use, and low cost relative to MRI make fascia can be viewed along the medial tubercle of thefollow-up of healing lesions practical. The majority of patients referred for evaluation of muscle lesions are athcalcaneus. The normal measurement for this location is 3.5 mm thick. Any inflammatory change increasing theletes. Several studies have demonstrated that approxi-

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mately 30% of all sports injuries are muscular in origintively freely, and it does not require sedation. Cost and (Peterson & Renstrom, 1986). In these patients the deciavailability factors also strongly favor ultrasound. sion of when to return to training or competition is extremely important. Recurrent injury resulting from early EVALUATION OF FOREIGN BODIES resumption of activity can be costly for both the individual One of the most frequent requests made of musculoskelathlete and the team. Repeated sonographic examinations etal radiologists in the emergency setting is the identifican evaluate accurately the stage of healing, significantly cation and localization of foreign bodies. The patient can decreasing the likelihood of recurrent damage. Because of the low cost of ultrasound and no contrain-give an indication of the likelihood of the presence of a foreign body, the material involved, and the general locadications or patient discomfort, sonography can be used tion. However, many of these patients may be children repeatedly to evaluate the various stages in muscle healing. and difficult to evaluate clinically. Barefoot children possess a magnetic attraction to foreign bodies. All inquiries MYOSITIS/MYOSITIS OSSIFICANS by the physician or parent about the accident are answered Myositis is a general term used to specify inflammationwith screaming and tears. Another challenge is the evalof muscle. Myositis ossificans, muscular contusion withuation for foreign bodies in patients involved in motor intramuscular hematoma, may calcify and then ossify.vehicle accidents. Commonly, they are under the influence These lesions are frequent findings in athletes involved in of alcohol, received intravenous (IV) analgesics, lost concontact sports such as rugby or football. sciousness during the accident, or have numerous injuries. The progression of myositis ossificans is easily fol-Frequently, foreign bodies in these patients go unidentilowed with ultrasound. Maturation of these lesions takesfied. Unrecognized foreign bodies will result in chronic approximately 5 to 6 months. Initially, within 3 weeks of draining wounds, abscesses, and persistent pain. Surinjury, the lesion is identified as a soft tissue mass withrounding infection can lead to devitalization of large disorganized inhomogeneous internal architecture. At thisamounts of tissue, joint destruction, and even limb loss stage, the lesion is indistinguishable sonographically from(Gooding, Hardiman, & Sumers, et al., 1987). a soft tissue neoplasm. Clinicians may refer to this lesion In looking for foreign bodies, radiographs alone are as gleosis, a palpable firm mass within muscle. This term not adequate (Gooding, Hardiman, Sumers, et al., 1987; comes from the Latingelare, to freeze. Anderson, Newmeyer, & Kilgore, 1982). A retrospective study of foreign bodies showed that the average time between injury and detection was 7 months; 38% of SONOGRAPHY OF RHEUMATOID DISEASES retained foreign bodies were overlooked on initial examEarly diagnosis, assessment ofammation, infl and detection ination (Anderson, Newmeyer, & Kilgore, 1982). Nonraof complications of rheumatoid disease are problems that diopaque foreign bodies and patients with orthopedic can be addressed using ultrasound. The use of noninvasive implants pose the greatest challenge. These are the cases techniques is especially important in patients with rheumain which ultrasound is the most beneficial. In general, the toid disease. Joint aspiration and arthrography are extremely use of ultrasound will increase the rate of success of painful when performed on an infl ammed joint. In addition, identifying and localizing foreign bodies by at least 20%. these procedures are associated with signifi cant risk of infection in this population due to immune suppression from chronic steroid therapy. Arthrography, arthroscopy, and jointCONCLUSION aspiration must be kept to an absolute minimum in these Sonography has demonstrated its cost-effective reliability patients (Moore, Sarti, & Lovie, et al., 1975). in the evaluation of numerous musculoskeletal disorders. Over the past 20 years, many noninvasive techniques The techniques are dif ficult to perform; however, this can have been proposed to evaluate cartilaginous involvement be minimized with proper training and standardized techof rheumatoid disease. Most recently, magnetic resonance nique. The role of sonography in the evaluation of the imaging (MRI) and sonography have come to the forefrontmusculoskeletal system is evolving. As technology conin the noninvasive evaluation of rheumatoid disease. Given tinues to improve and experience with this imaging modala perfect world scenario, both of these diagnostic studies ity increases, sonography will establish itself as the gold are equally suitable for the diagnosis and follow-up ofstandard for the diagnosis of musculoskeletal disorders rheumatoid disease. Sonography has a major advantage (Jacobson, 1998). over MRI in that the test can be conducted on the spot. Rheumatoid patients usually cannot tolerate lying motionACKNOWLEDGMENTS less on a hard table for the 60 to 90 minutes required for an MRI examination. In addition, during sonographic We would like to thank Marnix van Holsbeeck, M.D., examination the patient may move other extremities rela-Joseph H. Introcaso, and John Jacobson, M.D. of the

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Henry Ford Hospital/University of Michigan’ s Radiology Depalma, A.F. (1983). Biologic aging of the shoulder. In A.F. De Palma (Ed).Surgery of the shoulder. Philadelphia: Department, for their efforts in advancing the global availJ.B. Lippincott Co. ability of information on the topic of musculoskeletal ultraDillehay, G.L., Deschler, T., Rogers, L.F., et al. (1984). The sound. We have made numerous references to their work ultrasonographic characterization of tendons . Investigaand tried to make the appropriate references at all times. For tive Radiology, 19,338–341. more information from the Henry Ford Hospital/University Feretti, A., Puddu, G., Mariani, P.P., et al. (1985). The natural of Michigan, you may contact its website @ history of jumper’s knee. Patellar or quadriceps tendoniwww.med.umich.edu/rad/muscskel/mskus/index.html tis. International Orthopaedics, 8, 239–242. Fornage, B. (1986). Achilles tendon: U.S. examination. Radiology, 159,759–764. Gielen, J., van Holsbeeck, M., Hauglustaine, D., et al. (1990). REFERENCES Growing bone cysts in long-term hemodialysis. Skeletal Ahovuo, J., (1984). Single and double contrast arthrography in Radiology, 19,43–49. lesions of the gleohumeral joint. European Journal of Goldberg, B. (1997, December). Contrast-enhanced ultrasound Radiology, 4,237–240. to become dominant. Radiology in the 21st century, Ahovuo, J., Paavolaine, P., & Slatis, P. (1984).The diagnostic Supplement to Diagnostic Imaging . value of arthrography in rotator cuff tears. Acta OrthoGolding, F.C. (1962). The shoulder, the forgotten joint . British paedica Scandinavica, 55, 220–223. Journal of Radiology, 35 (41), 149–158. Aisen, A.M., McCune, W.J., McGuire, A., et al. (1984). Sono- Gooding, G.A.W., Hardiman, T., Sumers, M., et al. (1987). graphic evaluation of cartilage of the knee. Radiology, Sonography of the hand and foot in foreign body detec153, 781–784. tion. Journal of Ultrasound in Medicine, 6, 441–447. Anderson, M.A., Newmeyer, W.L., & Kilgore, E.S. (1982). Henderson, C.E., & Hopson, C.N. (1982). Pneumoscrotum as a Diagnosis and treatment of retained foreign bodies in complication of arthroscopy. Journal of Bone and Joint the hand.American Journal of Surgery, 144, 63. Surgery (U.S.A.), 64, 1238–1240. Batemen, J.E. (1983). Neurologic painful conditions affectingJacobson, J. (1998, May). Sonography: Ultrasound takes on musthe shoulder.Clinical Orthopaedics, 173,44–54. culoskeletal MRI.Diagnostic Imaging,49–57. Beltran, J., Gray, L.A., Bools, J.C., et al. (1986). Rotator cuffJeffries, J.T., Gainor, B.J., Allen, W.C., et al. (1987). Injuries to lesions of the shoulder: Evaluation by direct sagittal CT the popliteal artery as a complication of arthroscopic arthrography.Radiology, 160,161–165. surgery.Journal Bone and Joint Surgery (U.S.A.), 69, Blei, C.L., Nirschl, R.P., & Grant, E.G. (1986). Achilles tendon: 783–785. Ultrasound diagnosis of pathologic conditions . RadiolJobe, F.W., & Jobe, C.M. (1983). Painful athletic injuries of the ogy, 159,765–767. shoulder.Clinical Orthopaedics, 173,117–124. Bock, E., Cotroneo, A.R., et al. (1981). Xeroradiography of ten-Jobe, F.W., & Jobe, C.M. (1983). Painful athletic injuries of the domuscular traumatic pathologic conditions of the shoulder . Clinical Orthopaedics, 173,117–124. limbs. Diagnostic Imaging in Clinical Medical, 50, Lindenbaum, B.L. (1981). Complications of knee joint arthros235–248, 89. copy. Clinical Orthopaedics, 160,158. Bretzke, L.A., Crass, J.R., Craig, E.V., et al. (1985). Ultrasonog-Mack, L.A. (1988). Sonographic evaluation of the rotator . cuff raphy of the rotator cuff: Normal and pathologic anatRadiology Clinics of North America, (1), 26 161–177. omy. Investigative Radiology, 20, 311–315. Mack, L.A., Matsen, F.A., Kolcoyne, H.F., et al. (1985). U.S. Bruce, B.K., Hale, T.L., & Gilbert, S.K. (1982). Ultrasonograph evaluation of the rotator cuff. Radiology, 157,205–209. evaluation for ruptured Achilles tendon. Journal of the Middleton, W.D., Reinus, W.R., Totty, W.G., et al. (1986). UltraAmerican Pediatric Medical Association, 72, 15–17. sonic evaluation of the rotator cuff and biceps tendon. Canoso, J.J. (1981). Bursae, tendons and ligaments. Clinics in Journal of Bone and Joint Surgery (U.S.A.) 440–450. 68, Rheumatic Diseases, 189–221. 7, Moore, C.P., Sarti, D.A., & Lovie, S.S. (1975). Ultrasonographic Codman, E.A. (1931). The shoulder: Rupture of the supraspinademonstration of popliteal cysts in rheumatoid arthritis: tus tendon and other lesions in or about the subacromial A noninvasive technique. Arthritis and Rheumatism, 18, bursa. Boston: Thomas Todd Co. 557–580. Cofield, R.H. (1985). Rotator cuff disease of the shoulder. JourNeer, C.S. (1983). Impingement lesions. Clinical Orthopaedics, nal of Bone and Joint Surgery (U.S.A.), 67, 974–979. 173, 70–73. Crass, J.R. (1987). Ultrasonography of rotator cuff tears: AOgilvie Harris, D.J., & Wiley, A.M. (1986). Arthroscopic surgery review of 400 diagnostic studies (abstract ). Presented at of the shoulder.Journal of Bone and Joint Surgery the American Roentgen Ray Society Annual Meeting, (U.S.A.), 68,201–207. Miami Beach, Fl. Peterson, C.J., & Gentz, C.F. (1983). Ruptures of the supraspinaCrass, J.R., Craig, E.V., (1984). Thompson, R.C., et al. Ultratus tendon.Clinical Orthopaedics, 174,143–148. Peterson, L., & Renstrom, P. (1986). Sports injuries.Chicago: sonography of the rotator cuff: Surgical correlation . Yearbook Medical Publishers. Journal of Clinical Ultrasound, 12,487–491. Refior, H.F., Krodel, A., & Melzer, C. (1987). Examinations of Demarais, Y., Houles, J.P., Parier, J.H., et al. (1984). Echoscanthe pathology of the rotator cuff. Archives of Orthonographie dans les tendinites achilleennes et rotuliennes paedic and Traumatic Surgery, 106, 301–308. specialement chez le sportif. Cinesiologie, 23,249–256.

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Resnick, D., & Niwayama, G. (1988). Diagnosis of bone and van Holsbeeck, M., & Introcaso, J. (1989). Sonography of the postoperative shoulder. American Journal of Roentgenjoint disorders(2nd ed.). Philadelphia : W.B. Saunders. ology, 152–202. Roels J., & Martens, M. (1978). Patellar tendonitis (jumper’ s Musculoskeletal knee). American Journal of Sports Medicine, 6, van Holsbeeck, M., & Introcaso, J.H. (1989). ultrasound.St. Louis: Mosby Yearbook. 362–368. Musculoskeletal Teefey, S., Ashhfaq, H., Middleton, W., et al. (2000). Ultrasonog-van Holsbeeck, M., & Introcaso, J.H. (1991). ultrasound.St. Louis: Mosby Yearbook. raphy of the rotator cuff.Journal of Bone and Joint Surgery, 82-A,498–504.

87 Minimally Invasive Endoscopic Surgery for the Treatment of Lumbar Discogenic Pain Anthony T. Yeung, M.D. and John Porter, M.D. INTRODUCTION

spinal surgery finally solved the problem of traumatizing spinal muscle and ligament, destabilizing the spine, and The history of low back pain and sciatica dates back tocreating epidural and perineural scarring. This rapid ancient times. Domenico Cotugno first described “sciat-advance was further aided by the parallel evolution of ica” in its classic terminology in 1764 and believed thatradiologic imaging such as CT and MRI. pain was generated by the nerve itself. The big three Vs — Valliex, Virchow, and Von Luschka — introduced the possibility of structure-referred pain (i.e., vertebral, body,ENDOSCOPIC SPINE SURGERY: disc, or nerve) in the 1800s. With the advent of X-raysWHAT IS ITS ROLE? 100 years ago, imaging of spinal anatomy allowed corres role in lation of anatomic findings to conditions that explainedFew physicians question arthroscopic surgery’ advancing our understanding of knee and shoulder pain the origin of low back pain. The “Dynasty of Disc” began in the 1930s when Mix- and the treatment options arthroscopy affords. Endoscopic spinal surgery is poised to serve the same role (Kirkaldy). ter and Barr demonstrated that radicular pain was associated with disc herniation (Farlan, 1973). Attempts wereIntroduced in the United States by Kambin, the procedure made later to minimize the paradoxical effects of invadinghas evolved from a nucleotomy and targeted fragmentecthe spinal canal by utilizing smaller incisions and imagetomy to a surgical technique with the potential to offer a magnification. Although the overall result was not altered,minimally invasive approach to spinal conditions currently minimal invasiveness did reduce the morbidity of tradi-without a viable surgical alternative. The favorable ef ficacy of endoscopic lumbar distional approaches. cectomy compared to open discectomy, in a prospective Each change required a learning curve that initially randomized study, was published by Hermantin, Peters, was more difficult for the surgeon, but ultimately was Quartararo and Kambin in 1999. Endoscopic spine surembraced by surgeons because it was better for the gery, through the selective endoscopic discectomy techpatient. Endoscopic spine surgery continues this trend, nique, expands the endoscopic restrictions described in but recent experience has revealed a much greater benefit the article and does not excludeficult dif cases at L5-S1 that will ensure and secure the role of endoscopic spine surgery for the diagnosis and treatment of discogenicor extruded, migrated, recurrent, or sequestrated disc back pain. herniations. The technique also provides minimally This quantum leap from open decompression (lumbarinvasive access to degenerative conditions of the lumbar laminectomy) to micro-decompression with endoscopicspine.

