Somatic Presentations of Mental Disorders: Refining the Research Agenda for DSM-V

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SOMATIC PRESENTATIONS OF MENTAL DISORDERS Refining the Research Agenda for DSM-V

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SOMATIC PRESENTATIONS OF MENTAL DISORDERS Refining the Research Agenda for DSM-V Edited by

Joel E. Dimsdale, M.D. Yu Xin, M.D. Arthur Kleinman, M.D. Vikram Patel, Ph.D. William E. Narrow, M.D., M.P.H. Paul J. Sirovatka, M.S. Darrel A. Regier, M.D., M.P.H.

Published by the American Psychiatric Association Arlington, Virginia

Note: The authors have worked to ensure that all information in this book is accurate at the time of publication and consistent with general psychiatric and medical standards, and that information concerning drug dosages, schedules, and routes of administration is accurate at the time of publication and consistent with standards set by the U.S. Food and Drug Administration and the general medical community. As medical research and practice continue to advance, however, therapeutic standards may change. Moreover, specific situations may require a specific therapeutic response not included in this book. For these reasons and because human and mechanical errors sometimes occur, we recommend that readers follow the advice of physicians directly involved in their care or the care of a member of their family. The findings, opinions, and conclusions of this report do not necessarily represent the views of the officers, trustees, or all members of the American Psychiatric Association. The views expressed are those of the authors of the individual chapters. Copyright © 2009 American Psychiatric Association ALL RIGHTS RESERVED Manufactured with 100% wind energy in the United States of America on acid-free paper. 13 12 11 10 09 5 4 3 2 1 First Edition Typeset in Adobe’s Frutiger and AGaramond. American Psychiatric Association 1000 Wilson Boulevard Arlington, VA 22209-3901 www.psych.org Library of Congress Cataloging-in-Publication Data Somatic presentations of mental disorders : refining the research agenda for DSM-V / edited by Joel E. Dimsdale ... [et al.]. — 1st ed. p. ; cm. Presents a selection of articles reprinted from Psychosomatic medicine, v. 69, 2007. Includes bibliographical references and index. ISBN 978-0-89042-342-4 (alk. paper) 1. Somatoform disorders. I. Dimsdale, Joel E., 1947- II. American Psychiatric Association. III. Psychosomatic medicine. [DNLM: 1. Psychophysiologic Disorders–diagnosis–Collected Works. 2. Psychophysiologic Disorders–diagnosis–Congresses. 3. Somatoform Disorders–diagnosis–Collected Works. 4. Somatoform Disorders–diagnosis–Congresses. 5. Psychophysiologic Disorders–psychology–Collected Works. 6. Psychophysiologic Disorders–psychology–Congresses. 7. Psychosomatic Medicine-methods–Collected Works. 8. Psychosomatic Medicine–methods– Congresses. 9. Somatoform Disorders–psychology–Collected Works. 10. Somatoform Disorders–psychology–Congresses. WM 170 S6925 2009] RC552.S66S657 2009 616.85′24—dc22 2008048530 British Library Cataloguing in Publication Data A CIP record is available from the British Library.

CONTENTS CONTRIBUTORS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vii DISCLOSURE STATEMENT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xi FOREWORD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiii Darrel A. Regier, M.D., M.P.H. EVOLUTION OF PSYCHOSOMATIC DIAGNOSIS IN DSM . . . . . . . . . . . xix Donald Oken, M.D. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xxv Joel E. Dimsdale, M.D. Vikram Patel, M.B. Yu Xin, M.D. Arthur Kleinman, M.D.

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EPIDEMIOLOGY OF THE ASSOCIATION BETWEEN SOMATOFORM DISORDERS AND ANXIETY AND DEPRESSIVE DISORDERS . . . . . . . . . . 1 Roselind Lieb, Ph.D. Gunther Meinlschmidt, Ph.D. Ricardo Araya, Ph.D.

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THE ASSOCIATION OR OTHERWISE OF THE FUNCTIONAL SOMATIC SYNDROMES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Richard A.A. Kanaan, MRCPsych Jean Pierre Lepine, M.D. Simon C. Wessely, FRCPsych

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CULTURAL MODELS AND SOMATIC SYNDROMES. . . . . . . . . . . . . . . 19 Laurence J. Kirmayer, M.D. Norman Sartorius, M.D., Ph.D.

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INFLUENCE OF CULTURAL AND SOCIAL FACTORS ON THE EPIDEMIOLOGY OF IDIOPATHIC SOMATIC COMPLAINTS AND SYNDROMES. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Javier I. Escobar, M.D., M.S. Oye Gureje, Ph.D., D.Sc., FRCPsych

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ARE SOMATOFORM DISORDERS CHANGING WITH TIME? . . . . . . . . 53 Sing Lee, FRCPsych Arthur Kleinman, M.D.

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A BIOLOGICAL SUBSTRATE FOR SOMATOFORM DISORDERS . . . . . . 63 Joel E. Dimsdale, M.D. Robert Dantzer, D.V.M., Ph.D.

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SOMATOFORM AND SUBSTANCE USE DISORDERS . . . . . . . . . . . . . 75 Deborah Hasin, Ph.D. Hila Katz, B.A.

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STABILITY OF SOMATOFORM SYMPTOMS . . . . . . . . . . . . . . . . . . . . 89 Winfried Rief, Ph.D. Graciela Rojas, M.D.

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WHAT IS THE EVIDENCE FOR THE EFFICACY OF TREATMENTS FOR SOMATOFORM DISORDERS? . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 Athula Sumathipala, M.B.B.S., D.F.M., M.D., MRCPsych, Ph.D.

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ARE TREATMENTS FOR COMMON MENTAL DISORDERS ALSO EFFECTIVE FOR FUNCTIONAL SYMPTOMS AND DISORDER? . . . . . 131 Richard Mayou, B.M., FRCPsych, FRCP

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EFFICACY OF TREATMENT FOR SOMATOFORM DISORDERS. . . . . . 143 Kurt Kroenke, M.D.

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THE EVIDENCE FOR TREATMENTS FOR SOMATOFORM DISORDERS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165 Susan Levenstein, M.D. INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171

CONTRIBUTORS Ricardo Araya, Ph.D. Professor of Psychiatry, Academic Unit of Psychiatry, University of Bristol, United Kingdom Robert Dantzer, D.V.M., Ph.D. Professor of Psychoneuroimmunology, Department of Pathology (R.D.), University of Illinois College of Medicine, Urbana-Champaign, Illinois Joel E. Dimsdale, M.D. Distinguished Professor of Psychiatry, Department of Psychiatry, University of California, San Diego Javier I. Escobar, M.D., M.S. Associate Dean for Global Health and Professor of Psychiatry and Family Medicine, Department of Psychiatry, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey Oye Gureje, Ph.D., D.Sc., FRCPsych Professor and Head, Department of Psychiatry, University of Ibadan, University College Hospital, Ibadan, Nigeria Deborah Hasin, Ph.D. Professor of Clinical Public Health, Department of Psychiatry, College of Physicians and Surgeons and Department of Epidemiology, Mailman School of Public Health, Columbia University; Research Scientist, New York State Psychiatric Institute, New York, New York Richard A. A. Kanaan, MRCPsych Clinical Lecturer, King’s College London, Department of Psychological Medicine, Institute of Psychiatry, London, United Kingdom Hila Katz, B.A. Assistant Research Scientist, New York State Psychiatric Institute, New York, New York

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Laurence J. Kirmayer, M.D. James McGill Professor and Director, Division of Social and Transcultural Psychiatry, McGill University; Director, Culture and Mental Health Research Unit, Institute of Community and Family Psychiatry, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada Arthur Kleinman, M.D. Victor and William Fung Director of Harvard University Asia Center; Esther and Sidney Rabb Professor of Anthropology, Department of Anthropology in the Faculty of Arts and Sciences at Harvard University; Professor of Medical Anthropology and Professor of Psychiatry, Department of Global Health and Social Medicine, Harvard Medical School, Cambridge, Massachusetts Kurt Kroenke, M.D. Professor of Medicine, Division of General Internal Medicine and Geriatrics, Indiana University School of Medicine and Senior Scientist, Regenstrief Institute, Indianapolis, Indiana Sing Lee, FRCPsych Professor, Department of Psychiatry, The Chinese University of Hong Kong, Shatin, HKSAR Jean Pierre Lepine, M.D. Professor of Adult Psychiatry, Université Paris Descartes, Faculté de Pharmacie, Neuropsychopharmacologie des Addictions, CNRS, et Université Paris, France; INSERM, Paris, France; Assistance Publique-Hôpitaux de Paris, Hôpital Fernand Widal, Service de Psychiatrie, Paris, France Susan Levenstein, M.D. Aventino Medical Group, Rome, Italy Roselind Lieb, Ph.D. Professor, Department Epidemiology and Health Psychology, Institute of Psychology, University of Basel, Basel, Switzerland Richard Mayou, B.M., FRCPsych, FRCP Emeritus Professor of Psychiatry, Department of Psychiatry, Oxford University, Oxford, United Kingdom Gunther Meinlschmidt, Ph.D. Assistant Professor, Clinical Psychology and Psychotherapy, Institute of Psychology, University of Basel, Basel, Switzerland

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Donald Oken, M.D. Clinical Professor of Psychiatry, Department of Psychiatry, Pennsylvania Hospital, Philadelphia, Pennsylvania; Editor Emeritus of Psychosomatic Medicine Vikram Patel, M.B. Professor of International Mental Health and WellcomeTrust Senior Clinical Research Fellow in Tropical Medicine, London School of Hygiene and Tropical Medicine, London, United Kingdom Darrel A. Regier, M.D., M.P.H. Executive Director, American Psychiatric Institute for Research and Education, American Psychiatric Association, Arlington, Virginia Winfried Rief, Ph.D. Professor of Clinical Psychology, Department of Clinical Psychology and Psychotherapy, Philipps University of Marburg, Marburg, Germany Graciela Rojas, M.D. Directora, Departamento de Psiquiatría y Salud Mental, Clínica Psiquátrica Universitaria, Facultad de Medicina, Universidad de Chile, Santiago, Chile Norman Sartorius, M.D., Ph.D. Professor of Psychiatry, Culture and Mental Health Research Unit, Institute of Community and Family Psychiatry, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada; President of Association for the Improvement of Mental Health Care Programmes, Geneva, Switzerland Athula Sumathipala, M.B.B.S., D.F.M., M.D., MRCPsych, Ph.D Senior Lecturer, Kings College, University of London, International Mental Health, Department of Health Service Research, Institute of Psychiatry, United Kingdom; Honorary Director , Institute for Research and Development, Colombo, Sri Lanka Simon C. Wessely, FRCPsych Professor of Epidemiological and Liaison Psychiatry, King’s College London, Department of Psychological Medicine, Institute of Psychiatry, London, United Kingdom Yu Xin, M.D. Professor of Psychiatry, Peking University Institute of Mental Health, Beijing, China

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DISCLOSURE STATEMENT The research conference series that produced this monograph was supported with funding from the U.S. National Institutes of Health (NIH) Grant U13 MH067855 (Principal Investigator: Darrel A. Regier, M.D., M.P.H.). The National Institute of Mental Health (NIMH), the National Institute on Drug Abuse (NIDA), and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) jointly supported this cooperative research planning conference project. The conference series was not part of the official revision process for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V), but rather was a separate, rigorous research planning initiative meant to inform revisions of psychiatric diagnostic classification systems. No private-industry sources provided funding for this research review. Coordination and oversight of the overall research review, publicly titled “The Future of Psychiatric Diagnosis: Refining the Research Agenda,” were provided by an Executive Steering Committee composed of representatives of the several entities that cooperatively sponsored the NIH-funded project. Members of the Executive Steering Committee included: • American Psychiatric Institute for Research and Education—Darrel A. Regier, M.D., M.P.H. (P.I.), Michael B. First, M.D. (co-P.I.; consultant) • World Health Organization—Benedetto Saraceno, M.D., and Norman Sartorius, M.D., Ph.D. (consultant) • National Institutes of Health—Bruce Cuthbert, Ph.D., Wayne S. Fenton, M.D. (NIMH; consultant), Michael Kozak, Ph.D. (NIMH), Bridget F. Grant, Ph.D. (NIAAA), and Wilson M. Compton, M.D. (NIDA) • NIMH grant project officers were Lisa Colpe, Ph.D., Karen H. Bourdon, M.A., and Mercedes Rubio, Ph.D. • APIRE staff were William E. Narrow, M.D., M.P.H. (co-P.I.), Emily A. Kuhl, Ph.D., Maritza Rubio-Stipec, Sc.D. (consultant), Paul J. Sirovatka, M.S., Jennifer Shupinka, Erin Dalder-Alpher, Kristin Edwards, Leah Engel, Seung-Hee Hong, and Rocio Salvador

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The following contributors to this book have indicated financial interests in or other affiliations with a commercial supporter, a manufacturer of a commercial product, a provider of a commercial service, a nongovernmental organization, and/ or a government agency, as listed below: Robert Dantzer, D.V.M., Ph.D.—The author has received grant support from NIH. The author is a consultant for Astra-Zeneca, USA, and Danone Research, France. Joel E. Dimsdale, M.D.—The author is a consultant to Sepracor Pharmaceuticals. The author has received research support from Sepracor Pharmaceuticals and NIH. Javier I. Escobar, M.D., M.S.—The author has received grant support from NIMH. Deborah Hasin, Ph.D.—The author has received grant support from NIAAA and NIDA. Richard A.A. Kanaan, MRCPsych—The author has received support from the Biomedical Ethics Fellowship from the Wellcome Trust. Hila Katz, B.A.—The author has received grant support from NIAAA and NIDA. Laurence J. Kirmayer, M.D.—The author has received grant support from the Canadian Institutes of Health Research. Kurt Kroenke, M.D.—The author has been a consultant for Eli Lily, Pfizer, and Forest. The author has received grant funding from Pfizer. Donald Oken, M.D.—The author is Editor Emeritus of Psychosomatic Medicine. Darrel A. Regier, M.D., M.P.H.—The author, as Executive Director of American Psychiatric Institute for Research and Education, oversees all federal and industry-sponsored research and research training grants in APIRE but receives no external salary funding or honoraria from any government or industry. Winfried Rief, Ph.D.—The author has received support from the German Ministry of Research Education. The following contributors to this book do not have any conflicts of interest to disclose: Ricardo Araya, Ph.D. Oye Gureje, Ph.D., D.Sc., FRCPsych Arthur Kleinman, M.D. Sing Lee, FRCPsych Jean Pierre Lepine, M.D. Susan Levenstein, M.D. Roselind Lieb, Ph.D. Richard Mayou, B.M., FRCPsych, FRCP Gunther Meinlschmidt, Ph.D. Vikram Patel, M.B. Graciela Rojas, M.D. Norman Sartorius, M.D., Ph.D. Athula Sumathipala, M.B.B.S., D.F.M., M.D., MRCPsych, Ph.D. Simon C. Wessely, FRCPsych Yu Xin, M.D.

FOREWORD Darrel A. Regier, M.D., M.P.H.

Somatic Presentations of Mental Disorders: Refining the Research Agenda for DSM-V presents a selection of papers reporting the proceedings of a conference focused on somatic presentations of mental disorders. The conference was one in a series titled “The Future of Psychiatric Diagnosis: Refining the Research Agenda.” It was convened by the American Psychiatric Association (APA) in collaboration with the World Health Organization (WHO) and the U.S. National Institutes of Health (NIH), with funding provided by the NIH, and hosted by the Department of Psychiatry of Peking University, in Beijing, China.

Research Planning for DSM/ICD The APA/WHO/NIH conference series represents a key element in a multiphase research review process designed to set the stage for the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). In its entirety, the project entails eleven workgroups, each focused on a specific diagnostic topic or category, and two additional workgroups dedicated to methodological considerations in nosology and classification. Within the APA, the American Psychiatric Institute for Research and Education (APIRE), under the direction of the author (D. A. R.), holds lead responsibility for organizing and administering the diagnosis research planning conferences. Members of the Executive Steering Committee for the series include representatives of the WHO’s Division of Mental Health and Prevention of Substance Abuse and of three NIH institutes that are jointly funding the project: the National In-

This section is adapted from an editorial originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Regier DA: “Somatic Presentations of Mental Disorders: Refining the Research Agenda for DSM-V.” Psychosomatic Medicine 69:827–828 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Used with permission.

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stitute of Mental Health (NIMH), the National Institute on Drug Abuse (NIDA), and the National Institute on Alcohol Abuse and Alcoholism (NIAAA). APA published the fourth edition of DSM in 1994 1 and a text revision in 2000.2 Although DSM-V is not scheduled to appear until 2012, planning for the fifth revision began in 1999 with collaboration between APA and the NIMH designed to stimulate research that would address identified opportunities in psychiatric nosology. A first product of this joint venture was preparation of six white papers that proposed broad-brush recommendations for research in key areas. Topics included developmental issues, gaps in the current classification, disability and impairment, neuroscience, nomenclature, and cross-cultural issues. Each team that developed a paper included at least one liaison member from NIMH, with the intent—largely realized—that these members would integrate many of the workgroups’ recommendations into NIMH research support programs. These white papers were published in A Research Agenda for DSM-V.3 This volume more recently has been followed by a second compilation of white papers that outline diagnosis-related research needs in the areas of gender, infants and children, and geriatric populations.4 As a second phase of planning, the APA leadership envisioned a series of international research planning conferences that would address specific diagnostic topics in greater depth, with conference proceedings serving as resource documents for groups involved in the official DSM-V revision process. We, in collaboration with colleagues at WHO, developed a proposal for the cooperative research planning conference grant that NIMH awarded to APIRE in 2003, with substantial additional funding support from NIDA and NIAAA. The conferences funded under the grant are the basis for a monograph series and represent a second major phase in the scientific review and planning for DSM-V. The conferences that compose the core activity of this phase of preparation have multiple objectives. One objective is to promote international collaboration among members of the scientific community with the aim of eliminating the remaining disparities between DSM-V and the International Classification of Diseases (ICD)5 Mental and Behavioral Disorders section.6 The WHO launched the revision of ICD-10 that will lead to publication of the 11 th edition in approximately 2014. A second goal is to stimulate the empirical research necessary to allow informed decision-making regarding deficiencies identified in DSM-IV. A third objective is to facilitate the development of broadly agreed upon criteria that researchers worldwide may use in planning and conducting future research exploring the etiology and pathophysiology of mental disorders. Challenging as it is, this last objective reflects widespread agreement in the field that the wellestablished reliability and clinical utility of prior DSM classifications must be matched in the future by a renewed focus on the validity of diagnoses. APA attaches high priority to ensuring that information and research recommendations generated by each of the workgroups are readily available to investiga-

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tors who are concurrently updating other national and international classifications of mental and behavioral disorders. Moreover, given the vision of an ultimately unified international system for classifying mental disorders, members of the Executive Steering Committee have made strenuous efforts to realize the participation of investigators from all parts of the world in the project. Toward this end, each conference in the series had two co-chairs, drawn respectively from the United States and a country other than the United States. Approximately half of the experts invited to each working conference were from outside the United States, and half of the conferences were convened outside the United States.

Mind and Body, Health and Illness: Psychosomatic Disorders in DSM Recognition of the interaction of “psyche” and “soma” in health and illness dates to antiquity. Only within the past century and a half, however, have physicians developed and refined the vocabulary and concepts necessary to elucidate and, over time, systematically study the phenomena. Considerable early work in Europe and the United States reflected the strong influence of psychoanalytic thought7 that carried into the first edition of DSM. Donald Oken, a leading investigator in the field, emeritus editor of Psychosomatic Medicine (1982–1992), and former president of the American Psychosomatic Society, recently reviewed the evolution of DSM’s handling of psychosomatic disorders (Oken, unpublished manuscript). In the initial DSM, although the disorders were published under the rubric of “psychophysiological autonomic and visceral disorders,” the explanatory text described the conditions as “reactions [that] represent the visceral expression of affect which may be thereby largely prevented from being conscious.” This terminology was consistent, he noted, with “...the psychologism of the time: ‘with or without defined physical causes or structural change in the brain.’” He attributed this conceptualization to the influence on the DSM committee of Franz Alexander, then co-director of the Chicago Psychoanalytic Institute and a leading figure in the psychosomatic field. Of note, Dr. Oken said, was the prominent placement of this diagnostic category in the manual, at the center of the overall schema between psychotic and neurotic reactions. By the time DSM-II8 was published 16 years later, Dr. Oken recounts, doubts had begun to be voiced about the strong psychoanalytic tenor of the manual, accompanied by awareness of the value of controlled scientific research. Accordingly, the second edition retired the term “reactions” in favor of “disorders,” and deleted the “autonomic” and “visceral” modifiers, resulting in a new category called simply “psychophysiological disorders.” Growing interest in evidence-based diagnoses and empirical neurobiological research further emerged as driving forces in the development of DSM-III, which

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was published in 1980.9 Among the radically new features of this third revision were etiologic neutrality as evidenced by the listing of all conditions as “disorders”; the introduction of specific, defined criteria as the basis for diagnoses; the hierarchical organization of diagnostic categories; and, importantly, the use of a “multiaxial” format that promised great potential utility in describing nonlinear psychosomatic causal processes. The downside of the new formulation, in Dr. Oken’s view, was designation of the category as “psychological factors affecting physical condition,” implying a lesser, secondary, “modifier” status for psychological processes on health, and loss of any suggestion of the transactional nature of the relationship with the biological. In the subsequent, fourth revision of the manual,1 the category rubric was again changed, to “psychological factors affecting medical condition”—a further narrowing—and all of the conditions were listed as a subcategory of “other conditions that may be a focus of attention.” The sum effect of these and other changes in DSM-IV, Dr. Oken suggested, was to “further downgrade the role of psychological factors and, thus, to dilute the general concepts of psychosomatic processes.”

Toward DSM-V and ICD-11 The papers presented in this monograph make clear that “psychosomatic disorders”—a broad area billed in our APA/WHO/NIH conference as “somatic presentations of mental disorders”—remain a vital and important topic for psychiatry and all of medicine. Of particular import to this topic—and, hence, a primary justification for enlisting the assistance of our Chinese colleagues to convene this conference in Beijing—is the role and influence of cultural factors on the experience of mental disorders. The chance to interact with scientists from around the world in a setting far removed from the APA’s home base in the Washington, D.C., area was intellectually invigorating. We anticipate that the Beijing conference, and the research that it stimulates, will add rich material to Dr. Oken’s next review of the continuing evolution of this critical area of mental health care. We appreciate the enthusiastic interest of Joel E. Dimsdale, M.D. (co-chair of the Beijing conference), and David Sheps, M.D. (Editor-in-Chief of Psychosomatic Medicine), in ensuring the availability of these papers to a global readership. This volume will serve as a resource document for the DSM-V Task Force and disorderspecific workgroups. A summary report of the conference is available online at www.dsm5.org. The American Psychiatric Association greatly appreciates, as well, the contributions of all participants in the somatic manifestations research planning workgroup and the interest of our broader audience in this topic.

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References 1. 2.

3. 4.

5. 6.

7.

8. 9.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC: American Psychiatric Association; 1994. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed, Text Revision. Washington, DC: American Psychiatric Association; 2000. Kupfer DJ, First MB, Regier DA (eds). A Research Agenda for DSM-V. Washington, DC: American Psychiatric Association; 2002. Narrow WN, First MB, Sirovatka P, Regier DA (eds). Age and Gender Considerations in Psychiatric Diagnosis: A Research Agenda for DSM-V. Arlington, VA: American Psychiatric Association; 2007. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva: World Health Organization; 1992. World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: World Health Organization; 1992. Alexander FG, Selesnick ST. The History of Psychiatry: An Evaluation of Psychiatric Thought and Practice from Prehistoric Times to the Present. New York: Harper & Row, 1966; 388-401. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 2nd ed. Washington, DC: American Psychiatric Association; 1968. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: American Psychiatric Association; 1980.

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EVOLUTION OF PSYCHOSOMATIC DIAGNOSIS IN DSM Donald Oken, M.D.

Although recognition of the interaction of “psyche” and “soma” dates from antiquity, only in modern times have we developed the vocabulary and concepts to elucidate and then to systematically study its manifestations. With these developments came the notion of “psychosomatic disorders” (or “diseases”); however, the precise definition of these terms remained vague and holds true for all the “mental disorders.” Before the mid-20th century, psychiatric diagnoses were unstandardized, varying in part from hospital to hospital, although with fair agreement on the major categories, which were predominantly psychoses. “Hospital” is used deliberately, for it was in these primarily public mental hospitals that early psychiatry largely had existed. The first Diagnostic and Statistical Manual of Mental Disorders (DSM)1 was developed between 1946 and 1951, just after World War II. From that conflict had come a cadre of American medical officers who observed a host of nonpsychotic disorders arising in response to military service and combat. Many medical officers subsequently became psychiatrists, but not within state hospitals; instead they devoted themselves to treating nonpsychotic patients in ambulatory settings. Moreover, they came to understand the conditions they saw as largely psychological reactions to life experience requiring psychological treatment: psychotherapy. Most were influenced by psychoanalysis and a number became analysts, joining a group of European analysts who had fled to the United States.

This section is reprinted from an editorial originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Oken D: “Evolution of Psychosomatic Diagnosis in DSM.” Psychosomatic Medicine 69:830–831 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission.

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Those trends were abundantly reflected in DSM. With the exception of the organic brain disorders and mental “deficiency” (retardation), all mental disorders were denoted as “reactions.” Thus, the psychoses included affective and schizophrenic “reactions”; it was noted that these reactions could occur “with or without defined physical causes or structural change in the brain,” a statement consistent with the psychologism of the time. Immediately after the psychoses was the new rubric: “psycho-physiological autonomic and visceral disorders,” with an explanation that “This term is used in preference to ‘psychosomatic disorders’ since the latter refers to a point of view on the discipline of medicine as a whole rather than to certain specified conditions.” That is an important point to which we will return. The explanation went on to state that “these reactions represent the visceral expression of affect, which may be thereby largely prevented from being conscious. The symptoms are due to a chronic and exaggerated state of the normal physiological expression of emotion, with the feeling, or subjective part, repressed. Such long continued visceral states may eventually lead to structural changes.” This is not the place to dissect these interesting ideas. What is relevant is that this conceptualization is psychodynamic, psychoanalytic, and most specifically, the formulation of Franz Alexander.2 Alexander, Co-Director of the Chicago Psychoanalytic Institute and probably the most prominent figure in the psychosomatic field at that time, was for 3 years (1947–1950) a member of the committee that developed DSM; a combination of roles that makes full sense in the context of the history just elucidated. The psychophysiological disorders were subcategorized into “reactions” of various organ systems: musculoskeletal, cardiovascular, gastrointestinal, genitourinary, endocrine, etc. In each, examples of the conditions included ranged over a span from symptoms through demonstrable pathology such as backache, tension headache, asthma, constipation, colitis, hypertension, and dyspareunia. Of further note is the prominent locus of this category in the center of the overall schema between the psychotic and neurotic reactions. DSM-II was published 16 years later.3 By then, psychoanalysis had become established in American psychiatry, with an emphasis on clinical observation and the idiographic approach (idiographic: pertaining to or involving the study of cases or events as individual units, with a view to understanding each one separately). Analysts had assumed many chairs of medical school psychiatry departments. Even so, doubts had begun to increase, as had heightened awareness of the value of controlled scientific research in those academic departments. (An examination of the content of Psychosomatic Medicine and programs of the meetings of The American Psychosomatic Society during this period indicated that our field was at the cutting edge of this shift.) These doubts and increased emphasis on empirical research were reflected in the new DSM-II. Although its general features and categories were very similar to

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the original edition, the ubiquitous term “reactions” was dropped; conditions were now being referred to as neuroses, psychoses, or “disorders.” Psychosomatic conditions became “psychophysiological disorders,” with “autonomic and visceral” dropped, likely reflecting discomfort with being bound specifically to the concepts of Alexander. Subsequently, questions about psychoanalysis continued to increase, accompanied by advances in the basic and applied neurosciences relevant to mental disorders. American psychiatry became more scientific, with an emphasis on evidence-based diagnosis and treatment resting on data derived from appropriately designed research, and it became more neurobiological. Psychology was not entirely eschewed but was given less prominence, with psychoanalysis augmented or supplanted by behaviorism and cognitive science. Unfortunately, this new knowledge was applied within the tired old biomedical model rather than a “biopsycho-social”4 model. Even when psychological factors were deemed important, they were seen to operate in a concrete, linear way. All this was embodied in the vastly changed nature of DSM-III, which appeared 12 years later.5 Its major features included 1) the naming of conditions as “disorders,” a term chosen deliberately as etiologically neutral (although many subtle clues of biogenic bias were evident elsewhere); 2) the listing of sets of specific, defined criteria to be used as the basis for diagnosis; and 3) the organization of diagnostic categories in a hierarchy, with diagnoses of later categories often requiring the absence of earlier ones. Within the hierarchy of disorders, “psychophysiological disorders” was removed. Instead, there was a new category designated as “psychological factors affecting physical condition.” The nature of this category speaks for itself: Psychological processes can influence primarily physical, i.e., biological, conditions, but are modifiers operating in a lesser, secondary role. Nor is there any hint of their transactional relationship with the biological. This category was placed at the very end of the hierarchy, to many conveying its less important status. A new feature of DSM-III provided for diagnoses to be placed within a “multiaxial” format in which preexisting personality disorders or mental retardation, concomitant medical conditions, stressors, and functional capacity were included. With this incorporation of psychological, biological, and social factors into a dynamic framework, this system had the capacity to portray nonlinear psychosomatic causal adaptive processes.6 Unfortunately, perhaps because of its complexities, most psychiatrists paid lip service to the use of this novel, creative system. Fourteen years later, DSM-IV, with the same overall design as its predecessor, continued the same trends.7 Additional empirical data collected over the interval allowed for the refinement of diagnostic criteria, and a few disorders were added, dropped, relabeled, or reorganized, but the changes were minor. One subtle, but telling, shift was the dropping of the term “neurosis”—which implies psychogenesis—which had been left optional for a few disorders in DSM-III.

