Dimensional Models of Personality Disorders: Refining the Research Agenda for DSM-V

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DIMENSIONAL MODELS OF PERSONALITY DISORDERS Refining the Research Agenda for DSM-V

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DIMENSIONAL MODELS OF PERSONALITY DISORDERS Refining the Research Agenda for DSM-V Edited by

Thomas A. Widiger, Ph.D. Erik Simonsen, M.D. Paul J. Sirovatka, M.S. Darrel A. Regier, M.D., M.P.H.

Published by the American Psychiatric Association Washington, D.C.

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 © 2006 American Psychiatric Association ALL RIGHTS RESERVED Manufactured in the United States of America on acid-free paper 10 09 08 07 06 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 Dimensional models of personality disorders : refining the research agenda for DSM-V / edited by Thomas A. Widiger ... [et al.]. — 1st ed. p. ; cm. Includes bibliographical references and index. ISBN 0-89042-296-6 (pbk. : alk. paper) 1. Personality disorders—Classification. 2. Diagnostic and statistical manual of mental disorders. I. Widiger, Thomas A. [DNLM: 1. Personality Disorders—classification. 2. Models, Psychological. WM 15 D582 2006] RC554.D555 2006 616.85'8—dc22 2006014661 British Library Cataloguing in Publication Data A CIP record is available from the British Library.

This text is dedicated to the memory of Jerry S. Wiggins

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CONTENTS CONTRIBUTORS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xi DISCLOSURE STATEMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv FOREWORD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xvii Darrel A. Regier, M.D., M.P.H. PREFACE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xxi Thomas A. Widiger, Ph.D. Erik Simonsen, M.D. INTRODUCTION. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xxv Erik Simonsen, M.D. Thomas A. Widiger, Ph.D.

1

ALTERNATIVE DIMENSIONAL MODELS OF PERSONALITY DISORDER: Finding a Common Ground. . . . . . . . . . . . . 1 Thomas A. Widiger, Ph.D. Erik Simonsen, M.D.

2

COMMENTARY ON WIDIGER AND SIMONSEN: Toward a Consensus Personality Trait Structure. . . . . . . . . . . . . . . . . . 23 Lee Anna Clark, Ph.D.

3

COMMENTARY ON WIDIGER AND SIMONSEN: Working Out a Dimensional Framework . . . . . . . . . . . . . . . . . . . . . . . 29 John M. Oldham, M.D.

4

COMMENTARY ON WIDIGER AND SIMONSEN: From ICD-10 and DSM-IV to ICD-11 and DSM-V . . . . . . . . . . . . . . . . 33 Charles B. Pull, M.D., Ph.D.

5

BEHAVIORAL AND MOLECULAR GENETIC CONTRIBUTIONS TO A DIMENSIONAL CLASSIFICATION OF PERSONALITY DISORDER. . . . . 39 W. John Livesley, M.D., Ph.D.

6

COMMENTARY ON LIVESLEY: Genetic Contributions to a Dimensional Classification: Problems and Pitfalls . . . . . . . . . . . . . . 55 Peter McGuffin, M.D., Ph.D.

7

NEUROBIOLOGICAL DIMENSIONAL MODELS OF PERSONALITY: A Review of Three Models . . . . . . . . . . . . . . . . . . 61 Joel Paris, M.D.

8

COMMENTARY ON PARIS: Personality as a Dynamic Psychobiological System . . . . . . . . . . . . . . . 73 C. Robert Cloninger, M.D.

9

COMMENTARY ON PARIS: The Problem of Severity in Personality Disorder Classification . . . . . . . 77 Peter Tyrer, M.D.

10 TEMPERAMENT AND PERSONALITY AS BROAD-SPECTRUM ANTECEDENTS OF PSYCHOPATHOLOGY IN CHILDHOOD AND ADOLESCENCE . . . . . . . . . . . . . . . . . . . . . . . . 85 Ivan Mervielde, Ph.D. Barbara De Clercq, Ph.D. Filip De Fruyt, Ph.D. Karla Van Leeuwen, Ph.D.

11 COMMENTARY ON MERVIELDE ET AL.: Toward a Developmental Perspective on Personality Disorders . . . . . 111 Rebecca L. Shiner, Ph.D.

12 PERSONALITY DIMENSIONS ACROSS CULTURES . . . . . . . . . . . . . . . 117 Jüri Allik, Ph.D.

13 COMMENTARY ON ALLIK: The Lexical Approach to the Study of Personality Structure. . . . . . . . 133 Michael Ashton, Ph.D.

14 COMMENTARY ON ALLIK: A Historical Perspective on Personality Disorder . . . . . . . . . . . . . . . . 139 Juan J. López-Ibor, M.D.

15 COMMENTARY ON ALLIK: Cross-Cultural Diagnosis of Personality Disorders. . . . . . . . . . . . . . . 143 Yueqin Huang, M.D., M.P.H., Ph.D. Siu Wa Tang, M.B., Ph.D., F.R.C.P.(C.)

16 CONTINUITY OF AXES I AND II:

Toward a Unified Model of Personality, Personality Disorders, and Clinical Disorders . . . . . . . . . . 149 Robert F. Krueger, Ph.D.

17 COMMENTARY ON KRUEGER: What to Do With the Old Distinctions. . . . . . . . . . . . . . . . . . . . . . . . 163 M. Tracie Shea, Ph.D.

18 COMMENTARY ON KRUEGER: Traits Versus Types in the Classification of Personality Pathology . . . . 167 David Watson, Ph.D.

19 DIMENSIONAL MODELS OF PERSONALITY DISORDER: Coverage and Cutoffs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171 Timothy J. Trull, Ph.D.

20 COMMENTARY ON TRULL:

Drizzling on the 5 ± 3 Factor Parade . . . 189

Drew Westen, Ph.D.

21 COMMENTARY ON TRULL:

Just Do It: Replace Axis II With a Diagnostic System Based on the Five-Factor Model of Personality . . . 195 Paul Costa Jr., Ph.D.

22 COMMENTARY ON TRULL:

Reservations and Hopes . . . . . . . . . . . . 199

Carl C. Bell, M.D.

23 CLINICAL UTILITY OF DIMENSIONAL MODELS FOR PERSONALITY PATHOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203 Roel Verheul, Ph.D.

24 COMMENTARY ON VERHEUL: Focusing on the Clinician’s Need for a Better Model . . . . . . . . . . . . . 219 Erik Simonsen, M.D.

25 COMMENTARY ON VERHEUL: Clinical Utility of Dimensional Models for Personality Pathology . . . . 227 Theresa Wilberg, M.D., Ph.D.

26 PERSONALITY DISORDER RESEARCH AGENDA FOR DSM-V . . . . . . . 233 Thomas A. Widiger, Ph.D. Erik Simonsen, M.D. Robert F. Krueger, Ph.D. W. John Livesley, M.D., Ph.D. Roel Verheul, Ph.D. INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257

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CONTRIBUTORS Jüri Allik, Ph.D. Professor, Department of Psychology, University of Tartu, Estonia; Supervisor, Perception and Personality Research Team, The Estonian Center of Behavioral and Health Sciences, Tartu, Estonia Michael Ashton, Ph.D. Associate Professor, Department of Psychology, Brock University, St. Catharines, Ontario, Canada Carl C. Bell, M.D. C.E.O./President, Community Mental Health Council, Inc., Chicago, Illinois; Professor of Psychiatry and Public Health, Director of Public and Community Psychiatry, Department of Psychiatry, University of Illinois at Chicago Lee Anna Clark, Ph.D. Professor of Psychology, Department of Psychology, University of Iowa, Iowa City, Iowa C. Robert Cloninger, M.D. Wallace Renard Professor of Psychiatry and Genetics, Department of Psychiatry, Washington University Medical School, Saint Louis, Missouri Paul Costa Jr., Ph.D. Chief, Laboratory of Personality and Cognition, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland; Professor of Behavioral Biology, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine, Baltimore, Maryland Barbara De Clercq, Ph.D. Researcher, Department of Developmental, Personality and Social Psychology, Ghent University, Ghent, Belgium Filip De Fruyt, Ph.D. Professor, Department of Developmental, Personality, and Social Psychology, Ghent University, Ghent, Belgium xi

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Yueqin Huang, M.D., M.P.H., Ph.D. Professor, Institute of Mental Health, Peking University, Beijing, China Robert F. Krueger, Ph.D. Associate Professor, Department of Psychology, University of Minnesota, Minneapolis, Minnesota W. John Livesley, M.D., Ph.D. Professor, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada Juan J. López-Ibor, M.D. Chairman, Institute of Psychiatry and Mental Health, Hospital Clínica San Carlos, Universidad Complutense, Madrid, Spain Peter McGuffin, M.D., Ph.D. Director and Professor of Psychiatric Genetics, Medical Research Council Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King’s College London, United Kingdom Ivan Mervielde, Ph.D. Professor, Department of Developmental, Personality and Social Psychology, Ghent University, Ghent, Belgium John M. Oldham, M.D. Professor and Chairman, Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, South Carolina Joel Paris, M.D. Professor of Psychiatry, McGill University, Montreal, Quebec, Canada Charles B. Pull, M.D., Ph.D. Professor and Chairman, Department of Neurosciences, Centre Hospitalier de Luxembourg, Luxembourg, Grand-Duché de Luxembourg M. Tracie Shea, Ph.D. Professor, Department of Psychiatry and Human Behavior, Brown University Medical School, Veterans Affairs Medical Center, Providence, Rhode Island Rebecca L. Shiner, Ph.D. Associate Professor, Department of Psychology, Colgate University, Hamilton, New York

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Erik Simonsen, M.D. Associate Research Professor, University of Copenhagen, and Medical Director, Institute of Personality Theory and Psychopathology, Copenhagen, Denmark Paul J. Sirovatka, M.S. Associate Director for Research Policy Analysis, Division of Research/American Psychiatric Institute for Research and Education, Arlington, Virginia Siu Wa Tang, M.B., Ph.D., F.R.C.P.(C.) Professor and Head, Department of Psychiatry, The University of Hong Kong, Hong Kong, China Timothy J. Trull, Ph.D. Professor, Department of Psychological Sciences, University of Missouri at Columbia, Columbia, Missouri Peter Tyrer, M.D. Professor of Community Psychiatry, Department of Psychological Medicine, Imperial College London, United Kingdom Karla Van Leeuwen, Ph.D. Postdoctoral researcher, Department of Developmental, Personality and Social Psychology, Ghent University, Ghent, Belgium Roel Verheul, Ph.D. Professor of Personality Disorders, Department of Clinical Psychology, University of Amsterdam (UvA), Amsterdam, The Netherlands; Managing Director, Viersprong Institute for Studies on Personality Disorders (VISPD), Halsteren, The Netherlands David Watson, Ph.D. F. Wendell Miller Professor, Department of Psychology, University of Iowa, Iowa City, Iowa Drew Westen, Ph.D. Professor, Departments of Psychology and Psychiatry, Emory University, Atlanta, Georgia Thomas A. Widiger, Ph.D. Professor, Department of Psychology, University of Kentucky, Lexington, Kentucky Theresa Wilberg, M.D., Ph.D. Department for Research and Education, Psychiatric Division, Ulleval University Hospital, Oslo, Norway

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DISCLOSURE STATEMENT The research conference series that produced this monograph is supported with funding from the U.S. National Institutes of Health (NIH), Grant No. U13MH067855 (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 Institutes on Alcohol Abuse and Alcoholism (NIAAA) jointly support this cooperative research planning conference project. The Workgroup/Conference on Personality Disorders is not part of the official revision process for the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V), but rather is a separate, rigorous research planning initiative meant to inform revisions of psychiatric diagnostic classification systems. No private-industry sources provide funding for the research review. Coordination and oversight of the overall research review, publicly titled “The Future of Psychiatric Diagnosis: Refining the Research Agenda,” is provided by an Executive Steering Committee composed of representatives of the several entities that are cooperatively sponsoring the NIH-funded project. Present and former members are as follows: • American Psychiatric Institute for Research and Education—Darrel A. Regier, M.D., M.P.H.; support staff: William E. Narrow, M.D., M.P.H., Maritza Rubio-Stipec, Sci.D., Paul Sirovatka, M.S., Jennifer Shupinka, Rocio Salvador, and Kristin Edwards • World Health Organization—Benedetto Saraceno, M.D., and Norman Sartorius, M.D., Ph.D. (consultant) • National Institutes of Health—Wayne Fenton, M.D. (NIMH), Wilson Compton, M.D. (NIDA), and Bridget Grant, Ph.D. (NIAAA); NIMH grant project officers have included Bruce Cuthbert, Ph.D., Lisa Colpe, Ph.D., Michael Kozak, Ph.D., and Karen H. Bourdon, M.A. • Columbia University—Michael B. First, M.D. (consultant)

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

Dimensional Models of Personality Disorders: Refining the Research Agenda for DSM-V is the first in a series of volumes that collectively will summarize an international research-planning project undertaken to assess the status of scientific knowledge that is relevant to psychiatric classification systems and to generate specific recommendations for research to advance that knowledge base. As does the current volume, each forthcoming monograph in the series will report on a conference focused on a specific diagnostic topic or category, if not a delimited diagnosis. Titled “The Future of Psychiatric Diagnosis: Refining the Research Agenda,” the conference series is being convened by the American Psychiatric Association (APA) with the collaboration of the World Health Organization (WHO) and the U.S. National Institutes of Health (NIH). The APA/WHO/NIH conference series and monographs represent key elements in an extensive research review process designed to set the stage for the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). APA intends that information and recommendations developed as part of this process also should be available to scientific groups who are updating other national and international classifications of mental and behavioral disorders. Within the APA, the American Psychiatric Institute for Research and Education (APIRE), under the direction of Darrel A. Regier, M.D., M.P.H., holds lead responsibility for organizing and administering the diagnosis research planning conferences. Co-sponsors, and members of the Executive Steering Committee for the series, include representatives of the WHO’s Department of Mental Health and Substance Abuse and of three NIH institutes that are jointly funding the project: the National Institute 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 the DSM in 1994 and a text revision in 2000. With a target publication date of 2011 for DSM-V, we initiated planning for the fifth revision 12 years in advance, with the aim of stimulating research that would address identified opportunities as well as gaps in nosological research. The initial step was a 1999 collaboration between APA and NIMH that led to prepaxvii

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ration 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 programs. The volume A Research Agenda for DSM-V (Kupfer et al. 2002) more recently has been followed by a second compilation of white papers (Narrow et al., in press) that outline diagnosis-related research needs in the areas of gender, infants and children, and geriatric populations. As a second phase of planning, the APA leadership envisioned a series of 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. A prototype symposium on mood disorders was held in conjunction with the XII World Congress of Psychiatry in Yokohama, Japan, in late 2002. Presentations addressed diverse topics in depression-related research, including preclinical animal models, genetics, pathophysiology, functional imaging, clinical treatment, epidemiology, prevention, medical comorbidity, and public health implications of the full spectrum of mood disorders. This pilot effort underscored the importance of structuring multidisciplinary research planning conferences in a manner that would force interaction among investigators from different fields and elicit a sharp focus on the diagnostic implications of recent and planned research. These emphases strongly influenced the proposal for the cooperative research planning conference grant that NIMH awarded to APIRE in 2003, with substantial additional funding support from NIDA and NIAAA. Eleven conferences funded under the grant are the basis for this and future monographs in this series, and represent a second major phase in the scientific review and planning for DSM-V. Finally, a third major component of advance planning is the DSM-V Prelude Project, an APA-sponsored Web site designed to keep the DSM user community and the public informed about research and other activities related to the fifth revision of the manual. An “outreach” section of the site permits interested parties to submit comments about problems with DSM-IV and suggestions for DSM-V. All suggestions are being entered into the DSM-V Prelude database for eventual referral to the appropriate DSM-V Work Groups. This site and associated links can be accessed at www.dsm5.org. The conferences that comprise the core activity of the second phase of preparation have multiple aims. One is to promote international collaboration among members of the scientific community in order to increase the likelihood of developing a future DSM that is unified with other international classifications. A second aim is to stimulate the empirical research necessary to allow informed decision-making regarding crucial diagnostic deficiencies identified in DSM-IV. A

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third is to facilitate the development of consensus criteria that could be used by the research community as alternatives to the clinical DSM criteria for future research into 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 documenting the validity of diagnoses. Given the vision of an ultimately unified international classification system, members of the Executive Steering Committee have attached high priority to ensuring the participation of investigators from all parts of the world in the project. Toward this end, each conference in the series will have two co-chairs, drawn respectively from the United States and a country other than the United States; approximately half of the 25 experts invited to each working conference are from outside the United States; and half of the conferences are being convened outside the United States. Two leaders in the field of personality disorders research—Thomas Widiger, University of Kentucky, and Erik Simonsen, University of Copenhagen—agreed to help organize and co-chair the first conference. As evident in the contributions that follow, Drs. Widiger and Simonsen, working closely with the Executive Steering Committee, succeeded in inviting a stellar roster of participants for the conference. This monograph is the second of two reports derived from the conference on personality disorders. Earlier products included two successive issues of the Journal of Personality Disorders (Widiger and Simonsen 2005a, 2005b), which published eight of the papers presented in this monograph and which appear here with the permission of the journal.

References Kupfer DJ, First MB, Regier DA: Introduction, in A Research Agenda for DSM-V. Edited by Kupfer DJ, First MB, Regier DA. Washington, DC, American Psychiatric Association, 2002, pp xv–xxiii Narrow WN, First MB, Sirovatka P, et al. (eds): Age and Gender Considerations in Psychiatric Diagnosis: A Research Agenda for DSM-V. Arlington, VA, American Psychiatric Association (in press) Widiger TA, Simonsen E: Alternative dimensional models of personality disorder: finding a common ground. J Personal Disord 19:110–130, 2005a Widiger TA, Simonsen E: Personality disorder research agenda for DSM-V. J Personal Disord 19:315–338, 2005b

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PREFACE Thomas A. Widiger, Ph.D. Erik Simonsen, M.D.

I

n 1999, a DSM-V Research Planning Conference was held under joint sponsorship of the American Psychiatric Association (APA) and the National Institute of Mental Health (NIMH), the purpose of which was to set research priorities that might affect future classifications (McQueen 2000). One impetus for this conference was frustration with the existing nomenclature: In the more than 30 years since the introduction of the Feighner criteria by Robins and Guze, which eventually led to DSM-III, the goal of validating these syndromes and discovering common etiologies has remained elusive. Despite many proposed candidates, not one laboratory marker has been found to be specific in identifying any of the DSM-defined syndromes. Epidemiological and clinical studies have shown extremely high rates of comorbidities among the disorders, undermining the hypothesis that the syndromes represent distinct etiologies. Furthermore, epidemiological studies have shown a high degree of short-term diagnostic instability for many disorders. With regard to treatment, lack of treatment specificity is the rule rather than the exception. (Kupfer et al. 2002, p. xviii)

DSM-V Research Planning Work Groups were formed to develop white papers to guide research in a direction that would maximize impact on future editions of the diagnostic manual. The Nomenclature Work Group, charged with addressing fundamental assumptions of the diagnostic system, concluded that it is “important that consideration be given to advantages and disadvantages of basing part or all of DSM-V on dimensions rather than categories” (Rounsaville et al. 2002, p. 12). The Nomenclature Work Group recommended in particular that initial efforts toward a dimensional model of classification be conducted with the personality disorders. “If a dimensional system of personality performs well and is acceptable to clinicians, it might then be appropriate to explore dimensional approaches in other domains” (Rounsaville et al. 2002, p. 13). The white papers developed by the DSM-V Research Planning Work Groups were published in an APA monograph, edited by Drs. Kupfer, First, and Regier (Kupfer et al. 2002). The white paper addressing personality disorders provided xxi

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conceptual and empirical support for a dimensional model of classification (First et al. 2002). A closely related monograph concerned with dilemmas in psychiatric diagnosis (Phillips et al. 2003) was published by the APA the following year. This monograph included a chapter by Livesley (2003) that again provided conceptual and empirical support for a dimensional model of personality disorder classification. The white papers developed by the DSM-V Research Planning Work Groups are being followed by a series of international conferences that aim to further enrich the empirical data base in preparation for the eventual development of DSM-V (a description of this conference series can be found at www.dsm5.org). These conferences are being organized with the assistance and support of the World Health Organization and are co-funded by the NIMH, the National Institute on Alcohol Abuse and Alcoholism, and the National Institute on Drug Abuse. The principal purpose of each conference is to offer recommendations for, and stimulate the production of, research that would be of most use to the authors of DSM-V. The Executive Committee governing these conferences (i.e., Drs. William Compton, Bruce Cuthbert, Michael First, Bridget Grant, Darrel Regier, Benedetto Saraceno, and Norman Sartorious) decided to devote the first conference to reviewing the research and setting a research agenda that would be most useful and effective in leading the field toward a dimensional classification of personality disorder. This conference, “Dimensional Models of Personality Disorder: Etiology, Pathology, Phenomenology, and Treatment,” was held on December 1–3, 2004, at the APA headquarters in Arlington, Virginia. Members of the conference steering committee were Drs. Robert Krueger, John Livesley, Erik Simonsen (Co-Chair), Roel Verheul, and Thomas Widiger (Co-Chair). Topics covered were 1) alternative dimensional models of personality disorder (Drs. Thomas Widiger and Erik Simonsen), 2) behavioral genetics and gene mapping (Dr. John Livesley), 3) neurobiological mechanisms (Dr. Joel Paris), 4) childhood antecedents (Drs. Ivan Mervielde, Barbara De Clercq, Filip De Fruyt, and Karla Van Leeuwen), 5) crosscultural issues (Dr. Jüri Allik), 6) Axes I and II continuity (Dr. Robert Krueger), 7) coverage and cutoff points for diagnosis (Dr. Timothy J. Trull), and 8) clinical utility (Dr. Roel Verheul). The conference began with an introductory paper by Dr. Erik Simonsen, followed by the eight plenary papers that summarized the existing research and made recommendations for future research. Each plenary address was followed by brief discussant papers, provided by Drs. Michael Ashton, Carl Bell, Lee Anna Clark, Robert Cloninger, Paul Costa, Benjamin Greenberg, Deborah Hasin, Yueqin Huang, Juan J. López-Ibor, Peter McGuffin, John Oldham, Charles Pull, M. Tracie Shea, Rebecca Shiner, Erik Simonsen, Peter Tyrer, David Watson, Drew Westen, and Theresa Wilberg. Abbreviated versions of the plenary addresses were initially published across two special issues of the Journal of Personality Disorders (Widiger and Simonsen 2005). The Editor of Journal of Personality Disorders (Dr. John Livesley) and Guilford Publications graciously consented to allow abbreviated versions of the journal

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articles to be published together within this monograph. This monograph also includes abbreviated versions of the discussant papers by Drs. Michael Ashton, Carl Bell, Lee Anna Clark, Robert Cloninger, Paul Costa, Yueqin Huang, Juan J. LópezIbor, Peter McGuffin, John Oldham, Charles Pull, M. Tracie Shea, Rebecca Shiner, Erik Simonsen, Peter Tyrer, David Watson, Drew Westen, and Theresa Wilberg. One should not infer from the conference and this monograph publication that the existing categories of personality disorder will be replaced in the next edition of the diagnostic manual by a dimensional classification. There are arguments against making such a conversion. However, it is hoped that the publication of these papers will indeed provide further support for and stimulation toward the eventual adoption of a dimensional model of personality disorder by the American Psychiatric Association and the World Health Organization.