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CURRENT IMAGING METHODS

When compared with conditions diagnosed by spinal endoscopy, imaging studies are only about 70% accurate The posterolateral approach allows access to spinal structures such as the superior articular process, the pedicle and of specific (Yeung, 1999a; Kuslich, 1990). Conditions such as annular tears, rim tears with associated endplate the superior and inferior vertebra, the traversing and exitseparation, and various other discogenic pathologies are ing nerve root, and the annulus in the area of the foramen. missed almost a third of the time. Tears that are in the A newly developed spinal endoscopy system by ventral aspect of the disc are routinely missed by MRI Richard Wolf Surgical Instrument Company, the Yeung studies. Small disc herniations that protrude beyond the Endoscopic Spine System (Y.E.S.S.), features a multiouterfibers of the annulus may be missed. This is because channel scope and special access cannulas that allow the fragment may be flattened against the posterior longispinal probing in a conscious patient, diagnostic endostudinal ligament or nerve, looking like a swollen or copy, and t“ube surgery”with very little surgical morenlarged nerve. On the MRI, subligamentous herniations bidity. This technique revolutionizes the old concept that may appear as a thickened or bulged annulus. When the all disc surgery is really decompressive nerve surgery. It nerve is inflamed, the MRI may not be able to distinguish brings in a new era that will allow truedisc “ surgery” the enlarged nerve from a conjoined nerve, an anomalous and a more focused surgery at the tissue level such as branch, or a nerve with an adherent piece of disc. contracting and sealing annular tears, annular reinforce- Spinal endoscopy has allowed the endoscopic surment, and artifi cial discs. geon to identify the actual pathologic lesion, correlating The recent introduction of IDET (Intradiscal Elec- it with the imaging study, and making the clinician more trothermal Annuloplasty) provides another tool for treat-aware of the pitfalls of relying too much on imaging ing patients who suffer from back pain caused by annular alone. It is imperative that the patient be examined with tears, but IDET is another nonvisualized technique thatall these possibilities in mind to avoid labeling the patient will be noted for historical purposes as we now have thea “ head case. ” ability to do a “visualized IDET” under direct visual control. The history of minimally invasive spine surgery CLINICAL PRESENTATIONS CORRELATED supports the view that a visualized endoscopic procedure will eventually advance ablind” “ technique whose suc- WITH ENDOSCOPIC FINDINGS cess is dependent on very strict inclusion criteria, and When the disc tissue is in direct contact with the nerve, its eventual demise through overutilization by less expe-chemical irritation occurs and an infl ammatory memrienced and lesser trained clinicans. The role of IDETbrane forms. Even a large epidural venous plexus that is may be defined further by data gathered from visual inflamed can contribute to back pain and sciatica. When imaging of annular tears and correlating it with our cur-an inflammatory membrane is present ventral to the trarent imaging studies. versing and/or exiting nerve root, the clinical picture may not be clear. Spinal endoscopy has confirmed nondermatomal pain TEAM APPROACH in multiple patients with proximal thigh, buttock, and Due to the complexity of back pain, it is important to treatgroin pain at levels distal to the root origin of the anatomic area. These also include patients who are considered to the whole person. The medical team interfaces with the have spine pain by nonorganic physical signs. surgical team to obtain the best possible response and outcome for the patient (Yeung, 1999a). With the endoscopic spinal techniques described, the ability to identifyINCLUSION CRITERIA the tissue pain generator is available through spinal probAll disc herniations are amenable to selective endoscopic ing. Furthermore, a multidimensional treatment algorithm discectomy in a skilled endoscopic surgeon’ s hands. Each can be devised that will lead to improved outcomes and surgeon will select his or her patient dependent on his better patient selection for surgery. level of skill. Discogenic pain from internal disc disruption Patients not responding to standard conservative methand annular tears may benefit from thermal and chemical ods who may or may not be candidates for invasive surgery modulation of the disc. now have an opportunity for pain relief with endoscopic spine surgery. The endoscopic procedure, coupled with IDEAL INDICATION discography and spinal probing under local anesthesia, allows the patient to participate in his or her care (Kuslich,Perhaps the ideal lesion for selective endoscopic discectomy is the far lateral, extra-foraminal disc herniation. 1990; Yeung, 1999b).

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This type of herniation is the most ficult dif for the majority imaging studies identify these lesions as a high intensity of spinal surgeons. A skilled spinal surgeon can access the zone (HIZ), there is a high incidence of positive confirlateral zone of the disc with a paramedian incision, butmation by provocative discography. the posterior approach utilized by most traditional sur- Spinal endoscopy allows direct visualization of annugeons requires the removal of a significant amount of facet lar tears, identifying interpositional disc tissue as the sinto actually reach the herniation. This approach also causes gle most common finding preventing annular tears from extensive tissue trauma due to the dissection, which is healing. This approach may provide a possible alternative quite vascular. to fusion as a first line of surgical treatment for discogenic Our experience suggests that it is easier to access the pain with its origin from annular tears. extraforaminal zone with the endoscope. Endoscopically it is also more dif ficult than a contained herniation, but PROVOCATIVE DISCOGRAPHY the approach is much less traumatic for the patient. It is very important to remember that the success of any surOur clinic utilizes discography as an integral part of the gical procedure depends on proper patient selection, sursurgical workup. The literature supporting discography is geon skill, the correct use of treatment modalities, as well currently considered controversial in some circles. The conas the combined diagnostic and surgical skills of the treattroversy presents because of the high inter-observer variment team. ability by discographers in reporting the patient ’s subjective We have found that for the team diagnostic endoscopy pain. However, if the surgeon works closely on a team with confirms valuable information on predicted pain generaan experienced discographer, and there is ongoing commutors to actual sites. This approach also may alleviate the nication, we have found the two can help decrease the need for a surgical approach that is potentially destructive variability in the interpretation of the patient’ s response. to muscle and adjacent soft tissue when a less invasive or It is ideal for the surgeon to perform his or her own conservative treatment is available. discography, as he or she is the one who must take the Other validated indications include excisional biospy responsibility for deciding whether the patient will of spinal structures and tissue. A prime example is discitis. respond to endoscopic spine surgery. Furthermore, the Currently treated with long-term antibiotics, discitis is surgeon always repeats the discogram at the time of surmuch more effectively treated with endoscopic debridegery if the Selective Endoscopic Protocol that emphasizes ment and excisional biopsy of infected tissue. The initial vital dye staining of targeted tissue is used. clinical data results are promising, suggesting endoscopic excisional biopsy and debridement offer the optimal treat- The discogram can be used to predict the presence of a collagenized disc fragment vs. a soft herniation, and the ment option for this condition. extrusion of a disc fragment as a noncontained herniation. In addition, discography can diagnose the presence of the ALTERNATIVES TO FUSION type, grade, and location of painful vs. nonpainful annular tears (Yeung, 1995). Fusion has traditionally been reserved for spinal instability The senior author follows a classification for discoand deformity. More recently with the development of grams based on Adams, et al. (1986), Osti (1992), and fusion cages, patients have been offered fusion for discoSachs, et al. (1987). According to Adams, the basic pattern genic back pain without leg pain. The pain generators have is grades I to V. The radial extensions are per Dallas where been discovered to arise primarily from the annulus, but grade III is the extension to the inner annulus, grade IV also can involve the endplates and facet joints. up to the outer annulus, and grade V beyond the outer Patients with debilitating lumbar pain are currently annulus. The extension of circumferential tears is being offered surgical fusion as a treatment option to described per Osti. When this classification is used, the stabilize the motion segment. Pain nociceptors from the number of quadrants of involvement can be determined annulus which are innervated by branches of the sinuby discography alone, and it is not necessary to do a postvertebral nerve, have been shown to be deformed by heat discogram CT scan to get enough information to deterat least 42°C. When the heat is increased to 65°C, type mine the efficacy of endoscopic surgery. one collagen of the annulus contracts and thickens (Saal, Saal, and Ashley, 1997). Thermal therapy has been utilized The Revised Discogram Classification to tighten stretched ligaments and unstable joints. This approach is being applied to annular tears with favorable results. This type of lesion cannot always be 1. Cotton ball nucleus (normal cotton ball pattern). imaged, even with the most sophisticated techniques; however, provocative discography has demonstrated its 2. Oval nucleus and painless extension of fragability to diagnose such pathologies. Furthermore, when mentation beyond center.

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3. Radial fissured extension to the inner annulus with no circumferential extension and no disc protrusion. 4. Radial extension to the outer annulus and circumferential component to 1 to 4 quadrants and disc protrusion. 5. Radial tear past outer annulus, circumferential 1 to 4 quadrants, most variable and definite disc protrusion with possible extruded fragment.

results in a breakdown and restructuring of collagen fibers in the annulus. Proponents offer several explanations as to why this procedure might relieve pain attributed to the disc. It may be due to a stiffening of the disc itself, possibly alter the annular tears or, in fact, it may ablate nerve endings. Nevertheless, Saal, Saal, and Ashley (1997) report that 80% of the patients treated with IDET noted a signifi cant decrease in their back pain of at least 2 points on a 10-point analog scale, improvement in sitting tolerance, and reduction in medication usage. Clinically An SF-36 Questionnaire revealed a positive change of at least 7 points. • Grades 1 and 2 give no pain. Recent information from the International Society for • Grade 3: Pain present at moderate pressure. the Study of the Lumbar Spine (ISSLS) was critical of • Grade 4: Predominately back pain. Leg pain IDET. They cited the lack of high-quality scientific eviassociated with central and far lateral protru- dence exists in favor of this treatment. Furthermore, no sion, inflammatory membrane may be present. evidence in favor of IDET from randomized controlled • Grade 5: MRI can only detect in Zones I and trials, or from other published controlled studies about II, the central and foraminal zones (may be long-term safety, yet reports suggest over 20,000 patients associated with herniation). Possible prolonged have undergone this procedure. Caution is advised as with healing time up to 9 months, depending on the any procedure. These patients present with back pain withsize of the tear. out severe radiculopathy. Patients with severe radicular symptoms due to frank disc herniations are not candidates. The Technique Incorporates Adjunctive Modalities If there is any amount of disc protrusion or herniation, selective endoscopic discectomy would be the treatment 1. Flexible probes of choice. 2. Flexible mechanical instruments 3. Thermomodulation VISUALIZED THERMAL ANNULOPLASTY a. Radio frequency b. Laser The author’s choice of a visualized technique over the blind technique of a thermal resistive catheter is supported Since 1991 the senior author has treated over 1000 patients with a wide spectrum of disc herniations endo-by his success in converting failed IDET procedures to successful ones using the selective discectomy and visuscopically. These include extruded and sequestered fragalized thermal annuloplasty technique. In our experience ments. The success rate in the first 500 patients is an overall 86% good/excellent by MacNab Criteria. The suc-one of the most common findings with failed IDET is the presence of a disc fragment or interpositional disc tissue cess rate has continued to rise concurrent with diligence in the refinement of indications, techniques, and adjunc-fragment preventing shrinkage of the annular tear. On rare occasions one is able to find necrotic disc tissue (contive therapy. With the addition of a focused multidisciplinary firmed by pathology slides) in patients who have underteam that enjoys working together, it is our hope thatgone IDET treatment. with a coordinated team approach we can easily reach We feel strongly that direct visualization overcomes the 90% plus good/excellent outcome and avoid theboth conditions when visual control of tissue reaction to thermal energy allows the surgeon to avoid carbonization failed spine surgery syndrome so prevalent in today’ s of tissue and target the annular tear directly. In the Y.E.S.S. surgical environment. technique, inclusion of a side firing Ho:Yag laser also serves as the energy source that offers a tool that affects INTRADISCAL THERMAL THERAPY tissue shrinkage to the ablation of bone, just by controlling As of July, 2000, only one published study on the treat-the laser setting. Further advancement and application of these techment of back pain using Electrothermal Therapy (IDET) has been published. Electrothermal Annuloplastyniques will help expand the surgical capabilities of this (IDET) involves the insertion of an electrothermal cath-procedure, allowing for treatment of conditions in a degenerative spine that are painful, but not responding to coneter into a putatively painful disc underuoroscopic fl guidance. Thermal energy delivered by the catheterservative treatment.