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Two changes were made in the disorders of our current interest. “Psychological factors affecting medical condition” was substituted for “…physical condition,” a further narrowing. More significant, this rubric no longer had the status of a category in itself but became one of a series of subsections within the category “other conditions that may be a focus of attention,” grouped with medication-induced problems, relationship problems, abuse, etc: a step further down—or out. The subcategory also was broken down into several types: mental disorders…, psychological symptoms…, personality disorders or traits…, and stress responses…affecting medical conditions; and maladaptive health behaviors. All are reasonable, useful distinctions, but the overall effect was to further downgrade the role of psychological factors and thus dilute the concept of psychosomatic processes. As we look ahead toward the next DSM, we need to confront a fundamental and important question: Should there be a category for “psychosomatic disorders” at all? Psychological and biological factors are involved in all aspects of human function, healthy and disordered. All diseases, and health, are psychosomatic; there are no “psychosomatic disorders” because there are no non-psychosomatic ones. To be practical, there are situations in which biological factors play a more major role or are more pressing or amenable to treatment and thus must be the focus of diagnostic attention (noting that the same is true for psychological factors). Traumatic injuries must be treated on a gurney, not a couch. Such issues assume genuine importance when we shift our focus away from abstractions about the nature of disease to the concrete actualities of sick persons. In this sense, there is justification for having a rubric: “psychological factors affecting physical condition”— although an equal case can be made for adding a corresponding category of “physical disorders affecting a psychological condition.” But neither of these—nor any single diagnostic label—can adequately reflect the complex nature of human disease as an adaptive psychosomatic process. It may be that a better solution to the problem will be a broadened application of a multiaxial system,6 which can allow us to portray more accurately the array of specific psychological and somatic (biological) processes operating transactionally in a patient, reflecting the true psychosomatic nature of human disease.

References 1. 2. 3. 4.

American Psychiatric Association. Diagnostic and Statistical Manual: Mental Disorders. Washington, DC: American Psychiatric Association; 1952. Alexander F. Psychosomatic Medicine. New York: Norton and Company; 1950. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 2nd ed. Washington, DC: American Psychiatric Association; 1968. Engel GL. The need for a new medical model: a challenge for biomedicine. Science 1997;196:129–136.

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American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: American Psychiatric Association; 1980. Oken D. Multiaxial diagnosis and the psychosomatic model of disease. Psychosom Med 2000;62:171–175. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.

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INTRODUCTION Joel E. Dimsdale, M.D. Vikram Patel, M.B. Yu Xin, M.D. Arthur Kleinman, M.D.

Somatic Presentations of Mental Disorders: Refining the Research Agenda for DSM-V presents a series of brief overviews concerning one of the most challenging areas of psychiatric diagnosis. Somatic presentations are arguably present in virtually every psychiatric diagnosis, but they are particularly evident in the highly disparate diagnoses of somatization disorder, somatoform disorder, conversion disorder, pain disorder, hypochondriasis, body dysmorphic disorder, and psychological factors affecting medical conditions. How distress is “embodied” is one of the central challenges of contemporary psychiatry. Our epidemiological knowledge base is limited, particularly in the developing world. Thus, cross-cultural insights, although fervently desired, are based on limited data. Even in Europe and the United States, contemporary epidemiological studies rarely sample somatic issues thoroughly, instead focusing, if at all, on the relatively rare occurrence of somatization disorder. Studies describing and comparing the phenomenology, natural history, and treatment response of the current categories of mental disorders with prominent somatic presentations are scarce. Similarly, there are few studies utilizing contemporary neural imaging tools and neural immune probes for understanding these complex illnesses that are so frequently associated with relatively nonspecific somatic symptoms. The conceptual “borders” between these somatic presentations and other psychiatric disorders, such as depressive disorders, are also ill defined.

This section is reprinted from an editorial originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Dimsdale JE, Patel V, Xin Y, Kleinman A: “Somatic Presentations—A Challenge for DSM-V.” Psychosomatic Medicine 69:829 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission.

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This set of papers, written by international experts from different backgrounds, highlights some of the many challenges involved in diagnosing psychosomatic phenomena in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-V). In general, the papers stem from a landmark meeting in Beijing in September 2006. Two of the papers provide context for this special section. The chapter by Regier describes the overall process by which the American Psychiatric Association, the National Institutes of Health, and the World Health Organization are working together to craft the next DSM that will also be more convergent with International Classification of Diseases.1 The paper by Oken summarizes how psychosomatic disorders have been dealt with in successive versions of DSM.2 The rest of the papers discuss culture,3–5 epidemiology,6,7 comorbidity,8,9 biology,10 and treatment11–13 of these puzzling disorders. Efforts to standardize psychiatric diagnosis are relatively recent phenomena. As such, accumulating knowledge from the diverse disciplinary perspectives, which characterize modern psychiatry, and from across the world will determine our understanding of the diagnostic boundaries of somatoform presentations. We can perhaps have tolerance for the shortcomings of our efforts to achieve diagnostic clarity if we recall how long it has taken to map the world geographically. We hope that this book will provide some navigational assistance to the ongoing work in developing an improved DSM.

References 1. Regier D. Somatic presentations of mental disorders: refining the research agenda for DSM-V. Psychosom Med 2007;69:827–828. 2. Oken D. Evolution of psychosomatic diagnosis in DSM. Psychosom Med 2007;69:830–831. 3. Kirmayer L, Sartorius N. Cultural models and somatic syndromes. Psychosom Med 2007;69:832–840. 4. Lee S, Kleinman A. Are somatoform disorders changing with time? The case of neurasthenia in China. Psychosom Med 2007;69:846–849. 5. Escobar J, Gureje O. Influence of cultural and social factors on the epidemiology of idiopathic somatic complaints and syndromes. Psychosom Med 2007;69:841–845. 6. Kanaan R, Lepine JP, Wessely S. The association or otherwise of the functional somatic symptoms. Psychosom Med 2007;69:855–859. 7. Rief W, Rojas G. Stability of somatoform symptoms—implications for classification. Psychosom Med 2007;69:864–869. 8. Lieb R, Meinlschmidt G, Araya R. Epidemiology of the association between somatoform disorders and anxiety and depressive disorders: an update. Psychosom Med 2007;69:860–863. 9. Hasin D, Katz H. Somatoform and substance use disorders. Psychosom Med 2007;69:870–875.

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10. Dimsdale J, Dantzer R. A biological substrate for somatoform disorders: importance of pathophysiology. Psychosom Med 2007;69:850–854. 11. Mayou R. Are treatments for common mental disorder also effective for functional symptoms and disorders? Psychosom Med 2007;69:876–880. 12. Kroenke K. Efficacy of treatment for somatoform disorders: a review of randomized controlled trials. Psychosom Med 2007;69:881–888. 13. Sumathipala A. What is the evidence for the efficacy of treatments for somatoform disorders? A critical review of previous intervention studies. Psychosom Med 2007;69:889–900.

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1 EPIDEMIOLOGY OF THE ASSOCIATION BETWEEN SOMATOFORM DISORDERS AND ANXIETY AND DEPRESSIVE DISORDERS An Update Roselind Lieb, Ph.D. Gunther Meinlschmidt, Ph.D. Ricardo Araya, Ph.D.

This chapter succinctly reviews the epidemiological evidence on the comorbidity between somatoform disorders and anxiety and depressive disorders. Much interest in the associations between somatoform and anxiety and depressive disorders has arisen from observations in clinical samples that a substantial proportion of pa-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Lieb R, Meinlschmidt G, Araya R: “Epidemiology of the Association Between Somatoform Disorders and Anxiety and Depressive Disorders: An Update.” Psychosomatic Medicine 69:860–863 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association.

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tients with the Diagnostic and Statistical Manual of Mental Disorders (DSM) somatoform disorders also meet the criteria for DSM anxiety and/or depressive disorders.1–6 Less is known, however, about patterns of comorbidity in the general population. Why is it important to study comorbidity in the general population? As Kessler pointed out, patient samples do not reflect the natural patterns of comorbidity seen in the general population.7 One of the main reasons to explain this finding is that comorbidity is closely associated with treatment-seeking behavior.8 General population samples are less affected by illness behavior and thus data arising from these studies are less biased on patterns of comorbidity.

What Can We Learn From Population-Based Research? Based on data from the Epidemiological Catchment Area Program (ECA) carried out in the 1980s in the United States,9 Swartz et al.10 found that ECA respondents with a lifetime diagnosis of DSM-III11 somatization disorder, assessed with the Diagnostic Interview Schedule (DIS), had a much higher probability for having a lifetime history of DSM-III panic disorder (about 25 times higher), obsessivecompulsive disorder (about 12 times higher), and major depression (about 11 times higher) compared with those without this disorder. Because only somatization disorder was assessed within the ECA, no comorbidity patterns could be ascertained for other forms of DSM-III somatoform disorders, e.g., pain disorder, conversion disorder, or hypochondriasis. Escobar12 suggested an empirically validated form of a subsyndromal diagnostic category, the Somatic Symptom Index (SSI)4,6, which included four somatoform symptoms for men and six for women. ECA respondents fulfilling the SSI4,6 criterion also reported higher lifetime rates of DSM-III major depression and dysthymia, compared with the general population. Lieb et al.13 studied comorbidity between somatoform disorders and anxiety and depressive disorders on the basis of a representative community sample of 3,021 adolescents and young adults ages 14–24 years (the Early Developmental Stages of Psychopathology study). 14,15 Using a standardized diagnostic interview (Munich version of the Composite Diagnostic Interviews5–10,12–18), no respondent met the DSM-IV19 criteria for full-blown somatization disorder, but there was an association between the subsyndromal SSI4,6 and anxiety and depressive disorders. In this sample of adolescents and young adults, individuals with a lifetime diagnosis of SSI4,6 were more likely to report a lifetime DSM-IV anxiety disorder (OR =3.6; 95% CI=2.0–6.4) as well as any lifetime DSM-IV depressive disorder (OR =3.7; 95% CI =2.0–6.7). Interestingly, obsessive-compulsive disorders (OR =7.7; 95% CI =1.9–30.2) and posttraumatic stress disorder (PTSD) (OR=18.9; 95% CI=8.3–42.9) also showed increased likelihood of comorbidity with SSI4,6. As can be deduced from the wide

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confidence intervals for the latter two disorders, the accuracy of these estimates is affected by the low prevalence. It is also important to bear in mind that these associations were based on lifetime diagnoses reached through retrospective inquiry, which may affect the validity of the findings. Up to now, few studies have examined the comorbidity between DSM-IV pain disorder and depressive and anxiety disorders in representative population samples. Based on the Mental Health Supplement of the German National Health Interview and Examination Survey, 20 which involves a community-based sample of more than 4,000 participants ages 18–64 years, Fröhlich et al.21 reported that 33% of the men and 37% of the women with a 12-month diagnosis of DSM-IV pain disorder met the criteria for at least one of the assessed DSM-IV anxiety disorders. There was a strong association between pain and anxiety disorders for all specific anxiety diagnoses and in both genders. Among males with a 12-month history of DSM-IV pain disorder compared with those without this diagnosis, the increased likelihood ranged from an odds ratio of 13.0 (95% CI =5.1–33.2) for DSM-IV general anxiety disorder (GAD) to an odds ratio of 5.5 (95% CI =3.2–8.7) for DSM-IV specific phobia. Among females, these increased probabilities ranged from an odds ratio of 4.9 (95% CI=2.5–9.4) for GAD to an odds ratio of 2.1 (95% CI=1.5–3.2) for specific phobias. Similar results were found for major depression (OR=4.3; 95% CI =2.4–7.6) and dysthymia (OR=9.8; 95% CI=5.4–17.5) among males and females (major depression: OR = 2.4; 95% CI = 1.6–3.4 and dysthymia: OR =3.9; 95% CI =2.5–6.0). These findings support the view that comorbidity between pain disorder and anxiety/depressive disorder seems to be the rule rather than the exception. Lieb et al.13 found slightly different results for younger age in the previously described community-based study. Among 14- to 24-year-old persons, a lifetime diagnosis of DSM-IV pain disorder was significantly associated with a lifetime diagnosis of DSM-IV panic disorder (OR =4.5; 95% CI=3.2–22.2) as well as a lifetime DSM-IV PTSD (OR =4.5; 95% CI=1.2–16.7). Among depressive disorders, DSM-IV major depression but not DSM-IV dysthymia were strongly associated with pain disorder (OR =4.3; 95% CI=2.3–8.1). It is worth noting that, other than using a younger sample, these findings relate to lifetime diagnoses, whereas Fröhlich et al. utilized 12-month diagnoses. We are not aware of any other published population-based study on the association of other forms of DSM-somatoform disorders (e.g., hypochondriasis, conversion disorder, and body dysmorphic disorder) with anxiety and depressive disorders. In most surveys, these disorders were not assessed, whereas in others the prevalence rates of the full-blown diagnoses were too low to assess comorbidity.22–25 The lack of evidence is therefore a major obstacle to properly address this question. Ascertaining somatization disorders can be complex, and this may have gone against the inclusion of these disorders in some large surveys undertaken throughout the world.

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Why Is It Important to Evaluate the Associations Between Somatoform Disorders and Anxiety and Depressive Disorders? The limited but consistent population-based knowledge on the associations between somatoform disorders and anxiety and depressive disorders reported so far has concerned the lifetime or 12-month comorbidity. We have shown, on the basis of a few cross-sectional population-based surveys in which DSM somatoform disorders were assessed using standardized diagnostic interviews, that individuals who met the diagnostic criteria for some somatoform disorders (subclinical form SSI4,6 and pain disorder) showed high comorbidity rates with depressive and anxiety disorders. What does this mean and why is it important to look into the associations between somatoform and anxiety and depressive disorders? The occurrence of more than one disorder in the same individual may have clinical implications because treatment strategies may be different in patients affected by a single disorder rather than several disorders. Not only the comorbidity between different mental disorders but also the comorbidity with medical conditions can have an impact on treatment.26 Besides this practical clinical implication, the investigation of patterns of comorbidity may also provide valuable insight to understand etiological factors and ultimately assist improving the way we classify mental disorders. Ehlert et al.,27 for example, showed that patients with functional gastrointestinal disorders (FGD) (i.e., irritable bowel syndrome or nonulcer dyspepsia) but no mood alterations presented lower cortisol levels, whereas those with comorbid depressive mood had higher cortisol levels, suggesting some psychobiological substrate that could also help to identify subgroups of FGD patients. A better understanding of the underlying neurobiological underpinnings of frequently co-occurring disorders may also help to determine whether these are independent entities or not.28 As suggested by Kessler29 and Faraone et al.,30 several possibilities may explain some observed patterns of comorbidity between somatoform disorders and anxiety and depressive disorders: 1. The association is spurious, resulting from methodological problems; e.g., reporting or recall bias may explain the observed comorbidity or the same physical symptoms may account for more than one diagnosis. 2. Somatoform disorders may lead to the onset of anxiety and depressive disorders. 3. Anxiety and/or depressive disorders may lead, in a causal way, to the onset of somatoform disorders. 4. There are common causes, e.g., genetic or environmental factors, that lead to the onset of all three types of disorders. There is no etiological connection, but all these symptoms belong to a common diagnostic construct.

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5. There may be more complex associations; e.g., somatoform disorders may not influence the onset of anxiety and depressive disorders, but may influence remission or treatment responses (or vice versa).

Temporal Patterns of Comorbidity Population-based longitudinal cohorts that allow evaluating the temporal relationships between somatoform disorders and anxiety and depressive are lacking. Thus, there is no empirical evidence to answer the question whether primary somatoform disorders predict subsequent anxiety/depressive disorders or vice versa. Lieb et al., using retrospectively collected data, assessed the temporal priority of the first onset of somatoform disorders and depressive and anxiety disorders.13 As for the comorbidity with depressive disorders, their results suggested that DSM-IV pain disorder and SSI4,6 were usually reported as being the temporally primary conditions. More than three quarters (78%) of the respondents with a concomitant lifetime depression and pain disorder reported that the pain disorder had an earlier onset than the depressive disorder. Among those respondents with lifetime SSI4,6 and depression, 62% reported that the somatoform condition occurred before the onset of the comorbid depressive disorder. For anxiety disorders, the pattern was indistinguishable. Almost half of all individuals with pain or SSI4,6 somatization disorder reported that anxiety preceded these disorders and the other half the opposite. Across all analyses, the simultaneous (in the same year) onset of somatoform, depressive, and anxiety disorders was rare. Fröhlich et al. found similar results when using retrospective age of onset information.21 For instance, DSM-IV pain disorder was reported as the primary condition in 75% of those cases with comorbid depressive disorder. According to Fröhlich et al.,21 the observed temporal pattern seems to be in line with findings from other epidemiological studies.31 Although this may be a rather crude and biased way of establishing a temporal relationship between these conditions, at least it suggests there may be some temporal relationship that would need to be tested using better methodological designs. Equally, we are aware that even if we were able to demonstrate the presence of a temporal relationship, this would not necessarily represent an etiological, causal relationship. In one of the few prospective longitudinal studies that included the assessment of somatoform disorders, Lieb et al. investigated whether primary DSM-IV anxiety or depressive disorders predicted incident DSM-IV somatoform conditions during the 4-year follow-up of a young adult cohort.32 The results showed that anxiety and depressive disorders predicted the first onset of secondary somatoform conditions. In this study, anxiety and depressive disorder could be shown to increase the risk for somatoform conditions in this young sample. These findings would argue for a different temporal direction than that mentioned earlier. According to these findings, primary anxiety and depressive disorders would seem to

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be associated with secondary somatoform disorders. It is important to bear in mind that these findings arose from a more robust methodological design to test temporal relationships but are limited in view of the young sample involved. These findings hereby summarized show that the empirical evidence accumulated is far too sparse and limited to reach any firm conclusions on the patterns of associations between somatoform disorders and anxiety and depressive disorders. Existing results are inconsistent, suggesting temporal relationships in both directions, e.g., from primary somatoform conditions to secondary mood disorders and vice versa. More population-based longitudinal research is needed to shed light on the temporal patterns of comorbidity between somatoform conditions and anxiety and depressive disorders. Such studies may also help to explore the meaning of any observed temporal association between somatoform and anxiety and depressive disorders, for instance, whether these are causal relationships or simply associations underlying risk factors in the co-occurrence of these conditions.

Conclusions 1. There is a remarkable lack of data in this field, especially of large, populationbased longitudinal studies needed to establish temporal relationships between different conditions.33 In view of this, it is not surprising that a number of critical issues, such as the temporal relationship of this comorbidity, remain unresolved. All that can be said at this stage is that the comorbidity is highly common but the meaning of these associations remains unclear. 2. Despite the observed associations between somatoform conditions and depressive and anxiety disorders, the association patterns do not convincingly show that somatoform disorder may reflect subtypes of depression or anxiety. Findings do not provide strong arguments for either retaining or dismissing the group of somatoform disorders in future classification systems. 3. Because somatoform disorders include a broad variety of diagnoses and symptom clusters (e.g., hypochondriac anxiety, pain, gastrointestinal symptoms), future research should clarify the specificity of the comorbidity between individual somatoform symptom clusters and other mental disorders. 4. More and better epidemiological research is needed and should focus, among other things, on the meaning and implication of comorbidity and possible etiological relationships that may underline this comorbidity. 5. The inclusion of simple neurobiological assessments in population-based studies may help to understand better the biological mechanisms underlying the co-occurrence of somatoform disorders, depression, and anxiety.

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References 1. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry 1992;49:101–108. 2. Brown FW, Golding JM, Smith GR Jr. Psychiatric comorbidity in primary care somatization disorder. Psychosom Med 1990;52:445–451. 3. Katon W, Lin E, Von Korff M, Russo J, Lipscomb P, Bush T. Somatization: a spectrum of severity. Am J Psychiatry 1991;148:34–40. 4. Swartz M, Blazer D, George L, Landerman R. Somatization disorder in a community population. Am J Psychiatry 1986;143:1403–1408. 5. Escobar JI, Gara M, Waitzkin H, Silver RC, Holman A, Compton W. DSM-IV hypochondriasis in primary care. Gen Hosp Psychiatry 1998;20:155–159. 6. Ormel J, VonKorff M, Ustun TB, Pini S, Korten A, Oldehinkel T. Common mental disorders and disability across cultures. Results from the WHO collaborative study on psychological problems in general health care. JAMA 1994;272:1741–1748. 7. Kessler RC. Epidemiology of psychiatric comorbidity. In: Tsuang MT, Tohen M, Zahner GEP, editors. Textbook in Psychiatric Epidemiology. Wilmington, DE: WileyLiss; 1995:179–198. 8. Regier DA, Farmer ME, Rae DS, Locke BZ, Keith SJ, Judd LL, Goodwin FK. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the epidemiologic catchment area (ECA) study. JAMA 1990;264:2511–2518. 9. Robins R. Psychiatric Disorders in America. New York: Free Press; 1991. 10. Swartz M, Landerman R, George LK, Blazer DG, Escobar JI. Somatization disorder. In: Robins LN, Regier DA, editors. Psychiatric Disorders in America. New York: Free Press; 1991:220–257. 11. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association; 1980. 12. Escobar JI. Cross-cultural aspects of the somatization trait. Hosp Community Psychiatry 1987;38:174–180. 13. Lieb R, Pfister H, Mastaler M, Wittchen HU. Somatoform syndromes and disorders in a representative population sample of adolescents and young adults: prevalence, comorbidity and impairments. Acta Psychiatr Scand 2000;101:194–208. 14. Lieb R, Isensee B, von Sydow K, Wittchen HU. The early developmental stages of psychopathology study (EDSP): a methodological update. Eur Addict Res 2000;6:170–182. 15. Wittchen HU, Perkonigg A, Lachner G, Nelson CB. Early developmental stages of psychopathology study (EDSP): objectives and design. Eur Addict Res 1998;4:18–27. 16. Wittchen HU, Pfister H. DIA-X-Interviews: Manual für Screening-Verfahren und Interview; Interviewheft Längsschnittuntersuchung (DIA-X 12 Monate); Ergänzungsheft (DIA-X 12 Monate); PC-Programm zur Durchführung des Interviews (Längsund Querschnittsuntersuchung); Auswertungsprogramm. Frankfurt: Swets and Zeitlinger; 1997. 17. Wittchen HU, Lachner G, Wunderlich U, Pfister H. Test-retest reliability of the computerized DSM-IV version of the Munich composite international diagnostic interview (M-CIDI). Soc Psychiatry Psychiatr Epidemiol 1998;33:568–578.

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18. Reed V, Gander F, Pfister H, Steiger A, Sonntag H, Trenkwalder C, Sonntag A, Hundt W, Wittchen H-U. To what degree the composite international diagnostic interview (CIDI) correctly identifies DSM-IV disorders? Testing validity issues in a clinical sample. Int J Methods Psychiatric Res 1998;7:142–155. 19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC: American Psychiatric Association; 1994. 20. Jacobi F, Wittchen HU, Holting C, Sommer S, Lieb R, Hofler M, Pfister H. Estimating the prevalence of mental and somatic disorders in the community: aims and methods of the German national health interview and examination survey. Int J Methods Psychiatr Res 2002;11:1–18. 21. Fröhlich C, Jacobi F, Wittchen HU. DSM-IV pain disorder in the general population: an exploration of the structure and threshold of medically unexplained pain symptoms. Eur Arch Psychiatry Clin Neurosci 2006;256:187–196. 22. Canals J, Domenech E, Carbajo G, Blade J. Prevalence of DSM-III-R and ICD-10 psychiatric disorders in a Spanish population of 18-year-olds. Acta Psychiatr Scand 1997;96:287–294. 23. Faravelli C, Abrardi L, Bartolozzi D, Cecchi C, Cosci F, D’Adamo D, Lo Iacono B, Ravaldi C, Scarpato MA, Truglia E, Rosi S. The Sesto Fiorentino study: background, methods and preliminary results. Lifetime prevalence of psychiatric disorders in an Italian community sample using clinical interviewers. Psychother Psychosom 2004;73:216–225. 24. Kringlen E, Torgersen S, Cramer V. A Norwegian psychiatric epidemiological study. Am J Psychiatry 2001;158:1091–1098. 25. Martin A, Jacobi F. Features of hypochondriasis and illness worry in the general population in Germany. Psychosom Med 2006;68:770–777. 26. Iosifescu DV, Nierenberg AA, Alpert JE, Smith M, Bitran S, Dording C, Fava M. The impact of medical comorbidity on acute treatment in major depressive disorder. Am J Psychiatry 2003;160:2122–2127. 27. Ehlert U, Nater UM, Bohmelt A. High and low unstimulated salivary cortisol levels correspond to different symptoms of functional gastrointestinal disorders. J Psychosom Res 2005;59:7–10. 28. Nutt DJ, Stein DJ. Understanding the neurobiology of comorbidity in anxiety disorders. CNS Spectr 2006;11:13–20. 29. Kessler RC. The epidemiology of dual diagnosis. Biol Psychiatry 2004; 56:730–737. 30. Faraone A, Tsuang MT, Tsuang DW. Genetics of Mental Disorders. A Guide for Students, Clinicians and Researchers. New York: Guilford Press; 1999. 31. Fishbain DA, Cutler R, Rosomoff HL, Rosomoff RS. Chronic pain-associated depression: antecedent or consequence of chronic pain? A review. Clin J Pain 1997;13:116– 137. 32. Lieb R, Zimmermann P, Friis RH, Hofler M, Tholen S, Wittchen HU. The natural course of DSM-IV somatoform disorders and syndromes among adolescents and young adults: a prospective-longitudinal community study. Eur Psychiatry 2002;17:321–331. 33. Weich S, Araya R. International and regional variation in the prevalence of common mental disorders: do we need more surveys? Br J Psychiatry 2004;184:289–290.

2 THE ASSOCIATION OR OTHERWISE OF THE FUNCTIONAL SOMATIC SYNDROMES Richard A.A. Kanaan, MRCPsych Jean Pierre Lepine, M.D. Simon C. Wessely, FRCPsych

S

omatic symptoms without a clear medical explanation are common in the community and in medical settings.1–4 Many people report more than one such symptom,3,5 and these multiple symptoms are sometimes grouped together as the various “Functional Somatic Syndromes” (FSS). Of itself, this term tells us nothing about etiology—in particular, there is no implication that these symptoms arise through the hypothetical process of somatization. Simply put, these are clusters of physical symptoms occurring together for which no adequate medical ex-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Kanaan RAA, Lepine JP, Wessely SC: “The Association or Otherwise of the Functional Somatic Syndromes.” Psychosomatic Medicine 69:855–859, 2007. Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission. Richard A. A. Kanaan, MRCPsych, was supported by a Biomedical Ethics Fellowship from the Wellcome Trust (079743).

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planation has been found, and which doctors have grouped into syndromes. There is a long and changing list of these FSS, which currently includes chronic fatigue syndrome, irritable bowel syndrome, and multiple chemical sensitivity—every medical specialty has at least one (Table 2–1). There is much in common among these syndromes, epidemiologically, phenomenologically, and clinically, in terms of history, treatment, and doctor-patient relationships.6 Although the division of syndromes into the medically explained and unexplained is too simplistic for the complex etiology of modern medicine, it remains the case that no confirmed organic etiological markers have been found to distinguish the FSS. The lack of distinguishing pathophysiology, combined with the evidence of commonality, has led some researchers to propose that these syndromes may be manifestations of the same illness.6,7 In this article, we selectively review the evidence for and against that proposal.