References First MB, Bell CB, Cuthbert B, et al: Personality disorders and relational disorders: a research agenda for addressing crucial gaps in DSM, in A Research Agenda for DSM-V. Edited by Kupfer DJ, First MB, Regier DA. Washington, DC, American Psychiatric Association, 2002, pp 123–199 Kupfer DJ, First MB, Regier DA: Introduction, in A Research Agenda for DSM-V. Edited by Kupfer DJ, First MB, Regier DA. Washington, DC, American Psychiatric Association, 2002, pp xv–xxiii Livesley WJ: Diagnostic dilemmas in classifying personality disorder, in Advancing DSM: Dilemmas in Psychiatric Diagnosis. Edited by Phillips KA, First MB, Pincus HA. Washington, DC, American Psychiatric Association, 2003, pp 153–190 McQueen L: Committee on Psychiatric Diagnosis and Assessment update on publications and activities. Psychiatric Res Rep 16(2):3, 2000 Phillips KA, First MB, Pincus HA (eds): Advancing DSM: Dilemmas in Psychiatric Diagnosis. Washington, DC, American Psychiatric Association, 2003 Rounsaville BJ, Alarcon RD, Andrews G, et al: Basic nomenclature issues for DSM-V, in A Research Agenda for DSM-V. Edited by Kupfer DJ, First MB, Regier DA. Washington, DC, American Psychiatric Association, 2002, pp 1–19 Widiger TA, Simonsen E: Introduction to the special section: the American Psychiatric Association’s research agenda for DSM-V. J Personal Disord 19:103–109, 2005

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INTRODUCTION Erik Simonsen, M.D. Thomas A. Widiger, Ph.D.

Current Categorical Classification of Personality Disorders The personality disorder nomenclatures of the World Health Organization’s (WHO) International Classification of Diseases, 10th Revision (ICD-10; World Health Organization 1992) and the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM-IV-TR; American Psychiatric Association 2000) are quite similar. The notable exceptions are as follows: 1. ICD-10 schizotypy is consistent with DSM-IV (American Psychiatric Association 1994) schizotypal personality disorder but is included within the section for schizophrenia and schizotypal and delusional disorders. 2. DSM-IV narcissistic personality disorder is not included in ICD-10. 3. Some disorders have different names: DSM-IV borderline (ICD-10 emotional unstable), DSM-IV avoidant (ICD-10 anxious), and DSM-IV obsessive-compulsive (ICD-10 anankastic). Personality disorders are regarded as being among the more important diagnoses within the APA’s diagnostic nomenclature because they have the unique distinction of being placed on a separate diagnostic axis, thereby drawing the attention of many clinicians who may otherwise not have considered their presence. They were first placed on a separate axis in DSM-III (American Psychiatric Association 1980) in order to encourage clinicians to recognize the presence of maladaptive personality traits even when their attention is understandably drawn to a disorder of more immediate, pressing concern (Frances 1980; Spitzer et al. 1980): “This separation ensures that consideration is given to the possible presence of disorders that are frequently overlooked when attention is directed to the usually more florid Axis I disorder” (American Psychiatric Association 1980, xxv

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p. 23). The reason the authors of the multiaxial system of DSM-III wanted to draw attention to personality disorders was the “accumulating evidence that the quality and quantity of preexisting personality disturbance may...influence the predisposition, manifestation, course, and response to treatment of various Axis I conditions” (Frances 1980, p. 1050). DSM-IV and ICD-10 diagnose personality disorders categorically. The clinician determines whether the personality disorder symptomatology of a patient is sufficiently close to a particular diagnostic category to warrant the respective diagnosis. To facilitate the reliability and validity of this effort, DSM-IV includes specific and explicit diagnostic criteria sets (Spitzer et al. 1980). There are a number of advantages of the categorical approach to diagnosis (Frances 1993; Gunderson et al. 1991; Millon et al. 1996), including, for instance, their ease of use by clinicians who must make rapid diagnoses of a large number of patients whom they see briefly. The typologies are historically wellestablished syndromes, and they work as a standard reference for clinicians. All current and prior diagnostic systems have been categorical, and it would represent a major shift in clinical practice to convert to a dimensional model (Frances 1993). Clinicians must have a diagnostic system to guide their practice and facilitate their conceptualization of a patient’s pathology. They would otherwise be faced with repeated analyses that could not be generalized from one patient to another. Furthermore, clinicians are able to dig beyond the manifest and make interpretations from one behavior to another (Westen 1997). Finally, the typologies restore and recompose the unity of the self and constitute the patient as a person. Personality disorders, however, are among the more controversial and problematic disorders within the diagnostic manual. Maser et al. (1991) surveyed clinicians from 42 countries with respect to DSM-III-R (American Psychiatric Association 1987): “The personality disorders led the list of diagnostic categories with which respondents were dissatisfied” (p. 275). A number of reasons exist for this dissatisfaction with the existing diagnostic categories. We will summarize here some of the concerns regarding the categorical approach: 1) excessive diagnostic co-occurrence, 2) inadequate coverage, 3) heterogeneity within diagnoses, 4) arbitrary and unstable diagnostic boundaries, and 5) inadequate scientific base.

EXCESSIVE DIAGNOSTIC CO-OCCURRENCE ICD-10 and DSM-IV provide diagnostic criterion sets to help guide the clinician toward the correct diagnosis. The intention is to help determine which particular disorder is present, the selection of which would hopefully indicate the presence of a specific pathology that will explain the occurrence of the symptoms and suggest a specific treatment that would ameliorate the patient’s suffering (Frances et al. 1995). It is evident, however, that the diagnostic nomenclatures routinely fail in the goal of guiding the clinician to the presence of one specific personality dis-

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order. Studies have consistently indicated that many patients meet diagnostic criteria for an excessive number of personality disorder diagnoses (Bornstein 1998; Lilienfeld et al. 1994; Livesley 2003; Widiger and Trull 1998). The maladaptive personality functioning of patients does not appear to be adequately described by a single diagnostic category.

INADEQUATE COVERAGE In addition to the problem of excessive diagnostic co-occurrence, there is the opposing or complementary problem of inadequate coverage. Clinicians provide a diagnosis of personality disorder not otherwise specified (PDNOS) when they determine that a person has a personality disorder that is not adequately represented by any one of the 10 officially recognized diagnoses (American Psychiatric Association 2000). PDNOS is often the single most frequently used diagnosis in clinical practice, one explanation for which is that the existing categories are not providing adequate coverage (Verheul and Widiger 2004). Westen and Arkowitz-Westen (1998) surveyed 238 psychiatrists and psychologists with respect to their clinical practice and reported that “the majority of patients with personality pathology significant enough to warrant clinical psychotherapeutic attention (60.6%) are currently undiagnosable on Axis II” (p. 1769). The clinicians reported the treatment of commitment, intimacy, shyness, work inhibition, perfectionism, and devaluation of others that were not well described by any of the existing diagnoses. One approach to this problem is to add more diagnostic categories, but there is considerable reluctance to do so, in part because this would have the effect of increasing further the difficulties of excessive diagnostic co-occurrence and differential diagnosis (Pincus et al. 2003).

HETEROGENEITY WITHIN DIAGNOSES There are also important differences among the persons who share the same personality disorder diagnosis. Patients with the same diagnosis will vary substantially with respect to which diagnostic criteria were used to make the diagnosis, and the differences are not trivial. For example, only a subset of persons who meet the DSM-IV criteria for antisocial personality disorder will have the prototypic features of the callous, ruthless, arrogant, charming, and scheming psychopath (Hare 2003) and there are even important differences among the persons who would be diagnosed as psychopathic (Brinkley et al. 2004). The same point can be made for all of the other personality disorders (Millon et al. 1996), such as the differentiation of borderline psychopathology with respect to the dimensions of affective dysregulation, impulsivity, and behavioral disturbance (Sanislow et al. 2002), and the differentiation of dependent personality disorder into submissive, exploitable, and affectionate variants (Pincus and Wilson 2001).

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ARBITRARY AND UNSTABLE DIAGNOSTIC BOUNDARIES An additional problem has been establishing a nonarbitrary boundary with normal personality functioning. The existing diagnostic thresholds lack a compelling rationale (Tyrer and Johnson 1996). In fact, no explanation or justification has ever been provided for most of them (Widiger and Corbitt 1994). The thresholds for the DSM-III schizotypal and borderline diagnoses are the only two for which rationales have been provided. The DSM-III requirements that the patient have four of eight features for the schizotypal diagnosis and five of eight for borderline (American Psychiatric Association 1980) were determined on the basis of maximizing agreement with similar diagnoses provided by clinicians (Spitzer et al. 1979). However, the current diagnostic thresholds for these personality disorders bear little relationship with the original thresholds established for DSM-III. Blashfield et al. (1992) reported a kappa of only –.025 for the DSM-III and DSM-IIIR schizotypal personality disorders, with a reduction in prevalence from 11% to 1%. Seemingly minor changes to diagnostic criterion sets have resulted in unexpected and substantial shifts in prevalence rates across each edition of the diagnostic manuals that profoundly complicate scientific theory and public health decisions (Blashfield et al. 1992; Narrow et al. 2002).

INADEQUATE SCIENTIFIC BASE The fifth and final issue that we want to highlight is an inadequate scientific base. Blashfield and Intoccia (2000) conducted a computer search and concluded that there were “five disorders (dependent, narcissistic, obsessive-compulsive, paranoid, and passive-aggressive) that had very small literatures, averaging fewer than 10 articles per year” (p. 473). “The only personality disorder whose literature is clearly alive and growing is that of borderline personality disorder” (Blashfield and Intoccia 2000, p. 473). They characterized the research literature concerning the dependent, narcissistic, obsessive-compulsive, paranoid, passive-aggressive, schizoid, and histrionic personality disorders as being “dead” or “dying” (p. 473). The conclusions of Blashfield and Intoccia (2000) might have been overly negative. Their search appears to have been confined to studies that could be identified by the general index phrase “personality disorders,” and they may have missed the considerable research literature concerning psychopathy (Hare 2003); the many studies on sociotropy, dependency, and attachment (Bornstein 1992); and the many studies concerning narcissism and conflicted self-esteem published in the general personality literature (Widiger and Bornstein 2001). Nevertheless, their warning is well taken: “Disorders with literature growth that is dead or dying are not succeeding at accumulating new empirical knowledge, nor are they likely to be stimulating substantial clinical interest” (Blashfield and Intoccia 2000, p. 473). Most of the individual disorders included in DSM-IV have research programs and clinicians uniquely devoted to understanding their particular etiology, pathol-

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ogy, or treatment. This does not appear to be the case for many of the individual personality disorders, although there are notable exceptions (e.g., Bornstein 1992). Relative to many of the other diagnoses within the ICD-10 and DSM-IV nomenclatures, little progress is being made with respect to understanding the neurobiology, genetics, developmental antecedents, or treatment implications for many of the individual personality disorder diagnoses.

Alternative Dimensional Approach to the Classification of Personality Disorders The question of whether personality disorders are discrete clinical conditions or arbitrary distinctions along dimensions of general personality functioning has been a long-standing issue (Blashfield 1984; Kendell 1975; Schneider 1923). Proposals for a dimensional model of personality disorder have been made throughout the history of the American Psychiatric Association’s and the World Health Organization’s diagnostic manuals (e.g., Eysenck 1970; Presly and Walton 1973; Tyrer and Alexander 1979). DSM-III was quite innovative in many respects (Frances 1980; Millon et al. 1996), but it continued to diagnose personality disorders categorically despite the improvements in validity and clinical utility that would be obtained through a dimensional model of classification (Cloninger 1987; Eysenck 1987; Frances 1982; Kiesler 1986; Livesley 1985; Walton 1986; Widiger and Frances 1985; Wiggins 1982). The authors of DSM-III-R attempted to address some of the problems inherent to the categorical model by using polythetic criterion sets in which multiple diagnostic criteria are provided, only a subset of which are necessary for the diagnosis (Widiger et al. 1988). Compelling proposals for a more fundamental shift in how personality disorders are classified and diagnosed, however, continued to be made (e.g., Benjamin 1996; Clark 1992; Cloninger et al. 1993; Costa and McCrae 1990; Livesley et al. 1992; Oldham et al. 1992; Pincus and Wiggins 1990; Siever and Davis 1991; Stone 1993; Trull 1992; Tyrer 1988; Widiger 1993). The DSM-IV Personality Disorders Work Group considered proposals to include a dimensional model of classification within the diagnostic manual (Widiger and Sanderson 1995), but its final decision was to limit the presentation to simply a few sentences within the text of DSM-IV (American Psychiatric Association 1994, pp. 633–634). Further arguments and proposals for a more fundamental shift to a dimensional model of classification, however, continued to be provided (e.g., Clark et al. 1997; Cloninger and Svrakic 1997; Tyrer and Johnson 1996; Widiger and Costa 1994). There are arguments against making a conversion to a dimensional model, including (but certainly not limited to) the potential disruption to clinical practice of making a radical shift in how personality disorders are conceptualized and diag-

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nosed (e.g., see Frances 1993; Gunderson et al. 1991; Shedler and Westen 2004; Zimmerman 1988). Nevertheless, the field should be open to these alternative ways of enhancing clinical utility and improving the validity of our basic concepts in classification of personality disorder. It is our hope that the publication of these papers will indeed provide further support for and stimulation toward productive research that would lead to an eventual adoption by the APA and WHO of some kind of a dimensional model of personality disorder classification.

References American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition. Washington, DC, American Psychiatric Association, 1980 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised. Washington, DC, American Psychiatric Association, 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000 Benjamin LS: Interpersonal Diagnosis and Treatment of Personality Disorders, 2nd Edition. New York, Guilford, 1996 Blashfield RK: The Classification of Psychopathology. Neo-Kraepelinian and Quantitative Approaches. New York, Plenum, 1984 Blashfield RK, Intoccia V: Growth of the literature on the topic of personality disorders. Am J Psychiatry 157:472–473, 2000 Blashfield RK, Blum N, Pfohl B: The effects of changing Axis II diagnostic criteria. Compr Psychiatry 33:245–252, 1992 Bornstein RF: The dependent personality: developmental, social and clinical perspectives. Psychol Bull 112:3–23, 1992 Bornstein RF: Reconceptualizing personality disorder diagnosis in the DSM-V: the discriminant validity challenge. Clin Psychol-Sci Pr 5:333–343, 1998 Brinkley CA, Newman JP, Widiger TA, et al: Two approaches to parsing the heterogeneity of psychopathy. Clin Psychol-Sci Pr 11:69–94, 2004 Clark LA: Resolving taxonomic issues in personality disorders. J Personal Disord 6:360– 378, 1992 Clark LA, Livesley WJ, Morey L: Personality disorder assessment: the challenge of construct validity. J Personal Disord 11:205–231, 1997 Cloninger CR: A systematic method for clinical description and classification of personality variants. Arch Gen Psychiatry 44:573–588, 1987 Cloninger CR, Svrakic DM: Integrative psychobiological approach to psychiatric assessment and treatment. Psychiatry 60:120–141, 1997 Cloninger CR, Svrakic DM, Przybeck TR: A psychobiological model of temperament and character. Arch Gen Psychiatry 50:975–990, 1993 Costa PT Jr, McCrae RR: Personality disorders and the five-factor model of personality. J Personal Disord 4:362–371, 1990

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Eysenck HJ: A dimensional system of psychodiagnostics, in New Approaches to Personality Classification. Edited by Mahrer AR. New York, Columbia University Press, 1970, pp 169–207 Eysenck HJ: The definition of personality disorders and the criteria appropriate for their description. J Personal Disord 1:211–219, 1987 Frances AJ: The DSM-III personality disorders section: a commentary. Am J Psychiatry 137:1050–1054, 1980 Frances AJ: Categorical and dimensional systems of personality diagnosis: a comparison. Compr Psychiatry 23:516–527, 1982 Frances AJ: Dimensional diagnosis of personality—not whether, but when and which. Psychol Inq 4:110–111, 1993 Frances AJ, First MB, Pincus HA: DSM-IV Guidebook. Washington, DC, American Psychiatric Press, 1995 Gunderson JG, Links PS, Reich JH: Competing models of personality disorders. J Personal Disord 5:60–68, 1991 Hare RD: Hare Psychopathy Checklist Revised (PCL-R): Technical Manual. North Tonawanda, NY, Multi-Health Systems, 2003 Kendell RE: The Role of Diagnosis in Psychiatry. London, Blackwell Scientific, 1975 Kiesler DJ: The 1982 Interpersonal Circle: an analysis of DSM-III personality disorders, in Contemporary Directions in Psychopathology: Toward the DSM-IV. Edited by Millon T, Klerman G. New York, Guilford, 1986, pp 571–597 Lilienfeld SO, Waldman ID, Israel AC: A critical examination of the use of the term “comorbidity” in psychopathology research. Clin Psychol-Sci Pr 1:71–83, 1994 Livesley WJ: The classification of personality disorder, I: the choice of category concept. Can J Psychiatry 30:353–358, 1985 Livesley WJ: Diagnostic dilemmas in classifying personality disorder, in Advancing DSM: Dilemmas in Psychiatric Diagnosis. Edited by Phillips KA, First MB, Pincus HA. Washington, DC, American Psychiatric Association, 2003, pp 153–190 Livesley WJ, Jackson DN, Schroeder ML: Factorial structure of traits delineating personality disorders in clinical and general population samples. J Abnorm Psychol 101:432– 440, 1992 Maser JD, Kaelber C, Weise RF: International use and attitudes toward DSM-III and DSMIII-R: growing consensus in psychiatric classification. J Abnorm Psychol 100:271–279, 1991 Millon T, Davis RD, Millon CM, et al: Disorders of Personality: DSM-IV and Beyond. New York, John Wiley & Sons, 1996 Narrow WE, Rae DS, Robins LN, et al: Revised prevalence estimates of mental disorders in the United States: using a clinical significance criterion to reconcile 2 surveys’ estimates. Arch Gen Psychiatry 59:115–123, 2002 Oldham JM, Skodol AE, Kellman HD, et al: Diagnosis of DSM-III-R personality disorders by two semistructured interviews: patterns of comorbidity. Am J Psychiatry 149:213– 220, 1992 Pincus AL, Wiggins JS: Interpersonal problems and conceptions of personality disorders. J Personal Disord 4:342–352, 1990

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Pincus AL, Wilson KR: Interpersonal variability in dependent personality. J Pers 69:223– 251, 2001 Pincus HA, McQueen LE, Elinson L: Subthreshold mental disorders: nosological and research recommendations, in Advancing DSM: Dilemmas in Psychiatric Diagnosis. Edited by Phillips KA, First MB, Pincus HA. Washington, DC, American Psychiatric Association, 2003, pp 129–144 Presly AS, Walton HJ: Dimensions of abnormal personality. Br J Psychiatry 122:269–276, 1973 Sanislow CA, Morey LC, Grilo CM, et al: Confirmatory factor analysis of DSM-IV borderline, schizotypal, avoidant and obsessive-compulsive personality disorders: findings from the Collaborative Longitudinal Personality Disorders Study. Acta Psychiatr Scand 105:28–36, 2002 Schneider K: The Psychopathic Personalities. Vienna, Austria, Deuticke, 1923 Shedler J, Westen D: Dimensions of personality pathology: an alternative to the five-factor model. Am J Psychiatry 161:1743–1754, 2004 Siever LJ, Davis KL: A psychobiological perspective on the personality disorders. Am J Psychiatry 148:1647–1658, 1991 Spitzer R, Endicott J, Gibbon M: Crossing the border into borderline personality and borderline schizophrenia. Arch Gen Psychiatry 36:17–24, 1979 Spitzer RL, Williams JBW, Skodol AE: DSM-III: the major achievements and an overview. Am J Psychiatry 137:151–164, 1980 Stone MH: Abnormalities of Personality. Within and Beyond the Realm of Treatment. New York, WW Norton, 1993 Trull TJ: DSM-III-R personality disorders and the five-factor model of personality: an empirical comparison. J Abnorm Psychol 101:553–560, 1992 Tyrer P: What’s wrong with DSM-III personality disorders? J Personal Disord 2:281–291, 1988 Tyrer P, Alexander J: Classification of personality disorder. Br J Psychiatry 135:163–167, 1979 Tyrer P, Johnson T: Establishing the severity of personality disorder. Am J Psychiatry 153:1593–1597, 1996 Verheul R, Widiger TA: A meta-analysis of the prevalence and usage of the personality disorder not otherwise specified (PDNOS) diagnosis. J Personal Disord 18:309–319, 2004 Walton HJ: The relationship between personality disorder and psychiatric illness, in Contemporary Directions in Psychopathology. Toward the DSM-IV. Edited by Millon T, Klerman G. New York, Guilford, 1986, pp 553–569 Westen D: Divergences between clinical and research methods for assessing personality disorders: Implications for research and the evolution of Axis II. Am J Psychiatry 154:895–903, 1997 Westen D, Arkowitz-Westen L: Limitations of Axis II in diagnosing personality pathology in clinical practice. Am J Psychiatry 155:1767–1771, 1998 Widiger TA: The DSM-III-R categorical personality disorder diagnoses: a critique and an alternative. Psychol Inq 4:75–90, 1993

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Widiger TA, Bornstein RF: Histrionic, narcissistic, and dependent personality disorders, in Comprehensive Handbook of Psychopathology, 3rd Edition. Edited by Adams H, Sutker P. New York, Plenum, 2001, pp 507–529 Widiger TA, Corbitt E: Normal versus abnormal personality from the perspective of the DSM, in Differentiating Normal and Abnormal Personality. Edited by Strack S, Lorr M. New York, Springer, 1994, pp 158–175 Widiger TA, Costa PT Jr: Personality and personality disorders. J Abnorm Psychol 103:78– 91, 1994 Widiger T, Frances A: The DSM-III personality disorders: perspectives from psychology. Arch Gen Psychiatry 42:615–623, 1985 Widiger TA, Sanderson CJ: Towards a dimensional model of personality disorders in DSMIV and DSM-V, in The DSM-IV Personality Disorders. Edited by Livesley WJ. New York, Guilford, 1995, pp 433–458 Widiger TA, Trull TJ: Performance characteristics of the DSM-III-R personality disorder criteria sets, in DSM-IV Sourcebook, Vol 4. Edited by Widiger TA, Frances AJ, Pincus HA, et al. Washington, DC, American Psychiatric Association, 1998, pp 357–373 Widiger T, Frances A, Spitzer R, et al: The DSM-III-R personality disorders: an overview. Am J Psychiatry 145: 786–795, 1988 Wiggins JS: Circumplex models of interpersonal behavior in clinical psychology, in Handbook of Research Methods in Clinical Psychology. Edited by Kendall P, Butcher JN. New York, Wiley, 1982, pp 183–221 World Health Organization: The ICD-10 Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva, Switzerland, World Health Organization, 1992 Zimmerman M: Why are we rushing to publish DSM-IV? Arch Gen Psychiatry 45:1135– 1138, 1988

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1 ALTERNATIVE DIMENSIONAL MODELS OF PERSONALITY DISORDER Finding a Common Ground Thomas A. Widiger, Ph.D. Erik Simonsen, M.D.