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CHYMOPAPAIN

or nerve root block, the use of long-acting oral analgeTM ) will sics, and judicious use of gabapentin (Neurontin Low-dose chymopapain 500 units help “digest” the softmitigate this condition. herniation and treat the collagenized fragment for ease of We have noted the presence of dysesthesia as a delayed removal. The senior author uses chymopapain when disc response days and weeks after the procedure. Therefore, fragments are found to be extruded and migrated behind while we blame the use of laser and electrothermal therapy, the vertebral body. Other applications are when a recurrent the actual cause of this regional sympathetic condition is herniation exists. Chymopapain is used to decrease the still unknown. The incidence of dysesthesia is about 5%. recurrence rate and dissolve the missed fragments. ChyComplications of discitis, nerve injury, dural tear, and psoas mopapain is injected and left in the nucleus pulposus forhematoma total less than 1 to 2% overall. up to 5 minutes before endoscopic discectomy. When chymopapain is used as adjunctive therapy, we have had no adverse effects or allergic reactions, even REFERENCES when the discogram identifies leakage beyond the annular fibers into the epidural space. If the discogram demon-Adams, M.A., Dolan, P., & Hutton, W.C. (1986). The states of strates uptake by the venous plexus, if it is absorbed as disc degeneration as revealed by discograms. Journal of soon as it is injected, or if it communicates in any way Bone and Joint Surgery (Britain), (1), 68 36–41. with the thecal sac, demonstrating a communication withChoy, D.S. (1992). Percutaneous laser disc decompression. A new therapeutic modality. Spine, 17 , 949–956. the disc space, we have not injected chymopapain. As a Cresswell, C.C. (1992). Introduction to electrosurgery. Journal precaution against an allergic reaction, we routinely of British Podiatric Medicine , 47, 11–15. administer Benadryl™, 50 mg, and cimetidine, 300 mg Farlan, H.F. (1973).Mechanical disorder of the low back. PhilIV, before injecting the chymopapain. adelphia: Lea & Febiger. Fritsch, E.W., Heisel, J., & Rupp, S. (1996). The failed back INTRAOPERATIVE STEROIDS surgery syndrome: Reasons, intraoperative findings, and long-term results. A report of 182 operative treatments. Whenever an infl ammatory membrane was observed, Spine, 21 , 626–633. stimulation of the nerve and surrounding tissue elicitedHermantin, F.U., Peters, T., Quartararo, L., & Kambin, P. (1999). pain. When there is no inflammatory membrane, the nerve A prospective, randomized study comparing the results and annulus can be manipulated without eliciting pain. of open discectomy with those of video-assisted arthroscopic microdiscectomy. Journal of Bone and Joint SurWhen an inflammatory membrane is present, the patient’ s gery, 81(A), 958–965. pain is often considered out of proportion to the imaged pathology. When there is significant inflammation noted,Jacobson, J.H. (1997). The early days of microsurgery in Vermont. Mt. Sinai Journal of Medicine, 64 , 160–163. Depo-medrol® is placed intradiscally at the conclusion of Kambin, P., O’Brien, E., Zhou, L., & Schaffer, J.L. (1998). the procedure. Arthroscopic microdiscectomy and selective fragmentectomy.Clinical Orthopedics, 347 , 150–167. Kirkaldy, W.W. (1983). Managing low back pain.New York: RISKS AND COMPLICATIONS Churchill. Surgical risks and complications are real issues that need Kuslich, S.D. Microsurgical lumbar nerve root decompression to be weighed before considering any invasive procedure. utilizing progressive local anesthesia. In W. Williams, J. These include dural tear, nerve root damage, bleeding, or McCulouch, & P. Young (Eds.).Microsurgery of the lumbar spine.Rockville, MD: Aspen. infection. The authors have seen variations of nerve anatomy and distribution on the annulus, including conjoinedOsti, O.L., Vernon-Roberts, B., Moore, R., & Fraser, R.D. (1992). Annular tears and disc degeneration in the lumnerves not appreciated by imaging studies and accessory bar spine. A post mortem. Journal of Bone and Joint nerve branches that often connect the traversing with the Surgery (Britain), 74 (5), 678–682. exiting nerve. Removal of these branches usually do not Saal, J.A., & Saal, J.S. The use of a thermal resistive coil for affect the patient’ s clinical course. the treatment of discogenic pain. A preliminary report. The most common adverse effect of the use of elecSpine(in press). trothermal therapy is dysesthesia. Fortunately, most dysSaal, J.A., Saal, J.S., & Ashley, J. (1997). Targeted intradiscal esthesia will resolve completely, as in a second-degree thermal therapy: Preliminary feasibility studies. Issls controlled burn. Occasionally, there will be severe symconference, June 2–3. pathetic pain that will challenge post-operative painSachs, B., Vanharanta, H., Spivey, M.A., et al. (1987). Dallas management. A multidisciplinary team is extremely discogram description: A new classification of CT/dishelpful in assisting the patient to cope with the pain. cography in low back pain disorders. Spine, 12 (3), Usually good pain management with selective epidurals 287–294.

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Sauguaro, T., Oegeme, R.T., & Bradford, D.S. (1986). TheYeung, A.T. (2000). The evolution of percutaneous spinal endoscopy and discectomy: State of the Mt. art. Sinai Journal effects of chymopapain on prolapsed human interverteof Medicine, 67 , 327–332. bral disc: A clinical and correlate histochemical study. Yueng, A.T. (1999). Minimally invasive disc surgery with the Clinical Orthopedics, 213 , 223–231. Yeung Endoscopic Spine System (Y.E.S.S.). Surgical Yeung, A.T. (1995, March).The intraoperative discogram: Its Technology International VIII , 1–11. role in arthroscopic microdiscectromy. La Jolla, CA: International Intradiscal Therapy Society, Inc.

88 Phytomedicinal Approaches to Pain Management James Giordano, Ph.D. as assembled by PhytoPharm, U.S. Institute of PhytopharRecent medical practice has seen a phenomenal increase PDR for Herbal Medicines provides in the utilization of alternative and complementary maceuticals. The U.S. easy access for practitioners in an easy-to-read format for approaches by patients as well as physicians. One of the most dynamic and rapidly growing areas of complemen-herbs that are commercially available, as well as enhanced tary medical care involves herbal or phytomedicinal inter-research data on adverse effects, formulation, and safety. vention. In the United States, herbs and phytomedicinals Taken together, these documents demonstrate that are commercially available in accordance with the Dietarymany herbs contain potent ingredients capable of exerting Supplement and Health Education Act (DSHEA) of 1994.powerful biological effects. Also, active principal ingredients coupled with numerous constituent co-factors may This act offers the proviso that herbs sold as supplements set the stage for herb–drug interactions. Although consumcannot be marketed for diagnostic, therapeutic, or preveners may view herbs as simple nutritional supplements, the tive interventions for disease, and relegates them to the potencies of these pharmacologic actions are medically status of foods stuffs, additives, or (as the name would imply) nutritional supplements (or nutriceuticals). In this important. When properly utilized, herbs can serve as country, official governmental standards are not providedadjunctive or perhaps primary agents in pain management. for the production of herbal products and, therefore,It is important for the practitioner to recognize that herbs purity, potency, and viability can vary highly with regard often contain heterogeneous combinations of active principles. These can affect indication and use and may warto level of extract, contaminates, co-substances, and dose provided. Certainly this is not the case worldwide. Ofrant pharmacologic contraindications. Although many particular note are the actions of Germany’s “Commissionherbs possess few or no notable side effects, a knowledge of the possible range of effects is critical. Similarly, a E,” a subgroup of the German Federal Health Agency. This clinician must be aware that patients often maintain a organization has conducted an exhaustive study of over “microwave mentality, ” in which the assumption is erro350 common and medicinally used botanical preparations, neously made that an herb is a “natural” product, thereand has amassed basic scientific and clinical data that ” In accordance identify active constituents, chemical profiles, clinical fore, “a little is good…more must be better. with the aforementioned information, it is exceedingly applications, side effects, and contraindications for these possible that overdosing even relatively benign herbs can herbs. Thus, the Commission E monographs stand alone have serious consequences. It is important for practitioners as the most comprehensive and efficacious review of medicinal herbs currently available. Of equal importanceto be aware of not only active principles and constituents, is the currentPhysician’s Desk Reference for Herbal Med- but also to recognize viable dose ranges to maintain clinical icines. This volume provides a review of over 700 herbseffects. It should be noted, however, that both Commission 0-8493-0926-3/02/$0.00+$1.50 © 2002 by CRC Press LLC

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E and the U.S.PDR for Herbal Medicinesoffer very wellgenital urinary tract. In this regard, black cohosh has been defined caveats regarding the dosage of commerciallyhighly touted as an agent to relieve pain of premenstrual available herbs. Clinicians and consumers must be caudysmenorrhea and perimenopausal discomfort. tious in their utilization of herbs, because these substances In general, no overt side effects have been demonstrated are not under direct governmental control for qualityor reported with use of black cohosh within the therapeutic assurance, and doses of active and subconstituents can dose range, although some initial dyspepsia may occur in vary widely among preparations. sensitive individuals. Of particular note, however, is the This being the case, clinicians who look to integrateactivity of black cohosh in altering uterine smooth muscle herbal and phytomedicinal agents into their practice must motility; this agent is contraindicated during pregnancy due be very specific when questioning patients about herbs to a high potential for inducing uterine contractility and (with precise inquiry regarding brand, dose, frequency,evoking spontaneous abortion. The actions of the tripertene and combinations during initial assessments, follow-ups,glycosides can synergize the effect of antihypertensive medand discharge planning). It may be useful, if consideringications through relaxant effects on peripheral vascular integrating herbal preparations into practice, to procuresmooth muscle. Thus, the herb is contraindicated for use in the collaborative services of a compounding pharmacistindividuals who are pharmacologically maintained on antito assist in the acquisition of superior quality, “pure herbs, ” hypertensive medication (due to the risk of profound that are as close to pharmaceutical grade extract as conhypotension). Overdose in excess of 5 to 10 g per day has ceivably possible. For allopathic, osteopathic, and chiro-been reported to result in dizziness, orthostatic hypotension, practic practitioners, many medical associations offerdisorientation, headache, and vomiting, all apparently attribongoing continuing education in herbal treatments andutable to its vaso-relaxant mechanism and resultant central nutriceuticals that provides information on effects, indi- and peripheral hypotensive sequelae. cations/contraindications, and use of herbs for specific disorders. Interactive recruitment of a naturopathic physician also may be of critical benefit if an expanded, inte-BLACK PEPPER (PIPER NIGRUM) grative herbal practice is to be considered. Black pepper is an indigenous plant to the Indian continent The herbs considered in this chapter fall into the category of “occidental” herbal preparations, and it is beyondand is commercially cultivated in Asia and throughout the Caribbean. Berries of the pepper plant that have been the scope of this writing to address those herbs utilized in traditional Chinese, Indian, and various folk medicinalliberated from the pericarp and berry-like fruit parts are practices to treat pain. The U.S. PDR for Herbal Medi- utilized internally for stomach pain and are externally applied as a salve or ointment for neuralgia. Preparation cines addresses compounds that fall within these categoyields a volatile oil whose chief constituents include sabries, and the reader is referred to that document for approα- and β-pinene and∆priate review. Thus, while many herbs are capable ofineine, limonene, caryophyllene, affecting some component of pain symptoms, the follow-3 carene. Acidic amides include piperine, piperylin, piperolein A and B, and coumaperine. The plant also yields ing group represents those with specific well-documented fatty oils and polysaccharides. The mechanism of action actions on specific processes that mediate pain. These are involves both volatile oils and acid amides, although cerpresented alphabetically for ease of access and readability. tain glycosides (3,4-dyhydroxy phenyl ethanol glycoside, considered a substrate for enzymes responsible for proBLACK COHOSH (CIMICIFUGA RACEMOSA) ducing the color of the plant) may have some activity as A native plant of the North American continent, black well. Taken internally, black pepper activates buccal highcohosh is specifically cultivated as a medicinal herb inintensity thermal receptors and increases salivation. Europe. Alcohol-aqueous extract of icopropenolic extractWithin the alimentary tract, pepper increases secretion of gastric mucosal cells. When topically applied, volatile oils of the plant yields the active constituents of several types of triterpenes including triterpene glycoside, 27-deoxi-and acid amides act at ∆A-and perhaps C-thermosponsive actein, and simifugoside. Active quinolizidine alkaloids and polymodal afferents, either as a counterirritant or include cytisines and methyl cytisine and the phenyl pro-(indirect) secretogogue. Adverse side effects and contraindications have not pane derivatives including isoferulic acid. been reported for black pepper, nor have herb–drug interThe active constituents of the plant appear to be the triterpene glycosides that affect the activity of central andactions; black pepper appears to be safe and effective when used as an adjunctive agent in the treatment of peripheral estrogen receptors. Although equivocal evidence dyspeptic gastric pain (including NSAID-induced dyspepreports that LH levels are also affected by cohosh, studies sia due to decreased secretion of gastric mucosal cells) demonstrate the major action is through either a direct effect and as a topically applied agent for mild to moderate pain on estrogen receptors or an indirect estrogenic-like activity of triterpene glycoside on smooth muscle of the femaleof neuropathic etiology.

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BORAGE (BORAGO OFFICINALIS)

nal use or accidental contact with viable mucus membranes facilitating internal absorption, no direct contrainThe borage plant is indigenous to Central and Eastern dications for this substance exist. Health hazard and/or Europe where it is also cultivated commercially for culi- side effects for moderate external use of cajuput oil have nary and medicinal purposes. Explants of borage are now not been reported, although some individuals report an grown throughout Europe and in the United States and initial irritative dermatitis that subsequently dissipates. Canada. The medicinal components of the plant consist of dried flowers, leaves, stems, and seeds. Borage oil is the fatty extract derived from the seeds. The chief constit-CAYENNE (CAPSICUM VARIANTS) uent of the fatty oil isγ-linolenic acid, although linoleic Capsicum is native to Mexico, Central America, and the acid is found in lesser quantities. The borage leaf yields southern United States and is grown in numerous locations several active constituents including numerous pyrrolizifor both medicinal and culinary purposes. The active dine alkaloids (including supinin, lycopsamin, intermedin, ingredients are the capsacinoids (vanillyl amine amides), amabiline, and thesinine), a variably water-soluble silicic principally capsaicin and dihydrocapsaicin. Cayenne also acid, tannins, and mucilages. The oil is used in either contains carotinoids including violaxanthine, flavoniods liquid or capsular form for the treatment of neuroderma(apiin and luteolin-7-0-glucoside), and steroid saponins. titis, its therapeutic effect due to the activity of alkaloids The principal utility of capsicum is as a topical analgesic. and tannins. The leaf is used as an external astringent, The active moiety capsaicin, when afforded transdermal attributable to the tannins and mucilage. Of note is that the borage leaf contains hepatotoxicaccess (characteristically via delivery in a pluronic lecithin alkaloids, which although present in nominal quantities,organogel), binds to a vanilloid calcium-channel receptor on peripheral nociceptive C-fi ber afferents. Capsicum warrant against its internal use. An added caveat is that binding to this site facilitates an inward flux of calcium the borage leaf should be used as an external astringent leading to a rapid membrane depolarization and release for only brief periods of time, to lessen possible effects of these fi bers’ primary neurotransmitter, substance-P of the transdermal absorption of toxic alkaloids. Borage (please refer to Chapter 89 on the neurobiology of pain). oil has not been shown to be contraindicated when used Thus, capsicum acts as a secretogogue at peripheral Cwithin the therapeutic dose ranges and duration, and no fiber afferents. Capsicum binding appears to be long lastknown herb–drug interactions have been reported for the ing, thereby blocking the channel, depleting the C-fiber oil preparation. of substance-P, and producing a rightward shift in the stimulation-response curve of C-fiber afferents to thermal, CAJUPUT (MELALEUCA LEUCADENDRA) mechanical, and chemical noxious input. Commission E has approved the use of capsicum for pain of muscular This large tree is originally from southeastern Asia and (myoscitis, myofascitis) and rheumatic origin. the Australian continent, and grown commercially elseOf note is that use should be limited to 2 days, with where for medicinal purposes. The medicinal component a 10- to 14-day interval between applications. Prolonged is the oils of the fresh twigs and leaves, which are use of topical capsicum may cause festering dermatitis extracted, air dried, and steam distilled. This process yields active constituents of sineol, ± alpha terpineols,and ulceration. Capsicum should not be used on the peri± α-terpineols valerates, α-pinenes, and bicyclic sesquit- orbital skin, and should be discontinued should hypersensitivity, rhinoconjunctivitis, or dermatitis occur. It has erpenes. The oil is used externally as a salve or linament been suggested that hypersensitivity to capsicum is due for sprains, myofascitis, tendonous and ligamentous overexertion injury, and may be applied topically over arthritic infrequently to direct sensitization, but rather is a result joints. Mechanism of action appears to involve directof a generalized pollen hypersensitivity with cross-reacactivity of the terpineols with both anti-inflammatory and tivity to cayenne. perhaps mild muscular relaxant effects. The high sineol content yields toxicity if the drug is taken internally or is ENGLISH CHAMOMILE allowed to contact mucus membranes of the lips, eyes, or (CHAMAEMELUM NOBILE) nose. This latter effect is particularly viable in young children, in whom wherein facial application has beenEnglish chamomile, also known as Roman chamomile, documented to induce glottal, bronchial, and diaphrag-grows naturally in southern Europe and northern Africa, and matic spasm. As well, the high sineol content may induceis cultivated throughout Europe and the American continent. ower fl rapid overdose following internal consumption by adults.The medicinal oil extracted from the fresh or dried Profound hypotension, vascular and respiratory failure,heads contains volatile oils including the esters of angelic myoclonus and spasm, and electrolyte disruption have all and tiglic acid. Sesquiterpine lactones, including nobilin, been reported. Other than contraindications against interepinobilin and 4α hydroperoxy manolide. Flavoniods

