Somatoform Disorders (WPA Series in Evidence & Experience in Psychiatry Volume 9)

VOLUME

9 Somatoform Disorders Editors

Mario Maj University of Naples, Italy

Hagop S. Akiskal University of California, San Diego, USA

Juan E. Mezzich Mount Sinai School of Medicine, New York, USA

Ahmed Okasha Ain Shams University, Cairo, Egypt

WPA Series Evidence and Experience in Psychiatry

VOLUME

9 Somatoform Disorders

WPA Series Evidence and Experience in Psychiatry

Other Titles in the WPA Series Evidence and Experience in Psychiatry Volume 1—Depressive Disorders 1999 Mario Maj and Norman Sartorius ISBN 0471999059 Depressive Disorders, Second Edition 2003 Mario Maj and Norman Sartorius ISBN 0470849657 Volume 2—Schizophrenia 1999 Mario Maj and Norman Sartorius ISBN 0471999067 Schizophrenia, Second Edition 2003 Mario Maj and Norman Sartorius ISBN 0470849649 Volume 3—Dementia 1999 Mario Maj and Norman Sartorius ISBN 0471606987 Dementia, Second Edition 2003 Mario Maj and Norman Sartorius ISBN 0470849630 Volume 4—Obsessive-Compulsive Disorder 1999 Mario Maj, Norman Sartorius, Ahmed Okasha and Joseph Zohar ISBN 047187163X Obsessive-Compulsive Disorder, Second Edition 2003 Mario Maj, Norman Sartorius, Ahmed Okasha and Joseph Zohar ISBN 0470849665 Volume 5—Bipolar Disorder 2002 Mario Maj, Hagop S. Akiskal, Juan Jos´e L´opez-Ibor and Norman Sartorius ISBN 0471560375 Volume 6—Eating Disorders 2003 Mario Maj, Katherine Halmi, Juan Jos´e L´opez-Ibor and Norman Sartorius ISBN 0470848650 Volume 7—Phobias 2004 Mario Maj, Hagop S. Akiskal, Juan Jos´e L´opez-Ibor and Ahmed Okasha ISBN 0470858338 Volume 8—Personality Disorders 2005 Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha ISBN 0470090367 Volume 9—Somatoform Disorders 2006 Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha ISBN 0470016124

VOLUME

9 Somatoform Disorders Editors

Mario Maj University of Naples, Italy

Hagop S. Akiskal University of California, San Diego, USA

Juan E. Mezzich Mount Sinai School of Medicine, New York, USA

Ahmed Okasha Ain Shams University, Cairo, Egypt

WPA Series Evidence and Experience in Psychiatry

Copyright  2005

John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex PO19 8SQ, England Telephone (+44) 1243 779777

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Contents List of Review Contributors Preface

xiii xv

CHAPTER 1 SOMATIZATION AND CONVERSION DISORDERS

1.1 1.2

1.3 1.4 1.5

1.6 1.7 1.8

1.9

1.10

Somatization and Conversion Disorders: A Review Harold Merskey and Fran¸cois Mai COMMENTARIES From Hysteria to Somatization Francis Creed Somatoform and Conversion Disorders or Somatic Presentations of Mental Disorders? Javier I. Escobar Are Somatoform Disorders a Distinct Category? Gregory E. Simon Somatoform Disorders: Deconstructing a Diagnosis Oye Gureje The Psychobiology of Somatization and Conversion Disorders C. Robert Cloninger and Mehmet Dokucu Patient or Process? Linda Gask Reading the Body? Leslie Swartz Somatization and Conversion Disorders: A Forgotten Public Health Agenda? Shekhar Saxena A Cognitive Account on Conversion and Somatization Disorders Karin Roelofs Labelling the Unfathomable Bart Sheehan

1 1

23

26 29 31

34 38 40

42

44 47

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1.11 Somatization and Conversion: An Ongoing Controversy Carsten Spitzer and Hans J¨orgen Grabe 1.12 The Mind–Body Dualism and Conversion Disorders Carlo Faravelli and Massimo Lai 1.13 Concepts of Medically Unexplained Symptoms in Relation to Mind-Body Dualism Athula Sumathipala 1.14 A Challenge for Both Clinicians and Researchers Antonio Lobo 1.15 Somatization Disorders in the African Context Frank G. Njenga, Anna N. Nguithi and Rachel Kang’ethe 1.16 Somatization and Conversion Disorders: An Arab Perspective Tarek A. Okasha 1.17 Much Theory, but Little Agreement Alberto Perales and H´ector Chue CHAPTER 2 PAIN DISORDER

2.1

2.2

2.3 2.4 2.5

2.6 2.7

Pain Disorder: A Review Steven A. King COMMENTARIES The Major Paradigm Shift from the Biomedical Reductionist to the Biopsychosocial Approach to the Assessment and Treatment of Pain Robert J. Gatchel DSM and Pain: When (if Ever) Is Pain Truly a Psychiatric Disorder? Robert Boland Pain Disorder or Just Pain: Can We Escape Dualism? Robert G. Large and Tipu Aamir The Mind–Body Dichotomy in the Modern World Hans J¨orgen Grabe and Carsten Spitzer Chronic Pain: Towards a Biopsychosocial Perspective Michael Bach and Martin Aigner Pain Disorder: Where’s the Utility? Lance M. McCracken Patients Must Be at the Centre of Pain Management Joanna M. Zakrzewska

50 52

55 57 59

62 65

67 67

93

96 98 101

102 105 107

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2.8 Chronic Pain: the Importance of a Comprehensive History Gerald M. Aronoff 2.9 Psychological and Physiological Factors in Pain Disorder Morten Birket-Smith 2.10 Does the Somatoform Disorder Approach Broaden Our Perspective on Pain? Wolfgang Hiller and Paul Nilges 2.11 Diagnosis and Treatment of Pain: Consultation-Liaison Psychiatry Aspects Albert Diefenbacher 2.12 Pain: Suffering, Semantics, and Sensitization Jeffrey Rome 2.13 Subjectivity and Communitas: Further Considerations on Pain Etzel Cardena ˜ 2.14 The Relationship Between Pain and Anxiety Disorders Antonio Bulbena, Carlos Garcia Ribera and Lili Sperry 2.15 Gaps in Evidence Base of Pain Disorders Santosh K. Chaturvedi 2.16 Pain in General Practice Manuel Suarez Richards and Gustavo Alfredo Delucchi CHAPTER 3 HYPOCHONDRIASIS

3.1

3.2 3.3

3.4

Hypochondriasis: A Review Russell Noyes Jr. COMMENTARIES Hypochondriasis: Future Directions in Classification and Etiology Research Steven Taylor and Gordon J.G. Asmundson Making Sense of Hypochondriasis Jonathan S. Abramowitz Hypochondriasis: An Endless Source of Controversies? Vladan Starcevic Hypochondriasis: Defining Boundaries, Exploring Risk Factors and Immunology Eamonn Ferguson

110

112

114

117 119

121

123 125 127

129 129

161 164

167

170

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3.5 Hypochondriasis, Health Anxiety, and Cognitive-Behavioural Therapy Patricia Furer and John R. Walker 3.6 Progress with Hypochondriasis Theo K. Bouman 3.7 The Clinical Spectrum of Hypochondriacal Fears and Beliefs Giovanni A. Fava and Stefania Fabbri 3.8 A Nosological Nightmare Geoffrey G. Lloyd 3.9 Hypochondriacal Syndromes: Where Did They Go? Driss Moussaoui 3.10 Dimensional versus Categorical Approach to Obsessions, Delusions, and Hypochondriasis Joseph Zohar 3.11 The Nosographic Complexity of Hypochondriasis and the Ambiguity of the Body H´ector P´erez-Rinc´on 3.12 Hypochondriasis: Is There a Promising Treatment? Tewfik K. Daradkeh CHAPTER 4 BODY DYSMORPHIC DISORDER

4.1 4.2

4.3

4.4

4.5

Body Dysmorphic Disorder: A Review Giulio Perugi and Franco Frare COMMENTARIES The Complexity of Body Dysmorphic Disorder Vilma Gabbay and Rachel G. Klein Preoccupation with Appearance: Limitations of Our Understanding and Treatment Jon E. Grant Translational and Evolutionary Models of Body Dysmorphic Disorder Dan J. Stein Our Evolving Understanding of Body Dysmorphic Disorder Nancy J. Keuthen and Antje Bohne Is Body Dysmorphic Disorder a Culturally Determined Expression of a Body Image Disorder? David H. Gleaves and Suman Ambwani