The many limitations of the categorical model of personality disorder classification are well recognized. An obvious response to this recognition is the generation of proposals for dimensional classifications. If the authors of a future edition of the diagnostic manual shift toward a dimensional model, they will have quite a few alternative proposals to consider. The purpose of this presentation is twofold. We will first simply describe alternative proposals. More important, we will suggest that future research work toward an integration of these alternative models within a common hierarchical structure.

This chapter is an abbreviated version of a paper with the same title first published in the Journal of Personality Disorders (Volume 19, Issue 2, pages 110–130, 2005).

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Dimensional Models of Personality Disorders

Eighteen Proposals One approach to converting to a dimensional classification of personality disorder is to simply provide a dimensional profile of the existing (or somewhat revised) diagnostic categories (Widiger and Sanderson 1995). Three such proposals have been developed by Oldham and Skodol (2000), Tyrer and Johnson (1996), and Westen and Shedler (2000). An advantage of this approach is that it would retain the existing diagnostic constructs (e.g., antisocial), thereby easing the transition to a dimensional classification. A limitation of this approach is that there might be more fundamental dimensions of maladaptive personality functioning that cut across the existing personality disorders, contributing to their diagnostic co-occurrence. A second approach is to reorganize the existing (and perhaps expanded) diagnostic criterion sets into more clinically useful and empirically valid dimensions of maladaptive personality functioning. Four such proposals have been developed by Clark et al. (in press; assessed using the Schedule for Nonadaptive and Adaptive Personality [SNAP]), Harkness and McNulty (1994; assessed using the Personality Psychopathology—Five [PSY-5]), Livesley (2003; assessed using the Dimensional Assessment of Personality Psychopathology—Basic Questionnaire [DAPPBQ]), and Shedler and Westen (2004; assessed using the Shedler and Westen Assessment Procedure–200 [SWAP-200]). The three clusters included within DSMIV-TR (American Psychiatric Association 2000) could be said to represent a fifth version of this proposal, although the DSM-IV clusters do not in fact reorganize the criterion sets into a more coherent structure. Clark et al. (in press) include within their factor analyses of personality disorder symptoms traitlike manifestations of anxiety and mood disorders, because the diagnostic co-occurrence of personality with disorders on Axis I of DSM-IV could be due to the presence of common, underlying dimensions of maladaptive personality functioning. A third approach to a dimensional model of personality disorder is to identify spectra of dysfunction that cut across the existing personality, mood, anxiety, substance use, and other diagnostic classes. Two such proposals have been developed by Siever and Davis (1991) and Krueger (2002). Personality disorders may not only be on a continuum with Axis I disorders, they may also be on a continuum with general personality functioning, contributing to the absence of a clear boundary between normal and abnormal personality functioning and to the presence of a considerable amount of personality disorder symptomatology within the general population (Livesley 2003; Widiger and Sanderson 1995). A fourth approach is to integrate the classification of personality disorders with dimensional models of general personality structure. There are quite a few dimensional models of personality (Wiggins 2003). Eight that have been related explicitly to the DSM-IV personality disorders are those of Cloninger (2000; assessed using the Temperament and Character Inventory [TCI]), Costa and McCrae (1990; assessed using the Neuroticism–Extraversion–Openness Per-

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3

sonality Inventory—Revised [NEO PI-R]), Eysenck (1987; assessed using the Eysenck Personality Questionnaire [EPQ] or the Eysenck Personality Profiler [EPP]), the interpersonal circumplex (IPC; Benjamin 1996; Wiggins 2003), Millon et al. (1996; assessed using the Millon Index of Personality Styles [MIPS]), Tellegen (Watson et al. 1999; assessed using the Multidimensional Personality Questionnaire [MPQ]), Tyrer (2000; assessed using the Personality Assessment Schedule [PAS]), and Zuckerman (2002; assessed using the Zuckerman-Kuhlman Personality Questionnaire [ZKPQ]).

Toward an Integration of Alternative Models These proposals do vary in their empirical support as a dimensional model of personality disorder (e.g., O’Connor and Dyce 1998), and one of them is likely to have more validity and clinical utility than any one of the other 17. The additional papers within this text address (in part) research concerning behavioral genetics, neurobiological mechanisms, childhood antecedents, cross-cultural application, continuity with Axis I, coverage, and clinical utility of the alternative models. However, it may also be true that some common ground can be found among them. It appears to be the case, at least to us, that none of the models lacks any limitations that could not at times be well compensated through an integration with another model. Each model will have some flaws and deficits, and each model will likely have at least some useful features. The optimal decision for the authors of a future edition of the diagnostic manual might not be a zero-sum game, where one model is victorious and all other models are abandoned. Rather, the ideal solution might be to develop a common, integrative representation that includes the important contributions and potential advantages of each of the models.

COMMON HIGHER-ORDER DOMAINS Fortunately, most of the alternative models do appear to be readily integrated within a common hierarchical structure (Bouchard and Loehlin 2001; John and Srivastava 1999; Krueger and Tackett 2003; Larstone et al. 2002; Livesley 2003; Markon et al. 2005; Trull and Durrett 2005; Widiger and Mullins-Sweatt 2005; Zuckerman 2002). This should not be surprising, given that most of them are attempting to do largely the same thing (i.e., identify the fundamental dimensions of maladaptive personality functioning that underlie and cut across the existing diagnostic categories). We suggest more specifically that all but a few of the personality traits and behaviors contained within the 18 proposed models could be organized within a more fully developed, hierarchical structure. At the highest level could be the two clinical spectra of Internalization and Externalization identified by Krueger (2002) and Achenbach (1966). Immediately beneath the two dimensions of Internalization and Externalization would be three to five broad domains

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of personality functioning. Immediately beneath these broad domains would be personality trait scales, and at the lowest level would be the more behaviorally specific diagnostic criteria. Table 1–1 indicates how the broad domains of most of the models might be aligned with one another. We will discuss in more detail below the fit at this broad level of the DAPP-BQ, EPQ, IPC, MCMI-III, MPQ, NEO PI-R, PAS, PSY-5, SNAP, TCI, ZKPQ, and the Siever and Davis (1991) clinical spectra models. However, we want to acknowledge that a couple of the models do not as readily fit within this common structure, at least based on the existing research. For example, the SWAP-200 is not included in Table 1–1 because current research suggests that it does not have a congruent higher-order factor structure (Shedler and Westen 2004). The MIPS self–other, pleasure–pain, and active–passive polarity model of Millon et al. (1996) is not included, because its alignment with the other models is not readily apparent, and only one study has empirically related its polarities to any one of the other models (i.e., Millon [1994] reports correlations of the 6 MIPS scales with the NEO PI-R). On the other hand, factor analyses of the personality disorder scales of various editions of the Millon Clinical Multiaxial Inventory (MCMI-III; Millon et al. 1996) have produced solutions that do converge well with the four (or five) factor structure (e.g., Dyce et al. 1997; O’Connor and Dyce 1998; Simonsen 2005). An important focus of future research will be to determine whether the three (or six) polarities of the MIPS and the 12 scales of the SWAP-200 can be integrated with the higher-order structure of the DAPP-BQ, SNAP, MPQ, PSY-5, MCMI-III, IPC, NEO PI-R, EPQ, ZKPQ, and PAS, or whether the MIPS and SWAP-200 concern instead aspects of maladaptive personality functioning that are not commensurate with these other dimensional models. We do expect that a common structure is likely to be found, as the intention of these models is common: identify the fundamental dimensions of maladaptive personality functioning that underlie and cut across the existing diagnostic categories. We will also present below how the subscales of the SWAP-200 might in fact correspond with the subscales of the DAPP-BQ, EPP, MPQ, NEO PI-R, PAS, SNAP, and TCI.

Extraversion Versus Introversion It is evident from Table 1–1 that most if not all of the models include a domain that concerns Extraversion, also described as Sociability, Activity, Positive Emotionality, and (when keyed in the opposite direction) Inhibition, Introversion, or Withdrawal. This domain contrasts being gregarious, talkative, assertive, and active with being withdrawn, isolated, introverted, and anhedonic. The terms Extraversion and Positive Emotionality might appear to suggest different domains of personality functioning. However, many studies have confirmed that these are in fact the same domains (Bouchard and Loehlin 2001; Harkness et al. 1995; John and Srivastava 1999; Watson et al. 1994). The title Positive Affectivity is preferred

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by some, because it is believed that Positive Affectivity might be providing the motivating force for Extraversion, reflecting individual differences in a behavioral activation (or reward sensitivity) system (Depue and Collins 1999; Pickering and Gray 1999; Watson and Clark 1997). The interpersonal term of Extraversion is preferred by others in part because it is more simply descriptive of much of the behaviors that are included within the domain and it facilitates recognition of the association with the IPC domains of affiliation (Communion) and power (Agency) (Wiggins 2003). An important decision for the authors of the future edition of the diagnostic manual will be to select the optimal term(s) to characterize this (or any other) domain.

Antagonism Versus Compliance Most of the dimensional models also include traits referring to aggressive, dissocial, or antagonistic interpersonal relatedness at this higher-order level. This domain contrasts being suspicious, rejecting, exploitative, aggressive, antagonistic, callous, deceptive, and manipulative with being trusting, compliant, agreeable, modest, dependent, diffident, and empathic. This domain is represented more narrowly by the PSY-5 and the ZKPQ, as these versions of this domain are confined largely to interpersonal aggressiveness, whereas the other models include such additional components as mistrust, exploitation, suspiciousness, deception, and arrogance. Psychoticism from Eysenck’s dimensional model is not aligned perfectly with this domain, because he included within Psychoticism both interpersonal antagonism and impulsive disinhibition (Bouchard and Loehlin 2001; Clark and Watson 1999; Eysenck 1987; John and Srivastava 1999), comparable to the conceptualization of this domain by Siever and Davis (1991). A potential point of confusion of Table 1–1 is that Psychoticism scales are included in two different locations. This reflects the fact that this single term has been used to refer to quite different constructs. The Psychoticism of Eysenck’s (1987) EPQ is not the same as the Psychoticism of Harkness and McNulty’s (1994) PSY-5. As we just indicated, the Psychoticism of Eysenck (1987) refers to impulsive and aggressive behaviors, whereas the Psychoticism of the PSY-5 refers to cognitive and perceptual aberrations. The three-dimensional models of the MPQ and the SNAP do not include this domain of personality functioning at this higher-order level. The SNAP does include scales for mistrust, manipulativeness, and aggression, but these are placed within the domain of Negative Affectivity (Clark et al., in press), just as the MPQ includes an aggression scale within the domain of Negative Emotionality (A. Tellegen, N.G. Waller, “Exploring Personality Through Test Construction: Development of the Multidimensional Personality Questionnaire” [unpublished manuscript], Minneapolis, MN, 1987). Being mistrustful, aggressive, and manipulative does often (if not invariably) include a negative affect of angry hostility. However, joint-factor analyses of the DAPP-BQ and SNAP subscales have consistently

6

TABLE 1–1.

Alignment of alternative dimensional models: broad domains First

Second

Third

Fourth

DAPP-BQ

–Inhibition

Dissocial

Compulsivity

Emotional dysregulation

NEO PI-R

Extraversion

Antagonism

Conscientiousness

Neuroticism

SNAP and MPQ

Positive Affectivity

(Negative Affectivity)

Constraint

Negative Affectivity

PSY-5

Positive Aggressiveness Emotionality

Constraint

Negative Emotionality

Psychoticism

Agency

MCMI-III

–Withdrawn

EPQ and EPP

Extraversion

ZKPQ

Sociability

Communion Aggressiveness Constraint

Neuroticism

Psychoticism Aggression– Hostility

Neuroticism –Impulsive

Neuroticism

Activity PAS

–Withdrawn

Openness

Antisocial– Dependent

Inhibited

Dimensional Models of Personality Disorders

IPC

Fifth

Alignment of alternative dimensional models: broad domains (continued) First

Siever-Davis

TCI

(–Inhibition)

Second

Third Aggression– Impulsive

–Cooperativeness

Fourth

Fifth

Affective Instability Anxiety/ Inhibition

Cognitive– Perceptual

Persistence SelfHarm Novelty Seeking Directedness Avoidance

SelfTranscendence Reward Dependence

Note. Off-center scales lie between the domains defined by the adjoining columns. Italicized scales describe domains that are somewhat narrower in scope. Scales within parentheses are more strongly related to another domain. DAPP-BQ = Dimensional Assessment of Personality Psychopathology—Basic Questionnaire (Livesley 2003); EPQ = Eysenck Personality Questionnaire (Eysenck 1987); EPP = Eysenck Personality Profiler (Eysenck 1987); IPC = interpersonal circumplex model (Benjamin 1996; Wiggins 2003); MCMI-III = Millon Clinical Multiaxial Inventory—Third Edition (Millon et al. 1996); MPQ = Multidimensional Personality Questionnaire (Watson et al. 1999); NEO PI-R = Neuroticism–Extraversion–Openness (NEO) Personality Inventory—Revised (Costa and McCrae 1990); PAS = Personality Assessment Schedule (Tyrer 2000); PSY-5 = Personality Psychopathology—Five (Harkness and McNulty 1994); SNAP = Schedule for Nonadaptive and Adaptive Personality (Clark et al., in press); Siever-Davis = clinical spectra model (Siever and Davis 1991); SWAP-200 = Shedler and Westen Assessment Procedure–200 (Shedler and Westen 2004); TCI = Temperament and Character Inventory (Cloninger 2000); ZKPQ = Zuckerman-Kuhlman Personality Questionnaire (Zuckerman 2002).

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder

TABLE 1–1.

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yielded a four-factor solution (Clark and Livesley 2002; Clark et al. 1996) that corresponds to the first four domains of Table 1–1. As indicated by Watson et al. (1994), “extensive data indicate that...the Big Three and Big Five models define a common ‘Big Four’ space” (p. 24), consisting of Negative Affectivity (Neuroticism), Positive Affectivity (Extraversion), Antagonism, and Constraint.

Constraint Versus Impulsivity All but a couple of the models also include a domain concerned with the control and regulation of behavior, referred to as Constraint, Compulsivity, or Conscientiousness, or, when keyed in the opposite direction, Impulsivity or Disinhibition. It contrasts being disciplined, compulsive, dutiful, conscientious, deliberate, workaholic, and achievement-oriented with being irresponsible, lax, impulsive, negligent, and hedonistic (Constraint, as assessed by the SNAP and MPQ, also contain aspects of Antagonism). Dimensional models that do not include this domain of personality functioning are the IPC and the PAS. Tyrer (2000) places the symptoms of the obsessive-compulsive (anankastic) personality disorder within his PAS Inhibited domain, which is otherwise defined largely by traits of anxiousness and dysphoria (i.e., a somewhat different meaning for the term Inhibition than is used, for instance, for the DAPP-BQ). The IPC does not include Constraint versus Disinhibition, as it is a two-dimensional model confined to domains of interpersonal relatedness. An additional example of the same term having different meanings is the Harm Avoidance of the TCI and the MPQ. Harm Avoidance in the TCI refers to an anxious behavioral inhibition, whereas Harm Avoidance in the MPQ is a quite different construct, referring to a low Constraint (or behavioral disinhibition that is potentially fearless). The differences between TCI Harm Avoidance and MPQ Harm Avoidance are so striking that they are in fact placed within different broad domains.

Emotional Dysregulation Versus Emotional Stability Finally, it is also evident from Table 1–1 that all but one of the models include a broad domain of emotional dysregulation, otherwise described as Negative Affectivity or Neuroticism. It contrasts feeling anxious, depressed, angry, despondent, labile, helpless, self-conscious, and vulnerable with feeling emotionally stable, selfassured, invulnerable, calm, glib, shameless, and invincible. The only model not to include this domain of personality functioning is again the IPC. This fourth domain is also somewhat more narrowly defined by Siever and Davis (1991), as they separate anxiousness from affective instability. In sum, the predominant models of normal and abnormal personality functioning appear to converge upon four broad domains of personality functioning (Bouchard and Loehlin 2001; John and Srivastava 1999; Krueger and Tackett 2003; Larstone et al. 2002; Livesley 2003; Markon et al. 2005; Trull and Durrett

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder

9

2005; Watson et al. 1994; Widiger and Mullins-Sweatt 2005; Zuckerman 2002) that can be described as Extraversion versus Introversion, Antagonism versus Compliance, Constraint versus Impulsivity, and Emotional Dysregulation versus Emotional Stability. The authors of these various models would not all agree on the best names for each domain, due in part to the fact that 1) no single name is likely to optimally describe an entire domain; 2) some models place more emphasis on the normal variants (e.g., NEO PI-R and TCI), whereas other models place more emphasis on the abnormal variants (e.g., DAPP-BQ and SNAP); and, finally, 3) the models vary in how broadly or narrowly they define each domain. We have provided tentative names for each domain that emphasize (for the most part) the maladaptive variants, as these would be of most relevance and interest to clinicians. In any case, the convergence among the alternative models with respect to the existence of the four domains is quite evident. Empirical support for the convergence of these models has been provided in quite a number of studies (e.g., Austin and Deary 2000; Clark et al. 1996; Deary et al. 1998; Dyce et al. 1997; Livesley et al. 1998; Markon et al. 2005; Mulder and Joyce 1997; O’Connor and Dyce 1998).

Unconventionality Versus Closedness to Experience Only three of the models include a fifth broad domain, characterized within the NEO PI-R as Openness to Experience, described as unconventionality by Tellegen and Waller (A. Tellegen, N.G. Waller, “Exploring Personality Through Test Construction: Development of the Multidimensional Personality Questionnaire” [unpublished manuscript], Minneapolis, MN, 1987), identified within the PSY-5 as psychoticism (i.e., illusions, misperceptions, perceptual aberrations, and magical ideation), and identified within the clinical spectra of Siever and Davis (1991) as cognitive–perceptual aberrations. There are also subscales within the SNAP (e.g., eccentric perceptions), the DAPP-BQ (perceptual cognitive distortion), the MPQ (absorption), the PAS (eccentricity, rigidity), the SWAP-200 (thought disorder, dissociation), and the TCI (transpersonal identification, spiritual acceptance) that relate conceptual and empirically to this domain (Bouchard and Loehlin 2001; Clark and Livesley 2002). A domain of Unconventionality (or Openness) is obtained in joint factor analytic studies that provide sufficient representation (e.g., Clark and Livesley 2002; Costa and McCrae 1990; Wiggins and Pincus 1989). However, it appears to be the case that when this domain is narrowly defined as simply cognitive–perceptual aberrations, scales to assess it either load on other factors (typically negative affectivity) or define a factor that is so small that it might not appear to be worth identifying (Austin and Deary 2000; Clark et al. 1996; Larstone et al. 2002). Openness to Experience is itself the fifth and smallest domain of the Five-Factor Model (Ashton and Lee 2001). It is also possible that cognitive–perceptual aberrations do not belong within a dimensional model of abnormal personality functioning, consistent with the World Health Organization’s (1992) inclusion of DSMIV schizotypal personality disorder as a variant of schizophrenia.

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LOWER-ORDER TRAITS AND SYMPTOMS We now turn to the constructs and scales that might be included within each one of these four (or five) broad domains. This is facilitated by the fact that some of the dimensional models include lower-order scales that have been related empirically to one another. Consideration of the lower-order scales also provides a better understanding of the potential integration of the SWAP-200 within the hierarchical structure. Space limitations prohibit a presentation of lower-order scales for all four domains. Excluded from this presentation are the lower-order scales within the domain of Emotional Dysregulation versus Emotional Stability (this material is provided in the previously published version of this chapter [Widiger and Simonsen 2005]).

Constraint Versus Impulsivity Table 1–2 provides trait scales within a domain of Constraint versus Disinhibition (or Impulsivity). Normal and abnormal variants of constraint are readily identified, with a number of scales from the TCI, PAS, MPQ, and NEO PI-R that refer to normal, adaptive levels of Constraint (or Conscientiousness), such as dutifulness, conscientiousness, responsibility, ambitiousness, achievement, resourcefulness, deliberation, control, and self-discipline, and maladaptive variants of these traits emphasized by the DAPP-BQ, SWAP-200, EPP, and SNAP (i.e., compulsivity, obsessionality, workaholism, and propriety). We placed the TCI scales of perfectionism and work-hardened and the EPP scales of impulsivity, risk taking, and irresponsibility within the abnormal range, but these could just as well have been placed within the normal range. We are not suggesting, of course, that a future edition of the diagnostic manual provide all of the 30 scales included in Table 1–2. There is clearly substantial redundancy. Only a small subset would in fact be necessary, and an important issue for future research is which subset would represent the optimal choice. Considered in this selection might be extent of overlap, adequate coverage of the domain, representation of different dimensional models, clinical relevance, familiarity, and ease of use. An additional question for future research is the potential bipolarity of the hierarchical structure. The existing hierarchical structure of DSM-IV does not include any such bipolarities (e.g., there is no maladaptive variant of low compulsivity). However, we would suggest that this bipolarity is evident in other areas of medicine. For example, there are maladaptive consequences of both high and low blood pressure, with normal blood pressure occupying an intermediate ground. In addition, a bipolar structure appears to be inherent to any hierarchical organization of the adaptive and maladaptive personality scales included within the existing instruments. For example, in the higher-order structure of the SNAP, the SNAP Impulsivity scale loads negatively on the Constraint domain, whereas the

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder 11

TABLE 1–2.

Lower-order scales within a domain of Constraint versus

Impulsivity 1.

Version including all relevant scales from respective instruments Abnormally high traits DAPP-BQ: compulsivity SNAP: workaholism TCI: perfectionism, work-hardened SWAP-200: obsessionality Normal traits NEO PI-R: dutifulness, order, achievement-striving, selfdiscipline, deliberation, competence PAS: conscientiousness MPQ: achievement, control, traditionalism, harm avoidance SNAP: propriety TCI: resourcefulness, eagerness of effort, responsibility, ambitiousness, purposefulness Abnormally low traits SNAP: impulsivity TCI: impulsiveness, disorderliness PAS: irresponsibility, childishness, impulsiveness EPP: impulsivity, risk taking, irresponsibility

2.

Simplified version Abnormal Compulsivity Workaholism Obsessionality Impulsivity Irresponsibility Normal Dutifulness Achievement-striving Resourcefulness

Note. DAPP-BQ = Dimensional Assessment of Personality Psychopathology—Basic Questionnaire; EPP = Eysenck Personality Profiler; MPQ = Multidimensional Personality Questionnaire; NEO PI-R = Neuroticism–Extraversion–Openness (NEO) Personality Inventory—Revised; PAS = Personality Assessment Schedule; SNAP = Schedule for Nonadaptive and Adaptive Personality; SWAP-200 = Shedler and Westen Assessment Procedure– 200; TCI = Temperament and Character Inventory.

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SNAP Propriety and Workaholism scales load positively (Clark et al., in press). A comparable finding occurs for other domains. SNAP Exhibitionism loads positively on the domain of Positive Affectivity, whereas Detachment loads negatively (Clark et al., in press), just as the DAPP-BQ Stimulus Seeking scale loads positively on this domain and the DAPP-BQ Social Avoidance scale loads negatively (Livesley et al. 1998). The same finding also occurs when higher-order structures are developed with the DSM-IV personality disorder criterion sets. For example, in one of the initial efforts to integrate empirically the dimensional and categorical models of personality and personality disorder, Wiggins and Pincus (1989) indicated how the histrionic and narcissistic personality disorders loaded positively on an Extraversion dimension, whereas schizoid loaded negatively. Dependent personality disorder loaded positively on an Agreeableness factor, whereas the antisocial, paranoid, and narcissistic disorders loaded negatively. Comparable findings have occurred consistently in subsequent higher-order organizations of the DSMIV personality disorder constructs (Coker et al. 2002; O’Connor and Dyce 1998). A future diagnostic manual can avoid the conceptual complexity of this bipolarity, however, by simply excluding it from the visual presentation of the scales, consistent with how the personality disorders are currently presented. Table 1–3 also provides a much simplified version of the Constraint-versus-Impulsivity domain. Only a small subset of the constructs are provided within this simplified version, and the bipolarity is removed from the visual presentation. Note, however, that the scales included in the simplified version do not represent our suggestion of which scales should be included or excluded. Its intention is only to indicate visually that the presentation of the scales need not be as complex or burdensome as might be implied by the complete list.