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include anfemoside, cosmosioside, and caffeic and ferulic native plant. Active ingredients include the triterpene acid esters. The mechanism of action is not well docu-saponins; aglycone (20S)-protopanaxadiols including mented; however, the sesquiterpine lactones appear to act numerous ginsenosides (Ra1, Ra2, Ra3, Rb1, Rb2, and in the central nervous system, perhaps inducing the release Rb3); aglycone (20S) propanax triols including ginsenoof inhibitory neurotransmitters for central modulation of sides Re, Rf, and Rg, aglycone oneanolic acids of ginsepain. English chamomile has been used for treatment of nosides Ro, saponin V, Rb1 and Rb2, the water-soluble general headache, somatic distress, and premenstrual pain. polysaccharides panaxane (subtypes A-U) and several It has been suggested that use of English chamomile polyynes. The most active ingredients are the ginsenosmay result in sensitization reactions; however, no knownides, which act as steroidal saponins. One reported mechside effects or herb interactions have been documented. anism of ginseng’ s analgesic effect is through the reducIn light of the sparse documentation of potential interac-tion in platelet-derived serotonin. The ginsenosides Ro, tions and effects, the drug is not indicated for use duringRg1, and Rg2 inhibit platelet release reaction and thrompregnancy. boxane formation, thereby reducing platelet contribution to inflammatory and nocisponsive events. Saponin glycosides have been shown to stimulate corticotropin release, GERMAN CHAMOMILE which may mediate, at least in part, a component of neuro(MATRICARIA RECUTITA) endocrine analgesia. Although conflicting studies exist, Growing naturally throughout western Europe and culti-data exist that illustrate the direct CNS activity of ginsevated in North America, the flowers and entire herb arenosides Rg2 and Rg3 at nicotinic ACh receptors. It is unclear whether this constituent functions as a partial agoused as an infusion for inflammatory pain and pain-related anxiety. Active ingredients include the volatile oil consist- nist or mixed agonist-antagonist. By acting through central ing of (–) –α-bisabolor, chanazulene, and spathulenol.nicotinic ACh receptors, these ginsenosides appear to Bioactiveflavonoids include flavone glycosides, apigenin,mediate a limbic component of pain processing, and luteolin, flavinol glycosides including quercetin, and thereby affect pain perception. Ginsenosides Rg2 and 3 methoxylizedflavoniods including chrysosplenetin. Ger- may have activity at central GABA receptors, acting as man chamomile also contains phytomedicinal hydroxy-partial agonists or mixed agonist-antagonists, to mediate a component of nociceptive modulation. coumarins and mucilages. Analgesic effects are centrally mediated and are due to the activity of flavoniods: apige- In general, care should be taken when considering use of ginseng in patients with cardiovascular disease (due to nin is an agonist at CNS benzodiazepine receptors, and nicotinic stimulation) and/or diabetes (due to stimulation may potentiate binding at the benzodiazepine–chloride ion channel complex. Apigenin also appears to exert activityof insulin release and adrenergically mediated hypoglyceas a monoamine oxidase inhibitor, with specific activitymia). Thus, patients taking insulin or hypoglycemic agents should not employ ginseng as an adjunct analgesic. The at monoamine oxidase A, and lesser activity at monoamine use of nonsteroidal anti-inflammatory agents may be proboxidase B. Thus, both norepinephrine and serotonin conlematic due to the combined and potentiated anti-platelet centrations may be transiently elevated through the use of and thrombolytic activity of NSAIDs and ginseng. The chamomile. These latter effects subserve spinal and use of monoamine oxidase inhibitors with ginseng is consupraspinal mechanisms of analgesia. traindicated due to increased potential for sympathomiPatients who are hypersensitive to grass and mudwort pollen may exhibit cross-reactivity and sensitization tometic events (headache, tremor, hypertension). chamomile. Co-administration of CNS sedative agents including benzodiazepines, barbiturates, and ethanol SIBERIAN GINSENG should be avoided due to potentiation of central activity at benzodiazepine-binding sites and GABA potentiation.(ELEUTHEROCOCCUS SENTISOSUS) Concomitant use of monoamine oxidase inhibiting drugsThis plant is native to the Siberian regions of Russia, should be avoided due to the potential for sympathomi-Northern China, Mongolia, and Korea. It is grown in Japan metic and hypertensive effects. and North America. The dried roots and rhizomes are extracted for the production of the active compounds caffeic acid, hydroxycoumerins, several lignans including GINSENG sasamine, eleutheroside-d phytosteroids including β-sito(AMERICAN AND KOREAN PANAX GINSENG) sterol-3-O-β-D glucoside, rephinal acrylic acid eleutheroA native plant of China, Korea, and Japan, it is also cul-side B, several polysaccharides including eleutherane AG, steroid glycosides, and triterpene saponins (eleutherotivated for nutriceutical purposes in the United States. The sides I, K, L, and M). Siberian ginseng is used as an powdered preparation is used as either an infusion or in capsule form and is prepared from the dried root of theanalgesic against kidney pain, rheumatoid pain (primarily

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due to its immune modulating effect on T-lymphocytesexerting both a central and peripheral muscle relaxant and neural inhibitory effect. Desmethoxy yangonin, yangonin, induced by the eleutherane polysaccharides), and inflammatory pain. The latter effect is modulated by platelet-and kavain reversibly antagonize monoamine oxidase B, inhibiting actions mediated by hydroxycoumarins and tri-resulting in increased availability of synaptic serotonin at spinal and supraspinal sites. This increase in serotonin terpene saponins. The anti-platelet activity may reduce peripheral concentrations of platelet-derived serotoninsubserves the analgesic effect via inhibition of nociceptive that activate peripheral C-fibers in inflammatory pain. neurons in the spinal cord. Additional analgesic properties Due to the stimulating effects of caffeic acid and theare attributed to kavain, which can inhibit cyclo-oxygenplant steroids, the herb is contraindicated for patients withase 1 and perhaps cyclo-oxygenase 2 in peripheral tissues, as well as the CNS. By inhibiting formation of the prinhypertension. Possible interactions include a potentiated thrombolytic effect when used with nonsteroidals, salicy-cipal initiating enzyme of the archidonic acid cascade, kavain thus attenuates the formation of prostaglandins and lates, or anticoagulant agents. In addition, the hypoglycemic activity of the herb contraindicates its use for patientsthromboxane which act as potent inflammatory and nociceptive mediators. on hypoglycemic agents or insulin. As a mild depressant, the drug is contraindicated for patients with a history or current presentation of depresJAPANESE MINT sion. Initially, administration may lead to mild allergic (MENTHA ARVENSIS PIPERASCENS) hypersensitivity and dyspepsia; however, this appears to dissipate with repeated use. Some initial lethargy has also Indigenous to Europe, Asia, and commercially grown in been reported but this side effect also decreases with repetNorth America, the mint oil is obtained through distillation itive use. Based upon mechanism of actions, kava should of the flowering herb and removal of the active menthol not be used with alcohol due to reciprocal potentiation of ingredient. Chief components include menthol, menthone, effect, with benzodiazepines because of potentiation of limonene, neomenthol, and α and β pinene. It is used in benzodiazepine activity at GABA receptors, or with CNS Indian and Chinese medicine as a topical application ofdepressants (e.g., barbiturates) due to potentiated depresthe essential oil for joint pain, headache, myalgia, andsant effects. Patients taking SSRIs, tri- or heterocylic antiperipheral neuralgia. depressants should use kava with caution because of the Although Japanese mint, mint oil, and menthol can bepotential for enhanced psychotropic effects. There are used internally for the treatment of gastrointestinal pain,reports of dopaminergic antagonism occurring with kava; dyspepsia, and relief of respiratory congestion, the possithus, use of kava in Parkinsonian patients is contraindibility of hepatic insult and hepatotoxicity contraindicatescated. Similarly, cardiac patients should use kava with long-term internal use. As well, the cholagogic effect maycaution due to variable effects of kava on dopaminergic precipitate and worsen cholestatic disease in patients with control of the heart. Although these contraindications and this comorbidity. Topically applied, precautions and con-caveats are applicable to specific patient populations, a traindications are few; however, asthmatic patients maymore general precaution is that patients should use care have exacerbation of airway or bronchiolar spasm upon when operating heavy machinery or engaging ne in fi initiation of menthol application. Facial, perioral, and peri- motor tasks, particularly during the initial phase of kava nasal use of menthol oil is contraindicated in pediatrictherapy because of decreased motor coordination, patients because of increased risk of glottal and bronchial increased reaction time, and sedative effects. While these spasm. The anti-myospastic and neurotropic effects of may be transient, the early phase of therapy produces the topically applied menthol are due to the actions of mentholmost salient side effects for which the greatest precautions and menthone, perhaps as a counterirritant or through are a warranted. direct mechanism not completely understood.

KAVA KAVA (PIPER METHYSTICUM)

MARIJUANA (CANNABIS SATIVA)

Originating as a hashish derivative in the Near and Middle A native plant of Polynesia and the South Sea Islands, East,cannabisis cultivated throughout Europe, Asia, and kava kava is harvested for the dried rhisome and roots. North and South America as a substrate for illicit recreActive ingredients are the kava lactones including (+)-ational drug use. The active ingredients are the cankavain, yangonin, desmethoxy yangonin, kava pirones,naboids, mainly 9-tetrahydracanabinol and other bioand chalcones including flavokavain A and B. Used orally,active cannabinoids. The flavoniods canniflavone-1 and -2 kava lactones and pirones act at central GABA synapses are also present. The analgesic actions of the cannabinoids to potentiate GABA release or facilitate GABA binding appear to be due to binding at a discrete CNS receptor (primarily in brain). Kavain and dihydrokavain inhibit present in the thalamic, limbic, and cortical regions of the brain. Additionally, the effect of cannabinoids and voltage-dependent sodium and calcium channels, thus

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flavoniods on membrane lipid metabolism, specifically,SPRUCE (SPECIES OF PICEA) the diversion of fatty acid metabolism against archidonic Indigenous to north, central, and western Europe, spruce acid, appears to be a mechanism by which peripheral is grown worldwide. Medicinal oils are extracted from analgesic effects may be mediated. The legal implications needles, branches, and shoots. These yield needle oil conof cannabis use are obvious. It warrants mention that this taining bornoachinate, limonene, camphene, and pinene. agent has seen licit use as an analgesic, and may have Spruce shoots yield a volatile oil containing primarily utility as a marketed compound (dronabinol) for the treatlimonene, borniol, bornyl acetate, and ascorbic acid. ment of pain, AIDS-induced anorexia, and as an antiSpruce needle oil and spruce shoots are sanctioned by emetic for use during chemotherapy. Characteristically, Commission E for topical application in the treatment of cannabis is smoked (in cigarette or water-pipe form), neuralgia and rheumatic-type pain. Mechanism of action ingested (either directly or incorporated into sweets), or appears to be due to a secretolytic and tonic inhibitory taken in capsular form. Multiple effects are attributed to effect on peripheral nociceptive afferents. cannabis including vacillation of mood, lethargy, altered As with scotch pine oils, patients with skin trauma concentration, increased reaction time, and alteration of and injury should avoid use of spruce oil or use it causensations. Physiologically, cannabis induces bronchial tiously. Pediatric use is not recommended due to the dilation, mild to moderate immunosuppression, increased enhanced possibility of absorption and toxicity. cardiac chronotropy, and mild hypothermia. Although specific contraindications do not exist, the aforementioned side effects limit its utility and caveatsST. JOHN’S WORT against operating a motor vehicle or heavy equipment or (HYPERICUM PERFORATUM) engaging in complex tasks are afforded. Although regional Growing natively throughout Europe and North Africa, interest in legalizing cannabis use for general purposes (both medicinal and recreational) exists, marijuana stillthe plant has been introduced to Asia, the Australian continent, New Zealand, and is currently cultivated in remains an illegal substance with often dire penal conseNorth America. The specifi c medicinal utilization is of quences for possession and use. Thus, its use is limited to buds and flowers. These yield several active constituents; prescription dosing (dronabinol, marketed under the brand anthrosene derivatives include hypericin and pseudoname Marinol™) for appetite stimulation, anti-emetic hypericin. Active flavoniods include hyperosides, queraction, and as an analgesic adjuvant (generally employed citerin, rutin, and amentofl avone. Hypericum also conin end-stage terminal disease pain). tains zanthones, catechintannins, caffeic acid derivatives, and a volatile oil whose main constituents are aliphatic hydrocarbons and mono- and sesquiterpenes. The herb is SCOTCH PINE (PINUS) Commission E approved for treatment of depression, anxNative species are found in Europe, Siberia, the near iety, and may be used as an adjunct analgesic. These East, and Scotch pine is cultivated worldwide. Medic-properties are related to the activity of the flavone and inal components include tar extracted from the trunkflavinol derivatives. Hypericin has been shown to inhibit and branch, oil extracted from needles, and pine tipsreuptake of serotonin, norepinepherine, and dopamine from dried shoots. Active compounds include a volatileand may evoke pineal release of melatonin. The reuptake oil containing bornyl acetate, cadinene, and α tinnene, blocking effects of hypericum increase the synaptic availascorbic acid and several resins. The pine needle oil ability of serotonin and norepinepherine within the brain contains∆-3-carene and α- andβ-pinenes. A subspecies and spinal cord, mechanisms that facilitate supraspinal of pine, pinus sylvesteris , contains camphene, and centrifugal pain modulation. limonene, and terpinolene yielded from the raw turpen- Although no specific precautions are rendered against tine oil from the plant. Pine shoots are advocated bythe use of St. John’ s Wort, numerous side effects warrant Commission E for the treatment of neuralgia and oraldiscussion. Some patients experience paradoxical restlessinflammation. Pine needle oil and turpentine oil areness (initially thought to be a hypomanic effect somewhat externally used in the treatment of neuralgia and rheu-similar to that seen with SSRIs), while others experience matoid pain. These effects are due to its enzymaticfatigue and lethargy. Transient headache is also a reported actions that inhibit prostaglandin formation in periph- side effect, although this occurs in less than 10% of eral tissues. patients. Initially, patients may experience dyspepsia or No specific precautions are noted for external use ofGI pain with St. John’ s Wort use; this effect is transient. pine oils; however, patients with extensive skin injuries,Of note is that hypericum produces photosensitivity, paracute burns, and open wounds should avoid application. ticularly with higher doses, and patients should be cauProlonged and extensive use of pine-based turpentine oils tioned regarding ultraviolet light exposure (i.e., sun tanmay have nephrotoxic and peripheral neurotoxic potential.ning and/or tanning beds). The documented neurotropic

