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

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

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

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

Published by the American Psychiatric Association Arlington, Virginia

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

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

1

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

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

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

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

5

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

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

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

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

9

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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References 1. 2.

3. 4.

5. 6.

7.

8. 9.

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

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

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

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

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

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

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

References 1. 2. 3. 4.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

S

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

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

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

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

The Association or Otherwise of the Functional Somatic Syndromes

TABLE 2–1.

11

Some unexplained somatic syndromes by specialty

Specialty

Syndrome

Gastroenterology Gynecology Rheumatology Cardiology Infectious diseases Respiratory medicine Orthopedics Neurology Immunology

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

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

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

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

The Association or Otherwise of the Functional Somatic Syndromes

13

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

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

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

The Association or Otherwise of the Functional Somatic Syndromes

15

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

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

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

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

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

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

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

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

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

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

19

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

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

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21

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

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

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

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

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

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

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

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

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

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

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

Cultural Models and Somatic Syndromes

TABLE 3–1.

29

A typology of looping effects

Level

Description

1.

Attentional

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

2.

Emotional exacerbation (arousal-performance)

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

3.

Attributional

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

4.

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

5.

Help-seeking, health care services, iatrogenic

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

6.

Disability/avoidance

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

7.

Political economic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Are Somatoform Disorders Changing With Time?

Weakness symptoms

Emotional symptoms

Sleep disturbance

Excitement symptoms

Nervous pain

FIGURE 5–1.

Chinese symptom configuration of neurasthenia.

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

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

Somatic Presentations of Mental Disorders

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Muscular aches and pains Tension headaches

Irritability

Dyspepsia

FIGURE 5–2.

Dizziness FATIGUE OR WEAKNESS

Inability to relax

Sleep disturbance

Diagnostic and Statistical Manual of Mental Disorders symptom

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

Are Somatoform Disorders Changing With Time?

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

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

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

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

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

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

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

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

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

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

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

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

A

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

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

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

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

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TABLE 6–1. Subjective complaints

Epistemology: reconciling objective findings with subjective complaints Objective findings Present

Absent

Present

“Ideal” disease

Undiagnosed disease somatoform

Absent

Occult disease denial or stoicism

No disease

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

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

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

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A FIGURE 6–1.

B Symptom perceptions elicited by nails.

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

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

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

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

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

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FIGURE 6–2.

Somatic Presentations of Mental Disorders

Immune-to-brain communication.

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

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

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

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

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

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

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

S

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

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

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

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

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TABLE 7–1.

DSM-IV-TR symptoms of withdrawal from any substance

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

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

aSymptoms

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

bSymptoms

TABLE 7–2.

DSM-IV-TR symptoms of intoxication from any substance

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

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

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

bSymptoms

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

1,2

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

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

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

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

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

Study

Publication year

Follow-up period

Kent et al.14

1995

4 years

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

Simon and Gureje16

1999

1 year

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

Lieb et al.22

2002

4 years

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

Dickinson et al.28

2003

1–2 years

Jackson et al.34

2006

5 years

Patients with somatoform disorders are unlikely improved until follow-up

2006 (unpublished reanalysis)

6 months

Retest reliability of somatoform symptom count ranges from 0.72 to 0.75

Rief et

al.27

Stability of syndrome

Stability of Somatoform Symptoms

TABLE 8–1.

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

Leiknes et al.18

2006

11 years

Both somatic complaints and somatoform symptoms are unstable features

Arnold et al.15

2006

6 months

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

Bailer et al.25

2007

1 year

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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ferent medical settings and predicts certain outcomes (e.g., functional status, health care use) as well or better than does anxiety or depression.34,35 Moreover, somatoform symptoms have a specific impact on health services use that is not explained by depression or anxiety.36,37 Further, somatic complaints show different treatment responses in antidepressant trials compared with pure depression or anxiety disorders.38,39 Results on stability of somatic complaints show that individual symptoms vary tremendously over time, whereas polysymptomatic syndromes have stable features. This is a reason to distinguish monosymptomatic and polysymptomatic syndromes in the classification. Different proposals for polysymptomatic somatoform disorders have been presented.12,35,40 All of these diagnostic groups show considerable impairment,28 thus justifying classification as a disorder. However, the cutoffs for classification should be much lower than previously used for somatization disorder, as the diagnosis of somatization disorder covers only a very small part (<5%) of patients seeking medical help for multiple somatoform symptoms. 41 However, as soon as more than two symptoms are present, the syndrome seems to be stable over time.23 Although we favor a continuation of focusing on somatic complaints, we also feel that somatic complaints are not sufficient to justify a DSM Axis I or an International Classification of Disease (ICD)-10 section F diagnosis.42,43 Therefore, further psychological and behavioral features must be included to underline the relevance of these disorders under a psychosocial perspective. Examples for psychological and behavioral criteria can include symptom cognitions (selective attention, catastrophizing, focusing on organic explanations of the symptoms, expecting persistence of symptoms), affective aspects (e.g., demoralization, negative affectivity), or behavioral features (body checking, avoidance behavior, seeking for repeated testing). Most of these features have been shown to be specific for somatoform disorders44 and thus fulfill the necessity of classification criteria to be empirically based.

PRESENT STATE INSTEAD OF LIFETIME DIAGNOSES Considering the weakness associated with remembering long time periods, the reliability and validity of these diagnoses can be improved by focusing on present state symptoms. However, this does not mean that time issues should be omitted completely. Persistence of symptoms is still a feature increasing the stability of the diagnosis, and knowing about similar former symptoms can help to increase diagnostic confidence. However, the strong dependency on time issues longer than 2 years, as suggested in ICD-10 somatization disorder, or beginning of symptoms before the age of 30 years, as required for DSM-IV-TR somatization disorder, are unnecessary sources of unreliability. The impact of these time-based criteria should be reduced.

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REDUCE THE IMPACT OF DOCTORS’ ETIOLOGY ASSUMPTIONS SUBSTANTIALLY Doctors’ ratings that symptoms are “medically unexplained” is highly problematic. Physicians seem to differ substantially in the way they rate symptoms as due purely to organic processes versus psychologically influenced. Therefore, the impact of this source of variation should be reduced. In other examples, DSM-IV-TR uses the phrase “Symptoms are not better accounted for by another mental or physical disorder.” This seems to be less dependent on doctors’ causality ratings, although this should be tested in more detail. Moreover, the potential positive role of knowing about the medical records (e.g., history of symptoms, investigations, and treatments) might further improve diagnostic validity. Diagnosis should not only represent the result of a negative selection of excluded medical conditions; instead, positive and specific criteria to define the disorder must be included.43 This again is a plea for further psychological and behavioral classification criteria.

Summary While there is a substantial need to improve existing classification approaches for somatoform disorders, the reported results on stability aspects of classification criteria indicate ways to improve it. The health care relevance of these disorders necessitates feasible diagnoses with high interrater reliability. A diagnosis for patients with multiple somatic complaints is needed, and the inclusion criteria for this diagnosis should be broader than for somatization disorder. As these syndromes are under the section F (ICD-10) and Axis I of DSM, they should not only depend on physical symptoms but also on psychological and behavioral features characterizing these patients.

References 1. Kendell R, Jablensky A. Distinguishing between the validity and utility of psychiatric diagnoses. Am J Psychiatry 2003;160:4–12. 2. Robins LN. Using survey results to improve the validity of the standard psychiatric nomenclature. Arch Gen Psychiatry 2004;61:1188–1194. 3. Escobar JI, Burnam MA, Karno M, Forsythe A, Golding JM. Somatization in the community. Arch Gen Psychiatry 1987;44:713–718. 4. Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the national comorbidity survey replication. Arch Gen Psychiatry 2005;62:593–602,768. 5. Martin A, Jacobi F. Features of hypochondriasis and illness worry in the general population in Germany. Psychosom Med 2006;68:770–777.

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6. Fink P, Ornbol E, Toft T, Sparle KC, Frostholm L, Olesen F. A new, empirically established hypochondriasis diagnosis. Am J Psychiatry 2004;161:1680–1691. 7. Fink P, Rosendal M, Olesen F. Classification of somatization and functional somatic symptoms in primary care. Aust N Z J Psychiatry 2005;39:772–781. 8. Kroenke K, Price RK. Symptoms in the community. Prevalence, classification, and psychiatric comorbidity. Arch Intern Med 1993;153:2474–2480. 9. Wittchen HU, Jacobi F. Size and burden of mental disorders in Europe—a critical review and appraisal of 27 studies. Eur Neuropsychopharmacol 2005;15:357–376. 10. Rief W, Hessel A, Braehler E. Somatization symptoms and hypochondriacal features in the general population. Psychosom Med 2001;63:595–602. 11. American Psychiatric Association. DSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders. Washington, DC: American Psychiatric Association; 2000. 12. Escobar JI. Developing practical indexes of somatization for use in primary care. J Psychosom Res 1997;42:323–328. 13. Hiller W, Rief W, Fichter MM. Further evidence for a broader concept of somatization disorder using the somatic symptom index (SSI). Psychosomatics 1995;36:285–294. 14. Kent DA, Tomasson K, Coryell W. Course and outcome of conversion and somatization disorders. Psychosomatics 1995;36:138–144. 15. Arnold IA, De Waal MWM, Eekhof JAH, van Helmert AM. Somatoform disorder in primary care: course and the need for cognitive-behavioral therapy. Psychosomatics 2006;47:498–503. 16. Simon GE, Gureje O. Stability of somatization disorder and somatization symptoms among primary care patients. Arch Gen Psychiatry 1999;56:90–95. 17. Simon GE, Von Korff M. Recall of psychiatric history in cross-sectional surveys: implications for epidemiological research. Epidemiol Rev 1995;17:221–227. 18. Leiknes KA, Finset A, Moum T, Sandanger I. Methodological issues concerning lifetime medically unexplained and medically explained symptoms of the composite international diagnostic interview: a prospective 11-year follow-up study. J Psychosom Res 2006;61:169–179. 19. Kahnemann D, Fredrickson BL, Schreiber CA, Redelmeier DA. When more pain is preferred to less: adding a better end. Psychol Sci 1993;4:401–405. 20. Janca A, Isaac M, Bennett LA, Tacchini G. Somatoform disorders in different cultures—a mail questionnaire survey. Soc Psychiatry Psychiatr Epidemiol 1995;30:44– 48. 21. Interian A, Gara MA, Diaz-Martinez AM, Warman MJ, Escobar JI, Allen LA, ManettiCusa J. The value of pseudoneurological symptoms for assessing psychopathology in primary care. Psychosom Med 2004;66:141–146. 22. Lieb R, Zimmermann P, Friis RH, Höfler M, Tholen S, Wittchen H-U. The natural course of DSM-IV somatoform disorders and syndromes among adolescents and young adults: a prospective-longitudinal community study. Eur Psychiatry 2002;17:321–331. 23. Jackson JL, Passamonti M. The outcomes among patients presenting in primary care with a physical symptom at 5 years. J Gen Intern Med 2005;20:1032–1037.

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24. Fink P, Toft T, Hansen MS, Ørnbøl E, Olesen F. Symptoms and syndromes of bodily distress: an exploratory study of 978 internal medical, neurological, and primary care patients. Psychosom Med 2007;69:30–39. 25. Bailer J, Witthöft M, Bayerl C, Rist F. Syndrome stability and psychological predictors of symptom severity in idiopathic environmental intolerance and somatoform disorders. Psychol Med 2007;37:271–281. 26. Rief W, Hiller W, Heuser J. SOMS—Das Screening für Somatoforme Störungen. Manual zum Fragebogen (SOMS—The Screening for Somatoform Symptoms). Bern, Switzerland: Huber-Verlag; 1997. 27. Rief W, Martin A, Rauh E, Zech T, Bender A. Evaluation of a general practitioners’ training: how to manage patients with unexplained physical symptoms. Psychosomatics 2006;47:304–311. 28. Dickinson WP, Dickinson LM, DeGruy FV, Candib LM, Main DS, Libby AM, Rost K. The somatization in primary care study: a tale of three diagnoses. Gen Hosp Psychiatry 2003;25:1–7. 29. Slater ETO, Glithero E. A follow-up of patients diagnosed as suffering from “hysteria.” J Psychosom Res 1965;9:9–13. 30. Stone J, Smyth R, Carson A, Lewis S, Prescott R, Warlow C, Sharpe M. Systematic review of misdiagnosis of conversion symptoms and “hysteria.” Br Med J 2005;331;989. 31. Mayou R, Sharpe M, Kirmayer LJ, Simon G, Kroenke K. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162:847–855. 32. Smith RC, Gardiner JC, Lyles JS, Sirbu C, Dwamena FC, Hodges A, Collins C, Lein C, Given CW, Given B, Goddeeris J. Exploration of DSM-IV criteria in primary care patients with medically unexplained symptoms. Psychosom Med 2005;67:123–129. 33. Rief W, Henningsen P, Hiller W. Classification of somatoform disorders. Am J Psychiatry 2006;163:746–747. 34. Jackson J, Fiddler M, Kapur N, Wells A, Tomenson B, Creed F. Number of bodily symptoms predicts outcome more accurately than health anxiety in patients attending neurology, cardiology, and gastroenterology clinics. J Psychosom Res 2006;60:357– 363. 35. Kroenke K, Spitzer RL, deGruy FV, Hahn SR, Linzer M, Williams JBW, Brody D, Davies M. Multisomatoform disorder. An alternative to undifferentiated somatoform disorder for the somatizing patient in primary care. Arch Gen Psychiatry 1997;54:352– 358. 36. Barsky AJ, Orav J, Bates DW. Somatization increases medical utilization and costs independent of psychiatric and medical morbidity. Arch Gen Psychiatry 2005;62:903– 910. 37. Rief W, Martin A, Klaiberg A, Brähler E. Specific effects of depression, panic, and somatic symptoms on illness behavior. Psychosom Med 2005;67:596–601. 38. Karp JF, Scott J, Houck P, Reynolds III CF, Kupfer DJ, Frank E. Pain predicts longer time to remission during treatment of recurrent depression. J Clin Psychiatry 2005;66:591–597. 39. Hirschfeld RMA, Mallinckrodt C, Lee TC, Detke MJ. Time course for depressionsymptom improvement during treatment with duloxetine. Depress Anxiety 2005;21:170–177.

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40. Rief W, Hiller W. Toward empirically based criteria for somatoform disorders. J Psychosom Res 1999;46:507–518. 41. Escobar JI, Rubio-Stipec M, Canino G, Karno M. Somatic symptoms index (SSI): a new and abridged somatization construct. Prevalence and epidemiological correlates in two large community samples. J Nerv Ment Dis 1989;177:140–146. 42. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th Revision. Geneva, Switzerland: World Health Organization, 1992. 43. Rief W, Isaac M. Are somatoform disorders “mental disorders”? A contribution to the current debate. Curr Opin Psychiatry 2007;20:143–146. 44. Rief W, Broadbent E. Explaining medically unexplained symptoms—models and mechanisms. Clin Psychol Rev 2007;27:821–841.

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9 WHAT IS THE EVIDENCE FOR THE EFFICACY OF TREATMENTS FOR SOMATOFORM DISORDERS? A Critical Review of Previous Intervention Studies Athula Sumathipala, M.B.B.S., D.F.M., M.D., MRCPsych, Ph.D.

At least one-third of physical symptoms in medical care are medically unexplained.1 These symptoms are common all over the world, and their health consequences are not a peculiarity to just one culture.2–5 Patients with these symptoms place a heavy burden on the health system because of disproportionate consumption of health resources.3,4,6,7 Therefore, the need for more research on the best management of medically unexplained symptoms (MUS) has been stressed for decades.8,9 The importance of developing simple and feasible, but effective, inter-

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Sumathipala A: “What is the Evidence for the Efficacy of Treatments for Somatoform Disorders? A Critical Review of Previous Intervention Studies.” Psychosomatic Medicine 69:889–900 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. I thank Kethakie Sumathipala and Sudath Samereweera for their invaluable assistance in the literature search and help with the manuscript.

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ventions and demonstrating their effectiveness when applied in primary health care by a person without specialized psychiatric skills has also been reiterated.3 It is therefore important to review from time to time the gaps in the evidence of best management of this challenging group of patients. It is also important to review interventions in primary care and examine the evidence from the developed and developing world, as the available resources may be different in these settings. The symptoms unexplained by physical diagnosis are a heterogeneous group2 and occur with depression, anxiety, hypochondriasis, and the other somatoform disorders.2,3,10–13 But only half of the patients with MUS meet criteria for mood and anxiety diagnosis.14,15 Only a minority meet current Diagnostic and Statistical Manual (DSM) criteria for somatization disorder and less than 30% meet criteria for somatoform disorder.15 Many symptom syndromes (approximately 13), such as irritable bowel syndrome and chronic fatigue syndrome (CFS), are made up of combinations of MUS that cannot be assumed to be independent of one another. Overlap among these conditions is substantial.16–18 There are also patients with MUS who have neither physical disease nor severe mental illness.19 Lack of clear operational criteria for the entire category of somatoform disorders leaves a substantial proportion of patients who present with MUS without a clear indication for medication or psychotherapy.20 But individuals who fall below diagnostic criteria can have significant social, emotional, and behavioral problems21 that may respond to intervention. The difficulties in conceptualizing those presentations can affect the management of this group of patients. Hence, the term MUS and patients presenting with MUS were chosen to include all functional problems rather than the subgroups who met the operational criteria for somatization disorder, conversion disorder, or symptoms syndromes. In formulating the review question and searching for interventions, the aim was to look at the issues with the perspective of public health relevance because patients do present with symptoms rather than with specific diagnostic categories.

Aim This review attempted to answer the question, what is the highest level of evidence available for the efficacy of pharmaceutical and nonpharmaceutical interventions for patients with MUS, and where have these studies been carried out? The strength of evidence of the effectiveness of any intervention was assessed from a hierarchy based on study design. Search for evidence was confined to level I (systematic review) and level II (randomized controlled trial [RCT]) evidence. Adapting a hierarchical approach by examining the highest level of evidence was the aim. If evidence was present at level I, the review did not proceed further to obtain level II evidence. The aim was to identify the gaps and then to report any recent advances made since the last systematic review. Therefore, level II evidence

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(individual RCTs, published since last available systematic review) were also examined.

Methods SEARCH STRATEGY A comprehensive literature search was carried out using electronic databases: Cochrane library databases (up to 2007), MEDLINE (1966–2007), PsychINFO (1974–2006), and EMBASE (1980–2007). Searches were confined to literature in English. In Cochrane library databases (1971–2007), the search terms “medically unexplained symptoms,” “somatisation,” “somatization,” and “somatoform disorders” were used first for a simple search with each search term separately, followed by an advanced search combining all search fields with the Boolean operator “OR” in abstract, keywords, or title. These search terms were then used again with the Boolean operator “AND” with the search fields individually and in combinations; psychological therapies, cognitive behavior therapy, pharmacological therapies, management, therapy, drug therapy, and antidepressants. Results for Cochrane systematic reviews, other systematic reviews, and RCTs were scrutinized for suitable papers for this review (Table 9–1). Searches were repeated for MEDLINE (1966–2007) and PsychINFO (1974–2006) as well as EMBASE (1980–2007, week 26), using the OVID database. However, the search terms were modified to suit the search strategies for these databases. To ensure a comprehensive review, search for literature was supplemented by examining the reference lists of the papers generated from the original searches.