172 174

177 179 181

183

185 187

191

191

222

224

226

228

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4.6 Body Dysmorphic Disorder: Awareness Needed Don E. Jefferys 4.7 Recent Findings in Body Dysmorphic Disorder and Future Directions Sabine Wilhelm and Ulrike Buhlmann 4.8 Body Dysmorphic Disorder: Some Issues Concerning Classification and Treatment Fugen Neziroglu 4.9 Body Dysmorphic Disorder: The Antithesis of Narcissus Andrew A. Nierenberg 4.10 Playing the Devil’s Advocate: Is the Concept of Delusional Disorder, Somatic Type, Condemned to Extinction? Leonardo F. Fontenelle, Mauro V. Mendlowicz and Marcio Versiani 4.11 Advancing the Understanding of Body Dysmorphic Disorder Eric Hollander and Bernardo Dell’Osso 4.12 Is Body Dysmorphic Disorder More than a DSM Construct? Michel Botbol 4.13 Body Dysmorphic Disorder and Obsessive–Compulsive Disorder: More Similarities than Differences Euripedes C. Miguel, Albina R. Torres and Ygor A. Ferr˜ao CHAPTER 5 CHRONIC FATIGUE AND NEURASTHENIA Chronic Fatigue and Neurasthenia: A Review Michael C. Sharpe and Simon Wessely COMMENTARIES 5.1 From Neurasthenia to Chronic Fatigue Syndrome: A Journey, Not a Destination Kurt Kroenke 5.2 Tired People Challenge Medicine Stefan Priebe 5.3 Disease, Sickness or Illness: Which One Is Chronic Fatigue Syndrome and/or Neurasthenia? Bedirhan Ustun

ix

233

235

237

240

241

244

247

249

253

253

285 287

291

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5.4 Constructing Chronic Fatigue: Empiricism, Psychiatry, and Sociocultural Contexts Ren´ee R. Taylor 5.5 Chronic Fatigue Syndrome as a Paradigm for Psychosomatic Medicine James L. Levenson 5.6 Beyond Fashion Gordon Parker 5.7 Chronic Fatigue and Disembodied DSM Sing Lee and Arthur Kleinman 5.8 Problems of Definition, Etiological Approaches and Issues of Management in Chronic Fatiguing Disorders Anne Farmer and Tom Fowler 5.9 Chronic Fatigue Syndrome: Time to Concentrate on Fatigue, Not Chronicity Petros Skapinakis and Venetsanos Mavreas 5.10 Chronic Fatigue Syndrome: A Real Disease, A Real Problem Jonathan R. Price 5.11 The Specificity of Chronic Fatigue, Neurasthenia, and Somatoform Disorders Winfried Rief 5.12 Chronic Fatigue in Developing Countries Vikram Patel 5.13 Functional Somatic Syndromes: Many Names for the Same Thing? Marco Antonio Brasil, Jos´e Carlos Appolin´ario and Sandra Fortes 5.14 Recent Developments in Chronic Fatigue Syndrome Ruud C.W. Vermeulen 5.15 Does Neurasthenia Really Exist in this Century? Edmond Chiu CHAPTER 6 FACTITIOUS PHYSICAL DISORDERS Factitious Physical Disorders: A Review Stuart J. Eisendrath and John Q. Young COMMENTARIES 6.1 Wilful Deception as Illness Behaviour Christopher Bass

294

297 299 302

305

308

311

313 316

319

321 323

325

325

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CONTENTS

6.2 Factitious Disorders: Diagnosis or Misbehaviour? Charles V. Ford 6.3 Factitious Disorder and Malingering: The Doctor’s Dilemma Stephen M. Lawrie and Michael C. Sharpe 6.4 Factitious Physical Disorders: The Challenges of Efficient Recognition and Effective Intervention Lois E. Krahn 6.5 Some Aspects of Factitious Physical Disorders by Proxy Christopher Cordess 6.6 Inventing Illness: The Deviant Patient Don R. Lipsitt 6.7 Characterizing Factitious Physical Symptoms David G. Folks 6.8 Moral Constraints, Regret, and Remorse in Treating Patients with Factitious Disorder Ovidio A. De Le´on 6.9 Fact, Fiction, Factitious, or Fractious Disorders Dinesh Bhugra 6.10 Factitious Physical Disorders: A Strategy of Survival for Medically Trained Traumatized Borderlines? Ramon Florenzano 6.11 Factitious Physical Disorders and Malingering: The Hazardous Link Sa¨ıda Douki, Sara Benzineb and Fathy Nacef Index

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358

360

363 366 369

372 375

376

378

381

List of Review Contributors Stuart Eisendrath Langley Porter Psychiatric Hospital and Clinics, University of California at San Francisco, 401 Parnassus Avenue, San Francisco, CA 94143-0984, USA Franco Frare Adults Mental Health Unit, Pistoia Zone, Pistoia, Italy Steven A. King New York University School of Medicine, 308 E. 38th St., #19A, New York, NY 10016, USA Fran¸cois Mai Department of Psychiatry, Ottawa General Hospital, Medical Advisory Unit, 355 River Road, Ottawa, Ontario, K1A 0L1, Canada Harold Merskey University of Western Ontario, 71 Logan Avenue, London, Ontario, N5Y 2P9, Canada Russell Noyes Jr. Psychiatry Research, Medical Education Building, Iowa City, IA 52242-1000, USA Giulio Perugi Department of Psychiatry, University of Pisa, Via Roma 67, 56100 Pisa, Italy Michael C. Sharpe School of Molecular and Clinical Medicine and Symptoms Research, The Kennedy Tower, Royal Edinburgh Hospital, Edinburgh EH10 5HF, UK Simon Wessely King’s Centre for Military Health Research, Institute of Psychiatry, King’s College London, Weston Education Centre, Cutcombe Rd., London SE5 9RJ, UK John Q. Young Langley Porter Psychiatric Hospital and Clinics, University of California at San Francisco, 401 Parnassus Avenue, San Francisco, CA 94143-0984, USA

Preface This book reviews one of the most controversial and challenging areas of modern psychiatry. In fact, patients who present with somatic symptoms that remain ‘‘medically unexplained’’ pose a variety of conceptual and practical problems. First of all, they bring along the issue of Cartesian mind–body dichotomy, a conceptual frame that has been frequently criticized, but keeps on influencing our thinking and our nosology. This issue recurs in all the chapters of the book. In the chapter on pain disorder, several contributors emphasize the difficulty in evaluating, as requested by the DSM-IV, the relative role of physical and psychological factors in the genesis of pain, and underline the inadequacy of such a dualistic approach. In the chapter on somatization and conversion disorders, the high rate of neurological illness in patients receiving the diagnosis of conversion disorder is repeatedly emphasized. In the chapter on chronic fatigue and neurasthenia, the continuing oscillations between a predominantly biological and a predominantly psychogenic interpretation of the disorder, and their social and ‘‘political’’ implications, are clearly shown. The fact that both medically explained and medically unexplained somatic symptoms are frequently associated with mood and anxiety disorders is mentioned as a further evidence of the uncertainty of the boundary between the two categories of symptoms. The frequent ‘‘comorbidity’’ between somatoform disorders and other mental disorders (especially mood and anxiety disorders) poses the problem of whether the former category should be kept separate or should be subsumed under other diagnostic headings. This issue emerges in almost all the chapters of the book, in particular, in the discussion concerning the relationship between hypochondriasis and anxiety disorders, between body dysmorphic disorder and obsessive–compulsive disorder, and between somatization disorder and major depression. Many psychiatrists might suggest that somatization is an integral part of several mental disorders or an alternative manifestation of mood or anxiety disorders. However, in many instances, irrespective of one’s nosological assumptions, a clinical presentation with somatoform manifestations does raise therapeutic challenges beyond a classical mood or anxiety disorder. This may well be the reason why clinicians working in the interface of psychiatry and medicine find the concept of somatoform disorders still useful.

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PREFACE

The uncertainty of the boundary between conscious and unconscious production of somatic symptoms and signs, and the frequent switch of the same patient from unconscious ‘‘hysterical’’ behaviour to deliberate deception, is emphasized in the chapter on factitious disorders. This provides a rationale for the inclusion of these disorders in the volume, despite the fact that they are separated from somatoform disorders in current classification systems. On the practical side, the frustration often experienced by physicians when confronted with somatoform disorders and, at the same time, the need to establish an effective therapeutic relationship, including a legitimation of the patient’s symptoms, represents a recurring theme in the volume. The message that ‘‘management begins with examination’’ (i.e., management begins by showing that the time spent in history taking and examination is proportionate to the importance of the symptoms to the patient) is probably the one that emerges most frequently from the various chapters. The need for a sustained involvement of the physician and an ongoing health monitoring is repeatedly emphasized, as well as the requirement of the patient’s active collaboration for the success of cognitive–behavioural therapy. The comparison with the other volumes of the series ‘‘Evidence and Experience in Psychiatry’’ shows that somatoform disorders have been a relatively infrequent target for randomized controlled trials, both on the psychotherapeutic and the psychopharmacological sides, which clearly contrasts with their high prevalence and the very significant financial and emotional burden they place on the community. Probably due to this, and to the above-mentioned conceptual and practical problems posed by these disorders, the ‘‘experience’’ (as opposed to ‘‘evidence’’) component of this book is more substantial than in the other volumes of the series. This input may represent a stimulus for innovative research planning. The geographic representation in the authorship of this book is even broader than in the other volumes of the series: the contributors are from 35 different countries, representing all the continents and all the geographic zones of the WPA. This reflects the importance of the cultural dimension in the development and manifestation of somatoform disorders and emphasizes the need to take this dimension into account in future approaches to their diagnosis and classification. The paper on the diagnosis of neurasthenia in China is particularly instructive in this respect, as are the reports on somatization disorders from Arab countries. The readership of this book is expected to be slightly different from that of the other volumes of the series, including not only psychiatrists and other mental health workers, but also general practitioners and other medical specialists. These colleagues will probably appreciate the clinical orientation of all the chapters of the book and the deliberate attempt to avoid the use of a strictly psychiatric jargon.