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action of hypericum warrants precaution against several and 2-acetoxy-valerenic acid. Additionally, pyridine alkadrug interactions. Certainly, SSRIs used concomitantlyloids including valerianine and α-methyl tyrrylketone are with St. John’s Wort increase the potential for facilitated present. The valerenic acids inhibit the enzymatic degraserotonergic availability and the occurrence of serotonindation of GABA, thereby making this inhibitory neusyndrome (“wet dog shakes, ” diaphoresis, tremor, agita- rotransmitter more viable at supraspinal and spinal posttion, flushing). Similarly, the use of monoamine oxidasesynaptic binding sites. Nonselective GABA-A and inhibitors is contraindicated due to increased adrenergic GABA-B receptor effects are achieved through the use of neurotransmission and the possibility for hypertensive cri-valerian. Valerian also has a high content of glutamine, a sis and other sympathomimetic effects on the cardiovasmetabolic precursor to the glial GABA shunt for the biocular system. St. John’ s Wort induces hepatic cytochrome synthesis of GABA. This ultimately increases neuronal P450 enzyme activity; other drugs metabolized throughGABA content and potentiates post-synaptic GABA-ergic this pathway may have significant disruption of hepaticeffects further. The anxiolytic, muscle relaxant, and sedtransformation. Specifically, these include cyclosporineative effects are similar to those seen with administration (decreased serum concentration of cyclosporine followingof other GABA receptor agonists (e.g., the benzodiazconcomitant use of St. John’ s Wort), indinavir (greater epines). However, unlike benzodiazepines, tolerance, than 50% reduction in plasma concentration of indinavardependence, and withdrawal are rarely seen when utilizing with concomitant use of St. John’ s Wort), theophylline therapeutic doses of valerian. and digoxin (decreased area under-the-curve serum con- The activity at central GABA receptors contraindicentration digoxin with decreased digoxinficacy ef and cates the use of valerian with benzodiazepines or barbituanticipation of rising digoxin levels approaching toxicity rate agents that are also agonists at this multimolecular receptor site. As well, a caveat (particularly during the after discontinuation of St. John’ s Wort). initial use of valerian) against the operation of complex machinery or complex motoric tasks due to the spinal TURMERIC (CURCUMA DOMESTICA) motor inhibition, muscle relaxant, and CNS sedative Native to India, turmeric is grown throughout south easteffects should be noted. Asia and privately cultivated in the southern United States. Medicinally, the rhizome is stewed and dried to yield the WHITE FIR (ABIES ALBA) active volatile oilsα- andβ-tumerone, artumerone, α- and Indigenous to the Balkans, it is cultivated throughout γ-atlantone, zingiberene, and curcumol. The plant contains curcumoids including curcumin, demethoxycurcumin, Europe and in the United States as a domestic plant and and bidemethoxycurcumin. Turmeric is approved byfor phytomedicinal purposes. The timber yields an essential oil through extraction, with active compounds of Commission E for dyspepsia, loss of appetite, and abdomlimonene,α-pinene, champhene, bornyl acetate, and saninal pain. Prepared as a tea or in capsular form, it is taken internally after meals. Additionally, tincture of turmeric is tene. These oils may act as mild counter irritants initially, and perhaps as secretogogues to nociceptive afferents. used for anti-inflammatory effects and analgesia against inflammatory pain. It is believed that the tumerones, zin-White fir oil is approved by Commission E for topical application in treatment of neuralgia and rheumatic pain. giberene and curcumin, are the active moities in reducing the inflammatory cascade through direct stabilization of Like other essential oils of pine and fir trees, over membrane fatty acid content (thereby preventing biosyn-exposure to volatile oils may yield glottal and bronchial spasm. Thus, application to the face, periorbital, and perithesis of arachidonic acid and, subsequently, prostaglannasal regions and use in pediatric patients are contradins). This action may subserve analgesic effects as well. Although frank precautions or adverse effects are notindicated. known for tumeric, the use of this agent has been found to potentiate cholecystic disease in patients with premorWHITE WILLOW (SALIX) bid cholecystic pathology. Native to central Europe, the plant also is cultivated in the North American continent where the bark yields the active VALERIAN (VALERIANA OFFICINALIS) glycosides and salicylic acid. Additionally, white willow contains tannins andavoniods. fl White willow is approved Native to Europe and Asia, it is also cultivated in Japan and by Commission E for general treatment of pain andaminfl the United States for phytomedicinal purposes. The dried roots are utilized to yield the iridoids including the valepo-matory states. This is directly attributable to plant esters and glycosides that yield salicin, the metabolic precursor of saltriates, isovaltrate, and acevalterate. The volatile oil contains icylic acid. Salicylate is a potent inhibitor of cyclo-oxygenbornyl isovalerenate and valerenic acid. The plant yields the ase (both 1, and to a lesser extent, 2), thereby disrupting the sesquiterpenes of valerenic acid, 2-hydroxyvalerenic acid,

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TABLE 88.1 Suggested Dose, Utility and Precautions of Herbs with Pain-Modulating Activity Herb

Dose

Utility/Precautions

Black cohosh Borage

40–60 mg qd/bid or 60mg (2) bid 500 mg qd/bid as a capsule

Cajuput

1 g/cc topical oil

Cayenne

0.25%, 0.75% cream or topical transdermal gel (not to exceed 10 g/d)

Not to exceed 1–3 g/d Possible abortifacient Short-term internal use (1 week) Possibly hepatotoxic Not for facial use Not for pediatric use Use sparingly Short-term (2–3 days) use only Avoid oral, occular contact Avoid genital contact Not for use during pregnancy

English chamomile

1.5 g bid/tid Infusion 50–200 ml

Ginseng Korean

1–2 g/d as capsule (100–1250 mg available) or liquid Not to exceed 3 g/d (3 mg/ml) Contraindicated in cardiovascular, hypertensive diabetic patients Not for use during pregnancy Siberian 2–3 g/d root as extract (or capsule) Not for use in hypertensive or diabetic patients Japanese mint 2–3 drops extracted oil topically applied Not to exceed 3 times daily Not for orofacial use Not for pediatric use Kava kava 150–300 mg extract (capsular form) bid Best taken with food Not to exceed 600 mg/d Not for use in excess of 3 months without supervision Not for use during pregnancy/nursing Marijuana 2.5, 5.0, 10 mg capsules (Dronabinol: Marinol) Legal ramifications 2.5–10 mg bid-qid Not for prolonged use Precaution in motoric tasks/coordination-dependent activity Scotch pine 100 g alcohol extract bid; 20–50% topical cream, Not for orofacial use ointment, gel (1cc) tid Not for pediatric use Not for use in asthmatic patients Spruce 20–30% oil ointment (1cc) tid Not for orofacial use Not for pediatric use Not for use in asthmatic patients St. John’s Wort 125–500 mg (0.3% hypericin) capsules; Initial 6-week trial recommendation 200–300 mg tid Not for use with MAO-inhibitors, TCA, or SSRI/SNRI agents (potentiated effects) Photosensitizing: avoid UV exposure during use Induces hepatic microsomal P450 enzymes Turmeric 1.5–3.0 g/d Not for use in patients with premorbid or active cholecystic disease Not for use during pregnancy Valerian 100–1000 mg capsules; Titrate dose to effect 100–1000 mg qhs Not for use with alcohol, benzodiazepines, barbiturates May cause daytime drowsiness/lethargy Not for use during pregnancy or nursing

membrane arachidonic acid cascade that yields pro-infl amand/or dose escalation may yield salicylate toxicity (typically characterized by tinnitus and metabolic acidosis). matory and pro-nocisponsive prostaglandins. Although direct hazards and adverse side effects are In light of the salicylate content of white willow, concomitnot reported for therapeutic doses, patients who are hypertant use of nonsteroidal anti-infl ammatories or aspirin is sensitive to salicylates should not utilize white willow. As contraindicated. This is to avoid possible adverse hepatic well, pediatric use of white willow should be cautious dueeffects, concentration-induced toxic effects, and unwanted to possible occurrence of Reyes syndrome. Long-term use thrombolytic effects. There is equivocal evidence to suggest

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the utility and contraindication of white willow bark in REFERENCES patients with premorbid gastritis and/or history of peptic Almeida, J.C., & Grimsley, E.W. (1996). Coma from the health ulcer disease. Certainly, the use of this compound should food store: interaction between kava and alprazolam. be cautious in patients with co- or pre-morbid ulcer due Annals of Internal Medicine, 125, 940. to the systemic action of salicylate on prostaglandinAmmon, H.P., & Wahl, M.A. (1991). Pharmacology of curcuma induced mucus secretion in the stomach, thereby exacerlonga. Planta Medica, 57, 1. bating ulcerative symptomology. However, studies sug-Araya, O.S., & Ford, E.J. (1981). An investigation of the type gest the direct action of white willow on the gastric of photosensitization caused by the ingestion of St. mucosa may be considerably less than that of aspirin or John’s Wort (hypericum perforatum) by calves. Journal of Comparative Pathology, 91, 135. other nonsteroidals. Regardless, it is best to be prudent in the use of this compound in patients with peptic or duode-Attele, A.S., Wu, J.A., & Yuan, C.S. (1999). Ginseng pharmacology: Multiple constituents and multiple actions. Bional ulcerative disease.

chemical Pharmacology, 1, 58(11), 1685. Baldt, S., & Wagner, H. (1994). Inhibition of MAO by fractions and constituents of hypericum extract. Journal Geriatric SUMMARY Psychiatry and Neurology,(1), 7 57. The information contained in this chapter is provided asBennett, D. A., Phun, L., & Polk, J.F. (1998). Neuropharmacolan overview of those herbs identified to have viable, clinogy of St. John’ s Wort (hypericum).Annals of Pharmacotherapy, 32 (11), 1201. ically researched evidence for treatment of pain. Their use Biro, T., Acs, G., Acs, P., et al. (1997). Receptor advances and as primary and/or adjunctive analgesics requires considunderstanding of vanilloid receptors, a therapeutic target erable expertise and caution on the part of practitioners. for treatment of pain and inflammation in the skin. JourUnfortunately, precise pharmacokinetic parameters of nal of Investigative Dermatology, 2, 56. each herbal preparation are not completely understood. A Bonte, F., Noel-Hudson, M.S., Wepierre, J., & Meybeck, A. single herbal preparation may contain numerous active (1997). Protective effect of curcuminoids on epidermal principles that are differentially yielded based upon type skin cells under oxygen-free radical stress. Planta Medof preparation. Also, the actual concentration of the active ica, 8, 265. principles may vary widely based upon preparation, qual-Bradley, P.R. (Ed.). (1992). British herbal compendium, Dorset, ity of herb, season of herbal harvesting, as well as other U.K.: British Herbal Medicine Assn. factors. Accurate prediction of dose–response relation-Cowan, R.A., Heartnel, G., Lowdell, C., Baird, I., & Leak, A. (1984). Metabolic acidosis induced by carbonic anhyships, time course of effects, specific parameters for interdrase inhibitors and salicylates in patients with normal action and pharmacodynamic mechanisms and actions are renal function.British Medical Journal, 289,6441, 347. somewhat difficult to assess given available information. Daiber, W. (1983). Klimakterishe Beschwerden: Ohne Capital For the clinician considering integrating phytomedicinals Hormone zum Erfolg.Artzl. Praxis,35, 1946. to clinical practice, a working maxim would be to “start Davies, L.P., Drew, C.A., Duf field, P., et al. (1992). Kava pirones low and go slow” utilizing the purest form of the herb and resin: Studies on GABA-A, GABA-B, and benzocommercially available, at the lowest viable dose, incrediazepine binding in rodent brain. Pharmacology and mentally increasing that dose to effect, while observing Toxicology, 71 (2), 120. Boca for putative side effects and potential drug interactions. Duke, J.A. (1985).CRC handbook of medicinal herbs. Raton: CRC Press. To reiterate, recruiting the aid of a compounding pharmacist (to assist in obtaining the purest commercial formDuker, E.M., Kopanski, L., Jarry, H., & Wattke, W. (1991). Effects of extracts fromsimicifuga racemosaon gonaof herb), a naturopathic physician, and receiving specific dotropin release in menopausal women and ovariecto(advanced) training in phytomedicinal practice are mized rats.Planta Medica, 57,420. strongly advocated. Clinicians must be aware that simplyFaure-Raynaud, M. (1970). Study of volatile oil from abies alba because a substance is “natural” does not guarantee its miller. I. Study of raw material. Acta Poloniae Pharmasafety. Although herbs often provide a reasonable alternaceutica, 132 (B), 71. tive to commercially manufactured pharmaceutical prod-Furst, D.E., Sarkissian, E., Blocka, K., et al. (1987). Serum concentration of salicylate and naproxen during concurrent ucts, a complete understanding of their chemistry, phartherapy in patients with rheumatoid arthritis. Arthritis macologic mechanisms and effects, and potential and Rheumatism, 30 (10), 1157. physiologic and pharmacologic side effects and interacFusco, B. M., Fiore, G., Gallo, F., et al. (1994). Capsaicin-sensitive tions is mandatory. sensory neurons in cluster headache: Pathophysiological aspects and therapeutic indication. Headache, 34 (3) 132. Gleits, J., Beile, A., Peters, T., et al. (1995). (+/-)-kavain inhibits ACKNOWLEDGMENT in veratridine-activated voltage-dependent+-channels Na The author wishes to thank Connie Parker for her assissynaptosomes prepared from rat cerebral cortex. Neurotance in preparation of all phases of this manuscript. pharmacology, 34 (9), 1133.