Are There More Similarities Than Differences in the Phenomenology of the Functional Somatic Syndromes? A glance at Table 2–1 reveals a group of syndromes that would seem to have little in common, other than the absence of an accepted, clear-cut etiology. In particular, the symptoms after which most are named suggest little overlap, being segregated by physiological system. So it is perhaps surprising that anyone would think “irritable bowel syndrome” (IBS) an associate of “tension headache.” But the neat taxonomy suggested by Table 2–1 belies the diversity of symptoms involved in the presentation of these syndromes: it is extremely common for those with irritable bowel symptoms to also report headache,8 and vice versa.9 The lists of symptoms reported by patients with these conditions are long and overlap considerably. Furthermore, the etiological relationships suggested by such names as “tension headache” or “multiple chemical sensitivity” are either speculative or, as in “premenstrual syndrome,” descriptive. This is clearly seen when the names of these syndromes are compared across languages or cultures. The term for IBS is “spasmodic colitis” in French, for example, whereas hyperventilation syndrome is known as “spasmophilia.” The French terms suggest different pathophysiologies from their English counterparts. The names of our FSS may be suggestive, in short, but at present, none are etiological. Without the organizing principles afforded by determinate etiology or pathophysiology, the FSS are characterized by their symptoms. In the spirit popularized by Diagnostic and Statistical Manual, 3rd Edition (DSM-III),10 their diagnostic criteria tend to be given by checklists of these symptoms. One can therefore compare the phenomenology of the FSS by comparing their symptom checklists.

The Association or Otherwise of the Functional Somatic Syndromes

TABLE 2–1.

11

Some unexplained somatic syndromes by specialty

Specialty

Syndrome

Gastroenterology Gynecology Rheumatology Cardiology Infectious diseases Respiratory medicine Orthopedics Neurology Immunology

Irritable bowel syndrome Chronic pelvic pain Fibromyalgia Atypical chest pain (Postviral) fatigue syndrome Hyperventilation syndrome Chronic lower back pain Tension headache Idiopathic environmental intolerance

Do the Criteria Overlap? Wessely et al. considered this question in regard to twelve FSS for which criteria were available.6 They found considerable overlap in symptoms—bloating or abdominal distension in eight, headache in six, abdominal pain in six, fatigue in six, and so on. So it is unsurprising that an examination of symptom prevalence by syndrome reveals considerable overlap. Although all patients with chronic fatigue syndrome (CFS) report fatigue, for example, 86% of patients with fibromyalgia do as well; conversely, although all fibromyalgia patients report arthralgia, so do 88% of CFS patients.11 But what does this simple overlap tell us? Fatigue and pain are such ubiquitous features of illness that their involvement gives us few clues about disease processes: most diseases will have one or both as a symptom. Subarachnoid hemorrhage and meningitis may have almost 100% overlap in headaches without any suggestion that the boundary between them is blurred in any other important sense. Just sharing a symptom does not tell us much. A more useful way of looking at the overlap may come from dividing the criteria into essential features and supporting (or “accidental”) features. The essential features of subarachnoid hemorrhage and meningitis are blood in the cerebrospinal fluid and meningeal inflammation, respectively. A headache supports either diagnosis and may be a fundamental part of the patient’s experience, but it is not part of the diagnostic criteria: asymptomatic meningitis, for example, would be meningitis nonetheless. The situation for the FSS is different because the lack of discrete pathology means both essential and supporting features will be symptoms. Still, it makes sense that fatigue should be the essential symptom of CFS, for example, and arthralgia should be a symptom that supports the diagnosis but is not

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required. This structuring of criteria has been used in most FSS, which do not adopt simple checklists but rather “Chinese menu”-style criteria in which some symptoms are essential, and others are merely supportive. The 1994 Centers for Disease Control (CDC) criteria for CFS,12 for example, require at least 6 months of persistent fatigue (essential feature) plus four or more (supporting) features from a list including sore throat, tender glands, headaches, and so on. Fibromyalgia, by contrast, is diagnosed solely by two essential features—musculoskeletal pain and the presence of tender points13—and all other reported symptoms, such as fatigue, may support the diagnosis but are not required. This is an attractive approach to classification, but it conceals a problem. The division into essential and accidental features comes originally from Aristotle,14 who argued that man, for example, was essentially rational but only accidentally bipedal. Although this makes good sense for “man,” it makes much less sense for any particular man, who is both bipedal and rational, to ask which is essential to him—his being bipedal is essential to him being “ambulatory,” for example.15 Similarly, for any patient or group of patients, it is not clear why any symptom should be considered essential, unless it is to some prior conception or some purpose. The meningeal inflammation is essential to meningitis because it provides an explanatory basis for the whole clinical picture of symptoms and therapeutics. But why should a patient’s fatigue be essential and not his or her pain? It might seem obvious that fatigue should be essential to CFS, but we must remember that “chronic fatigue syndrome” was constructed on the basis of symptom profiles, and for every symptom considered essential to that construct, there were equally many symptoms rejected.16 Why should we not consider this construct to be arbitrary? Several reasons suggest themselves. First, the construct might reliably identify a separate group of patients from the symptom combinations of other FSS. Second, the group identified might differ from other FSS groups in other ways—epidemiologically, physiologically, or therapeutically. Third, the groups might differ in some important psychological respects. We consider each of these in turn.

If You Fulfill Criteria for One Syndrome, Do You for Others? If fibromyalgia and CFS were really (aspects of ) the same underlying condition, then a high degree of comorbidity would be expected but could not be explained by simple overlap of the diagnostic criteria. For meningitis and subarachnoid hemorrhage, focusing on the essential features of the disease rather than the headache identifies separate groups of patients, with almost no diagnostic overlap—no comorbidity of hemorrhage and meningitis: does the same hold for FSS? Patients with one FSS almost universally report symptoms of others.11 Wessely et al. drew attention to the literature reporting the symptomatic overlaps between,

The Association or Otherwise of the Functional Somatic Syndromes

13

on the one hand, CFS and, on the other hand, fibromyalgia, tension headache, multiple chemical sensitivity, food allergy, premenstrual syndrome, and IBS.6 IBS was likewise associated with symptoms of hyperventilation syndrome, fibromyalgia, CFS, tension headache, atypical facial pain, noncardiac chest pain, chronic pelvic pain, nonulcer dyspepsia, and premenstrual syndrome. Wessely et al. considered symptoms, however, not diagnostic criteria, which are more complex for a variety of reasons—the structuring into essential and supporting symptoms, the time course requirements, and the requirement for severity or functional impairment. Fortunately, many other studies have used diagnostic criteria rather than symptoms. Aaron and Buchwald reviewed 53 studies where patients with one FSS were assessed by the formal diagnostic criteria for another.17 They found that 35%–70% of patients with CFS met the criteria for fibromyalgia, 58%–92% met the criteria for IBS, and 53%–67% showed multiple chemical sensitivity. Similarly, 75% of patients with fibromyalgia met the criteria for temporomandibular disorder, 32%–80% met the criteria for IBS, and 55% described multiple chemical sensitivity. Equally high rates were found for IBS, but for other, less studied disorders, such as temporomandibular disease and interstitial cystitis, the rates of concordance seemed to be lower. In a more recent large Swedish twin study, Kato et al. looked at the comorbidities of chronic widespread pain as the cardinal symptom of fibromyalgia.18 They reported considerable co-occurrences with CFS (OR =23.2), depressive symptoms (OR=7.4), and IBS (OR =5.3). The authors used co-twin analysis to demonstrate that these associations were extensively mediated by unmeasured genetic and family environment factors. However, although these fully explained the psychiatric comorbidity, odds ratios remained greater than 3 for CFS and IBS. There is still something about (meeting the criteria for) one FSS that makes another comorbid FSS more likely. So it seems that not only do the criteria for FSS often overlap, but so do the patients identified by those diagnoses. Even in cases where the diagnostic criteria do not refer to the essential features of another disorder, the criteria continue to identify the same patients: 70% of patients with fibromyalgia meet the criteria for CFS,19 even though pain and tenderness do not appear in the essential criteria for CFS. As long as these syndromes are defined solely on the basis of symptom profiles, it can seem that the same patients, with the same symptoms, are being diagnosed one way or another on the basis of some arbitrary selection of these symptoms. But even diagnostic criteria do not fully exhaust the factors that enter into making a diagnosis: the judgment of doctors and the presentation of patients will both have an impact. So, it is possible that when it comes to making an actual diagnosis that some factor in the clinic room determines that a patient has CFS or IBS. Yet even where recent, large-scale studies have looked at the rates of comorbid diagnoses actually made, they still find increased rates of, for example, fibromyalgia in IBS patients (OR =1.8)20 and vice versa (risk ratio of 4.4 in women, 3.9 in men).21 These results are striking because one would expect physicians to avoid

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making multiple diagnoses where possible. However, cohort studies of this kind are less good at detecting true comorbidity because they do not rely on primary clinical data. The increased rates may therefore represent a degree of pathoplasticity, or changes in diagnosis, rather than true comorbidity. Although there is some evidence of pathoplasticity,22 population-based studies16,23,24 find that the fatigue syndrome, for example, is stable. We should acknowledge the interest of the specialist physician here. The same patient could be diagnosed with temporomandibular disorder by the oral surgeon and then with fibromyalgia by the rheumatologist; thus, the apparent diversity of syndromes may be no more than an artifact of medical specialization.6,19 In summary, at every level of clinical-phenomenological assessment—symptoms, criteria, and actual diagnoses—there are greatly increased rates of comorbidity, of overlap. This lends support, as far as it goes, for those who would argue that the FSS are all one, or at least closely related. But the phenomenological is only one consideration—the FSS may differ in many other respects.

Do the Syndromes Differ in Other Ways? The perceived commonalities of epidemiology, psychosocial risks, management, and outcome, when combined with the absence of pathognomonic tests and overlapping symptoms, have historically led some researchers to suggest that the similarities outweigh the differences between these syndromes. Freud’s is perhaps the most famous attempt to group medically unexplained symptoms under a single model,25 although it was not the first, or the last. More recently, it has been argued that the FSS are still substantially similar in these respects,6 although not everyone is persuaded.26 These other aspects are explored in this book. Suffice it to say, the commonalities remain impressive, and the increasing number of differences is intriguing. The interpretation of these, however, is more complex still. Let us consider one illustrative recent finding that different infective organisms differentially precipitate CFS and IBS.27 This is clear evidence that CFS and IBS are different. But different in what way? In the way that a staphylococcal dermatitis differs from a streptococcal dermatitis? Or in the way that a streptococcal dermatitis differs from a streptococcal meningitis? In both of these senses, there are important differences and important commonalities; whether we want to consider a streptococcal dermatitis different from a meningitis depends on our purpose: the way we classify is ultimately instrumental. Classifying by infective organism is no more “real” than classifying by organ system—they each have their utility. What purpose, then, could it serve to consider CFS and IBS the same, if their etiological risks are essentially different and their symptoms perhaps only accidentally similar? One answer could be that it may serve to describe a commonality of disease process, of the psychosocial role in the generation, maintenance, and treatment of symptoms.

The Association or Otherwise of the Functional Somatic Syndromes

15

Does This Mean They Are All Psychosomatic? No. Although a psychosomatic view of FSS has been popular in the past, it is by no means implied by the “one syndrome” hypothesis26—even if, as seems probable, the psychosocial is relevant to the etiology, pathophysiology, and management of FSS. The relationship of the psychosocial and psychiatric with FSS is explored elsewhere in this book. But the same sorts of questions of overlap that we have discussed here have been explored with respect to the FSS, anxiety, and depression. There is no doubt that there is a relationship between them, although it is complex.28 For CFS, there is a linear relationship between the number of CDC symptoms and psychiatric morbidity,16 and this cannot be explained simply as a psychological reaction to physical illness and/or disability.28 But the high rates of psychiatric morbidity are far from sufficient to explain the prevalence of FSS. Another clear relevance of the psychosocial view is in treatment, where cognitive-behavioral therapies have shown success in a number of FSS.29 These therapies offer cognitive-behavioral models for symptom persistence and, in some cases, symptom generation. More generally, it is a platitude that all symptoms are cognitively mediated. But this is not the same as a “psychosomatic” or “imaginary” model: sleep in CFS really is disturbed, and may have been provoked by any number of organic illnesses, for all that a cognitive-behavioral cycle can be argued to sustain the disturbance. The patient’s beliefs about his or her illness play a key role in the cognitive model and in the presentation of that illness.30 This idea of the centrality of the psychosocial role may serve as a kind of grouping principle, as an important way in which the FSS are importantly thought to be the same; but equally, the specific psychosocial roles in each FSS reveal another way in which they differ.

The Patient’s Perspective In this discussion of the different perspectives from which the FSS may be considered, we finally come around to the patient’s perspective. Giving a diagnostic label has potentially huge significance for the patient,31 and which particular diagnostic label may make a considerable difference.32 This is not to reanimate the moribund antipsychiatry view that the label is all. Disposing of the schizophrenia label does not abolish psychosis or the problems of patients with psychotic symptoms. But we do accept that labels shape and reflect how patients respond to illness. CFS and fibromyalgia, for example, are the syndromes for which there is arguably the greatest overlap, including in their response to graded exercise,33,34 yet a glance at online discussion groups reveals dramatically different views on its application between the two disorders. If a diagnostic system divided along the lines of medical specialties seems arbitrary, one that accords with patients’ views is the height of pragmatism.35 Where

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diagnoses are contentious, and the evidence base for one system or another is limited, a classification that minimizes conflict may serve far more effectively as a platform for recovery.31

The Same but Different For all the commonality, the differences between the FSS cannot be ignored. Although there are substantial overlaps in symptoms and patients, these are far from universal. A latent variable analysis of patients with somatic symptoms36 suggested a best fit of a five-factor model—CFS-like, IBS-like, fibromyalgia -like, depression, and anxiety—but also a large common factor: yes, they had much in common, and no, they are not the same. For some classificatory purposes, it may be best to consider the FSS as the same, and for other purposes as different. Although this may seem pusillanimous, we should remember that all our scientific classifications are instrumental: light is both a wave and in other contexts a particle, and with our current understanding, there is simply no better, no more truthful way to describe it.37 In the FSS, a diagnosis that respects the patient’s view of his or her illness stands to be both instrumentally and pragmatically apt.

References 1. Kroenke K, Price RK: Symptoms in the community: prevalence, classification, and psychiatric comorbidity. Arch Intern Med 1993;153:2474–2480. 2. Khan AA, Khan A, Harezlak J, Tu W, Kroenke K: Somatic symptoms in primary care: etiology and outcome. Psychosomatics 2003;44:471–478. 3. Kroenke K, Mangelsdorff AD: Common symptoms in ambulatory care: incidence, evaluation, therapy, and outcome. Am J Med 1989;86:262–266. 4. Nimnuan C, Hotopf M, Wessely S: Medically unexplained symptoms: an epidemiological study in seven specialities. J Psychosom Res 2001;51:361–367. 5. Kroenke K, Spitzer RL, deGruy FV III, Swindle R: A symptom checklist to screen for somatoform disorders in primary care. Psychosomatics 1998;39:263–272. 6. Wessely S, Nimnuan C, Sharpe M: Functional somatic syndromes: one or many? Lancet 1999;354:936–939. 7. Barsky AJ, Borus JF: Functional somatic syndromes. Ann Intern Med 1999;130:910– 921. 8. Whorwell PJ, McCallum M, Creed FH, Roberts CT: Non-colonic features of irritable bowel syndrome. Gut 1986;27:37–40. 9. Mongini F, Rota E, Deregibus A, Ferrero L, Migliaretti G, Cavallo F, Mongini T, Novello A: Accompanying symptoms and psychiatric comorbidity in migraine and tension-type headache patients. J Psychosom Res 2006;61:447–451. 10. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition. Washington, DC: American Psychiatric Association; 1980.

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11. Aaron LA, Burke MM, Buchwald D: Overlapping conditions among patients with chronic fatigue syndrome, fibromyalgia, and temporomandibular disorder. Arch Intern Med 2000;160:221–227. 12. Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A: The chronic fatigue syndrome: a comprehensive approach to its definition and study. International chronic fatigue syndrome study group. Ann Intern Med 1994;121:953–959. 13. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P, Fam AG, Farber SJ, Fiechtner JJ, Franklin CM, Gatter RA, Hamaty D, Lessard J, Lichtbroun AS, Masi AT, McCain GA, Reynolds WJ, Romano TJ, Russell IJ, Sheon RP: The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicenter criteria committee. Arthritis Rheum 1990;33:160–172. 14. Aristotle, Lawson-Tancred HC: The Metaphysics. London: Penguin; 1998. 15. Quine WVO. Two dogmas of empiricism. The Philosophical Review 1951;60:20–43. 16. Wessely S, Chalder T, Hirsch S, Wallace P, Wright D: Psychological symptoms, somatic symptoms, and psychiatric disorder in chronic fatigue and chronic fatigue syndrome: a prospective study in the primary care setting. Am J Psychiatry 1996;153:1050–1059. 17. Aaron LA, Buchwald D: A review of the evidence for overlap among unexplained clinical conditions. Ann Intern Med 2001;134:868–881. 18. Kato K, Sullivan PF, Evengard B, Pedersen NL: Chronic widespread pain and its comorbidities: a population-based study. Arch Intern Med 2006;166:1649–1654. 19. Buchwald D, Garrity D: Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Arch Intern Med 1994;154:2049–2053. 20. Cole JA, Rothman KJ, Cabral HJ, Zhang Y, Farraye FA: Migraine, fibromyalgia, and depression among people with IBS: a prevalence study. BMC Gastroenterol 2006;6:26. 21. Weir PT, Harlan GA, Nkoy FL, Jones SS, Hegmann KT, Gren LH, Lyon JL: The incidence of fibromyalgia and its associated comorbidities: a population-based retrospective cohort study based on International Classification of Diseases, 9th Revision codes. J Clin Rheumatol 2006;12:124–128. 22. Stewart DE: The changing faces of somatization. Psychosomatics 1990;31:153–158. 23. Hickie I, Koschera A, Hadzi-Pavlovic D, Bennett B, Lloyd A: The temporal stability and co-morbidity of prolonged fatigue: a longitudinal study in primary care. Psychol Med 1999;29:855–861. 24. Merikangas K, Angst J: Neurasthenia in a longitudinal cohort study of young adults. Psychol Med 1994;24:1013–1024. 25. Freud S. Studies in Hysteria. London: Hogarth Press; 1895. 26. Wessely S, White PD:. There is only one functional somatic syndrome. Br J Psychiatry 2004;185:95–96. 27. Moss-Morris R, Spence M: To “lump” or to “split” the functional somatic syndromes: can infectious and emotional risk factors differentiate between the onset of chronic fatigue syndrome and irritable bowel syndrome? Psychosom Med 2006;68:463–469. 28. Henningsen P, Zimmermann T, Sattel H: Medically unexplained physical symptoms, anxiety, and depression: a meta-analytic review. Psychosom Med 2003;65:528–533.

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29. Kroenke K, Swindle R: Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom 2000;69:205–215. 30. Butler S, Chalder T, Ron M, Wessely S: Cognitive behaviour therapy in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry 1991;54:153–158. 31. Huibers MJ, Wessely S: The act of diagnosis: pros and cons of labelling chronic fatigue syndrome. Psychol Med 2006;36:895–900. 32. Hamilton WT, Gallagher AM, Thomas JM, White PD: The prognosis of different fatigue diagnostic labels: a longitudinal survey. Fam Pract 2005;22:383–388. 33. Moss-Morris R, Sharon C, Tobin R, Baldi JC: A randomized controlled graded exercise trial for chronic fatigue syndrome: outcomes and mechanisms of change. J Health Psychol 2005;10:245–259. 34. Richards SC, Scott DL: Prescribed exercise in people with fibromyalgia: parallel group randomised controlled trial. BMJ 2002;325:185. 35. Engel CC: Explanatory and pragmatic perspectives regarding idiopathic physical symptoms and related syndromes. CNS Spectr 2006;11:225–232. 36. Robbins JM, Kirmayer LJ, Hemami S: Latent variable models of functional somatic distress. J Nerv Ment Dis 1997;185:606–615. 37. Heisenberg W. Physics and Philosophy: The Revolution in Modern Science. London: Penguin; 1989.

3 CULTURAL MODELS AND SOMATIC SYNDROMES Laurence J. Kirmayer, M.D. Norman Sartorius, M.D., Ph.D.

The somatoform disorders bring together three conceptually distinct sets of clinical problems: 1) patients with excessive bodily preoccupation, illness worry, or the unwarranted conviction that they are ill; 2) patients with medically unexplained symptoms or functional somatic syndromes (e.g., fibromyalgia, irritable bowel syndrome, chronic fatigue, nonulcer dyspepsia, and various chronic idiopathic pain syndromes) that are presumed to be due to psychological factors; and 3) patients who present clinically with somatic symptoms or concerns but who can be diagnosed with another psychiatric or psychological disorder (e.g., major depressive disorder or panic disorder) that accounts for their bodily symptoms.1 Although these problems often co-occur and each can lead to the other, they can also occur in iso-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Kirmayer LJ, Sartorius N: “Cultural Models and Somatic Syndromes.” Psychosomatic Medicine 69:832–840 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission. The study was supported by Senior Investigator Award MSS 55123 (L.J.K.) from the Canadian Institutes of Health Research on “the integration of culture in psychiatric theory and practice.” We thank Suparna Choudhury and Andrew Ryder for helpful comments on earlier drafts.

19

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lation, suggesting that distinct mechanisms are involved. There is evidence that cultural ways of understanding the body, interpreting symptoms, and expressing distress can shape each of these problems.2,3 In this chapter, we explore some implications of work on cultural models for rethinking the nature of somatoform disorders and for research that can inform future revisions of diagnostic systems.

Culture in a Globalizing World Any discussion of cultural models must begin with a consideration of what the term culture means in the contemporary world. Although in much psychological and sociological work on illness behavior, culture has been conflated with ethnicity, race, or geographic origins, in the contemporary world, every society, geographic region, and ethnic group participates in multiple coexisting, intertwined cultural systems. Current anthropological views emphasize that cultures are fluid, heterogeneous, hybrid systems of knowledge, institutions, discourse, and practices that vary over time and location.4,5 Contemporary views of culture recognize the dynamic interplay between individuals’ agency and social processes of discursive and institutional power, often expressed through the control of technical knowledge and professional authority.6–8 Cultures function as both resources for and constraints on individuals’ constructions and construals of experience. Research that compares ethnic or cultural groups in terms of group means is ill suited to capture this process of cultural shaping of illness experience. The majority of epidemiological studies that report on ethnoracial blocs in the United States (e.g., African-American, Hispanic, Asian American) or some other crudely defined ethnic group cannot shed much light on the impact of culture on psychopathological processes. Specifying ethnicity more precisely does not get at the real issue, which is the heterogeneity within even well-defined ethnic groups. More proximal measures of the impact of culture on symptom reporting and illness behavior are needed. For research to advance on cultural variations in psychopathology, we need to go beyond conventional group labels to examine the specific biological, psychological, or social mediators of cultural difference. For example, if cultures differ in the categories and concepts they provide to interpret and explain physical symptoms, we need to examine individuals’ use of these attributions directly rather than simply using ethnocultural identity as a proxy for the specific cultural factors that underlie the attribution. This is a crucial shift in paradigm from group comparisons based on ethnic identity toward careful measurement of potential mediators of cultural influences on behavior, which include bodily processes, cognitive models, modes of expression and narration of distress, social interactions, and institutional practices. It requires using measures that have been validated across cultures but has the potential to yield much more consistent and useful results, not only to

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21

guide cross-cultural applications of nosology but also to advance the basic science of psychiatry and psychosomatic medicine. Cultural knowledge about illness is encoded, maintained, and transmitted in a variety of different ways with corresponding differences in how it can be accessed and how it may influence psychopathology. Some knowledge is encoded in cognitive schemas of various types that may include explicit models of physiological process or mechanisms, networks of associations, or systems of propositions that constitute diagnostic criteria and ways of deducing the consequences of events (e.g., “if you have a stuffy nose, you may have a cold”). This is the sort of knowledge that contributes to explanatory models from which one reasons “logically.” Such reasoning is not usually via strict syllogism but follows a variety of judgment heuristics using “bounded rationality”—rules of thumb for estimating the consequences of actions that have built into them various cognitive and affective biases.9 The explanatory model perspective in medical anthropology, developed by Arthur Kleinman and associates, has established the importance of causal attributions and more elaborate ethnophysiological theories in illness experience, symptom-reporting, help-seeking behavior, and treatment response.10–13 Cultural knowledge about illness is also conveyed in salient prototypes or exemplars: images and stories of others’ experience or of one’s own past experiences that are used to reason analogically about one’s current situation.14 These prototypes may be salient because they are personally meaningful and emotionally vivid, they are given social authority through the status of the exemplars, or they are consonant with other cultural values or institutions. The explanatory model perspective in medical anthropology assumes that cultural knowledge is largely explicit and can be accessed by asking individuals what they think. However, knowledge is also encoded in various implicit ways; e.g., patterns of association that are acquired outside of conscious awareness and that result in dispositions to respond to events in particular ways. This implicit knowledge can be measured by observing individuals’ behavior or by analyzing illness narratives for their underlying structure.15,16 Cultural knowledge is also socially embodied, residing in social institutions and their associated rules, roles, and practices. These social institutions and practices may be expressed through explicit directives, discourse, and technologies or contribute to tacit background knowledge.17 Social background knowledge may be hard for individuals to become aware of and articulate both because it is taken for granted and because it is distributed—that is, not held by any single individual but parceled out among many actors and emergent from their cooperative interaction. In addition to the impact of culture on basic psychophysiological processes, it is important to recognize that classifications of mental disorders, diagnoses, and related professional practices also are part of cultural systems. Hence, to create useful diagnostic systems and guidelines for practice, we need to consider the impact of local and international professional agendas and health care systems and the ways

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in which professional models are appropriated by pharmaceutical marketing, promoted through mass media, and turned into popular models that individuals use to understand their illness.

Impact of Explanatory Models on Symptom Reporting The semiotics of biomedicine assumes that complaints about bodily function are more or less direct indices of impairments of organ tissue or function, neglecting the fact that these complaints emerge from processes of attention, interpretation, labeling, and social presentation.18 The translation or transduction of a bodily process into a salient experience and a verbal report is mediated by perceptual, cognitive, interpersonal, and social processes. A minimal set of these mediators would include attentional strategies (e.g., focused attention, distraction, or dissociation); symptom and illness attributions or interpretations in terms of cognitive models or schemas; processes of organizing experience in terms of narratives that locate distress in temporal accounts of causes, consequences, and implications for health and identity; and processes that include culturally shaped ways of understanding and communicating one’s experience and the response of others within family, work, health care, and other social contexts.2,19,20 This cognitive and social shaping of somatic distress is crucial for understanding the exaggerated bodily concern and somatic complaints that characterize the somatoform disorders. Ordinary fluctuations in somatic regulatory systems as well as states of strong emotion or stressful life events give rise to transient experiences of bodily distress that can be interpreted as symptoms of illness. To become chronic and disabling, however, additional processes must come into play to create vicious circles of symptom amplification. These positive feedback loops are mediated by the meanings ascribed to symptoms. Acute symptoms and distress prompt a search for meaning.21 Every culture provides explanations and causal attributions for somatic symptoms.22 These explanations, in turn, set up expectations that influence the ways that individuals attend to their bodies and the sorts of symptoms they recognize and report to others. Symptom attributions and interpretations are not static but dynamic and malleable, reorganized cognitively and renegotiated with others in ongoing processes of psychological adaptation and social positioning. The meanings inherent in cultural models may amplify distress or lead individuals to ignore or deny specific symptoms, which are threatening or stigmatizing.23 Although the body is the vehicle for our engagement with the world, producing the basic conceptual models and metaphors we use to think with,24 the healthy body is largely absent from awareness.25 The body becomes an object of attention in itself mainly at moments of unusual pleasure, effort, or discomfort. Bodily sen-

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sations or experiences may become salient for a variety of reasons: 1) unusual quality or intensity; 2) functional impairment; 3) contiguity or association with other salient events; and 4) availability of treatment or other plans of action. Cultural models also may lead individuals to search for and identify specific symptoms and syndromes that fit salient templates. The body produces a constant “white noise” of somatic sensations that are potential symptoms, and this background noise increases as we age.26 Physiological perturbations, emotional arousal, and social conflict can all intensify these sensations so that they cross a perceptual threshold and are perceived as disturbing. Symptom schemas assign meaning to sensations, and illness schemas organize patterns of symptoms into coherent entities according to folk knowledge.27 Such schemas may be anchored in causal explanations, but they also reflect the sociomoral and cultural meanings of distress. Explanatory models include explicit notions of cause, course, appropriate proper treatment, and likely outcome. The models may be specific to particular symptoms, syndromes, or disorders or may cut across whole categories of problem. Some, like “stress,” serve as all-purpose explanations. 28 Explanatory models are shaped by local theories of the body (ethnophysiology), person (ethnopsychology), and the nature of health problems and adversity, which often includes social, moral, and spiritual ideas.27,29 Qualitative health research shows that people bring multiple models to bear to explain distress and decide what to do about it.30 In a community study of people with medically unexplained symptoms, most participants were able to give multiple explanations for symptoms their doctors had not explained.31,32 These typically included stressful social circumstances that they had not brought to their doctor’s attention because they felt there was a lack of opportunity, interest, or relevance to the biomedical agenda. In addition to explanatory models identified in medical anthropology, individuals may reason about their condition in terms of salient prototypes drawn from their own previous experience, family members, friends, mass media, and popular culture.33 Prototypes are images or models that are used to reason analogically about current illness experience. Prototypes may or may not include explicit causal attributions or ideas about mechanism but may nonetheless convey ideas about what the appropriate treatment would be for a problem and its likely outcome. A study of patients with medically unexplained symptoms identified by their primary care providers as high utilizers found that many had prototypes for their illness that were very compelling, such as the sudden death of a relative after suffering from symptoms that resembled the patients’ symptoms. This prototype was the source of persistent concern.34 Such prototypes may function as “rogue representations”35—persistent disturbing images and ideas that are not readily refuted or displaced by medical explanation or reassurance and that therefore contribute to persistent somatic preoccupation, concern, and help seeking.