Extraversion Versus Introversion Table 1–3 provides possible scales for a domain of Extraversion versus Introversion. At one pole could be maladaptive scales from the DAPP-BQ (Stimulus Seeking), SNAP (Exhibitionism), TCI (Extravagance), and SWAP-200 (Histrionic Sexualization); at the opposite pole could be the maladaptive scales from the DAPP-BQ (Intimacy Problems, Social Avoidance), SNAP (Detachment), PAS (Aloofness), and SWAP-200 (Schizoid Orientation). In between could be the normal variants of these constructs, as represented by the NEO PI-R scales concerning Gregariousness, Assertiveness, Activity, Excitement-Seeking, and Positive Emotionality; the MPQ scales of Social Potency and Social Closeness; the TCI scales of Exploratory Excitability and Sociability; and the EPP scales of Sociability, Assertiveness, and Activity. It is also important to note that much of the existing personality disorder diagnostic criteria would be easily included within this hierarchical structure. Each of the abnormal trait scales would include items for their assessment, and in most in-

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder 13 stances these items would resemble closely the existing personality disorder diagnostic criteria. In fact, the existing personality disorder diagnostic criteria are already included within the DAPP-BQ, SNAP, and SWAP-200 scales. In sum, clinicians familiar with the existing diagnostic criterion sets would readily identify much (if not all) of the existing personality disorder symptoms within the dimensional hierarchical structure. The dimensional model will have simply reorganized the criterion sets into a more coherent and empirically supported structure. In addition, the diagnostic manual could go further by providing guidelines for a profile matching with which clinicians could recover the DSM-IV diagnostic constructs (e.g., antisocial or borderline). For example, what was identified in DSM-IV as schizoid personality disorder could be diagnosed by elevations on the detachment and aloofness scales. Research has indicated that these profile-matching algorithms reproduce well the findings that are currently obtained with the existing diagnostic constructs (e.g., Miller and Lynam 2003; Trull et al. 2003).

Antagonism Versus Compliance Table 1–3 also provides a description of how the respective lower-order personality trait scales from the PAS, DAPP-BQ, SNAP, TCI, NEO PI-R, MPQ, and SWAP200 might be aligned with one another within a domain of antagonism versus compliance. Scales from the NEO PI-R and TCI refer largely to normal variants (i.e., being trusting, compliant, straightforward, altruistic, modest, helpful, compassionate, sentimental, or empathic), whereas scales from the DAPP-BQ, SWAP200, PAS, and SNAP refer largely to abnormal, maladaptive variants of these same traits (i.e., being dependent, diffident, gullible, sacrificial, meek, docile, submissive, or self-denigrating). The Antagonism versus Compliance domain is useful in illustrating the close relationship of the normal and abnormal variants of these traits, as some scales are difficult to even classify (e.g., MPQ scale for aggression), consistent with the considerable amount of research indicating a continuum between normal and abnormal personality functioning (Cloninger 2000; Livesley 2001; Reynolds and Clark 2001; Saulsman and Page 2004; Trull and Durrett 2005; Tyrer 2001; Widiger and Costa 2002). A decision for the authors of a future edition of the diagnostic manual will be whether to include normal variants of each of the domains of personality functioning. There are arguments against doing so (e.g., the argument that the diagnostic manual is not for the purpose of describing normal psychological functioning). However, there are also compelling arguments for including normal personality scales—for example, their inclusion will allow for the provision of a more comprehensive description of a patient’s entire personality functioning; will facilitate an integration of the diagnostic manual with basic science research on general personality functioning; and may be helpful clinically by identifying adaptive personality traits that contribute to treatment responsivity.

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TABLE 1–3.

Lower-order scales within the domains of Extraversion versus Introversion and Antagonism versus Compliance 1.

Extraversion versus Introversion Abnormally high traits DAPP-BQ: SNAP: TCI: SWAP-200:

stimulus seeking exhibitionism, (entitlement) extravagance (histrionic sexualization)

Normal traits NEO PI-R: MPQ: TCI: EPP: PAS:

gregariousness, assertiveness, activity, excitementseeking, positive emotionality (warmth) social potency, social closeness, well-being exploratory excitability, sociability, (attachment) sociability, assertiveness, activity (optimism)

Abnormally low traits DAPP-BQ:

intimacy problems, social avoidance, restricted expression SNAP: detachment PAS: aloofness, (shyness) TCI: (shyness) SWAP-200: schizoid orientation 2.

Antagonism versus Compliance Abnormally high traits DAPP-BQ:

narcissism, suspiciousness, interpersonal disesteem, conduct problems, passive oppositionality, rejection SNAP: mistrust, manipulativeness, aggression, entitlement MPQ: aggression, (alienation) PAS: suspiciousness, aggression, callousness SWAP-200: narcissism, psychopathy Normal traits NEO PI-R: TCI: MPQ:

trust, straightforwardness, altruism, compliance, modesty, tender-mindedness, agreeableness helpfulness, compassion, pure-hearted, sentimentality, empathy, social acceptance, attachment (social closeness)

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder 15

TABLE 1–3.

Lower-order scales within the domains of Extraversion versus Introversion and Antagonism versus Compliance (continued) 2.

Antagonism versus Compliance (continued) Abnormally low traits DAPP-BQ: SNAP: PAS: TCI:

diffidence, insecure attachment (dependency) dependence, submissiveness dependence

Note. Some scales are noted parenthetically because they include aspects of personality function from another domain. DAPP-BQ = Dimensional Assessment of Personality Psychopathology—Basic Questionnaire; EPP = Eysenck Personality Profiler; MPQ = Multidimensional Personality Questionnaire; NEO PI-R = Neuroticism–Extraversion–Openness (NEO) Personality Inventory—Revised; PAS = Personality Assessment Schedule; SNAP = Schedule for Nonadaptive and Adaptive Personality; SWAP-200 = Shedler and Westen Assessment Procedure–200; TCI = Temperament and Character Inventory.

As we discuss further below, future research might indicate that some of our scale placements are inaccurate or at least not optimal. For example, a number of studies have placed Dependency scales within a domain of Neuroticism or Emotional Instability (e.g., Clark and Livesley 2002; Clark et al. 1996; De Clercq and De Fruyt 2003; Trull 1992). However, quite a few studies have placed Dependency scales within a domain of Agreeableness (e.g., Blais 1997; Coker et al. 2002; Costa and McCrae 1990; Dyce and O’Connor 1998; Haigler and Widiger 2001; Hyer et al. 1994; Lynam and Widiger 2001; Pincus and Gurtman 1995; Sprock 2002; Wiggins and Pincus 1989; Zuroff 1994). The IPC dimensional models consistently place Dependency scales within an Agreeableness (or Compliance) domain (Pincus and Gurtman 1995; Widiger and Hagemoser 1997), as the IPC dimensional models do not include a Neuroticism (or Negative Affectivity) domain. The inconsistency in placement is perhaps due largely to the complexity of the dependent personality disorder construct (i.e., involving traits of both Neuroticism and Agreeableness).

Conclusion and Recommendations In sum, we suggest that an important goal of future research will be the identification of a common ground among the alternative dimensional models of personality disorder. We recognize that future research will continue to focus on the particular strengths, nuances, and advantages of alternative models. The respective validity and clinical utility of each alternative model would be informative to the

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Dimensional Models of Personality Disorders

authors of a future edition of the diagnostic manual in making decisions regarding which specific components of each model to include within an integrative structure. However, we would also encourage researchers to themselves consider the possibility of working toward a more unified, integrative model. Given that these models are all attempting to do largely the same thing, it would seem likely that they share common ground. It is possible that the authors of a future edition of a diagnostic manual will come to the decision that one particular model is preferable to all of the others. However, it is our opinion that it is unlikely that any one particular model will lack any redeeming or useful features or, conversely, that any one particular model will be without any meaningful faults or limitations. We would therefore suggest that research that leads to an integrative structure will be particularly informative to the authors of this future diagnostic manual. It is also possible that a common, integrative structure will not resemble closely the illustrative model we provided. Our integrative model is guided by a considerable amount of supportive research (e.g., Austin and Deary 2000; Clark et al. 1996; Clark et al. 1993; Costa and McCrae 1990; Deary et al. 1998; De Clercq and De Fruyt 2003; De Fruyt et al. 2000; Duijsens and Diekstra 1996; Dyce et al. 1997; Livesley et al. 1998; Markon et al. 2005; Mulder and Joyce 1997; O’Connor and Dyce 1998; Ramanaiah et al. 2002; Reynolds and Clark 2001; Schroeder et al. 1992; Trull 1992; Trull et al. 1995; Zuckerman 2002), but admittedly there are some studies that suggest that some of the existing dimensional models might not be well integrated within this structure (e.g., Shedler and Westen 2004) and that the placement of some models (e.g., PAS) is based on only a limited amount of research. Our placements of some of the PAS, DAPP-BQ, SNAP, TCI, NEO PI-R, MPQ, and SWAP-200 scales might also be disputed. Perhaps we have misunderstood the constructs assessed by these scales or the research that has been conducted to date. Some of the placements (e.g., those placed parenthetically) were difficult because the constructs appear to contain aspects from more than one domain. Future research could help determine how these alternative dimensional models of personality disorder could be best integrated into a common, unified, hierarchical structure. The devil, of course, could be in the details. It is apparent that the illustrative model includes considerable redundancy (a direct effect of the alternative efforts to describe a common ground) and uncertain labeling. If the authors of a future diagnostic manual prefer to use an integrative, hierarchical structure, they will need to decide which scales and constructs will be optimal for inclusion, and how best to represent them. Considered in this selection could be extent of overlap, adequate representation of different models, adequate coverage of the domain, clinical relevance, familiarity, and ease of usage. Last but not least is whether the diagnostic manual should include normal, adaptive traits. We again argue for the importance of their inclusion. The inclusion of normative, adaptive traits will facilitate the provision of a more comprehensive (and accurate) description of each

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder 17 patient’s general personality structure; it will facilitate an integration of the diagnostic manual with basic science research on general personality structure; and it will facilitate treatment decisions through the recognition of traits that contribute to an understanding of treatment responsivity. Even if the diagnostic manual does not explicitly include normal personality traits, it should be closely coordinated with them so that the American Psychiatric Association diagnostic manual of personality disorders is itself well integrated and coordinated with basic science research on general personality structure.

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Trull TJ: DSM-III-R personality disorders and the five-factor model of personality: an empirical comparison. J Abnorm Psychol 101:553–560, 1992 Trull TJ, Durrett CA: Categorical and dimensional models of personality disorder. Annu Rev Clin Psychol 1:355–380, 2005 Trull TJ, Useda JD, Costa PT Jr, et al: Comparison of the MMPI-2 Personality Psychopathology Five (PSY-5), the NEO-PI, and the NEO PI-R. Psychol Assess 7:508–516, 1995 Trull TJ, Widiger TA, Lynam DR, et al: Borderline personality disorder from the perspective of general personality functioning. J Abnorm Psychol 112:193–202, 2003 Tyrer P (ed): Personality Disorders. Diagnosis, Management, and Course, 2nd Edition. London, Arnold, 2000 Tyrer P: Personality disorder. Br J Psychiatry 179:81–84, 2001 Tyrer P, Johnson T: Establishing the severity of personality disorder. Am J Psychiatry 153:1593–1597, 1996 Watson D, Clark LA: Extraversion and its positive emotional core, in Handbook of Personality Psychology. Edited by Hogan R, Johnson J, Briggs S. New York, Academic Press, 1997, pp 767–793 Watson D, Clark LA, Harkness AR: Structures of personality and their relevance to psychopathology. J Abnorm Psychol 103:18–31, 1994 Watson D, Wiese D, Vaidya J, et al: The two general activation systems of affect: structural findings, evolutionary considerations, and psychobiological evidence. J Pers Soc Psychol 76:820–838, 1999 Westen D, Shedler J: A prototype matching approach to diagnosing personality disorders: toward DSM-V. J Personal Disord 14:109–126, 2000 Widiger TA, Costa PT Jr: Five factor model personality disorder research, in Personality Disorders and the Five Factor Model of Personality, 2nd Edition. Edited by Costa PT Jr, Widiger TA. Washington, DC, American Psychological Association, 2002, pp 59–87 Widiger TA, Hagemoser S: Personality disorders and the interpersonal circumplex, in Circumplex Models of Personality and Emotions. Edited by Plutchik R, Conte HR. Washington, DC, American Psychological Association, 1997, pp 299–325 Widiger TA, Mullins-Sweatt SN: Categorical and dimensional models of personality disorder, in The American Psychiatric Publishing Textbook of Personality Disorders. Edited by Oldham JM, Skodol AE, Bender DS. Washington, DC, American Psychiatric Publishing, 2005, pp 35–53 Widiger TA, Sanderson CJ: Towards a dimensional model of personality disorders in DSMIV and DSM-V, in The DSM-IV Personality Disorders. Edited by Livesley WJ. New York, Guilford, 1995, pp 433–458 Widiger TA, Simonsen E: Alternative dimensional models of personality disorder: finding a common ground. J Personal Disord 19:110–130, 2005 Wiggins JS: Paradigms of Personality Assessment. New York, Guilford, 2003 Wiggins JS, Pincus AL: Conceptions of personality disorders and dimensions of personality. Psychol Assess 1:305–316, 1989 World Health Organization: (The ICD-10 Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva, Switzerland, World Health Organization, 1992

Widiger and Simonsen: Alternative Dimensional Models of Personality Disorder 21 Zuckerman M: Zuckerman-Kuhlman Personality Questionnaire (ZKPQ): An alternative five-factorial model, in Big Five Assessment. Edited by de Raad B, Perugini M. Kirkland, WA, Hogrefe & Huber, 2002, pp 377–397 Zuroff DC: Depressive personality styles and the five-factor model of personality. J Pers Assess 63:453–472, 1994

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2 COMMENTARY ON WIDIGER AND SIMONSEN Toward a Consensus Personality Trait Structure Lee Anna Clark, Ph.D.

W

idiger and Simonsen (Chapter 1 in this volume) have summarized a great deal of information to present a compelling, dimensional, hierarchical model of adaptive and maladaptive personality traits that can serve as the common basis for integration of at least 12 of 18 existing models of personality dysfunction. Lowerorder scales from a 13th model can be placed within the common structure, a 14th model emerges easily from combinations of the 4 higher-order dimensions of the common structure, and all that remain are 4 models tied directly to the DSM, which the common structure replaces. Thus, this common structure encompasses all currently well-known non-DSM models of personality pathology to some degree and, in most cases, to quite a large degree. Therefore, the primary intent of this comment is to further the thrust of Widiger and Simonsen’s argument by proposing solutions to certain difficulties they pose or do not address; offering a different viewpoint on the relation of measures to the higher-order structure; suggesting alternative placements of lower-order dimensions within the common structure; and discussing the next challenge facing the intertwined fields of personality and personality pathology. First, Widiger and Simonsen indicate that the clinical spectra of internalizing and externalizing exist at the highest level of the structure, and from them emerge the “three to five broad domains of personality functioning” (Chapter 1, pp. 3–4). However, they do not specify the relation of these three to five domains to the two 23

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clinical spectra. I suggest that internalizing and externalizing are not a higher level of abstraction than the three to five higher-order domains, but rather result from combinations of these domains. Specifically, internalizing and externalizing are correlated through the common factor of Neuroticism/Negative Affectivity/Emotionality (hereafter, N/NA/NE). Internalizing combines N/NA/NE with low Extraversion/Positive Affectivity/Emotionality (E/PA/PE), whereas externalizing is a combination of Antagonism and Impulsivity, with N/NA/NE as a secondary, but still important, component (Krueger and Tackett 2003). In this context it is worth noting that selecting “the optimal term(s) to characterize this (or any other) domain” is more important politically than scientifically, and far less important than clarifying both the core and, to the extent possible, the boundaries of the respective domains. That is, the concepts Extraversion and Positive Emotionality both contribute to defining the same broad domain. Whether sociability, agency, or emotionality—or all three conjointly—will prove to be the core construct(s) of the domain is an empirical question whose answer awaits further research, and it will be more fruitful to devote our efforts to designing and conducting that research than to arguing over the domain name. Second, Widiger and Simonsen go to some pains to align 12 of the models in the common structure presented in their Table 1–1 (see Chapter 1, p. 7, for key to instrument abbreviations used here). Remarkably, I have only one quibble with their placement, and that is that the SNAP and MPQ structures are highly convergent with those of the EPQ and the EPP (Markon et al. 2005), which is not well reflected in the table. Specifically, the SNAP–MPQ Constraint (vs. Disinhibition) factor falls between the table’s Second and Third factors, just as do Eysenck’s (1997) Psychoticism and Siever and Davis’s (1991) Aggression-Impulsive. Similarly, I feel sure enough of the data to take public exception to only one placement in Table 1–3, and to offer a suggestion for Table 1–2. In Table 1–3, the parentheses around Entitlement belong under Antagonism versus Compliance, not under Extraversion versus Introversion (Clark et al., in press; Markon et al. 2005). In Table 1–2, “spontaneous” would be a good addition to the Normal list of the Simplified Version. I have some questions about a few other placements as well, but more data are needed to answer them. For a field about which many outside observers believe there is great chaos and contention, this level of agreement is nothing short of extraordinary. Much more important than any of these quibbles, however, are the realization that 1) there may be no need to shoehorn these measures into a single “three to five” domain structure and 2) the attention of the field needs now to turn to clarifying the lower levels of the hierarchy. I discuss each of these in turn. First, as Markon et al. (2005) demonstrate clearly, many of the measures in Table 1–1 fit quite neatly into a hierarchical structure with four levels of two to five factors, respectively (see Chapter 1, p. 7, for key to instrument abbreviations used here). The SNAP/MPQ/EPQ three factors spawn the four-factor DAPP-BQ/MCMI-III/

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ZKPQ by the splitting of (EPQ) Psychoticism versus Constraint into Antagonism–Aggression and Conscientiousness versus Impulsivity. In turn, the fifth factor in five-factor models (e.g., PSY-5, NEO PI-R) emerges by (PSY-5) Psychoticism–Openness splitting off from a broader Extraversion factor. At the top of this hierarchy are Digman’s (1997) Alpha (N/NA/NE + EPQ Psychoticism vs. Constraint) and Beta (E/PA/PE + Openness) factors. Once this multilevel hierarchical structure is acknowledged, the need for Widiger and Simonsen to discuss how Eysenck’s Psychoticism and the three-dimensional models of the MPQ and SNAP relate to Antagonism versus Compliance (see Chapter 1 subsection titled “Antagonism Versus Compliance”) simply disappears. The answer is that they exist at the three-factor level, whereas Antagonism versus Compliance only emerges at the four-factor level. It is extremely important in this context not to begin the debate with whether the 3- or 4- or 5- or 20-factor model is the “right” or “true” model. It may well be that one, or some subset, of models ultimately will prove to be the most useful, for example, in terms of its reflecting most closely brain structures, genetic architecture, or cultural patterns of reinforcement. But these are larger empirical questions that cannot be resolved by debate or psychometric refinements, no matter how sophisticated. Nor can they be resolved if—either by explicit agreement or simply by default—all personality disorder research is conducted only at one level of the hierarchy. Rather, I contend that the field will be best served by a strong consensus that a relatively well-defined hierarchical structure exists, and that both existing and new measures should be examined in the context of the structure as a whole—unless, of course, the research is designed explicitly to test the robustness of the structure itself, either internally or in relation to a clear external set of correlates. We now have enough data to be reasonably sure that working within this broad structure will not lead us far astray for the foreseeable future, and that much is to be gained by everyone pulling in the same general direction with an interrelated set of tools. Accordingly, the next challenge facing the field of personality—both adaptive and maladaptive—today is not the higher-order structure, but rather clear, coherent, and consistent delineation of the lower-order structure of the model, from 6 through 20 or 30 factors. It is unlikely (and probably unnecessary as well) that every level of the structure can be spelled out with the same degree of precision that characterizes the 2- through 5-factor structures. However, for measures that fall into roughly the same level of the overall hierarchy, it would be useful to work toward a consensus set of dimensional constructs at that level. For example, the 15 scales of the SNAP might be studied conjointly with the 18 scales of the DAPP-BQ to arrive at a consensus set of lower-order constructs at this middle level of specificity. To illustrate, two DAPP-BQ scales—Diffidence and Insecure Attachment— both correlate moderately strongly with SNAP Dependency. A focused study could determine the empirical value of these scales, investigating such questions as whether SNAP Dependency lacks important content covered by one or the other

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of the DAPP scales (and vice versa); whether the two DAPP scales have more, the same, or less predictive power than the one SNAP scale for specified relevant variables; and whether the two DAPP scales have differential correlates, justifying their existence as separate traits, or whether they each correlate similarly with the same set of variables, raising questions about the utility of having separate scales. Such investigations would clarify—and, ideally, yield a consensus regarding—each focused portion of the hierarchical structure. Furthermore, in cases such as dependency, for which the placement of the subdomain relative to the higher-order structure is unclear, such research would address this question. Moreover, this research will need to address additional questions such as those raised by Widiger and Simonsen, including whether the traits are bipolar in nature, how best to assess the continuum of traits from normality into psychopathology, and even how traits may combine to form “true” categorical entities which are more than the sum of their parts. Newer, more sophisticated methods such as item response theory (IRT) modeling and taxometrics will be of value in these investigations. The end result of such research might be 1) a single consensus set of X traits, with each instrument adding constructs it previously lacked, 2) a single consensus set of Y traits, with some realignment of the scales’ variables (e.g., the item content of the three scales Diffidence, Insecure Attachment, and Dependency might be realigned into a cleaner two-trait set), or 3) some other outcome not yet envisioned. In addition, we might expect increased clarity regarding where the resultant traits fit in the hierarchical structure and the nature of the traits, including their potential bipolarity, relations between normal and abnormal variants, and the possibility of emergent categories. Widiger and Simonsen suggest that a future DSM would provide a set of lowerorder traits such as those just discussed, and that the selection of traits to be included would be based on “extent of overlap, adequate coverage of the domain, representation of different dimensional models, clinical relevance, familiarity, and ease of use” (Chapter 1, p. 10). This implies that a future committee would be choosing from among a cacophony of extant variables and measures. What I am suggesting here is that determining an optimal set of lower-order traits, such as those shown in Widiger and Simonsen’s Tables 1–2 and 1–3, for inclusion in a future DSM is work that is too important to leave to a selection committee. Rather, we must take responsibility as researchers to provide the committee with sufficient data to determine which traits to include in the next DSM. Widiger and Simonsen have started us in the right direction. We must now take up the baton and do our part.