PREFACE

xvii

It is our hope that this volume will be useful to psychiatric and nonpsychiatric professionals in their clinical practice and will contribute significantly to the ongoing debate on this challenging area of psychiatry and public health. Mario Maj Hagop S. Akiskal Juan E. Mezzich Ahmed Okasha

CHAPTER

1 Somatization and Conversion Disorders: A Review Harold Merskey1 and Fran¸cois Mai2 1 2

University of Western Ontario, 71 Logan Avenue, London, Ontario, N5Y 2P9, Canada Department of Psychiatry, Ottawa General Hospital, Medical Advisory Unit, 355 River Road, Ottawa, Ontario, K1A 0L1, Canada

INTRODUCTION Most bodily symptoms in the present categories of somatization fall into two groups. One group comprises symptoms that are involuntary and automatic, depending on arousal in the autonomic nervous system. They often appear with depression as well as anxiety. The second group of symptoms depends upon thoughts or embodies intentions, and yet these thoughts and ideas are not recognized, or are not acknowledged, by the patient. In discussing this topic, it helps to distinguish these two groups of symptoms both phenomenologically and aetiologically. Allocating a symptom to the second group, however, may be difficult because, sometimes, autonomic symptoms can be adopted and utilized as reflecting ideas. Cardiac palpitations are a good example, particularly if associated with chest discomfort. In that case what perhaps begins as an autonomic response may become a response, or a cognitive event, permitting retreat or escape from a difficult cognitive problem. Because our present notions exist in a changing framework of concepts and observations, it helps to discuss the meaning of the physical symptoms of psychological origin as it has evolved sequentially. We begin with the term hysteria, which is much older than conversion disorder, which in turn is older than somatization.

HISTORICAL BACKGROUND The recognition of hysterical symptoms is thought to date back to Hippocrates. The evidence for this is limited. The Hippocratic Collection of Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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writings contains a number of entries that describe treatments that would assist the womb to return to its place. Sometimes these treatments were provided from below, that is, through the vagina, and sometimes they were provided from above, whether through the nostrils or as liquids. Medieval theorists held that the Greeks believed in a migration of the womb, downwards or upwards, sometimes by virtue of unsatisfied sexual drive. Historians, for example Veith [1], wrote that these ideas were obtained from the ancient Egyptians, but re-reading the available texts from the Papyri that were supposed to provide this information leaves considerable doubt as to whether the Egyptians had such ideas at all [2], and claims about the Greek belief are also uncertain. There is no full English version of the Hippocratic Collection, but the French version by Littr´e [3] described several phenomena that could be diagnosed as ‘‘hysterical’’, including hysterical suffocation (‘‘hysterike pnix’’). This phenomenon gave rise to the idea that the womb could move around the body, block the channels of respiration and cause ‘‘suffocation’’. However, King [4] pointed out that the Littr´e translation introduced headings to organize the concept of hysteria as hysterical suffocation, an organization absent from the original material. Micale [5] remarked that the Littr´e edition contains ‘‘no coherent clinical syndrome in the modern sense but only the most casual enumeration of symptoms including laboured breathing, loss of voice, neck pain, heart palpitations, dizziness, vomiting, and sweating’’ and that there was no clear reference to globus hystericus or hyperesthesia. King [4] further noted that ‘‘suffocation of the womb’’ was probably an incorrect translation, and that the original Greek ‘‘hysterike pnix’’ more likely means stifling and implies heat as well as difficulty in breathing. Galen, the leading anatomist of ancient times, concluded that the womb was fixed and did not move about the body. It seems that the descriptions of the womb moving around were a dramatic elaboration of the fact that sometimes the womb might swell, as in pregnancy, or drop, as in prolapse. Supposedly, hysterical symptoms could come and go and often did move away, or return under the influence of particular psychological circumstances, so that the idea developed that they might be due to witchcraft. This idea was widespread through Europe. Protestant pastors, like Roman Catholic priests, exorcised devils to cure distressed young women [6]. Charcot, as an early nineteenth-century neurologist, was similarly keen to show that medicine could provide a better explanation of ‘‘possession’’ than the Church [7]. An explanation of hysterical symptoms as a consequence of psychological trauma was provided by Sydenham [8], the leading British physician of his day: ‘‘When the mind is disturb’d by some grevious Accident, the animal Spirits run into disorderly motions. . . .Whatsoever part of the body the Disease doth affect (and it affecteth many) immediately the symptoms that

SOMATIZATION AND CONVERSION DISORDERS: A REVIEW

3

are proper to that Part appear; in the Head, the Apoplexy, which ends in a Palsy of one half of the Body. . . sometimes they are seiz’d with Convulsions, that very much resemble the Epilepsy. . . At other times they are miserably tormented with the Hysterical Clavus [nail], in which there is a most vehement pain in the Head. . .’’. Sydenham mentioned other pains in addition to the hysterical clavus, and also diarrhoea, dropsy (oedema), tears, and laughter. Nowadays, we would recognize some of these changes as due to the presence of brain damage or as related to anxiety or depression. According to Micale [5], ‘‘In the 18th century the disorder slid imperceptibly into hypochondria, the vapours, and in the 19th century it often overlapped with neurasthenia, nymphomania, general nervousness. . . Many. . . have used the word in reference to any nervous malady with convulsive complications. . . Many physicians have complained vociferously about the vagueness and indefinability of hysteria’’. By the mid-nineteenth century, the concept of hysteria involved numerous bodily symptoms, often with episodic exacerbations [9, 10]. By the time of Paul Briquet [11], hysteria was considered to be a life-long disorder, cerebral in origin, almost always found in young women, characterized by pains in any part of the body, paralysis of limbs, anaesthesias, certain types of fits, dyspnea, pharyngeal globus, dysphagia, hiccup, vomiting, meteorism, dysuria, and urinary retention. Briquet published an extensive clinical and demographic study [12, 13] and described the clinical patterns in detail under seven headings. He associated the disorder with a ‘‘neurosis of the brain’’ and emphasized the importance of heredity. More astutely, Sir Benjamin Brodie [14] observed that there was no clear organic cause for hysterical complaints but ‘‘. . .it is not the muscles which refuse to obey the will, but the will itself which has ceased to work’’. Ideas about hysteria fluctuated during the nineteenth century. This is the period, however, in which many of our existing concepts seem to have grown strong. In particular, there was an increasing recognition of the fact that socalled hysterical symptoms appeared to be related to ideas. The first to bring this out explicitly was Sir John Russell Reynolds [15], and his views were quickly adopted and assimilated by Charcot, the leading French neurologist of his day. These insights were stimulated by increasing neurological skill in the evaluation of symptoms. Sigmund Freud made the last apparent major nineteenth century contribution to hysteria by explaining physical symptoms that seemed to be due to the loss of the patient’s will as caused by the repression of ideas into the unconscious. That view is now vigorously challenged because of increasing doubts about the value of psychoanalysis, its lack of empirical support, and even the truthfulness of Freud’s original accounts [16, 17]. The term somatization is more recent. Wilhelm Stekel [18] wrote of ‘‘organspr¨ache’’, or ‘‘organ speech’’, which was translated as ‘‘somatization’’,

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possibly a mistranslation [19]. The word became popular when Lipowski [20] offered a definition that he later amended to read ‘‘the tendency to experience and communicate somatic distress and symptoms unaccounted for by pathological findings, to attribute them to physical illness and to seek medical help for these’’ [21].

THE CONCEPT OF CONVERSION DISORDER The central issue in understanding and appraising physical symptoms with presumed psychological causes concerns the nature of their development. Are they a consequence of psychophysiological events, or do they follow from a process through which ideas give rise to complaints? The way in which the latter conclusion is reached depends particularly on neurological examination. For example, if a patient reports that he or she cannot move a leg, the neurologist who tests motor power will determine if there are obvious signs of physical difficulty, for example, spasticity, clonus, a positive Babinski test or signs of parkinsonism and extra-pyramidal rigidity, or a flaccid paralysis, as after spinal cord injury. If the limb appears to be healthy, but is still unable to move, the neurologist will undertake a procedure such as the Hoover test, in which one hand is placed under the affected heel and the patient asked to lift the leg or press down, and no response is found. Thereafter, the patient will be asked to lift the good leg while the hand remains under the original heel. If there is motor power in the leg where the patient thinks it has been lost, the synergistic action of the musculature will cause the patient to press down with the supposedly paralysed leg and the pressure will be felt by the examining hand underneath the heel. This kind of evidence was called positive signs of hysteria by Head [22]. In the case of the special senses, it is relatively easy to establish positive tests of visual or auditory function that will belie the patient’s claims. With other sensory conditions, the commonest error is to attribute regional pain or regional loss of sensation to hysterical mechanisms. Regional symptoms may correspond to an idea in the mind of the patient and for this reason diffuse anaesthesia or a regional pain in a limb were taken as an example of hysterical complaints. Increasing knowledge has shown that pain interferes with light touch and other cutaneous sensations and that both pain and light touch may have a regional distribution resulting from alterations in the activity of the nervous system. While some anaesthetic lesions correspond to dermatomal distributions or nerve root patterns, other patterns of pain often develop from organic disease. This happens also with pain affecting the musculature, or with pain affecting a limb, so that the appearance of a regional pain due to thoughts may be mimicked although the physiological situation is abnormal [23].