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Knowledge about illness is also encoded in “chain complexes”: schemas based on associative chains that are based on the contiguity of experiences, actions, and events. These schemas may be acquired through “Hebbian learning,” in which salient sensations and events that co-occur repeatedly become associatively linked.36–38 Hebb conjectured that neurons or “cell assemblies” (small neural networks) would tend to become functionally linked if they were repeatedly activated at the same time.36 There is now evidence for this type of associative learning by contiguity in a variety of neural systems (e.g., long-term potentiation in the hippocampus), and it provides a potential mechanism for the acquisition of rudimentary sensorimotor schemas through simple exposure to sequences of sensations, actions, and events.39 A similar mechanism may operate to organize social knowledge in terms of the parallels between our own actions and experiences and our perceptions of the actions and experiences of others (including somatic sensations and emotions), as suggested by recent work on mirror neurons.40 Importantly, for our understanding of the embodiment of cultural models, these schemas may be implicit (i.e., acquired unintentionally, activated automatically, and not directly accessible to awareness). Chain complexes may link a variety of somatic sensations, actions, and expected outcomes in ways that influence illness behavior even though the person cannot give an explicit account of a cultural model. The models that individuals use to make sense of bodily experience may vary with social context.30 Thus, the same person may think about and present their problem in one way in the physician’s office and another way at work or at home. The organization of the health care system itself may have a significant impact on the use of cultural models. The finding that, in health care systems where primary care physicians have a more personal and ongoing relationship to patients, there is a lower prevalence of somatoform diagnoses41 points to the notion that when there is trust and open communication, it is easier to find explanations for distress— whether that involves explaining somatic symptoms in terms of distributed psychophysiology or acknowledging the social and psychological factors that contribute to making bodily symptoms intolerable.30

Cultural Models and Symptom Experience These considerations on the nature of cultural models are pertinent to understanding the impact of culture on somatic distress. There is evidence for cultural influences on symptom experience and reporting at multiple levels, including psychophysiology, attention, symptom attribution and interpretation, modes of coping, and help seeking and treatment. These cultural influences are reflected in a range of phenomena relevant to psychiatric nosology, including culture-specific symptoms and syndromes as well as styles of clinical presentation. Cultural explanations may give rise to unique symptoms and concerns like semen loss, genital shrinking, or heat in the head. The prevalence of explanatory

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models and prototypes may also influence the prevalence of specific clinical presentations of symptoms and syndromes. Finally, explanatory models indicate the significance and seriousness of symptoms, determining whether bodily symptoms will give rise to anxiety, help seeking, and disability. Specific somatic symptoms are associated with prevalent cultural explanations that have been described in terms of somatic syndromes. For example, losing semen in the urine is associated with “dhat syndrome” in India, based on the notion that semen concentrates vital energy; 42,43 epigastric burning is associated with hwa-byung in Korea (“fire illness”), based on the notion of an imbalance of “fire” as a basic constituent of the body;44,45 heat in the head is a nonspecific symptom commonly reported in equatorial Africa, based on notions of the importance of central heat in the constitution of the person.46,47 Certain symptoms may be more prevalent because they form part of an illness prototype. For example, loss of consciousness was reported more frequently in the Puerto Rican Epidemiologic Catchment Area Study than elsewhere in North America, and this has been traced to the influence of the cultural template for ataque de nervios, an “attack of nerves” that may be associated with a wide range of symptoms including shouting, crying, and dissociative behaviors including apparent loss of consciousness.48–50 Cultural models not only shape symptom reporting but also can contribute to psychopathological processes. For example, in an important body of work on panic and anxiety disorders among Southeast Asian migrants in the United States, Hinton and colleagues described a series of culture-specific vicious circles in which ethnophysiological notions interact with memories and bodily conditioning to give rise to disabling symptoms.51–57 Catastrophizing interpretations of sensations associated with orthostatic hypotension, dizziness, and other common sensations can lead to vicious circles with panic attacks or anxiety about somatic illness. Understanding the social and psychological processes that reinforce or stabilize particular symptom and illness meanings and that make them resistant to change may lead to a useful nosology that is keyed to differential therapeutics. In addition to understanding the individual psychological dynamics of managing the meaning of distress in terms of the maintenance of self-esteem, self-efficacy, and avoiding stigma or the fearsome implications of illness and mortality, we need to consider the social consequences of construing symptoms in particular ways. Social and cultural processes may amplify and spread particular meanings and models of distress and may modulate attention to the body and help seeking. Cultural models, whether encoded in individuals’ cognitive schemas, in body practices, or in social roles, discourse, and institutions can have an impact on psychological processes of attention, interpretation, and coping. Through these psychological processes, cultural models can regulate symptom experience, reporting, help seeking, adaptation, treatment response, and disability.

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Locating Somatic Distress: From Psychosomatics to Sociosomatic Theory Although the notion of culture-bound syndromes has dominated an older literature in cultural psychiatry, more recent ethnographic research makes it clear that many of the conditions labeled “culture-bound syndromes” were not syndromes but rather metaphorical descriptors or everyday terms, causal attributions or explanations, or cultural idioms of distress that can be used to describe a wide range of different somatic experiences of varying pathological significance.58 This is the case for many somatic “syndromes” including dhat and hwa-byung. Such culturally shaped categories and ways of describing the bodily distress can influence somatic symptom experience and illness behavior but do not, in themselves, constitute discrete syndromes or disorders. Cultural idioms of distress are culturally prescribed modes of understanding and narrating health problems and broader personal and social concerns.59 They usually do not indicate psychopathology and may be linked to popular explanatory models or to sociosomatic theory.31 Cultural idioms may reflect more elaborate cultural models or employ evocative metaphors without a well-worked-out conceptual model. For example, the notion of “nerves” has been a popular idiom in many cultures going back to the late 19th century.60 The concept of “cultural idioms of distress” was introduced to draw attention to the fact that reports of bodily distress can serve a communicative function.59 Somatic distress may be a way to express dissatisfaction with living conditions or legitimate difficulties in performing social roles, and to allow the individual to seek outside help through the health care system. If the social conditions that give rise to distress are implacable and persistent, then the person may present with persistent symptoms. The social meaning of somatic symptoms includes their use as ways of talking about or alluding to other forms of distress. For example, talk of burning in the epigastrium may be an indication of reflux esophagitis or other upper gastrointestinal problem, but it is also part of the Korean understanding of hwa-byung, fire illness, in which anger, usually from interpersonal conflicts or injustices, manifests itself as a physiological imbalance with corresponding symptoms.44 This sort of link between a symptom and an ethnophysiological theory may reflect an explicit explanatory model, but it can also follow from more analogical reasoning based on the natural metaphoricity of sensory and affective experiences.61,62 Hence, anger is associated with heat because of the flushing that can accompany the emotion, and sensations of burning resemble tactile sensations of heat. The connections do not require an explanatory model. The process runs the other way: bodily experiences provide analogies that give rise to metaphors, which in turn are elaborated in explicit conceptual models and illness narratives over time.63 Whether they reflect elaborate models or more partial and temporary metaphors, cultural idioms may create the impression that a problem is fundamentally

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somatic and may lead to iatrogenic somatization when the clinician ignores the socioemotional dimensions of distress and pursues somatic explanations. When medical investigations fail to provide an explanation, physicians may view patients as somatizing when, in fact, the patients were aware of the social and emotional antecedents of their bodily distress from the start. Many patients with somatic cultural idioms of distress will acknowledge the social problems that exacerbate their symptoms if they find a sympathetic listener.30,64,65 In biomedical health care settings, however, they may downplay or deny the social dimensions of their distress either because they view it as inappropriate to discuss with a medical practitioner or because they fear stigmatization. Diagnostic systems are also cultural artifacts. In addition to serving as a guide to differential therapeutics, diagnostic labeling provides meaning for suffering, indicates its seriousness and significance to others, and maps its social consequences. In the absence of a clear diagnosis or effective treatment, patients suffer from uncertainty and may engage in efforts to find a definite diagnosis and legitimization for their suffering. Absent, equivocal, and contested diagnoses pose special dilemmas for patients, and some of what is seen as psychopathology may reflect this social predicament.66,67 Although psychological explanations for persistent symptoms are always available, framed in terms of the impact of stress and difficult life circumstances, they may be unsatisfying to patients for many reasons: 1) they may seem obvious and be part of taken-for-granted conditions of social adversity; 2) they can imply a degree of personal weakness; 3) they are associated with other highly stigmatized psychiatric conditions; and most importantly, 4) they may not lead to significant relief.68,69 Even when models are popular and widely shared, others may contest them. The dynamics of this conflict and contest of models have important implications for health and illness. For example, challenges to the legitimacy of a symptom or condition may put the suffering individuals in the position of having to prove the veracity, severity, and seriousness of their complaints. Chronic fatigue syndrome provides a good example of a situation in which many individuals faced with disbelief and the potential for psychological stigmatization have tended to emphasize the gravity of their illness and reject any psychological dimension as a threat to the legitimacy of their suffering.70 As a result, patients with chronic fatigue syndrome are less willing to endorse psychological contributors to their condition than are patients with other conditions such as rheumatoid arthritis.71

A Typology of Looping Effects: Varieties of Somatic Amplification A variety of factors contribute to amplifying or intensifying symptom experience and associated illness behavior through direct effects (e.g., anxiety leads to in-

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creased somatic symptoms); only when these processes feed back into or reinforce themselves in some way do they become the vicious circles that characterize looping effects. A consideration of the varieties of looping effect could lead to a nosology of somatic syndromes based on mechanisms rather than symptom counts or clusters. These loops can be characterized in terms of the pivotal processes forming the feedback loops that amplify distress (Table 3–1). Current evidence would suggest the following factors that may contribute to the intensity and persistence of somatic symptoms and that may become involved in feedback loops: 1) physiological perturbation (as a result of functional disturbances of autonomic and other regulatory systems, affecting visceromotor, pain, and other sensorimotor systems); 2) emotional distress (in the form of an affective or anxiety disorder or other forms of emotional arousal and distress that do not reach the threshold for clinical diagnosis in their own right); 3) disturbances of attention (leading to increased bodily focused attention or, in contrast, ignoring sensations or dissociation); 4) misattribution (linking sensations to pathological causes); 5) catastrophizing or other types of pathologizing cognitions that undermine coping and elaborate negative expectations associated with symptoms; 6) interpersonal responses that may reinforce specific verbal and behavioral expressions of bodily distress; 7) health care, disability, and other systemic responses that investigate, diagnose, legitimate, and ratify symptoms and syndromes of bodily distress; and 8) larger social and cultural models and institutions that sanction specific modes of talking about and responding to bodily illness. These processes all participate in the ordinary regulation of symptom experience; when they exceed normal parameters, all can be etiological factors in giving rise to persistent bodily preoccupation or somatic distress syndromes. Hypochondriacal worry may arise from loops that resemble those of panic disorder: emotional arousal (anxiety) gives rise to somatic sensations, which are interpreted as evidence of a threat to one’s health, which gives rise to more emotional arousal and hence more intense symptoms. In the case of panic disorder, the interpretation is that something catastrophic is about to happen. In the case of hypochondriasis, the feared outcome may be less immediate and result in less intense anxiety, but there is more persistent concern to collect information, focus on, and monitor one’s body and seek reassurance from health providers (which is often perfunctory and unsatisfactory), resulting in increased conviction that something is wrong.72 A variety of isolated bodily complaints may be driven by attentional processes that increase body focus and hence lead to more symptom reports. Attention to the body may raise awareness of one’s mortality and hence be a source of anxiety in itself.73 Attentional processes may also lead to ignoring distress and hence to delays in help seeking or lack of adherence to treatment regimens. In the case of conversion symptoms, symptoms may arise and persist because of dissociative processes that divert attention from symptom and illness representations.35,74

Cultural Models and Somatic Syndromes

TABLE 3–1.

29

A typology of looping effects

Level

Description

1.

Attentional

Attention to sensations increases their salience and intensity, leading to greater and more focused attention.

2.

Emotional exacerbation (arousal-performance)

Emotional arousal interferes with functioning, leading to performance decrements, negative self-appraisal, and greater emotional arousal.

3.

Attributional

Attributing sensations to pathology leads to the conviction that one is ill, increasing the tendency to attribute sensations to pathology.

4.

Family system and Reactions of others to distress reinforce the interpersonal interaction experience and expression of distress.

5.

Help-seeking, health care services, iatrogenic

Availability of health care services and caregiving increases the tendency to seek care.

6.

Disability/avoidance

Disability sanctions the avoidance of unpleasant circumstances and hence reinforces disability.

7.

Political economic

Marketing of pharmaceuticals influences the availability of specific diagnostic labels and treatments, which are applied to patients who then become consumers of medications, increasing economic demand and encouraging further marketing.

Ways of coping with symptoms may inadvertently lead to exacerbations. For example, many people with symptoms of chronic fatigue may tend to reduce their activity and engage in prolonged bed rest, thereby leading to physical deconditioning and exacerbating symptoms of fatigue, weakness, and exercise intolerance.70 Similar behaviors can exacerbate other physiological systems, resulting in symptoms such as orthostatic dizziness. Personality and social factors interact with ways of coping.75 For example, rather than adopting a gradual and graded process of increasing their activity, some patients with chronic fatigue or pain may overexert themselves in initial efforts to push past their symptoms, giving rise to new or intensified symptoms. Social influences come into play when prevalent cultural models or the response of others suggest that such recurrent symptoms are signs of serious exacerbation or new injury and must be avoided.

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The social reinforcement of a specific bodily complaint may increase bodily attention, in effect, encouraging people to look for, notice, and label the sensation, to interpret it as worrisome, and to seek medical attention. Parental modeling of symptoms during childhood and current reinforcement contingencies (including verbal expressions of sympathy, release from responsibilities, and assistance given when sick) influence symptom reporting, even when life stressors and illness attitudes are statistically controlled.76,77 Labeling sensations in terms of psychological or somatic schemas itself is also shaped by reinforcement contingencies. 78 In chronic pain, the response of others may reinforce pain behavior and experience. Spouses’ positive attention to their partners’ display of pain can inadvertently increase reported pain, pain behaviors, and disability.79,80 Differences in spouse response may account for difficulties in coping with chronic pain and levels of disability.81 Such responses to social reinforcement contingencies can occur without conscious awareness. Social contingencies are also associated with specific roles and statuses. The “sick role,” described by Parsons, exempts the ill individual from certain responsibilities and offers him or her care and concern.82 These social responses may reinforce sick behavior. Again, this can occur unintentionally and outside of conscious awareness. Professional diagnostic practices are important elements in this process of social shaping of distress. The experience with repetition strain injury in Australia illustrates this social looping effect.83–86 Finally, there are larger institutional forces, including political economic considerations such as the structure of health insurance and compensation systems and the marketing of specific disease entities and treatments. All of these social factors give rise to what the philosopher Ian Hacking has called an ecosocial “niche.”87 Hacking pointed out that psychiatric diagnostic categories can become part of social looping effects in which a variety of contingencies reinforce the existence and prevalence of the disorder.88 The protean forms of hysteria or mass psychogenic illness described over the years are a prime example of this social looping effect. It is possible to describe hysteria at a sufficiently abstract or general level that it transcends specific cultural and historical forms. To do this, though, hysteria must be characterized not by its symptoms, which vary with cultural models and modes of expressing distress, but by some more general characteristic or index of underlying mechanism. Hacking described social looping effects in very broad terms as resulting from the existence of a social or “ecological” niche consisting of an available label, prescribed role, social institution, and economic factors that encourage patients and physician to populate this category. We need to understand this and make the links back to specific psychological processes to identify the points at which those social factors exert their influence on the individual through the dynamics of meaning in illness experience.

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Conclusion Increasing knowledge of the nature of cultural models and their influence on bodily experience has implications for research on somatic distress syndromes and for efforts to rethink the nosology of somatoform disorders.

EPIDEMIOLOGICAL RESEARCH Epidemiology and clinical diagnosis both assume an indexical relationship between symptom reports and underlying physiology and illness experience, but the relationship is embedded in and mediated by cognitive and social processes. Symptoms can exist in the absence of cultural models and can be elicited and counted by suitable questions and probes, but their recognition, salience, significance, and organization into syndromes reflects cultural models rather than purely physiological processes. Epidemiological research must be designed not simply to identify some putative universal configuration of somatic distress but to tease apart the psychophysiological and sociophysiological processes that contribute to somatic distress. Standard symptom indices do not canvas the wide range of symptoms found in diverse cultural groups, some of which may be important indicators of coexisting affective and anxiety disorders, others of which constitute significant health concerns in their own right. We can only accrue knowledge about cultural syndromes and explanations if we ask the right questions. We need to use expanded symptom inventories that canvas symptoms relevant to specific cultural contexts. We need more research on the ways in which culture and context shape the somatic clinical presentations of the range of psychiatric disorders. We need integrated epidemiological and ethnographic research, both in the community and the clinic, to examine the relationship between cultural idioms of distress and clinical syndromes. The extensive work on ataques de nervios in Latin populations is exemplary in this regard.48,49,89–91 We need to study the impact of introducing new labels and categories in specific social contexts. The history of repetition strain injury is a striking example of how changes in diagnostic fashion can interact with social stressors to give rise to a social looping effect that greatly increases the prevalence of a specific somatic distress syndrome.92

RESEARCH ON THE MECHANISMS OF SOMATIC DISTRESS SYNDROMES Looping effects are core mechanisms of psychopathology that can be studied in their own right. However, they require methods of study that go beyond self-report measures. Recent studies using functional brain imaging hold the prospect of allowing more direct study of attentional mechanisms and other processes that un-

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derlie implicit learning. Attributional processes have been studied with explicit questions but can also be elicited in indirect ways that may yield better measures of automatic thoughts and implicit associations. Coping strategies can be studied in laboratory analogues or in daily life with behavioral diaries or experiential sampling. All of these methods go beyond self-reports, which are close to the outcome of symptom reporting and may not capture mediating mechanisms.

EPISTEMOLOGY, POLITICS, AND PRAGMATICS OF SOMATIC DIAGNOSIS The category of somatoform disorders, based on symptom counts and the absence of medical explanation or the presumption of psychological mechanisms, has had limited utility in primary care and other medical settings where most patients with somatic concerns are seen.93 The somatoform disorders are part and parcel of a dualistic medical system that requires diagnoses for patients who fall through the cracks of biomedical diagnosis. The somatoform category serves a useful administrative and organizational function in general hospital psychiatry because the availability of these diagnostic labels ensures that everyone can get a diagnosis: idiopathic pain becomes pain disorder, unexplained symptoms become undifferentiated somatoform disorder, and so on. Psychiatric labeling of these conditions assigns clinical responsibility but does not necessarily indicate any increase in understanding or guide to effective therapeutics. Instead, the diagnosis of a somatoform disorder conveys psychiatric stigma, perplexes patients because it implies their problems are mental rather than physical, and justifies therapeutic nihilism on the part of clinicians. The existing classification of somatoform disorders has also not served to capture the important cultural variations in modes of somatic expression of distress, which do not reflect discrete disorders but rather the use of cultural idioms to signal concerns that are not only about bodily health but also are linked to social predicaments. The existence of the whole category of somatoform disorders is largely the consequence of a dualistic ontology and epistemology that is reflected in the structure of biomedical health care. The category may introduce new problems in health care systems not founded on this dualism. Exporting the somatoform disorders across cultures, therefore, seems to be a poor idea for several reasons: 1) it exports an ontological dualism that other systems of medicine may not have; 2) it confounds the notion of a cultural idiom of distress or mode of suffering with a disorder; and 3) it ignores the specificity of somatic symptoms and syndromes, which may make more sense to people in the clinical negotiation and which can guide the clinician in a symptom-focused approach to distress.

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RETHINKING THE NOSOLOGY OF SOMATOFORM DISORDERS In current nosology, somatoform disorders are defined in largely negative terms as “medically unexplained symptoms.” This label names a social predicament rather than a discrete syndrome or disorder and hence should really be classified as a V-code in DSM. The identification of somatoform disorders as a distinctive form of psychopathology rests on the assumption that there are specific psychological processes that give rise to symptoms or amplify distress and maintain help seeking and disability. However, the same processes of symptom perception and interpretation that influence somatic syndromes also affect help seeking and health care utilization more generally.94 Similarly, the same social and cultural factors that shape illness experience and expression in the somatoform disorders contribute to the wide variations in coping and adaptation to other medical and somatic conditions. This suggests that it may be helpful to develop a description of various dimensions of illness cognition, behavior, and interaction under the rubric of “psychological factors affecting medical conditions.”95 Much of what is currently diagnosed as a somatoform disorder would then be described as somatic symptoms or syndromes on Axis III (i.e., a medical condition), qualified by a description on Axis I of the various psychological and social factors that may be leading to symptom amplification (or minimization and denial), poor coping, excessive health care utilization, functional impairment, and disability. A revised nosology should make it possible to characterize these aggravating factors independently of the original causes or precipitants of somatic distress. Developing a separate scheme for psychological factors that affect medical conditions could serve the function of linking diagnosis to differential therapeutics, at the same time avoiding the negative effects of labeling such problems as discrete psychiatric disorders. Looping effects that create vicious circles of amplifying somatic preoccupation, distress, and disability could be made central to a revised nosology. A typology of looping effects could be keyed to specific interventions targeted at modifying attentional strategies, emotional arousal, reattributing symptoms, reducing catastrophizing, and improving coping with distress.96 Finally, there is a need for a social and cultural approach to the phenomenon of somatization that goes beyond the model of diseases and disorders. If the somatoform disorders reflect “abnormal illness behavior,” this is not a single construct or closely related family of constructs but a normative distinction that groups together a broad set of disparate conditions and predicaments on the basis of their contravening tacit medical or social norms for appropriate behavior when sick.97–99 Grouping these dimensions of illness behavior as a family of disorders justifies an approach to research that searches for intrinsic characteristics of patients and deflects attention from understanding how problematic behavior emerges out of interactions with clinicians and a health care system unable to respond to these common predicaments. An alternative approach based on identifying and mea-

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suring psychological and social factors, including interactional problems that modulate bodily experience, may have more utility for researchers, clinicians, and patients. This could be recognized in psychiatric nosology by creating a place for the assessment of “psychological and social factors affecting bodily condition.”

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57. Hinton D, Hinton S. Panic disorder, somatization, and the new cross-cultural psychiatry: the seven bodies of a medical anthropology of panic. Cult Med Psychiatry 2002;26:155–178. 58. Kirmayer LJ. Cultural psychiatry in historical perspective. In: Bhugra D, Bhui K, editors. Textbook of Cultural Psychiatry. Cambridge, UK: Cambridge University Press; 2007:3–19. 59. Nichter M. Idioms of distress: alternatives in the expression of psychosocial distress: a case study from South India. Cult Med Psychiatry 1981;5:379–408. 60. Low S. Embodied metaphors: nerves as lived experience. In: Csordas T, editor. Embodiment and Experience: The Existential Ground of Culture and Self. Cambridge, UK: Cambridge University Press; 1994:139–162. 61. Kirmayer LJ. The body’s insistence on meaning: metaphor as presentation and representation in illness experience. Med Anthropol Q 1992;6:323–346. 62. Kirmayer LJ. On the cultural mediation of pain. In: Shelemay K, Coakley S, editors. Pain and Its Transformations: The Interface of Biology and Culture. Cambridge, MA: Harvard University Press; 2007:363–401. 63. Kövecses Z. Metaphor and Emotion: Language, Culture, and Body in Human Feeling. Cambridge, UK: Cambridge University Press; 2000. 64. Salmon P, Dowrick CF, Ring A, Humphris GM. Voiced but unheard agendas: qualitative analysis of the psychosocial cues that patients with unexplained symptoms present to general practitioners. Br J Gen Pract 2004;54:171–176. 65. Salmon P, Ring A, Dowrick CF, Humphris GM. What do general practice patients want when they present medically unexplained symptoms, and why do their doctors feel pressurized? J Psychosom Res 2005;59:255–260. 66. Kirmayer LJ. Broken narratives: clinical encounters and the poetics of illness experience. In: Mattingly C, Garro L, editors. Narrative and the Cultural Construction of Illness and Healing. Berkeley: University of California Press; 2000:153–180. 67. Fletcher CM. Environmental sensitivity: equivocal illness in the context of place. Transcult Psychiatry 2006;43:86–105. 68. Kirmayer LJ. Mind and body as metaphors: hidden values in biomedicine. In: Lock M, Gordon D, editors. Biomedicine Examined. Dordrecht, Netherlands: Kluwer; 1988:57–93. 69. Raguram R, Weiss MG, Channabasavanna SM, Devins GM. Stigma, depression, and somatization in South India. Am J Psychiatry 1996;153:1043–1049. 70. Wessely S, Hotopf M, Sharpe M. Chronic Fatigue and Its Syndromes. Oxford, UK: Oxford University Press; 1998. 71. Looper KJ, Kirmayer LJ. Perceived stigma in functional somatic syndromes and comparable medical conditions. J Psychosom Res 2004;57:373–378. 72. Kirmayer LJ, Looper KJ. Hypochondriasis in primary care. In: Starcevic V, Lipsitt DR, editors. Hypochondriasis: Modern Perspectives on an Ancient Malady. New York: Oxford University Press; 2001:155–180. 73. Goldenberg JL, Pyszczynski T, Greenberg J, Solomon S. Fleeing the body: a terror management perspective on the problem of human corporeality. Pers Soc Psychol Rev 2000;4:200–218.

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74. Brown RJ, Schrag A, Trimble MR. Dissociation, childhood interpersonal trauma, and family functioning in patients with somatization disorder. Am J Psychiatry 2005;162:899–905. 75. Kirmayer LJ, Robbins JM, Paris J. Somatoform disorders: personality and the social matrix of somatic distress. J Abnorm Psychol 1994;103:125–136. 76. Schwartz SM, Gramling SE, Mancini T. The influence of life stress, personality, and learning history on illness behavior. J Behav Ther Exp Psychiatry 1994;25:135–142. 77. Whitehead WE, Crowell MD, Heller BR, Robinson JC, Schuster MM, Horn S. Modeling and reinforcement of the sick role during childhood predicts adult illness behavior. Psychosom Med 1994;56:541–550. 78. Lam K, Marra C, Salzinger K. Social reinforcement of somatic versus psychological description of depressive events. Behav Res Ther 2005;43:1203–1218. 79. Kremer EF, Sieber W, Atkinson JH. Spousal perpetuation of chronic pain behavior. Int J Fam Ther 1985;7:258–270. 80. Turk DC, Kerns RD, Rosenberg R. Effects of marital interaction on chronic pain and disability: examining the down side of social support. Rehab Psychol 1992;37:259– 274. 81. Thieme K, Spies C, Sinha P, Turk DC, Flor H. Predictors of pain behaviors in fibromyalgia syndrome. Arthritis Rheum 2005;53:343–350. 82. Parsons T. The Social System. Glencoe, IL: The Free Press; 1951. 83. Miller MH, Topliss DJ. Chronic upper limb pain syndrome (repetitive strain injury) in the Australian workforce: a systematic cross sectional rheumatological study of 229 patients. J Rheumatol 1988;15:1705–1712. 84. Hall W, Morrow L. ‘Repetition Strain Injury’: an Australian epidemic of upper limb pain. Soc Sci Med 1988;27:645–649. 85. Bammer G, Martin B. Repetition strain injury in Australia: medical knowledge, social movement, and de facto partisanship. Soc Probl 1992;39:219–237. 86. Hopkins A. The social recognition of repetition strain injuries: an Australian/American comparison. Soc Sci Med 1986;30:365–372. 87. Hacking I. Mad Travelers: Reflections on the Reality of Transient Mental Illnesses. Charlottesville, VA: University Press of Virginia; 1998. 88. Hacking I. The Social Construction of What? Cambridge, MA: Harvard University Press; 1999. 89. Lewis-Fernandez R, Guarnaccia PJ, Martinez IE, Salman E, Schmidt A, Liebowitz M. Comparative phenomenology of ataques de nervios, panic attacks, and panic disorder. Cult Med Psychiatry 2002;26:199–223. 90. Guarnaccia PJ, Rogler LH. Research on culture-bound syndromes: new directions. Am J Psychiatry 1999;156:1322–1327. 91. Interian A, Gara MA, Diaz-Martinez AM, Warman MJ, Escobar JI, Allen LA, Manetti-Cusa J. The value of pseudoneurological symptoms for assessing psychopathology in primary care. Psychosom Med 2004;66:141–146. 92. Kirmayer LJ. Rhetorics of the body: Medically unexplained symptoms in sociocultural perspective. In: Ono Y, Janca A, Asai M, Sartorius N, editors. Somatoform Disorders—A Worldwide Perspective. Tokyo: Springer-Verlag; 1999:271–286.