References Clark LA, Simms LJ, Wu KD, Casillas A: Schedule for Nonadaptive and Adaptive Personality. Minneapolis, MN, University of Minnesota Press, in press

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Digman JM: Higher-order factors of the Big Five. J Pers Soc Psychol 73:1246–1256, 1997 Eysenck HJ: Personality and experimental psychology: the unification of psychology and the possibility of a paradigm. J Pers Soc Psychol 73:1224–1237, 1997 Krueger RF, Tackett JL: Personality and psychopathology: working toward the bigger picture. J Personal Disord 17:109–128, 2003 Markon KE, Krueger RF, Watson D: Delineating the structure of normal and abnormal personality: an integrative hierarchical approach. J Pers Soc Psychol 88:139–157, 2005 Siever LJ, Davis KL: A psychobiological perspective on the personality disorders. Am J Psychiatry 148:1647–1658, 1991

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3 COMMENTARY ON WIDIGER AND SIMONSEN Working Out a Dimensional Framework John M. Oldham, M.D.

The paper by Widiger and Simonsen is a careful, elegant, and thoughtful review of 1) proposed modifications of the current DSM diagnostic system for the personality disorders, 2) potential ways to dimensionally reorganize personality disorder symptoms, 3) the relative merits of clinical spectra models, and 4) dimensional models that encompass general personality functioning. The authors propose four to five broad domains of personality functioning, emphasizing 1) Extraversion versus Introversion, 2) Antagonism versus Compliance, 3) Constraint versus Impulsivity, 4) Emotional Dysregulation versus Emotional Stability, and possibly 5) Unconventionality versus Closedness to Experience. Each domain is then displayed as a “bipolar system,” implying a continuum with normal personality traits in the midzone and pathology on the high and low ends of each continuum; estimates of which assessment instruments best capture which parts of each continuum are presented. Presumably, what would be measured would be behaviorally specific criteria reflecting an attempt to quantify the amount of a specific personality trait present or absent, which, if “too much” or “too little,” would define a component of pathology. For clinicians, some DSM-IV-TR (American Psychiatric Association 2000) personality disorder categories might be rather easily reconceptualized using one of the five domains proposed by Widiger and Simonsen. For example, schizoid personality disorder might naturally be understood as a condition characterized by 29

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a high degree of introversion. Other familiar conditions, such as borderline personality disorder, might need to be “unpacked” into subtypes, such as one subtype characterized by impulsivity and another subtype characterized by emotional dysregulation. In other cases, such as narcissistic personality disorder, it is not clear how current DSM-defined categories could be translated into this dimensional model, or even whether there are sufficient data supporting its construct validity to justify doing so. Relying solely on an evidence base to establish validity is complicated, however, since research data that inform us about personality pathology are mostly derived from clinical populations. It may be misleading, therefore, to judge the relative “validity” of a given DSM-defined personality disorder based on the number of published research studies and clinical case reports on the disorder, since the volume of published studies in the literature may reflect who comes for treatment, or who comes to public or institutional attention. Borderline personality disorder, by this measure, would naturally be the subject of many studies, since these patients are highly prevalent within clinical populations. Patients with antisocial personality disorder, though not necessarily high on the treatment-seeking list, contribute quite significantly to social cost and burden, and they populate correctional systems at great expense. However, patients with paranoid or schizoid personality disorder may avoid treatment settings, even when significantly symptomatic, by the very nature of their conditions, as could be the case for other personality disorders such as dependent or obsessive-compulsive. In other cases, features of given personality disorders may be widely accepted as “facts,” even though the data vary greatly depending on the population studied. Borderline personality disorder, for example, is frequently described as a condition more common in women than in men (Gunderson 2001), whereas population-based studies report even distribution of the disorder between women and men (Torgersen 2001). We know that DSM-defined borderline personality disorder is an enormously heterogeneous category, perhaps partially explaining the apparent discrepancy among reported borderline personality disorder populations, and patterns of comorbidity could vary as well—high percentages of women with borderline personality disorder might have comorbid major depressive disorder and might be likely to seek treatment, whereas high percentages of men with borderline personality disorder might have comorbid antisocial personality disorder, and their more characteristic impulsivity could land them in correctional settings more often than treatment settings. It is important to underscore, as the authors point out, that DSM-IV-TR is not a textbook about the nonpathological biology and psychology of motivated human behavior. Instead, it is used to define illness (i.e., abnormality), which then presumably guides treatment planning. Practically and inevitably, as well, it also guides health policy, coding, reimbursement, and legal and forensic arguments. At least some of the DSM-defined categories of personality disorders—such as paranoid personality disorder, schizoid personality disorder, antisocial personality dis-

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order, and obsessive-compulsive personality disorder—have been stable and persistent, appearing in every edition of the DSM, perhaps reflecting a longitudinal clinical consensus that conveys some sense of “real world” validity. Other personality disorders have been proposed and later have been judged to be invalid (e.g., aesthenic personality disorder) or have been reconceptualized as Axis I disorders (e.g., cyclothymic disorder), and still others have been introduced in one of the later editions of the DSM (e.g., borderline personality disorder). One could argue that this process of reevaluation and revision is appropriate and is mirrored by a similar process for Axis I conditions. Whatever diagnostic system for the personality disorders eventually achieves consensus, there will still need to be a way to define the threshold or “cut point” that differentiates normal traits from pathology, and this applies for dimensional systems as well (Rothschild et al. 2003). Such a differentiation would have to be worked out if a system similar to that proposed by Widiger and Simonsen were adopted. For example, how much or how little of a particular trait on a continuum would define pathology? Would a hypothetical individual be judged to have “antagonistic personality disorder” if above and “compliant personality disorder” if below particular cut points on an Antagonism-versus-Dependency scale? If so, what evidence would guide such delineation? If, instead of radical revision, a modification of the current DSM-IV-TR system were introduced, a dimensional framework could be worked out (Oldham and Skodol 2000) identifying a designated number of criteria to define trait, subthreshold, threshold, or prototypic levels of a given personality disorder, as Widiger (1993) and Widiger and Sanderson (1995) previously proposed. Finally, new data are raising questions about the long-term stability of the personality disorders (Grilo et al. 2004; Paris and Zweig-Frank 2000; Zanarini et al. 2003), perhaps challenging the current inclusion of “stable and of long duration” as one of the DSM-IV-TR generic defining features for all personality disorders. The now clearly established fluctuation in reported levels of symptoms over time in patients with personality disorders might argue in favor of a dimensional, continuum model, to some degree analogous to the exacerbations and remissions of Axis I disorders. One could still use a stratified, combined, categorical/dimensional system, but the lack of longitudinal stability may argue against a fundamental difference between Axis I and Axis II disorders.

References American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000 Grilo C, Sanislow CA, Gunderson JG, et al: Two-year stability and change of schizotypal, borderline, avoidant and obsessive-compulsive personality disorders. J Consult Clin Psychol 72:767–775, 2004

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Gunderson JG: Borderline Personality Disorder: A Clinical Guide. Washington, DC, American Psychiatric Publishing, 2001 Oldham JM, Skodol AE: Charting the future of Axis II. J Pers Disord 14:17–29, 2000 Paris J, Zweig-Frank H: A 27-year follow-up of patients with borderline personality disorders. Psychiatr Q 71:291–307, 2000 Rothschild L, Cleland C, Haslam N, et al: A taxometric study of borderline personality disorder. J Abnorm Psychol 112:657–666, 2003 Torgersen S, Kringlen E, Cramer V: The prevalence of personality disorders in a community sample. Arch Gen Psychiatry 58:590–596, 2001 Widiger TA: The DSM-III-R categorical personality disorder diagnoses: a critique and an alternative. Psychol Inq 4:75–90, 1993 Widiger TA, Sanderson CJ: Toward a dimensional model of personality disorder, in The DSM-IV Personality Disorders. Edited by Livesley WJ. New York, NY, Guilford, 1995, pp 433–458 Zanarini MC, Frankenburg FR, Hennen J, et al: The longitudinal course of borderline psychopathology: 6-year prospective follow-up of the phenomenology of borderline personality disorder. Am J Psychiatry 160:274–283, 2003

4 COMMENTARY ON WIDIGER AND SIMONSEN From ICD-10 and DSM-IV to ICD-11 and DSM-V Charles B. Pull, M.D., Ph.D.

As a member of the overall World Health Organization (WHO) Task Force that coordinated the development of ICD-10 (World Health Organization 1992), the author of this discussant paper participated in many of the meetings that were convened to compare the successive drafts developed for the classification and description of personality disorders in ICD-10 and DSM-IV (American Psychiatric Association 1994). It became rapidly apparent to the members of the ICD-10 and the DSM-IV Task Forces that there was little evidence to rely on for making fundamental decisions, e.g., for deciding what categories of personality disorders to include in the ICD-10 or DSM-IV, or for choosing the number and content of individual diagnostic criteria defining each individual disorder. As such, members of the two tasks forces had to rely heavily on considerations that were based, not on scientific evidence, but on the traditions of various schools of psychiatry or psychology, as well as on the expert opinion of specialists. Many of the final decisions in either system were, in fact, consensus decisions taken by the respective ICD-10 or DSM-IV committees. The main data that were used to finalize the ICD-10 criteria sets came from the results of the International Pilot Study on Personality Disorders (IPSPD), which included centers from 11 countries in North America, Europe, Africa, and 33

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Asia (Loranger et al. 1994; World Health Organization 1997). In the IPSPD, personality disorders were assessed with the International Personality Disorder Examination (IPDE). The IPDE is a semistructured diagnostic interview that contains a prescribed set of carefully selected and researched questions for the assessment of each criterion provided for each personality disorder in either system (draft criteria of ICD-10 and DSM-III-R [American Psychiatric Association 1987] criteria in the original version, final ICD-10 and DSM-IV criteria in the current version of the instrument). Although the principal objectives of the study were to determine the cultural applicability, user friendliness, and interrater reliability of the instrument, the results also provided information on the interrater reliability and temporal stability of personality disorder diagnoses, on the co-occurrence of personality disorders in the same patients, and on the overlap of ICD-10 and DSM-IV diagnoses. The results of the IPSPD revealed major difficulties in the diagnosis of personality disorders in both ICD-10 and DSM-III-R. First, administration of the IPDE took a long time (usually between 2 and 3 hours). Second, interrater agreement and temporal stability of IPDE diagnoses were far from perfect. For interrater agreement, the overall weighted kappa values for definite and definite/probable diagnoses were .57 and .69 in DSM-III-R and .65 and .72 in ICD-10, respectively. For temporal stability, the overall weighted kappa values for the definite and definite/probable diagnoses were .50 and .53 in DSMIII-R and .54 and .53 in ICD-10, respectively. Third, a substantial number of patients had more than one diagnosis of personality disorder. Of the patients with a DSM-III-R personality disorder diagnosis, 30.3% had more than one personality disorder, including 15.0% with two, 8.7% with three, and 6.6% with more than three disorders. Of the patients with an ICD10 personality disorder diagnosis, 33.9% had more than one type of disorder, including 20.1% with two, 9.5% with three, and 4.2% with more than one disorder. Fourth, there was substantial disagreement regarding the cases of personality disorders identified by ICD-10 and DSM-III-R. The question of whether the two classification systems identified the same patients as having a particular disorder was addressed by calculating an overall weighted kappa based on all of the disorders, regardless of whether they met the criterion of a 5% base rate. The kappa was .54, an indication of moderate agreement. The results of the IPSPD led to a number of modifications in the criteria that were retained for the diagnosis of the different personality disorders in ICD-10 and DSM-IV, concerning in particular the thresholds required for a positive diagnosis in either system, and the content or formulation of several of the initial criteria. There remained, however, substantial differences between the final ICD-10 and DSM-IV criteria for most of the personality disorders in either system (Pull and Pull 2002).

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In some instances, the differences are such that the diagnosis of a given personality disorder may be met according to the criteria in one of the systems, while none of the criteria from the other system are met for the same disorder. An example of this extreme situation is provided by paranoid personality disorder (Table 4–1). In both ICD-10 and DSM-IV, a diagnosis of paranoid personality disorder can be made when (at least) 4 out of 7 criteria are met. Four of the ICD-10 criteria (criteria 1, 4, 6, and 7) are not part of the DSM-IV criteria, and in the same way, four of the DSM-IV criteria (criteria 2, 3, 4, and 6) are not part of the ICD-10 criteria. Since a diagnosis of paranoid personality disorder can be made when only ICD-10 criteria 1, 4, 6, and 7 (or DSM-IV criteria 2, 3, 4, and 6) are met, it is quite possible (at least on a theoretical level), to make a diagnosis of the disorder according to the criteria in either of the systems, even when no single criterion for the same disorder is present from the other. Similar considerations apply to the criteria of dissocial (ICD-10) and antisocial (DSM-IV) personality disorder. Other major differences between ICD-10 and DSM-IV personality disorders include discrepancies in the criteria for anankastic (ICD-10) and obsessive-compulsive (DSM-IV), anxious (ICD-10), and avoidant (DSM-IV) and dependent personality disorders. All along, the members of both the ICD-10 and the DSM-IV task forces were fully aware of the existence of dimensional models of personality disorder and, over the years when the two systems were developed, the option to replace diagnostic categories by dimensions was discussed many times. In both groups, however, the general opinion prevailed that it was too early to make this kind of radical change at that time. The diagnostic criteria defining the various types of personality disorder in the current classification systems translate enduring patterns of thinking, feeling, and behaving. According to the dimensional model, personality disorders represent maladaptive variants of personality traits. While it would be difficult to accommodate criteria defining patterns of behaviors within a dimensional model, most other current diagnostic criteria in ICD-10 and DSM-IV-TR could in fact easily be viewed as combinations of abnormal high or abnormal low traits or facets within a small number of fundamental dimensions or domains, such as those that are identified in the five-factor model (Widiger and Costa 2002). The masterly and comprehensive review by Drs. Simonsen and Widiger show that the field has considerably evolved during the past decade and that significant advances have been made in the development of dimensional models of personality as well as of personality disorder. Drs. Widiger and Simonsen have described 18 alternative proposals and suggested, quite convincingly, that these alternative models might be integrated within a common hierarchical structure. In fact, they provide an illustration of how this could be accomplished. Considering the data that Drs. Widiger and Simonsen have presented, the time may now be ripe to make those radical changes that could not be made a decade ago. The task ahead is obviously a formidable challenge, but certainly worth the try.

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TABLE 4–1.

A comparison of ICD-10 and DSM-IV criteria for paranoid personality disorder ICD-10 criteria

DSM-IV criteria

At least four of the following must Four or more of the following: be present: 1. excessive sensitivity to setbacks _____ and rebuffs 2. tendency to bear grudges 5. persistently bears grudges, i.e., persistently, e.g., refusal to forgive is unforgiving of insults, insults, injuries, or slights injuries, or slights 3. suspiciousness and a pervasive 1. suspects, without sufficient tendency to distort experience by basis, that others are misconstruing the neutral or friendly exploiting, harming, or actions of others as hostile or deceiving him or her contemptuous 4. a combative and tenacious sense of _____ personal rights out of keeping with the actual situation 5. recurrent suspicions, without 7. has recurrent suspicions, justification, regarding sexual fidelity without justification, of spouse or sexual partner regarding fidelity of spouse or sexual partner 6. persistent self-referential attitude, _____ associated particularly with excessive self-importance 7. preoccupation with unsubstantiated _____ “conspiratorial” explanations of events either immediate to the patient or in the world at large _____ 2. is preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or associates _____

3. is reluctant to confide in others because of unwarranted fear that the information will be used maliciously against him or her

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TABLE 4–1.

A comparison of ICD-10 and DSM-IV criteria for paranoid personality disorder (continued) ICD-10 criteria

DSM-IV criteria _____

_____

4. reads hidden demeaning or threatening meanings into benign remarks or events 6. perceives attacks on his or her character or reputation that are not apparent to others and is quick to react angrily or to counterattack

References American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised. Washington, DC, American Psychiatric Association, 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994 Loranger AW, Sartorius N, Andreoli A, et al: The International Personality Disorder Examination: the World Health Organization/Alcohol, Drug Abuse, and Mental Health Administration International Pilot Study of Personality Disorders. Arch Gen Psychiatry 51:215–224, 1994 Pull CB, Pull MC. Conceptions typologiques des troubles de la personnalité: critères diagnostiques des troubles de la personnalité, in Les troubles de la personnalité. Edited by Féline A, Guelfi JD, Hardy P. Paris, France, Médecine-Sciences Flammarion, 2002, pp 81–97 Widiger TA, Costa PT: Five factor model personality disorder research, in Personality Disorders and the Five Factor Model of Personality, 2nd Edition. Edited by Costa PT, Widiger TA. Washington, DC, American Psychological Association, 2002, pp 59–87 World Health Organization: The ICD-10 Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva, Switzerland, World Health Organization, 1992 World Health Organization: Assessment and Diagnosis of Personality Disorders: The ICD10 International Personality Disorder Examination (IPDE). Edited by Loranger AW, Janca A, Sartorius N. Cambridge, UK, Cambridge University Press, 1997

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5 BEHAVIORAL AND MOLECULAR GENETIC CONTRIBUTIONS TO A DIMENSIONAL CLASSIFICATION OF PERSONALITY DISORDER W. John Livesley, M.D., Ph.D.

The central argument advanced in this chapter is that it is feasible to construct an etiologically informed dimensional classification of personality disorder that addresses many of the limitations of current categorical systems. The evidence shows that personality disorders are best represented by behavioral continua continuous with normal personality variation and that current diagnoses are not natural kinds that “carve nature at its joints” but rather artifactual kinds—contrived constructs used to organize clinical information. When constructing a dimensional alternative, the challenge is to construct a system based on natural kinds. Accumulating knowledge on the genetic etiology of personality disorder makes this an achievable

This chapter is an abbreviated version of a paper with the same title first published in the Journal of Personality Disorders (Volume 19, Issue 2, pages 131–155, 2005).

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goal. The intent of this chapter is not to review the genetics of personality in detail but to consider how genetic research may help taxonomic endeavors. For this reason, the chapter begins by briefly considering the classification of personality disorder and what is needed to build a valid system.

The Classification of Personality Disorder A dimensional classification requires two components (Livesley 2003). First, a definition of personality disorder is needed to diagnose the disorder because extreme variation alone does not necessarily imply disordered functioning (Wakefield 1992). Second, constructs are needed to represent individual differences in personality pathology. Ideally, the definition of personality disorder should be based on an understanding of disturbances in normal personality functioning. Consequently, the category of personality disorder is an artifactual kind—a construction for organizing information about mental disorders. Hence, genetic research probably has little to contribute to its definition. Genetic information can, however, make a substantial contribution to delineating the constructs needed to represent individual differences. Most models of individual differences assume that traits are hierarchically organized with secondary traits subdividing into multiple primary traits. Common models of personality such as Eysenck’s three-component model as assessed by the Eysenck Personality Questionnaire (EPQ; Eysenck and Eysenck 1992) and the five-factor model as assessed with the Neuroticism–Extraversion–Openness Personality Inventory—Revised (NEO PI-R; Costa and McCrae 1992) differ in the number and nature of the constructs used to represent personality. Nevertheless, there is considerable agreement that four secondary dimensions underlie personality disorder (Mulder and Joyce 1997). These dimensions may be labeled: anxious-submissive, psychopathic, socially withdrawn, and compulsive. They resemble the five-factor dimensions of neuroticism, (dis)agreeableness, introversion, and conscientiousness (clinical studies consistently fail to find a component corresponding to openness) and Eysenck’s neuroticism, extraversion, and psychoticism dimensions. The difference is that Eysenck considers compulsivity to be a facet of psychoticism rather than a secondary domain (Eysenck 1991, 1992). Despite this convergence, debate continues on the number of factors needed to represent broad differences in personality. Although this issue is relatively unimportant for many research purposes—because it is often useful to vary level of analysis according to the research question under investigation—it is important when constructing a dimensional classification because secondary traits are a useful way to organize personality descriptors. For this reason, we need to resolve discrepancies across models. Disagreement stems partly from the failure to differentiate secondary and primary traits. What is a primary trait to one theorist is a

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secondary trait to others, as illustrated by the disagreement between Costa and McCrae and Eysenck over whether conscientiousness is a secondary domain or merely a facet of psychoticism. Moreover, broad agreement on the secondary dimensions masks disagreement on the primary traits defining each domain. For example, there is agreement that sociability and affiliation are major components of extraversion but not on the importance of agency, activation, impulsivity, sensation seeking, positive emotions, or optimism (Depue and Collins 1999). Similar problems occur with other secondary traits (e.g., whether impulsivity is a feature of neuroticism or of psychoticism). To construct a dimensional classification that integrates current models, we need to specify the difference between secondary and primary traits, determine the number and content of secondary domains, and develop a procedure for identifying and defining primary traits. The failure of standard psychometric studies to resolve these issues suggests that psychometric criteria alone may be insufficient for this purpose (Eysenck 1991, 1992). Hence, it seems appropriate to consider whether a genetic perspective can clarify the structure of personality and whether it is possible to construct what Tsuang and colleagues (1993) referred to as a “genetically informed nosology.” The foundations for such a system would be provided by evidence that 1) genetic factors have an extensive influence on personality disorder; 2) behaviors used to classify individual differences arise primarily from genetic influences and that the environment does not produce new personality structures, or at least not structures that are pertinent to classification; and 3) the classification incorporates phenotypes that reflect the etiological structure of personality disorder.

Genetic Approaches to Personality Considerable progress has been made recently in molecular genetic and behavioral genetic research on personality. The search for personality genes was stimulated by Cloninger’s (1987; Cloninger et al. 1993) innovative hypotheses about the neurotransmitters associated with personality including the putative association between novelty seeking and dopamine. The dopamine receptor DRD4 was known to exist in short and long forms with the shorter form coding for a receptor that is more efficient in binding dopamine. Cloninger and colleagues (1996) hypothesized that individuals with the long allele seek novelty to increase dopamine release. Consistent with the hypothesis, the initial reports showed that novelty-seeking scores were significantly higher in individuals with the long form of the allele (Benjamin et al. 1996; Ebstein et al. 1996). Unfortunately, subsequent studies yielded inconsistent results and meta-analyses concluded that the mean association was nonsignificant and similar in magnitude to the association with other temperament scales, namely, harm avoidance and reward dependence (Kluger et al. 2002; Schinka et al. 2002). As a result, Kluger and colleagues suggested that “researchers in the field have to

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assess whether or not variable small true association between DRD4 and NS is theoretically meaningful” (Kluger et al. 2002, p. 715). Studies using other measures and candidate genes also produced conflicting results. Despite extensive investigation of associations between polymorphisms and personality, meta-analyses find scant evidence of significant effects (Munafò et al. 2003). Whatever relationships exist, most effects are probably small and relatively nonspecific. Future classifications may well be profoundly influenced by specification of the genes of personality. However, the absence of consistent findings limits the immediate nosological value of molecular genetic studies. A second important development in molecular genetic studies of personality is work on gene–environment interaction in the development of antisocial behavior by Caspi and colleagues (2002). They noted that although in boys, childhood maltreatment is a major risk factor for conduct disorder, antisocial behavior, and violent offending, not all maltreated children develop antisocial behavior. Based on observations that the monoamine oxidase A gene (MAOA) is associated with aggressive behavior, they hypothesized that the MAOA genotype can modulate the influence of maltreatment. In a large sample, they found that maltreated children with the genotype that conferred high levels of MAOA expression were less likely to develop antisocial behavior. Identification of a gene that modulates the effects of developmental adversity suggests that future classifications of mental disorders will probably need a provision for coding genotypes that are associated with increased likelihood of disorder and those that are protective. Indeed, Gottesman (2002) recently envisioned a sixth axis for DSM-V to record relevant genotypic information. In contrast to molecular studies, behavioral genetic research is beginning to provide the information needed to construct a dimensional classification of personality disorder. Behavioral genetics has progressed beyond simple heritability analyses that estimate the magnitude of genetic and environmental influences on personality to the use of more sophisticated multivariate genetic techniques that permit exploration of the etiological factors responsible for observed patterns of trait covariation. Although it has been suggested that the advent of molecular genetics has rendered behavioral genetics less useful because behavioral genetics can only infer genetic effects using well-established statistical methods whereas molecular genetics specify the actual genes associated with phenotypic variability (Faraone et al. 1999), behavioral genetic methods can play a useful role in clarifying personality phenotypes.