SELECTION OF STUDIES The author, with another colleague, jointly scanned the abstracts identified by the electronic searches to select the potentially suitable papers. Abstracts eligible for inclusion were systematic reviews or randomized trials of a psychological (Table 9–2), pharmacological, or any other type of intervention involving an adult, with patients defined as medically unexplained symptoms, unexplained symptoms, somatoform disorders, somatisation, somatization, functional somatic symptoms, and the abstract had to be written in the English language.

DATA EXTRACTION Initially, all abstracts that appeared relevant were selected as potentially suitable. The same two assessors then scrutinized them more carefully for definitive inclusion. All abstracts selected were checked for duplications, which, if found, were excluded. Systematic reviews or RCTs exclusively on symptom syndromes, such as

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TABLE 9–1.

Search results from Cochrane Library Cochrane reviews

Medically unexplained symptom/s Somatization

One relevant protocol on One on CBT for MUS23 22 consultation letter One review on psychosocial Nil intervention by GP not relevant Nil One—CBT for somatization and symptom syndromes24 Two—one on psychodynamic 10 in total but only 3 were psychotherapies for common relevant: CBT for MUS,23 CBT for somatization and symptom mental disorders, one on psychosocial intervention by GP; syndromes,24 and psychosocial interventions for MUS25 both not relevant Three identified but only one 10 identified, only 3 suitable23–25 relevant protocol on consultation letters for MUS22

Somatization Somatoform disorder/s

Combination of MUS, somatisation, somatization, somatoform disorders

Other reviews

RCT 20 total but 12 were potentially suitable 20 total but 3 were potentially suitable 188 total but 29 were potentially suitable 193 total but 78 were potentially suitable

355 but 311 potentially suitable

Note. CBT= cognitive-behavioral therapy; GP=general practitioner; MUS =medically unexplained symptoms; RCT = randomized controlled trial.

Somatic Presentations of Mental Disorders

Search field(s)

Summary of the findings of systematic reviews on psychological interventions

Review author(s)

Patient group

O’Malley

MUS including Antidepressants symptoms syndromes Somatization, Individual or group somatoform disorders, CBT or persistent symptoms Somatization Individual or group CBT

Kroenke and Swindle24 Blankenstein26

Nezu et al.23

Allen et al.25

Looper and Kirmayer28

Intervention

MUS, somatization, Individual or group somatoform disorders, CBT or symptom syndromes Somatization, Psychosocial somatoform, interventions psychogenic, functional somatic syndrome Different diagnostic CBT categories or symptom syndromes

Conclusions by authors Effective in improving outcome, including symptoms and disability CBT effective for patients with somatization or symptom syndromes; reduction of physical complaints could occur whether or not psychological distress CBT effective for somatization and symptom syndromes but the evidence for the effectiveness of CBT for somatization was limited CBT effective for all 4 categories of patients; improvement on physical symptoms and associated mood disturbances, and overall physical and social functioning for patients with MUS and CFS Effect sizes are modest at best. Although beneficial, have not shown a lasting influence on the physical complaints of polysymptomatic somatizers Most studies used multiple treatment strategies but studies support the efficacy of individual CBT for symptom syndromes and MUS

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Note. CBT= cognitive-behavioral therapy; CFS=chronic fatigue syndrome; MUS = medically unexplained symptoms.

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TABLE 9–2.

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irritable bowel syndrome, CFS, and fibromyalgia, were excluded. Systematic reviews of MUS incorporating symptom syndromes, however, were included. Papers focusing on children and adolescents were also excluded.

Results Cochrane searches aggregated to 13 abstracts on systematic reviews and 421 RCTs during simple search. The combined search of all search words yielded 13 abstracts of systematic reviews and 355 of RCTs. The cases were performed in primary, secondary, or tertiary care. The therapists ranged from medical specialists, psychiatrists, and psychologists to primary care physicians. Search results from MEDLINE, PsychINFO, and EMBASE did not yield any suitable systematic reviews. However, there were RCTs; 12, 6, and 8 from these respective databases. Full-text papers of six potentially relevant systematic reviews were studied in detail. One paper on antidepressants and two on psychological interventions were excluded as they were not strictly systematic reviews even though they were otherwise valuable reviews. One systematic review from a thesis26 and two other systematic reviews27,28 were known to the author through previous work. Six systematic reviews were finally included in the review. The last systematic review was published in 2002 and reviewed studies up to 2000. Two assessors identified 108 abstracts of RCTs that were retrieved for further scrutiny. Seventeen duplicate publications were identified and excluded. Fourteen trials published since 2000 were selected for this review.

LEVEL I EVIDENCE (SYSTEMATIC REVIEWS) Pharmacological Therapy Only one systematic review on antidepressant medication including a meta-analysis qualified. Antidepressant medication. O’Malley et al. 27 identified papers by searching MEDLINE (1966–1998), PsychLIT (1974–1998), EMBASE/Excerpta Medica (1974–1998), the Cochrane Library, the Federal Research in Progress database, and bibliographies of relevant articles. The emphasis was on adults with MUS but mainly those with at least one of six symptom syndromes: headache, fibromyalgia, functional gastrointestinal syndromes, idiopathic pain, tinnitus, and chronic fatigue. Ninety-four RCTs compared antidepressant medications: tricyclic antidepressants, selective serotonin reuptake inhibitors with placebo, and nonantidepressant medications. The majority of participants were women. Sixty-four (69%) studies demonstrated improvement of one or more of the following outcomes: global assessment (patient or physician), summary symptom index score, or pain severity score.

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A meta-analysis showed benefits from antidepressant medication; the standard mean difference was 0.87 (95% CI, 0.59–1.14), or dichotomized outcomes of improvements, odds ratio of 3.4 (95% CI, 2.6–4.5). The absolute percentage difference in improvement was 32%, and the number needed to treat for the benefit of one additional patient was four. O’Malley et al.27 concluded that antidepressant medication could be effective in improving outcome, including symptoms and disability. However, high withdrawal rates were seen in 63% of the studies. Side effects were reported only in 37% of the studies.

Psychological Therapy Cognitive-behavioral therapy. Five systematic reviews have shed light on the use of cognitive-behavioral therapy (CBT) showing varying success in the management of patients with MUS. Kroenke and Swindle searched for studies published between 1966 and 1999.24 The studies were either RCTs or nonrandomized trials of CBT or cognitive therapy for somatization, somatoform disorders, or persistent symptoms or symptom syndromes. All these trials (randomized or not) included a control group not receiving CBT or cognitive therapy interventions. Of 31 trials reviewed, 29 were randomized. Eleven were performed in the United States, seven in the United Kingdom, five in Netherlands, four in Australia, three in Sweden, and one in Germany. Twenty-five studies targeted specific symptom syndromes: irritable bowel, back pain, CFS, chest pain, tinnitus, or fibromyalgia. Only six focused on general somatization, three of those were on patients with MUS and three on those with hypochondriasis. Most studies (n =29) included patients referred to secondary or tertiary care. Only two trials were carried out in primary care: those reported by Speckens et al.29 and van Dulmen et al.30 Of 1,689 patients, the majority were women, and 803 received CBT. Primary outcomes were physical symptoms, psychological distress studies, or functional status but some had more than one primary outcome. Physical symptoms appeared to be the most responsive. CBT patients improved more than control subjects did in 71% of the studies. Group therapy, as brief as five sessions, was reported to be efficacious, and its benefits were sustained for up to 12 months. Kroenke and Swindle concluded that CBT, both individual and group therapy, could be an effective treatment for patients with somatization or symptom syndromes.24 Benefits in reduction of physical complaints could occur whether or not psychological distress was ameliorated. Kroenke and Swindle recommended further evaluations on optimal sequencing of CBT in treating primary care patents and identification of those most likely to accept and respond to therapy.24 Other issues identified were the need for flexible interventions having varying degrees of emphasis on cognitive and behavioral components, different numbers of sessions provided, therapists in most studies were mental health professionals, and mostly short-term follow-up on referred populations.

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Blankenstein26 carried out a systematic review of all randomized trials of treatment for somatization, which were either performed in or applicable to general practice. Only 10 trials were identified as appropriate for the review. Three studies reported using CBT, one of which was group CBT; all were identified as carried out in primary care.29,31,32 Blankenstein concluded that CBT could be an effective treatment for somatization and symptom syndromes.26 However, he also noted that the number of trials was small and methodological quality was mediocre; thus, the evidence for the effectiveness of CBT for somatization was limited. Looper and Kirmayer28 reviewed studies from 1970 to February 2001 having possible overlap with Kroenke and Swindle.24 The difference of this review is that the analysis was carried out separately for the different diagnostic categories and symptom syndromes. Evidence for the effectiveness was found by the following: 1. Four RCTs using relatively brief individual CBT were effective for hypochondriasis;33–36 2. Four RCTs for body dysmorphic disorders;37–40 3. Four RCTs on “undifferentiated somatoform disorder”: CFS;41–44 4. Four RCTs on “undifferentiated somatoform disorder”; noncardiac chest pain;45–48 5. Four RCTs on “undifferentiated somatoform disorders”; MUS. All four studies were categorized as primary care based.29,31,32,49 Looper and Kirmayer28 concluded that there has been considerable progress in establishing the efficacy of CBT for the treatment of somatoform disorders and that the evidence supports the efficacy of individual CBT for the treatment of hypochondriasis, body dysmorphic syndrome, chronic fatigue, noncardiac chest pain, and MUS. The efficacy of group therapy was also demonstrated in body dysmorphic syndrome and somatization disorder. Effects were of moderate to large magnitude, and the authors recommend CBT as the first line of treatment. However, they noted that the optimal and minimum duration of treatment and value of maintenance therapy need to be established. They identified many important methodological considerations. Nonavailability of standardized treatment manuals, not making a blind-rating outcome, and use of intention to treat analysis were the other issues highlighted. Nezu et al. reviewed 37 studies, but only 19 were randomized trials.23 Nine had targeted MUS, seven on CFS, sixteen on fibromyalgia, and five on noncardiac chest pain. Significantly, a larger number of studies used group therapy. Five of the nine studies on MUS were performed in the United Kingdom and Sweden. Nezu et al. also analyzed studies separately for the different diagnostic categories and symptom syndromes. 23 Of nine studies on MUS, only six were RCTs.29,31,49,50–52 The authors concluded that CBT seems effective for reduction

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of a wide range of physical symptoms and physical and social functioning. Of seven studies on CFS, five were RCTs.41,42,44,53,54 CBT improved CFS symptoms, activity, function, and distress. Of the above highly mixed group of sixteen studies, three were group interventions, four were individual RCTs, and one was inpatient care; even the treatment methods were highly variable. Nonetheless, the authors concluded that CBT was beneficial in decreasing psychological and physical symptoms distress and increasing quality of life. Five studies were identified on undifferentiated somatoform disorder: noncardiac chest pain;45,47,48,55,56 one included group therapy. CBT was beneficial in reducing chest pain and distress. The overall duration of sessions ranged from six 40-minute sessions to eight 3-hour group sessions for MUS; 30- to 60-minute outpatient interventions to 10 weeks of inpatient treatment for CFS; nine sessions over 3–14 weeks of triweekly intervention for studies of fibromyalgia syndrome (FMS); and 4–12 weeks for studies of noncardiac chest pain. The review concluded that, overall, CBT appeared to be effective for all four categories of patients, with improvement on a wide range of physical symptoms and associated mood disturbances and overall physical and social functioning for patients with MUS and CFS. There was a significant decrease in certain psychological and physical symptoms, including improved quality of life, pain, tender points, physical condition, emotional distress, and self-efficacy beliefs in patients with fibromyalgia, and decreased chest pain, activity limitation, and emotional distress in patients with noncardiac chest pain. Allen et al. searched the literature from 1966 through January 2001.25 Studies were selected if they compared any psychosocial intervention with a control intervention in the treatment of multiple unexplained physical symptoms. Interestingly, the authors used the term “polysymptomatic somatizers” and included only multiple medically unexplained symptoms, an extreme group, and selected 34 RCTs for their review. These studies included 2 on somatization disorder, 15 on irritable bowel, 5 on CFS, and 12 on FMS. Allen et al. used the term “psychosocial interventions” instead of psychological. Outcome measures were intensity and frequency of physical symptoms, physical distress, psychological distress, and functional impairment. They observed methodological shortcomings and lack of evidence on long-term outcome in over 75% of studies. Their conclusion was that “although seemingly beneficial, psychosocial treatments have not yet been shown to have a lasting and clinically meaningful influence on the physical complaints of polysymptomatic somatizers.”25

Psychodynamic Psychotherapy There were no systematic reviews on psychodynamic psychotherapy.

Family Therapy There were no systematic reviews on family therapy.

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Other Interventions Consultation letters. There was no systematic review on consultation letters, but a Cochrane protocol was available proposing to assess the effectiveness of consultation letters to assist general practitioners or occupational health physicians in the treatment of patients with multiple MUS in primary care. There were no other systematic reviews.

LEVEL II EVIDENCE: INDIVIDUAL RCT Psychodynamic Psychotherapy Guthrie57 identified three studies using psychodynamic psychotherapy for patients with “somatisation disorders”58–60 and concluded that the small number of studies makes it difficult to generalize the results to other somatic conditions. Bassett and Pilowsky58 reported an RCT that compared 12 sessions of psychodynamic psychotherapy with six sessions of supportive therapy for patients in a pain clinic. A small difference in pain reduction was shown between the treatment and control groups. Svedlund compared the effectiveness of routine medical treatment with dynamic therapy for patients with irritable bowel syndrome from an outpatient clinic.59 Patients who received 12 sessions of psychotherapy showed a significantly greater reduction in gastrointestinal symptoms. Guthrie et al.60 reported a placebo-controlled trial involving 100 patients with chronic unresponsive symptoms of irritable bowel syndrome. The treatment of seven sessions of exploratory psychotherapy was compared with the control of seven sessions of supportive listening. They reported significantly greater improvement in the treatment group in reduction of symptoms.

Family Therapy Empirical studies using family therapy for MUS or symptom syndromes are almost nonexistent. Real et al.61 reported a study that used brief family therapy for 18 patients who suffered from somatoform disorder for at least 1 year. A general practitioner trained in short family therapy applied therapy under the supervision of a trained psychologist. Only the abstract is available, and it reports 61.1% “therapeutic success.”61

Reattribution The reattribution model consists of an interview with an assessment and a management part. There are three phases in the session, with the patient 1) feeling understood, 2) changing the agenda, and 3) making the link.62 Evaluation of the teaching package on the reattribution model revealed that the skills can be effectively learned.63 Training family practitioners in reattribution to manage patients

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with MUS is feasible and acceptable, and its effectiveness is measurable in routine primary care.64 Larisch et al.65 in a two-level cluster randomized trial compared psychosocial interventions based on the modified reattribution model for somatizing patients in general practice with those of nonspecific psychosocial primary care alone. Fortytwo general practices were randomized; 23 to intervention and 19 to the control arm. In total, 127 patients were included. Primary outcome measures were somatoform symptoms and quality of life. These revealed a reduction of physical symptoms (P =0.007), an improvement in physical functioning (P=0.0172), and a reduction of depression (P=0.0211) and anxiety (P=0.0388) in the intervention group compared with in the control group at the 3-month follow-up. Results no longer remained significant after controlling for baseline and covariate variables for most of these variables, although physical symptoms were still reduced at 6-month follow-up (P=0.029). Compared with nonspecific psychosocial primary care, the effects of reattribution techniques were small and limited to physical symptoms.

Problem-Solving Approach Wilkinson and Mynors-Wallis66 reported a pilot study of problem-solving therapy for the treatment of MUS in 11 primary care patients. Ten of the 11 patients completed between 7 and 10 treatment sessions. The mean Symptom Checklist (SCL)-90 score was 90 before the treatment and fell to 50 after the treatment (t=5.4; P <0.001); the mean Whitley Index score was 8.9 before treatment and dropped to 5.1 (t =3.1; P <0.005), and the mean number of visits to general practitioner reduced from 4.9 to 2.1.

Therapeutic Benefits Arising From an Assessment/Consultation Patients with MUS who were randomized to receive “positive” suggestion (told that they had a definite diagnosis and they would be better soon) compared with “negative” suggestion (that their diagnosis and outcome were uncertain) did significantly better in terms of both satisfaction and subjective improvement (64% vs. 39%; P=0.001) than the negative group did.67 Smith et al.8 in a crossover RCT tested the efficacy of a psychiatric consultation in reducing the medical costs of patients with somatization. Thirty-eight patients in intervention or control arms were followed up for 18 months. The intervention consisted of a psychiatric consultation leading to suggestions on the management for the primary care physicians. After the psychiatric consultation, the quarterly health care charges for the first treatment group declined by 53% (P<0.05). The quarterly charges in the control group were significantly higher than those in the treatment group (P <0.05). After the control group crossed over, their quarterly charges declined by 49% (P<0.05). The reductions in expenditures in both groups were due largely to decreases in hospitalization. They concluded that psychiatric

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consultation reduced subsequent health care expenditures of patients with somatization disorder without affecting changes in health status or the patients’ satisfaction with their health care.