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93. Mayou R, Kirmayer LJ, Simon G, Kroenke K, Sharpe M. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162:847–855. 94. Frostholm L, Fink P, Christensen KS, Toft T, Oernboel E, Olesen F, Weinman J. The patients’ illness perceptions and the use of primary health care. Psychosom Med 2005;67:997–1005. 95. Fava GA, Fabbri S, Sirri L, Wise TN. Psychological factors affecting medical condition: a new proposal for DSM-V. Psychosomatics 2007;48:103–111. 96. Looper KJ, Kirmayer LJ. Behavioral medicine approaches to somatoform disorders. J Consult Clin Psychol 2002;70:810–827. 97. Kirmayer LJ, Looper KJ. Abnormal illness behaviour: physiological, psychological and social dimensions of coping with distress. Curr Opin Psychiatry 2006;19:54–60. 98. Pilowsky I. Abnormal illness behaviour. Br J Med Psychol 1969;42:347–351. 99. Pilowsky I. Abnormal Illness Behaviour. West Sussex, UK: John Wiley and Sons; 1997.

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4 INFLUENCE OF CULTURAL AND SOCIAL FACTORS ON THE EPIDEMIOLOGY OF IDIOPATHIC SOMATIC COMPLAINTS AND SYNDROMES Javier I. Escobar, M.D., M.S. Oye Gureje, Ph.D., D.Sc., FRCPsych

There seems to be a universal tendency to experience and communicate psychological distress in the form of physical symptoms and seek medical attention for them.1 In most cultures, these complaints and syndromes tend to be associated with increased medical visits, unnecessary medical tests, and the performance of

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Escobar JI, Gureje O: “Influence of Cultural and Social Factors on the Epidemiology of Idiopathic Somatic Complaints and Syndromes.” Psychosomatic Medicine 69:841–845 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission. Partially supported by Grant P20MH074634–01 from the National Institute of Mental Health.

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procedures that may result in iatrogenic complications.2,3 There are many terms used in the literature to label these somatic presentations. These include “somatization symptoms,” “unexplained symptoms,” “medically unexplained symptoms,” “functional somatic symptoms,” “somatic presentations,” “idiopathic physical symptoms,” and many others. The association of these symptoms with psychiatric disorders follows the frequent coexistence of both types of phenomena and the evidence for psychogenesis in some instances. However, these symptoms most frequently arise spontaneously or stem from rather obscure, unknown causes. Moreover, what distinguishes these patients from others is not the symptoms per se but how they interpret them. For the purpose of this review, we felt it appropriate to use “idiopathic somatic complaints and syndromes” (ISCS) instead of some of the other terms listed because many of the international studies discussed herein elicited the presence of physical symptoms that seemed to be medically unexplained but without clear reference to their etiology or pathophysiology.4 Besides bringing some conceptual clarity to the field, invoking the “idiopathic” label in this instance may fit current thinking in the psychosomatic field, such as the distinction of “neuropathic,” “inflammatory,” “nociceptive,” and “idiopathic” pain.5 In this selective review, we examine how these symptom presentations are distributed in different countries, cultures, and ethnic groups, and we assess the impact of social and cultural factors on their form, frequency, and correlates. The main question we are trying to address is whether there are consistent and meaningful cultural differences in type and frequency of ISCS. In comparative studies, there is a need to clarify what exactly is being measured and determine whether these studies are measuring the same thing. There is also a need to examine whether there is any evidence that these ISCS represent hidden psychopathology or serve a symbolic function in some cultures (idioms of distress). Finally, on the basis of this review, we make some recommendations for future classification of these syndromes, in particular, how empirically validated cultural/social factors may be reflected in future diagnostic systems such as the fifth edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-V).

Brief History ISCS of presumed psychological origin have always mystified the medical establishment and taken new forms as cultures evolve and medical paradigms shift.6 Psychiatric syndromes with outstanding somatic manifestations, such hysteria and hypochondriasis, were key syndromes in traditional psychopathology and remained influential in medical discourse at the turn of the 20th century. As reviewed by Merskey and Mai,7,8 the idea that psychological processes are involved in certain somatic experiences seems to have ancient origins but waxed and waned periodi-

Influence of Cultural and Social Factors on Somatic Complaints and Syndromes 43 cally. In the 17th century, Sydenham was reputed to have ascribed not only pain and convulsions but diarrhea and dropsy to disturbance of the mind.9 In the mid19 th century, Briquet described a syndrome of multiple somatic symptoms to which he gave the name “hysteria.”10 Briquet gave an extensive clinical description of the syndrome, situating its origin in the brain and associating it with young women. Rightly or wrongly, Stekel11 has been credited with the coinage of the term “somatization,” but its entry into popular medical discourse is probably due to the work of Lipowski in the mid- to late-20th century.12 By the time “somatization” became a full diagnostic category in psychiatric classificatory systems, an extensive body of research, principally conducted in tertiary care settings of North America, had produced empirical evidence for the utility of its forebear, hysteria.13,14

Phenomenology The different symptom thresholds proposed throughout the years to elicit these syndromes, such as somatization disorder (SD), abridged somatization (AS), multisomatoform disorder, and other syndromes rely mainly on a number of symptoms presented.15 Psychological causation or modulation as well as behavioral and attitudinal aspects of these syndromes have been neglected in recent diagnostic systems, possibly because they are difficult to define operationally. In an influential book, McHugh and Slavney stated that somatic presentations (hysteria in this instance) “is not something the patient has; it is something the patient does; that is, it is a behavior.”16 Some useful models to practically dissect these ambiguous somatic syndromes have been recently proposed. For example, Brown separated these symptoms according to three explanatory themes, namely, “dissociation, conversion, and somatization.”17 Merskey and Mai distinguished two types of somatic symptom presentations.7 The first comprises symptoms, such as unexplained pain and “functional” cardiovascular/gastrointestinal symptoms, which are involuntary, automatic, related to autonomic arousal, and manifest in temporal relationship to the experience of “stress” or jointly with depression/anxiety syndromes. This type seems particularly common in primary care. The other and more ambiguous set depends on thoughts, embodied intentions, or ideas that are not recognized or acknowledged, expressed as unexplained neurological symptoms. This subtype may represent the more severe, polymorphous, treatment-refractory syndromes that are more likely to be seen in specialty mental health environments but are also seen in medical and surgical tertiary care centers. Although these models make sense intuitively, they have not been assessed in systematic studies. A recent European study showed that physical and psychological complaints are ubiquitous from an early age and that they seem to follow separate paths regarding their expression, evolution, and recognition.18

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Psychiatric Nosologies and ISCS Despite the common joint occurrence of psychological and physical symptoms, patients with ISCS seem to focus selectively on the physical component and seem reluctant to accept a psychological etiology and even less a psychiatric diagnosis. This confronts clinicians with the often difficult decision of whether or not to attach a psychiatric label to a person with ISCS. Modern psychiatric nomenclatures, such as DSM-IV 19 and International Classification of Disease (ICD)-10,20 have relegated somatic phenomena to a secondary level, and classify ISCS of presumed psychological origin under the heading of “somatoform disorders”—a category that is hierarchically inferior to other categories included in these nosologies (e.g., mood disorders). Although the creation of the somatoform category has been lauded as a nosological advancement by some investigators, in the “real world,” patients with ISCS rarely fit neatly into the taxonomies provided by the DSM and ICD systems. Even when somatoform criteria are met, there is also significant overlap with several other psychiatric syndromes, a reminder that nosologies are still imperfect and in need of continuous distillation. In classifying ISCS, the problems in applying current diagnostic criteria in primary care and community studies (e.g., the restrictive quality of categorical diagnoses that would leave out many of the “cases”) led investigators in this field to propose the use of broad, dimensional categories as an alternative for research.15,21,22 For example, in the late 1980s, the senior author proposed an abridged construct of somatization,15 which has been found of value for international comparative studies. Also, in primary care, rather than categories, the use of dimensional constructs and concepts of somatization seems to have better utility.21,22 It would seem from current literature that there are two main dimensions, which may have practical value; one dimension is characterized by high levels of physical symptoms (somatization), whereas the other dimension is characterized by somatic amplification (hypochondriasis or health anxiety). In our view, this dimensional approach should be taken into account for future nosological revisions.

Epidemiology Worldwide, a large majority of the comparative surveys that examined ISCS have consisted mainly of counts of physical symptoms with some effort made to rule out medical explanations.23–25 In these studies, the presence of high levels of ISCS has been generally derived from physical symptom inventories included in instruments, such as the Symptom Checklist 90 (SCL-90), General Health Questionnaire (GHQ), and particularly the Diagnostic Interview Schedule (DIS) and the Composite International Diagnostic Interview (CIDI). ISCS have been often articulated as either “full” or “abridged” somatization disorder. Problems with these

Influence of Cultural and Social Factors on Somatic Complaints and Syndromes 45 studies include variations in key instruments, ways of survey administration, format of answers, and the reliance on lifetime rather than current symptoms. In general, ISCS have been reported to be more common among females, individuals from lower socioeconomic strata, and, in the United States at least, among people from certain ethnic groups, such as Latinos. Also, the comorbidity of ISCS and psychiatric syndromes, such as depression, has been well documented for most cultures and ethnic groups, although there seems to be cross-cultural variation in frequency and severity of the associated physical symptoms.

General Populations Studies in the United States, Puerto Rico, Germany, and Italy found lifetime prevalence rates of full SD ranging from 0.1% in the United States26 to 0.8% in Germany,27 whereas lifetime rates of AS ranged between 5.6% in Germany27 and 19% in Puerto Rico. 23 Much larger prevalence rates have been reported for more broadly defined ISCS. For example, 22% of the general population in Germany reported at least one unexplained physical symptom leading to severe impairment,27 and in Switzerland, 80% of young adults reported sleep disorders, backache, headache, and stomach or bowel complaints.18 However, these studies included various somatization criteria (ICD, DSM-III-R,28 DSM-IV), different constructs, and concepts, and they used different methodologies for assessment. Unfortunately, some of the most recent, large-scale, epidemiological studies, such as the National Epidemiologic Survey of Alcohol and Related Conditions (NESARC), either did not assess unexplained physical symptoms at all or, such as the World Mental Health Surveys, assessed only chronic pain complaints,29 possibly due to the time and effort it takes to probe through long physical symptom inventories.

Primary Care The primary care setting has been dubbed the “de-facto mental health system,” and because this is more readily available across cultures than the more formal mental health system, comparative international studies have often taken place there. Studies in primary care are also of particular importance in regard to ISCS because physical symptoms at this level can be taken to have clinical importance to the person experiencing them. Overall, it has been estimated that, for as many as two-thirds of patients presenting to primary care, no allopathic disease entity can be differentially diagnosed and unequivocally established as the principal determinant of a given patient’s presenting somatic complaints.30 In the United States, our group reported a 3% prevalence of SD and a 20% prevalence of AS in patients presenting to primary care.31 In this study, immigrants to the United States seemed to have higher rates of ISCS than the U.S.-born residents. We also found that about

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20% of primary care patients had high levels of ISCS and that 75% of them met the criteria for a major psychiatric disorder, leading us to posit that ISCS may be the most typical way for common psychiatric disorders, such as depression and anxiety, to manifest in primary care. A study in Spain estimated that about 1/1,000 of the population presenting to outpatient clinics met the criteria for full SD and about 20% met the criteria for AS. 32 An international study sponsored by the World Health Organization (WHO) that took place in 14 different countries examined somatic symptoms as well as various concepts of somatization in primary care and how these related to depression and other syndromes.22,29,33,34 This study found that ISCS—defined as SD or AS—were very common (range =53%–65%). Denial of psychiatric symptoms differed across sites with rates ranging from 3% in Brazil to 26% in Berlin. No major differences were noted across countries when somatization was defined as either denial of psychological symptoms or reporting of medically unexplained somatic symptoms. However, when somatization was defined according to presenting symptoms, they found greater variation among the centers. An important observation of this study was confirming that reports on lifetime somatic symptoms are unstable, particularly when somatic symptom thresholds are high (SD). Lower symptom counts (AS) fared better, but half of the symptoms reported at the initial interview were still forgotten 1 year later.34 According to this research, because diagnoses based on lifetime recall seem to rest on an unreliable foundation, the use of current rather than lifetime somatic symptoms should be considered for future endeavors. An important but poorly studied methodological issue is whether or not reported differences in rates of somatic presentations reflect “culture” as commonly conceptualized or, rather, the nature in which the patient-provider interaction is conducted. ISCS may thus reflect the availability of particular health services in a given region. An indication that this may be the case stems from other findings of the previously cited WHO collaborative study showing that variation in the rates of somatization across sites reflects the way in which services were organized and provided in the clinics studied. Thus, there is some evidence that there are fewer “somatizers” in settings where more personalized type of care is common than in those where it is rare.22

Culture-Specific Somatic Symptoms? Clinical presentations dominated by physical symptoms have been suggested to represent “idioms of distress” and lay explanations embedded in culture concerning the origin of behavioral symptoms may play a relevant role in their form and intensity. These variations in symptom presentation are likely the result of the interaction of multiple factors within cultural contexts that affect how individuals identify and classify bodily sensations, perceive illness, and seek medical attention. Because physical symptoms are easy to scrutinize, they provide a useful construct

Influence of Cultural and Social Factors on Somatic Complaints and Syndromes 47 for international comparison. Unfortunately, comparative studies have used different methodologies for symptom assessment and symptom thresholds. Assessment strategies have varied widely, and the use of lifetime instead of current ISCS makes results of many studies questionable. According to the ICD-10 manual, the most common ISCS worldwide are gastrointestinal complaints and abnormal skin sensations. However, the type of symptoms representing “idioms of distress” may vary across cultural groups. In a review of the literature on cross-cultural aspects of somatization performed by the senior author, it was found that, in Latin America and the Caribbean, a repertoire of ISCS including dissociative features (trance, possession states) such as ataque de nervios, susto, el espanto, el duende and other incubi, and mal de ojo have been described for many years and that high levels of ISCS have also been reported among Latin American patients with depression.3 The review also found that commonly reported somatic symptoms in Africa and India seemed to be different from those in Europe and the Americas. For example, common symptoms in Africa were “feeling of heat,” “peppery and crawling sensations,” and “numbness,” and in India, they included “burning hands and feet” and “hot, peppery sensations in head.”3 In western countries, such as the United States, Canada, and Europe, there also seems now to be a tendency for patients to present with clusters suggestive of immunologically based disorders.2,35 The evidence, therefore, suggests that the type of somatic symptoms presented may vary across cultures. On the other hand, when identical ascertainment tools have been used, there are only very minimal and, albeit, inconsistent differences across cultures in regard to the frequency of ISCS. Thus, other than a tendency for much higher rates in Latin American sites, the WHO collaborative primary care study found no consistent differences in rates between sites in regard to the occurrence of somatization, hypochondriasis, or pain syndromes, however each of these was defined.22

Type of Symptoms and Psychopathology Unexplained physical symptoms mimicking neurological disease (previously called “pseudoneurological”) seem to have a long tradition in psychopathology. They were the focus of the original construct of hysteria/Briquet’s syndrome.14 Studies employing cluster analytic methods have shown that high levels of these symptoms are a reliable marker for severe psychopathology. Thus, patients reporting high levels of neurological symptoms seem more likely than patients with other physical symptoms to meet the criteria for AS and SD as well as other Axis I disorders and to score higher on dimensional measures of depression, anxiety, and physical functioning. In addition, these patients are much more likely to meet the criteria for culturally related syndromes, such as ataque de nervios.36 A factor analytic study of somatization symptoms in a large primary care sample in Ibadan, Nigeria found that the factor with the highest Eigen value loading included a diagnostically im-

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portant group of neurological (or conversion) symptoms, suggesting that these symptoms may have broad cross-cultural diagnostic utility.37 We believe that the presence of high levels of unexplained neurological symptoms should be taken into account in new classifications systems.

Somatic Symptom Clusters Naturally occurring somatic symptom clusters have been characterized in community studies using data from the Epidemiologic Catchment Area Study (ECA) and the Puerto Rican Epidemiologic Survey employing statistical clustering techniques. However, a “unique” somatic symptom factor that included abdominal pain, nausea, vomiting, excessive gas, dyspnea, chest pain, palpitations, unusual spells, amnesia, paralysis, dizziness, fainting, and muscle weakness was found exclusively among Puerto Rican respondents.38 Interestingly, the clinical manifestations of ataque de nervios (headache, trembling, heart palpitations, stomach disturbances, a sensation of heat rising to the head, numbness of extremities, and at times, pseudoseizures, fainting, and unusual spells) look strikingly similar to those symptoms included in the symptom cluster derived from the epidemiological sample in Puerto Rico.39

Conclusions In responding to the specific queries posed at the outset, this brief review has shown the following: 1. Although there may be differences across cultures in type and frequency of ISCS, methodological issues do not allow firm conclusions on this because comparative studies may not have been measuring the same thing (lifetime versus current symptoms, different instruments, different symptom thresholds, different interviewing formats, etc.). 2. Culture influences symptom formation. In most cultures, ISCS accompany psychopathology most of the time, and psychopathology is often relegated to a secondary level due to stigma and other factors. However, in most instances, psychopathology can be elicited on proper scrutiny. 3. ISCS may serve a symbolic function in some cultures more than they do in others and, in that instance, they are likely to represent idioms of distress. However, current evidence is not conclusive about this. 4. In making recommendations for future classification of ISCS, cognizance should be taken of the widespread dissatisfaction with the current somatoform categories in DSM-IV and ICD-10. The inconsistency of invoking etiology at times (as in conversion disorder), but otherwise pretending to be descriptive or

Influence of Cultural and Social Factors on Somatic Complaints and Syndromes 49 “atheoretical” (as in SD), and the ignorance of physiological influences and the contributions of psychosomatic research have been highlighted.40 A number of investigators have proposed the elimination of the SD category altogether from Axis I in DSM-V and recommended placing them in Axis III.41–43 We believe, however, that a dimensional approach should remain in Axis I at least for high levels of somatic symptoms (somatization) and somatosensory amplification (hypochondriasis or health anxiety). The specific thresholds would have to be carefully defined, and only current symptoms should be included to improve reliability. In addition, other behavioral/attitudinal features should be incorporated into the criteria. 5. Regarding social and cultural factors in DSM-V, several recommendations related to culture and psychiatric diagnosis have already been made elsewhere.44 We wish to add the following caveats: a. The ethnicity concept has to be defined more precisely. For example, ethnicity can be characterized according to the group to which that person most closely relates, their ancestry, the language spoken by their parents, and the language most commonly spoken at home. b. In analyses of ethnic influences on ISCS, we recommend that these elements be entered as discrete variables rather than one overarching “ethnic group” variable. c. Mexican-Americans, Puerto Ricans, Cubans, South Americans, and other Latino populations in the United States should not continue to be blended into a “Hispanic” group for the sake of convenience, because research is showing significant differences among these groups in prevalence of DSM-IV disorders, use of services, and other outcomes. d. Recommendations on sociocultural elements in diagnosis should be research based and testable. Much needed research in this area should be articulated in a more practical, hierarchical fashion so that these goals can become attainable in stages. At the current level of knowledge, a well-defined research program is needed to support and justify a cultural axis with practical utility or scientific validation. e. Efforts should be made to provide crisp, practical ethnic/cultural examples, including illustrative clinical vignettes in key areas. The use of brief, precise, illustrative appendices may be helpful. Meaningful cultural annotations and a glossary of cultural terms that are applicable in daily clinical practice and not limited to infrequently encountered syndromes (culture-bound) would be highly desirable. Of practical value for practitioners would be explanations of words used in different cultures to express signs and symptoms of specific DSM disorders and information about cultural assumptions regarding psychologically based ISCS and related behaviors and impairments.

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In closing, we strongly recommend that in developing and assessing new diagnoses relevant to ISCS, those working in the mental health field should maintain a close collaboration with many other international colleagues as well as members of key disciplines, such as general health and primary care.

References 1. Murphy M. Somatization: embodying the problem. BMJ 1989;293:328–332. 2. Payer L. Medicine and Culture. New York: Henry Holt and Co.; 1988. 3. Escobar JI. Transcultural aspects of dissociative and somatoform disorders. Psychiatr Clin North Am 1995;18:555–569. 4. Escobar JI, Interian A, Diaz-Martinez A, Gara M. Idiopathic physical symptoms: a common manifestation of psychiatric disorders in primary care. CNS Spectr 2006;11:201–210. 5. Moeller Gorman R. The body in pain. Proto, Massachusetts General Hospital Dispatches from the Frontiers of Medicine [serial online]. Spring 2007;23–7. Available at: http://www.mghproto.com/issues/2007_spring/ body_pain_print.html. Accessed October 17, 2007. 6. Shorter E. From the Mind into the Body: The Cultural Origin of Psychosomatic Symptoms. New York: Free Press, 1994. 7. Merskey H, Mai F. Somatoform and conversion disorders: a review. In: Maj M, Akiskal HS, Mezzich JE, Okasha A, editors. Somatoform Disorders: WPA Series, Evidence and Experience in Psychiatry. Vol 9. London: John Wiley and Sons, Ltd.; 2005:1–22. 8. Mai F, Merskey H. Briquet’s treatise on hysteria. Arch Gen Psychiatry 1980;37:1401– 1405. 9. Sydenham T. Discourse concerning hysterical and hypochondriacal distempers. In: Dr. Sydenham’s Complete Method of Curing Almost All Diseases, and Description of Their Symptoms, to Which Are Now Added Five Discourses of the Same Author Concerning Pleurisy, Gout, Hysterical Passion, Dropsy and Rheumatism. 3rd ed. London: Newman and Parker; 1697. 10. Briquet P. Traité clinique et Thérapeutique de l’Hystérie. Paris: Baillière; 1859. 11. Stekel W. The Interpretation of Dreams. New York: Liveright; 1943. 12. Lipowski ZJ. Somatization: the concept and its clinical application. Am J Psychiatry 1988;145:1358–1368. 13. Guze SB, Woodruff RA, Clayton PJ. A study of conversion symptoms in psychiatric out-patients. Am J Psychiatry 1971;128:643–646. 14. Bibb RC, Guze SB. Hysteria (Briquet’s syndrome) in a psychiatric hospital: the significance of secondary depression. Am J Psychiatry 1972;129:224–228. 15. Escobar JI, Burnam A, Karno M, Forsythe A, Golding J. Somatization in the community. Arch Gen Psychiatry 1987;44:713–718. 16. McHugh PR, Slavney PR. The Perspectives of Psychiatry. Baltimore, MD: The Johns Hopkins University Press; 1998.

Influence of Cultural and Social Factors on Somatic Complaints and Syndromes 51 17. Brown RJ. Psychological mechanisms of medically unexplained physical symptoms. Psychol Bull 2004;130:739–812. 18. Ajdacic-Gross V, Horvath S, Canjuga M, Gamma A, Angst J, Rössler W, Eich D. How ubiquitous are physical and psychological complaints in young and middle adulthood? A longitudinal perspective. Soc Psychiatry Psychiatr Epidemiol 2006;41:881–888. 19. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC: American Psychiatric Association; 1994. 20. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva, Switzerland: World Health Organization, 1992. 21. Kirmayer LJ, Robbins JM. Three forms of somatization in primary care: prevalence, cooccurrence and sociodemographic characteristics. J Nerv Ment Dis 1991;79:647–655. 22. Simon GE, Von Korff M, Piccinelli M, Fullerton C, Ormel J. An international study of the relation between somatic symptoms and depression. N Engl J Med 1999;341:1329– 1335. 23. Canino GJ, Bird HR, Shrout PE, Rubio-Stipe M, Bravo M, Martinez R, Sesman M, Guevara LM. The prevalence of specific psychiatric disorders in Puerto Rico. Arch Gen Psychiatry 1987;44:727–735. 24. DeWaal WM, Arnold IA, Eekhof JAH, Van Hemert AM. Somatoform disorders in general practice. Br J Psychiatry 2004;184:470–476. 25. Kirmayer LJ, Groleau D, Looper KJ, Dao MD. Explaining medically unexplained symptoms. Can J Psychiatry 2004;49:663–672. 26. Swartz M, Landerman R, George L, Blazer D, Escobar JI. Somatization disorder. In: Regier D, Robins LN, editors. Psychiatric Disorders in America. New York: The Free Press; 1990:220–237. 27. Hiller W, Rief W, Braler E. Somatization in the population: from mild bodily misperceptions to disability symptoms. Soc Psychiatry Psychiatr Epidemiol 2006;41:704– 712. 28. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed Revised. Washington, DC: American Psychiatric Association; 1987. 29. Gureje O, Von Korff M, Kola L, Demyttenaere K, He Y, Posada-Villa J, Lepine JP, Angermeyer MC, Levinson D, de Girolamo G, Iwata N, Karam A, Luiz Guimaraes Borges G, de Graaf R, Browne MO, Stein DJ, Haro JM, Bromet EJ, Kessler RC, Alonso J. The Relation Between Multiple Pains and Mental Disorders: Results from the World Mental Health Surveys. Pain 2008;135:82–91. 30. Gureje O. What can we learn from a cross-national study of somatic distress? J Psychosom Res 2004;56:409–412. 31. Escobar JI, Waitzkin H, Gara M, Holman A, Cohen-Silver R. Abridged somatization: a study in primary care. Psychosom Med 1998;60:466–472. 32. Garcia-Campayo J, Lobo A, Echeverria J, Campos R. Three forms of somatization presenting in primary care settings in Spain. J Nerv Ment Dis 1998;186:554–560. 33. Gureje O, Simon G, Ustun TB, Goldberg DP. Somatization in cross-cultural perspective: a World Health Organization study in primary care. Am J Psychiatry 1997;154:989–995.

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34. Simon GE, Gureje O. Stability of somatization disorder and somatization symptoms among patients in primary care. Arch Gen Psychiatry 1999;56:90–95. 35. Shorter E. From Paralysis to Fatigue. New York: Free Press; 1992. 36. Interian A, Guarnaccia PJ, Vega WA, Gara M, Like RC, Escobar JI, Diaz-Martinez A. The relationship between ataque de nervios and unexplained neurological symptoms: a preliminary analysis. J Nerv Ment Dis 2005;193:32–39. 37. Gureje O, Obikoya B. Somatization in primary care: pattern and correlates in a Nigerian clinic. Acta Psychiatr Scand 1992;86:223–227. 38. Rubio-Stipec M, Shrout PE, Bird H, Canino G, Bravo M. Symptom scales of the diagnostic interview schedule: factor analytic results in Hispanic and Anglo samples. Psychol Assess 1989;1:30–34. 39. Guarnaccia PJ. Ataques de nervios in Puerto Rico: culture-bound syndrome or popular illness? Med Anthropol 1993;15:157. 40. Martin RD. The somatoform conundrum: a question of nosological values. Gen Hosp Psychiatry 1999;21:177–186. 41. Sharpe M, Mayou R. Somatoform disorders: a help or hindrance to good patient care. Br J Psychiatry 1994;184:465–467. 42. Mayou R, Kirmayer LJ, Simon G, Kroenke K, Sharpe M. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162:847–855. 43. Kroenke K. Physical symptom disorder: a simpler diagnostic category for somatization spectrum disorders. J Psychosom Res 2006;60:335–339. 44. Alarcon RD, Alegria M, Bell CC, Boyce C, Kirmayer LJ, Lin KM, Lopez S, Üstün TB, Wisner KL. Beyond the funhouse mirrors: research agenda on culture and psychiatric diagnosis. In: Kupfer D, First MB, Regier DA, editors. A Research Agenda for DSM-V. Washington, DC: American Psychiatric Press; 2003:219–281.

5 ARE SOMATOFORM DISORDERS CHANGING WITH TIME? The Case of Neurasthenia in China Sing Lee, FRCPsych Arthur Kleinman, M.D.

Categories are the outcomes of historical development, cultural influence, and political negotiation. Psychiatric categories—though mental illness will not allow us to make of it whatever we like—are no exception. Arthur Kleinman, Rethinking Psychiatry (1988, p. 12)

Although it is not widely recognized, the professional classification of mental illness is subject to no less sociocultural influence than the symptoms or experience of the illness itself.1–3 This is partly because mental disorders are complex in etiol-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Lee S, Kleinman A: “Are Somatoform Disorders Changing With Time? The Case of Neurasthenia in China.” Psychosomatic Medicine 69:846–849 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission.