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5

The late Patrick Wall and many of his colleagues working on the neurophysiology of pain repeatedly demonstrated that the spread of regional pain and sensitivity to noxious stimulation or light touch could be linked with pathophysiological mechanisms (24, 25). A number of physical signs have been said to be ‘‘non-organic’’ in patients with musculoskeletal complaints, but Gordon Waddell [26], who extensively investigated these signs, reached the conclusion that they could not be taken as particular evidence of psychological illness and were more likely to be related to severity of pain. The diagnosis of conversion disorder has been complicated by many extraneous impressions, in addition to the difficulty in obtaining consistency as to what is meant by the condition. Concepts such as belle indiff´erence, meaning that the patient seems to be not bothered about a disabling symptom, were popular because they seemed to fit well with a psychodynamic explanation. Since the symptoms solved the problem, the patient would feel happy. But often patients do not feel happy and some leading examples of belle indiff´erence probably involved patients with multiple sclerosis who suffered from difficulties in movement that were thought to be psychological and had frontal lobe lesions that left them more happy than the average patient with paralysis [27, 28]. Gould et al. [29] examined 30 patients with acute neurological illness (29 of them with stroke) and noted the evidence for seven supposedly typical markers of hysteria in these patients. The seven markers were as follows: a history suggestive of hypochondriasis, potential secondary gain, belle indiff´erence, non-anatomical patchy sensory loss, changing boundaries of hypoalgesia, sensory loss (to pinprick or vibratory stimulation) that splits at the midline, and giveaway weakness. The mean number of positive items per patient was 3.4. It was evident that none of these items could provide a consistently reliable basis for diagnosis. There is still a dispute as to whether some tonic contractions may be regarded as due to conversion disorder, particularly if they are not associated with other signs that may be organic, and if they occur in some situations where potential benefit may accrue to the patient from being disabled. This argument arises about ‘‘writer’s cramp’’ and the repetitive pain syndromes that may be found in workers using computers. The commonest current interpretation seems to be that repetitive use syndromes are better regarded as aberrant habits of muscular usage than as being due to a motivated loss of use or function. It is generally accepted that classical conversion disorders are now rare in developed societies. When they occur, they are most often diagnosed (whether correctly or otherwise) in individuals who have compensation claims, or who find themselves in difficult social situations. In developing societies, classical conversion disorder persists [30].

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The diagnosis, and even the terminology for hysteria, has been disputed over many years. The word was rejected in DSM-III and avoided thereafter in ICD-9 and ICD-10, but still figures commonly in historical writings and in the topics favoured by social historians. Instead of hysteria, it has become customary to write of conversion disorders, that is, those involving bodily complaints, and dissociative disorders, that is, those involving loss of the mental function, particularly, memory or awareness of special events. Dissociative disorders are dealt with elsewhere in this series, but the same principles apply to their labelling (which will be in need of change) as they apply here to the labelling of conversion disorders. They too can be understood to reflect ideas that patients have about their condition. In response to difficulties with theories of repression affecting the concepts of both conversion disorders and dissociative disorders, Merskey [31] suggested that we should use the term ‘‘doxogenic disorders’’ for both the groups. This term refers to complaints caused by having the idea of a particular symptom or disorder. A more neutral term, ‘‘doxomorphic disorders’’ [32], might be further preferred since it merely indicates complaints having the form of a symptom related to an idea.

THE CONCEPT OF SOMATIZATION DISORDER As originally described in DSM-III, somatization disorder was based upon the earlier work of Cohen et al. [33] and Perley and Guze [34]. The manual required a history of many physical complaints over several years, beginning before age 30. The patient had to have sought treatment or shown significant impairment in social, occupational or other important areas of functioning, and had to present at least 14 symptoms if female and 12 if male, from a list of 37 items. Symptoms had to be found in each of seven groups: feeling sickly, conversion or pseudo-neurological symptoms, gastrointestinal symptoms, female reproductive symptoms, psychosexual symptoms, pain, and cardiopulmonary symptoms. The DSM-IV criteria for somatization disorder are much less stringent. There have to be four pain symptoms related to at least four different sites, two gastrointestinal symptoms other than pain, one sexual symptom other than pain, and one pseudo-neurological symptom or deficit suggesting a neurological condition not limited to pain. The symptoms are not to be fully explicable by a known general medical condition or the direct effects of a substance. When there is a related general medical condition, the physical complaints or resulting social occupational impairment have to be in excess of what would be expected from the history, physical examination or laboratory findings. The symptoms are not to be produced by a factitious disorder or malingering. The history of physical complaints should begin before age 30, occurring over a period of several years and resulting in treatment being

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sought or significant impairment occurring in social, occupational or other important areas of functioning. ICD-10 requires ‘‘cases’’ of somatization disorder to show at least two years of multiple and variable physical symptoms for which no adequate physical explanation has been found, persistent refusal to accept the advice or reassurance of several doctors, and some degree of impairment of social and family function attributable to the nature of the symptoms and resulting behaviour. This classification does not provide a cut-off for the diagnosis. This is not necessarily an undesirable approach to providing diagnostic guidelines. The concept of somatization disorder remains controversial. According to Kirmayer [35], somatization is neither a discrete clinical entity nor the result of a single pathological process, but cuts across diagnostic categories. Kirmayer and Robbins [36] proposed three operational definitions of somatization: a) high levels of functional somatic distress, measured by a somatic symptom index; b) hypochondriasis, measured by high scores on a measure of illness, worry, and the absence of evidence of serious illness; c) exclusively somatic presentations among patients with current major depression or anxiety. The three forms of somatization are associated with different sociodemographic and illness behaviour characteristics. The majority of patients meet criteria for only one type of somatization, suggesting that distinct pathogenic processes may be involved with each of the three types. In addition, somatization appears to be more, rather than less, likely in the presence of organic disease. According to Merskey [23], in clinical practice and in research reports, the term somatization is evidently used in a variety of ways, which can be summarized approximately as follows: a) somatization disorder; b) conversion symptoms; c) hypochondriasis; d) heightened bodily awareness (alerting) resembling hypochondriasis but, unlike the latter, responding to reassurance on examination or investigation; e) psychophysiological events associated with anxiety or depression; f) certain types of somatic complaints in schizophrenic patients, perhaps with a delusional basis, for example hypochondriacal psychosis; g) any of the above, combined with organic disease. This variety of meanings rivals the number of meanings or subdivisions that have historically been offered for hysteria, despite the fact that somatization is a far younger term.

EPIDEMIOLOGY OF CONVERSION DISORDER A study of the incidence of hysterical neurosis, conversion type, or conversion disorder in terms of DSM-III, compared findings in Monroe County, New York, and in Iceland, based upon the same 10 years [37]. In Monroe County, a retrospective examination of case records from hospitals and practitioners was undertaken, while the Icelandic figures were taken from a psychiatric register. The overall rate in Monroe County was 22/100,000 per annum,

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while in the second half of the period it was only 15/100,000 per annum. In Iceland, the rate was 11/100,000 per annum. The rate fell year by year throughout the 10 years in Monroe County, and there was a small similar change in the annual rates in the Icelandic figures. In both the countries, it was thought that the continuing fall in the rates might have been partly influenced by increasing scepticism with respect to the diagnosis of hysteria. The rates were twice as high for men as for women in Monroe County and almost 5 times as high for women in Iceland. A third group of subjects was also studied, namely, a series of 64 patients seen in the psychiatric service of a university general hospital whose records were also examined for the same time period, 1960–1969. Among these individuals with diagnoses of hysterical neurosis, conversion type, or a conversion disorder, 39 had pain and 32 were overtly or covertly depressed. Eight were considered to be misdiagnosed. A good prognosis is reported from developing countries [30, 37], while, in Western society and tertiary practice, patients tend to have a poor prognosis unless they are very early cases. The largest follow-up study is by Ljungberg [38], in a highly selected group from the practice of the University Hospital in Stockholm. After one year, 43% of men and 35% of women were still symptomatic. By five years, the figures were 25% and 22%, respectively. On the other hand, acute cases may recover very promptly with limited treatment. The sample and selection are immensely important in determining the outcome, and population studies are infrequent. Epidemic hysteria has long been known [39]. Outbreaks still occur, even in developed societies, and many examples have been recognized since the early nineteenth century. Modern examples were provided by cargo cults in Melanesia when islanders abandoned their normal activities because of a prophecy that a ship or an aeroplane would arrive laden with many welcome goods. The ship was expected to be manned by the benevolent spirits of ancestors [40]. Psychological contagion was considered to characterize these events. In Western society, Sirois [41] reported two epidemics in schools in Quebec and surveyed altogether 70 reports out of 78 that had appeared in the world literature from 1872 to 1972.

EPIDEMIOLOGY OF SOMATIZATION DISORDER Using criteria based on DSM-III, Escobar et al. [42] reported that the lifetime prevalence of somatization disorder varied between 0.2% and 2% in women, while in men it was likely to be less than 0.2%. Similar data were reported by Canino et al. [43]. Farley et al. [44] found one case in a sample of 100 post-partum women, agreeing with similar findings by Majerus et al. [45] and Murphy et al. [46].