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(2000). Hasmeda, M., & Polya, G.M. (1996). Inhibition of cyclic AMP- Physician’s desk reference for herbal medicines. Montvale, NJ: Medical Economics Co. dependent protein kinase by curcumin. Phytochemistry, Ridel, E., Hansel, R., & Ehrke, G. (1982). Hemmung des 42, 599. Gamma-aminobuttersaureabbaus durch ValerensaureHernandez, M.L., Garcia-Gile, L., Berrendero, F., Ramos, J.A., derivate.Planta Medica, 46,219. and Fernandez-Ruiz, J.J. (1997). Delta 9-tetrahydrocanapinol increases activity of tyrosine hydroxylise in Ruh, N.F., Taylor, J.A., Howlett, A.C., & Welshons, W.V. (1996). The volatile oil composition of fresh and air-dried buds cultured fetal mesencephalic neurons. Journal of Molecof cannabis sativa . Journal of Natural Products, 53, 49. ular Neuroscience, 8,83. Hiller, K.O., & Zetler, G. (1996). Neuropharmalogical studies Schirrmacher, K., Busselberg, D., Langlasch, J.M., et al. (1999). Effects of (+/-)-kavain on voltage-activated inward curon ethanol extracts of valeriana officinalis: Behavioral, rents of dorsal root ganglion cells from neonatal rats. anti-convulsive properties. Phytotherapy Research, 10, European Neuropsychopharmacology, (1–2), 9 171. 145. Schmidt, B., & Heide, L. (1995). The use of salicis cortex in Hoffman, D. (1988).The herbal handbook: A user’ s guide to rheumatic disease: Phytotherapy with known mode of medicinal herbalism.Rochester, VT: Healing Arts action?Phytomedicine, 61,94. Press. Huang, H.C., Jan, T.R., & Yeh, S.F. (1992). Inhibitory effect of Seizt, U., Schule, A., and Gleitz, J. (1997). [3H]-Monoamine uptake inhibition properties of kava pirones. Planta curcumin, an anti-inflammatory agent on vascular Medica, 63(6), 548. smooth muscle cell proliferation. European Journal of Srivastava, K.C., Bordia, A., & Verma, S.K. (1995). Curcumin: Pharmacology, 54,381. A major component of food spice turmeric curcuma ( Ippen, H. (1995). Gamma-linolensure besser aus nachtkerzenlonga) inhibits aggregation and alters eicosanoid metaboder aus borretschol? Zeitschrift Pflanz u Phytotherapie, olism in human blood platelets. Prostaglandins Leukot16(3) 167. rienes and Essential Fatty Acids, 52, 232. Isaacs, O. (1993). Chamaemelum nobile. Zeitschrift Pflanz u Steinegger, E., & Hanscl, R. (1980). Pharmakognosie(p. 258). Phytotherapie, 14 (4) 212. Heidelberg: Springer-Verlag. Jamieson, D.D., & Duf field, P.H. (1990). The anti-nociceptive Teng, C.M., Kuo, S.C., Ko, F.N., et al. (1989). Anti-platelet actions of kava components in mice., Clinical and actions of panaxynol and ginsenosides isolate from ginExperimental Pharmacology and Physiology,(7), 17 seng.Acta Biochemica et Biophysica, 990 (3), 315. 495. Biogene gifte: Biologie Kohane, D., Kuang, Y., Lou, N., et al. (1999). Vanilloid receptor Teuscher, E. & Lindquist, U. (1994). Chemie, Pharmakologie . Stuttgard: Fischer Verlag. agonists potentiate the in vivo local anesthetic activity of percutaneously injected type-1 sodium channelThomas, D.F., Adams, I.B., Mascareloa, S.W., Martin, B.R., & Razdan, R.K. (1996). Structure-activity analysis of blockers.Anesthesiology, 90 (2), 524. anandamide analogs: Relationship to a cannabinoid Kuo, S.C., Teng, C.M., Lee, J.C., et al. (1990). Anti-platelet pharmacophore.Journal of Medicinal Chemistry, 58, components in panax ginseng. Planta Medica,56 (2) 471. 164. Leung, A.Y. (1980).Encyclopedia of common natural ingredi- Tyler, V.E. (1994).Herbs of choice: The therapeutic use of phytomedicinals. Binghamton: Pharmaceutical Products ents used in food, drug and cosmetics. New York: John Press. Wiley and Sons, Inc. Lewis, R., Wake, G., Court, G., et al. (1999). Non-ginsenosideUebelhick, R., Frank, L., & Schewe, H.J. (1998). Inhibition of platelet MAO-B by kava pirone-enriched extract from nicotinic activity in ginseng species. Phytotherapy piper methysticum forster(kava kava).PharmacopsyResearch,13(1), 59. chiatry, 31(5), 187. Liske, E. (1998). Therapeutic ficacy ef and safety ofsimicifuga racemosafor gynecologic disorders. Advanced Thera- Wheatley, D. (1998). Hypericum extract: Potential in the treatment of depression. CNS Drugs, 9, 431. peutics, 15 (1), 45. Mackie, K., & Hille, B. (1992). Cannabinoids inhibit N-type Wichtl, M. (1994). Herbal drugs and phytopharmaceuticals. Boca Raton: CRC Press. calcium channels in neuroblastoma-glioma cells. Proceedings of the National Academy of Science (U.S.A.),Yamamoto, I., Matsunaga, T., Kobayashi, H., Watanabe, K., & Yoshimura, H. (1991). Analysis and pharmacotoxicity 89, 3825. of feruloyltyramine as a new constituent and p-coumaMuller, W.D., & Rossol, R. (1994). Effects of hypericum extract royltyramine in cannabis sativa. Pharmacology, Bioon the expression of serotonin receptors. Journal Gerichemistry, and Behavior, 40, 465. atric Psychiatry and Neurology,(1), 7 63. Yun-Choi, H.S., Kim, J.H., & Lee, J. (1987). Potential inhibitors Newall, C.A., Anderson, L.A., & Phillipson, J.D. (1996). Herbal of platelet aggregation from plant sources. Journal Natmedicine: A guide for healthcare professionals. London: ural Products, 50 (6), 1059. Pharmaceutical Press.

89 The Neurobiology of Pain James Giordano, Ph.D. Pain is a most beguiling clinical problem. With both sub-Serotonin may work directly upon the terminals of free nerve +) and/or calcium (Ca ++) jective and objective components, pain becomes a unique endings to initiate a sodium (Na experience for each individual. The neural substrates that current leading to heightened excitation. are involved in processing noxious input contribute to both The burning sensation that often accompanies highthe sensation and perception of pain. By understanding intensity mechanical and thermal stimulation may be the components of the pain transmitting and modulatingindicative of the sequential activation of discrete populasystems we may gain insight toward the development oftions of differentially sensitive nociceptor nerve endings therapeutic strategies against chronic pain. (and their associated primary afferents): first by the stimulus directly, followed by the resultant chemical changes in the affected tissue. NOCICEPTORS The free nerve endings subserving the transduction of noxious stimuli are responsive to high-intensity mechanThe first step in the nociceptive sensory pathway is the ical input (i.e., pinch, squeeze, intense pressure), hightransduction of noxious stimuli to a relevant neural signal. intensity thermal input (e.g., noxious heat in excess of In cutaneous, muscle, and visceral tissues, free nerve end45°C), mixed high-intensity mechanothermal input, and ings of nocisponsive primary afferents are responsible for chemical stimulation (disturbance of the local chemical this transduction step. It remains somewhat unclear or ionic environment and presence of various pro-nocicewhether the free nerve endings respond to the actual noxptive substances). Transduction occurs as these stimuli ious stimulus or to evoked changes in the tissues which evoke changes in the neural membrane integrity, producthey innervate. In the latter case, noxious stimuli incur a ing a inward sodium and/or calcium current. The receptor cascade of cellular damage evoking the release of fatty acids and free ions from cell membranes. Among the fattypotential for free nerve endings appears to be a graded response, with time- and intensity-dependence of the acids, arachidonic acid serves as the initiative substrate for induction of the enzymes cyclooxygenase 1 and 2 tomembrane polarity. Subsequent to transduction, the nociceptive signal is transmitted from free nerve endings in catalyze the inflammatory cascade (subsequently mediated the periphery (or viscera) along what appears to be stimby prostaglandins and leukotrienes). Change in local tissue ulus-specific, labeled lines of nociceptive primary afferent pH and the concentration of various ions, such as potassium (K +), serves to directly affect membrane polarity of freefibers. There are two type of primary nociceptive afferents, A-delta and C-fibers. These subtend distinct types of noxnerve endings in the affected tissue as well as altering vascular permeability and mast cell degranulation. Degranula-ious input (e.g., thermal, mechanical, polymodal) and are responsible for differing subjective qualities of fast (i.e., tion of mast cells causes release of histamine and serotonin, which exacerbate vasodilatory and inflammatory effects.“first”) and slow (i.e., “second”) pain, respectively.

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thresholds for mechanical and chemical stimuli by noxious heat. However, unlike thermal sensitization of mechA-DELTA FIBERS anosponsive A-delta fibers, C-fibers are sensitized by noxious heat of lower intensity (48 to 50°C). This may account These fibers are small, thinly myelinated neurons 1 to for both the persistent second pain and hyperalgesia that 5 µm in diameter, with conduction velocities in the range of 5 to 30 m/sec. The rapid rate of conduction is respon-occur following a milder burn injury. In this light, C-fibers sible for the initial sensation of pain (first pain) typically may contribute to multiple sensations from a painful region. C-fibers also innervate muscle tissue, localized to described as sharp, localized, and well defined. A-delta fibers have small receptive fields and are relatively modal-the intrafibril matrix, tendons, and areas surrounding the ity specific. A-delta thermosponsive fibers respond to vascular walls. C-fiber muscle afferents are polymodal, and are responsible for the nociceptive response to intense extremes of temperature. One population is activated by noxious heat, with an initial response threshold in themechanical stimulation, numerous chemicals (including lactic acid), and heat. Although not directly activated by range of 40 to 45°C. Response function increases directly, muscular contraction or the stretch reflex, intramuscular although not necessarily linearly, as a consequence of C-fibers can be sensitized (under ischemic conditions) to temperature elevation, with maximal responses occurring respond to even small myofibril contraction, and may at temperatures of 46 to 53°C. These responses subserve both the rapid, demonstrably painful response to an initialrespond vigorously to excessive stretch. This sensitization presentation of noxious heat and the ability to quicklyhelps to explain the diffusely painful response to both discriminate the extent of thermal pain as a function ofpassive and active movement of over-exerted, traumatized, heat intensity. A second population, high-threshold coldor ischemic skeletal muscle. afferents, respond to cold temperatures at or below a VISCERAL PRIMARY NOCICEPTIVE AFFERENTS threshold of approximately 20°C. A-delta mechanoreceptive afferents are activated by Primary afferent innervation of the viscera is not comhigh-intensity mechanical stimulation (deep pressure, pletely understood. Conflicting evidence exists regarding stab, pinch), although these fibers may be sensitized by the potential for nociceptive transmission from the viscera. and become secondarily responsive to noxious heat. Numerous stimuli are capable of producing visceral pain. Unlike A-delta thermal afferents, sensitized A-delta mechDistention, compression, and chemical and tactile irritaanoreceptive afferents respond to suprathreshold heat tion of several visceral structures have all been shown to (usually in excess of 50 to 55°C) and/or repetitive presenelicit distinct and quantifiable pain responses in humans tation of noxious heat, rather than to a singular exposure that are often accompanied by reports of localized somatic to a heat stimulus at or above the nociceptive threshold. and cutaneous pain. The diversity of responsiveness to The sensitization of this second population to nociceptive various types of noxious stimuli suggests the presence of A-delta afferents is thought to underlie clinical patterns afferents with polymodal qualities. Taken with the diffuse, of hyperalgesia (increased sensation of pain) seen followpoorly localized quality that often accompanies visceral ing heat and burn injury. pain, such findings implicate the involvement of C-fibertype innervation. C-fiber-type afferents innervate several C-FIBERS visceral structures, although studies also have demonC-fibers are small, unmyelinated afferents. With fiberstrated the presence of A-delta fibers with polymodal sensitivity, particularly in the testes and structures surrounddiameters ranging from 0.25 to 1.5 µm, the absence of myelin leads to slower conductance velocities that varying the heart. As well, a small, unmyelinated J-fiber has been identified in the parenchyma of the lung. J-fibers from 0.5 to 2 m/sec. This slower conductance subserves “second pain, ” a diffuse, poorly localized burning, throb- have structural properties, receptive fields, and conducbing, and/or gnawing sensation that follows, and is tem-tance velocities similar to C-fibers and respond to highporally and qualitatively distinct from the initial sensation intensity mechanical changes in lung volume (i.e., distenammation, and exogenous of first pain. Numerically, C-fibers constitute the majority tion and compression), infl of primary nociceptive afferents found in cutaneous tissue.chemical irritants (e.g., acidic and basic substances). C-fibers are polymodal, and can be activated by thermal, Nociceptive afferent innervation of visceral structures mechanical, and chemical stimuli. In addition to respond-has several characteristics that are markedly distinct from ing to noxious (thermal, mechanical, and chemical) stim-those in cutaneous and muscle tissues. First, nociceptive uli, C-fiber polymodal afferents may be activated by cer-afferent innervation of the viscera is relatively sparse, with tain types of non-noxious, low-intensity stimulation. C- considerable diffusion at projection sites at second-order neurons within the spinal dorsal horn. Thus, nociceptive fiber thresholds to such non-noxious stimuli can be sensitized by high-intensity heat, pressure, or chemical dis-input from the viscera may not evoke strong, well-localized turbance. Similarly, C-fibers may be sensitized to lowervolleys of excitation capable of spatially and/or temporally