Consultation Letter Smith et al.68 conducted another RCT with 51 physicians treating 56 somatizing patients who had a history of seeking help for 6–12 unexplained physical symptoms. At the start of the experiment, physicians randomized to the treatment condition received a psychiatrist’s consultation letter recommending a specific management approach. Physicians randomized to the control then crossed over to receive this letter after 12 months. Data on health outcomes and charges were collected every 4 months for up to 2 years. Patients in the intervention arm reported significantly increased physical functioning and remained stable during the year after the intervention. The intervention reduced annual medical care charges by $289 (95% CI, $40–$464) in 1990, which equates to a 32.9% reduction in the annual median cost of their medical care. Somatizing patients with a lifetime history of 6–12 medically unexplained symptoms benefited by the treatment based on the recommendations after a psychiatric consultation. The consultation is cost effective and reduces subsequent charges for medical care and improves health outcomes in a chronically impaired population. Rost et al.69 performed an RCT in which 59 primary care physicians received a psychiatric consultation letter providing treatment recommendations for 73 patients either at baseline or at the end of the year-long study. Patients of doctors receiving the consultation letter reported greater physical capacity than did patients of control physicians (mean difference=17.9; 95% CI, 1.0–34.9) with a $466 reduction (95% CI, $132–$699) in health care charges. In addition to a net 21% reduction in health care charges for the typical somatization disorder patient, the consultation letter improved physical functioning in a group of highly impaired subjects. Psychiatric consultation letters are also associated with reduction of health costs either as part of individual care70 or with additional group therapy.52

PROGRESS MADE OVER THE LAST DECADE RCTs carried out since the last systematic review in 2002 (RCTs up to 2001) are presented in Table 9–3. Overall, there were fourteen RCTs that qualified for the review; seven from primary care, five from secondary care, and three from tertiary care. All were from the developed world and were selected samples of defined study populations introducing some selection bias. Three drug trials were double blind.72,74,79 Understandably, none of the psychotherapy trials could be double blinded, but the efforts to mask the assessors were described in six trials.65,71,76,77,80,81 Prior power calculations were reported in five studies,73,74,76,80,83

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effect sizes of treatment difference were reported in seven,73,74,76,78,80,82,83 and long-term outcome in three studies.73,82,83

Discussion The review reveals that two types of interventions, antidepressant medication and CBT, are supported by level I evidence as benefiting patients with MUS. In addition, there is limited level II evidence for other pharmacological and psychological interventions: assessment or consultation including collaborative care model, consultation letter, reattribution, bioenergetics exercise, St. John’s wort extract (LI 160), and levosulpiride. However, there were no studies comparing the efficacy between pharmacological and psychological treatments for MUS. All six systematic reviews reached similar conclusions: that CBT may be efficacious for these disorders whether defined as symptom syndromes or grouped under the broader heading of MUS. The impact of CBT has been shown to range from reduction of physical symptoms to psychological distress and disability. However, all reviews recommended further high-quality studies and noted the low number of studies in primary care. There has been a positive trend over the last decade toward more studies being performed in primary care, but still, there is a crucial and significant deficit of intervention research for MUS in the developing world. Only one study has been reported to date.32 It could be because of the publication divide84 or simply a result of limited research capacity in the developing world.85

ANTIDEPRESSANT MEDICATION Evidence for the effectiveness of antidepressants is available for different subgroups of somatoform disorders. There isn’t much new evidence on other medication. The O’Malley et al.27 review did not comprehensively address the issue of side effects. Only 37% of the studies covered had examined the issue of side effects, and the high withdrawal rates of 63% in such studies may be an indicator of this problem. The potential for side effects is a serious consideration when using antidepressants, particularly tricyclics, for patients with MUS because the side effects in response to medication may be misinterpreted as worsening of symptoms. In a commentary on the work of O’Malley et al.,27 Price86 concluded that for MUS or symptoms syndromes, antidepressant medication could be effective in improving outcome, including symptoms and disability. However, Price noted that for antidepressants there was as yet no information on the optimum dose, duration of treatment, or long-term outcome, and there was no firm evidence that antidepressants or any other pharmaceutical agent can be regarded as the best approach for treating MUS.

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TABLE 9–3.

Randomized clinical trials since 2001

N

Population

Treatment condition

Control condition

Reported results and conclusions by authors

Studies in primary care 161

Frequent attendees with Disclose emotionally somatizing symptoms important events in from 10 general practices their life

Volz et al.72 2002 Germany

151

ICD-10 somatization St. John’s wort Placebo disorder, Hypericum extract LI undifferentiated 160, 600 mg/day somatoform disorder, or somatoform autonomic dysfunctions from 21 general practices

Normal care from 85% completed the trial and doctor’s GP disclosure had no effect on the subjective health, use of medical services, or sick leave Primary outcome; Hamilton Anxiety Scale, subfactor somatic anxiety (HAMA-SOM) decreased from 15.39 (SD 2.68) to 6.64 (4.32) in Hypericum group and from 15.55 (2.94) to 11.97 (5.58) in the placebo group (p=0.001); somatization disorder efficacy independent of depressive symptomatology

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Schilte et al.71 2001 Netherlands

Randomized clinical trials since 2001 (continued)

N

Population

Treatment condition

Control condition

Reported results and conclusions by authors

Studies in primary care (continued) Dickinson et al.73 2003 USA

188

12-month intervention effect on the Multisomatoform disorder Care recommendation CR letter intervention on physical functioning (PCS) scale of from 3 family practices (CR) letter the SF-36 was 5.5 points patients intervention on patients immediately 12 months after (p<0.001); CR letter has favorable impact on physical impairment enrollment after enrollment

Müller et al.74 2004 Germany

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ICD-10 somatization disorder, undifferentiated somatoform disorder, and somatoform autonomic dysfunction without major depression

300 mg of St. John’s wort extract LI 160 twice daily

Placebo

Primary outcome measures including somatic subscores significantly better than for placebo. St. John’s wort patients, 45.4% were classified as responders compared with 20.9% with placebo (p=0.0006); effective and safe for somatoform disorders of mild to moderate

What Is the Evidence for the Efficacy of Treatments for Somatoform Disorders?

TABLE 9–3.

117

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TABLE 9–3.

Randomized clinical trials since 2001 (continued) Treatment condition

Control condition

Reported results and conclusions by authors

N

Population

10

Alexithymia and high Jungian psychotherapy No Treatment feasible, able to engage patients in a trusting therapeutic scores on somatization in for 6 months psychotherapy primary care but contact as relationship. No definite before with their conclusions can be drawn GP

Studies in primary care (continued) Posse75 2004 Sweden

van der FeltzCornelis et al.76 2006

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Somatizing patients in general practice

Persistent medically 81 unexplained symptoms from 36 practices

Psychosocial Nonspecific interventions based psychosocial on the modified primary care reattribution model (PPC) alone A collaborative care model of training and psychiatric consultation

Compared with nonspecific PPC, the effects of reattribution techniques were small and limited to physical symptoms

Training plus care Intervention group, severity of the as usual by the main MUS decreased by 58%. A GP collaborative care model combining training with psychiatric consultation in the GP setting is an effective intervention for MUS

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Larisch et al.65 2004 Germany

Randomized clinical trials since 2001 (continued)

N

Population

Treatment condition

Control condition

Reported results and conclusions by authors

Stretching

Aerobic exercise offers no benefits over nonaerobic exercise but primary health care use was reduced

Studies in secondary care Peters et al.77 2002 UK

228

Nanke and Rief78 2003 Germany

50

Symptoms of chronic Aerobic exercise fatigue and fibromyalgia Somatization syndrome

Biofeedback treatment Relaxation group Biofeedback modified patients’ cognitive schemata: patients with somatization syndrome of the biofeedback group showed a greater reduction of catastrophizing of somatic sensations and higher acceptance of psychosocial causal attributions than the control group did

What Is the Evidence for the Efficacy of Treatments for Somatoform Disorders?

TABLE 9–3.

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120

TABLE 9–3.

Randomized clinical trials since 2001 (continued) Treatment condition

N

Population

Altamura et al.79 2003

78

Somatoform disorders; Levosulpiride 50 mg somatoform disorders bid for 4 weeks diagnosed according to ICD-10 and DSM-III-R criteria

Allen et al.80 2006 USA

84

Somatization disorder

Control condition

Reported results and conclusions by authors

Placebo

Levosulpiride significantly reduced the number of somatization disorder symptoms compared with those of placebo (p=0.007) after 4 weeks of treatment

Studies in secondary care (continued)

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At 15 months from baseline, Standard medical care 10-session, somatization symptoms augmented by a manualized, psychiatric consulindividual CBT significantly reduced in CBT group tation intervention; by psychologists (0.84 points on the CGI-SD patients’ primary added to the 7-point scale) (p<.001). CBT was psychiatric associated with greater care physicians receive the consultation improvements in self-reported intervention; psychiatric functioning, somatic symptoms, PCL consultation letter and a greater decrease in health costs (PCL)

Randomized clinical trials since 2001 (continued)

N

Population

Treatment condition

Control condition

Reported results and conclusions by authors

Studies in secondary care (continued) Smith et al.81 2006 USA

Medically unexplained symptoms

A behaviorally defined Usual care patient-centered method consisting of CBT, pharmacological, and other treatment by nurse practitioners

Relative risk for improvement was 1.47 (CI: 1.05–2.07), and the number needed to treat was 6.4 (95% CI: 0.89–11.89).

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Somatization syndrome, DSM-IV somatoform symptoms

Individual therapy and 34 waiting list problem-focused controls group therapy, assertiveness training and, for other therapy modules focusing on comorbid disorders

Long-term improvements in number of somatoform symptoms, subjective health status, life satisfaction, visits, anxiety, and depression

Studies in tertiary care Bleichhardt et al.82 2004 Germany

121

206

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TABLE 9–3.

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TABLE 9–3.

Randomized clinical trials since 2001 (continued)

N Studies in tertiary care (continued) Nickel et al.83 2006 Germany

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Population

Turkish immigrants with chronic somatoform disorders

Treatment condition

Control condition

Bioenergetics exercises Gymnastic (BE) exercises

Reported results and conclusions by authors

Note. CBT=cognitive behavioral therapy; CGI-SD =Clinical Global Impression Scale for Somatization Disorder; GP=general practitioner; ICD-10=International Statistical Classification of Diseases and Related Health Problems, 10th Revision; MUS =medically unexplained symptoms; PCL=psychiatric consultation letter; SD =standard deviation.

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BE appears to improve symptoms of somatization, social insecurity, depression, anxiety, and hostility in the inpatient therapy of subjects with chronic somatoform disorders

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There were two recent trials on St. John’s wort72,74 reporting efficacy for MUS independent of depressive mood. Werneke87 discussed some methodological issues of the Müller study,74 including exclusion of placebo responders after the placebo run-in phase, leading to a bias in favor of St. John’s wort, and that the trial was conducted over a shorter period of 6 weeks. Therefore, more replication studies were recommended.

COGNITIVE-BEHAVIORAL THERAPY There is more level I evidence for CBT compared with for other approaches, and the evidence is increasing. CBT seems to be effective in the reduction of a wide range of physical symptoms and associated mood disturbance, as well as in producing improvements in overall physical and social functioning. Antidepressants are moderately effective for MUS, and effect sizes are homogenous across functional syndromes, but no trials have compared antidepressants with CBT. However, there are other reasons, beyond efficacy and empirical evidence, for the choice of CBT over antidepressants. Fewer than 50% of patients with chronic diseases maintain compliance in the longer term.88,89 Compliance by patients with MUS will be a particular problem as they seek treatment from many different categories of therapists. The cognitive-behavioral model accommodates each factor that contributes to the patient’s distressed state. Working with this model, the therapist is able to go beyond the medical model that searches for a physical cause and treatment by prescription of medication, which has so far failed to help the patient. Another possible advantage is, in contrast to antidepressant medication, patients do not experience unwanted side effects from CBT. Lack of clarity on what interventions qualify to be defined as CBT remains a problem. Although Nezu et al.’s23 review claimed to be on CBT, the interventions reported were diverse and may not strictly fall under the category of CBT. Relaxation training, problem-solving training, assertiveness training, visualization, use of behavioral experiments, graded increases in activity level, coping-skills training, education, biofeedback, exercise, and breathing training were included as variants of CBT. Ismail et al.90 categorized psychological therapies into four groups: supportive or counseling therapy, CBT, psychoanalytically informed therapies, and family systems therapy, and some of the above techniques were classified as counseling. On the contrary, Allen et al.25 used the definition “psychosocial interventions” instead of psychological. However, from the results it seems they have included trials using short-term dynamic psychotherapy, relaxation, cognitive therapy, behavioral therapy, and individual and group CBT. Hence, it may be misleading to categorize them together as psychosocial interventions. Existing evidence on brief dynamic psychotherapies is very limited for MUS. Dynamic psychotherapy has still not shown convincingly better results than placebo or good clinical care do, but harm may also occur from dynamic interven-

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tion.91 Although there are elements common to both these therapies, there are differences too. CBT focuses more on practical methods of managing current symptoms, whereas dynamic psychotherapy concentrates on the historical origin of symptoms and on relationships, including that of the patient with the therapist.

OTHER INTERVENTIONS Assessment As an Intervention An assessment itself without formal psychotherapy has therapeutic effects.86 A rounded clinical assessment might modify such cognitive factors as symptom attribution and improve outcome.92 The trials that include a comprehensive assessment thus seem to have a positive impact on the outcome of patients with physical symptoms whether they are medically explained or unexplained. The factor influencing the outcome may be a result of change in cognition.

LIMITATIONS OF THE INTERVENTION STUDIES CARRIED OUT TO DATE Most of the studies have adopted divergent selection procedures, interventions, outcome measures, and instruments, and these clinical and methodological differences hamper comparison of treatment effects. Many issues remain unanswered, and most trials have assessed short-term outcomes only. Although MUS are common in primary care, most studies up to 2000 were not carried out in primary care. However, it is encouraging to see that over the last few years more studies have been conducted in primary care; but it is striking that evidence from the developing world is very limited. Many studies have not provided equal time for the control subjects and for the intervention group. Finally, another limitation of this review is that it is confined to literature in English.

IMPLICATIONS FOR CLASSIFICATION The challenges posed by the existing systems on classifying MUS pose similar challenges and limitations in reviewing intervention studies on MUS as well. The variation of the numbers of reviews and RCTs retrieved by using different search words for the same problem is a good example. The limitations imposed by these divergent criteria seriously hamper a comparison of the reported work. Maybe the terms “thick folder patients,” “crocks,” “hysterics,” “the terror of the doctor,” “problem patients,” “painful woman,” “hypochondriac,” and “amplifiers”93 are replaced with the more sophisticated MUS, somatization, somatoform disorders, and functional syndromes, but the alternatives are still diverse.

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DIRECTIONS FOR FUTURE RESEARCH Treatment of patients with MUS involves a complex intervention, consisting of different components, which may act both independently and interdependently94 but the active component may not be easily defined. Therapists’ and patients’ characteristics, delivery, frequency, timing of trial procedures, recruitment into a trial per se, availability of information leaflets, the consent process, nonspecific effects of structured appointments, and the regular structured follow-up assessment, all may be part of active components. Hence, future research should consider using factorial designs; compare the efficacy of CBT with other alternative treatment, antidepressants in particular and combinations;78 group and individual CBT therapy;28 other combined regimes;81 or stepped care.95 Optimum treatment intensity or duration (i.e., dosage) and place of booster sessions28 should be considered. Qualitative work to identify strategic components to develop a culturally sensitive and patient friendly intervention should also be embedded with RCTs.94 As most studies used short-term benefits, it is crucial to monitor longer-term benefits.80 Even if evidence exists for efficacy, we need more pragmatic controlled trials to have a chance of implementing these therapies in more realistic clinical settings16,23 and that can be carried out with relevance to accessibility.96 More studies are warranted in the developing world with more locally sensitive and culturally appropriate interventions. Evidence-based guidelines on treatment will be useful only if the subjective elements of patients’ preferences and values are acknowledged and explored.89

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44. Lloyd AR, Hickie I, Brockman A, Hickie C, Wilson A, Dwyer J, Wakefield D. Immunologic and psychologic therapy for patients with chronic fatigue syndrome: a doubleblind, placebo-controlled trial. Am J Med 1993;94:197–203. 45. Klimes I, Mayou RA, Pearce MJ, Coles L, Fagg JR. Psychological treatment for atypical non-cardiac chest pain: a controlled evaluation. Psychol Med 1990;20:605–611. 46. Mayou RA, Bryant BM, Sanders D. A controlled trial of cognitive behavioural therapy for non cardiac chest pain. Psychol Med 1997;27:1021–1031. 47. van Peski-Oosterbaan AS, Spinhoven P, van Rood Y, van der Does JW, Bruschke AV, Rooijmans HG. Cognitive-behavioral therapy for noncardiac chest pain: a randomized trial. Am J Med 1999;106:424–429. 48. Potts SG, Lewin R, Fox KA, Johnstone EC. Group psychological treatment for chest pain with normal coronary arteries. QJM 1999;92:81–86. 49. MacLeod CC, Budd MA, McClelland DC. Treatment of somatisation in primary care. Gen Hosp Psychiatry 1997;19:251–258. 50. Harrison S, Watson M, Feinmann C. Does short-term group therapy affect unexplained medical symptoms? J Psychosom Res 1997;43:399–404. 51. Hellman CJ, Budd M, Borysenko J, McClelland DC, Benson H. A study of the effectiveness of two group behavioral medicine interventions for patients with psychosomatic complaints. Behav Med 1990;16:165–173. 52. Kashner TM, Rost K, Cohen B, Anderson M, Smith GR Jr. Enhancing the health of somatization disorder patients. Effectiveness of short-term group therapy. Psychosomatics 1995;36:462–470. 53. Butler S, Chalder T, Ron M, Wessely S. Cognitive behaviour therapy in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry 1991;54:153–158. 54. Friedberg F, Krupp LB. A comparison of cognitive behavioral treatment for chronic fatigue syndrome and primary depression. Clin Infect Dis 1994;181:105–110. 55. Mayou R, Bryant B, Forfar C, Clark D. Non-cardiac chest pain and benign palpitations in the cardiac clinic. Br Heart J 1994;72:548–553. 56. Van Peski-Oosterbaan AS, Spinhoven P, Van der Does AJ, Bruschke AV, Rooijmans HG. Cognitive change following cognitive behavioural therapy for non-cardiac chest pain. Psychother Psychosom 1999;68:214–220. 57. Guthrie E. Psychotherapy for somatisation disorders. Curr Opin Psychiatry 1996;9:182–187. 58. Bassett DL, Pilowsky I. A study of brief psychotherapy for chronic pain. J Psychosom Res 1985;29:259–264. 59. Svedlund J. Psychotherapy in irritable bowel syndrome. A controlled outcome study. Acta Psychiatr Scand 1983;306:81–86. 60. Guthrie E, Creed F, Dawson D, Tomenson B. A controlled trial of psychological treatment for the irritable bowel syndrome. Gastroenterol 1991;100:450–457. 61. Real PM, Rodriguez-Arias PML, Cagigas VJ, Apariciao Sanz MM, Real Pérez MA. Brief family therapy: an option for the treatment of somatoform disorders in primary care. (Abstract) Atencian Primaria 1996;17:241–246. 62. Goldberg D, Gask L, O’Dowd T. The treatment of somatization: teaching techniques of reattribution. J Psychosom Res 1989;33:689–695.