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Guze [47], using very strict diagnostic criteria, found somatization disorder in 5–11% of a sample of psychiatric outpatients (according to our interpretation of their paper). About 10% of psychiatric inpatients in a university hospital were reported to be similarly affected [48]. The epidemiology of somatization disorder thus depends greatly upon the mode of definition, but most community physicians with, say, 1,000 patients can expect five or 10 patients satisfying relatively weak criteria to exist in their practices. Not all of them may be recognized and some physicians may attract more such patients than others. The broader term of somatization is applied to many physical symptoms at large when they lack full explanation. In a recent review, Kirmayer et al. [49] summarized knowledge on medically unexplained symptoms and estimated that they comprised 15 to 30% of all primary care consultations. Not all of these should necessarily be regarded as having what has been called somatization disorder. Kirmayer pointed out that physicians often assume that psychological factors account for these symptoms, but current theories of psychogenic causation and somatic amplification could not fully account for common unexplained symptoms. Kirmayer also argued that psychological explanations are often not communicated effectively, do not address patients’ concerns and may lead patients to reject treatment or referral because of potential stigma. Many systems of medicine in different cultures provide social and somatic explanations linking problems in the family and the community with bodily distress. Accordingly, most patients could have culturally based explanations available for their symptoms. Once the bodily nature and the cultural meaning of their suffering is validated, most patients will acknowledge that stress, social conditions and emotions have an effect on their physical condition. Using a telephone survey in a community sample of 2,400 individuals, Kirmayer et al. [50] reported that 10.5% of respondents had at least one unexplained symptom in the last 12 months. The most common symptoms reported were similar in both sexes and these corresponded to symptoms found in other studies of primary care. Musculoskeletal pain affected 30.3% of the respondents; abdominal pain and other gastrointestinal symptoms affected 17.7%; ear, nose and throat symptoms affected 7.8%; fatigue affected 3.9%; and dizziness affected 3.5%. Their sample included five groups with different ethno-cultural background and migration history: anglophone-Canadian born, francophoneCanadian born, immigrants from the Caribbean, immigrants from Vietnam, and immigrants from the Philippines. There was no difference across cultural groups but, when results were stratified by sex, Vietnamese men were significantly more likely to report unexplained symptoms than were women (18.3% versus 7.2%). This is in marked contrast to the usual finding that

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such symptoms are more common among women, and the authors argue that this may reflect the high rates of exposure to trauma in this sample, which included many refugees, combined with male reticence in reporting psychosocial and emotional distress that would help explain the symptoms. If we compare these cases from no-man’s land with the criteria for somatization disorder in DSM-IV, it is noteworthy that the latter system requires that each symptom must have been appropriately investigated and cannot fully be explained by a known general medical condition or the direct effects of a substance and that, where there is a related general medical condition, the physical complaints should be in excess of what would be expected from the history of physical examination or laboratory findings. In the DSM-IV, the residual category exists of ‘‘undifferentiated somatoform disorder’’. Like all residual categories in classification systems that have to provide for all cases, the criteria are less stringent than for the index condition. An extended use of the notion of undifferentiated somatoform disorder is demonstrated in a paper by DeWaal et al. [51] on somatoform disorders in general practice. In this study, the authors arranged a standardized diagnostic interview in which they recorded a prevalence of somatoform disorders of 16.1% among 1,046 consecutive patients of general practitioners. The prevalence increased to 21.9% when comorbid disorders were included, and ‘‘comorbidity of somatoform disorders and anxiety/depressive disorders was 3.3 times more likely than expected by chance’’. These results could only be achieved by assuming that the ‘‘comorbid somatoform’’ condition was to be diagnosed even in the presence of mood or anxiety disorders. In reaching these figures, the authors sidestepped the hierarchical DSM-IV rule that undifferentiated somatoform disorders should not be diagnosed in the presence of another mental illness (including an anxiety disorder or mood disorder) which would better account for the condition. Even if this rule were to be observed, their findings would suggest that, after deducting the individual frequencies of anxiety and depressive disorders, 6.5% of all cases in general practice would still meet their criteria for somatization disorder or undifferentiated somatoform disorder (8.1% if one includes also ‘‘mild’’ cases). This study mostly seems to tell us that physical symptoms are common, but does not give us the true proportion of physical symptoms that may have to be explained in some purely psychological fashion without the psychophysiological explanations that could apply in the presence of anxiety or depression. Overall, broader criteria obviously enlarge the scope of the diagnosis and increase the frequency or number of diagnoses to be anticipated. They have been used by Kirmayer et al. [49] and by Mai [52] to develop information about the social and individual factors which influence the presentation of somatic symptoms in medical practice. The same may apply to the study by De Waal et al. [51]. This benefit is achieved at a price, which is the risk

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that all these numerous somatic and incompletely explained symptoms will continue to be interpreted in traditional psychodynamic terms. We agree with Sharpe and Mayou [53], who emphasized the limitations of the somatoform disorder classification, for example, the evidence suggesting that its aetiology is likely to be multi-factorial, including physiological as well as psychological and social factors [54]. Curiously, epidemiological studies have found a higher prevalence of somatization disorder when the interviewers are physicians. Perhaps this finding indicates that an interviewee is more likely to describe a medical history to a physician than to a non-physician. It has also been found that the prevalence is higher when the assessment interview is done face-to-face than when it is done by telephone. These factors must be taken into consideration when comparing epidemiological surveys and may, at least in part, explain the differences in prevalence that have been found in different studies.

ECONOMIC AND SOCIAL COSTS A retrospective study of 13,314 consultations in a consultation-liaison service found that somatization disorder caused disability and unemployment more frequently than any other psychiatric disorder [55]. Bass et al. maintained that somatization disorder has ‘‘few peers’’ in terms of morbidity and cost to society and health care services [56]. This cost is aggravated by the fact that these patients are frequently poorly managed by their physicians [57]. The huge expense and poor outcome of invasive surgical and medical procedures have been well-documented [58, 59]. Some argue that these problems and the increased utilization of health care services are aggravated by the progressive medicalization of physical distress, in which uncomfortable bodily states are reclassified as diseases for which medical treatment is sought [60]. Another study of frequent medical attenders at a health clinic found that patients with medically unexplained symptoms had greater costs of medical investigations than did other frequent attenders [61]. An unusual approach that connected somatization and health care utilization was taken by Ciechanowski et al. [62]. They hypothesized that there would be a link between attachment style and somatization. They identified two attachment styles, preoccupied and fearful, and found that, although both correlated with somatization, only the preoccupied style was associated with increased utilization. The fearful style, in fact, correlated with decreased utilization. Although both attachment styles were associated with increased dependency on others, only the fearful was coupled with avoidance of caregivers. The authors made practical recommendations: for example, they recommended that patients with preoccupied attachment require regularly scheduled, frequent brief visits that could be carried out more cost-effectively

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by nurses, nurse practitioners, and social workers. Patients with fearful attachment may work better with a group of health care providers such as may be found in a cohesive clinic. Although these findings are tentative, they are novel and deserving of further study. There appear to be four reasons why these patients are poorly managed by physicians: ignorance of the condition, the drive to rule out organic disease, the discomfort of many physicians when exploring psychological issues, and the fear of missing an organic disease [63]. To these may be added the inability of many physicians to live with uncertainty, and the unwillingness to go with their judgement [64].

BIOLOGICAL CORRELATES At first sight, it may seem surprising that we are even discussing the biological correlates of conditions that, for many years, have been the focus of intensive psychodynamic speculation. However, when one examines the issues carefully, a connection between somatization and organicity could be expected, and it may take one or more of the following three forms. Biological changes and organic conditions may be part of the antecedent stimuli that precipitate somatization, or a pre-existing pathophysiological change may lower the threshold for the development of a somatic symptom, or biological changes may be the consequence of functional impairment that may accompany somatization. The most frequent correlate described in the literature is with disturbed cerebral function, but there are pathophysiological correlates with other organs and systems. In addition, a genetic component to somatization and conversion has been identified. An association between hysteria as historically defined and cerebral pathology has been described by a number of authors. Both Slater [65] and Merskey and Buhrich [66] found that a high proportion of people with hysteria had associated cerebral pathology, in particular, epilepsy and multiple sclerosis. However, these authors were studying patients in a neurological hospital setting. In a comparable study of hysteria patients in a psychiatric hospital setting, Roy found that only 3% had identifiable cerebral pathology [67]. Flor–Henry et al. found that patients with ‘‘hysteria’’ (with chronic multiple symptoms) were more likely to have cerebral impairment, particularly affecting the non-dominant hemisphere, than healthy controls, and a comparable group of patients with a psychiatric illness [68]. It has also been proposed that both hysteria and hypochondriasis are cerebral dysfunctions associated with inhibition of afferent stimulation interfering with attention and recent memory [69]. A retrospective study of 21 ‘‘hysterics’’ found that six had objective evidence of brain dysfunction: in four, there was clinical or neurological evidence of cognitive impairment, one had encephalitis, and one dyslexia [70].