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ogy and dimensional in nature (e.g., normal sadness versus depression; existential angst versus generalized anxiety disorder). The lack of biological markers that precludes an etiological diagnosis is another recognized reason. These facts about diagnostic categories in psychiatry produce tensions with practical needs in clinical practice and professional training that focus on “making the correct diagnosis.” Nonetheless, it is sobering to remember that physical diseases that are complex in manifestations and etiology (e.g., autoimmune diseases) or dimensional in nature (e.g., hypertension) do not run into the same amount of nosological and diagnostic controversies as mental disorders do. Like mental disorders, many well-recognized physical diseases do not have clear-cut biological markers (e.g., epilepsy, trigeminal neuralgia, and irritable bowel syndrome). This suggests that the classification and definition of mental disorders may be especially susceptible to nonscientific influences and may serve diverse purposes for different parties. Yet we should not forget that scientific categories (and with them measurement devices and the findings they produce) also change and can be influenced by economics, politics, and culture.4 From this perspective, the professional transformation of neurasthenia in China illustrates such a connection between psychiatric diagnosis and social change.1

Origin of Somatoform Disorder in DSM-III Despite the frequent reference to “somatization” among Chinese people in the Western psychiatric literature, traditional Chinese medicine does not contain an equivalent conceptual category to describe the loosely understood phenomenon in which patients preferentially present their distress as somatic rather than psychic symptoms.5 Specifically, the ontological view of disease that certain symptoms are more real than others, or “core” rather than “peripheral” (as is used in the Diagnostic and Statistical Manual of Mental Disorders (DSM) configuration of symptom hierarchy, viz., operationally defining one to two mandatory symptoms as pathognomonic and treating the other symptoms as less specific and optional), is nonexistent in traditional Chinese medicine. Because traditional Chinese medicine was the source of knowledge about health and medicine for Chinese people over the millennia, its nondualistic approach to symptoms was also the way that Chinese culture has addressed this issue. As a result, the conventional Western cultural approach embodied in DSM was foreign to Chinese society (as it was to pre-DSM-III6 Western psychiatric nosology, such as DSM-II7). It was also alien to the clinical cognitive schema of Chinese psychiatrists. Instead, the latter treated varying clusters of somatic and psychic symptoms as occurring simultaneously in the conceptualization of diseases including neurasthenia (shenjing shuairuo, a culture-syntonic term that means “weakness of nerves”) (Figure 5–1). Somatoform disorder, which was first created in DSM-III, marginalized somatic distress and gave primacy to psychological symptoms in the configuration of

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Are Somatoform Disorders Changing With Time?

Weakness symptoms

Emotional symptoms

Sleep disturbance

Excitement symptoms

Nervous pain

FIGURE 5–1.

Chinese symptom configuration of neurasthenia.

mood and anxiety disorders. There it was a residual category that should only be diagnosed when all shades of other Axis I disorders (usually with core psychic symptoms) were excluded. Unlike the Chinese conceptualization of neurasthenia, somatoform disorder should have a dominant somatic symptom. Even if mood and other nonsomatic symptoms are present, they should not be severe enough to reach the diagnostic threshold of the anxiety and depressive disorders (Figure 5–2). Thus defined, the category of somatoform disorder was new to the Chinese epistemological theory of disease.5

Origin of Neurasthenia in China The term neurasthenia was revived by the New York neurologist George Beard in 1869 to denote a variable syndrome of lassitude, poor concentration, headache,

Somatic Presentations of Mental Disorders

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Muscular aches and pains Tension headaches

Irritability

Dyspepsia

FIGURE 5–2.

Dizziness FATIGUE OR WEAKNESS

Inability to relax

Sleep disturbance

Diagnostic and Statistical Manual of Mental Disorders symptom

configuration of neurasthenia as a somatoform disorder. sleep disturbance, and more than 50 other symptoms. The term steadily acquired popularity with both physicians and the general public in North America up to the early years of the 20th century. The term was probably introduced to China from Japan in the early 1900s and is rendered semantically into the Chinese language as shen jing shuai ruo. In Japan, the term neurasthenia is translated as shinkei suijaku and gained currency after the Meiji period (1868–1912). Although this is pronounced differently from shenjing shuairuo, the two terms are ideographically identical. In all likelihood, the written Chinese term was adopted from Japanese sources.1 Shen may be translated as “spirit” and is emblematic of vitality, the capacity of the mind to form ideas, and the desire of the person to live life. Jing originally refers to the meridians or channels that carry qi (“vital energy”) and xue (“blood”) through the body. Conceptually, shenjing is treated by both Chinese physicians and

Are Somatoform Disorders Changing With Time?

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lay people as one term that may mean “nerve,” “neurological,” or “nervous.” Shenjing can decline (shuai) and weaken (ruo) after nervous excitement, resulting in various symptom complexes. This connotation of nervous weakness in shenjing shuairuo resonates with a number of ancient conceptual categories that signify weakness (xu) or the deficiency of a vital essentialism in traditional Chinese medicine, such as the depletion of qi that follows overstraining or the stagnation of qi when one overly worries. The term is readily distinguishable from the folk expression of jingshen bing, which refers to insanity and promises severe social stigma. Subjects with shenjing shuairuo are, ipso facto, not deranged in mind and not dangerous to others.4 As a euphemistic term, shenjing shuairuo is easily graspable by Chinese people, including doctors, to connote “excessive stress in a susceptible person” and/or “nervous disposition” in addition to “neurological weakness.” The fact that it is also nonstigmatizing allows it to infiltrate social relations and to encourage private distress to be elaborated into a public form. Regarding its professional definition, shenjing shuairuo included a variety of symptoms much like those described by Beard.2

Three Periods of Transformation Under the joint influence of DSM-III and other sociocultural forces, the Chinese concept of neurasthenia has transformed in remarkable ways that have brought it into conformity with DSM-III-based epistemology. The process of transformation can be divided into three main periods during which the disease acquired a different identity.

PREREFORM PERIOD (BEFORE 1980)— “NEURASTHENIA AS IT IS” In a review of psychiatric epidemiological surveys in the early 1980s, Cheung found that neurasthenia was by far the most common neurotic disorder in China.8 In the clinical setting, as many as 80%–90% of Chinese psychiatric outpatients received the diagnosis of neurasthenia from the 1950s to 19809—indicating that the disease was a broad category for nearly all nonpsychotic disorders and resembled the old Western concept of neurosis or “general neurotic syndrome.”10 Clinically, psychiatrists made no attempt to differentiate the condition into specific types of anxiety and depressive disorders as we understand them today. In contemporary nosological terms, neurasthenia therefore encompassed most, if not all, of the (syndromal and subsyndromal) depressive and anxiety disorders. This was possible because its definition at the time was not based on any symptom hierarchy. Its symptom configuration attached equal diagnostic weight to the constituent symp-

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toms that could be somatic, cognitive, or emotional in nature (Figure 5–1). As such, it was not the same thing as the DSM-III somatoform disorder (Figure 5–2). When applied to the Chinese context, the DSM-III criteria may constitute a category fallacy, which is the imposition of a conceptual category from one culture to another without proper regard for its contextual validity in the latter.4 Nonetheless, neurasthenia is frequently equated to a somatoform disorder and at times to chronic fatigue syndrome in the Western psychiatric literature.3,11 The end of the prereform period witnessed the development of DSM-III and Chinese psychiatrists’ increased opportunity for international engagement.

REFORM PERIOD (1980s–1995)— IMPACT OF DSM-III AND KLEINMAN’S STUDY During the earlier part of the reform period, neurasthenia was still defined as a variable somato-affective syndrome. 12 At least two events alerted and later obliged Chinese psychiatrists to reconsider how they should reconceptualize the disease. First, the rejection of neurasthenia by DSM-III and DSM-III-R 13 (where the term was cursorily mentioned as a somatoform disorder in an appendix of the respective manual) and the DSM hierarchical approach to configuring symptoms for diagnosis rendered neurasthenia an unreal disease. Second, the concern over the nosological legitimacy of neurasthenia was fueled by the publication of Kleinman’s widely cited study in Hunan, which indicated that 87% of Chinese patients with the illness could be rediagnosed as having DSM-III depression and responded favorably to tricyclic pharmacotherapy.9 Inasmuch as neurasthenia was the most common psychiatric diagnosis made by Chinese psychiatrists at the time of the study, this high rate of rediagnosis suggested that they had flagrantly missed patients with “major” depression. This was a grave matter because depression, unlike neurasthenia, was proven to respond favorably to tricyclic antidepressant therapy.1 Although few Chinese psychiatrists read Kleinman’s scholarly work in its entirety, the study created several years of heated debate and at times mistrust among Chinese psychiatrists. Nonetheless, a subsequent series of Chinese studies “confirmed” that a substantial proportion (30%–70%) of patients with neurasthenia did have depression.14 This failure of neurasthenia to fulfill contemporary tests of reliability and validity set the stage for the next period of transformation when Chinese psychiatrists began to rediagnose patients with familiar neurasthenic symptoms as having depression. Under the additive impact of pharmaceutical marketing, neurasthenia was marginalized as a crude or even “wrong” clinical diagnosis.1

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POSTREFORM PERIOD (AFTER 1995)— THE BURIAL OF NEURASTHENIA During this period of rapid social change in China, there has been an active exchange of Chinese psychiatrists with Western psychiatry on multiple fronts as well as a powerful influence of the pharmaceutical industry. The latter has marketed depression as a common mental disorder and repackaged neurasthenia as a pharmacoresponsive form of depression.1 The result is a rapid assimilation of the latest DSM system. A deep transformation in clinical diagnostic style has followed. There has been a national system of psychiatric classification known as the Chinese Classification of Mental Disorders (CCMD) in China. The first edition dated back to 1981, whereas the second (CCMD-2), second-revised (CCMD2R), and third (CCMD-3) editions were published in 1989, 1995, and 2001, respectively.15 Notably, the CCMD-2 includes a cautionary statement that neurasthenia “has aroused international disputes, and there was a previous tendency for overdiagnosis to occur in China. Therefore, other forms of neurotic and psychophysiological disorders should be prudently excluded before the diagnosis is made.”16 CCMD-3 is the longest of all editions and the first to use a symptom hierarchy, like that of DSM, in establishing psychiatric diagnosis. Although Chinese psychiatrists are unfamiliar with the concept of somatoform disorder, pressure to unify the CCMD with globally accepted systems such as DSM-IV17 and International Classification of Diseases—10th Revision (ICD-10)18 has resulted, for the first time in China, in the inclusion of the category of somatoform disorder in CCMD-3.1 At the same time, the application of hierarchical rules requires that neurasthenia can only be diagnosed after all anxiety and depressive disorders are excluded. Neurasthenia received a code of 43.5 in the CCMD-3 and even ranks after the various somatoform disorders and somatization disorder (43.4x) in the new Chinese diagnostic hierarchy. An anticipated consequence is that neurasthenia is rarely diagnosed (or diagnosable) by Chinese psychiatrists nowadays, at least in urban China where professional awareness of international practice is greater and the CCMD-3 is followed more rigorously. Those who do diagnose neurasthenia may be considered outdated if not deficient in clinical skills. It should be noted, however, that the pace of change in diagnostic practice is uneven in China. The diagnostic category of neurasthenia is still widely used by general physicians and psychiatric practitioners outside of urban areas. It is also widely understood in both urban and rural China, although the term for depression is gaining usage among better educated, middle-class Chinese and younger people generally. Some are now suggesting that stigma associated with depression may be lessening among this growing group, leading to greater willingness to reveal dysphoria and thus more accurate estimates of the prevalence of depression among younger cohorts of people in urban China.19

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Has the DSM-ization of Neurasthenia Made a Difference to Treatment? As Chinese psychiatrists abandon the diagnosis of neurasthenia, the clinical diagnosis of depression has increased. However, whether this merging of diagnostic practice with international practice leads to better access to treatment or better treatment outcome is another matter. A recent community epidemiological survey conducted in Beijing and Shanghai indicated that 96.6% of Chinese people with any 12-month DSM-IV disorder and 80.2% of those with moderate and severe disorders in Beijing and Shanghai received no treatment in the previous 1 year.20 This enormous treatment gap exists despite the fact that these two major cities in China already have a higher-thanaverage concentration of health care resources, including better-trained psychiatrists. Moreover, of those individuals who sought help, they did so primarily from nonpsychiatrists who pay little attention to complex diagnostic systems such as DSM-IV or CCMD-3. Because of the greatly limited access to health care, it can be argued that the reconceptualization of neurasthenia in China has resulted in limited impact on the rate of treatment of depression among Chinese people. Regarding psychiatric practice, a critical question that matters to patients’ welfare is whether the demonstrable change in diagnostic practice has led to better outcome of psychiatric treatment. This is hard to answer because modern psychopharmacological agents, such as the selective serotonin reuptake inhibitors (widely adopted by psychiatrists in urban China, provided patients are covered by insurance or can pay for the medications), have been effectively used across the entire spectrum of anxiety, depressive, and impulse-control disorders. Moreover, because of the demise of professional interest in neurasthenia, no systematic research has been done to examine the efficacy of these medications in neurasthenia. A diagnosis of neurasthenia (especially in a general medical setting) nonetheless confers far less stigma than one of depression.

Implications for DSM-V as a Global Diagnostic System From a cross-cultural perspective, it could be considered that the category of somatoform disorders was created to accommodate the somatic presentations of mental disorders in non-Western communities where depression was reportedly rare. Ironically, the diagnosis remains rarely used in the clinical practice of nonWestern psychiatrists, who have increasingly used depression as a clinical label. To Chinese general physicians who see patients with somatoform disorders (e.g., chronic pain), somatoform disorder remains a bewildering term compared with fa-

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miliar categories such as irritable bowel syndrome, tension headache, fibromyalgia, and the like. It is thus paradoxical that a disease category that marginalizes somatic distress in the DSM-III system and is believed to be common in non-Western communities has been marginalized by non-Western psychiatrists themselves. Additionally, such marginalization is shared by psychiatrists in the West. For example, recent community psychiatric epidemiological surveys using the Composite International Diagnostic Interview in many countries, including the United States and China, do not include somatoform disorders.20,21 The story of neurasthenia in China and the social context in which neurasthenia is contested, marginalized, and reconstituted as the popular Western disease of depression among Chinese psychiatrists is at once unique and shared. It may, to some extent, guide our attempt to understand the social (disappearing) course of culture-bound syndromes in diverse communities (e.g., dhat syndrome in India, hwa-byung in Korea, and Taijin-kyofusho in Japan) where psychiatry is also undergoing transformation under global forces, such as the DSM system, and pharmaceutical marketing is making the previously Western culture-bound syndrome of “depression” a master narrative among clinicians.22 At this stage, the usefulness of the diagnosis of somatoform disorder remains to be evaluated from public health, clinical, and biological perspectives. Apart from the need to solve certain conceptual problems of the category (e.g., the validity of completely dichotomizing bodily and psychic symptoms associated with human suffering in addition to the stated feature of a refusal to acknowledge psychological causes among affected people), we believe that socioeconomic forces (definitely) and empirical evidence (hopefully) will mold its future course.

References 1. Lee S. Diagnosis postponed: shenjing shuairuo and the transformation of psychiatry in post-Mao China. Cult Med Psychiatry 1999;23:349–380. 2. Ware N, Weiss M. Neurasthenia and the social construction of psychiatric knowledge. Transcult Psychiatry 1994;31:101–123. 3. Ware N, Kleinman A. Culture and somatic experience: the social course of illness in neurasthenia and chronic fatigue syndrome. Psychosom Med 1992;54:546–560. 4. Kleinman A. Rethinking Psychiatry: From Cultural Category to Personal Experience. New York: Free Press; 1988. 5. Fabrega H Jr. The concept of somatization as a cultural and historical product of Western medicine. Psychosom Med 1990;52:653–672. 6. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association; 1980. 7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 2nd ed. Washington, DC: American Psychiatric Association; 1968.

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8. Cheung P. Adult psychiatric epidemiology in China in the 80s. Cult Med Psychiatry 1991;15:479–496. 9. Kleinman A. Neurasthenia and depression: a study of somatization and culture in China. Cult Med Psychiatry 1982;6:117–190. 10. Tyrer P. Classification of Neurosis. Chichester, UK: John Wiley and Sons; 1989. 11. Lee S, Yu H, Wing YK, Chan C, Lee AM, Lee DTS, Chen CN, Lin KM, Weiss M. Psychiatric morbidity and illness experience of primary care patients with chronic fatigue in Hong Kong. Am J Psychiatry 2000;157:380–384. 12. Lee S. The vicissitudes of neurasthenia in Chinese societies: where will it go from the ICD-10? Transcult Psychiatry 1994;31:153–172. 13. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed Revised. Washington, DC: American Psychiatric Association; 1987. 14. Zhang MY. The diagnosis and phenomenology of neurasthenia: a Shanghai study. Cult Med Psychiatry 1989;13:147–161. 15. Lee S. Cultures in psychiatric nosology: the CCMD-2-R and international classification of mental disorders. Cult Med Psychiatry 1996;20:421–472. 16. Young D. Chinese Diagnostic Criteria and Case Examples of Mental Disorders. Hunan, China: Hunan University Press; 1989. 17. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC: American Psychiatric Association; 1994. 18. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva, Switzerland: World Health Organization, 1992. 19. Lee S, Tsang A, Zhang MY, Huang YQ, He YL, Liu ZR, Shen YC, Kessler RC. Lifetime prevalence and inter-cohort variation in DSM-IV disorders in metropolitan China. Psychol Med 2007;37:61–71. 20. Shen YC, Zhang MY, Huang YQ, He YL, Liu ZR, Cheng H, Tsang A, Lee S, Kessler RC. Twelve month prevalence, severity, and unmet need for treatment of mental disorders in metropolitan China. Psychol Med 2006;26:257–267. 21. Kessler RC, Üstün TB. The World Mental Health (WMH) survey initiative version of the World Mental Health Organization (WHO) composite international diagnostic interview (CIDI). Int J Methods Psychiatr Res 2004;13:93–121. 22. Lee S. Sociocultural and global health perspectives of the development of future psychiatric diagnostic systems. Psychopathology 2002;351:152–157.

6 A BIOLOGICAL SUBSTRATE FOR SOMATOFORM DISORDERS Importance of Pathophysiology Joel E. Dimsdale, M.D. Robert Dantzer, D.V.M., Ph.D.

A

t the heart of every clinical interchange is the doctor’s attempt to reconcile the patient’s subjective complaints with the objective findings, a 2×2 table, so to speak (Table 6–1). Medicine is typically most comfortable when these two areas are in agreement. When, for instance, objective findings and subjective complaints are present, one recognizes an “ideal disease.” Similarly, when neither objective findings nor subjective complaints are present, one happily recognizes “no disease.” Unfortunately, it is not uncommon to have disparities between findings and complaints. The bulk of this chapter discusses the situation in which objective findings

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Dimsdale JE, Dantzer R: “A Biological Substrate for Somatoform Disorders: Importance of Pathophysiology.” Psychosomatic Medicine 69:850–854 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. This research has been supported by Grants HL36005, HL44915, CA23100, R01 MH71349, and MH-079829 from the National Institutes of Health.

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are absent but subjective complaints are present. This situation may be viewed either as “undiagnosed disease” or alternatively as “somatoform disorder.” Somatoform disorders represent a very heterogeneous group of patient presentations, ranging from conversion disorder to hypochondriasis to somatization disorder to body dysmorphic disorder to pain disorder, etc. The neologism was introduced in Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition1 in the hopes of finding a neutral-sounding all-encompassing diagnostic label and in the recognition that many patients present with somatic distress that does not “fit” in the rubric of anxiety, mood, or psychotic disorders. Like Wilsonian efforts to redraw the map of Europe after World War I, this diagnostic category grouped together some uneasy companions. For the purpose of this paper, we use “somatoform” to refer to one segment of this disorder—psychiatric patient presentations associated with significant somatic distress (e.g., pain, fatigue). It is the thesis of this paper that a substantial reservoir of undiagnosed disease is found in somatoform disorders. Before developing this premise, however, it is necessary to complete the 2×2 table. There is one further cell of the table that is at least as troubling as the somatoform disease category. Not infrequently, physicians encounter objective findings in the absence of subjective complaints. Such a situation is common in occult disease and is also common in denial or stoicism. A great deal could be written on this latter cell, but this chapter focuses primarily on the cell wherein the diagnosis of somatoform disease is typically made.

Four Ways That Unrecognized Diseases Get Labeled as Somatoform Diseases First, it is by no means unlikely that patients’ illnesses get labeled as somatoform diseases because the doctor has simply missed the diagnosis by insufficient attention to the history, physical examination, or adjunctive laboratory tests. This happens rather more often than one would like. Hong and Dimsdale recently carried out a pilot study of exercise as a treatment of fatigue in breast cancer patients (unpublished). They recruited a small number of breast cancer survivors who had devastating amounts of fatigue and who were willing to try an exercise regimen. As part of the baseline data, they obtained basic relevant laboratory studies and found that 40% of the patients were frankly hypothyroid. How did it come about that this eminently treatable cause of fatigue was not diagnosed? Breast cancer survivors are typically passed back and forth between oncologist and primary care provider. Neither of these physician pairs worked up the patients for their fatigue. Rather, they both assumed the fatigue was a result of chemotherapy or perhaps was a form fruste of depression in response to the stress of illness. A second way that unrecognized diseases get labeled as somatoform diseases is by not relying on contemporary diagnostic techniques. There have been astonish-

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TABLE 6–1. Subjective complaints

Epistemology: reconciling objective findings with subjective complaints Objective findings Present

Absent

Present

“Ideal” disease

Undiagnosed disease somatoform

Absent

Occult disease denial or stoicism

No disease

ing breakthroughs in clinical chemistry as well as anesthesia, imaging, and medical instrumentation. As a result, we are now recognizing a huge reservoir of unrecognized diseases because we previously lacked the techniques to study them. Obstructive sleep apnea (OSA), first discussed in a fascinating case report 50 years ago, is now recognized as an extremely prominent sleep disorder. Whereas the initial diagnosis of OSA was confined to rare “zebra” presentations marked by profound obesity and somnolence, contemporary diagnosis, made possible by ever smaller sleep monitoring systems, reveals that OSA is prevalent in 4%–9% of the population, depending on population characteristics and definitional cut points.2 Similarly, celiac disease, once diagnosed as a rare malabsorption disorder in infancy, is now recognized as prevalent in 1% of the population. Accompanied by ill-defined findings and symptoms such as mild anemia and fatigue, the diagnosis can now be made thanks to progress in clinical chemistry, such as development of endomysial antibody tests3 and pharmacological developments to make possible conscious sedation as well as biomedical instrument development to facilitate endoscopy. We now know that a huge population has an eminently treatable disease, if only we stop to think about the possibility of that diagnosis. We mention OSA and celiac disease in this context because both are characterized by fatigue and emotional distress and thus could readily be misdiagnosed as a somatoform disorder. There is a third way that unrecognized diseases get labeled as somatoform diseases. Insights from basic science research can have profound ramifications for clinical symptoms. Symptoms, such as pain and fatigue, are core presentations in many patients with somatoform illness. However, those symptoms are tightly related to each other and have the potential to be worsened by iatrogenic factors. Fundamental research in sleep, for instance, has demonstrated that sleep disruption lowers pain threshold. Other work demonstrates that opioids—the mainstay for treatment of severe pain—disrupt sleep.4 Thus, one has the potential for a vicious circle in the treatment of pain. We treat the pain with opioids, thereby interrupting sleep and increasing daytime fatigue, thereby ensuring a need for more opioids, etc. How many of our pain patients who bear a label as “somatoform disorder” patients do so

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as a result of well-intended clinical interventions that have unexpected adverse outcomes? Finally, it is important to acknowledge, as Pliny the Elder stated in 75 A.D. that “new diseases, unknown in past years, have come….” Hepatitis C with its unpleasant cargo of fatigue and depression is perhaps one of the clearest instances of such new diseases. Unrecognized until sensitive laboratory tests were developed, this disease is currently found in approximately 4% of individuals age 40 years or older in the United States population,5 and again, the early symptoms are invariably illdefined subjective complaints—a setup for (mis)diagnosing somatoform diseases.

Getting Beyond the Black Box of Symptom Reporting The “mischief ” comes from relying solely on self-report for symptom verification. Self-report is at the heart of all medical complaints, but in the absence of physical findings, understanding the meaning of self-report gets very complicated. Oddly enough, three developments in contemporary medicine allow a new “window” on self-report. One involves a refreshingly new way of looking at symptom reporting. Another involves contemporary neural imaging studies to shed light on self-report of symptoms. A third applies contemporary insights on neural immune properties as a way of understanding paradoxical self-report of symptoms. Together, the three approaches amount to a challenge of the “black box” that has historically characterized symptom reporting, a black box that has heretofore defied efforts at understanding the psychology and physiology of such reports. Arthur Barsky and others asked, “What determines the ‘volume’ level of symptoms, how is it that some people amplify their symptoms and others de-amplify them?”6 This is a felicitous approach in that it carries no implicit assumptions of underlying neuroticism, etc., but rather asks the question from a cognitive neural science perspective. Do some individuals “amplify” their symptoms characteristically or, perhaps, under unusual stressors? Is that “amplification” neurally driven? Does the amplification reflect the fact that patients have different explanatory models for understanding the significance of their symptoms? Oddly enough, two brief case reports involving construction injuries with nails demonstrate the phenomenon beautifully. In one report, Fisher et al. described the case of a builder who jumped down onto a 7-inch nail, which pierced his boot at the toe level (Figure 6–1, left panel).7 The man was in pain and required intravenous sedation in the emergency department. However, when the boot was cut away, it turned out that the nail had fortunately passed between his toes as opposed to its apparent impaling of the foot. The man’s agonizing pain was elicited solely by his misperception—a case of somatic amplification. On the other hand, a report in USA Today described a construction worker who had unknowingly shot himself

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A FIGURE 6–1.

B Symptom perceptions elicited by nails.

Figure 6–1A exemplifies somatic amplification; Figure 6–1B exemplifies somatic deamplification. Source. Figure 6–1A reprinted from Fisher JP, Hassan DT, O’Connor N. Minerva. Br Med J 1995;310:70, with permission from BMJ Publishing Group Ltd. Figure 6–1B reprinted with permission from Associated Press, Wide World Photos. 1/16/05.

in the head with a nail gun (Figure 6–1, right panel) and who was unaware of the injury. He perceived a toothache and went to a dentist 6 days later, wherein the cause of the rogue toothache was discovered. In this case, one would conclude that somatic deamplification was at work. The patient was unaware of the injury and attributed the sensation to more familiar sources. Neural imaging studies have taken up the quest for understanding symptom perception. Raij et al. used functional magnetic resonance imaging to examine how the brain responded to painful heat laser stimulation to the hand versus to the hypnotic suggestion of laser stimulation.8 In healthy subjects tested repeatedly, they observed many common neural patterns of response to the two pain stimuli. The next step was made by Coghill et al., who contrasted individuals’ neural imaging responses to thermal stimuli.9 In this case, the stimuli were identical, but normal individuals were contrasted in terms of whether they reported high versus low selfreport of pain sensitivity. Individuals with high sensitivity had increased activation of the anterior cingulate cortex, somatosensory cortex, and prefrontal cortex, but there was no difference in the thalamic response between the high pain sensitivity and the low pain sensitivity subjects. Sadly, this sort of study has not been made of patients with somatoform disorders. Do these patients have a different pattern of response to painful stimuli? If so, what are the implications for etiology and treatment of the symptoms? Most astute clinicians do not question the authenticity of patients’ complaints of pain. Rather, they try to understand its origins and direct interventions that help manage the pain. Pain is inherently subjective. It can be treated with analgesic medication, distraction, hypnosis, etc., regardless of whether there is a known focal stimulus for the pain. The case reports of nail injuries, to-

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gether with the neural imaging studies, suggest that a helpful focus for future clinical interventions in patients with somatoform illness must include an analysis of how their symptoms are perceived, interpreted, and amplified by the brain. The focus on neutral terms such as somatic amplification as well as the employment of neural imaging probes may help shed light on the “black box” area of symptom reporting in somatoform disorders. Other developments in physiology may similarly help expose a somatopsychic as well as a psychosomatic underpinning of these disorders. One of the most dramatic areas of knowledge advances has come with our understanding of neural immune trafficking. Immune factors may underpin subtle perception of pain, fatigue, depression—what some have called “sickness behavior.”