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63. Gask L, Goldberg D, Porter R, Creed F. The treatment of somatization: evaluation of a teaching package with general practice trainees. J Psychosom Res 1989;33:697–703. 64. Morriss R. Specific psychosocial interventions for somatizing patients by the general practitioner: a randomised controlled trial. J Psychosom Res 2004;57:515–556. 65. Larisch A, Schweickhardt A, Wirsching M, Fritzsche K. Psychosocial interventions for somatizing patients by the general practitioner: a randomized controlled trial. J Psychosom Res 2004;57:507–714. 66. Wilkinson P, Mynors-Wallis L. Problem-solving therapy in the treatment of unexplained physical symptoms in primary care: a preliminary study. J Psychosom Res 1994;38:591–598. 67. Thomas KB. General practice consultations: is there any point in being positive? BMJ 1987;294:1200–1202. 68. Smith GR, Rost K, Kashner TM. A trial of the effect of a standardized psychiatric consultation on health outcomes and costs in somatizing patients. Arch Gen Psychiatry 1995;52:238–243. 69. Rost K, Kashner TM, Smith RG. Effectiveness of psychiatric intervention with somatization disorder patients: improved outcomes at reduced costs. Gen Hosp Psychiatry 1994;16:381–387. 70. Kashner TM, Rost K, Smith GR, Lewis S. An analysis of panel data. The impact of a psychiatric consultation letter on the expenditures and outcomes of care for patients with somatization disorder. Med Care 1992;30:811–821. 71. Schilte AF, Portegijs PJ, Blankenstein AH, van Der Horst HE, Latour MB, van Eijk JT, Knottnerus JA. Randomised controlled trial of disclosure of emotionally important events in somatisation in primary care. BMJ 2001;323:86–89. 72. Volz HP, Murck H, Kasper S, Möller HJ. St John’s wort extract (LI 160) in somatoform disorders: results of a placebo-controlled trial. Psychopharmacol 2002;164:294– 300. 73. Dickinson WP, Dickinson LM, deGruy FV, Main DS, Candib LM, Rost K. A randomized clinical trial of a care recommendation letter intervention for somatization in primary care. Ann Fam Med 2003;4:228–235. 74. Müller T, Mannel M, Murck H, Rahlfs VW. Treatment of somatoform disorders with St. John’s wort: a randomized, double-blind and placebo-controlled trial. Psychosom Med 2004;66:538–547. 75. Posse M. Jungian psychotherapy for somatization. Eur J Psychiatry 2004;18:23–29. 76. van der Feltz-Cornelis CM, van Oppen P, Ader HJ, van Dyck R. Randomised controlled trial of a collaborative care model with psychiatric consultation for persistent medically unexplained symptoms in general practice. Psychother Psychosom 2006;75:282–289. 77. Peters S, Stanley I, Rose M, Kaney S, Salmon P. A randomized controlled trial of group aerobic exercise in primary care patients with persistent, unexplained physical symptoms. Fam Pract 2002;19:665–674. 78. Nanke A, Rief W. Biofeedback-based interventions in somatoform disorders: a randomized controlled trial. Acta Neuropsychiatrica 2003;15:4,249–225.

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79. Altamura AC, Di Rosa A, Ermentini A, Guaraldi GP, Invernizzi G, Rudas N, Tacchini G, Pioli R, Meduri M, Coppola MT, Tosini V, Proto E, Bolognesi E, Marchio B. Levosulpiride in somatoform disorders: a double- blind, placebo-controlled cross-over study. Int J Psychiatry Clin Pract 2003;7:155–159. 80. Allen LA, Woolfolk RL, Escobar JI, Gara MA, Hamer RM. Cognitive-behavioral therapy for somatization disorder: a randomized controlled trial. Arch Intern Med 2006;166:1512–1518. 81. Smith RC, Lyles JS, Gardiner JC, Sirbu C, Hodges A, Collins C, Dwamena FC, Lein C, William Given C, Given B, Goddeeris J. Primary care clinicians treat patients with medically unexplained symptoms: a randomized controlled trial. J Gen Intern Med 2006;21:671–677. 82. Bleichhardt G, Timmer B, Rief W. Cognitive-behavioural therapy for patients with multiple somatoform symptoms—a randomised controlled trial in tertiary care. J Psychosom Res 2004;56:449–454. 83. Nickel M, Cangoez B, Bachler E, Muehlbacher M, Lojewski N, Mueller-Rabe N, Mitterlehner FO, Leiberich P, Rother N, Buschmann W, Kettler C, Pedrosa Gil F, Lahmann C, Egger C, Fartacek R, Rother WK, Loew TH, Nickel C. Bioenergetic exercises in inpatient treatment of Turkish immigrants with chronic somatoform disorders: a randomized, controlled study. J Psychosom Res 2006;61:507–513. 84. Patel V, Sumathipala A. International representation in psychiatric literature: survey of six leading journals. Br J Psychiatry 2001;178:406–409. 85. World Health Organization. Investing in health research and development. Report of the ad hoc committee on health research relating to future intervention options. Geneva: World Health Organization; 1996. 86. Price J. Review: antidepressants are effective for clinical unexplained symptoms and syndromes. Evid Based Ment Health 2000;3:84. 87. Werneke U. St John’s wort improves somatoform disorders. Evid Based Ment Health 2005;8:13. 88. House WC, Pedleton L, Parker L. Patients’ versus physicians’ attributions of reasons for diabetic patients’ non-compliance with diet. Diabetes Care 1986;4:434–436. 89. Jones G. Editorial: Prescribing and taking medicines. BMJ 2003;327:819. 90. Ismail K, Winkley K, Rabe-Hesketh S. Systematic review and meta-analysis of randomised controlled trials of psychological interventions to improve glycaemic control in patients with type 2 diabetes. Lancet 2004;15:1589–1597. 91. Andrews G. Psychotherapy: from Freud to cognitive science. Med J Aust 1991;16:845–848. 92. Petrie K, Moss-Morris R, Weinman J. The impact of catastrophic beliefs on functioning in chronic fatigue syndrome. J Psychosom Res 1995;39:31–37. 93. Pilowsky I. Abnormal illness behaviour: a 25th anniversary review. Aust N Z J Psychiatry 1994;28:566–573. 94. Medical Research Council. Framework for Development and Evaluation of RCTs for Complex Interventions to Improve Health. London: Nuffield Council; 2000. 95. Kroenke K. Patients presenting with somatic complaints: epidemiology, psychiatric comorbidity and management. Int J Methods Psychiatr Res 2007;12:32–43. 96. Hotopf M, Churchill R, Lewis G. Pragmatic randomised controlled trials in psychiatry. Br J Psychiatry 1999;175:217–223.

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

This book is concerned with the very large clinical and public health problem of persistent and limiting somatic symptoms that are not explained by organic pathology.1,2 They rarely present to psychiatrists and psychologists, being mainly treated in primary care and outpatient clinics where they are regarded as difficult to treat. Consultation with alternative, complementary, and nonmedical healers is also very frequent. The large size of the clinical problem means that the few of us with specialist skills need to set out the evidence base and its implications for the whole range of treatments that can be used by nonspecialists in all medical settings in all cultures. This chapter concentrates on “nonspecific” treatments and delivery in routine care. The latter means placing a much greater emphasis than at present

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Mayou R: “Are Treatments for Common Mental Disorders Also Effective for Functional Symptoms and Disorder?” Psychosomatic Medicine 69:876–880 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission.

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on simple early interventions and also on better methods to identify those requiring more intensive treatments. It raises issues about the greater use of specialist expertise to develop and evaluate care programs and to train and supervise nonspecialists. Our answers to the question posed in the title of this chapter depend on first clarifying the nature of the clinical problems, etiology, and the many approaches to treatment in specialist and nonspecialist settings.3–5

Nomenclature, Classification, and Treatment Priorities Somatoform complaints are known under a bewildering variety of other names, for example, somatization and medically unexplained symptoms, or as we prefer, “functional symptoms and syndromes.” 5 Most presenting complaints are short lived, and there is usually no additional psychiatric disorder, but the more persistent and disabling problems are likely to be associated with one or more diagnosable Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV)6 disorders: • Anxiety, depression, or other well-established mental disorders (including personality disorder); • Somatoform disorder; • Somatoform plus another psychiatric disorder. The authors of somatoform disorders for DSM-III7 focused on what they believed to be uncommon and specific subcategories, such as hypochondriasis and somatization disorder. In practice (and with a considerable widening of diagnostic concepts in DSM-III-R8), it has become apparent that almost all persistent functional or physically unexplained symptoms satisfy criteria for somatoform disorder, most usually the nonspecific categories that are defined only in terms of physical symptoms—undifferentiated somatoform disorder, pain disorder, somatoform disorder not otherwise specified. Because these latter conditions are very frequent in clinical practice, they deserve to be a priority in the program leading up to DSM-V and International Classification of Diseases-11 (ICD-11).

Etiology Traditionally DSM, ICD, and Western clinical practice have, despite protestations to the contrary, been dualist in their separation of mind and body explanations. Although this has resulted in much uncertainty and acrimony about the

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causes of functional syndromes and symptoms, it is encouraging that it is now widely accepted that etiology should be seen as an interaction between bodily perceptions (physiological or minor pathological) and psychological interpretation or attribution.3,5 Cognitive interpretations are affected by culture and social setting, personality, health beliefs and experience, mental state, and the reactions of others, including doctors. Complaints and disability are maintained by physiological, psychological, behavioral, iatrogenic, and social variables. In addition, it is ever more apparent that mental states often have physiological consequences. There is no division in this etiological model between physically “explained” and “unexplained” categories, rather a spectrum from the largely physical (myocardial infarction) to the largely psychological (conversion, palpitation as a symptom of panic). Many conditions are intermediate (low back pain, irritable bowel); some, like chronic fatigue, are highly controversial, with vocal lay groups unwilling to accept that psychological variables make any contribution to perception of symptoms or to disability. The model also makes explicit the close similarities in the patterns of psychological reactions to whole spectrum of somatic complaints from those of entirely psychological origin to those associated with major organic pathology. This means that, in working with our patients, whether or not there is probable pathology, we can combine from the outset appropriate physical investigation with efforts to minimize psychologically determined distress and disability. A more dispassionate and open-minded understanding of etiology is basic to devising and implementing more effective treatments. It provides a rationale, which is clearly understandable and acceptable to patients, for all those attempting to treat them and allows us target treatments on modifying causal “biopsychosocial” variables.

Treatment Priorities Other chapters in this book provide valuable systematic reviews of the evidence of treatment efficacy largely based on randomized clinical trials of specialized interventions in selected populations with diagnosed somatoform disorder or with common symptoms. The complementary standpoint of this chapter emphasizes the urgent public health need to develop and evaluate both efficacy and pragmatic effectiveness for treatments, which can be delivered to very large numbers of people. This will need to be provided by primary care practitioners and their teams without expert psychological or psychiatric knowledge. There are four main clinical priorities: • Newly presenting functional symptoms in primary and outpatient care, most of which have a good prognosis. Patients need appropriate investigation accompanied by explanation, reassurance, and advice that will minimize distress and

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reduce the risk of persistent distress and disability for a clinically significant minority. • More persistent problems that could be effectively treated by nonspecialists. • Chronic and recurrent problems requiring specialist “biopsychosocial” treatments. • Evidence that recurrent and persistent adult functional symptoms are predicted by childhood variables9 indicates the need (as yet hardly formulated) for preventative interventions in childhood and adolescence.10

Evidence About Treatment In contrast to the very considerable evidence about treatments for common mental disorders (i.e., anxiety and depression), we know little about their effectiveness for functional symptoms not accompanied by conspicuous psychological features. Kroenke in Chapter 11 considers the modest evidence relating to populations defined in terms of somatoform diagnoses, such as somatization disorder, hypochondriasis, and body dysmorphic disorder, but finds no studies of the much more frequent nonspecific somatoform categories.11 We must therefore rely on the findings of clinical trials relating to individual types of functional symptoms (e.g., dizziness) and syndromes (e.g., chronic fatigue) and on a very few accounts of consecutive clinic attenders with mixed types of symptoms.12–14 Although diagnoses are usually not specified in these studies, we can reasonably assume most participants could have been given somatoform or other psychiatric diagnoses. Whereas systematic reviews of the management of functional problems have necessarily focused on specialist interventions, we must keep in mind the whole range of potential treatments. These can be classified into five groups: • Symptomatic treatments that provide relief from pain and distress; • Relatively “specific” psychiatric interventions—pharmacological treatments (mainly antidepressant medication) and the more precisely formulated psychological treatments; • A wide range of nonspecific psychosocial interventions; • The many interventions used by complementary medicine and traditional healers; • Organized stepped care programs that include multiple elements and are often multidisciplinary.

Symptomatic Treatments Symptomatic measures are common in treating common mental disorder, for example, anxiolytic and hypnotic medication and practical help and advice. They

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have a similar role in managing distress associated with functional symptoms. In addition, physical symptomatic treatments, such as analgesics, have an important role in relieving pain and other somatic symptoms and promoting recovery. However, they are largely ineffective in modifying inappropriate cognitions and behaviors. For example, diagnosing and treating esophagitis is helpful in many of those who present with chest pain, but it is only a partial answer when such patients are convinced that their symptoms are due to heart disease.

“Specific” Treatments Interventions that are “specific” in that they are precisely targeted at psychological states and processes are effective in the treatment of common mental disorders; they are also effective for some functional conditions (as reviewed elsewhere in this book). For example, antipsychotic drugs are useful in the symptomatic management of delusional health beliefs, and antidepressant medication is effective in the treatment of some functional symptoms, especially where there is clear evidence of a depressive disorder.13 However, the latter are not, in fact, specific to low mood in that they have other therapeutic actions and are effective in some pain syndromes. Effective cognitive-behavioral therapy (CBT) treatments of anxiety and other disorders are highly specific treatments with their components targeted to psychological symptoms and processes. They are often similarly effective when directed to functional symptoms, not only for the somatic symptoms of anxiety and depressive disorders but also for somatoform problems, such as hypochondriasis and chronic pain.11,14 The effectiveness of relatively “specific” treatments for some functional symptoms leads to several conclusions: 1. The significance of mood and anxiety (whether or not symptoms are severe enough to satisfy diagnostic criteria) in the causation of somatic symptoms; 2. The possibility that some somatoform problems that respond to specific treatments (for example, hypochondriasis and body dysmorphic disorder) might best be reassigned to other established psychiatric categories; 3. Possible psychological and physiological etiological mechanisms underlying some types of functional complaint.

Nonspecific Treatments Nonspecific elements are fundamental to all good medical care. They have a major role in the treatment of mental disorders, and our textbook of psychiatry for medical students states (p. 256): “Certain basic procedures are involved in all psychological treatment whatever additional techniques may be employed” and then lists: devel-

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oping a therapeutic relationship; listening to patients’ concerns; provision of information; explanation and advice; allowing the release of emotion; improving morale; reviewing and developing assets and encouragement of self-help.15 These procedures depend on the fundamental importance of doctor-patient communication16 and encouraging self-care17 and family involvement. Similar methods seem to be equally effective for functional symptoms and in managing maladaptive responses to major physical conditions. Despite the clinical importance of nonspecific elements, the extent and the quality of evidence about their specification and delivery are limited.4 Even so, it is very clear that even though nonspecific in their applications, they need to be as clearly specified, evaluated, and delivered as all other treatments. It is evident that some apparently common-sense and widely recommended measures, such as giving out information booklets and simple reassurance, are largely ineffective.18 Nonspecific interventions should not be taken for granted as within the basic skills of all physicians, but deserve much greater attention and more critical evaluation, followed by better training.

Complementary Medicine and Traditional Healers Complementary and alternative treatments are very commonly used in Western countries;19 elsewhere, traditional therapies are both widely practiced and generally accepted as being valuable. For example, traditional herbal medicine is an integral part of Chinese medical services. Although these treatments do not have the specific therapeutic actions that are claimed for them, some of their components are similar to those of orthodox psychological therapies. Jerome Frank powerfully argued that patients may be helped by the sympathetic reassurance and encouragement that traditional therapies usually offer, but he also pointed out that they may also suffer as a result of harmful advice and by being dissuaded from seeking effective orthodox care.20 For countries with few health services, it is an important public health issue as to how traditional healing can be encouraged to complement and promote the best use of scarce specialist medical and psychological resources. More generally, it is worrying that the failure of orthodox medicine to convince patients has allowed far too many people to turn to expensive and ineffective alternative practitioners.

Organization of Care The efficient organization of care is essential if we are to help much greater proportions of those who need and would benefit from treatment. Stepped care4 is considered to be the most effective and efficient way of delivering care for individ-

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uals with potentially chronic physical and mental problems, for example, the treatment of depression in those with diabetes.21 • The first step for newly presenting problems is sympathetic nonspecialist routine care, which makes the maximum use of self-help materials and offers good information, explanation, advice, and reassurance.4,22 It also requires clear communication between all those involved in care, as has been notably shown for somatization disorder.23 • The succeeding steps for persistent symptoms are progressively more intensive and specialist. Each step requires systematic reassessment. • There is some evidence that good organization and delivery can improve outcomes for functional symptoms and syndromes in everyday clinical practice; perhaps the best examples relate to the treatment of chronic pain and especially low back pain.22 Implementing better delivery depends on our being able to demonstrate that it is possible to teach primary care doctors and teams to provide more effective care for somatic symptoms and to do so within a very restricted time for consultation. There is some encouraging evidence. 24,25 However, it is worrying that this and other research has consistently found that willingness and aptitude to modify clinical skills cannot be taken for granted.

Example of Noncardiac Chest Pain The management of the functional symptom of noncardiac chest pain provides a good example of the general issues. It is very frequent and more common in almost all clinical settings than angina. It is most likely to be due to minor, often unidentified, physical causes such as muscle strain or esophagitis. A 30-year program of research has consistently found that, despite reassurance, a sizable proportion of patients continue to have pain and disability and believe that they have undiagnosed heart disease.26,27 The characteristics, associations, and clinical course have many similarities with angina. Chronic pain is due to an interaction of chest sensations attributable to physiological or minor pathology and psychological, behavioral, and social factors. Iatrogenic factors are prominent in maintaining maladaptive beliefs and behaviors. Psychological assessment indicates that in addition to this Axis III diagnosis, Axis I psychiatric diagnoses are common: occasionally depression, more often anxiety disorder or somatoform disorder. There may be no psychiatric diagnosis. Interventions for persistent symptoms that have been proven in randomized clinical trials include • Symptomatic treatments of any underlying pathology (for example, esophagitis);

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• Antidepressant medication, especially for the small minority with clinical depression; • Anxiolytic drugs useful for symptomatic relief but relatively ineffective in modifying cognitions; • CBT derived from methods for anxiety disorder both for those with panic disorder and the greater number without panic.26 Overall, we can conclude that antidepressant medication can be useful in the minority of subjects with diagnosable depressive or panic disorder. More importantly, psychological treatments based on CBT principles are effective with a greater number of patients with maladaptive beliefs and behaviors, whether or not they also suffer from a psychiatric disorder. Such findings lead to recommendations for stepped care as a basis for routine care: • Step 1: Reassurance, advice, and explanation in the medical clinic; • Step 2: Reassessment, more extended CBT-based discussion, and encouragement of self-help; • Step 3: Reassessment, sessions of CBT or other specialist care. In recent research, we have been interested in developing treatment packages that address the conspicuous failures of reassurance and communication in managing newly presenting patients; these communication failures seem to maintain and even exacerbate misinterpretations, symptoms, and disability. Qualitative studies in a rapid access chest pain clinic have shown that simple changes to the presentation of explanation and advice with encouragement of self-help and improved discharge letters resulted in both improved outcome and satisfaction.27 We also found that the same approach was valuable in treating psychological aspects of newly presenting angina, with patients reporting themselves as being much more satisfied after the changes were made to clinic organization and communication.27 In other research, we described the poor outcome of another common and rather similar functional presentation to cardiologists—benign palpitation. A randomized controlled trial demonstrated the significant benefit of a further appointment with a cardiac nurse, who offered well-specified explanation, discussion, and advice. Also, a 3-month follow-up assessment enabled professionals to identify those patients who required more specialist psychological treatment. 28 Further studies have confirmed that early rehabilitation by nurses and CBT after patients had suffered myocardial infarction resulted in reduced worry and more rapid return to full activities.29 A final worthwhile conclusion from such evaluations of psychological interventions is that they provide us with information about the psychological processes underlying symptom formation and maintenance and determining interpretation and behavior.