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Another controlled study of 17 hospitalized patients with conversion hysteria showed that they had heightened suggestibility, greater field dependency, and greater impairment of recent memory, vigilance, and attention [71]. Abnormalities of motor evoked potentials have been found in patients with phantom limb pain compared to amputees who do not have pain [72]. Impaired neuropsychological performance in patients with somatoform disorder has been confirmed in a more recent controlled study [73]. On the other hand, Meyer found that magnetic evoked potentials in patients with limb weakness caused by psychogenic factors were normal, contrary to patients with weakness caused by organic disease [74]. With reference to non-cerebral conditions, Kristal–Boneh [75] carried out 24-h blood pressure monitoring in 114 healthy, normotensive men. They were also interviewed as to the presence of somatic symptoms. A positive association was found between systolic blood pressure and somatic complaints score. Another study found that cortisol levels and heart rates were elevated in patients with somatic symptoms compared to normal controls [76]. Recently, it has been found that tryptophan, branched chain amino acids, and other serotoninergic amino acids were decreased in patients with somatoform disorders, even when no depression was present [77]. These studies suggested that physiological changes accompany the activation associated with somatization. Such physiological changes may even help to perpetuate the condition by making the individual more conscious of bodily function. A problem exists with all these studies in disentangling the cause-effect, post hoc-propter hoc phenomenon. Finding a pathophysiological abnormality in a group of patients with somatization or conversion disorder does not prove that the organic abnormality preceded, and therefore might have caused the condition. The physical finding may have been a consequence of ‘‘somatization’’, or it may even have been a coincidental finding. There is a great need for longitudinal studies, particularly those where a physical assessment preceded the onset of the condition. Genetic factors may also contribute to the development of somatization disorder and conversion disorder, although the research findings are not consistent [78–80]. In the nineteenth century, Paul Briquet found a strong tendency for family clustering to occur in hysteria [11–13]. This may be the result of either genetic or environmental influences and it is likely that both play a role. Cloninger et al. [81] found that male relatives of a patient with Briquet’s syndrome had increased prevalence of antisocial personality and alcoholism and that female relatives of a male prison population revealed a high prevalence of Briquet’s syndrome [82]. These authors found that hysteria in women was a more prevalent and less deviant manifestation of the same process that causes sociopathy in men and that somatization disorder had a different familial pattern in women, compared to men. Another study of women (n = 859) who had been adopted at an early age by non-relatives

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found that the adoptees had a significant excess of somatizers, compared with a non-adopted control group. The parents of the adoptees were known to have excess numbers who showed criminal or psychotic behaviour [83]. We infer from these studies that, although genetic factors play a role in these conditions, the effect is a limited one. The specific mode of inheritance is not known, but it is most likely polygenic.

MANAGEMENT A summary of the principles governing the management of somatization disorder can be found in Table 1.1. The management of these conditions begins with the examination. The first essential is to demonstrate that the extent of the history-taking, the examination, and the investigation are all appropriate

T A B L E 1.1

Management of somatization disorder

General principles a) Perform a comprehensive clinical assessment (history, mental state, and physical examination) b) Interview key family member c) Minimize number of clinicians involved. Ensure a consistent, coordinated management plan d) Minimize invasive diagnostic/therapeutic procedures e) Ensure regular, structured sessions. Avoid unnecessary visits to doctors and emergency departments f) Recognize reality of symptoms and provide diagnostic feedback to both patient and family member. Where appropriate, link symptoms to stressful life events g) Identify and minimize secondary reinforcers h) Treat associated medical and psychiatric conditions appropriately. Cognitive behavioural therapy i) Develop treatment ‘‘contract’’ (approximate frequency, duration, and number of sessions) j) Set realistic short- and long-term goals. Review these regularly k) Focus on practical ways of coping with symptoms and limitations l) Encourage patient to keep daily log of thoughts, feelings, and coping behaviours. Review these regularly m) Promote daily physical, social, recreational, and occupational activities n) Promote daily relaxation activities and exercises o) Promote patient control and autonomy. Pharmacotherapy p) Minimize use of habit-forming drugs q) Avoid unnecessary medication r) Use antidepressant medication where appropriate. Reproduced from [52] by permission of the Canadian Journal of Psychiatry

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to the importance of the symptoms to the patient. Some temporary somatic symptoms will respond to reassurance after history-taking and focussed physical examination. At all stages in this process, the patient should be encouraged to feel that the symptoms are being taken seriously, both for their psychological importance and their physical potential. This is no more than good practice, but it helps to maintain a relationship with the patient that can carry through to guidance in different life situations that may contribute to the patient’s state. Most types of discussion of ‘‘worries’’ that might be troubling the patient can be used sympathetically to evaluate circumstances that may have promoted a problem. Pharmacological interventions should be considered if the somatic complaint is associated with depressed mood or anxiety, even if the symptom is of the conversion type. Thus, a patient with a moderately severe depressive disorder and a complaint of weakness, thought to be somatoform in nature, or dizziness, or even paralysis of a limb, should be provided with antidepressants. Patients who are being treated for physical illness with medication that may influence their mental status will require specific attention. For example, increased serum levels of anticonvulsants such as phenytoin, above the normal upper limit, may be associated with a conversion disorder paralysis that remits with little problem once the serum level of the anticonvulsant has been adjusted [84]. Likewise, a patient who has taken an overdose of medication and developed what is apparently a psychological ataxia may recover promptly once the intoxication is reduced. Many types of suggestion have been employed for patients with conversion disorders or physical symptoms that are thought to have a conversion basis. Commonly, such measures as hypnosis, relaxation, physiotherapy, including massage or exercises encouragement, ‘‘retraining’’, and a variety of other supportive techniques have been used to provide improvement. Improvement may result from a direct emotional benefit through medical support, or from the passage of time and a natural cure of some symptoms or situations. Patients may turn up feeling much better after a brief course of treatment and disclose that in the interim worry over something has been resolved, an unpleasant colleague has moved, a debt has been paid, a partner has changed attitudes, and so forth, without themselves tying the improvement to what seems an obvious potential cause for a change in feelings. Even changes in administrative procedures have been found to affect utilization. Zhang et al. found that implementation of a Medicare prospective payment scheme decreased hospital admissions and health expenditure, but it is not clear from this study whether this change also improved health and well-being [85]. Behavioural measures, including cognitive behavioural therapy, are often recommended, and we favour the cognitive element more than

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the behavioural one, as do most psychologists currently in the Englishspeaking world. Indeed, cognitive behavioural therapy is the most efficacious treatment in somatization disorder. A critical review of 31 controlled studies published prior to 2000 concluded that cognitive behavioural therapy should be used either as the first-line treatment or as treatment for patients who fail simpler strategies [86]. The cost-effectiveness of short-term group psychotherapy [87], training family doctors in specific intervention techniques [88], short-term intervention [89], and a single psychiatric consultation including specific recommendations to the family physician [90] have all been demonstrated. Hiller et al. carried out a controlled study using a cognitive behavioural therapy program on a group of 172 patients with various forms of somatoform disorder. Prior to their treatment, the somatoform patients’ costs were 2.2 times higher than average for patients in the system. At two year follow-up, after cognitive behavioural therapy, outpatient costs were reduced by 24.5%, and inpatient costs by 36.7%. Indirect socio-economic costs due to lost days from work decreased by 35.3%, and per patient savings of 63.9% were achieved in a subgroup of high utilizers [91]. There is still an important place for supportive psychotherapy. This is best carried out by a physician who is sympathetic and understanding toward the patient’s particular difficulties and who is able to respond appropriately to both the physical and emotional problems presented. The advantage of the therapist being a physician arises particularly from the fact that most patients with somatization disorder will be more comfortable with explanations that come from a medical source than from one that is purely psychological. Group sessions in this situation must be regular, structured, and consistent and have to focus on understanding the symptom and the patient’s circumstances. So long as patients feel that they have had a thorough evaluation of their physical problems, management of their psychological status becomes more feasible. There will always be some patients, however, who have a need for long-term support, which may not have to be more frequent than once a month or even once in two months, but whose symptoms are kept in abeyance and become less troublesome so long as they have a friendly authority figure to whom they feel they can turn. There may be a need for treatment goals and sometimes a treatment contract in which aims such as the number and frequency of sessions and a requirement to do homework may be stated clearly. For homework, patients can be asked to read certain relevant literature, to keep a diary, to record their feelings and thoughts, and to bring these copies back to the treatment session for discussion. Quite frequently it may be appropriate to work with the patient’s spouse and family. In more intractable cases, particularly those in which conversion disorder is diagnosed rather than somatization disorder, very special techniques may be used. One of the most sympathetic and perceptive approaches has

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been described by a distinguished neurologist who demonstrated how it was possible to manage a patient with a paralysis of the legs which was apparently relieved by hypnosis and then relapsed. Gentle enquiry into the ultimate basis for the patient’s symptoms—which solved a psychosocial problem for her—led to a social adjustment with face-saving provisions for the patient, who was able to ‘‘resume’’ normal health [92]. In another approach to such cases, Shapiro and Teasell [93] employed a double-bind method in which the patient’s physician and a psychologist provided contrasting views to the patient. One (the physician) told the patient he thought that the condition was psychological and that the patient would not get better. The other argued that it was not a psychological disorder but a physical one from which recovery was possible with physiotherapy. Each of the two therapists would minimize the importance of his colleague’s belief to the patient. Thirteen out of 21 patients with highly intractable motor disorders recovered with the use of this regime. The difficulty with this approach is that it involves deception and deliberate misleading of patients. The benefit is that it provides an effective technique for otherwise persistently disabled individuals to lose their symptom with the help of subsequent management and adaptation. More discussion of the justification for this approach is desirable.