Insights From the Psychoneuroimmune Perspective Psychoneuroimmunology studies the interactions between the central nervous system and the immune system. The field has made major advances in understanding how brain functions can modulate the activity of the immune system and the discovery (particularly relevant for this chapter) that mediators produced by cells of the immune system exert profound influences in the brain. As a typical example, many breast cancer survivors experience persistent fatigue up to 5–10 years after diagnosis despite the termination of chemotherapy and radiotherapy. Fatigued breast cancer survivors display increased inflammatory biomarkers.10 Similar associations between self-reports of fatigue and inflammatory markers have been reported in patients with coronary heart disease.11 The cooccurrence of decreasing energy, general malaise, and minor depression in the weeks that precede a myocardial infection has been termed “vital exhaustion.”12 High levels of inflammatory biomarkers have been found in apparently healthy patients who scored high on vital exhaustion.13 The mechanisms that are responsible for the association between subjective health complaints and inflammation have been elucidated over the last decade.14,15 Activation of the innate immune system by pathogen-associated molecular patterns induces the local production of proinflammatory cytokines. These molecules are responsible for the development of the local inflammatory response and the systemic response to inflammation. This acute-phase reaction includes the production of acute-phase proteins by hepatocytes and the occurrence of fever, which is a regulated metabolic response to pathogens. The fever is “coordinated” in the anterior preoptic area of the hypothalamus and is triggered by the action on the brain of proinflammatory cytokines that are released at the periphery. Proinflammatory cytokines do not need to enter the brain to target the hypothalamus because the brain is able to form a cellular and molecular representation of

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the peripheral immune response (Figure 6–2). During the course of an inflammatory response, brain innate immune cells produce proinflammatory cytokines. These cytokines are produced in response either to blood-borne pathogen-associated molecular patterns or to circulating proinflammatory cytokines that are sensed by macrophage-like cells residing in circumventricular organs. Because circumventricular organs have a deficient blood-brain barrier, they are able to monitor changes in the composition of the internal milieu. The cytokines that are produced in the circumventricular organs gradually diffuse into the brain side of the blood-brain barrier and recruit microglial cells in the brain parenchyma. Another important pathway of communication from the immune system to the brain is represented by the afferent nerves that innervate the bodily site in which the inflammation is taking place. Activation of these afferent nerves promotes the perception of the sensory components of inflammation (calor or heat and dolor or pain) and the expression of brain proinflammatory cytokines in response to peripheral inflammatory cytokines. A bilateral section of the vagus nerves blocks the immune-to-brain transmission of inflammation that takes place in the abdominal cavity,16,17 whereas the section of the trigeminal nerves does the same for an oral inflammation.18 In addition to their role in the genesis of fever, brain proinflammatory cytokines are also responsible for the subjective and behavioral components of illness, which accounts for why one feels sick and behaves in a sick way when one is ill. Conversely, sickness symptoms that develop during the course of a peripheral activation of the innate immune system can be blocked by administration of various cytokine antagonists in the brain.19 Studies of the brain effects of cytokines have shown that, although cytokineinduced sickness behavior is normally reversible on the resolution of the infectious episode, it persists when the innate immune system is chronically activated and can even culminate in major depression in vulnerable individuals.20,21 Psychological symptoms of depression (e.g., anhedonia, depressed mood, irritability) coexist with neurovegetative signs of depression (e.g., fatigue, reduced appetite) in vulnerable patients whose immune system is chronically activated. Patients with more depressive symptoms are more likely to become depressed in response to an activation of the immune system than those who have fewer such symptoms.22 The same applies to patients whose pituitary-adrenal axis is more responsive to the immune stimulation.23 An important aspect of the pathophysiology of immune-to-brain communication is the existence of a cross-sensitization process between stressors and cytokines. Exposure to inescapable electric shocks, for instance, sensitized the peripheral and central cytokine response to lipopolysaccharide in rats for a minimum of 4 days after stress.24 Reciprocally, a prior episode of interleukin (IL)-1-induced sickness sensitized the pituitary-adrenal response to inescapable electric shock up to 2–3 weeks after the cytokine treatment.25 Sensitization can also occur when the

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FIGURE 6–2.

Somatic Presentations of Mental Disorders

Immune-to-brain communication.

Proinflammatory cytokines are produced at the periphery by innate immune cells in response to pathogen-associated molecular patterns or to danger signals, such as heat shock proteins released by dying cells. Peripheral proinflammatory cytokines induced the production of the same proinflammatory cytokines in the brain. The brain proinflammatory cytokines acting on various brain areas induce nonspecific symptoms of sickness, such as fatigue, depressed mood, and altered cognition. The production and action of proinflammatory cytokines are regulated both at the periphery and in the central nervous system by a number of opposing molecules including anti-inflammatory cytokines, steroid hormones such as glucocorticoids, and neuropeptides such as α-melanotropin (α-MSH) and vasopressin (AVP).

same cytokine is administered twice at an interval of several days or weeks, and it affects both cytokine-sensitive neurotransmitter metabolism and pituitary-adrenal responsiveness to cytokines.26 These protracted effects of stressors and cytokines on brain functions likely play an important role in the pathophysiology of somatic amplification. The clearest demonstration of the clinical relevance of the sensitizing effects of cytokines is in the field of pain. The perception of pain is strongly amplified under the effect of proinflammatory mediators produced by activated glial cells in the spinal cord.27 It is important to note that glial activation is not restricted to the spinal cord but also occurs in the brain in situations of chronic inflammation associated, for instance, with progressive neurodegeneration,28 obesity,29 or aging.30 In these conditions, the brain cytokine system seems to be sensitized in that it responds to a greater ex-

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tent to a further activation of the peripheral innate immune system, resulting in a more intense cytokine-induced sickness behavior and/or a delayed recovery from sickness. The main medical implication of this view is that many somatization symptoms, including depressed mood, fatigue, and pain, may represent the expression of a previously sensitized brain cytokine system that is reactivated by infectious or noninfectious trauma. At the clinical level, there is not yet consensus as to which biomarkers best relate somatization symptoms to inflammation. Only peripheral markers of inflammation are currently available. Circulating levels of acute-phase proteins (e.g., C-reactive protein) provide a gross index of the inflammatory response that can be refined using plasma levels of cytokines, such as IL-6 together with its soluble receptor. Because most other cytokines act in a paracrine/autocrine manner rather than as hormones, the production of cytokines by stimulated monocytes in culture is a better index of activity of the innate immune system than circulating levels that only reflect overflow of local cytokines. Because cytokines are produced by many cell types other than innate immune cells, it can be useful to more precisely assess the involvement of macrophages in the inflammatory response by measuring circulating levels of neopterin. Last but not the least, the possible impact of immune activation on serotoninergic neurotransmission can be studied by measuring the circulating concentrations of kynurenine, the main metabolite of tryptophan. At the therapeutic level, treatments that specifically target activation of the brain cytokine system are not yet available. However, there is already evidence that pharmacological (e.g., antidepressants)30 and nonpharmacological (e.g., aerobic exercise)31 therapies are able to attenuate some somatic symptoms by down-regulating inflammation.

Conclusion Although medicine’s goal is always to allay suffering, there is no one universal remedy other than courtesy and respect and kindness. Specific remedies may be applied only when an accurate diagnosis has been made. Somatoform disorders are among the hardest disorders to diagnose and thus to treat. This chapter suggests two rather different conclusions. First, somatoform disorder may be misdiagnosed due to complex factors that lead to underrecognition of another underlying disorder other than somatoform disorder. Second, one must study the underlying physiology of symptoms in somatoform disorder in terms of the cognitive processes involved in recognition of symptoms and the complex physiology of distress, increasingly recognized as immune in nature, which augments nonspecific symptoms.

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References 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association; 1980. 2. Caples SM, Gami AS, Somers VK. Obstructive sleep apnea. Ann Intern Med 2005;142:187–197. 3. Reddick BK, Crowell K, Fu B. Clinical inquiries: what blood tests help diagnose celiac disease? J Fam Pract 2006;55:1088,1090–1093. 4. Dimsdale J, Norman D, Dejardin D, Wallace MS. The effects of opioids on sleep architecture. J Clin Sleep Med 2007;3:33–36. 5. Armstrong GL, Wasley A, Simard EP, McQuillan GM, Kuhnert WL, Alter MJ. The prevalence of hepatitis C virus infection in the United States, 1999 through 2002. Ann Intern Med 2006;144:705–714. 6. Barsky A, Wyshak G, Klerman G. The somatosensory amplification scale and its relationship to hypochondriasis. J Psychiatr Res 1990;24:323–334. 7. Fisher JP, Hassan DT, O’Connor N. Minerva. BMJ 1995;310:70. 8. Raij TT, Numminem J, Narvanen S, Hiltunen J, Hari R. Brain correlates of subjective reality of physically and psychologically induced pain. Proc Natl Acad Sci 2005;102:2147–2151. 9. Coghill RC, McHaffie JG, Yen YF. Neural correlates of interindividual differences in the subjective experience of pain. Proc Natl Acad Sci 2003;100:8538–8542. 10. Collado-Hidalgo A, Bower JE, Ganz PA, Cole SW, Irwin MR. Inflammatory biomarkers for persistent fatigue in breast cancer survivors. Clin Cancer Res 2006;12:2759– 2766. 11. Janszky I, Lekander M, Blom M, Georgiades A, Ahnve S. Self-rated health and vital exhaustion, but not depression, is related to inflammation in women with coronary heart disease. Brain Behav Immun 2005;19:555–563. 12. Appels A. Mental precursors of myocardial infarction. Br J Psychiatry 1990;156:465– 471. 13. Wirtz PH, von Kanel R, Schnorpfeil P, Ehlert U, Frey K, Fischer JE. Reduced glucocorticoid sensitivity of monocyte interleukin-6 production in male industrial employees who are vitally exhausted. Psychosom Med 2003;65:672–678. 14. Konsman JP, Parnet P, Dantzer R. Cytokine-induced sickness behaviour: mechanisms and implications. Trends Neurosci 2002;25:154–159. 15. Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends Immunol 200;27:24–31. 16. Bluthe RM, Michaud B, Kelley KW, Dantzer R. Vagotomy blocks behavioural effects of interleukin-1 injected via the intraperitoneal route but not via other systemic routes. Neuroreport 1996;7:2823–2827. 17. Laye S, Bluthe RM, Kent S, Combe C, Medina C, Parnet P, Kelley K, Dantzer R. Subdiaphragmatic vagotomy blocks induction of IL-1 beta mRNA in mice brain in response to peripheral LPS. Am J Physiol 1995;268:R1327–1331. 18. Navarro VP, Iyomasa MM, Leite-Panissi CR, Almeida MC, Branco LG. New role of the trigeminal nerve as a neuronal pathway signaling brain in acute periodontitis: participation of local prostaglandins. Pflugers Arch 2006;453:73–82.

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19. Dantzer R. Cytokine-induced sickness behavior: where do we stand? Brain Behav Immun 2001;15:7–24. 20. Capuron L, Ravaud A, Dantzer R. Early depressive symptoms in cancer patients receiving interleukin 2 and/or interferon alfa-2b therapy. J Clin Oncol 2000;18:2143– 2151. 21. Constant A, Castera L, Dantzer R, Couzigou P, de Ledinghen V, Demotes-Mainard J, Henry C. Mood alterations during interferon-alfa therapy in patients with chronic hepatitis C: evidence for an overlap between manic/hypomanic and depressive symptoms. J Clin Psychiatry 2005;66:1050–1057. 22. Capuron L, Ravaud A. Prediction of the depressive effects of interferon alfa therapy by the patient’s initial affective state. N Engl J Med 1999; 340:1370. 23. Capuron L, Raison CL, Musselman DL, Lawson DH, Nemeroff CB, Miller AH. Association of exaggerated HPA axis response to the initial injection of interferon-alpha with development of depression during interferon-alpha therapy. Am J Psychiatry 2003;160:1342–1345. 24. Johnson JD, O’Connor KA, Deak T, Stark M, Watkins LR, Maier SF. Prior stressor exposure sensitizes LPS-induced cytokine production. Brain Behav Immun 2002;16:461–476. 25. Tilders FJ, Schmidt ED, Hoogendijk WJ, Swaab DF. Delayed effects of stress and immune activation. Baillieres Best Pract Res Clin Endocrinol Metab 1999;13:523–540. 26. Anisman H, Merali Z, Hayley S. Sensitization associated with stressors and cytokine treatments. Brain Behav Immun 2003;17:86–93. 27. Watkins LR, Hutchinson MR, Ledeboer A, Wieseler-Frank J, Milligan ED, Maier SF. Glia as the “bad guys”: implications for improving clinical pain control and the clinical utility of opioids. Brain Behav Immun 2007;21:131–146. 28. Bluthe RM, Michaud B, Delhaye-Bouchaud N, Mariani J, Dantzer R. Hypersensitivity of lurcher mutant mice to the depressing effects of lipopolysaccharide and interleukin-1 on behaviour. Neuroreport 1997;8:1119–1122. 29. O’Connor JC, Satpathy A, Hartman ME, Horvath EM, Kelley KW, Dantzer R, Johnson RW, Freund GG. IL-1beta-mediated innate immunity is amplified in the db/ db mouse model of type 2 diabetes. J Immunol 2005;174:4991–4997. 30. Davidson KW, Kupfer DJ, Bigger JT, Califf RM, Carney RM, Coyne JC, Czajkowski SM, Frank E, Frasure-Smith N, Freedland KE, Froelicher ES, Glassman AH, Katon WJ, Kaufmann PG, Kessler RC, Kraemer HC, Krishnan KR, Lesperance F, Rieckmann N, Sheps DS, Suls JM, National Heart, Lung, and Blood Institute Working Group. Assessment and treatment of depression in patients with cardiovascular disease: National Heart, Lung, and Blood Institute Working Group Report. Psychosom Med 2006;68:645–650. 31. Woods JA, Vieira VJ, Keylock KT. Exercise, inflammation, and innate immunity. Neurol Clin 2006;24:585–599.

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7 SOMATOFORM AND SUBSTANCE USE DISORDERS Deborah Hasin, Ph.D. Hila Katz, B.A.

S

omatoform disorders are generally characterized by somatic symptoms that are unaccounted for by a medical condition, a direct substance-related effect, or another psychiatric disorder. These disorders include somatization disorder, body dysmorphic disorder, pain disorder, hypochondriasis, conversion disorder, as well as undifferentiated somatoform disorder and somatoform disorder not otherwise specified. Because somatoform symptoms overlap with the symptomatology of numerous other conditions, clinicians and researchers often encounter difficulty assigning a somatic symptom to an appropriate diagnostic category and they have trouble consequently in diagnosing a somatoform disorder. After the publication of Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition (DSM-III),1

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Hasin D, Katz H: “Somatoform and Substance Use Disorders.” Psychosomatic Medicine 69:870–875 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission. This research was supported, in part, by Grant K05 AA014223 from the National Institute on Alcoholism and Alcohol Abuse and Grant RO1 DA018652 from the National Institute on Drug Abuse and support from New York State Psychiatric Institute.

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relatively little attention has focused on the overlap of symptoms and comorbidity between somatoform and substance use disorders. This review addresses two main issues. The first issue is the potential for diagnostic difficulties posed by the overlap in somatoform symptoms and symptoms of substance use disorders, including acute intoxication or withdrawal. The second issue is what is known about the comorbidity between somatoform disorders and substance use, abuse, and dependence. In DSM-IV2 and DSM-IV-TR 3, two main substance use disorders are included—abuse and dependence. The DSM-IV-TR dependence diagnosis includes seven criteria. Meeting three or more of these criteria results in a diagnosis of dependence. One of these dependence criteria is withdrawal. DSM-IV-TR also lists withdrawal symptoms separately for each major substance category (stimulants, alcohol, etc.). Table 7–1 presents all DSM-IV-TR withdrawal symptoms that are included for any substance category. Table 7–1 also indicates which of these are included as symptoms of at least one somatoform disorder. Several of the 18 withdrawal symptoms overlap with symptoms of a somatoform disorder. Given the high levels of depressive or anxiety symptoms noted among individuals with somatoform disorders or subclinical manifestations,4,5 the withdrawal symptoms of anxiety, depression, insomnia, hypersomnia, restlessness, or psychomotor retardation can also be perceived as overlapping with symptoms commonly seen in patients manifesting what seems to be a somatoform condition. Even substance use that does not meet the criteria for dependence can produce various side effects, such as abdominal pains, impaired coordination, hallucinations, and sexual dysfunction; somatoform symptoms overlap with multiple DSM-IV-TR symptoms for intoxication in any substance category (Table 7–2). All these symptoms thus have the potential to create diagnostic difficulties, especially if a patient has a pattern of unrecognized alcohol or illicit substance use or is using medication prescribed to alleviate pain. Both somatoform disorders and substance use disorders incur a great burden of health care costs5–7 and may greatly impair physical health, quality of life, and psychological well-being. We therefore reviewed the research conducted to date on the comorbidity of the two classes of disorders, how they might possibly interact, and what difficulties and limitations hinder the research. To our knowledge, such a review has not previously been undertaken.

Methods We conducted online literature searches, primarily via PubMed, using combinations of keywords related to both somatoform disorders and substance use disorders. Keyword combinations comprised general terms such as “substance use disorders” and “somatoform disorders,” specific terms such as “conversion disorder”

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TABLE 7–1.

DSM-IV-TR symptoms of withdrawal from any substance

Anxietyb Insomniab Vivid or unpleasant dreams Hallucinationsa Restlessnessb Shakingb Depressed moodb Hypersomniab Psychomotor retardation b

Feeling weak or tireda Bad headachesa Muscle cramps Runny eyes or nose Yawning Nauseaa Sweating Fever Seizurea

aSymptoms

overlapping directly with somatoform symptoms. that may additionally overlap with somatoform symptoms due to the extensive comorbidity between somatoform, depressive, and anxiety disorders.

bSymptoms

TABLE 7–2.

DSM-IV-TR symptoms of intoxication from any substance

Slurred speech Incoordinationa Unsteady gait Nystagmus Impairment in attention/memory Stupor or coma Tachycardiab or brachycardia Pupillary dilation Elevated or lowered blood pressure Perspiration or chillsb Nausea/vomitinga Psychomotor agitation/retardationb Flushed faceb Gastrointestinal disturbanceb Twitching musclesa Palpitationsb Dizzinessb Blurred vision a Ataxiaa Muscle rigidity Increased appetiteb aSymptoms

Chest paina Cardiac arrythmiaa Respiratory depression Muscular weakness Restlessnessb Nervousnessb Excitement Insomniab Dystonia Dyskinesiaa Confusion Seizurea Diuresis (increased urine discharge) Rambling thought and speech Dry mouth Tremorsa Tirednessa Numbnessb Dysarthria Hyperacusis (abnormally acute hearing)a Conjunctival injection (red/bloodshot eyes)

overlapping directly with somatoform symptoms. that may additionally overlap with somatoform symptoms due to the extensive comorbidity between somatoform, depressive, and anxiety disorders.

bSymptoms

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and “alcohol,” and pairings of general and specific terms such as “somatization” and “opiates.” The keywords included the following: somatoform disorder, somatization, somatization disorder, body dysmorphic disorder, pain disorder, conversion disorder, hypochondriasis, undifferentiated somatoform disorder, somatoform disorder not otherwise specified, substance use, substance abuse, dependence, withdrawal, substance use disorder, drugs, alcohol, drinking, nicotine, smoking, cocaine, cannabis, heroin, opiates, and medication. The search encompassed family history studies, epidemiological studies, and patient-based studies whose purpose was to investigate comorbidity between substance use disorders and somatoform disorders or that provided information on this topic through an assessment procedure that was explicitly described in the article. Through articles found in this manner, we also identified additional papers through the citations of the articles found via PubMed.

Results Our search uncovered few papers on the comorbidity of substance use disorders or even substance use and somatoform disorders. We review these papers by type of study design.

EPIDEMIOLOGIC STUDIES Three German general population studies suggested a significant association between substance use disorders and somatoform disorders. Among 4,074 German adults, drinkers meeting the criteria for DSM-IV alcohol abuse and at-risk drinkers (men and women consuming >30 and >20 g ethanol/day, respectively) had significantly higher rates of somatoform, affective, and anxiety disorders than abstainers and moderate drinkers.8 Among females, 16.1% of moderate drinkers and abstainers were diagnosed with a lifetime somatoform disorder as opposed to 26.3% and 33.3% of the at-risk drinkers and alcohol abusers, respectively. Among men, the rate of lifetime somatoform disorder was 7.1% for moderate drinkers, 13.8% for at-risk drinkers, and 11.6% for alcohol abusers. In another study comparing smokers and nonsmokers, German female daily smokers had higher odds of somatoform disorders (OR = 1.8) as well as higher odds for anxiety disorders (OR = 1.9), affective disorders (OR =2.1), and other substance use disorders (OR =3.0).9 Additionally, nicotine dependence and withdrawal symptoms were associated with all psychiatric disorders, including somatoform disorders. Finally, among Germans ages 14–24 years, substance dependence was significantly associated with conversion disorder (OR =8.19).10 Substance dependence was also associated with the subthreshold somatoform condition known as SSI4,6, a Somatic Symptom Index category requiring at least four somatization symptoms among

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men and at least six among women.11 An odds ratio of 3.53 was found for the association between substance dependence and SSI4,6.10 In contrast to the German findings, data from the U.S. Epidemiologic Catchment Area (ECA) study,12 a large-scale study carried out in five sites in the United States, found that somatization symptoms were correlated most weakly with substance abuse symptoms and most strongly with symptoms of major depression and anxiety disorders.13 Among a subset of ECA participants with five or more current somatization symptoms, the prevalence of drug abuse/dependence and alcohol abuse/dependence was 2.2% and 7.4%, respectively, compared with 45.2% for phobia, 17.8% for panic disorder, and 14.8% for major depression. However, a more recent study drawing on data from four ECA sites broadened its analyses to include somatization symptoms of lesser severity (coded as nondisruptive of daily life) and found that a greater number of somatization symptoms was associated with an increasingly elevated risk of comorbid “extreme alcohol use,” which was defined as drinking 7 or more drinks per day for at least 2 weeks or binge-drinking 20 beers a day (or its alcoholic equivalent) more than once.14 A Canadian general population study conducted among 1,015 13- to 16-yearolds did not find a significant relationship between high levels of somatization symptoms and the development of alcohol or drug abuse/dependence 4 years later.15 However, high levels of somatization symptoms predicted greater risk of depression and panic attacks at the 4-year follow-up. The studies conducted in Germany produced different results than the studies conducted in North America. Whereas studies in the United States and Canada produced mixed findings, the studies in Germany, conducted among both adults and adolescents, consistently suggested that somatization and substance disorders are comorbid. The reason for the discrepancies is unclear and merits further study.

PATIENT/TREATMENT SAMPLES Several studies conducted among patient samples indicated an association between substance use disorders and somatoform disorders. Among patients diagnosed with body dysmorphic disorder, lifetime rates of substance use disorders ranged from 25% to 49%.16,17 Higher levels of somatization symptoms were also associated with craving for benzodiazepines in Dutch general practice patients, 113 of whom were current long-term benzodiazepine users and 80 of whom were former users.18 British ecstasy users (n =53) who reported that their ecstasy use caused problems in their lives had significantly higher scores on somatization, depression, and anxiety scales than several comparison groups, including nonproblem ecstasy users, past illicit drug users who did not use ecstasy, and past users of alcohol and nicotine only.19 In a U.S. study that compared 119 primary care patients with somatization disorder and a community sample, the patients had a higher rate of alcohol abuse and dependence but not of drug abuse.20

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In contrast, other patient-based studies had negative results. Among psychiatric outpatients in Greece diagnosed with somatoform disorders, very few were diagnosed with substance abuse, although the patients had high rates of major depression, dysthymia, and panic disorder.21 In a small sample (n=50) of patients with body dysmorphic disorder, only 2% were diagnosed with substance dependence, whereas the rates of dysthymia and social phobia were 18% and 16%, respectively.22 Few reports on the comorbidity between somatoform and substance disorders are available, in contrast to many hundreds of articles on other aspects of comorbidity in clinical samples. The few studies available are contradictory, although the larger studies tended to report that somatoform and substance use disorders were associated. The reasons for the inconsistencies are unclear and may involve measurement issues as well as true variation in the comorbidity depending on unspecified aspects of the patients studied or the countries in which the studies were conducted.

FAMILY HISTORY STUDIES In the 1980s, the Stockholm Adoption Study23–25 examined the intergenerational relationship between somatization and parental criminality and alcohol abuse; the latter was defined by registrations at the Swedish temperance board for alcohol-related offenses, hospitalizations, and duration of treatment for alcoholism. Compared with female adoptees of non-alcohol-abusing and noncriminal biological parents, female adoptees whose biological parents abused alcohol or exhibited criminal behavior showed increased risk of somatization,25,26 defined by the frequency, diversity, and duration of symptoms reported on medical records, as well as an increased number of absences from work.23 Also, the biological parents of somatizing adoptees manifested significantly higher rates of alcohol abuse and criminal behavior than the biological parents of nonsomatizers.25 Female somatizers were divided into two types—“high frequency” and “diversiform” somatizers, based primarily on the number and kinds of symptoms they exhibited. Both groups of somatizing adoptees had higher rates of alcohol abuse and criminality than nonsomatizers.24 Similar findings arose in two smaller family studies. One study found that the relatives of primary care patients with full or subthreshold somatization (n=99) presented with higher rates of alcohol use disorders and depression than relatives of community residents without psychiatric disorders.27 In another study, antisocial symptoms, substance use, and somatization in parents were all linked to higher rates of somatization in children.28 A third family study compared relatives of 35 substance-abusing adolescent males with delinquent behavior and relatives of 35 control subjects.29 Relatives of the two groups did not differ in somatization symptoms, but the sample was small. Thus, the family studies have tended to sug-

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gest associations between somatoform disorders and symptoms and substance abuse problems.

Discussion Although the research to date suggests the possibility of an association between substance use disorders and somatoform disorders, the scarcity of research and inconsistent findings preclude strong conclusions about their relationship. However, the literature reviewed suggests that somatoform and substance use disorders may be more highly associated than is commonly believed. A number of methodological issues in the studies that are available contribute to the lack of clarity about the comorbidity of somatoform and substance use disorders and symptoms.

FAILURE TO CONTROL FOR DEPRESSIVE OR ANXIETY COMORBIDITY The available studies typically included analyses of depressive and anxiety disorders, which were common. Somatoform disorders and subthreshold somatization symptoms usually show a stronger association with depression and anxiety than with substance use disorders. Because of a failure to control for the comorbidity of depression and anxiety, the studies are not clear about whether substance disorders are associated with the actual somatization of the subjects, or rather with the high levels of concomitant depression and anxiety commonly comorbid with somatization.

HIGH DIAGNOSTIC THRESHOLDS Another methodological issue is the high symptom threshold for some somatoform disorders and their consequent low prevalence, regardless of the population studied. For example, a comparison of psychiatric disorders in 8,296 relatives of alcoholic probands and 1,654 control subjects did not identify enough cases of DSM-III-R 30 somatization disorder for analysis.31 In another example, in the population-based study of Germans ages 14–24 years, too few cases of hypochondriasis and somatization disorder emerged for meaningful analysis.10 However, when this study broadened its inclusion criteria for somatoform conditions by using the SSI4,6, an association with substance dependence was found. The impact on prevalence of a lower diagnostic threshold was shown in a general population sample that yielded a rate of 0.03% for somatization disorder and a rate of 4.4% for SSI4,6.32 Comorbidity research on somatoform and substance use disorders typically has not used less restrictive disorders, such as the SSI4,6. Using categories with lower thresholds seems to be a useful approach in studying the comorbidity of

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substance and somatoform disorders, as may be the elimination of categories entirely and the use instead of a dimensional approach. However, a consensus on the validity of lower threshold categories of somatoform disorders or on an entirely dimensional approach has not yet been reached. Another low-threshold somatoform condition is undifferentiated somatoform disorder (USD). USD is included in DSM-IV but, unlike somatization disorder, does not require a specific number or type of symptoms and requires only that the unexplained symptoms be present for at least 6 months; prevalence rates for USD in the general population have been found to be as high as 19.7%.33 A caution for studies based on USD is that this category may encounter reliability and validity problems due to the lack of specificity in its definition.

POOR RECALL OF SYMPTOMS The problem of symptom recall, particularly as applied to lifetime symptoms, is exemplified by an assessment of longitudinal data from a World Health Organization study, which found that 61% of medically unexplained lifetime symptoms reported at baseline were not reported in a 12-month follow-up that also assessed lifetime symptoms.34 In research investigating the lifetime comorbidity of substance use disorders and somatization disorders or symptoms, this could lead to an underestimation of the relationship of somatoform symptoms or disorders to alcohol or drug disorders.