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Conclusions We have considered a wide range of clinical impressions and research of rather varied quality which, taken as a whole, leads to generally encouraging conclusions about the benefits of psychological and psychiatric treatments of functional symptoms: 1. Most functional symptoms seen in general medical care are transient and not associated with psychiatric disorder. Simple routine measures are appropriate. 2. “Specific” interventions that are effective with mental disorders are also effective for some functional symptoms and syndromes in which psychological features are not prominent. 3. “Nonspecific” interventions can also be effective whether or not there is associated psychiatric disorder. Such treatments require much greater definition and critical evaluation. Similar nonspecific interventions are also effective in managing psychologically determined complications of physical disorders. 4. “Traditional” therapies include useful nonspecific components but can also be unhelpful or harmful. 5. Better organized early interventions for functional disorder could prevent chronicity and iatrogenic complications and also enable much earlier recognition of those requiring more specialist and intensive care. Care might best be delivered according to stepped care principles. 6. Treatment research provides valuable information about underlying psychological processes.

IMPLICATIONS FOR CLASSIFICATION It is often argued that the introduction of the category of somatoform disorder in DSM-III has been useful in drawing attention to common and important clinical problems. This may be true for psychiatrists and psychologists, who are usually concerned with a more chronic and severe minority who usually have an additional psychiatric diagnosis. In contrast, the majority of primary care doctors and others who treat the very large majority of functional problems do not understand or use the terminology and classification. We must both revise our classifications and (equally important) present them in a manner that helps rather than hinders the choice, design, and delivery of treatments and that is understood and accepted by patients. It has been argued elsewhere that the fundamental problems of the present DSM and ICD classifications are not due to lack of evidence but are conceptual and can be resolved.3 The evidence reviewed here (and elsewhere in this book) suggests that it would be helpful for DSM-V and ICD-11

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• To accept that it must complement the separate medical classification of all functional symptoms and syndromes, for example, chest pain, irritable bowel, chronic fatigue, and low back pain. In the minority for whom an additional DSM Axis I psychiatric diagnosis is appropriate and helpful, the descriptive medical diagnosis will be recorded on Axis III. • To include categories of psychiatric disorder for the psychological processes associated with most chronic functional symptoms. In addition to anxiety and mood mental disorders, there should be categories for clinical problems now covered by somatoform disorder but that have an etiologically neutral nomenclature and criteria referring to probable abnormalities of perception, interpretation, and behavior. • To use experience from clinical practice and treatment research as valuable guidance when writing criteria that reflect underlying psychological processes. • To be accompanied by a radically revised text that promotes a more modern understanding of the etiology of functional symptoms and also the delivery of effective nonspecific and specific interventions. • To enable similar psychological consequences of functional disorder and of major physical pathology to be classified in a similar manner.

IMPLICATIONS FOR RESEARCH There is a pressing need for more and better quality clinical trials of the whole range of types of intervention. This chapter argues that such research should place a greater emphasis on simple early treatments (specific and nonspecific) that could be used by nonspecialists. This means more evaluation in primary care populations and a greater interest in guided self-help and other interventions not dependent on scarce specialist skills and greater cultural awareness. Evaluations of efficacy must lead to pragmatic research on effective delivery. This inevitably means large, multicenter, randomized trials. Their findings should be a basis for changes to training of specialists and nonspecialists in all relevant health professions. They will also require those of us who have a special expertise to modify our clinical practice and to develop considerably our contributions as teachers and supervisors of others. These final conclusions on developing much better training for all involved in care are perhaps the most important of all in that they are basic to change but have received far too little attention.

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22. Von Korff M, Moore C. Stepped care for back pain: activating approaches for primary care. Ann Intern Med 2001;134:911–917. 23. Morriss R, Gask L. Treatment of patients with somatized mental disorder: effects of reattribution training on outcomes under the direct control of the family doctor. Psychosomatics 2002;43:394–399. 24. Smith GR, Rost K, Kashner TM. A trial of the effect of standardized psychiatric consultation on health outcomes and costs in somatizing patients. Arch Gen Psychiatry 1995;52:238–243. 25. Morriss R. Specific psychosocial interventions for somatizing patients by the general practitioner: a randomised controlled trial. J Psychosom Res 2004;57:507–514. 26. Bass C, Mayou R. ABC of psychological medicine: chest pain. Br Med J 2002;325:588– 591. 27. Price JR, Mayou RA, Bass CM, Hames R, Sprigings D, Birkhead JS. Developing a rapid access chest pain clinic. Qualitative studies of patients’ needs and experiences. J Psychosom Res 2005;59:237–246. 28. Mayou R, Sprigings D, Birkhead J, Price J. A randomized controlled trial of a brief educational and psychological intervention for patients presenting to a cardiac clinic with palpitation. Psychol Med 2002;32:699–706. 29. Mayou RA, Thompson DR, Clements A, Davies CH, Goodwin SJ, Normington K, Hicks N, Price J. Guideline-based early rehabilitation after myocardial infarction. A pragmatic randomised controlled trial. J Psychosom Res 2002;52:89–95.

11 EFFICACY OF TREATMENT FOR SOMATOFORM DISORDERS A Review of Randomized Controlled Trials Kurt Kroenke, M.D.

S

omatoform disorders are among the most prevalent mental disorders seen in the general medical setting, present in 10%–15% of primary care patients.1–4 The functional impairment associated with somatoform disorders is comparable with that seen in depressive and anxiety disorders.5,6 Moreover, clinically significant somatization leads to excessive health care use, costing the U.S. health care system an estimated $100 billion annually.7 Also, somatoform disorders are among the most frustrating mental disorders for clinicians to manage and also result in high levels of patient dissatisfaction.5,8–10 Finally, there is greater skepticism regarding the treatability of somatoform disorders compared with the confidence practitioners have regarding the treatment of depression and anxiety. It is likely that if evidence-based treatments existed and were more uniformly applied, the adverse consequences of somatoform disorders, including disability, costs, and dissatisfaction, would be reduced.

This chapter is reprinted from an article originally co-published by Psychosomatic Medicine and the American Psychiatric Association: Kroenke K: “Efficacy of Treatment for Somatoform Disorders: A Review of Randomized Controlled Trials.” Psychosomatic Medicine 69:881–888 (2007). Copyright © 2007 by the American Psychosomatic Society and the American Psychiatric Association. Reprinted with permission.

143

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Somatic Presentations of Mental Disorders

There have been several evidence-based reviews of psychological treatments for somatic symptoms and functional somatic syndromes.11–15 However, the overlap between these symptom-based general medical disorders and somatoform disorders remains controversial. Therefore, a critical review of the literature was undertaken to determine which treatments are efficacious for somatoform disorders and to ascertain the strength of evidence for particular treatments. The purpose is both to guide current practice as well as to identify gaps in the evidence to inform future treatment research.

Methods A MEDLINE search of articles published in English from 1966 to 2006 was conducted, using the following search terms: randomized clinical trial, somatoform disorders, somatization disorder, undifferentiated somatoform disorder, hypochondriasis, conversion disorder, pain disorder, and body dysmorphic disorder. Potential studies were also identified from bibliographies of retrieved articles as well as several recent reviews of selected treatments.12,14,16,17 Prepost studies (i.e., where outcomes were assessed in a single group of patients before and after an intervention) were excluded. Also excluded were studies that focused on specific symptoms (e.g., back pain, headache) or functional somatic syndromes (e.g., irritable bowel syndrome, fibromyalgia). Data were abstracted on the following key variables: somatoform disorder category, sample size, type of intervention, number and duration of sessions, type of control group, duration of follow-up, outcomes evaluated, and treatment effect. The following types of patient-centered outcomes were evaluated: 1) symptoms (i.e., the study’s main measure of somatic symptom count and/or severity); 2) functional status (i.e., the study’s main measure of functional impairment or quality of life); and 3) psychological (i.e., either a domain specific to the disorder, such as hypochondriacal or body dysmorphic beliefs and behaviors, or a generic measure of depression, anxiety, or psychological distress). For each trial, these three outcomes were assessed as positive (outcome was better in the treatment group than the control group), equivocal (there was a trend favoring the treatment group but the group difference was not statistically significant), negative (the groups did not differ), or not assessed. Secondary variables for which data were abstracted include patient demographics (age, gender, educational level, race) and country as well as type of clinic in which the study was conducted. A standard meta-analytic approach to aggregate the reported data on efficacy was not possible because of the small number of trials for a given intervention within broad treatment classes; substantial differences in the definition and types of reported outcomes; and considerable variation in the reporting of statistical details, such as exact P values and standard deviations. Moreover, many studies nei-

Efficacy of Treatment for Somatoform Disorders

145

ther stated what the primary outcome was nor prespecified the sample size needed to adequately test for a primary outcome. Therefore, similar to several previous literature syntheses of mental health interventions across multiple conditions,12,18 a vote-counting approach19 was used to classify each trial as positive or negative. Any trial that reported statistically significant improvement in at least one of the three patient-centered outcomes was operationally defined as a positive trial.

Results SOMATOFORM DISORDERS STUDIED IN THE RANDOMIZED CLINICAL TRIALS A total of 34 randomized clinical trials (RCTs) involving 3,922 patients were included (Table 11–1). Two-thirds of the studies involved somatization disorder (SD) (n= 4 studies)20–23 and lower threshold variants, such as abridged versions of SD (n =9)24–32 and medically unexplained symptoms (n=10).33–42 There were five studies of hypochondriasis, 43–47 three of conversion disorder,48–50 and three of body dysmorphic disorder (BDD).51–53 Three of the trials included patients with undifferentiated somatoform disorder (USD) but did not report the results separately for USD.30–32 Also, most or all of the patients in the 9 studies of abridged versions of SD and the 10 studies of medically unexplained symptoms would likely meet the criteria for USD. Finally, although there are a large number of RCTs in the literature focused on patients with specific pain conditions or chronic pain in general, there were no studies of Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV)54 pain disorder per se.

TREATMENTS STUDIED IN THE RCTs Cognitive-behavioral therapy (CBT) was the treatment studied in 13 trials, antidepressants in 5, and other treatments in 16 (Table 11–2). Twelve of the 16 trials involving other treatments were conducted in patients with SD and its lower threshold variants and evaluated a psychiatric consultation letter (n=4) to the patient’s primary care physician (PCP), training PCPs how to better manage somatizing patients (n =3), non-CBT psychotherapy (n =2), a multicomponent nurse care management intervention (n=1), aerobic exercise (n=1), and writing disclosure (n=1). There were studies of hypnosis (n=2) and paradoxical intention (n =1) in conversion disorder and explanatory therapy (n=1) in hypochondriasis. The median number of subjects and range per study by type of treatment are shown in Table 11–2. There were a few studies with very small samples (<40 subjects), and the several largest studies focused on general practitioner training, where patients enrolled were clustered within a modest number of physicians, potentially

146

TABLE 11–1.

Summary of 34 randomized clinical trials testing treatments for somatoform disorders Outcomesc

Reference

Treatment, na Disorder(s) # sessions 38

SD

73

SD

70

SD

Allen et al. 200623

84

SD

Smith et al. 199524 Sumathipala et al. 200025

56

ASD

68

ASD

Schilte et al. 200126

137 ASD

Followupb Symptoms

Functional Psychologic Comments

Usual care

18

−

−

↓ Costs

Usual care

12

+

−

↓ Costs

Consult letter to PCP CBT, 10 (1 hr) Consult letter to PCP Consult letter Usual care to PCP CBT, 6 (1/2 hr) Usual care

12

+

+

↓ Costs

−

Response difference=35%; ↓ costs ↓ Costs

+

↓ Utilization

−

No effect on utilization

Consult letter to PCP Consult letter to PCP Psychotherapygroup, 8 (2 hr)

Writing disclosure, 2 (1.5 hr)

Usual care

15

+

+

+

24 3

+

24

−

−

Somatic Presentations of Mental Disorders

Smith et al. 198620 Rost et al. 199421 Kashner et al. 199522

Control

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions

Control

Followupb Symptoms +

Functional Psychologic Comments −

−

+

−

127 ASD or greater

PCP training in PCP reattribution trained in (12 hr) psychosocial care

6

Used active instead of usual care comparator. Patients in each group got mean of 4.5 sessions 5.5↑PCS score (ES=0.48); change similar for SD and ASD Pain improved, but not total somatic symptom score

Dickinson et al. 200328

111 MSD

Consult letter to PCP

Usual care

24

Kroenke et al. 200629

112 MSD

Venlafaxine

Placebo

3

±

+

Volz et al. 200030 Volz et al. 200231

200 SD, USD, SAD 149 SD (108) USD (7) SAD (38)

Opipramol

Placebo

1/12

+

+

ES<St. John’s wort trials

St. John’s wort

Placebo

1/12

+

+

Independent of depression improvement

147

Larisch et al. 200427

Efficacy of Treatment for Somatoform Disorders

TABLE 11–1.

148

TABLE 11–1.

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions 173 SD (67) St. John’s wort USD (30) SAD (90)

Hellman et al.a 199033

61

MUS

CBT-group, 6 (1.5 hr)

Speckens et al. 199534

79

MUS

CBT, 6 to 16 (1 hr)

Lidbeck 199735

50

MUS

McLeod et al.a 199736

82

MUS

CBT-relaxation therapy, 8 (3 hr) CBT-group, 6

Followupb Symptoms

Functional Psychologic Comments

Placebo

1/12

+

+

Stress management Usual care

6

+

+

12

+

Wait list

6

Wait list

6

+

±

Response difference=25%; excluded major depression ↓ Utilization; ES=0.38–0.88

−

Response difference=18%; ES=0.54 and 36 (6 and 12 months)

−

↓ HC; ↓ medications

+

ES=0.43

Somatic Presentations of Mental Disorders

Muller et al. 200432

Control

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions

Control

Followupb Symptoms

Functional Psychologic Comments

Peters et al. 200237

228 MUS

Exercise, 20 (1 hr)

Stretching, 20 (1 hr)

6

−

Kolk et al. 200438

98

Psychotherapy, ≤12 (1 hr)

Usual care

12

−

Smith et al. 200639

200 MUS

Bundled: CBT Usual care and/or antidepressant

12

Rosendal et al. 200740

667 MUS

Usual care

12

−

Rief et al. 200641 Martin et al. 200742

295 MUS ≥2

GP training in reattribution (25 hr) GP training (8 hr) CBT-group, 1 (3.5 hr)

Usual care

6

−

−

↓ Utilization

Wait list

6

±

−

↓ Utilization; ↓ medications; mixed somatization results

MUS

140 MUS ≥2

−

−

− +

−

Active instead of usual care comparator. Both groups improved Low power— imbalanced groups (only 18 controls) Response difference=16%

Efficacy of Treatment for Somatoform Disorders

TABLE 11–1.

−

149

150

TABLE 11–1.

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions

Control

Followupb Symptoms

Functional Psychologic Comments

32

HC

CBT, 16

Wait list

7

+

48

HC

CT or stress management, 17 (1 hr)

Wait list

12

+

Fava et al. 200045

20

HC

Explanatory, 8 (1/2 hr)

Wait list

6

+

↓ HC cognitions/ behaviors; ↓ utilization

Visser et al. 200146

78

HC

CT or exposure therapy, 12 (1 hr)

Wait list

7

+

Barsky et al. 200447

187 HC

↓ HC cognitions/ behaviors; CT=exposure in efficacy ↓ HC cognitions/ behaviors; no effect on HC somatic symptoms

CBT, 6 (1.5 hr) Usual care

12

+

+

+

↓ HC cognitions/ behaviors ↓ HC cognitions/ behaviors; CT=stress management in efficacy

Somatic Presentations of Mental Disorders

Warwick et al. 199643 Clark et al. 199844

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions

Control

Followupb Symptoms

Functional Psychologic Comments

45

Inpatient CD (motor) Inpatient treatment for treatment for 12 12 weeks plus weeks hypnosis, 8 (1 hr)

8

−

Moene et al. 200349

44

CD (motor) Hypnosis, 10 (1 hr)

6

±

−

Ataoglu et al. 200350

30

CD (pseudoseizures)

1.5

±

+

Rosen et al. 199551

54

BDD

Wait list

Diazepam Paradoxical intention twice daily for 3 weeks as inpatient CBT w/ expoWait list sure therapy, 8 (2 hr)

6

Hypnosis provided no added benefit to inpatient treatment

+

+

↓ Motor signs using video rating scale immediately post treatment but not assessed at follow-up 1/15 versus 6/15 seizures (p=0.08)

↓ Obsessive-compulsive BDD beliefs and behaviors

151

Moene et al. 200248

Efficacy of Treatment for Somatoform Disorders

TABLE 11–1.

152

TABLE 11–1.

Summary of 34 randomized clinical trials testing treatments for somatoform disorders (continued) Outcomesc

Reference

Treatment, na Disorder(s) # sessions

Control

Followupb Symptoms

19

BDD

CBT, 12

Wait list

3

Phillips et al. 200253

67

BDD

Fluoxetine

Placebo

3

+

+

↓ Obsessive-compulsive BDD beliefs and behaviors

+

↓ Obsessive-compulsive BDD beliefs and behaviors

Note. ASD =abridged somatization disorder; BDD= body dysmorphic disorder; CBT= cognitive-behavioral therapy; CD=conversion disorder; CT= cognitive therapy; ES= effect size (mean group difference÷SD); GP = general practitioner; HC= hypochondriasis; MSD =multisomatoform disorder; MUS= medically unexplained symptoms; PCP =primary care physician; SAD= somatoform autonomic dysfunction; SD= somatization disorder; USD= undifferentiated somatoform disorder. aDrop-outs are not included in n if not included in the analysis of the original paper. bFollow-up measured in number of months. c+ =treatment group was better than control group on this outcome; ± = there was a trend favoring the treatment group but the difference was not statistically significant; −= the groups did not differ on this outcome.