SUMMARY Consistent Evidence Symptoms of ‘‘somatization’’ or ‘‘conversion’’ are more common in women than in men. Epidemic hysteria occurs most often in relatively undeveloped, underprivileged or immature populations. Motor conversion symptoms can be diagnosed consistently with some neurological techniques. Conversion disorders of the special senses can be consistently diagnosed. The prognosis for the majority of cases of acute conversion disorder is good. The management of conversion and dissociative disorders requires the exclusion of organic disease and recognition that many symptoms are unexplained, or only incompletely explained, and cannot automatically be assumed to be psychological in origin. It requires the provision of psychological support. Powerful methods of suggestion help many patients, but a small group of intractable cases remains. Many somatic symptoms form part of anxiety, depressive or other recognizable psychological or physical conditions and will improve with appropriate treatment of the concomitant or originating psychiatric or physical conditions.

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Incomplete Evidence Epidemiological figures for somatoform disorder, conversion disorder, and medically unexplained or incompletely explained symptoms are inconsistent, varying with the criteria employed. The level of somatization diagnosed increases with the liberality of the diagnostic procedures. Biological factors may precipitate or promote conversion type symptoms. This occurs particularly in patients with pre-existing physical illness affecting the nervous system. The evidence that cognitive and behavioural techniques are effective remains incomplete.

Areas Still Open to Research The frequency of so-called ‘‘somatization’’ symptoms and their characteristics are both open to much further research, as are the diagnostic procedures for somatization and conversion disorders. The evidence for the mechanisms of production of conversion disorders is poor. The effects of selection on the effectiveness of cognitive and behavioural techniques in somatization disorders require further study.

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Veith I. (1965) Hysteria: The History of a Disease. University of Chicago Press: Chicago. Merskey H., Potter P. (1989) The womb lay still in ancient Egypt. Br. J. Psychiatry 154: 751–753. Littr´e E. (1839–1861) Oeuvres Compl`etes d’Hippocrate. Bailli`ere: Paris. King H. (1994) Once upon a text: the Hippocratic origins of hysteria. In: Hysteria in Western Civilization, S. Gilman, H. King, R. Porter, G. Rousseau, E. Showalter (Eds). University of California Press: Berkeley, pp. 3–90. Micale I. (1989) Hysteria and its historiography: a review of past and present writings. Hist. Sci. 27: 223–261. Walker D.P. (1981) Unclean Spirits: Possession and Exorcism in France and England in the Late and Early XVIIth Centuries. Scholar Press: London. Goldstein J. (1987) Console and Classify. The French Psychiatric Profession in the 19th Century. Cambridge University Press: New York. Sydenham T. (1697) Discourse concerning hysterical and hypochondriacal distempers. In: Dr. Sydenham’s Completa 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., Newman and Parker: London. Dubois d’Amiens E.F. (1833) Histoire Philosophique de l’Hyst´erie. Deville Cavellin: Paris.

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Cloninger R.C., Reich T., Guze S. (1995) The multifactorial model of disease transmission: III. Familial relations between sociopathy and hysteria (Briquet’s syndrome). Br. J. Psychiatry 127: 23–32. Sigvardsson S., Von Knorring A.L., Bohman M., Cloninger R.C. (1984) An adoption study of somatoform disorders. 1: The relation of somatization to psychiatric disability. Arch. Gen. Psychiatry 41: 853–859. Niedermeyer E., Blumer D., Holscher E., Walker B.A. (1970) Classical hysterical seizures facilitated by anticonvulsant toxicity. Psychiatr. Clin. 3: 71–84. Zhang M., Booth B., Smith G. (1998) Services utilization before and after prospective payment system by patients with somatization disorder. J. Behav. Health Serv. Res. 25: 76–82. Kroenke K., Swindle R. (2000) Cognitive-behavioural therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother. Psychosom. 9: 205–215. Kashner T., Rost K., Cohen B., Anderson M., Smith G.R. Jr. (1995) Enhancing the health of somatization disorder patients: effectiveness of short-term group psychotherapy. Psychosomatics 36: 462–470. Morriss R., Gask L., Ronalds C., Downes-Grainger E., Thompson H., Leese B., Goldberg D. (1998) Cost-effectiveness of a new treatment for somatized mental disorder taught to GPs. Fam. Pract. 15: 119–125. Matalon A., Nahmani T., Rabin S., Maoz B., Hart J. (2002) A short-term intervention in a multidisciplinary referral clinic for primary care frequent attenders: description of the model, patient characteristics and their use of medical resources. Fam. Pract. 19: 251–256. Smith C., Monson R., Ray D. (1986) Psychiatric consultation in somatization disorder. N. Engl. J. Med. 14: 1407–1413. Hiller W., Fichter M., Rief W. (2003) A controlled study of somatoform disorders including analysis of health care utilization and cost effectiveness. J. Psychosom. Res. 54: 369–380. Symonds C. (1979) Hysteria: an address given by Sir Charles Symonds at the National Hospitals for Nervous Diseases, Queen Square, London, 27th February 1970. In: The Analysis of Hysteria, H. Merskey (Ed). Gaskell: London, pp. 407–413. Shapiro A.P., Teasell R.W. (2004) Behaviour interventions in the rehabilitation of acute versus chronic non-organic conversion/factitious motor disorders. Br. J. Psychiatry 185: 140–146.

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Commentaries 1.1 From Hysteria to Somatization Francis Creed1 The area of psychiatry covered by Merskey and Mai’s review is riddled with definition difficulties. The terms ‘‘somatization disorder’’ and ‘‘somatization’’ probably cause the greatest confusion. The authors rightly point out that the concept of ‘‘somatization disorder’’, as embodied in DSM-III and DSM-IV, has its roots in the early studies of patients attending specialized clinics. These disorders are defined by an early age of onset and a very large number of bodily symptoms, which are disabling but unexplained by an underlying medical disorder. The relevance of such a concept to modern epidemiological investigations, however, may be negligible [1]. The term ‘‘somatization’’ is used in an entirely different way to indicate numerous bodily symptoms, which are attributed to physical illness and reported to doctors, but whose cause is unknown. Only sometimes can these be shown to be an expression of distress [2]. The term ‘‘medically unexplained symptoms’’ may be preferable in the sense that it is accurate—patients with these symptoms go to doctors, who conclude that the symptoms cannot be explained by an underlying organic disease. A change of terminology, however, is unlikely to rescue us from the difficulties in conceptualizing these disorders. A fresh approach is required, such as that provided by studies in population-based and primary care samples. ‘‘Medically unexplained symptoms’’ is a negative definition reflecting the rather narrow role of some branches of modern medicine that are concerned only with medically explained symptoms. A more positive approach is required to explain why the essentially normal experiences of bodily sensations and illness worry become so prominent in a minority of people. Recent psychological and sociological investigations have provided much useful information. Primary care–based studies have identified three overlapping groups of patients: a) those with somatic symptoms associated with clear anxiety and depression, b) those with a high level of illness worry, and c) those who 1

School of Psychiatry and Behavioural Sciences, University of Manchester, UK

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report high levels of bodily symptoms, but in whom no clear underlying psychological process could be identified [2]. The second group corresponds to hypochondriacal disorder [3] and the first and third groups correspond to somatization disorder. Whether these disorders share a common aetiology with each other and with conversion disorder is still not clear. Clinical reports emphasize their common risk factors, including a female sex predominance, a strong association with anxiety and depression, concurrent chronic physical illness, and stressful life events, but population-based studies do indicate some differences. In population or primary care–based studies, the presence of numerous bodily symptoms, but fewer than those required to diagnose somatization disorder (‘‘abridged somatization disorder’’), occurs in 10–15% of respondents and is associated with female sex (but less strongly than in clinic studies), few years of education and low socio-economic status [1]. It is also associated with impaired health-related quality of life, even after adjusting for other psychiatric disorders and increased health care use [4, 5]. Illness worry, less severe than that defined as hypochondriacal disorder, occurs in 6–7% of the population [1]. It is not associated with female sex, but is closely associated with depression and chronic physical illness and with disability and high health care use [1, 6]. High scores on a dissociative experiences questionnaire are also found in approximately 6% of the general population; they are associated with childhood physical abuse and adult psychiatric disorder [7]. It is not clear how these measures of bodily symptoms, illness worry and dissociation relate to the clinical disorders of somatization, hypochondriacal and conversion disorders in DSM-IV, but the relationship is probably close [3]. The association between hypochondriasis, somatization and conversion with reported childhood abuse found in clinic samples is finding some support from population-based studies [4, 7]. In addition to the existence of such a link, the mediators involved illustrate the importance of adult relationships, including attachment style [8, 9], hypnotic susceptibility [10], dissociation [11], and adult psychiatric disorder. Even after controlling for psychiatric disorders, there is some evidence of a direct association between childhood adversity and the outcomes of high health care use and disability [7, 12]. In fact, psychotherapy leads to a very pronounced improvement in people with reported childhood abuse and irritable bowel syndrome [13]. Future studies will need to take into account also personality and genetic factors, which predispose to develop these states [14, 15]. Finally, a firmer psychological theoretical basis for understanding these processes is developing [16, 17]. Increasingly, it appears that there are greater similarities than differences between conversion, somatization and hypochondriasis ‘‘disorders’’ and these might turn out to be related responses to stress, with the different