PROBLEMS ARISING FROM MISATTRIBUTION OF THE CAUSE OF THE SYMPTOMS In studies of somatoform symptoms and disorders, the need for symptoms to have the lack of an explanation has the potential to cause bias due to misattribution of the cause (or lack thereof ) of the symptoms. For example, a subject may feel that a symptom has no explanation but therefore fails to correctly attribute it to a substance-related effect arising from alcohol, drug, and/or medication use, masking a symptom of substance use. The reverse is possible as well, with subjects incorrectly reporting substance use as the cause of what is actually an unexplained somatic symptom. Whereas some somatoform symptoms such as urogenital complaints are not typically associated with a substance use effect or disorder, other somatoform symptoms are more closely associated with substance intoxication or withdrawal; for example, cardiological symptoms such as chest pain and a racing heartbeat may result from cocaine or amphetamine intoxication. Over the course of many years, patients with multiple medically unexplained somatic symptoms may receive variable diagnoses influenced by the specialties of the many different doctors or departments that the patients consult.35 In addition, among patients with somatic complaints, physicians may not probe to determine

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patterns of substance use, abuse, and/or dependence or verify subject self-reports with tests or with collateral information from a significant other; the reverse is also possible, with a current substance use disorder masking an earlier manifestation of multiple unexplained somatic symptoms. Diagnoses may not only vary based on the clinician’s own area of specialty or interest, but may also be influenced by the patient’s gender, class, and/or race, as has been found for other disorders such as posttraumatic stress disorder.36 Methodological studies are needed to clarify the extent to which these types of misattribution occur. A specific example of the potential for symptom misattribution may have occurred in the ECA study, where the lay-administered diagnostic assessment procedure used a probe flow chart to determine the source (i.e., the attribution of cause) of all psychiatric symptoms.37 In a validity study of this procedure via comparison of its results to assessments by psychiatrists, the greatest discrepancies involved somatization disorder, which was underdiagnosed.37 The failure to detect somatoform disorders in the ECA may have led to inaccurate findings on the weakness of their relationships to substance use disorders.13 Although a more recent ECAbased study suggested an association between somatization symptoms and heavy alcohol use, the study did not examine the prevalence of alcohol abuse and dependence among the heavy drinkers and the possible relationship of those disorders with somatization symptoms, nor did it take into account other factors potentially associated with both extreme alcohol use and somatization, such as drug use disorders, depression, and anxiety.14 The weak relationships initially found between somatoform and substance use disorders from the ECA may have led (at least in part) to the lack of research on this aspect of comorbidity since then. If so, it is possible that an important association between two diagnostic categories of major interest has been missed. Additional studies addressing some of the methodological shortcomings reviewed above would yield crucial information on this topic, both in the ECA data and in data from new studies.

OVERLY LARGE ASSESSMENT BURDEN DUE TO LARGE NUMBER OF DIAGNOSTIC SYMPTOMS Diagnostic accuracy might be improved by condensing symptom checklists used for somatoform disorder diagnoses.38,39 A reason somatoform disorders may have been omitted so often from large studies is that the battery of symptoms required to make a full diagnosis of the somatoform disorders is so large. Trimming the battery via statistical analyses to a smaller subset of highly relevant symptoms would considerably aid future comorbidity research by enabling more studies to include the most common, relevant, and widely exhibited somatoform symptoms and determine if substance use disorders are comorbid with these.

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FUTURE RESEARCH In addition to the numerous methodological and assessment issues identified above, an important area barely addressed in the research to date is the issue of prescription and nonprescription medications. Some evidence suggests that, in addition to making more frequent use of primary care doctors, hospitals, and outpatient services,5 patients diagnosed with somatization disorder also use higher levels of medication than patients without somatization disorder.40 Although patients with unexplained somatic symptoms may not always explicitly ask for medication, they might indirectly pressure physicians to prescribe drugs by describing their symptoms in graphic and highly emotional terms.41 Even if patients do not succeed in obtaining a prescription from their doctors, they might turn to the Internet, where drugs such as benzodiazepines and opiates are increasingly available online,42,43 leading to concerns about the misuse and abuse of these drugs due to lax regulation at online pharmacies and the improper dispensation of drugs by unlicensed and uncertified distributors. Future research could explore a possible link between somatoform disorders or subthreshold somatization and the abuse/dependence of painkillers and other medications; a challenge for both researchers and clinicians would also be to tease apart the side effects of such medications and the symptoms attributed to the somatoform disorder. More information is also needed on whether specific somatoform disorders are associated more strongly with certain substances, or if certain somatoform disorders are generally more significantly comorbid with substance use disorders regardless of the substance. The somatoform category encompasses disorders that differ markedly from each other in clinical presentation, progression, and appropriate treatments. Therefore, future comorbidity studies should address specific disorders or subthreshold manifestations of the disorders rather than aggregating all disorders within the category as a whole. For example, one study comparing patients with somatization disorder (n=65) and patients with conversion disorder (n =51) at a large American medical center found a significantly higher level of substance abuse among the somatization disorder patients.44 In another example, a study of substance abusers treated in a drug-free residential community, residents reporting marijuana and hallucinogens as their greatest drug use problem experienced higher levels of somatization than residents with cocaine or heroin as their greatest drug use problem.45 However, very few such studies have been conducted. More information of this type would aid greatly in understanding the specificity or generality of any associations between somatoform and substance use disorders. This could help explain, in turn, some of the inconsistencies in the associations found to date.

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References 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. Washington, DC: American Psychiatric Association; 1980. 2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994. 3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. DSM-IV-TR. 4th ed. Text Revision. Washington, DC: American Psychiatric Association; 2000. 4. Henningsen P, Jakobsen T, Schiltenwolf M, Weiss MG. Somatization revisited: diagnosis and perceived causes of common mental disorders. J Nerv Ment Dis 2005;193:85– 92. 5. Barsky AJ, Orav EJ, Bates DW. Somatization increases medical utilization and costs independent of psychiatric and medical comorbidity. Arch Gen Psychiatry 2005;62:903– 910. 6. Hasin D, Stinson F, Ogburn E, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: results from the national epidemiologic survey on alcohol and related conditions. Arch Gen Psychiatry 2007;64:830–842. 7. Compton WM, Thomas YF, Stinson FS, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry 2007;64:566–576. 8. Bott K, Meyer C, Rumpf HJ, Hapke U, John U. Psychiatric disorders among at-risk consumers of alcohol in the general population. J Stud Alcohol 2005;66:246–253. 9. John U, Meyer C, Rumpf HJ, Hapke U. Smoking, nicotine dependence and psychiatric comorbidity—a population-based study including smoking cessation after three years. Drug Alcohol Depend 2004;76:287–295. 10. Lieb R, Pfister H, Mastaler M, Wittchen HU. Somatoform syndromes and disorders in a representative population sample of adolescents and young adults: prevalence, comorbidity and impairments. Acta Psychiatr Scand 2000;101:194–208. 11. Escobar JI, Rubio-Stipec M, Canino G, Karno M. Somatic symptom index (SSI): a new and abridged somatization construct. Prevalence and epidemiological correlates in two large community samples. J Nerv Ment Dis 1989;177:140–146. 12. Regier DA, Farmer ME, Rae DS, Locke BZ, Keith SJ, Judd LL, Goodwin FK. Comorbidity of mental disorders with alcohol and other drug abuse. Results from the epidemiologic catchment area (ECA) Study. JAMA 1990;264:2511–2518. 13. Simon GE, VonKorff M. Somatization and psychiatric disorder in the NIMH epidemiologic catchment area study. Am J Psychiatry 1991;148:1494–1500. 14. Tien AY, Schlaepfer TE, Fisch HU. Self-reported somatization symptoms associated with risk for extreme alcohol use. Arch Fam Med 1998;7:33–37. 15. Zwaigenbaum L, Szatmari P, Boyle MH, Offord DR. Highly somatizing young adolescents and the risk of depression. Pediatrics 1999;103:1203–1209. 16. Gunstad J, Phillips KA. Axis I comorbidity in body dysmorphic disorder. Compr Psychiatry 2003;44:270–276.

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17. Grant JE, Menard W, Pagano ME, Fay C, Phillips KA. Substance use disorders in individuals with body dysmorphic disorder. J Clin Psychiatry 2005;66:309–316. 18. Mol AJ, Gorgels WJ, Oude Voshaar RC, Breteler MH, van Balkom AJ, van de Lisdonk EH, Kan CC, Zitman FG. Associations of benzodiazepine craving with other clinical variables in a population of general practice patients. Compr Psychiatry 2005;46:353–360. 19. Soar K, Turner JJ, Parrott AC. Problematic versus non-problematic ecstasy/MDMA use: the influence of drug usage patterns and pre-existing psychiatric factors. J Psychopharmacol 2006;20:417–424. 20. Brown FW, Golding JM, Smith GR. Psychiatric comorbidity in primary care somatization disorder. Psychosom Med 1990;52:445–451. 21. Garyfallos G, Adamopoulou A, Karastergiou A, Voikli M, Ikonomidis N, Donias S, Giouzepas J, Dimitriou E. Somatoform disorders: comorbidity with other DSM-IIIR psychiatric diagnoses in Greece. Compr Psychiatry 1999;40:299–307. 22. Veale D, Boocock A, Gournay K, Dryden W, Shah F, Willson R, Walburn J. Body dysmorphic disorder: a survey of fifty cases. Br J Psychiatry 1996;169:196–201. 23. Sigvardsson S, von Knorring AL, Bohman M, Cloninger R. An adoption study of somatoform disorders, I: the relationship of somatization to psychiatric disability. Arch Gen Psychiatry 1984;41:853–859. 24. Cloninger CR, Sigvardsson S, von Knorring AL, Bohman M. An adoption study of somatoform disorders, II: identification of two discrete somatoform disorders. Arch Gen Psychiatry 1984;41:863–871. 25. Bohman M, Cloninger R, von Knorring AL, Sigvardsson S. An adoption study of somatoform disorders, III: cross-fostering analysis and genetic relationship to alcoholism and criminality. Arch Gen Psychiatry 1984;41:872–878. 26. Cloninger CR, Bohman M, Sigvardsson S, von Knorring AL. Psychopathology in adopted-out children of alcoholics. The Stockholm adoption study. Recent Dev Alcohol 1985;3:37–51. 27. Golding JM, Rost K, Kashner TM, Smith GR. Family psychiatric history of patients with somatization disorder. Psychiatr Med 1992;10:33–47. 28. Livingston R, Witt A, Smith GR. Families who somatize. J Dev Behav Pediatr 1995;16:42–46. 29. Taylor J, Carey G. Antisocial behavior, substance use, and somatization in families of adolescent drug abusers and adolescent controls. Am J Drug Alcohol Abuse 1998;24:635–646. 30. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 3rd ed Revised. Washington, DC: American Psychiatric Association; 1987. 31. Nurnberger JI, Wiegand R, Bucholz K, O’Connor S, Meyer ET, Reich T, Rice J, Schuckit M, King L, Petti T, Bierut L, Hinrichs AL, Kuperman S, Hesselbrock V, Porjesz B. A family study of alcohol dependence: coaggregation of multiple disorders in relatives of alcohol-dependent probands. Arch Gen Psychiatry 2004;61:1246– 1256. 32. Escobar JI, Burnam MA, Karno M, Forsythe A, Golding JM. Somatization in the community. Arch Gen Psychiatry 1987;44:713–718.

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33. Grabe HJ, Meyer C, Hapke U, Rumpf HJ, Freyberger HJ, Dilling H, John U. Specific somatoform disorder in the general population. Psychosomatics 2003;44:304–311. 34. Simon GE, Gureje O. Stability of somatization disorder and somatization symptoms among primary care patients. Arch Gen Psychiatry 1999;56:90–95. 35. Fink P, Rosendal M, Olesen F. Classification of somatization and functional somatic symptoms in primary care. Aust N Z J Psychiatry 2005;39:772–781. 36. Seng JS, Kohn-Wood LP, Odera LA. Exploring racial disparity in posttraumatic stress disorder diagnosis: implications for care of African American women. J Obstet Gynecol Neonatal Nurs 2005;34:521–530. 37. Robins LN, Helzer JE, Croughan J, Ratcliff KS. National Institute of Mental Health Diagnostic Interview Schedule: its history, characteristics, and validity. Arch Gen Psychiatry 1981;38:381–389. 38. Kroenke K, Spitzer RL, deGruy FV 3rd, Swindle R. A symptom checklist to screen for somatoform disorders in primary care. Psychosomatics 1998;39:263–272. 39. Fink P, Ewald H, Jensen J, Sorensen L, Engberg M, Holm M, Munk-Jorgensen P. Screening for somatization and hypochondriasis in primary care and neurological inpatients: a seven-item scale for hypochondriasis and somatization. J Psychosom Res 1999;46:261–273. 40. Ladwig KH, Marten-Mittag B, Erazo N, Gundel H. Identifying somatization disorder in a population-based health examination survey: psychosocial burden and gender differences. Psychosomatics 2001;42:511–518. 41. Ring A, Dowrick C, Humphris G, Salmon P. Do patients with unexplained physical symptoms pressurise general practitioners for somatic treatment? A qualitative study. BMJ 2004;328:1057. 42. Forman RF, Woody GE, McLellan T, Lynch KG. The availability of web sites offering to sell opioid medications without prescriptions. Am J Psychiatry 2006;163:1233– 1238. 43. Manchikanti L. Prescription drug abuse: what is being done to address this new drug epidemic? Testimony before the subcommittee on criminal justice, drug policy and human resources. Pain Physician 2006;9:287–321. 44. Tomasson K, Kent D, Coryell W. Somatization and conversion disorders: comorbidity and demographics at presentation. Acta Psychiatr Scand 1991;84:288–293. 45. Metrikin AS, Galanter M, Dermatis H, Bunt G. Somatization, anxiety and depression in a drug-free residential therapeutic community. Am J Addict 2003;12:60–70.

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8 STABILITY OF SOMATOFORM SYMPTOMS Implications for Classification Winfried Rief, Ph.D. Graciela Rojas, M.D.

The stability of a diagnosis is suggested as one of the major criteria for validity.

1,2

Patients with one diagnosis should not fall into the category of another diagnosis at follow-up assessment. Robins2 felt that accurate diagnoses should show that the disorder predicts course and does not predict different disorders over time. Diagnostic stability is desirable to buttress validity, although it should be kept in mind that some syndromes are not stable and vary by nature (e.g., manic episodes, transient ischemic attacks); yet nobody questions the validity of these episodic syndromes. Therefore, stability of a syndrome should not be considered as sine qua non for defining classification criteria. However, information on stability of symp-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Rief W, Rojas G: “Stability of Somatoform Symptoms—Implications for Classification.” Psychosomatic Medicine 69:864–869 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission. The mentioned studies from Dr. Rief et al. were funded from the German Ministry of Research and Education (BMBF). There were no significant other sources of funding or support that might have influenced the content of this manuscript.

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toms and syndromes is important, as it can point to weaknesses of some criteria. Low stability of diagnoses can be caused by low reliability of some criteria, although other criteria are reliable and should be maintained in future classification attempts. Therefore, stability results can offer guidelines on how to improve classification rules. In this chapter, we summarize studies presenting data on the stability of criteria for the classification of somatoform syndromes. Unfortunately, the large epidemiological surveys did not address the question of stability of somatoform complaints adequately (e.g., Epidemiological Catchment Area study)3 or even disregarded these frequent health problems (National Comorbidity Survey);4 thus, the empirical basis for our analyses is limited to smaller longitudinal studies. We focus on studies providing data on the classification of multiple somatic symptoms. The discussion of validity criteria of other somatoform disorders such as hypochondriasis can be found elsewhere.5–7 From all subgroups of somatoform disorders, those patients with multiple somatic complaints seem to be the most costly subgroup.8–10 Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR)11 offers the diagnosis of somatization disorder for patients with multiple somatic complaints. The diagnosis of somatization disorder has been criticized frequently,12,13 because this diagnosis does not apply for most patients with multiple somatic complaints. Beside the overexclusiveness of this category, we also outline additional factors that reduce the stability of the diagnostic result.

Overview of Studies Investigating Stability of Criteria of Somatoform Disorders Table 8–1 presents an overview of studies investigating stability aspects of the classification of multiple somatoform symptoms. Study selection resulted from a PubMed/MEDLINE search (search items “somatoform” and “stability”) as well as from individual literature search. It is obvious that many studies confirm the stability of the syndrome, whereas some studies found unexpected changes in symptoms or diagnoses. We highlight two extremes: 1) The study of Kent et al.14 investigated 38 patients with somatization disorder per interview and chart review. Four years later, interviewers blind for the former diagnoses were able to confirm the diagnosis in 37 (97%) of the 38 patients. 2) Arnold et al. found that, even for patients with general somatoform disorders (not only somatization disorder), the syndromes were stable.15 In contrast to these encouraging results, a study of the World Health Organization including 15 study sites in 14 countries found 74 patients with somatization disorder at first assessment, but confirmed this diagnosis only for 21 (28%) 12 months later, whereas 49 patients were newly diagnosed with somatization disorder at follow-up.16 The divergence of the results of the studies mentioned in Table 8–1 are used in this article to analyze sources of unreliability.

Overview on studies investigating the stability of syndromes characterized by multiple somatic complaints

Study

Publication year

Follow-up period

Kent et al.14

1995

4 years

Somatization disorder is very stable (97% of diagnoses confirmed 4 years later), conversion disorder is less stable

Simon and Gureje16

1999

1 year

Symptom report is very unstable (61% of medically unexplained lifetime symptoms were not recalled 1 year later); prevalence rate of syndrome was stable

Lieb et al.22

2002

4 years

Somatization syndrome is as stable as depression and more stable than anxiety disorders

Dickinson et al.28

2003

1–2 years

Jackson et al.34

2006

5 years

Patients with somatoform disorders are unlikely improved until follow-up

2006 (unpublished reanalysis)

6 months

Retest reliability of somatoform symptom count ranges from 0.72 to 0.75

Rief et

al.27

Stability of syndrome

Stability of Somatoform Symptoms

TABLE 8–1.

Reductions of physical quality of life associated with somatoform symptoms is stable or even worse at follow-up

Leiknes et al.18

2006

11 years

Both somatic complaints and somatoform symptoms are unstable features

Arnold et al.15

2006

6 months

From 99 patients with somatoform disorders, the diagnosis was confirmed in 69 patients 6 months later

Bailer et al.25

2007

1 year

86% of patients with multiple somatoform symptoms (>3) were reclassified correctly 1 year later

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Lifetime Versus Present State Diagnosis Somatization disorder according to DSM-IV-TR requires “a history of many physical complaints beginning before the age of 30 years….”11 Thus, somatization disorder is a lifetime disorder, not a present state diagnosis. This has several implications. A key question is whether people can ever be cured of this disorder, as the history of symptoms always remains. Moreover, this diagnosis requires that patients remember symptoms correctly over many years. Finally, remembering the onset of symptoms if the onset was months or years ago is definitely a source of erroneous reports.17 The difference between lifetime symptom report and present state symptoms in somatoform disorders is impressive. Simon and Gureje found that 61% of medically unexplained lifetime symptoms were not reported 1 year later.16 Although the prevalence rates of current somatization syndromes were comparable between the two assessment points, many people were not able to remember the symptoms they reported 1 year ago. However, it is unclear whether inaccurate recall is restricted to somatoform symptoms or whether this holds true for the lifetime report of symptoms in general. Another study demonstrated that the report of physical complaints is erroneous in general, not only in medically unexplained symptoms.18 In an 11-year follow-up study, the authors found that lifetime symptom report is unreliable both for medically unexplained and medically explained symptoms. If classification depends on memory of past symptoms, typical memory errors occur. Symptom report of past symptoms is highly dependent on current symptoms and current symptom intensity. People seem to remember former physical complaints better if they (still) suffer from these symptoms at present. Furthermore, if symptoms are currently very intense, their course is remembered as being longer and their duration is overestimated. An experimental investigation has shown that unpleasant medical procedures are remembered as less unpleasant if they are followed by a more positive procedure compared with no subsequent procedure.19 Thus, current body sensations including severity and how recently they have occurred may influence the accuracy of symptom recall.

Culture-Specific Aspects Influencing Stability Another problem when using long time frames for classification is the fact that the use of terms for time periods is partially culture bound. Although number of years, day of birth, etc., are important and frequently used anchors of time ratings in most developed countries, some languages of developing countries do not even have terms for time periods such as month or year and do not register birthdays. If people do not know their birthday or their age, they cannot remember whether symptoms were present before the age of 30 years, as requested for somatization

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disorder according to DSM-IV-TR; thus, this time criteria opens the door for cultural differences in the validity of diagnostic classification. Another source of culture-bound instability of the diagnosis of somatoform disorders is the list of symptoms that are included. The frequency of individual symptoms varies substantially between cultures,20,21 although grouping of symptoms might increase stability and also might reduce cultural differences. The only study in Table 8–1 that includes not only developed but also developing countries was the one demonstrating low stability of somatization disorder.16 The other studies investigated samples from the United States, The Netherlands, Scandinavia, and Germany. Therefore, there is a substantial need to investigate more systematically cultural issues in future studies.

Stability of Somatoform Disorders in Younger People Most mental disorders develop in youth and adolescence. Therefore, the longitudinal investigation of symptoms and syndromes in this age group challenges the aspect of stability the most, as symptoms are not yet chronic and symptom recovery is more likely during adolescence than it is later. A very sound epidemiological survey investigating psychiatric symptoms by means of structured clinical interviews was done in Germany.22 The authors assessed anxiety, depressive, and somatoform symptoms in 2,548 adolescents and young adults. In this 4-year follow-up study, the authors found that somatization syndrome was as stable as depression and more stable than anxiety disorder. About half of the young people describing depression or multiple somatic complaints confirmed these syndromes 4 years later. Thus, although there is some variation, the present state diagnosis of somatization syndrome seems to be in the stability range of other psychiatric disorders.

Minimum Duration of 6 Months For the diagnosis of undifferentiated somatoform disorders or somatoform pain disorder, a minimum symptom duration of 6 months is required. Although the use of this time period leads to culture-dependent variations of stability, it seems to have stability-increasing effects in many countries. When all currently presented symptoms in primary care are considered, many symptoms improve or disappear in subsequent months or years.23 However, if only patients with a minimum symptom duration of 6 months are included, somatoform symptoms are more likely to persist until follow-up.15 Therefore, it seems to make sense to distinguish spontaneously resolving symptoms from more persistent bodily complaints. However, it should be kept in mind that primary care doctors also need terms or diagnoses to

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describe patients requesting investigations because of nonpersistent physical complaints;24 such a diagnosis, however, is unstable per definition.

Stability of Single Symptoms Versus Syndromes Many patients have various coexisting somatic symptoms (“somatoform syndromes”) instead of single symptoms. If syndromes instead of single symptoms are considered, the stability is much higher. For the discussion of this issue, two types of stability must be distinguished: a) the stability of the symptom report of individual patients, and b) the stability of overall prevalence rates in large samples. Even the provocative results of the Simon and Gureje trial demonstrated that the present state prevalence rate of somatoform syndromes was the same at first assessment and 1 year later, although the individuals fulfilling the criteria were different at the two assessment points. Leiknes et al. investigated stability within individual patients and reported that the grouping of symptoms improved substantially the stability of symptom report.18 Using the Composite International Diagnostic Interview, the researchers found that between 22% and 100% of individual symptoms were lost to recall at follow-up 11 years later; this rate was substantially lower for groups of symptoms. Interestingly, the rate of forgetting symptoms was influenced by age and gender, with men tending to forget more symptoms, and younger respondents remembering slightly better at follow-up. The increase of stability when grouping symptoms with a syndrome of polysymptomatic somatoform disorder has been shown impressively in another study investigating primary care patients.23 In a 5-year follow-up study of 500 patients, the authors showed that individual symptoms have high rates of resolution in the upcoming months and years. However, if patients had multisomatoform disorder, they were less likely to improve than patients with fewer medically unexplained symptoms. Sixty-seven percent of patients who had two or more bothersome symptoms at baseline still had bothersome symptoms 5 years later. This rate increased to 94% of patients with bothersome symptoms 5 years later, if they had five or more bothersome symptoms at baseline. These results are confirmed by a recently published study showing that 86% of patients with multiple somatoform symptoms (at least three symptoms) were reclassified correctly 1 year later.25 To summarize, there is evidence that grouping of individual symptoms with syndromes increases the stability at follow-up. Probably even other diagnoses that are based on symptom counts (e.g., panic attacks, major depression) may not have stability of individual symptoms, but patients could still meet the criteria for the disorder although specific symptoms have changed over time.

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Doctors’ Rating of Origin of Symptoms; Self-Rating Versus Expert Rating of Symptoms The diagnosis of somatization disorder requires that physicians rate the origin of the physical complaints as “not fully explained by a known general medical condition.” Therefore, physicians’ ratings about the origin of the symptoms are crucial for the diagnosis. However, this seems to be a substantial source of instability, as doctors vary tremendously in their rating systems. Fink, Rosendal, and Olesen have shown that 37 general practitioners rated the prevalence of medically unexplained symptoms in their patients very differently (from 4% to 33%).7 However, this huge variation of ratings did not reflect real prevalence differences between medical offices, as the somatization scale of the Symptom Check List indicated a constant rate of about 30% of patients with increased somatization scores in all general practitioner offices. Therefore, it can be postulated that doctors’ ratings about the origin of physical complaints is a substantial source of unreliability. Considering cultural issues, doctor’s assumptions about etiology lead to further interrater differences. In developing countries, doctors’ possibilities for expensive medical examinations are limited. They must decide about the origin of the symptoms with much less diagnostic information than a doctor who has access to multiple, highly sophisticated, and expensive examination results. As long as the diagnosis of somatoform disorder primarily depends on excluded organic conditions, this might be a further reason for cultural variations. Despite this fact, expert ratings on the number of somatoform symptoms correlate substantially with self-ratings of patients (r=0.73).26 However, in the above study, experts used a structured and standardized interview to diagnose somatoform symptoms and were familiar with the medical charts. The study aimed to analyze whether expert ratings and patient ratings about the number of somatoform symptoms have different reliability. We reanalyzed the data of a sample described in a recently published study,27 including 295 primary care patients. The 6 months retest correlation for the number of somatoform symptoms is in the range of r=0.72 (somatoform symptom count according to expert interview) and r=0.75 (according to self-rating), which can be considered as substantially high. Thus, the variable “somatoform symptom count” reveals stable scores in both self-ratings and in expert ratings.

Stability of Associated Disability It is not only the syndrome that seems to be stable but also the associated physical functioning and quality of life. This was shown in a study by Dickinson and others using the self-rating scale SF-36.28 Patients with multiple somatoform symptoms were in the lowest quartile of physical functioning at first assessment and at 1 and

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2 years later. Thus, multiple somatoform symptoms are associated with persistent reduction in quality of life and continuing disability.

Are Somatoform Disorders Misdiagnosed Organic Conditions? The detection of a medical disease that explains all the somatic complaints could be one reason for reduced stability of the diagnosis of somatoform disorders. The scientific community was alarmed after Slater and Glithero published that many patients with “conversion or hysteria” had misdiagnosed serious, sometimes even life-threatening diseases.29 However, a reanalysis of all trials on misdiagnosed patients initially diagnosed as “conversion” or “hysteria” has shown that the majority of studies reported misdiagnosis rates of less than 10%. Studies published from 1980 showed a mean rate of misdiagnoses of 4%.30 For somatization disorder, 1 of 37 patients with this disorder was detected as misdiagnosed 4 years later.14 In one of our studies, 6 (2%) of 295 primary care patients with multiple somatoform symptoms were found as possible misdiagnosed organic condition during follow-up.27 Although misdiagnoses rates should always be minimized, for somatoform disorders this rate is in the range of misdiagnoses that are found for other mental or physical disorders.

Implications for Revising the Somatoform Disorders Category to DSM-V The existing criteria for somatoform disorders are an issue for debates,31–33 and most experts agree that there is a substantial need for improving the classification of people with multiple somatic complaints not better explained by a known medical condition. Whereas some authors favor an abolition of this category and moving these diagnoses to other mental or physical disorders, others argue to improve the existing category. This overview on stability aspects of classification criteria offers some aspects that help to improve the quality of these diagnoses. The implications for the planning of future classification systems are outlined below.

FOCUSING ON MULTIPLE SOMATIC COMPLAINTS Despite the critique of some experts31,32 on the category of somatoform disorders in general, we suggest continuing to focus on somatic complaints when classifying these disorders and not to merge this category under affective or anxiety disorders. The number of bodily symptoms is a relevant predictor of outcome in many dif-

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ferent medical settings and predicts certain outcomes (e.g., functional status, health care use) as well or better than does anxiety or depression.34,35 Moreover, somatoform symptoms have a specific impact on health services use that is not explained by depression or anxiety.36,37 Further, somatic complaints show different treatment responses in antidepressant trials compared with pure depression or anxiety disorders.38,39 Results on stability of somatic complaints show that individual symptoms vary tremendously over time, whereas polysymptomatic syndromes have stable features. This is a reason to distinguish monosymptomatic and polysymptomatic syndromes in the classification. Different proposals for polysymptomatic somatoform disorders have been presented.12,35,40 All of these diagnostic groups show considerable impairment,28 thus justifying classification as a disorder. However, the cutoffs for classification should be much lower than previously used for somatization disorder, as the diagnosis of somatization disorder covers only a very small part (