Somatic Presentations of Mental Disorders

Veale et al. 199652

Functional Psychologic Comments

153

Efficacy of Treatment for Somatoform Disorders

TABLE 11–2.

Selected characteristics of trials by type of treatment for somatoform disorder

Characteristic of trial Number of trials Sample size, n subjects Median Range Total (all trials) Duration of follow-up, n trials <6 months 6–11 months ≥12 months

Cognitivebehavioral therapy

Antidepressants

Other therapy

13

5

16

68 19–187 982

149 67–200 701

86 20–667 2239

2 7 4

5 0 0

1 6 9

diminishing the study power. All five antidepressant trials had 3 months or less of follow-up, whereas the duration of follow-up tended to be longer in the studies of nonpharmacological interventions.

TREATMENT INTENSITY FOR INTERVENTION GROUP AND TYPES OF CONTROL GROUPS Data could be abstracted for 24 studies (Table 11–1) on the number of sessions and total contact hours provided for subjects in the intervention arm (it was not relevant and therefore not provided for five antidepressant trials, four trials of a consultation letter to the PCP, and one trial of a bundled CBT/antidepressant trial). The median number of sessions was 8 (range=1–30), and the median number of total contact hours was 12 (range =3–25). Subjects in the control arm were assigned to treatment as usual in 12 trials, a wait list in 10, an active comparator in 7, and placebo (all drug trials) in 5. The active comparator was a psychiatric consult letter to the PCP in two trials, and stress management, stretching exercises, diazepam, psychiatric inpatient treatment, or specialized PCP psychosocial training in one trial each.

SECONDARY STUDY CHARACTERISTICS Slightly more than half (n=18) of the trials reported enrollment rates. In these trials, the median proportion of eligible subjects enrolled was 76% (range=30%–100%).

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Somatic Presentations of Mental Disorders

In the seven CBT trials that reported enrollment rates, the median was 81% (range=30%–87%). All trials reported the proportion of women, the median being 75% (range=45%–100%). All trials also reported the average patient age, the median being 43 years (range of average ages=27.0–50.6 years). Ten trials (all from the United States) reported on race/ethnicity, with the median proportion of minority subjects enrolled being 19% (range =10%–37%). In the 16 trials that reported educational status, the variable ways of reporting years of schooling made precise pooled estimates difficult. Nonetheless, the median educational level achieved approximated a high school education. Of the 34 trials, 13 were conducted in the United States,20–24,28,29,33,36,39,47,51,53 6 in Germany,27,30–32,41,42 6 in the Netherlands,26,34,38,46,48,49 4 in the United Kingdom,37,43,44,52 and 1 each in Denmark,40 Italy,45 Sri Lanka,25 Sweden,35 and Turkey.50 The treatment was administered by a mental health professional in 22 trials, a primary care provider in 9 trials,20,21,24,27–29,39–41 and other types of providers in 3 trials.26,35,37 Of the 22 trials involving an intervention delivered by a mental health professional, 10 enrolled subjects solely or predominantly from primary care,22,23,25,33,34,36,38,42,45,47 and the mental health professionals were psychiatrists in 16 trials,22,23,25,30–32,34,43–45,47–50,52,53 psychologists in four trials,38,42,46,51 and behavioral medicine specialists in two trials.33,36 Finally, the vast majority of studies were published in the past decade with 22 published since 2000, 9 studies between 1995 and 1999, 2 studies between 1990 and 1994, and only 1 study before 1990.

OUTCOMES IN GENERAL Outcomes of individual trials are summarized in Table 11–1. Of the 20 studies assessing somatic symptom outcomes, 10 (50%) were positive trials whereas 4 were equivocal and 6 were negative. Of the 14 studies assessing functional status, 8 (57%) were positive trials, whereas 1 was equivocal and 5 were negative. Of the 32 studies assessing psychological distress, 18 (56%) were positive trials whereas 14 were negative. Of the 10 trials in which somatic symptoms improved, depression and/or psychological distress also improved in 7 trials, did not improve in 2 trials, and was not assessed in 1 trial. Improvement in the primary outcome measure was independent of depression status or change in the 6 studies where this was assessed.31,32,39,44,45,53 A secondary outcome highly relevant to somatoform disorders is health care use and/or costs, and 10/11 studies assessing this outcome showed reduction in health care use (5 trials) or costs (5 trials).

OUTCOMES BY TREATMENT TYPE Table 11–3 shows the proportion of positive trials by major treatment category. A positive study was defined as one in which the treatment group fared better than

155

Efficacy of Treatment for Somatoform Disorders

TABLE 11–3.

Outcomes of 34 randomized clinical trials for somatoform disorders

Disorder

Cognitivebehavioral therapy

Somatization disorder

1/1

Lower threshold somatization disorder Medically unexplained symptoms Hypochondriasis Conversion disorder Body dysmorphic disorder Total

1/1

Antidepressants

Other therapy 2/3

3/4

3/4

3/5

1/5

4/4

1/1 1/3

2/2

1/1

11/13

4/5

8/16

Positive trials/total trials.

the control group on at least one of the three patient-centered outcomes. The one treatment for which there seems to be convincing evidence is CBT, which proved beneficial for at least one outcome in 11/13 trials. Of the five trials examining antidepressants, four were positive (two trials of St. John’s wort and one of opipramol for SD-spectrum disorders and one trial of fluoxetine for BDD), whereas one was equivocal for the primary outcome but positive for at least one secondary patientcentered outcome (venlafaxine for SD-spectrum disorders). It should be noted that all antidepressant trials specified a primary outcome, whereas many nonpharmacological studies did not specify a primary outcome but simply reported multiple outcomes. Of the other treatments, only two were evaluated in more than one or two studies. Three of the four trials examining the effectiveness of providing a simple psychiatric consultation letter to PCPs were positive; the benefits were in terms of improved functional status (3/4 positive for this outcome) rather than reduced psychological distress (0/4 positive). Somatic symptom outcomes were not assessed in any of these four studies, although there were cost savings in all three studies that examined this outcome. Only one of the three trials examining the effectiveness of providing specialized training to PCPs in managing the somatizing patient proved positive.

156

Somatic Presentations of Mental Disorders

OUTCOMES BY SOMATOFORM DISORDER CATEGORY Somatization Disorder and Its Lower Threshold Variants CBT was effective in five of seven trials, and antidepressants in three of four trials. A psychiatric consultation letter to the PCP was effective in three of four trials, whereas providing specialized training to the PCP was effective in only one of three trials. A multicomponent nurse-administered intervention, using a type of CBT and antidepressants as indicated, was beneficial in one trial, whereas one of two trials using non-CBT psychotherapy was positive. Finally, one trial found aerobic exercise ineffective (although an active comparator of muscle stretching was used in the control group), and emotional disclosure through writing was ineffective in a single trial.

Hypochondriasis CBT proved consistently effective (4/4 trials involving a total of 345 patients) for hypochondriasis. One pilot study of explanatory therapy in 20 patients was also positive. All five trials also showed benefits in terms of hypochondriacal cognitions and behaviors.

Body Dysmorphic Disorder CBT was effective in two of two trials involving a total of 73 patients with BDD, and fluoxetine was effective in a single trial involving 67 patients. All three trials also showed benefits in terms of obsessive-compulsive BDD beliefs and behaviors.

Conversion Disorder There were only three small studies of conversion disorder (two using hypnosis and one using paradoxical intention), and the results were inconclusive.

Discussion This literature synthesis allows one strong and several tentative conclusions regarding the efficacy of treatment for somatoform disorders. First, CBT is consistently effective (11/13 trials) across a spectrum of somatoform disorders including SD and its lower threshold variants, hypochondriasis and BDD. Second, a psychiatric consultation letter to the primary care physician about strategies for managing the somatizing patient seems to improve physical functioning (3/4 trials) and reduce costs, although surprisingly the effect on somatic symptoms themselves has not been reported. Third, although there is preliminary evidence that antidepressants may be beneficial, the degree to which this is a general effect mediated through reduced depression and anxiety versus a specific effect on somatic symptoms needs to

Efficacy of Treatment for Somatoform Disorders

157

be better ascertained. A variety of other treatments have been evaluated for which the results have been either negative or inconclusive. All trials except three were published in the past decade. This could be due to a number of factors ranging from substantial changes in classification, a paucity of interest in somatoform disorders, lack of clinical trial funding for these disorders, and the fact that most somatizing patients present in primary care and fewer are referred to mental health specialists than patients with other mental disorders. Although somatoform disorders are just as common as depression and anxiety in primary care, the number and quality of trials to inform our treatment of somatoform disorders are far less. The literature reviewed has important limitations, which in turn weaken the conclusions we can draw, except for the likely efficacy of CBT. First, the heterogeneity of conditions, disease definitions, treatments, intervention type and intensity, outcomes, and duration of follow-up precluded quantitative pooling of study data. Thus, we had to resort to a crude vote-counting approach of characterizing studies as positive or negative, and a narrative synthesis rather than a formal metaanalysis. Second, most trials measured multiple outcomes and reported neither which outcome was primary nor a prespecified sample size. Therefore, our operational definition of a positive trial as needing to show benefit for only one of the three patient-centered outcomes could overestimate treatment benefits because multiple outcomes were often assessed and analyses were not typically adjusted for multiple hypothesis testing. On the other hand, many studies had small sample sizes meaning the differences that were found had to be of at least a moderate magnitude to be statistically significant. Third, the comparison arm for most studies was a usual care, wait list, or active comparator rather than placebo control. Consequently, blinding of the patient was impossible in many of these studies, and blinding of the outcome assessment was often not specified. Functional somatic syndromes (e.g., irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome) and individual chronic symptoms (e.g., headache, low back pain) were not the subject of this review but exhibit considerable overlap with somatoform disorders55 as well as depression and anxiety.56 It is therefore notable that evidence-based reviews have established the efficacy of both CBT and antidepressants for these somatic conditions.11–15,57 Additionally, it seems the effect of CBT and antidepressants on somatic symptoms is not entirely mediated through reduction of depression and psychological distress.11,12 On the other hand, depression and anxiety frequently co-occur in patients with functional somatic syndromes as well as somatoform disorders.4,58 and some studies have suggested that somatic symptoms may improve to a lesser degree than emotional symptoms.59,60 Regarding type of treatment, the strongest and most consistent evidence exists for CBT. In contrast, the number of antidepressant trials was small. Of these five trials, four were positive for the prespecified primary outcome, whereas the other was positive for one of the other patient-centered outcomes considered primary for

158

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this review. Compared with the nonpharmacological treatment studies, antidepressants had on average larger patient samples, had a prespecified primary outcome, and were placebo-controlled; the latter two factors would tend to increase the likelihood of a negative trial. On the other hand, antidepressant trials tended to have shorter follow-up periods, leaving unanswered questions about the persistence of benefits and the need for chronic therapy. Also, the three antidepressant trials, which showed benefits for SD-spectrum disorders, were all conducted in Germany and used either St. John’s wort or opipramol rather than antidepressants typically prescribed in the United States. Much stronger evidence is needed regarding the efficacy of pharmacotherapy, including the magnitude and sustainability of its benefits for somatic symptoms as well as its independent effect not mediated by improvement of comorbid depression and anxiety. Ironically, a psychiatric consultation letter provided to PCPs was effective in three of four trials, but specialized PCP training was effective in only one of three trials. Although substantial differences between trials make comparisons difficult, several points should be mentioned. First, although the consultation letter trials showed modest improvement in physical functioning, none of the trials reported on somatic symptom outcomes, which is notable in that all four trials were performed in SD or its lower threshold variants. Second, the consultation letter trials were all performed by the same group and had small sample sizes. Nonetheless, the fact that PCP training trials have not shown a convincing effect means further work is needed to determine the optimal balance between PCP care, collaborative care, or referral for CBT for improving outcomes of somatoform disorders in primary care. In terms of type of somatoform disorder, the most evidence (23/34 trials; Table 11–3) exists for the family of related disorders including SD, its abridged or subthreshold variants, and medically unexplained symptoms. Clinical trial evidence for the treatment for other somatoform disorders ranges from modest to limited. The evidence supporting CBT in hypochondriasis is consistent across four trials. Two trials of CBT and one trial of fluoxetine were beneficial in BDD. A metaanalysis of treatments for BDD61 included, in addition to the RCTs reported here, three case series and one crossover trial of antidepressants (three with selective serotonin reuptake inhibitors, one with clomipramine) involving 89 patients, and eight case series of psychological treatments (four with behavioral therapy, three with CBT, and one with cognitive therapy) involving 85 patients. Including all studies where the effect size could be derived from the published data, the mean effect sizes were 0.92 for antidepressants (five studies), 1.43 for behavioral therapy (four studies), and 1.78 for CBT (five studies). Effect sizes of 0.8 or greater are considered large therapeutic effects.62 Finally, the three small trials in conversion disorder were inconclusive, yet they are the only trials that qualified for inclusion in a recent Cochrane Collaboration review.63 Although we found no trials focusing on DSM-IV pain disorder or undifferentiated pain disorder per se, previous evidencebased reviews of antidepressants, CBT, and other psychological treatments for

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159

functional symptoms had patient samples where pain was often a cardinal symptom.11–15,57 Also, many of the trials in our review that focused on patients with lower-threshold SD and/or medically unexplained symptoms likely included many patients with pain symptoms or undifferentiated SD. Despite the evidence for some potentially effective treatments, many clinicians find somatoform disorders and medically unexplained symptoms among the most difficult conditions to treat, both in terms of outcomes as well as clinician-patient interactions.10,64 The reasons for this may be multifactorial including lack of clinician knowledge about evidence-based treatments, lack of access to or inadequate reimbursement for CBT and other psychotherapeutic interventions, concomitant personality disorders, and limited time in busy outpatient encounters with other competing demands. Also, there may be selection bias in published trials. For example, despite the consistent evidence supporting CBT, many such patients seen in clinical practice may refuse referral to mental health providers. Those with somatoform disorders who are convinced their problems are “physical” may be less likely to enroll in studies of “psychological” treatments. In summary, there is strong evidence supporting the efficacy of CBT across several types of somatoform disorders, and moderate evidence supporting a psychiatric consultation letter in SD and its lower threshold variants. Antidepressants also seem promising, particularly for functional somatic syndromes, but require further study in somatoform disorders per se. The most prevalent type of somatoform disorder is the family of conditions that includes SD, its lower threshold variants including medically unexplained symptoms, USD, and pain disorder. The overlap along a continuum of these disorders with one another and with functional somatic syndromes has important implications for revised classification in DSM-V as well as common treatments.55,65 Also, psychotherapeutic interventions other than CBT (e.g., interpersonal therapy, problem-solving therapy, brief psychodynamic therapy) as well as treatments outside of what are traditionally considered “psychological” (e.g., optimizing analgesics, the use of pain self-management programs) merit further study for somatoform disorders. Finally, most trials have studied single treatments, whereas it is likely that combining treatments may be necessary in patients with chronic somatic conditions. Because somatoform disorders are as prevalent as depression and anxiety in primary care and account for considerable disability and costs, enhancing treatment outcomes for this oftenneglected category of mental disorders should be a priority.

References 1. Spitzer RL, Williams JB, Kroenke K, Linzer M, deGruy FV III, Hahn SR, Brody D, Johnson JG. Utility of a new procedure for diagnosing mental disorders in primary care. The PRIME-MD 1000 study. JAMA 1994;272:1749–1756.

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2. Ormel J, Vonkorff M, Ustun TB, Pini S, Korten A, Oldehinkel T. Common mental disorders and disability across cultures. Results from the WHO collaborative study on psychological problems in general health care. JAMA 1994;272:1741–1748. 3. Kroenke K, Spitzer RL, Williams JBW. The PHQ-15: validity of a new measure for evaluating the severity of somatic symptoms. Psychosom Med 2002;64:258–266. 4. Kroenke K, Rosmalen JG. Symptoms, syndromes, and the value of psychiatric diagnostics in patients who have functional somatic disorders. Med Clin North Am 2006;90:603–626. 5. Kroenke K, Spitzer RL, deGruy FV, Hahn SR, Linzer M, Williams JBW, Brody D, Davies M. Multisomatoform disorder: an alternative to undifferentiated somatoform disorder for the somatizing patient in primar y care. Arch Gen Psychiatry 1997;54:352–358. 6. de Waal MW, Arnold IA, Eekhof JA, van Hemert AM. Somatoform disorders in general practice: prevalence, functional impairment and comorbidity with anxiety and depressive disorders. Br J Psychiatry 2004;184:470–476. 7. Barsky AJ, Orav EJ, Bates DW. Somatization increases medical utilization and costs independent of psychiatric and medical comorbidity. Arch Gen Psychiatry 2005;62:903–910. 8. Hahn SR, Thompson KS, Wills TA, Stern V, Budner NS. The difficult doctor-patient relationship: somatization, personality and psychopathology. J Clin Epidemiol 1994;47:647–657. 9. Hahn SR, Kroenke K, Spitzer RL, Brody D, Williams JB, Linzer M, deGruy FV III. The difficult patient: prevalence, psychopathology, and functional impairment. J Gen Intern Med 1996;11:1–8. 10. Jackson JL, Kroenke K. Difficult patient encounters in the ambulatory clinic: clinical predictors and outcomes. Arch Intern Med 1999;159:1069–1075. 11. O’Malley PG, Jackson JL, Santoro J, Tomkins G, Balden E, Kroenke K. Antidepressant therapy for unexplained symptoms and symptom syndromes. J Fam Pract 1999;48:980–990. 12. Kroenke K, Swindle R. Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom 2000;69:205–215. 13. Jackson JL, O’Malley PG, Kroenke K. Antidepressants and cognitive-behavioral therapy for symptom syndromes. CNS Spectr 2006;11:212–222. 14. Allen LA, Escobar JI, Lehrer PM, Gara MA, Woolfolk RL. Psychosocial treatments for multiple unexplained physical symptoms: a review of the literature. Psychosom Med 2002;64:939–950. 15. Raine R, Haines A, Sensky T, Hutchings A, Larkin K, Black N. Systematic review of mental health interventions for patients with common somatic symptoms: can research evidence from secondary care be extrapolated to primary care? BMJ 2002;325:1082. 16. Mayou R, Bass C, Sharpe M, editors. Treatment of Functional Somatic Symptoms. Oxford: Oxford University Press; 1995. 17. Looper KJ, Kirmayer LJ. Behavioral medicine approaches to somatoform disorders. J Consult Clin Psychol 2002;70:810–827.