Genetic Structure of Personality Behavioral genetic research provides convincing evidence of extensive genetic influences on individual differences in normal and disordered personality. Heritability is typically estimated in the 40%–60% range and environmental influences are largely confined to nonshared effects. All traits are subject to genetic influences, nonherit-

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able traits have not been identified (Plomin et al. 1990), heritability does not differ significantly across traits, and heritability estimates are not appreciably influenced by method of measurement: the results are similar when based on ratings by cotwins (Heath et al. 1992) and peers (Riemann et al. 1997). Estimates of the broad heritability of Eysenck’s dimensions of neuroticism, extraversion, and psychoticism are 36%, 53%, and 39%, respectively (Tambs et al. 1991). Studies of the NEO PIR yielded values of 41%, 55%, 58%, 41%, and 37% for neuroticism, extraversion, openness, agreeableness, and conscientiousness, respectively (Jang et al. 1996). The temperament and character domains of Cloninger’s Temperament and Character Inventory (TCI; Cloninger et al. 1994) are equally heritable with estimates ranging from 49% for self-directedness to 34% for novelty seeking (Ando et al. 2004). Similarly, Torgersen and colleagues (2000) reported that the heritability of DSM-III-R (American Psychiatric Association 1987) personality disorders ranged from 79% to 28%. The heritability of secondary factors of personality disorder traits assessed with the DAPP were 53%, 50%, 51%, and 38% for emotional dysregulation, dissocial behavior, inhibitedness, and compulsivity, respectively, and the heritability of the 18 basic traits ranged from 56% to 35% (Jang et al. 1996; Livesley et al. 1993). Heritability estimates are similar throughout the trait hierarchy: 24 of the 30 NEO PI-R facets are heritable (Jang et al. 1996) as are the 24 facets of the TCI (Ando et al. 2004) and all but 3 of the 69 of the subtraits defining the 18 basic DAPP-BQ dimensions (Jang et al. 1996). Evidence that all personality disorder traits are heritable provides the basis for a genetically informed nosology: evidence that some traits were forged by experience would reduce the taxonomic value of genetic information. However, the results of heritability studies have limited value in organizing a classification because they only provide information on relative contributions of genes and environment to a given trait. They do not provide information on whether the trait is subject to a single or multiple sources of genetic influence or whether genetic influences are specific to that trait or shared with other traits. This information, which is needed to organize traits on the basis of a shared etiology, is provided by multivariate genetic analyses that explore the etiology of the covariance structure underlying multiple traits at different levels of the trait hierarchy (Carey and DiLalla 1994). Multivariate genetic analyses extend univariate analysis of etiological influences on a single trait to estimate genetic and environmental contributions of the covariation between two or more traits. The degree to which genetic and environmental effects on two variables are correlated is indexed by genetic and environmental correlation coefficients. Genetic and environmental correlation or covariance matrices may then be factored to provide information on underlying structures (Crawford and DeFries 1978). The approach permits estimation of separate genetic and environmental common and specific factor loadings. Information about common sources of genetic variation underlying a set of traits is useful in clarifying the secondary structure of personality and information about specific sources of variance

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should help to clarify the relationship between secondary and primary traits and determine whether primary traits are etiologically distinct from secondary traits. Multivariate analyses are also useful in exploring the relationship between the phenotypic and etiological structure of personality. A crucial question when developing a dimensional classification is the extent to which trait structure reflects an underlying biological structure. This question may be explored by comparing matrices of genetic and environmental correlations with a matrix of observed or phenotypic correlations computed between subscales of a personality measure. High congruency between genetic and observed structures permits the use of genetic information to help resolve seemingly intractable problems of the number and contents of secondary domains and develop a classification based on natural kinds.

Genetic Contributions to Trait Covariance The evidence indicates substantial convergence between the phenotypic and genetic structure of personality. In an early investigation of the genetic structure underlying a set of personality traits, Loehlin (1987) identified four factors from the genetic correlation matrix computed for item clusters from the California Psychological Inventory that resembled Neuroticism, Extraversion, Openness, and Conscientiousness of the five-factor model. The apparent congruence between the phenotypic and genetic structure of the five-factor model was subsequently confirmed using the NEO PI-R. Jang and colleagues (2002) reported that analysis of the genetic covariance matrix for NEO PI-R facets yielded five factors. Congruence coefficients computed between genetic factors and published normative structure ranged from .92 to 70. A similar study by Ando and colleagues obtained congruence coefficients greater than .95 (J. Ando, S. Yamagata, A. Suzuki, et al.: “Cross-National Generalizability of Personality Trait Structure: Psychometric and Biometrical Support From Europe, Asia, and North America” [unpublished manuscript]). These values were probably higher than those in the previous study because genetic structures were compared with phenotypic structures based on the study samples rather than normative structure. There is also high congruence between genetic and phenotypic factor structures of the DAPP-BQ (Livesley et al. 1998): congruence coefficients were .97, .97, .98, and .95 for emotional dysregulation, dissocial, inhibition, and compulsivity, respectively. The TCI is an exception to this pattern: evaluations of the extent to which the seven dimensional phenotypic structure of the TCI reflects the genetic architecture of personality have yielded mixed results. Genetic analyses of the seven dimensions of the TCI show considerable overlap among them. The temperament and character traits are not as etiologically distinct as the theory postulates: temperament accounts for 26%, 37%, and 10% of additive genetic variance in the character dimensions of self-directedness, cooperativeness, and self-transcendence,

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respectively (Gillespie et al. 2003). Also, the assumption that temperament traits are based on independent genetic factors was not supported for reward dependence—28% of the variance in this dimension was explained by other temperament scales and the genetic correlation with novelty seeking was .42. Despite these findings, Gillespie and colleagues concluded that the seven component structure is justified by evidence of considerable specific genetic variance for all dimensions. This conclusion differs from that of Ando and colleagues (2002). Unlike Gillespie et al., they examined the genetic structure of the TCI facets scales employing the methods used to examine the structure of the NEO-PI-R and DAPPBQ. A five-factor model provided the best fit. A subsequent study using a larger sample (Ando et al. 2004) yielded a four-component structure in which temperament and character scales often loaded on the same component. Ando and colleagues (2004) used these results to reorganize the temperament scales to provide a better match to genetic structure. Genetic intercorrelations among the revised scales were small, ranging from .02 to –.23. The lack of congruence between genetic and hypothesized phenotypic structure of the TCI probably occurs because the phenotypic structure of TCI is theoretically rather than empirically derived. The phenotypic analyses of the TCI do not support the hypothetical seven-factor structure (Herbst et al. 2000) and suggest that the seven dimensions fit the fivefactor framework (De Fruyt et al. 2000). Overall, the evidence suggests high correspondence between genetic and empirically derived phenotypic factor structures—a finding with important implications for classification.

Nosological Implications of Phenotype– Genotype Congruence The higher-order genetic analyses of normal and disordered personality traits suggest that a few general genetic factors account for observed trait covariation and that personality is subject to extensive pleiotropic effects (a single genetic entity influences distinct phenotypes). The high genotype–phenotype correspondence for personality disorder contrasts with the poor genotype–phenotype correspondence observed with many psychiatric disorders (Merikangas 2002). Evidence that trait structure primarily reflects genetic influences forms an additional component to the foundation for a genetically informed classification. Although environmental influences on personality traits are similar in magnitude to genetic influences, the congruence of genetic and phenotypic structures suggests that these effects do not change the structure of trait covariation. Instead, environmental events and the extensive interplay between genes and environment probably consolidate pleiotropic effects. Since environmental influences do not give rise to new traits or substantially change trait structure, they have fewer implications for conceptualizing this level of a personality nosology.

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When discussing the potential contributions of genetic research for psychiatric classification, Merikangas (2002) suggested that phenomena such as pleiotropy compromise the nosological value of genetic findings. While this may be the case with disorders associated with genes of large effect, with personality disorder, pleiotropic effects may help to organize the secondary structure of the system along etiological lines and resolve persistence problems with domain definition.

Defining Secondary Traits A few general genetic factors may account for the secondary structure of personality. This would suggest that a secondary domain could be defined as a cluster of primary traits that share a common genetic influence that is distinct from the general genetic factors influencing other secondary domains (Livesley et al. 2003). Defined in this way, the secondary domains would “carve nature at its joints” because they involve etiologically and functionally distinct behaviors. This does not mean that the secondary domains are distinct in the sense that a given individual will only exhibit pathology in a single secondary domain. Rather, they are distinct in the sense that respiratory and cardiac disorders are distinct—they involve anatomically and functionally separate systems even though they may show symptomatic overlap and co-occur. With this approach, the goal would be to define a set of secondary domains with minimal genetic intercorrelations. Ando and colleagues’ (2004) reorganization of the TCI to yield scales with genetic intercorrelations ranging from .02 to –.23 and the low genetic correlations among DAPP secondary domains (range: –.10 to .21 before scale modification using genetic information) suggest that this is an achievable goal. This definition of a secondary domain provides a genetic criterion to supplement the usual statistical criteria to determine the number and content of secondary constructs. The secondary structure of a classification would be determined by the number of general genetic factors required to account for the variation among a comprehensive set of primary traits representing individual differences in personality pathology. The location of a given primary trait within the trait hierarchy would be determined by its loadings on common genetic factors and the pattern of genetic correlations with other primary traits. For example, disagreement persists as to whether sensation seeking and impulsivity are distinct traits belonging to the separate domains of neuroticism and extraversion as in the NEO PI-R (Costa and McCrae 1992) or whether they are related and part of the psychoticism/dissocial domain (Eysenck 1992; Livesley et al. 1998). These would be resolved by examining the genetic correlations between these traits, their genetic correlations with the primary traits defining these domains, and their loadings on the respective general genetic factors.

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Genetic Influences on Primary Traits Identification of a few general genetic factors that account for trait covariation raises questions about whether these factors also explain all sources of genetic influence. This in turn raises questions about the etiology of primary traits and their role in models of normal and disordered personality. Originally, primary traits were thought to be heritable simply because they are components of secondary traits that are heritable (Loehlin 1982). This assumption is questioned by the finding that basic traits have a specific heritable component when the effects of higherorder factors are partialled out and standard heritability analyses are applied to the residuals (Jang et al. 1998; Livesley et al. 1998). For example, 11 of 18 traits assessed by the DAPP-BQ had substantial residual heritability ranging from .48 for conduct problems to .26 for intimacy problems (Livesley et al. 1998). These findings were confirmed with multivariate genetic analyses of the subscales defining the 18 basic dimensions of the DAPP-BQ (Livesley et al. 2003). For 12 scales, a single common genetic factor was identified in addition to the general genetic factor that contributes to trait covariation. The remaining scales were influenced by two or three factors. The 30 NEO-PI-R facet scales showed even greater evidence of specificity of genetic influences, with 26 scales showing residual heritability ranging from .21 to .37 (Jang et al. 1998). The specific nature of genetic influences emphasizes the importance of primary traits for a dimensional classification. A set of precisely defined primary traits would facilitate biological research by providing more homogeneous targets than the traits that have been the focus of attention. It would also enhance clinical utility by increasing the value of the classification in treatment planning (Livesley 2003). Psychosocial and pharmacological interventions increasingly focus on specific components of personality pathology rather than global diagnoses. This does not mean, however, that the secondary trait level is unimportant. Secondary traits impose meaningful structure on what would otherwise be merely a list of primary traits and for many purposes secondary traits are the most appropriate level of description and evaluation. However, given the importance of primary traits, greater attention needs to be given to how primary traits should be defined and assessed. Despite the etiological importance of primary traits, the establishment of a comprehensive set of primary traits has been a challenge for personality research (Costa and McCrae 1998). A behavioral genetic approach would begin by defining a primary trait as a class of behaviors that index a single, specific source of genetic variance. Personality measures are usually constructed using psychometric criteria to select items that form homogeneous scales. Incorporation of a genetic perspective into this process would also involve selecting items that index a specific genetic dimension. Two methods are available for this purpose. The first is to use multivariate genetic analysis at the item level. Heath and colleagues (Heath and Martin 1990; Heath et al. 1989a, 1989b) used this approach to analyze the genetic

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structure of the EPQ. They showed that Neuroticism and Extraversion were influenced by common genetic and environmental factors, indicating that these scales are etiologically homogeneous. Less evidence was found for a common genetic factor for Psychoticism (Heath and Martin 1990; Heath et al. 1989a, 1989b). Items related to cruelty, suspiciousness, and hostility loaded positively on a general genetic factor, and items related to conventional behavior loaded negatively. These findings are consistent with phenotypic analyses showing that the Psychoticism scale is heterogeneous (Heath and Martin 1990; Heath et al. 1988). A second method would be to select items based on their association with the underlying genetic factor. This approach is made possible by the development of methods to estimate genetic and environmental factor scores (Sham et al. 2001; Thomis et al. 2000). With this method, factor scores would be computed for genetic factors contributing to a set of scales and correlating each item with each genetic component. For example, disagreements about the nature of impulsivity could be explored by estimating the genetics underlying a set of impulsivity scales and related measures. Item factor score correlations could then be used to select items that index a specific genetic factor. The value of this approach is that it fits well with standard item analysis: items would be selected according to their correlation with the total scale score and the genetic factor score to foster phenotypically and genetically coherent scales.

Toward a Genetically Informed Taxonomic Research Strategy A genetically informed dimensional classification for DSM-V could be developed using a “winner takes all” approach in which different models are evaluated using genetic and phenotypic criteria. The problem with this approach is that the different models not only have some features in common but also incorporate specific constructs not included in other models. None offer a comprehensive account of normal and disordered personality. Even the more comprehensive models of normal personality do not provide an empirically derived set of primary traits that capture all aspects of personality pathology that clinicians consider important. These considerations suggest that a better approach would be to construct an integrated taxonomy by using the results of genetic research to help identify similarities and resolve discrepancies across models. Although a genetically informed approach is likely to facilitate taxonomic endeavors, it needs to be considered within the context of the overall framework for developing a classification. The optimal approach probably remains the construct validation approach used in test construction (Blashfield and Livesley 1991; Livesley and Jackson 1992). Traditionally, construct validation has relied on psychometric methods to develop valid measures. Genetic methods could, however, be

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readily incorporated into the approach. As conceptualized by Loevinger (1957), construct validity has three components. First, a theoretical classification needs to be constructed that defines diagnostic entities and items. This would be based on the findings of genetic and phenotypic analyses of normal and disordered personality with especial emphasis on ensuring comprehensive representation of clinical concepts. Agreement across models makes it possible to develop a preliminary theoretical taxonomy based on four secondary factors that combines elements of different models and provides a comprehensive representation of the domain. In addition to substantial evidential support, the four factor structure has the advantage of incorporating biological distinctions into the basic structure of the system. The structure also resembles the more prevalent and valid DSM-IV (American Psychiatric Association 1994) diagnoses of borderline, antisocial, schizoid-avoidant, and obsessive-compulsive personality disorders, thereby creating a degree of continuity with the present classification. Greater continuity may be difficult to achieve without sacrificing validity given the serious flaws with current categorical models. The next step would be to determine the primary traits that define each secondary trait. Here there are considerable divergences across models. For this reason, the initial list of primary traits should be comprehensive and incorporate considerable redundancy by including all primary or facet traits from the different models. The second step in construct validation is to demonstrate that diagnostic items combine empirically to form the diagnostic entities proposed in the theoretical taxonomy. This would involve a combination of phenotypic and genetic analyses, including genetic item analysis, of data collected within a genetically informed design such as a twin study. Third, relationships between constructs and external criteria need to be established, although the use of genetic methods would reduce the need for some forms of external validation. The three stages form an iterative process in which empirical evaluations of the theoretical structure are used to modify this structure. Successive iterations lead increasingly to a valid system.

Conclusion The essential argument in this paper is it is possible to construct an etiologically informed classification of personality disorder by incorporating behavioral genetic methods within the construct validation framework. Genetic research does, however, raise some conceptual problems that need to be addressed. One is the relative importance of secondary and primary dimensions—an issue that is basic to the organization and application of a dimensional system. Attention needs to be given to the circumstances that require an assessment at the primary as opposed to the secondary trait level. Should the diagnostic process focus on evaluating only primary traits so that secondary trait assessment is simply a summary of primary trait endorsement? Or, should the system incorporate diagnostic items to assess second-

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ary traits directly since this more parsimonious approach may provide sufficient information for many purposes? This essay has focused almost exclusively on the implications of the findings of genetic research for classification. However, behavioral genetic research also highlights the importance of the environment. Indeed, environmental influences account for the greatest part of the variation in personality traits. The ability to estimate genetic and environmental factor scores raises the issue of whether diagnostic items should reflect genetic or environmental influences. The use of diagnostic items with high genetic loading may be preferable for molecular genetic and other biological investigations. On the other hand, items saturated with environmental variance may be more useful when investigating psychosocial factors and perhaps treatment outcomes. Although this seems a major conceptual issue, it may not be a practical problem since it seems difficult to identify items that capture only genetic or environmental variance. Finally, there is the problem of gender differences. There is good evidence of sex differences in personality disorder phenotypes and gender-specific genetic and environmental influences. It is not clear whether these differences affect the structures that would form the basis of a classification. These unresolved conceptual problems should not, however, detract from the recognition that the information is available to construct an integrated dimensional classification that reflects the phenotypic and etiological structure of personality disorder. The major constructs are well established and the procedures for integrating different systems are readily available and relatively straightforward.

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Plomin R, Chipuer HM, Loehlin JC: Behavioral genetics and personality, in Handbook of Personality: Theory and Research. Edited by Pervin LA. New York, NY, Guilford, 1990, pp 225–243 Riemann R, Angleitner A, Strelau J: Genetic and environmental influences on personality: a study of twins reared together using the self- and peer report NEO-FFI scales. J Pers 65:449–476, 1997 Schinka JA, Letsch EA, Crawford FC: DRD4 and novelty seeking: results of meta-analyses. Am J Med Genet 114:643–648, 2002 Sham PC, Sterne A, Purcell S, et al: GENESiS: creating a composite index of the vulnerability to anxiety and depression in a community-based sample of siblings. Twin Research 3:316–322, 2001 Tambs K, Sundet JM, Eaves L, et al: Pedigree analysis of Eysenck Personality Questionnaire (EPQ) scores in monozygotic twin families. Behav Genet 21:369–382, 1991 Thomis MA, Vlietnick RF, Maes HH, et al: Predictive power of individual genetic and environmental factor scores. Twin Research 3:99–108, 2000 Torgersen S, Lygren S, Oien PA, et al: A twin study of personality disorders. Compr Psychiatry 41:416–425, 2000 Tsuang MT, Faraone SV, Lyons MJ: Identification of the phenotype in psychiatric genetics. Eur Arch Psychiatry Clin Neurosci 243:131–142, 1993 Wakefield JC: The concept of mental disorder: on the boundary between biological facts and social values. Am Psychol 47:373–388, 1992

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6 COMMENTARY ON LIVESLEY Genetic Contributions to a Dimensional Classification: Problems and Pitfalls Peter McGuffin, M.D., Ph.D.

Dr. Livesley has provided a scholarly and thoughtful account of the possible utility of molecular and behavioral genetic approaches in arriving at a new classification of personality disorder, one that is based on dimensions and takes etiological factors into account. The article assumes in the reader a fairly sophisticated understanding of quantitative genetics but does not go into detail about the complications and difficulties that arise from behavioral genetic models and the problems that may occur if some of the implicit simplifying assumptions are incorrect. This brief commentary will attempt to explicate such problems in a nontechnical way for the general reader.

Heritability as an Indicator of Validity Heritability is strictly defined as the proportion of phenotypic variance that is explained by additive genetic factors. It has been suggested in the past (e.g., Farmer et al. 1987) that finding a definition of a disease that describes an entity with high heritability may be one way of validating diagnostic criteria. Livesley points out that diagnostic systems based on high genetic loading are likely to be preferable for studies where the aim is to discover the biological or molecular basis of a disorder, but that one may also wish to explore diagnostic items that are more highly loaded on environmental influences for studies of psychosocial etiology. The inherent 55

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limitation in estimating heritability is that the results are applicable only to a particular population at a specific time point. Although there is evidence, for example, that disorders such as schizophrenia, defined using modern criteria, are roughly as heritable in Europe as they are in Japan (Cardno and Gottesman 2000), one cannot assume that uniformity of heritability across all populations for all disorders necessarily applies. Some societies may show greater variability than others in relation to exposure to environmental factors. Societies in which there is much environmental variation will then tend to have higher phenotypic variation overall, and there will tend to be lower heritability than would be found in a society where the environmental variation is more restricted. Other complications arise because of nonadditive effects. Most of the quantitative genetic models applied in the studies reviewed by Livesley, especially those looking at multivariate effects, assume genetic additivity—that is, that genes of small effect sum together to contribute to a dimension—termed in quantitative genetics a liability—to a disease. However, genes may interact within a locus—the phenomenon of dominance—or between loci—the phenomenon called epistasis. If it is assumed that there is no dominance or epistasis when in fact these phenomena exist, heritability will tend to be overestimated from twin data. It is also generally assumed in basic twin models that genes and environment coact—that is, that they combine in a straightforward additive way. This, again, may not be the case. In particular, gene–environment interaction and gene–environment covariation may occur.