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target for glutamate binding. Glutamate-induced AMPA summating at spinal relays. Second, the nature of visceral receptor activation evokes a ligand-gated sodium current afferents is such that sensitization by chemical mediators in post-synaptic second-order neurons of the dorsal horn and/or sympathetic activity (see below) appears to be required for their sustained firing. Given the sparse distri-that produces a rapid, depolarization. Glutamate is also bution of these fibers throughout the viscera and the dif-capable of binding to a second site, the NMDA (N-methylfuse connections with nociceptive units of the spinal cord,D-aspartate) receptor. It appears that AMPA receptors either directly or indirectly modulate activation of NMDA it appears that this sustained firing is responsible for the activation of second-order spinal afferents, and ultimatelyreceptors by glutamate through allosteric modulation of the transmission of visceral nociceptive signals. The per-magnesium binding to a shared or cooperative domain of ception of visceral nociception is vague, becoming morethe NMDA receptors. With persistent AMPA receptor activation, the rise in intracellular sodium displaces a magneintense (and better localized) as increased painful activity sium “gate” from the NMDA receptor, thereby increasing in the innervated structure(s) sensitizes the involved afferents. Third, nociceptive afferent innervation of the visceraits sensitivity or releasing it from an inaccessible configis often structurally co-localized with sympathetic afferenturation to actively bind glutamate. It is hypothesized that (and perhaps efferent) neurons. Noxious stimulation fromthis molecular change on the receptor level subserves a the viscera can lead to concurrent excitation of both vis-component of the altered neurological responses from ceral nociceptive afferents and sympathetic innervation,acute to chronic pain. Glutamate binding at the NMDA capable of producing retrograde sympathetic outflow andreceptor is responsible for mediating an inward calcium sympathetically maintained regional hyperalgesia. Last,current that initiates a protein kinase-C to catalyze the induction of the enzyme nitric oxide (NO) synthase visceral nociceptive afferents are often integrated anatomically with somato-cutaneous nociceptive afferents withinrequired for the intracellular production of NO. dorsal root ganglia or within the neuropil of second-order Protein kinase-C is also capable of catalyzing other afferents of the spinal cord. Reciprocal sensitizationintracellular enzymatic reactions that stimulate protein within the dorsal root ganglion and the overlap of second-synthesis in the second-order neuron. These glutamatedependent protein kinase-C related reactions may be order receptive fields for visceral and somato-cutaneous responsible for the production of new membrane-bound input subserve the somatic referred component that is characteristic of much of visceral pain. In this regard itcalcium channels and “new” NMDA receptors that may mediate or prolong sensitization of second-order afferents becomes clinically relevant to understand the convergence to input from nociceptors. It also has been posited that of visceral and somato-cutaneous afferents when attempting to predicting involvement of visceral structures in these molecular changes subserve, at least in part, secondorder afferent sensitization to subthreshold primary afferpatterns of referred somatic pain. ent input, thereby producing hyperalgesic and perhaps allodynic responses. There is further evidence to suggest PROJECTIONS TO THE SPINAL DORSAL HORN that prolonged activation of newly synthesized NMDA Although a small number of nociceptive afferents synapse receptors may instigate protein kinase-C mediated nuclear within the ventral spinal cord, the vast majority of somato-reactions that may affect cell vitality and viable function (i.e., induction of apoptotic mechanisms of programmed cutaneous and visceral nociceptive primary afferent fibers cell degeneration and death). project to defined areas of the superficial dorsal horn. This area has been anatomically distinguished into discrete Primary afferent nociceptors also release the undecapeptide substance-P. It is unclear whether substance-P zones, known as the laminae of Rexed. The laminae, or is released directly following depolarization of primary layers, are numbered consecutively from dorsal to ventral afferents or as a consequence of feedback stimulation regions. Both A-delta and C-fibers have been shown to terminate on specific populations of second-order spinalfollowing glutamate release. Substance-P binds post-synneurons in laminae I, II, IIa, and V, which are the origins ofaptically to neurokinin-1 (NK-1) receptors on secondorder dorsal horn neurons. Prolonged activation of neurothe ascending spinal pathways critical to pain transmission. kinin receptors has been shown to result in the initiation and accumulation of a stimulatory proto-oncogene, c-fos NEUROCHEMISTRY OF PRIMARY AFFERENT and its protein product. c-fos proto-oncogene appears to PAIN TRANSMISSION be responsible for mediating increased metabolic activity The principal neurochemical mediator at the synaptic cleftwithin the second-order neuron. Also, c-fos may interact between primary afferent nociceptors and dorsal horn cells on a molecular level to induce or increase the production appears to be glutamate. Post-synaptically, glutamate of is other proto-oncogenes, namely, ras and perhapsjun. capable of binding to two sets of discrete receptors. The Together, these proto-oncogenes may be responsible for AMPA (α-amino-3-hydroxy-5-methyl-isoxazole-4 propi- promoting nuclear mechanisms that code for novel (and onic acid) receptor appears to be the initialrst or molecular fi perhaps aberrant) structural and functional proteins

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involved in remodeling second-order neurons that areWIDE DYNAMIC RANGE NEURONS actively processing chronic pain. In addition, sensitized primary afferents are capableWide dynamic range (WDR) neurons are localized with of anti-dromic or retrograde release of neurochemicalthe highest concentrations in laminae I, II, V, and VI, with mediators of the infl ammatory response. Prolonged acti- greatest numbers found in the latter levels. Although WDR vation of primary afferent A-delta, and particularly C- neurons receive input from low-threshold cutaneous mechanoreceptor afferents (Aβ type), they are also a site fibers, has been shown to evoke an anti-dromic release of convergence for both A-delta and C-fiber nociceptive of substance-P. Substance-P provokes degranulation of afferents. WDR neurons that are driven by nociceptive mast cells in peripheral tissue leading to the release of input are organized hierarchically within the dorsal horn, several potent vasoactive and pro-infl ammatory mediawith the majority of primary A-delta and C-fiber afferent tors including histamine and serotonin. Substance-P also input occurring in laminae V. The size and responsivity of may act directly as a vasodilator. In addition to antiWDR neuron receptive fields increases progressively from dromic release of substance-P, primary afferent nocicelaminae I to V: WDR units in laminae I and II have smaller ptors release calcitonin gene-related peptide (CGRP) from terminal branches to affect distal peripheral (and/orreceptive fields that are sensitive to gentle mechanical stimuli, those of laminae V have larger, overlapping recepvisceral) tissues. CGRP activates the enzyme NO synthase from the vascular endothelium leading to antive fields with graded sensitivities containing small, disincrease production of nitric oxide and, ultimately, crete regions excited by non-nociceptive input and broad vasodilatation. Taken together, the effects of histamine,regions that are maximally sensitive to high-threshold nociceptive stimulation. mast cell-derived serotonin, substance-P, and CGRP proWDR neurons are not individually sensitive to speduce potent peripheral vasodilatory effects that lead to cific types of stimuli. Rather, individual WDR neurons, extravasation of chemical mediators that both propagate based upon response properties within their receptive the inflammatory response and are directly pro-nocisponfields, function to discriminate stimulus intensity. sive. These include vasoactive intestinal peptide (VIP), Increases in stimulus intensity activate coexistent areas bradykinin, and platelet-derived serotonin. Of particular of receptive fields of numerous WDR neurons. This patinterest is the effect of rising concentrations of serotonin tern of engagement would involve slight differences in in extra-vascular tissue from mast cells and degranulated temporal activation, with individual WDR responses platelets. Our research has demonstrated that as periphbecoming phase-shifted. The activation of greater numeral serotonin concentrations rise, serotonin 5-HT 3 bers of WDR neurons by high-intensity nociceptive stimreceptors on terminals of C-fi ber primary afferents uli would, therefore, result in spatial and temporal sumbecome directly stimulated, facilitating an increase in Cmation of these responses. fiber depolarization and continuity of this cycle. These mechanisms help to explain how prolonged primary NOCICEPTIVE SPECIFIC (NS) NEURONS afferent activity can transform acute and subacute pain into a chronic condition with distinct neurologic and In contrast to the anatomical distribution of WDR neurons, neurochemical properties. nociceptive specific (NS) neurons are found in highest concentrations in laminae I and II, with lesser numbers in laminae V. NS neurons receive excitatory input from ASECOND-ORDER AFFERENTS delta fibers and polymodal C-fiber afferents. Generally, The dorsal horn of the spinal cord is a critical site for theNS neurons have small, non-overlapping receptive fields convergence and neural processing of nociceptive infor-with a well-defined, center-surround organization. The mation from peripheral primary afferent fibers. A-delta central region is maximally excited by high intensity stimand C-fibers form synaptic connections upon distinct uli, while the outer region is differentially excited by freclasses of wide dynamic range (WDR) and nociceptive-quency-based repetitive stimulation. This outer region specific (NS) neurons within the spinal cord whose func-may be inhibited by non-noxious input. The homogeneity tional properties contribute to spatial and temporal trans-of input from nocisponsive primary afferents and the small formations of the afferent input. These second-order neusize and nociceptive selectivity of their receptive elds fi prorons aggregate in the dorsal horn, project contralaterally, vide evidence that NS neurons appear to function in localand ascend within the anterolateral quadrant(s) as the ization, and perhaps qualitative discrimination of particular spinothalamic tract (STT) to sites within the brainstem,types of noxious input (i.e., noxious pressure and/or heat). midbrain, and thalamus. The unique physiologic charac- Although painful sensations and responses can be teristics of WDR and NS neurons encode specific qualities evoked by WDR neuron excitation alone, WDR and NS of intensity, modality, and localization to the nociceptive activity appears to be necessary for the constellation of signal that is transmitted to supraspinal targets. spatial and temporal qualities ascribed to pain. This

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becomes apparent when the convergent inputs of A-delta neurons are in smaller numbers within these laminae and and C-fibers upon WDR and NS neurons are considered. they comprise only a minority of NSTT fibers. Recall that The unique properties of the primary afferents and theNS neurons receive almost completely homogeneous second-order neurons essentially assemble the neurologic input from A-delta and high-threshold polymodal C-fiber pain signal. For example, the sensation of first pain as afferents, and encode stimulus localization and modality. punctate, well-localized, and temporally well-defined is aTherefore, the main role of the NSTT appears to involve function of the response characteristics of both rapidlytransmission of these signal qualities to the thalamus. conducting A-delta primary afferents and their excitation The PSTT is composed of axons from second-order of WDR and NS neurons. In contrast, second pain, a more neurons arising in lamina V of the spinal cord. WDR diffuse, long-lasting nociceptive sensation that follows theneurons constitute the majority of cells from this lamina, initial stimulus is the result of the threshold, firing and with only a smaller number of NS neurons contributing conduction properties of C-fibers sustained by local tissue to the axonal pool of the PSTT. Heterogeneous input to damage and/or chemical change, as well as patterns lamina of V WDR neurons from both nocisponsive and nontemporal and spatial summation of C-fiber inputs by WDRnocisponsive primary afferents contributes to the transand NS neurons. Both WDR and NS neurons are capable mission of some non-nociceptive signals along the PSTT. of after-responses that persist as a consequence of nociWDR neurons of lamina V also send axons ipsilaterally ceptive afferent volley number and frequency; factorsto ascend within the dorsal column medial lemniscal tract. related to nociceptive stimulus intensity and continuity. This latter pathway is responsible for the transmission of The anatomic and physiologic properties of second-light touch, vibration, and other low-threshold stimuli. order afferents also subserve the phenomenon of referred Given the role of lamina V WDR neurons to encode noxpain. As previously discussed, primary afferent innerva-ious stimulus intensities, the co-localized transmission of tion of visceral and deep muscular structures is organized nociceptive and non-nociceptive afferent information so that these fibers converge upon WDR and NS neurons within the PSTT appears to serve a stimulus discriminathat also receive input from primary nociceptive (and non-tory function. This is further supported by the properties nociceptive) afferents from specifi c somato-cutaneous of PSTT WDR neurons to accumulate strong afterregions. The convergence of visceral and cutaneous afferresponses following nociceptive input. Such afterents from a given somatotome upon second-order WDR responses override weaker impulses evoked by non-nociand NS neurons underlies patterns of clinical referred pain ceptive afferent stimuli, and produce temporally sumsyndromes. Thus, sensory information from the viscera is mated volleys within the PSTT. These events are correoften interpreted subjectively as afferent information fromlated to, and appear to subserve the qualities and subjective a cutaneous structure within the corresponding somatotome. characteristics of clinically relevant, second, and/or chronic pain. Unlike the NSTT, the PSTT is not a direct thalamic SPINOTHALAMIC TRACT(S) pathway. PSTT fibers project to several supraspinal sites The majority of WDR and NS neurons project contralat-that are involved in (nociceptive) sensory processing and erally within the spinal cord and ascend within the ante-that may exert pain modulatory control. The PSTT may rolateral quadrant, forming the spinothalamic tract(s)be divided into spinoreticular, spinotectal, and ultimately (STT). A minority of fibers remain ipsilateral, and ascendspinothalamic projections. Spinoreticular pathways outside of the STT within the ventrolateral white matterproject to areas of the brainstem reticular formation. These include the raphe nuclei of the rostroventral medulla and to supraspinal sites that correspond to the contralateral anterolateral quadrant projections. Anatomically, axonsthe nuclei reticularis gigantocellularis (NRGC) and paragigantocellularis (NRpG) of the caudal pons. from second-order neurons in the superficial dorsal horn (laminae I and II) are segregated from those of deeper Spinotectal projections terminate within the tectum laminae (lamina V). This provides anatomical separationand periaqueductal grey (PAG) region of the midbrain. between the neospinothalamic (NSTT) and paleo-The spinoreticular and spinotectal circuits function in censpinothalalmic (PSTT) tracts. While both the NSTT andtrifugal pain control and ascending neurons from these PSTT may be considered “labeled-lines” for the transmis-sites serve as relays between spinal pathways and higher sion of pain signals, the differential localization of NS centers that mediate the perceptual and affective dimensions of pain. Of particular note are defined tracts from neurons to laminae I and II, in contrast to a greater abundance of WDR neurons in lamina V, subserves functionalthe reticular formation to several regions of the limbic foredistinctions in the type of nociceptive information that is brain, and a reciprocal neuraxis involving the PAG, the periventricular gray region (PVG), and hypothalamus. Thatransmitted in these pathways. The NSTT projects directly to the ventroposterior lat- lamic projections of the PSTT differ from those of the NSTT; eral (VPL) nuclei of the thalamus and is composed pre-PSTTfibers project diffusely to the thalamus, with terminadominately of NS neurons from lamina I and II. WDR tions at several intralaminar nuclei. (See Figure 89.1.)

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serotonin may bind to serotonin 5-HT1 b receptors on processes of second-order nociceptive neurons. As well, serotonin may bind to 5-HT1 b receptors on an interneuron pool in several laminae of the dorsal horn to disinhibit the release of the inhibitory transmitter gamma-amino-butyric acid (GABA) and enkephalin to produce graded inhibition of second-order pain-transmitting afferents. PAG-NRGC connections involve a release of opioids from the periacqueductal grey that disinhibit noradrenergic neurons of the reticular formation (whose axons similarly descend in the dorsal lateral funiculi) to evoke a release of norepinephrine in laminae II and V. Norepinephrine binds to α2 receptors on primary (and perhaps second-order afferents) to produce a graded hyperpolarizing inhibitory current, thereby toning down these neurons and producing an analgesic response. Whether these distinctions actually subserve modality specifi city or reflect differential activation based upon stimulus intensity remains speculative. Although stimulus or intensity differences in the involvement of particular reticular nuclei exist, it is unlikely that any further discriminative processing of the nociceptive signal occurs at the reticular level. PSTT excitation of reticular neurons also activates neural systems involved in pain-related aversive and arousal responses.