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18. Kroenke K, Taylor-Vaisey A, Dietrich AJ, Oxman TE. Interventions to improve provider diagnosis and treatment of mental disorders in primary care: a critical review of the literature. Psychosomatics 2000;41:39–52. 19. Light RJ, Pillemer DB. Summing Up: The Science of Reviewing Research. Cambridge, MA: Harvard University Press; 1984. 20. Smith GR, Monson RA, Ray DC. Psychiatric consultation in somatization disorder: a randomized, controlled study. N Engl J Med 1986;314:1407–1413. 21. Rost K, Kashner TM, Smith GR. Effectiveness of psychiatric intervention with somatization disorder patients: improved outcomes at reduced costs. Gen Hosp Psychiatry 1994;16:381–387. 22. Kashner TM, Rost K, Cohen B, Anderson M, Smith GR Jr. Enhancing the health of somatization disorder patients. Effectiveness of short-term group therapy. Psychosomatics 1995;36:462–470. 23. Allen LA, Woolfolk RL, Escobar JI, Gara MA, Hamer RM. Cognitive-behavioral therapy for somatization disorder: a randomized controlled trial. Arch Intern Med 2006;166:1512–1518. 24. Smith GR, Rost K, Kashner TM. A trial of the effect of a standardized psychiatric consultation on health outcomes and costs in somatizing patients. Arch Gen Psychiatry 1995;52:238–243. 25. Sumathipala A, Hewege S, Hanwella R, Mann AH. Randomized controlled trial of cognitive behaviour therapy for repeated consultations for medically unexplained complaints: a feasibility study in Sri Lanka. Psychol Med 2000;30:747–757. 26. Schilte AF, Portegijs PJ, Blankenstein AH, Der Horst HE, Latour MB, van Eijk JT, Knottnerus JA. Randomised controlled trial of disclosure of emotionally important events in somatisation in primary care. BMJ 2001;323:86. 27. Larisch A, Schweickhardt A, Wirsching M, Fritzsche K. Psychosocial interventions for somatizing patients by the general practitioner: a randomized controlled trial. J Psychosom Res 2004;57:507–514. 28. Dickinson WP, Dickinson LM, deGruy FV, Main DS, Candib LM, Rost K. A randomized clinical trial of a care recommendation letter intervention for somatization in primary care. Ann Fam Med 2003;1:228–235. 29. Kroenke K, Messina N, III, Benattia I, Graepel J, Musgnung J. Venlafaxine extended release in the short-term treatment of depressed and anxious primary care patients with multisomatoform disorder. J Clin Psychiatry 2006;67:72–80. 30. Volz HP, Moller HJ, Reimann I, Stoll KD. Opipramol for the treatment of somatoform disorders results from a placebo-controlled trial. Eur Neuropsychopharmacol 2000;10:211–217. 31. Volz HP, Murck H, Kasper S, Moller HJ. St John’s wort extract (LI 160) in somatoform disorders: results of a placebo-controlled trial. Psychopharmacology (Berl) 2002;164:294–300. 32. Muller T, Mannel M, Murck H, Rahlfs VW. Treatment of somatoform disorders with St. John’s wort: a randomized, double-blind and placebo-controlled trial. Psychosom Med 2004;66:538–547.

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33. Hellman CJC, Budd M, Borysenko J, McClelland DC, Benson H. A study of the effectiveness of two group behavioral medicine interventions for patients with psychosomatic complaints. Behav Med 1990;16:165–173. 34. Speckens AEM, van Hemert AM, Spinhoven P, Hawton KE, Bolk JH, Rooijmans GM. Cognitive behavioural therapy for medically unexplained physical symptoms: a randomized controlled trial. BMJ 1995; 311:1328–1332. 35. Lidbeck J. Group therapy for somatization disorders in general practice: effectiveness of a short cognitive-behavioural treatment model. Acta Psychiatr Scand 1997;96:14–24. 36. McLeod CC, Budd MA, McClelland DC. Treatment of somatization in primary care. Gen Hosp Psychiatry 1997;19:251–258. 37. Peters S, Stanley I, Rose M, Kaney S, Salmon P. A randomized controlled trial of group aerobic exercise in primary care patients with persistent, unexplained physical symptoms. Fam Pract 2002;19:665–674. 38. Kolk AM, Schagen S, Hanewald GJ. Multiple medically unexplained physical symptoms and health care utilization: outcome of psychological intervention and patientrelated predictors of change. J Psychosom Res 2004;57:379–389. 39. Smith RC, Lyles JS, Gardiner JC, Sirbu C, Hodges A, Collins C, Dwamena FC, Lein C, Given CW, Given B, Goddeeris J. Primary care clinicians treat patients with medically unexplained symptoms: a randomized controlled trial. J Gen Intern Med 2006;21:671–677. 40. Rosendal M, Olesen F, Fink P, Toft T, Sokolowski I, Bro F. A randomized controlled trial of brief training in the assessment and treatment of somatization in primary care: effects on patient outcome. Gen Hosp Psychiatry 2007;29:364–373. 41. Rief W, Martin A, Rauh E, Zech T, Bender A. Evaluation of general practitioners’ training: how to manage patients with unexplained physical symptoms. Psychosomatics 2006;47:304–311. 42. Martin A, Fichter MM, Rauh, E, Rief W. A one-session treatment for patients suffering from medically unexplained symptoms in primary care: a randomized clinical trial. Psychosomatics 2007;48:294–303. 43. Warwick HM, Clark DM, Cobb AM, Salkovskis PM. A controlled trial of cognitivebehavioural treatment of hypochondriasis. Br J Psychiatry 1996;169:189–195. 44. Clark DM, Salkovskis PM, Hackmann A, Wells A, Fennell M, Ludgate J, Ahmad S, Richards HC, Gelder M. Two psychological treatments for hypochondriasis. A randomised controlled trial. Br J Psychiatry 1998;173:218–225. 45. Fava GA, Grandi S, Rafanelli C, Fabbri S, Cazzaro M. Explanatory therapy in hypochondriasis. J Clin Psychiatry 2000;61:317–322. 46. Visser S, Bouman TK. The treatment of hypochondriasis: exposure plus response prevention vs cognitive therapy. Behav Res Ther 2001;39:423–442. 47. Barsky AJ, Ahern DK. Cognitive behavior therapy for hypochondriasis: a randomized controlled trial. JAMA 2004;291:1464–1470. 48. Moene FC, Spinhoven P, Hoogduin KA, van DR. A randomised controlled clinical trial on the additional effect of hypnosis in a comprehensive treatment programme for in-patients with conversion disorder of the motor type. Psychother Psychosom 2002;71:66–76.

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49. Moene FC, Spinhoven P, Hoogduin KA, van DR. A randomized controlled clinical trial of a hypnosis-based treatment for patients with conversion disorder, motor type. Int J Clin Exp Hypn 2003;51:29–50. 50. Ataoglu A, Ozcetin A, Icmeli C, Ozbulut O. Paradoxical therapy in conversion reaction. J Korean Med Sci 2003;18:581–584. 51. Rosen JC, Reiter J, Orosan P. Cognitive-behavioral body image therapy for body dysmorphic disorder. J Consult Clin Psychol 1995;63:263–269. 52. Veale D, Gournay K, Dryden W, Boocock A, Shah F, Willson R, Walburn J. Body dysmorphic disorder: a cognitive behavioural model and pilot randomised controlled trial. Behav Res Ther 1996;34:717–729. 53. Phillips KA, Albertini RS, Rasmussen SA. A randomized placebo-controlled trial of fluoxetine in body dysmorphic disorder. Arch Gen Psychiatry 2002;59:381–388. 54. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed. Washington, DC: American Psychiatric Association; 1994. 55. Mayou R, Kirmayer LJ, Simon G, Kroenke K, Sharpe M. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry 2005;162:847–855. 56. Henningsen P, Zimmermann T, Sattel H. Medically unexplained physical symptoms, anxiety, and depression: a meta-analytic review. Psychosom Med 2003;65:528–533. 57. Nezu AM, Nezu CM, Lombardo ER. Cognitive-behavior therapy for medically unexplained symptoms: a critical review of the treatment literature. Behav Ther 2001;32:537–583. 58. Kroenke K. Patients presenting with somatic complaints: epidemiology, psychiatric comorbidity and management. Int J Methods Psychiatr Res 2003;12:34–43. 59. Greco T, Eckert G, Kroenke K. The outcome of physical symptoms with treatment of depression. J Gen Intern Med 2004;19:813–818. 60. Lin EH, Katon W, Von Korff M, Tang L, Williams JW Jr, Kroenke K, Hunkeler E, Harpole L, Hegel M, Arean P, Hoffing M, Della PR, Langston C, Unutzer J. Effect of improving depression care on pain and functional outcomes among older adults with arthritis: a randomized controlled trial. JAMA 2003;290:2428–2429. 61. Williams J, Hadjistavropoulos T, Sharpe D. A meta-analysis of psychological and pharmacological treatments for Body Dysmorphic Disorder. Behav Res Ther 2006;44:99–111. 62. Kazis LE, Anderson JJ, Meenan RF. Effect sizes for interpreting changes in health status. Med Care 1989;27:S178–S189. 63. Ruddy R, House A. Psychosocial interventions for conversion disorder. Cochrane Database Syst Rev 2005;(4):CD005331. 64. Hahn SR. Physical symptoms and physician-experienced difficulty in the physicianpatient relationship. Ann Intern Med 2001;134:897–904. 65. Kroenke K, Sharpe M, Sykes R. Revising the classification of somatoform disorders: key questions and preliminary recommendations. Psychosomatics 2007;48:277–285.

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12 THE EVIDENCE FOR TREATMENTS FOR SOMATOFORM DISORDERS A View From the Trenches Susan Levenstein, M.D.

The somatizing patient can be the nemesis of the primary care physician. A good proportion of our patients may seem to us to have inappropriate worries about their health—what makes an otherwise competent adult come to the doctor’s office for a runny nose?—but among them are a hardcore few who occupy a vastly larger space in our cumulative frustration quota than their numbers would suggest. Out of the 10,000 or so patients I’ve seen during 30 years of practicing general internal medicine, I’d say that I have seen several hundred with persistently exaggerated somatic concerns, and that the couple of dozen with true somatization disorder or unshakeable single-symptom conditions are permanently etched on my memory. What makes these patients so frustrating is our inability to make a satisfying medical diagnosis combined with our fear of missing one (at least one of my “somatizing” patients turned out to have multiple sclerosis), the great difficulty in getting any improvement, and the hostility and otherwise distorted illness behavior that are often on display. The result is that patients who desire particularly much attention and emotional support from their physicians1 receive particularly little.2 Formulating a somatoform diagnosis can be a double-edged sword for physicians on the front line. On the negative side, it may breed diagnostic sloppiness and

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therapeutic nihilism, leading to overemphasis on the psychological components in so-called “functional” disorders and underemphasis on interactions between mind and body in organic disorders such as coronary artery disease. The very line between “organic” and “functional” is becoming blurred as we recognize, for instance, that migraine can cause stroke and that the symptoms of many “irritable bowel syndrome” patients are demonstrably caused by lactose intolerance, mild celiac disease, or microscopic colitis. “Medically unexplained” can be a code word for our exasperation and/or ignorance, and unreasonable distress related to physical symptoms can exist in all kinds of disorders including the most anatomically severe. On the positive side, diagnosing a patient as having the psychological characteristics of somatization disorder or undifferentiated somatoform disorder can be invaluable. For one thing, it validates the clinician’s frustration. The cognitive reframing can defuse some negative attitudes and enable the physician to shift his or her aims from diagnosis and cure toward management, a more feasible goal. It can open the way toward focused and specific approaches toward management. In addition, recognizing the centrality of a disturbed physician-patient relationship may increase the chances of restructuring that relationship in a constructive direction. Controlled treatment trials of treatments for somatoform disorders, as summarized by Dr. Sumathipala, highlight the successes of cognitive-behavioral therapy and other psychological approaches. From the primary care practitioner’s point of view, the major problem with this literature is its emphasis on therapies provided by psychiatrists or psychologists—in our own experience, on the contrary, the major burden of managing these patients lies on us. Even when patients are undergoing cognitive-behavioral therapy, it is our waiting rooms they will haunt when they feel unwell; the research literature tends to leave us in the lurch. If there is as yet no clear evidence-based treatment strategy for the practitioner at the point of first impact, what approach can he or she use? Fortunately many accomplished clinicians have published their advice,3–5 and drawing on their experience, as well as my own, I would propose: 1. Patience. Somatization disorders are deeply rooted, resistant to change, and embedded in destructive and often mutually suspicious physician-patient relationships, so it is essential for the physician to take a long-term perspective about achieving any improvement. 2. Selective referral. Patience and selectivity are particularly important when it comes to referring somatization disorder spectrum patients for psychologically based treatments. In my experience it is generally best, unless you know a patient very well indeed, to reserve referral of these patients to psychiatrists or psychotherapists for the usual indications of subjective psychological distress, not for what is perceived by the physician as excessive somatic concerns. Difficult somatizing patients are not likely to accept psychiatric referral, and the attempt can damage the rapport between the patient and the referring physi-

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4. 5.

6.

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cian to the point of driving the patient away altogether—which may sometimes be the physician’s half-unwittingly desired outcome. “Consultation letter” principles. When somatizing patients do receive and accept a psychiatric referral they frequently return from the consultant with standard recommendations for the referring practitioner that reflect the general concepts listed in Smith’s “consultation letter”:6 legitimize the patient’s physical symptoms, avoid extensive examinations and unnecessary tests, give appointments at regular intervals, perform repeated brief physical examinations, provide frequent reassurance, and invite the patient to talk about personal issues. Given the wide applicability of these simple principles of management and their reported potential for improving both health outcomes and medical costs,7,8 educators should try to ensure that they are familiar to all medical graduates. Don’t miss depression, which not infrequently manifests as excessive somatic concerns. Consider antidepressants. They may play a useful role even if the patient is not depressed, since selective serotonin reuptake inhibitors and especially tricyclic drugs can be effective for irritable bowel syndrome, migraine, and a variety of undiagnosed pain symptoms, often in doses that would be subtherapeutic for psychiatric indications.9 Make common cause with your patient. The statement that a strong therapeutic alliance is the key to management of somatizing patients is likely to draw ironic shrugs from primary care practitioners, who are accustomed to trying and awkward relationships with these patients that can verge at times on the reciprocally antagonistic.10 But a physician who accomplishes the difficult task of transforming his or her relationship with a somatization disorder patient into a collaborative one will find the endeavor highly rewarding in terms of therapeutic results as well as in terms of the reduction in anger and frustration on both sides. A solid alliance means that both sides have accepted the other’s good will. Once that has been established, the patient is more likely to accept psychiatric referral and perhaps more likely to benefit from cognitive-behavioral therapy or other psychologically based treatments, if indeed these are still necessary.

The physician him- or herself often needs some cognitive restructuring to make the shift from a conflictual to a collaborative relationship; there is some evidence that this skill can be taught.11 The chances of success are greatest if the physician takes the patient’s symptoms seriously and empathizes with suffering; expresses interest in the patient’s life situation and psychological state; inquires directly and nonjudgmentally about the possible influence of stress and distress on physical symptoms; refrains from pressing to detect links between psyche and soma and doesn’t rush to communicate even those links that seem apparent; provides medications for supportive symptomatic treatment, a concrete sign of caring; and encourages patients to participate actively in treatment decisions.

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What are the prospects for cure? The somatization spectrum disorders tend to be chronic and treatment resistant, at least when not secondary to a depressive disorder. In rare instances, however, even deep-rooted somatization disorders can enter prolonged remission. These cases can be instructive, even though our usual therapeutic aim will still remain limited to management, symptom control, and cost containment. The few patients of my own who have achieved what could be called a cure of their somatization disorder had all undergone profoundly lifealtering experiences that loosened the grip of their intense focus on bodily functioning. One such experience whose curative effect I have observed has been traditional psychoanalysis—somewhat surprising since depth psychotherapy is often held to be inappropriate and fruitless for most somatizers. Others have included religious conversion, the assumption of caretaking for a family member with severe chronic disease, and in one case the impact of the September 11 terror attacks. But what, finally, are the risks of inappropriately high somatic concern? Frustration, misery, and wasted resources. And what about the risks of inappropriately low somatic concern? This is a disorder that is less present in the diagnostic classifications, and yet it can be much more serious: every physician has seen nonchalant self-neglect lead to severe illness, even death. Perhaps this paradoxical thought can be of some consolation to practitioners struggling to handle their somatization disorder patients on the front lines. Patients get the best care and physicians get the most satisfaction when the patients have the “right balance” between somatic attention and somatic denial.

References 1. Salmon P, Ring A, Dowrick CF, Humphris GM. What do general practice patients want when they present medically unexplained symptoms, and why do their doctors feel pressurized? J Psychosom Res 2005;59:255–260, discussion 61–62. 2. Epstein RM, Shields CG, Meldrum SC, Fiscella K, Carroll J, Carney PA, Duberstein PR. Physicians’ responses to patients’ medically unexplained symptoms. Psychosom Med 2006;68(2):269–276. 3. Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med 1999;130:910– 921. 4. Yeung A, Deguang H. Somatoform disorders. West J Med 2002;176:253–256. 5. Spratt EG, DeMaso DR. Somatoform disorder: somatization. May 30, 2006. Available at: http://www.emedicine.com/ped/topic3015.htm. Accessed May 7, 2007. 6. Smith GR Jr, Monson RA, Ray DC. Psychiatric consultation in somatization disorder. A randomized controlled study. N Engl J Med 1986;314:1407–1413. 7. Smith GR Jr, Rost K, Kashner TM. A trial of the effect of a standardized psychiatric consultation on health outcomes and costs in somatizing patients. Arch Gen Psychiatry 1995;52:238–243.

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8. Dickinson WP, Dickinson LM, deGruy FV, Main DS, Candib LM, Rost K. A randomized clinical trial of a care recommendation letter intervention for somatization in primary care. Ann Fam Med 2003;1:228–235. 9. O’Malley PG, Jackson JL, Santoro J, Tomkins G, Balden E, Kroenke K. Antidepressant therapy for unexplained symptoms and symptom syndromes. J Fam Pract 1999;48:980–990. 10. Salmon P, Peters S, Clifford R, Iredale W, Gask L, Rogers A, Dowrick C, Hughes J, Morriss R. Why do general practitioners decline training to improve management of medically unexplained symptoms? J Gen Intern Med 2007;22:565–571. 11. Rosendal M, Bro F, Sokolowski I, Fink P, Toft T, Olesen F: A randomised controlled trial of brief training in assessment and treatment of somatisation: effects on GPs’ attitudes. Fam Pract 2005;22:419–427.

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INDEX Page numbers printed in boldface type refer to tables or figures.