Nonadditive Gene–Environment Interplay Gene–environment interaction is present if a particular genotype confers special sensitivity to a particular environmental effect. Several lines of evidence suggest that gene–environment interaction may exist for personality traits, particularly those associated with antisocial behavior. For example, Cadoret et al. (1995) studied adoptees raised apart from parents who did or did not have a history of antisocial behavior or substance abuse. The authors found that although family disharmony predicted antisocial behavior in the adoptees, the effect was small and nearly negligible in those without a biological antisocial background and marked in those whose biological parents were themselves antisocial. A somewhat different pattern, but again one suggesting gene–environment interaction, was found recently by Button et al. (2005), who studied symptoms of conduct disorder or antisocial behavior in a population-based sample of adolescent twins. The specific environmental factor was parent-reported family disharmony. There were main effects of both family discord and genes but also evidence of a highly significant interaction between these two factors. Such studies of twins and adoptees deal with inferred, unobserved genotypes, but, as Livesley notes, studies now have looked at a specific genotype and a measured

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environment. The specific genotype in question is monoamine oxidase A (MAOA), an X-linked gene that has a common variation in the promoter region that confers either high or low enzyme activity. Previous work on a family segregating a mutated form of MAOA that completely disrupts enzyme activity and on knockout mice lacking the MAOA gene has indicated that complete absence of MAOA activity is associated with aggressive behavior. However such mutations in humans appear to be extremely rare, and the evidence as to whether the promoter variant affects levels of aggression in humans has been inconsistent. Caspi et al. (2002) studied a cohort of men from New Zealand for whom there were excellent longitudinal data, including information on convictions and antisocial or aggressive behavior up to the age of 26 years. These investigators found that although there was no main effect of MAOA genotype on antisocial behavior, regardless of how it was measured, there was a striking interaction effect between early maltreatment and MAOA, in that only those with a low-activity genotype showed a significant association between antisocial or aggressive behavior and early maltreatment. This pattern, using somewhat different environmental measures, has subsequently been replicated by an independent study conducted in the United States (Foley et al. 2004). Gene–environment correlation for personality traits has yet to be equally well explored, but there are three possible mechanisms by which it can arise (Plomin et al. 2001). The first is passive—that is, parents pass on both genes and environmental influences to their offspring. Second, particular behaviors that are genetically influenced may evoke certain responses from parents or other adults involved in a child’s upbringing or education. Thus, a well-behaved child may evoke more favorable and encouraging responses from adults than a frequently naughty child, toward whom carers may be more punitive. Third, there may be active gene–environment covariation such that, for example, a child who is intellectually curious may seek out environments that facilitate learning more often than does a child who is innately less open to new ideas. Part of the reason that gene–environment covariation has been little studied in behavioral genetics is that until comparatively recently, methods have not been available to reliably detect it. Such difficulties are now gradually being overcome, and, for example, twin models that incorporate gene–environment covariation have been developed (Purcell and Sham 2002).

Are the Extremes the Same as the Middle? A final complication to address in applying genetic approaches to the classification of personality is crucial to the question of whether categories really can be abolished in favor of dimensions. In fact, modern quantitative genetic studies in general make an assumption that disorders are nothing more than the extremes of dimensions. Thus, the prevalent model for familial diseases is the liability threshold model (Falconer 1965; Reich et al. 1972), in which it is assumed that multiple en-

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vironmental and genetic effects contribute to a continuum of liability that tends to have a normal distribution, and that only those individuals who at some point exceed a certain threshold manifest the disorder. Relatives of affected individuals have on average an increased liability compared with the population mean, and thus more of them lie beyond the threshold for being affected. Knowing the proportion of the population affected and the proportion in a certain class of relatives allows a correlation in liability to be calculated. This is a useful measure of familiality that forms the starting point for structural equation model fitting. For most diseases, liability is unobserved, but for personality disorders there is at least the potential that personality dimensions can be sufficiently well measured that scores on a trait or set of trait measures will be more useful than simply categorizing individuals as affected or unaffected. This, however, presupposes that the same etiological factors operate at the ends of a distribution as are operating in the middle, which may not always be the case. Although this author knows of no examples relating to personality, there are instances for other behavioral traits, such as language acquisition, where the lower end of the distribution shows higher heritability than is found in the middle (Dale et al. 1998).

Conclusion Dr. Livesley’s general thesis that genetic studies are likely to be of help in improving our understanding of personality disorder and arriving at a sounder, more etiologically based classification must be seen as broadly correct. The general approach offers one of the best ways forward, and it is apparent that genetics cannot be ignored in attempts to devise an improved classificatory scheme for personality disorders. Nevertheless, there are complications and inherent limitations in the genetic approach that need to be taken into account and can potentially lead to major errors if they are overlooked.

References Button TM, Scourfield J, Martin N, et al: Family dysfunction interacts with genes in the causation of antisocial symptoms. Behav Genet 35:115–120, 2005 Cadoret RJ, Yates WR, Troughton E, et al: Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Arch Gen Psychiatry 52:916–924, 1995 Cardno AG, Gottesman II: Twin studies of schizophrenia: from bow-and-arrow concordances to star wars Mx and functional genomics. Am J Med Genet (Semin Med Genet) 97:12–17, 2000 Caspi A, McClay J, Moffit TE, et al: Role of genotype in the cycle of violence in maltreated children. Science 297:851–854, 2002

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Dale PS, Simonoff E, Bishop DV, et al: Genetic influence on language delay in two-yearold children. Nat Neurosci 1(4):324–328, 1998 Falconer DS: The inheritance of liability to certain diseases, estimated from the incidence among relatives. Ann Hum Genet 29:51–76, 1965 Farmer AE, McGuffin P, Gottesman II: Twin concordance for DSM-III schizophrenia. Scrutinizing the validity of the definition. Arch Gen Psychiatry 44:634–641, 1987 Foley DL, Eaves LJ, Wormley B, et al: Childhood adversity, monoamine oxidase a genotype, and risk for conduct disorder. Arch Gen Psychiatry 61:738–744, 2004 Plomin R, DeFries JC, McClearn GE, et al: Behavioral Genetics, 4th Edition. New York, Worth, 2001 Purcell S, Sham P: Variance components models for gene-environment interaction in quantitative trait locus linkage analysis. Twin Research 5:572–576, 2002 Reich T, James JW, Morris CA: The use of multiple thresholds in determining the mode of transmission of semi-continuous traits. Ann Hum Genet 36:163–184, 1972

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7 NEUROBIOLOGICAL DIMENSIONAL MODELS OF PERSONALITY A Review of Three Models Joel Paris, M.D.

Background and Guiding Principles Personality disorders can be understood as reflecting pathological amplifications of personality trait profiles (Costa and Widiger 2002; Depue and Lenzenweger 2001; Livesley et al. 1998; Paris 2003; Siever and Davis 1991). All of psychopathology, whether on Axis I or Axis II, need not necessarily fall into categories, and could reflect interactions between a few broad dimensions (Krueger 1999). Historically, there have been two approaches to defining personality dimensions. One is primarily empirical, based on the results of factor analysis of selfreport data, yielding broad traits that are relatively independent of each other and that can be further subdivided into narrower facets or subtraits. Building a model of disorders using this approach could be described as “bottom-up,” and this method characterizes the Five-Factor Model (FFM; Costa and Widiger 2002) as well as the work of other researchers (Clark and Livesley 2002; Livesley et al. 1998).

This chapter is an abbreviated version of a paper first published in the Journal of Personality Disorders (Volume 19, Issue 2, pages 156–170, 2005).

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Alternatively, one might develop a “top-down” approach, linking traits with neurobiological measures. Gray (1991) proposed one of the earliest of these systems, using three brain systems: 1) approach (response to positively reinforcing stimuli), 2) fight–flight (response to negatively reinforcing stimuli), and 3) behavioral inhibition. However, although this model resembles some of the schema to be reviewed here, it has been tested primarily in animal models and has not been operationalized for humans using standard measurements.

CLONINGER MODEL The original model proposed by Cloninger (1987) was tridimensional, describing three dimensions of temperament, each of which was hypothesized to be linked to a specific neurotransmitter system: Novelty Seeking, linked to dopamine; Harm Avoidance, linked to serotonin; and Reward Dependence, linked to norepinephrine. A revised model (Cloninger et al. 1993) included a fourth temperamental dimension of Persistence, as well as three “character” dimensions: Self-Directedness, Cooperativeness, and Self-Transcendence, with Self-Directedness and Cooperativeness being broad measures of personality disturbance. The investigators proposed that the three characterological dimensions are less rooted in temperament. All seven dimensions can be assessed with a self-report instrument, the Temperament and Character Inventory (TCI). Because a large amount of data support the FFM as reflecting the basic structure of personality (Costa and Widiger 2002), one might ask whether the TCI has any specific advantages. Temperamental and characterological profiles derived from the model can be used to describe many of the same phenomena as Axis II diagnoses (Svrakic et al. 2002), but this has also been shown for the FFM (Costa and Widiger 2002). The temperamental factors in this model generally resemble four of the five factors on the FFM (Extraversion, Neuroticism, Agreeableness, and Conscientiousness), although they do not map personality in quite the same way. The factors in the TCI are not fully independent of each other (Herbst et al. 2000), but this is also true of the FFM (Costa and Widiger 2002). There is substantial overlap between these two systems (Macdonald and Holland 2002), and the TCI can be factor-analyzed to yield the FFM (Ramanaiah et al. 2002). The main question is whether the Cloninger model can truly be described as neurobiological. Whereas the original theory on the links between temperament, neural pathways, and neurotransmitters were very specific, the evidence in support of these associations has not been consistent. Perhaps this lack of supporting data explains why these links have not been emphasized in later publications (e.g., Cloninger 2004). In retrospect, one might conclude that the original schema was heuristic but speculative, and that it has not been shown to be consistent with the ways behavioral systems are organized at the neurobiological level.

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Nonetheless, a large amount of research has been published using the Cloninger schema, largely because the scales purport to provide a measure of temperament. In this review, my focus will be on whether biological research supports the model. Peripheral measures of neurotransmitters can be used to test neurobiological associations with personality dimensions. A few studies support a relationship between peripheral measures of serotonin receptor binding and TCI Harm Avoidance (Nelson et al. 1996; Peirson et al. 1999). This finding is consistent with frequent reports of a relationship between serotonin levels and impulsivity (Coccaro 2004). However, Gerra et al. (1999) reported that Novelty Seeking was associated with plasma norepinephrine (rather than dopamine, as predicted by the theory). A second method involves molecular genetics. A number of studies have looked for linkages between candidate genes and the TCI scales. Quite a few have reported negative or unclear results (Gebhart et al. 2000; Ham et al. 2004; Herbst et al. 2000; Jonsson et al. 2003; Suzuki et al. 2003; Thierry et al. 2004). In a multivariate study of 59 traits against all seven dimensions, Comings et al. (2000) noted that their findings showed “different ratios of functionally related groups of genes, and of different genotypes of the same genes, for different traits” (p. 375). In relation to Novelty Seeking, some molecular genetic studies have supported the model, while others have not. A relationship between the D4 dopamine receptor gene (DRD4) and Novelty Seeking was reported by Cloninger et al. (1996) and replicated by Benjamin et al. (1996), by Ebstein et al. (1996), and by KeltikangasJarvinen et al. (2003). However, this association was not found by Ebstein et al. (1997), Gebhardt et al. (2000), Herbst et al. (2000), Malhotra et al. (1996), Pogue-Geile et al. (1998), or Vandenbergh et al. (1997). Ronai et al. (2001) found a relation between the DRD4 and Novelty Seeking, as the theory would predict, but the link was also significant only in females. Benjamin et al. (2000) suggested that more variance might be accounted for by considering interactions between the serotonin transporter gene (5-HTT) and DRD4, indicating that this trait may not be related to a single neurotransmitter system. Finally, reviews (Lusher et al. 2001; Patterson et al. 1999) and meta-analyses (Kluger et al. 2002; Munafò et al. 2003; Schinka et al. 2002) of the relationship between DRD4 and Novelty Seeking suggest that there is at best only a weak relationship between them. In relation to Harm Avoidance, there is some evidence for a link with 5-HTT, the serotonin transporter gene (Melke et al. 2003). However, other studies (Ham et al. 2004; Jonnson et al. 2003; Kusumi et al. 2002; Samochowiec et al. 2001; Soyka et al. 2002) failed to confirm this relationship. One study (Lee et al. 2003) found that the relationship between 5-HTT and Harm Avoidance might apply only to women. This observation would be in concordance with recent evidence that serotonergic pathways in the brain are different in men and women (Soloff 2004). There have been fewer studies of Reward Dependence, and no confirmation that it is related, as the theory predicts, to norepinephrine. In another report that

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points to the importance of gender differences in neurobiological correlates of personality, Itoh et al. (2004) found a relationship between brain-derived neurotrophic factor and Reward Dependence that was significant only in females. The other dimensions of the model have an even smaller base of empirical data. A sib-pair study (Farmer et al. 2003) was supportive of the overall model in that it suggested that the character traits of the TCI (particularly Self-Directedness) have genetic loadings that could be accounted for by the original group of temperamental dimensions. However, in the study by Comings et al. (2000), the DRD4 gene was linked to Self-Transcendence, suggesting that the “character” dimensions must also reflect temperament. Behavior genetics has provided support for the temperamental nature of the original four dimensions: Stallings et al. (1996) used a twin sample to show that the four dimensions in the Cloninger model are genetically independent; in a Japanese sample, Ando et al. (2002), using multivariate genetic analysis, found no significant associations between Novelty Seeking, Harm Avoidance, and Reward Dependence, as the theory predicts, while the genetic components of Persistence, Self-Directedness, and Cooperativeness were derived from the temperament dimensions. However, Ando et al. (2004) also found that the character scales had a similar genetic contribution as the temperamental scales. In addition, multivariate analyses obtained four factors that did not correspond to the current TCI. In neuroimaging findings, a functional magnetic resonance imaging study (Gusnard et al. 2003) found an association between the Persistence dimension and activity in orbitofrontal and adjacent ventromedial cortex. In a positron emission tomography (PET) study of normal volunteers, Youn et al. (2002) noted specific differences in activity in different brain regions in relation to TCI scores. Suhara et al. (2001) found differences in D2 receptor binding in insular cortex related to Novelty Seeking, a finding that supports the original theoretical model. Neurophysiological markers suggest that Self-Directedness correlates with event-related brain potentials (Vedeniapin et al. 2001). A similar finding was reported by Hansenne et al. (2000), but the authors noted a failure to find strong correlations. In summary, research findings concerning links between the Cloninger model and neurobiological variables are highly inconsistent and often negative. Although the model has generated a large body of research, theoretical concepts have not been supported by data. Thus, the claim that the Cloninger model is neurobiological is not justified by the existing evidence. It shows no superiority to the FFM in describing personality or personality disorders.

DEPUE MODEL Depue and Lenzenweger (2001) have developed an overall model of personality and personality disorders. They propose that personality is built on four higher-

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order trait dimensions, the first three of which are associated with specific transmitters that modulate brain systems, although they acknowledge that personality traits cannot be modeled on single neurotransmitters. The higher-order traits that appear in virtually every taxonomy are Extraversion and Neuroticism. The FFM and most other schema include dimensions of Agreeableness and Conscientiousness. Depue and Lenzenweger divided Extraversion into two components, one related to Affiliation (sociability), and the other to Agency (social dominance), and these facets can in turn be divided into lower-order components. Depue and Lenzenweger distinguish between Neuroticism (anxiety) and Harm Avoidance (fear), which some behavioral genetic studies (Tellegen et al. 1988) have indicated to be independent traits. Depue and Lenzenweger also argue that Impulsivity is a heterogeneous cluster of lower-order traits, as opposed to a single higher-order trait, redefining this construct as nonaffective constraint to separate it from behavioral disinhibition that is not related to emotional states. Depue and Lenzenweger (2001) propose a biological basis for Extraversion and Neuroticism. Extraversion would be related to dopaminergic brain systems. Depue and Collins (1999) have provided a detailed neurobiological theory of this trait, which they consider to be a measure of positive incentive motivation. Depue and Collins note parallels between Extraversion (particularly its Agency component) and a mammalian behavioral approach system based on positive incentive motivation, implicating specific neuroanatomic networks and modulatory neurotransmitters in its processing. Thus, the corticolimbic-striatal-thalamic network carries out functions that include 1) integrating salient incentive context in the medial orbital cortex, amygdala, and hippocampus; 2) encoding intensity of incentive stimuli in a motive circuit composed of the nucleus accumbens, ventral pallidum, and ventral tegmental area dopamine projection system; and 3) creating an incentive motivational state that can be transmitted to the motor system. Individual differences in the functioning of this network could arise from functional variation in the ventral tegmental area dopamine projections directly involved in coding the intensity of incentive motivation. The other aspect of Extraversion is Affiliation, which concerns neurobiological processes that promote longer-term affective bonds. Research by Insel (1997) suggests that neuropeptides such as oxytocin and vasopressin play important roles in this process. In the Depue model, Neuroticism and Harm Avoidance are hypothesized to be independent, but with norepinephrine playing a role in both. One key anatomical structure here is the locus coeruleus, which innervates all brain regions. It is suggested that fear responses are coordinated by the amygdala, while anxiety is related to a different subcortical structure (the bed nucleus of the stria terminalis). Nonaffective Constraint describes the response threshold of brain systems. It is hypothesized to be related to serotonergic brain systems, associated with the wide innervation of brain structures by the dorsal raphe.

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Depue and Lenzenweger (2001) describe how these five dimensions can account for features of the personality disorder diagnoses. They suggest that this model can explain a number of puzzling phenomena about personality disorders, ranging from gender differences in prevalence to unclear relationships with genes and biological markers. We require much more data before we can evaluate this model. Like the Cloninger model, it is consistent with some current research but may not account for inconsistent findings, not to speak of research that is likely to appear in the future. Although there is much evidence that dopamine is related to reward systems, we need more confirmation about whether it is the major neurotransmitter associated with Extraversion and whether the specific pathways suggested for its action are operative and unique to this trait. In summary, the Depue model is well thought out but has not generated specific instruments for measuring the precise dimensions it postulates. With the exception of preliminary studies (e.g., Lenzenweger et al. 2004), the model has not been the subject of a large body of empirical research.

SIEVER AND DAVIS MODEL The model of Siever and Davis (1991) was designed to describe neurobiological dimensions that underlie all categories of psychopathology, both on Axis I and Axis II. Four dimensions are described: 1. Cognitive/Perceptual—based on brain systems for attention and response. The mechanism is hypothesized to be dopaminergic. Evidence derives from studies of schizophrenic and schizotypal patients, with abnormalities in homovanillic acid (HVA) related to other biological markers, such as eye-movement dysfunction. 2. Impulsivity/Aggression—based on brain systems related to the capacity to inhibit behavior. The mechanism is hypothesized to be serotonergic. Evidence derives from the relationships between impulsivity and aggression and measures of 5-hydroxyindoleacetic acid (5-HIAA), neuroendocrine challenge tests, and PET studies. 3. Affect Regulation—based on brain systems related to stability of mood. In the original publication, it was proposed that this system relates to noradrenergic– cholinergic balance, but this hypothesis may have been discarded due to lack of supporting evidence. 4. Anxiety/Inhibition—based on brain system for assessing danger, and associated with high arousal. In the original publication, it was proposed that this system relates to reduced dopaminergic and increased serotonergic activity. The Siever and Davis model focuses on clinical phenomena rather than normal variations, and there is no theory to establish linkages between them. There

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remains a lack of consistent evidence that neurotransmitter variations consistently correspond to these trait dimensions. Few specific empirical tests have been applied to the model. Like the Cloninger model, the Siever and Davis model is somewhat simplistic in linking behavioral traits to neurotransmitter systems. The best and most robust data support a relationship between impulsivity/aggression and serotonin (Coccaro 2004; Mann 1998; Paris et al. 2004; Siever et al. 1998), although even here, correlations have not demonstrated a simple linear relationship. On the other hand, there is evidence disconfirming the proposal that affect regulation in personality disorders is related to a defect in noradrenergic–cholinergic balance (Paris et al. 2004). Depue and Lenzenweger (2001) point out that the dimensions seen in psychopathology may not be primary, but rather might reflect secondary interactions between more basic processes. Moreover, levels of neurotransmitters such as serotonin are not specific to one dimension but have widespread effects on behavior, including impulsivity, aggression, arousal, and emotional regulation. The Siever and Davis (1991) model has not generated standard instruments for measuring its dimensions, although it has stimulated research, using other measures on the dimension of affective instability (Henry et al. 2001). Like the Cloninger model, most of the hypothesized relationships between dimensions and neurotransmitters have not been supported by research, with the important exception of links between impulsivity and central serotonin activity.

What Research Is Needed to Develop a Better Model? Researchers will continue to look for associations between trait dimensions and neurobiological measures. It is possible that this approach could bear fruit. But it is also possible that it will continue to provide us with ambiguous data. Although a few findings in the literature have been robust (e.g., links between serotonin with impulsive aggression or harm avoidance), most have not shed great light on these relationships. It may well be that our understanding of brain mechanisms is at too early a stage to conduct this research program successfully. Until we know more about the neuroscience of emotions and behaviors, attempts to develop a neurobiological model linked to personality dimensions are premature. Neurobiological research has rarely supported simple reductionistic models. There is virtually no brain function that is strictly limited to one brain site or to one type of neuron: modulation and interaction are the rule for virtually anything one wishes to study (Andreasen 2001). We are a long way from being able to map out such brain systems, either anatomically or functionally. The question is whether the data are sufficient to show that any specific trait is strongly linked to

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any specific biological mechanism. It is not sufficient that links be plausible; they must also be solidly established. The literature on neurotransmitters reveals an astonishing level of complexity. The monoamines, which have been the main subject of research, serve to modulate the effects of other neurons that use glutamine and gamma-aminobutyric acid (GABA) as transmitters (Cooper et al. 2003), so that their effects on behavior are far from linear; the same receptors could have entirely different effects in different brain locations, and serotonin may have as many as 15 receptor sites (Kroeze et al. 2002). These findings make it unlikely that we can find one-to-one correspondence between any single neurotransmitter and any single neurophysiological mechanism, not to speak of behavioral traits. Moreover, if such associations are found in the future, they are likely to be related to narrower dimensions rather than the broader traits that are currently being investigated (Livesley et al. 1998). Thus, although it is useful in principle to define traits that have a “genetic architecture,” it is not likely that we will find robust correlates associated with just a few dimensions, given the multiplicity and complexity of brain systems. Even if we could identify traits that have a specific genetic architecture, it does not follow that they will be associated with unique neurotransmitters. Neuroscience has tended to focus on neurochemistry, probably because this is the area in which the most dramatic progress has been made. But neurotransmitters have different effects, depending on brain anatomy and physiology. Future models will probably depend on advances in the understanding of neurocircuitry. Finally, the models reviewed here need to be compared with other measures of personality dimensions, some of which have their own neurobiological literature. For example, impulsive aggression, which may be related to Novelty Seeking and Harm Avoidance, has shown consistent (although not always strong) relationships with serotonergic dysfunction and with polymorphisms of the 5-HTT gene, at least when operationally defined by self-report measures (such as the Barratt Impulsivity Scale; Coccaro 2004). Personality traits are powerful constructs that predict a wide range of behavioral patterns, but there is little evidence that personality dimensions correspond in any predictable way to brain systems (Matthews et al. 2003; Zuckerman 1991). Instead, traits can be thought of as complex outcomes of interactions between many systems. In summary, although research should continue on the relationship between personality traits and neurobiology, it is premature for psychiatry to adopt a neurobiologically based system to describe the disorders currently classified on Axis II. If we decide to replace categories with dimensions, we would probably be better off using a factor analytically derived schema. Moreover, these dimensions could be revised at some later point in the light of further progress in research on the links between brain and behavior.