MIDBRAIN NOCICEPTIVE MECHANISMS Anatomical evidence demonstrates that PSTT fibers project to the midbrain PAG both directly and through interneuronal pathways from the reticular formation. Studies suggest that the PAG is somatotopically and perhaps stimulus-specifically organized. Somatotopic organization FIGURE 89.1 Cross-sectional schematic representation (not to scale) of spinothalamic tracts projecting to supraspinal locicorresponds to the ascending hierarchy of PSTT afferents from progressively rostral somatotomes: the posterior involved in nociceptive processing. PAG receives input from PSTT fibers of the caudal spinal cord while the anterior PAG receives PSTT projections BRAINSTEM NOCICEPTIVE NEURAXES from more rostral regions. Stimulus-specific organization of the PAG seems to PSTT neurons differentially project to specifi c sites within the brainstem. Some stimulus specifi city exists in PSTT be a function of the population characteristics of PSTT activation of raphe and/or NRGC/NRpG neurons. InputWDR or NS neurons that are selectively excited by from NS and/or WDR units excited by thermosponsive pri-mechanical, thermal, or polymodal primary afferents. While it is difficult to determine whether absolute stimumary afferents appears to evoke greater excitation of raphe circuitry, while WDR and NS neurons driven by mechano-lus-specific organization exists, it is likely that regions of sponsive input elicit somewhat greater activation of thethe PAG respond to somatotopic innervation of the periphNRGC/NRpG. Both circuits are apparently engaged byery and would thus be maximally excited by input from chemosponsive or polymodal C-fi ber afferent activation of a particular modality or intensity. WDR or NS neurons. It has been suggested that such stim- Although the function of the PAG in centrifugal pain ulus specificity is maintained at the midbrain level, and may control is clear, the role of the PAG in afferent processing be involved in the differential activation of PAG-raphe or of the nociceptive signal remains more enigmatic. Pathways exist between the PAG and hypothalamus and sevPAG-NRGC centrifugal analgesic systems. The former system involves a release of opioids from the PAG that disin-eral structures of the forebrain. Stimulation of the PAG or fibers within this pathway elicit an array of arousal and hibits serotonergic cells of the raphe nuclei, thereby causing behavioral activation responses that have distinct aversive an increased turnover and release of serotonin in pathways or frightening emotional content. It is not completely that descend in the dorsal lateral funiculi. These serotonergic understood whether the PAG mediates these responses fibers synapse heterogeneously in laminae I, II, and V, where

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alone, or acts in concert with reticular structures, higherin S-I (and to a lesser extent S-II areas) of the somatosensory cortex. Thalamo-corticalbers fi from the intralaminar brain structures of the limbic system, or both. nuclei, driven by the PSTT, project more diffusely, with only a small number terminating in S-I or S-II. The somaTHE THALAMUS totopic organization of the thalamus is preserved in corThe NSTT and PSTT project to different nuclei within the tical projections, and nociceptive input contributes to distinct regions of somatosensory dominance within the thalamus. NSTT neurons project to a caudal area of the homunculus, “ ” the spaventroposterior lateral nucleus (VPLc). Nociceptive inputscortex (i.e., the so-called sensory tial representation of bodily structures across the cortical from the NSTT are arranged in columnar zones that are somatotopically organized. Thalamic neurons within thesesensory field). Somatosensory cortical regions are arranged in vertical dominance columns in which hierarzones retain many response characteristics of WDR and NS chical processing of afferent input occurs. Only a small units. Thalamic wide-range neurons have center-surround receptivefields with distinct, small areas sensitive to low- percentage of nociceptive input constitutes each given cortical column. Nociceptive thalamo-cortical input is threshold excitation and a broad area that is excited by highficial threshold nociceptive input. Thalamic NS neurons, like theirdistributed differentially within each column. Super cortical layers receive thalamic input from non-nocicepspinothalamic counterparts, have smaller receptive eldsfithat are excited by high-intensity mechanical or thermal input. tive pathways, while WDR- and NS-activated inputs are WDR and NS neurons of the VPLc summate concentrated throughout the deeper cortical layers. Thus, for any given bodily region represented in a cortical colresponses as a function of stimulus frequency and intenumn there is an array of non-noxious information (relayed sity. Slow temporal and spatial summation is accompanied through medial lemniscal tracts) and nociceptive inforby a prolonged firing phase that exceeds the actual noxious mation (relayed through the STTs) that creates the stimulus and primary and secondary afferent discharges. This transformation parallels the time-course for the“ depiction” of sensations that determines the subjective sensory experience. The integrity of the pain signal, and human experience of pain. It is probable that the temporal aspects of painperception reflect serial processing of the unique qualities of its duration and intensity are a afferent information from the peripheral to the thalamicfunction of the additive transformation of afferent volleys levels, with progressive extension of after-dischargesfrom primary nociceptors through multiple processing ultimately terminating in cortical neurons. The slow adapalong the pathway. It is tempting to speculate that such tation, long after-discharges, and spatial summation of effects may “match” sensory, arousal, and environmental cortical S-I and S-II neurons represent the nalfiand most cues in establishing conditioned responses to circumdirect contribution to the temporal and intensity dimenstances surrounding painful stimuli. sions of pain perception. Therefore, the experience of The PSTT projects to several intralaminar thalamic pain is not only individually variant, but may vary accordnuclei, including the nucleus centralis lateralis and mediing to myriad combinations of exteroceptive circumalis dorsalis. Most of the neurons within these thalamic stances for each individual. areas are of the wide-range type, sensitive to both nociThe multiple intra-cortical projections from S-I/S-II ceptive and non-nociceptive activation and with extensive to other parietal, frontal, and temporal regions most proboverlapping input from cutaneous and visceral innervaably engage these brain areas in discriminatory, cognitive, tion. These units do not have the adaptive properties of and affective dimensions of pain. neurons of the VPLc; intralaminar neurons summate responses, but response patterns do not reflect direct spatial or temporal transformation of increments in stimulusPAIN MODULATING SYSTEMS frequency or intensity. Unlike neurons of the VPLc, CORTICAL INHIBITORY PROCESSING intralaminar neurons appear to be arranged inlooser” a “ somatotopic pattern and project diffusely to several regions Neurons of the sensory cortex are capable of inhibitory of the cortex. The response patterns of individual intralam-control over the thalamo-cortical units of STT origin that inar neurons, together with their anatomic distribution andproject to them (although cortico-thalamic inhibition can cortical projections, suggest that thalamic connections of the also occur over neurons of the medial lemniscal tract that PSTT act more as a relay to engage cortical systems involved are non-nocisponsive). The extent of inhibition appears to in behavioral activation associated with nociception. vary with the frequency and intensity of thalamo-cortical input. For nociceptive input that is both rapidly temporally and spatially summating, a greater level of inhibition CORTICAL PROJECTIONS exists. Cortical inhibition involves normalization” “ or Neurons from the NSTT project to the VPLc of the thal-“stabilization” of afferent volleys. This compensates for amus; thalamo-cortical bers fi from this region terminate differences in response characteristics between thalamic

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and cortical neurons and ultimately enhances the inputgroup of the pons, consisting of the nucleus reticularis response function of thalamically driven nociceptive cor-gigantocellularis (NRGC), nucleus reticularis paragigantical inputs. In this way, a more direct transformation oftocellularis (NRpG), and the nucleus paragigantocellularis the incoming signal is generated without over-summation.lateralis (NpGL). These sites are often referred to as the Cortical neurons also can excite thalamo-cortical fibersreticular magnocellular nuclei (RMC). In the rostro-venand STT units directly. This inhibition and excitation servetral medulla. PAG-originating interneurons synapse on a modulatory role over afferent information that affectsneurons of the raphe nuclei, including the nuclei raphe cortical circuitry. Cortical neurons can discriminately alatus and raphe lateralis. These sites are combined when amplify or reduce the extent of nociceptive input. Suchreferring to the nucleus raphe magnus (NRM). The NRM modifications strengthen the signal-to-noise ratio of par-and RMC directly receive efferent input from the PAG ticular afferent volleys and facilitate discrimination of sen- and afferent input from the PSTT. Both neuraxes are capasory input. As well, this alternate excitation/inhibition may ble, either alone or in concert, of exciting NRM or RMC neurons to elicit centrifugal pain modulation. Inhibitory subserve changes in the nociceptive sensorium as a consequence of levels of cortical activity (e.g., sleep, hypno-connections between these groups of brainstem nuclei exist as well. This inter-brainstem inhibition appears to sis, biofeedback, etc.). determine the relative participation of NRM, RMC, or both groups in bulbospinal analgesia; moderate levels of MIDBRAIN PAIN MODULATION activity within the RMC inhibit the NRM. In contrast, higher levels of RMC activity excite certain NRM neurons. There is considerable evidence to show that the midbrain Projections from the NRM and RMC descend in the dorsoPAG is a principal site for endogenous pain control. Efferlateral funiculi (DLF) of the spinal cord and terminate in ent projections from mesolimbic structures and the hypodense synapticelds fi within laminae I, II, and V of the dorsal thalamus are capable of exciting PAG opioid neurons, as horn. Synaptic connections within these layers involve do inputs from the PSTT. The PAG exerts pain modulation polysynaptic circuits of multiple spinal interneurons, as well by centrifugal inhibition of the PSTT and NSTT via disas monosynaptic contacts with wide dynamic range, nociinhibition of bulbospinal projections from the raphe nuclei ceptive-specifi c and primary afferent neurons. and NRGC/NRpG. Defined pathways from the PAG to the Spinal interneurons receiving efferent projections raphe nuclei and NRGC/NRpG are activated by high-from the brainstem synapse on WDR and NS second-order threshold, high-frequency afferent volleys from the PSTT.neurons as well as the terminals of primary afferent fibers. Mechanical, thermal, or polymodal nocisponsive units ofThese interneurons are neurochemically heterogeneous, the PSTT appear to differentially stimulate discrete areas many release the inhibitory transmitter glycine, while othof the PAG to activate the raphe nuclei, NRGC/NRpG, orers release the opioids enkephalin and/or dynorphin. These both. It is not fully understood whether selective PAGinterneuronal contacts provide selective, multi-focal inhiengagement of raphe-spinal or NRGC/NRpG-spinalbition of specific groups of nociceptive afferents. neuraxes is dependent upon the modality, frequency, or Synaptic connections between bulbospinal and intensity of the evoking afferent input. WDR, NS, and perhaps primary afferent neurons exist The connections between the PAG and brainstem are in laminae I, II, and V. A single ber fi from the brainstem polysynaptic, involving one or more pools of interneu- may synapse on several second-order afferents within a ronal relays. These multiple circuits function in levels of given lamina. The differential projection of NRM or modulation that have the capacity for both serial and conRMC terminals onto discrete populations of mechanocomitant activation. This type of “volume control” is a sponsive, thermosponsive, or polymodally driven WDR function of the nature of the afferent nociceptive stimulus,and NS neurons in laminae I, II, and V further suggests the extent of PAG activation by PSTT (and perhaps hypo-that some stimulus- or modality-specifi city may exist in thalamic and mesolimbic) neurons, and the excitation orthe analgesic axis that originates from these brainstem inhibition of specific neural circuits to the brainstem. nuclei. Figure 89.2 provides a schematic representation Thus, the PAG can discriminately recruit bulbospinal sub-of this possible organization. strates whose net output determines the extent and properties of centrifugal pain modulation.

INTRASPINAL PAIN MODULATION

In addition to descending analgesic systems from the brainstem, pain modulation can occur through the actiProjections from the PAG synapse upon interneurons with vation of local circuits within the spinal dorsal horn. terminations in the ventromedial pons and rostro-ventralInterneurons that receive collateral projections from primary A-delta and C-fi bers are found in laminae I, II, medulla of the brainstem. These are the subcerulear nuclear

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sively studied. Dynorphin binds post-synaptically with κ-opioid receptors. There is some heterogeneity in κ-receptor populations; however, most found in the spinal cord are negatively coupled to N-type calcium ionic channels. Dynorphin binding at these κ-sites on primary or second-order afferents closes the calcium channel thereby producing a hyperpolarizing inhibitory current, essentially“ tuning down” or “shutting off” the transmission of nociceptive information along this neuraxis. This local circuit inhibition modulatesring fi of primary A-delta and C-fibers afferents; a particular pattern of primary afferent firing may excite populations of local interneurons to exert recurrent inhibition. Similarly, primary afferent activity may evoke local spinal inhibition of certain populations of WDR and NS neurons. Low-threshold mechanosponsive dorsal column afferents, driven by a Aβ mechanoreceptors, also exert modulatory influence over WDR and NS neurons that comprise the STT. Interneurons in laminae IIa, III, and IV with synapticfields linking the dorsal columns and STT evoke brief inhibitory post-synaptic potentials (IPSPs) in STT cells following dorsal column excitation by low-intensity mechanical stimuli. These IPSPs persist after termination FIGURE 89.2 Schematic depiction of putative analgesic of the low intensity stimulus, and cause a brief, rightward neuraxes modulating thermal and mechanical noxious input.shift in both the time- and threshold-based stimulus Thermosponsive A-delta and C-fi ber afferents may engage a response function of the affected WDR and NS cells descending serotonergic circuit (either directly or via activa-within the STT. In other words, low-level mechanical tion of opioid neurons in the PAG/PVG that inhibit interneu- stimulation of the dorsal column tract is capable of overrons to disinhibit raphe-spinal mechanisms). 5-HT releasedriding or de-sensitizing WDR and NS activity within the from raphe-spinal neurons may (a) directly inhibit pain-transSTT. This phenomenon subserves the clinical ficacy ef of mitting afferents; (b) act at (excitatory) 5-HT 3 receptors on low-frequency transcutaneous electrical nerve stimulation spinal opioid, GABA, and glycine interneurons to evoke release of the transmitters and modulate activity of primary(TENS), and helps to explain the somewhat beneficial effect of rubbing a painful area. or secondary nociceptive afferents. Mechanosponsive A-delta and C-fibers appear to engage a descending noradrenergic neuraxis (from the magnocellular reticular formation) either SUMMARY directly or indirectly via PAG/PVG activation. Norepinephrine released from reticulo-spinal neurons acts α2at receptors The anatomical and physiologic systems that subserve to modulate activity of primary and second-order nociceptivepain and analgesia are complex. Heterogeneous populaafferents. DLF = dorso-lateral funiculus; Dyn = dynorphin; tions of neurons from the periphery, through the spinal Enk = leu/met-enkephalin; GABA =γ-amino butyric acid; cord, brainstem, thalamus, and ultimately the cortex with gly = glycine; (+) = excitatory synapse(s); ) (– = inhibitory discrete neurochemical and physiological properties, all synapse(s).

contribute to the amalgam of sensations that compromise the constellation of features known as pain. By underand V. These interneurons form reciprocal synapses standing the structure and function of this system, we may upon primary afferent(s) and, in certain cases, secondorder WDR and NS neurons. The majority of such inter-develop enhanced therapeutic approaches to acute and neuronal connections are found within a given horizon-chronic pain that target these substrates more effectively tal section of the spinal cord, although some interneu-and selectively, thereby reducing deleterious side effects rons have terminal elds fi that are trans-segmental. while facilitating an enhanced quality of life. Pharmacologic and electrophysiologic evidence has demonstrated that these interneurons are inhibitory.ACKNOWLEDGMENTS Many produce and release the inhibitory transmitter glycine, as well as the opioid peptide dynorphin. TheThe author wishes to acknowledge the untiring assistance of Connie Parker in the preparation of this manuscript. pharmacology of this latter compound has been exten-

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TABLE 89.1 Physiologic and Pharmacologic Properties of Primary Afferent Nociceptors Type

Stimulus

Anatomy

Diameter

Conduction/Properties

A-delta

High threshold Mechanical Thermal (>45°C) (