Assertiveness training, 121, 123 Assessment, as intervention technique, 124 Ataque de nervios, 25, 31, 47, 48 Attentional processes, and cultural influences on symptom experience, 28, 29 Attribution, and cultural influences on symptom experience, 28, 29, 32. See also Reattribution model Avoidance, and cultural influences on symptom experience, 28, 29

Abridged somatization (AS), 43 Afferent nerves, and immune-to-brain communication, 69 Africa, and cultural models for symptom experience, 25, 47 Age, and diagnostic stability of somatoform disorders, 93 Alexithymia, 118 Amplification, of symptom self-reports, 66, 68, 70 Analgesics, 135 Anthropology, and views of culture, 20, 21, 23 Antidepressants evidence-based studies of treatment and, 145, 149, 153, 155, 156, 157–158, 159 for functional symptoms and syndromes, 135, 138 for medically unexplained symptoms (MUS), 107, 108–109, 115, 123 noncardiac chest pain and, 138 recommendations on treatment and, 167 Antipsychotic drugs, 135 Anxiety disorders comorbidity with somatoform disorders, 1–6 noncardiac chest pain and, 137 Anxiolytic drugs, 138 Aristotle, 12 Arthralgia, and fibromyalgia, 11–12 Asian Americans, and cultural influences on symptom experience, 25

Barsky, Arthur, 66 Beard, George, 55 Behavior brain proinflammatory cytokines and illness-related, 69 cultural influences on, 20 Behavioral therapy, and evidence-based studies of treatments, 158. See also Cognitive-behavioral therapy Benzodiazepines, 79 Biofeedback treatment, 119, 123 Bioenergetics exercises (BE), 122 Body dysmorphic disorder cognitive-behavioral therapy for, 110 comorbidity with substance use disorders, 79, 80 evidence-based studies of treatment for, 145, 155, 156, 158 Brazil, and epidemiology of idiopathic somatic complaints and syndromes, 46

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Breast cancer, and fatigue, 64, 68 Briquet, P., 43 Canada, and comorbidity of substance abuse with somatoform disorders, 79 Celiac disease, 65 Centers for Disease Control (CDC), 12 Chain complexes, and cultural knowledge about illness, 24 Chest pain. See Noncardiac chest pain China approach to symptoms in traditional medicine of, 54, 57 neurasthenia in, 55–61 Chinese Classification of Mental Disorders (CCMD), 59 Chronic fatigue syndrome. See also Functional somatic syndromes aerobic exercise and, 119 cognitive-behavioral therapy for, 110, 111 controversies on, 133 criteria overlap with fibromyalgia, 11, 12, 13 culture and explanatory models for, 27 differences and commonalities with other functional somatic syndromes, 14 medically unexplained symptoms (MUS) and, 104 Classification. See also DSM-III; DSMIII-R; DSM-IV; DSM-IV-TR; DSM-V cultural models and rethinking of, 33– 34 of idiopathic somatic complaints and syndromes, 44 treatment efficacy studies and, 124, 139–140 Clinical vignettes, and ethnic/cultural examples, 49 Clomipramine, 158 Cochrane Library databases, 105, 106, 158 Cognitive-behavioral models, for functional somatic syndromes, 15

Cognitive-behavioral therapy (CBT) evidence-based studies of treatment and, 145, 146–152, 153, 154, 155, 156–159 for functional symptoms and syndromes, 135, 138 for medically unexplained symptoms (MUS), 106, 107, 109–111, 121, 123–124, 125 for noncardiac chest pain, 138 Cognitive restructuring, and recommendations on treatment, 165, 167 Comorbidity of anxiety and depressive disorders with somatoform disorders, 1–6 of idiopathic somatic complaints and syndromes and psychiatric disorders, 45 of substance use disorders with somatoform disorders, 76–84 Composite Diagnostic Interview (CDI), 2, 94 Composite International Diagnostic Interview (CIDI), 44, 61 Consultation letters evidence-based studies of treatment and, 145, 146–147, 158 for medically unexplained symptoms (MUS), 106, 112, 114, 117, 118, 120 treatment recommendations and, 167 Conversion disorder diagnostic stability of, 91 evidence-based studies of treatment for, 145, 155, 156, 158 Coping strategies, and cultural influences on symptom experience, 29, 32 Coronary heart disease, 68 Culture. See also China; Ethnicity definitions of terms, 20–22 diagnostic stability and, 92–93 epidemiological research on, 31–32 explanatory models on symptom reporting and, 22–24

Index idioms of distress and, 26–27 idiopathic somatic complaints and syndromes, 46–50 influence of on symptom experience, 24–25 looping effects and somatic amplification, 27–30 neurasthenia in China and, 60–61 Cytokines, studies on brain effects of, 69. See also Proinflammatory cytokines Dependence, and substance use disorders, 76 Depression Chinese concept of neurasthenia and, 58, 59, 60 chronic fatigue syndrome and cooccurrence of , 13 comorbidity of with somatoform disorders, 1–6 diabetes and, 137 immune system and, 69 noncardiac chest pain and, 137 recommendations on treatment and, 167 Dhat syndrome, 25, 26, 61 Diabetes, and depression, 137 Diagnosis cultural influences on systems of, 27 difficulty of formulating, 165–166 misdiagnosis of somatoform disorders and, 71, 96 patient’s perspective on functional somatic syndromes and, 15 stability of symptoms and, 89–98 symptom threshold for somatoform disorders and, 81–82 Diagnostic Interview Schedule (DIS), 44 Disability cultural influences on symptom experience and, 28, 29 diagnostic stability and, 95–96 Distress, cultural idioms of, 26–27, 31– 32, 46, 47, 48 DSM-III

173 Chinese concept of neurasthenia and, 56, 57, 58 functional somatic syndromes and, 10 introduction of somatoform disorders in, 54–55, 56, 64, 75, 132, 139 DSM-III-R, and neurasthenia, 58 DSM-IV functional symptoms and syndromes in, 132 idiopathic somatic complaints and syndromes in, 44 substance use disorders in, 76 undifferentiated somatoform disorder in, 82 DSM-IV-TR diagnosis of somatization disorder in patients with multiple somatic complaints and, 90 medical explanations for symptoms and, 98 substance use disorders in, 76, 77 DSM-V concepts of somatoform disorders in China and, 59, 60–61 diagnostic stability and, 96–98 evidence-based studies of treatments and, 159 functional symptoms and syndromes in, 132, 139–140 idiopathic somatic complaints and syndromes in, 49 Duration, of symptoms and diagnostic stability, 93–94 Dysthymia, and comorbidity with somatoform disorders, 2, 3, 80 Early Developmental Stages of Psychopathology study, 2 Economic factors, and cultural influences on symptom experience, 28, 29 Ecstasy (drug), 79 EMBASE, 105, 108 Emotional exacerbation, and cultural influences on symptom experience, 28, 29

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Epidemiological Catchment Area (ECA) study, 2, 25, 48, 79, 83 Epidemiology. See also Prevalence of comorbidity of anxiety and depressive disorders with somatoform disorders, 2–6 of comorbidity of substance use disorders with somatoform disorders, 78–81 of idiopathic somatic complaints and syndromes, 44–46 research on cultural models and, 31–32 Ethnicity. See also Asian Americans; Culture; Hispanic Americans need for more precise definition of concept, 49 research on culture and, 20 Etiology, of functional symptoms and syndromes, 132–133 Exercise evidence-based studies of treatment for, 145, 149, 156 as treatment for medically unexplained symptoms (MUS), 119, 122, 123 Explanatory model, for cultural influences on symptom reporting and experience, 21, 22–25 Explanatory therapy, 145, 150, 156 Exposure therapy, 150, 151 Family, and cultural influences on symptom experience, 28, 29. See also Family therapy; Parental modeling Family history studies, of comorbidity of substance abuse with somatoform disorders, 80 Family therapy, for medically unexplained symptoms (MUS), 112 Fatigue, and breast cancer, 64, 68. See also Chronic fatigue syndrome Fibromyalgia aerobic exercise and, 119 cognitive-behavioral therapy for, 110, 111 overlap of criteria with chronic fatigue syndrome, 11, 12, 13

Five-factor model, of functional somatic syndromes, 16 Fluoxetine, 152, 155, 156, 158 Freud, Sigmund, 14 Functional gastrointestinal disorder (FGD), 4 Functional somatic syndromes (FSS) complementary and traditional medicine for, 136 definition of, 9–10 etiology of, 132–133 fulfillment of criteria for multiple syndromes, 12–14 organization of care for, 136–137 patient’s perspective on, 15–16 psychosomatic view of, 15 question of overlap in criteria for, 11–12 similarities and differences in phenomenology of, 10, 14, 16 specific and nonspecific treatments for, 135–136, 139 symptomatic treatments for, 134–135 taxonomy of, 11 treatment priorities for, 133–134 use of term, 132 General anxiety disorder (GAD), and comorbidity with pain disorder, 3 General Health Questionnaire (GHQ), 44 German National Health Interview and Examination Survey, 3 Germany comorbidity of substance use disorders with somatoform disorders, 78– 79 prevalence of somatization disorder in, 45, 46 Greece, and comorbidity of substance use disorders with somatoform disorders, 80 Group therapy evidence-based studies of treatment and, 148, 149 for medically unexplained symptoms (MUS), 109, 110, 111, 121, 125

175

Index Hacking, Ian, 30 Hamilton Anxiety Scale (HAMA), 116 Health care. See also Illness; Medical diseases; Medical specialization; Primary care cost of somatoform disorders in, 143 cultural influences on symptom experience and, 28, 29 limited access to in China, 60 Hebbian learning, and cultural knowledge about illness, 24 Hepatitis C, 66 Herbal medicine, 136. See also St. John’s wort Hispanic Americans, and countries of origin, 49 Hwa-byung (fire illness), 25, 26, 61 Hypochondriasis cognitive-behavioral therapy for, 110 cultural influences on symptom experience and, 28 evidence-based studies of treatment for, 145, 155, 156, 158 Hypnosis, 145, 151 Hysteria, 30, 43 Idiopathic somatic complaints and syndromes (ISCS) brief history of concept, 42–43 culture-specific somatic symptoms and, 46–50 epidemiology of, 44–46 psychiatric nosologies and, 44 Illness. See also Medical diseases brain proinflammatory cytokines and behavioral components of, 69 cultural knowledge about, 21 Immune factors, and somatic symptoms, 68–71 India, and cultural influences on symptom experience, 25, 47 International Classification of Diseases10th Revision (ICD-10), 44, 47, 59 International Classification of Diseases11th Revision (ICD-11), 132, 139–140

Interpersonal interaction, and cultural influences on symptom experience, 28, 29 Intoxication, and substance use disorders, 77 Irritable bowel syndrome. See also Functional somatic syndromes cognitive-behavioral therapy for, 111 differences and commonalities among functional somatic syndromes and, 14 medically unexplained symptoms (MUS) and, 104 overlap of criteria with chronic fatigue syndrome and fibromyalgia, 13 psychodynamic psychotherapy for, 112 Japan, and neurasthenia, 56 Kleinman, A., 58 Knowledge, and cultural influences on beliefs about illness, 21 Korea, and Hwa-byung, 25, 26 Levosulpiride, 120 Lifetime disorders, versus present state diagnosis, 92, 97 Looping effects, and cultural influences on somatic amplification, 27–30, 31– 32, 33 Major depression, and comorbidity with somatization disorder, 2, 3 Medical anthropology, 21, 23 Medical diseases, misdiagnosis of somatoform disorders as, 96. See also Illness Medically unexplained symptoms (MUS) antidepressants for, 107, 108–109, 115, 123 consultation letters and, 114 psychological therapy for, 106–107, 109–114, 123–124 use of term, 103–104, 166 Medical specialization, and functional somatic syndromes, 14

176

Somatic Presentations of Mental Disorders

Medications, use of by patients with somatization disorder, 84 MEDLINE, 90, 105, 108, 144 Memory, and reports of past symptoms, 82, 92 Meningitis, 11, 12 Multicomponent nurse care management intervention, 145, 156 Multiple chemical sensitivity, 13. See also Functional somatic syndromes Multisomatoform disorder, 43, 94, 117 National Epidemiologic Survey of Alcohol and Related Conditions (NESARC), 45 Neural imaging studies, and understanding of symptom perception, 67–68 Neurasthenia, in China, 55–61 Nigeria, and cultural influences on symptom experience, 47–48 Noncardiac chest pain cognitive-behavioral therapy for, 110, 111 esophagitis and, 135, 137 as example for treatment of functional symptoms and syndromes, 137–139 Obsessive-compulsive disorder, and comorbidity with somatization disorder, 2 Obstructive sleep apnea (OSA), 65 One syndrome hypothesis, for functional somatic syndromes, 15 Opipramol, 147, 155, 158 OVID database, 105 Pain and pain disorder. See also Noncardiac chest pain association between anxiety and depressive disorders and, 3, 5 as inherently subjective, 67–68 sleep disruption and threshold for, 65 somatic amplification and perception of, 70

Panic disorder comorbidity of with somatization disorder, 2, 3 cultural influences on symptom experience in, 28 Paradoxical intention, 145, 151 Parental modeling, and cultural influences on symptom experience, 30. See also Family Pathophysiology, and immune-to-brain communication, 68–71 Pathoplasticity, of functional somatic syndromes, 14 Patience, and treatment recommendations, 166 Personality, and coping strategies, 29 Pliny the Elder, 66 Political factors, and cultural influences on symptom experience, 28, 29 Polysymptomatic somatizers, 111 Population-based research, on comorbidity of anxiety and depressive disorders with somatoform disorders, 2–3 Posttraumatic stress disorder (PTSD), and comorbidity with somatization disorder, 2, 3 Present state diagnosis, versus lifetime disorder, 92, 97 Prevalence. See also Epidemiology of somatization disorder, 45 of undifferentiated somatoform disorder, 82 Primary care. See also Health care dimensional constructs and concepts of somatization in, 44 epidemiology of idiopathic somatic complaints and syndromes and, 45–46 Problem-solving approach, for medically unexplained symptoms (MUS), 113, 123 Proinflammatory cytokines, and immune system, 68–71, 70

Index Prototypes, and cultural knowledge about illness, 21, 23 PsychINFO, 105, 108 Psychodynamic psychotherapy, for medically unexplained symptoms (MUS), 106, 112, 123–124. See also Psychotherapy Psychological therapy, for medically unexplained symptoms (MUS), 109–111 Psychoneuroimmunology studies, of somatic symptoms, 68–71 Psychosocial factors, in functional somatic syndromes, 15 Psychosocial interventions, for medically unexplained symptoms (MUS), 106, 107, 111, 113, 118, 123 Psychotherapy. See also Cognitivebehavioral therapy; Family therapy; Group therapy; Psychodynamic psychotherapy evidence-base studies of treatment and, 146, 149 for medically unexplained symptoms (MUS), 118 PubMed, 76, 78, 90 Puerto Rico cultural influences on symptom experience in, 25, 48 prevalence of somatization disorder in, 45 Reassurance, and noncardiac chest pain, 138 Reattribution model. See also Attribution evidence-based studies of treatment and, 149 for medically unexplained symptoms (MUS), 112–113, 118 Relaxation therapy, 119, 123, 148 St. John’s wort, 116, 117, 123, 147, 148, 155, 158 Selective referral, and treatment recommendations, 166–167

177 Selective serotonin reuptake inhibitors (SSRIs) evidence-based studies of treatments and, 158 psychiatry in China and, 60 Shenjing shuairuo. See Neurasthenia Sick role, and cultural influences on symptom experience, 30 Side effects, of substance use, 76 Sleep and sleep disturbance chronic fatigue syndrome and, 15 pain threshold and, 65 Social factors, and strategies of coping, 29, 30 Social institutions, and cultural knowledge about illness, 21 Social phobia, 80 Sociocultural approach, to phenomenon of somatization, 33–34 Somatic amplification, and cultural influences on symptom experience, 27–30 Somatic distress, and cultural idioms, 26– 27, 31–32 Somatic Symptom Index (SSI), 2, 78, 81 Somatization disorder (SD) biofeedback treatment for, 119 comorbidity of with psychiatric disorders, 2, 3 diagnostic stability of, 90, 91, 92 evidence-based studies of treatments for, 155, 156 patience in treatment of, 166 phenomenology of, 43 prevalence rates for, 45 psychiatric consultation for, 120 psychosocial interventions for, 111 psychotherapy for, 121 use of medications by patients with, 84 Somatoform disorders. See also Classification; Comorbidity; Culture; Diagnosis; Functional somatic syndromes; Idiopathic somatic complaints and syndromes; Symptoms; Treatment

178

Somatic Presentations of Mental Disorders

Somatoform disorders (continued) complex factors in misdiagnosis of, 71 definition of, 75 diagnostic accuracy and symptom checklists for, 83 distinct sets of clinical problems concerning, 19–20 dualistic medical system and, 32 heterogeneity of patient presentations, 64 importance of in general medical setting, 143 introduction of in DSM-III, 54–55, 56, 64, 75, 132, 139 neurasthenia in China and, 55–61 self-reporting of symptoms in, 66–68 unrecognized diseases labeled as, 64–66 Spain, and study of idiopathic somatic complaints and syndromes, 46 Specialist physicians, and functional somatic syndromes, 14 Specific treatments, for functional symptoms and syndromes, 135, 139 Stepped care, for functional symptoms and syndromes, 136–137 Stockholm Adoption Study, 80 Stress management, 150 Subarachnoid hemorrhage, 11, 12 Substance use disorders, overlap of symptoms and comorbidity with somatoform disorders, 76–84 Subtypes, of somatization disorder, 43 Sweden, and comorbidity of substance abuse with somatoform disorders, 80 Sydenham, T., 43 Symptom(s). See also Diagnosis; Medically unexplained symptoms (MUS) cultural models and experience of, 24–30 diversity of in functional somatic syndromes, 10 explanatory model for cultural influences on reporting of, 21, 22– 24 misattribution of cause of, 82–83 recall of past, 82, 92 self-reporting of, 66–68, 95

threshold for diagnosis of somatoform disorders and, 81–82 Symptom Checklist 90 (SCL-90), 44, 95, 113 Temporal patterns, of comorbidity between anxiety and depressive disorders and somatoform disorders, 5–6 Temporomandibular disorder, 13 Therapeutic alliance, and recommendations on treatment, 167 Traditional medicine, for functional symptoms and syndromes, 136. See also China Treatment, studies on efficacy of. See also Antidepressants; Cognitivebehavioral therapy; Psychosocial interventions; Psychotherapy evidence-based reviews of psychological interventions, 144– 159 functional symptoms and syndromes in primary and outpatient settings, 133–140 noncardiac chest pain and, 137–139 pharmaceutical and nonpharmaceutical interventions for medically unexplained symptoms (MUS), 105–125 recommendations for evidence-based methods of, 166–168 Undifferentiated somatoform disorder (USD), 82, 145 Validity, and diagnostic stability, 89 Venlafaxine, 147, 155 Whitley Index, 113 Withdrawal, and substance use disorders, 76, 77 World Health Organization (WHO), 46, 47, 82, 90 World Mental Health Surveys, 45 Writing disclosure, as treatment technique, 145, 146