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References Ando J, Ono Y, Yoshimura K, et al: The genetic structure of Cloninger’s seven-factor model of temperament and character in a Japanese sample. J Pers 70:583–609, 2002 Ando J, Suzuki A, Yamagata S, et al: Genetic and environmental structure of Cloninger’s temperament and character dimensions. J Personal Disord 18:379–393, 2004 Andreasen NC: Brave New Brain: Conquering Mental Illness in the Era of the Genome. New York, Oxford University Press, 2001 Benjamin J, Patterson C, Greenberg BD, et al: Population and familial association between the D4 receptor gene and measures of novelty seeking. Nat Genet 12:81–84, 1996 Benjamin J, Osher Y, Kotler M, et al: Association between tridimensional personality questionnaire (TPQ) traits and three functional polymorphisms: dopamine receptor D4 (DRD4), serotonin transporter promoter region (5-HTTLPR) and catechol-Omethyltransferase (COMT). Mol Psychiatry 5:96–100, 2000 Clark LA, Livesley WJ: Two approaches to identifying the dimensions of personality disorder: convergence on the five-factor model, in Personality Disorders and the Five-Factor Model of Personality, 2nd Edition. Edited by Costa PT Jr, Widiger TA. Washington, DC, American Psychological Association, 2002, pp 161–176 Cloninger CR: A systematic method for clinical description and classification of personality variants. A proposal. Arch Gen Psychiatry 44:573–588, 1987 Cloninger CR: Feeling Good. New York, Oxford University Press, 2004 Cloninger CR, Svrakic DM, Pryzbeck TR: A psychobiological model of temperament and character. Arch Gen Psychiatry 50:975–990, 1993 Cloninger CR, Adolfsson NM, Svrakic DM: Mapping genes for human personality. Nat Genet 12:3–4, 1996 Cloninger CR, Svrakic NM, Svrakic DM: Role of personality self-organization in development of mental order and disorder. Dev Psychopathol 9:881–906, 1997 Coccaro EF: Intermittent explosive disorder and impulsive aggression: the time for serious study is now. Curr Psychiatry Rep 6:1–2, 2004 Comings DE, Gade-Andavolu R, Gonzalez N, et al: A multivariate analysis of 59 candidate genes in personality traits: the temperament and character inventory. Clin Genet 58:375–385, 2000 Comings DE, Gonzales N, Saucier G, et al: The DRD4 gene and the spiritual transcendence scale of the character temperament scale. Psychiatr Genet 10:185–189, 2000 Cooper JR, Bloom FE, Roth RH: The Biochemical Basis of Neuropharmacology, 8th Edition. New York, Oxford University Press, 2003 Costa PT Jr, Widiger TA (eds): Personality Disorders and the Five Factor Model of Personality, 2nd Edition. Washington, DC, American Psychological Association, 2002 Depue RA, Collins PF: Neurobiology of the structure of personality: dopamine, facilitation of incentive motivation, and extraversion. Behav Brain Sci 22:491–517, 1999 Depue RA, Lenzenweger M: A neurobehavioral dimensional model, in Handbook of Personality Disorders: Theory, Research, and Treatment. Edited by Livesley WJ. New York, Guilford, 2001, pp 137–176

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Ebstein RP, Novick O, Umansky R, et al: Dopamine receptor (D4R) exon III polymorphism associated with the human personality trait of novelty seeking. Nat Genet 12:78–80, 1996 Ebstein RP, Gritsenko I, Nemanov L, et al: No association between the serotonin transporter gene regulatory region polymorphism and the Tridimensional Personality Questionnaire (TPQ) temperament of harm avoidance. Mol Psychiatry 2:224–226, 1997 Farmer A, Mahmood A, Redman K, et al: A sib-pair study of the Temperament and Character Inventory scales in major depression. Arch Gen Psychiatry 60:490–496, 2003 Gebhardt C, Leisch F, Schussler P, et al: Non-association of dopamine D4 and D2 receptor genes with personality in healthy individuals. Psychiatr Genet 10:131–137, 2000 Gerra G, Avanzini P, Zaimovic A, et al: Neurotransmitters, neuroendocrine correlates of sensation-seeking temperament in normal humans. Neuropsychobiology 39:207–213, 1999 Gray JA: Neural systems, emotion, and personality, in Neurobiology of Learning, Emotion and Affect. Edited by Madden J. New York, Raven, 1991, pp 273–306 Gusnard DA, Ollinger JM, Shulman GL, et al: Persistence and brain circuitry. Proc Natl Acad Sci U S A 100:3479–3484, 2003 Ham BJ, Kim YH, Choi MJ, et al: Serotonergic genes and personality traits in the Korean population. Neurosci Lett 354:2–5, 2004 Hansenne M, Pitchot W, Pinto E, et al: P300 event-related brain potential and personality in depression. Eur Psychiatry 15:370–377, 2000 Henry C, Mitropoulou V, New AS, et al: Affective instability and impulsivity in borderline personality and bipolar II disorders: similarities and differences. J Psychiatr Res 35:307– 312, 2001 Herbst JH, Zonderman AB, McCrae RR, et al: Do dimensions of the temperament and character inventory map a simple genetic architecture? Evidence from molecular genetics and factor analysis. Am J Psychiatry 157:1285–1290, 2000 Insel T: A neurobiological basis of social attachment. Am J Psychiatry 154:726–735, 1997 Itoh K, Hashimoto K, Kumakiri C, et al: Association between brain derived neurotrophic factor 196 G/A polymorphism and personality traits in healthy subjects. Am J Med Genet 124B:61–63, 2004 Jonsson EG, Burgert E, Crocq MA, et al: Association study between dopamine D3 receptor gene variant and personality traits. Am J Med Genet 117B:61–65, 2003 Keltikangas-Jarvinen L, Elovainio M, Kivimaki M, et al: Association between the type 4 dopamine receptor gene polymorphism and novelty seeking. Psychosom Med 65:471– 476, 2003 Kluger AN, Siegfried Z, Ebstein RP: A meta-analysis of the association between DRD4 polymorphism and novelty seeking. Mol Psychiatry 7:712–717, 2002 Kroeze WK, Kristiansen K, Roth BL: Molecular biology of serotonin receptors structure and function at the molecular level. Curr Top Med Chem 2:507–528, 2002 Krueger RF: The structure of common mental disorders. Arch Gen Psychiatry 56:921–926, 1999 Kusumi I, Suzuki K, Sasaki Y, et al: Serotonin 5-HT(2A) receptor gene polymorphism, 5HT(2A) receptor function and personality traits in healthy subjects: a negative study. J Affect Disord 68:235–241, 2002

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Lee HJ, Lee HS, Kim YK, et al: D2 and D4 dopamine receptor gene polymorphisms and personality traits in a young Korean population. Am J Med Genet 121B:44–49, 2003 Lenzenweger MF, Clarkin JF, Fertuck EA, et al: Executive neurocognitive functioning and neurobehavioral systems indicators in borderline personality disorder: a preliminary study. J Personal Disord 18:421–438, 2004 Livesley WJ, Jang KL, Vernon PA: Phenotypic and genetic structure of traits delineating personality disorder. Arch Gen Psychiatry 55:941–948, 1998 Lusher JM, Chandler C, Ball D: Dopamine D4 receptor gene (DRD4) is associated with novelty seeking and substance abuse: the saga continues. Mol Psychiatry 6:497–499, 2001 MacDonald DA, Holland D: Examination of relations between the NEO Personality Inventory—Revised and the Temperament and Character Inventory. Psychol Rep 91:921–930, 2002 Malhotra A, Virkkunen M, Ronney W, et al: The association between the dopamine D4 receptor (D4DR) 16 amino acid repeat polymorphism and novelty seeking. Mol Psychiatry 1:388–391, 1996 Mann JJ: The neurobiology of suicide. Nat Med 4:25–30, 1998 Matthews G, Deary IJ, Whiteman MC: Personality Traits, 2nd Edition, New York, Cambridge University Press, 2003 Melke J, Westberg L, Nilsson S, et al: Polymorphism in the serotonin receptor 3A (HTR3A) gene and its association with harm avoidance in women. Arch Gen Psychiatry 60:1017–1023, 2003 Munafò MR, Clark TG, Moore LR, et al: Genetic polymorphisms and personality in healthy adults: a systematic review and meta-analysis. Mol Psychiatry 8:471–484, 2003 Nelson EC, Cloninger CR, Pryzbeck TR, et al: Platelet serotonergic markers and Tridimensional Personality Questionnaire measures in a clinical sample. Biol Psychiatry 40:271–278, 1996 Paris J: Personality Disorders Over Time: Precursors, Course, and Outcome. Washington, DC, American Psychiatric Press, 2003 Paris J, Zweig-Frank H, Ng F, et al: Neurobiological correlates of diagnosis and underlying traits in patients with borderline personality disorder compared with normal controls. Psychiatry Res 121:239–252, 2004 Patterson AD, Sunohara GA, Kennedy JL: Dopamine D4 receptor gene: novelty or nonsense? Neuropsychopharmacol 21:3–16, 1999 Peirson AR, Heuchert JW, Thomala L, et al: Relationship between serotonin and the Temperament and Character Inventory. Psychiatry Res 89:29–37, 1999 Pogue-Geile M, Ferrell R, Deka R, et al: Human novelty-seeking personality traits and dopamine D4 receptor polymorphisms: a twin and genetic association study. Am J Med Genet 81:44–48, 1998 Ramanaiah NV, Rielage JK, Cheng Y: Cloninger’s temperament and character inventory and the NEO Five-Factor Inventory. Psychol Rep 90:59–63, 2002 Ronai Z, Szekely A, Nemoda Z, et al: Association between novelty seeking and the -521 C/ T polymorphism in the promoter region of the DRD4 gene. Mol Psychiatry 6:35–38, 2001

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Samochowiec J, Rybakowski F, Czerski P, et al: Polymorphisms in the dopamine, serotonin, and norepinephrine transporter genes and their relationship to temperamental dimensions measured by the Temperament and Character Inventory in healthy volunteers. Neuropsychobiology 43:248–253, 2001 Schinka JA, Letsch EA, Crawford FC: DRD4 and novelty seeking: results of meta-analyses Am J Med Genet 114:643–648, 2002 Siever LJ, Davis KL: A psychobiological perspective on the personality disorders. Am J Psychiatry 148:1647–1658, 1991 Siever LJ, New AS, Kirrane R, et al: New biological research strategies for personality disorders, in Biology of Personality Disorders. Edited by Silk KR. Washington, DC, American Psychiatric Press, 1998, pp 27–62 Soloff P: Impulsivity and suicide: review and update of research in BPD. Presentation to the European Congress on Personality Disorders, Zaragoza, Spain, June 2004 Soyka M, Preuss UW, Koller G, et al: Dopamine D4 receptor gene polymorphism and extraversion revisited: results from the Munich gene bank project for alcoholism. J Psychiatr Res 36:429–35, 2002 Stallings MC, Hewitt JK, Cloninger CR, et al: Genetic and environmental structure of the Tridimensional Personality Questionnaire: three or four temperament dimensions? J Pers Soc Psychol 70:127–140, 1996 Suhara T, Yasuno F, Sudo Y, et al: Dopamine D2 receptors in the insular cortex and the personality trait of novelty seeking. Neuroimage 13:891–895, 2001 Suzuki E, Kitao Y, Ono Y, et al: Cytochrome P450 2D6 polymorphism and character traits. Psychiatr Genet 13:111–113, 2003 Svrakic DM, Draganic S, Hill K, et al: Temperament, character, and personality disorders: etiologic, diagnostic, treatment issues. Acta Psychiatr Scand 106:189–195, 2002 Tellegen A, Lykken DT, Bouchard TJ, et al: Personality similarity in twins reared apart and together. J Pers Soc Psychol 54:1031–1039, 1998 Thierry N, Willeit M, Praschak-Rieder N, et al: Serotonin transporter promoter gene polymorphic region (5-HTTLPR) and personality in female patients with seasonal affective disorder and in healthy controls. Eur Neuropsychopharmacol 14:53–58, 2004 Vandenbergh DJ, Zonderman AB, Wang J, et al: No association between novelty seeking and dopamine D4 receptor (DRD4) exon III seven repeat alleles in Baltimore Longitudinal Study of Aging participants. Mol Psychiatry 2:417–419, 1997 Vedeniapin AB, Anokhin AP, Sirevaag E, et al: Visual P300 and the self-directedness scale of the Temperament and Character Inventory. Psychiatry Res 101:145–156, 2001 Youn T, Lyoo IK, Kim JK, et al: Relationship between personality trait and regional cerebral glucose metabolism assessed with positron emission tomography. Biol Psychol 60:109–120, 2002 Zuckerman M: The Psychobiology of Personality. New York, Cambridge University Press, 1991

8 COMMENTARY ON PARIS Personality as a Dynamic Psychobiological System C. Robert Cloninger, M.D.

The choice of a model for describing human personality is clinically important because personality defines a perspective that shapes the way clinicians understand and treat their patients. Consequently, there is not one standard by which to judge alternative approaches, because people differ in their interests and perspectives about personality and psychopathology. Clinicians become familiar with particular ways of evaluating and treating patients, and it requires effort to switch to alternative models of personality and psychopathology. Nevertheless, there is reason to be optimistic, because alternative approaches show extensive convergence in ways that may allow a widespread consensus in improving the assessment of personality. Trait descriptions of the observable personality differences between individuals became dominant before there was any possibility of identifying specific psychological processes underlying motivated behavior by functional brain imaging and related techniques. Psychodynamic psychiatrists and social-cognitive psychologists have long criticized personality theorists for focusing on differences between the traits of individuals while treating the mind as a black box. The concern of clinicians about between-person models of traits is the absence of attention to the dynamic processes within the person that predict response to treatment and personality development within a social context. When I developed the Temperament and Character Inventory (TCI), I deliberately measured psychobiologically defined traits that provided an explanation of the dynamics of personality development, thereby providing a model of both within-person and between-person differences. Subsequent research has confirmed strong correlations (r > .7) between 73

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TCI dimensions and the activation of specific brain networks under psychologically specific conditions, as described in detail elsewhere (Cloninger 2004). In order to account for both within-person and between-person differences, it is necessary to recognize the nonlinearity of the relations between temperament and character and to decompose traits like Extraversion into multiple processes that have distinct psychology, biology, and sociology. For example, NEO Personality Inventory—Revised (NEO PI-R; Costa and McCrae 1992) Neuroticism correlates strongly with both high TCI Harm Avoidance and low TCI Self-Directedness, even though these two TCI dimensions are correlated with activity in different brain networks. Fortunately, the between-person model of traits measured by the NEO PI-R and the within-person model of dynamic processes measured by the TCI are strongly convergent statistically (Table 8–1). Table 8–1 summarizes the correlations between the seven TCI higher-order dimensions and the five NEO PI-R higher-order factor scores, along with the multiple correlations of each trait with the scores from the other model. The agreement is strong for all traits, except NEO Openness and TCI Self-Transcendence, which show moderate overlap. When facet scales are used, the multiple correlations of individual NEO scales predicted by TCI subscales are .71 to .80; those of TCI scales predicted by NEO facets are .64 to .80. Such agreement is remarkable, given that the tests were administered more than a year apart in a community sample of 662 individuals in Oregon by Goldberg (1999). Therefore, we can confidently say that both the NEO and TCI provide a reliable and thorough coverage of human personality, although they organize the self-reported information according to different perspectives. The difference in the perspective provided by the TCI can be important clinically. For example, TCI Self-Directedness, but not Harm Avoidance, predicts response to cognitive-behavioral therapy (Cloninger 2000). Essentially, character traits like Self-Directedness measure higher-order cognitive processes involving the prefrontal cortex, whereas temperament traits like Harm Avoidance depend on emotional processes involving limbic networks. These processes are clinically dissociated in that whereas all individuals with a personality disorder are low in SelfDirectedness, some may be in the anxious cluster (i.e., high in Harm Avoidance) while others may be low in anxiety-proneness (i.e., low in Harm Avoidance). Conversely, all individuals with an anxiety disorder are high in Harm Avoidance, but they may vary in degree of maturity of their character. The clinical importance of the within-person dynamic perspective of the TCI is also shown by findings that the TCI temperament dimensions have a simple and direct relationship to the traditional clusters of personality disorder recognized in DSM-IV (American Psychiatric Association 1994). The four TCI temperaments define individuals who are high in Harm Avoidance (i.e., pessimistic and anxietyprone, as in the anxious or DSM cluster C); high in Novelty Seeking (i.e., impulsive and anger-prone, as in the erratic or DSM cluster B); low in Reward Depen-

Correlation coefficients and multiple-correlation coefficients of TCI scales with NEO PI-R scales (N = 662) TCI variables

NEO PI-R variables

NS

HA

RD

PS

SD

CO

ST

Mult-R

N E

.06 .40

.63 –.55

–.02 .52

–.20 .40

–.62 .25

–.28 .19

.06 .22

.75 .77

O

.43

–.25

.25

.07

.12

.20

.37

.54

CN

–.34

–.26

.00

.51

.41

.15

–.10

.70

A

–.23

.02

.40

.01

.31

.61

.20

.66

.65

.76

.68

.60

.67

.65

.45

Mult-R

Cloninger: Commentary on Paris

TABLE 8–1.

Note. Temperament and Character Inventory (TCI) variables: NS=Novelty Seeking; HA=Harm Avoidance; RD=Reward Dependence; PS=Persistence; SD=Self-Directedness; CO=Cooperativeness; ST=Self-Transcendence. NEO Personality Inventory—Revised (NEO PI-R) variables: N=Neuroticism; E=Extraversion; O=Openness; CN =Conscientiousness; A=Agreeableness.

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dence (i.e., aloof and cold-hearted, as in the odd or DSM cluster A); and high in Persistence (i.e., determined and perseverative, if a fourth cluster for obsessive personalities is included) (Cloninger 2000). In contrast, Extraversion is a particularly bad fit to the erratic or impulsive cluster. As can be seen in Table 8–1, NEO Extraversion is more strongly correlated with measures of sociability and warmth (as measured by high TCI Reward Dependence) than with high TCI Novelty Seeking, which defines the B cluster well, along with its comorbidity with substance dependence. Fortunately, in defining consensus measures of personality, we can be guided by the convergence of clinical tradition with the results of psychobiological research.

References American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994 Cloninger CR: A practical way to diagnosis of personality disorder: a proposal. J Personal Disord 14:99–108, 2000 Cloninger CR: Feeling Good: The Science of Well-Being. New York, Oxford University Press, 2004 Costa PT Jr, McCrae RR: Revised NEO Personality Inventory (NEO PI-R) and NEO FiveFactor Inventory (NEO-FFI) Professional Manual. Odessa, FL, Psychological Assessment Resources, 1992 Goldberg LR: A broad-bandwidth, public domain, personality inventory measuring the lower-level facets of several five-factor models, in Personality Psychology in Europe, Vol 7. Edited by Mervielde I, Deary I, DeFruyt F, et al. Tilburg, The Netherlands, Tilburg University Press, 1999, pp 7–28

9 COMMENTARY ON PARIS The Problem of Severity in Personality Disorder Classification Peter Tyrer, M.D.

The valuable articles in this series omit one consideration that is very important in clinical practice: They do not address the question of severity. In this paper, I argue that the measure of severity, using what are described as hybrid models, is a critical component of practice and can be recorded easily using standard systems, both existing and planned. In arguing this case, I will use an exemplar, the Personality Assessment Schedule (PAS), mainly because we have so much data from this instrument. I would emphasize, however, that other assessment procedures can be easily adapted to produce similar severity assessments.

Origins of Personality Assessment Schedule The Personality Assessment Schedule was developed in 1976 and published in 1979. It rates 24 personality traits on a nine-point dimensional scale, depending on the degree of social maladjustment created by the personality characteristics.

This chapter is an abbreviated version of a paper with the same title first published in the Journal of Personality Disorders (Volume 19, Issue 3, pages 309–314, 2005).

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This has an algorithm leading to a four-cluster classification (Tyrer and Alexander 1979) but also has modifications to allow International Classification of Diseases, 10th Revision (ICD-10; World Health Organization 1992) and Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV; American Psychiatric Association 1994) diagnoses to be created. In addition to recording categories, we also recorded severity in our earlier studies, using a five-point scale derived from our algorithm (no personality disorder, personality difficulty, personality disorder, severe personality disorder, and gross personality disorder) (Tyrer et al. 1990). However, we quickly realized from analyzing the first sets of data in clinical practice that this was not a true dimensional scale. “Severe personality disorder” in one personality domain was less of a handicap in short- and long-term outcome and treatment response than were relatively milder personality disorders when they covered more than one cluster (what Oldham and his colleagues call “extensive personality disorder”) (Oldham and Skodol 2000; Oldham et al. 1992). We therefore adjusted this to a four-point (later a five-point) scale of severity (Table 9–1), in which the separation of simple and complex personality disorder is determined by the number of clusters containing one or more personality disorders. The lowest level of personality abnormality—personality difficulty—is accounted for by subthreshold personality disorders (i.e., those that do not quite meet the criteria using standard procedures). Since the original publication in 1996, we also have added an extra level—severe personality disorder—which includes those with the most antisocial personalities who are at risk to a much wider group in society. There is no good theoretical reason why overlapping dimensions of personality should be equated with severity, but in practice this seems to have empirical justification. Because of the degree of overlap between the criteria for existing personality disorders (Livesley et al. 1992), the choice of clusters for combining severity was a natural decision. We wanted to extend the clusters to four to accommodate the original ones identified in the PAS (passive-dependent, sociopathic, withdrawn, and inhibited), but we felt it necessary to stick to the original DSM cluster model (in which cluster C includes both passive-dependent and inhibited groups) in fitting the system to existing structures. Some details of studies with the PAS are illustrated in Table 9–2 using the severity coding system in a wide range of patients. These give at least face validity to the system, as there is a graded increase in the influence of personality pathology in all studies.

STUDY 1—NOTTINGHAM STUDY OF NEUROTIC DISORDER This is a study in which patients with anxiety and depressive disorders (generalized anxiety disorder, dysthymic disorder, and panic disorder) have their personality assessed at the beginning of treatment and treatment impact determined at intervals

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TABLE 9–1. Level of severity

Dimensional system of classifying personality disorders Description

Definition by categorical system

0

No personality disorder

1

Personality difficulty

2

Simple personality disorder

3

Complex (diffuse) personality disorder

4

Severe personality disorder

Does not meet actual or subthreshold criteria for any personality disorder Meets subthreshold criteria for one or several personality disorders Meets actual criteria for one or more personality disorders within the same cluster Meets actual criteria for one or more personality disorders within more than one cluster Meets criteria for creation of severe disruption to both individual and to many in society

Source.

After Tyrer and Johnson 1996 and Tyrer 2000, pp. 129–130.

up to 12 years later. Persistent social dysfunction (Seivewright et al. 2004) and general outcome (Tyrer et al. 2004a) were well predicted by personality status. Unsurprisingly, most people with personality disorder at baseline had abnormalities in the cluster C grouping, but in follow-up there was a considerable shift from cluster C to cluster A (Seivewright et al. 2002). Despite this, the severity coding at baseline was a remarkably robust predictor of outcome and was of much greater value than the category coding (incidentally suggesting that those who change in personality status when severely disordered do so by crossing clusters rather than improving to no personality disorder). The patients with complex personality disorder had the worst outcome and after 12 years were marginally worse than at baseline, illustrating the contention that if personality disorder is ignored, patients will apparently have “resistant” affective disorders.

STUDY 2 AND 3—PERSONALITY DISORDER IN RECURRENT PSYCHOSIS Personality is more difficult to assess in recurrent psychotic disorders than in many other patients but we have also found exactly the same findings in this group. Those with complex personality disorders respond less well to treatment and have more problems in the community with regard to violence and other antisocial behavior leading to contacts with the police (see Table 9–1) (Gandhi et al. 2001;

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TABLE 9–2.

Examples of severity model of recording personality abnormality in predicting the effect of personality abnormality in the presence of other symptoms and behavior No personality disorder

Personality difficulty

Simple personality disorder

Complex (diffuse) personality disorder

1.7

2.1

2.3

3.7