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manifestations reflecting different developmental experiences. Indeed, in countries where conversion disorders are frequent, there is evidence of considerable similarity between conversion and somatization disorders [18] and studies from such countries challenge the existing diagnostic schema [18–21]. As our understanding of the aetiology of these disorders develops, we are likely to see them less as distinct disorders and more as overlapping psychological responses; that is when our treatment will substantially improve.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Creed F., Barsky A. (2004) A systematic review of the epidemiology of somatisation disorder and hypochondriasis. J. Psychosom. Res. 56: 391–408. Kirmayer L.J., Robbins J.M. (1991) Three forms of somatization in primary care: prevalence, co-occurrence, and sociodemographic characteristics. J. Nerv. Ment. Dis. 179: 647–655. Gureje O., Ustun T.B., Simon G.E. (1997) The syndrome of hypochondriasis: a cross-national study in primary care. Psychol. Med. 27: 1001–1010. Walker E.A., Gelfand A., Katon W.J., Koss M.P., Von Korff M., Bernstein D., Russo J. (1999) Adult health status of women with histories of childhood abuse and neglect. Am. J. Med. 107: 332–339. Walker E.A., Unutzer J., Rutter C., Gelfand A., Saunders K., Von Korff M., Koss M.P., Katon W. (1999) Costs of health care use by women HMO members with a history of childhood abuse and neglect. Arch. Gen. Psychiatry 56: 609–613. Barsky A.J., Ettner S.L., Horsky J., Bates D.W. (2001) Resource utilization of patients with hypochondriacal health anxiety and somatization. Med. Care 39: 705–715. Mulder R.T., Beautrais A.L., Joyce P.R., Fergusson D.M. (1998) Relationship between dissociation, childhood sexual abuse, childhood physical abuse, and mental illness in a general population sample. Am. J. Psychiatry 155: 806–811. Ciechanowski P.S., Walker E.A., Katon W.J., Russo J.E. (2002) Attachment theory: a model for health care utilization and somatization. Psychosom. Med. 64: 660–667. Biggs A.M., Aziz Q., Tomenson B., Creed F. (2004) Effect of childhood adversity on health related quality of life in patients with upper abdominal or chest pain. Gut 53: 180–186. Roelofs K., Keijsers G.P., Hoogduin K.A., Naring G.W., Moene F.C. (2002) Childhood abuse in patients with conversion disorder. Am. J. Psychiatry 159: 1908– 1913. Salmon P., Skaife K., Rhodes J. (2003) Abuse, dissociation, and somatization in irritable bowel syndrome: towards an explanatory model. J. Behav. Med. 26: 1–18. Kapur N., Hunt I., MacFarlane G., McBeth J., Creed F. (2004) Childhood experience and health care use in adulthood: nested case-control study. Br. J. Psychiatry 185: 134–139. Creed F.H., Guthrie E., Ratcliffe J., Fernandes L., Rigby C., Tomenson B., Read N., Thompson D.G. (2005) Reported sexual abuse predicts impaired functioning but a good response to psychological treatments in patients with severe irritable bowel syndrome Psychosom. Med. 67: 490–499.

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Gillespie N.A., Gillespie N.A., Zhu G., Heath A.C., Hickie I.B., Martin N.G. (2000) The genetic aetiology of somatic distress. Psychol. Med. 30: 1051–1061. Noyes R.J., Watson D.B., Letuchy E.M., Longley S.L., Black D.W., Carney C.P., Doebbeling B.N. (2005) Relationship between hypochondriacal concerns and personality dimensions and traits in a military population. J. Nerv. Ment. Dis. 193: 110–118. Brown R.J. (2004) Psychological mechanisms of medically unexplained symptoms: an integrative conceptual model. Psychol. Bull. 130: 793–812. Holmes E.A., Brown R.J., Mansell W., Fearon R.P., Hunter E.C., Frasquilho F., Oakley D.A. (2004) Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin. Psychol. Rev. 25: 1–23. Guz H., Doganay Z., Ozkan A., Colak E., Tomac A., Sarisoy G. (2004) Conversion and somatization disorders: dissociative symptoms and other characteristics. J. Psychosom. Res. 56: 287–291. Kuloglu M., Atmaca M., Tezcan E., Gecici O., Bulut S. (2003) Sociodemographic and clinical characteristics of patients with conversion disorder in Eastern Turkey. Soc. Psychiatry Psychiatr. Epidemiol. 38: 88–93. Alexander P.J., Joseph S., Das A. (1997) Limited utility of ICD-10 and DSM-IV classification of dissociative and conversion disorders in India. Acta Psychiatr. Scand. 95: 177–182. Syed E.U., Atiq R., Effendi S., Mehmud S. (2001) Conversion disorder: difficulties in diagnosis using DSM-IV/ICD-10. J. Pak. Med. Assoc. 51: 143–145.

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1.2 Somatoform and Conversion Disorders or Somatic Presentations of Mental Disorders? Javier I. Escobar1 Following the Linnaean tradition, medical taxonomies allocate patients into non-overlapping categories on the basis of signs, symptoms and clinical observations authenticated by a set of biological correlates. The definition of disease, disorder or abnormality is a critical element for classification systems. Of several models for psychological abnormalities that exist in the literature, Wakefield’s ‘‘harmful dysfunction analysis’’ [1] was the one incorporated in modern nosologies such as DSM-IV. Such a model implies a subjective element (condition seen as harmful or undesirable) as well as objective features (identification of a malfunctioning internal mechanism). Obviously, the latter remains quite elusive in psychiatry, where, in the absence of objective signs, markers, or biological correlates, we continue to build syndromes (almost 400 in DSM-IV!) on the basis of phenomenological attributes. The ‘‘epidemics’’ of comorbidity plaguing our field is simply a 1 Department of Psychiatry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, New Jersey 08854-5635, USA

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reminder that our syndromes are still imperfect and in need of continuous distillation and that premature closure of nomenclatures is unwarranted. The diagnostic issues enumerated above are particularly pungent in the case of the ‘‘somatoform’’ syndromes. Merskey and Mai provide us with an excellent review of these disorders, and give us particular details on their history with emphasis on traditional syndromes. They distinguish two major forms of somatic presentations that may have phenomenological and aetiological relevance. The first comprises symptoms that are involuntary and automatic, depending on arousal in the autonomic nervous system, which often appear with depression and anxiety disorders. One assumes these may be the less severe syndromes often seen in primary care that may be responsive to psychiatric treatments. The second and more ambiguous form depends upon thoughts, embodied intentions, or ideas that are not recognized or acknowledged, likely representing the more severe, comorbid, treatment refractory syndromes seen in specialty mental health clinics. It can be stated that, in all their forms, ‘‘somatizing’’ patients are the bane of modern medicine. Not fitting anywhere, they land in the vortex of the centuries-old mind/body debate. Somatic presentations have been well documented throughout the years, have always baffled the medical establishment, and have metamorphosed with cultural evolution and the changing perspectives of the medical paradigms [2]. What is intriguing is that these disorders, once so central to traditional psychopathology, fell into disrepute in recent times, being overtaken by other more ‘‘fashionable’’ diagnoses. For example, in primary/specialty care, more ‘‘medicalized’’ labels such as ‘‘chronic fatigue’’, ‘‘temporo-mandibular joint syndrome’’, ‘‘fibromyositis’’, ‘‘environmental disease’’, ‘‘multiple chemical sensitivity’’, ‘‘irritable bowel’’, and many others are now used to classify the ‘‘hysterics’’ and ‘‘hypochondriacs’’ of yesteryear. Somatic presentations add complexity to psychopathology. Morrison and Herbstein [3] first reported that patients diagnosed simultaneously with somatization disorder and affective disorder were more impaired than those who only had affective disorder, an observation confirmed by our group in the case of depressive and anxiety syndromes [4]. Thus, when somatization is present, any comorbid disorder (e.g., depression, diabetes) is rendered much more disabling and difficult-to-treat than when such a disorder is present without somatization. A number of British authors have proposed to eliminate altogether the category of somatoform disorders from current nomenclatures and advise placing this feature in a secondary axis [5]. While not advocating abolition of these diagnoses, our group proposes viewing somatization dimensionally, rather than categorically, arguing that somatic presentations ‘‘color’’ the phenomenology of depression and anxiety disorders, as well as that of ‘‘bona-fide’’ physical disorders [6].

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Primary care is the ‘‘de facto’’ mental health system worldwide. The overwhelming tendency for people with common mental disorders such as depression and anxiety to go to primary care providers and present with physical symptoms is well documented everywhere [7–10]. While some of the people presenting to primary care with somatic symptoms acknowledge psychological issues as contributing factors [11], many others vigorously reject any such labels. These two groups may represent Mersky and Mai’s somatic symptom dichotomy in a primary care setting. Mersky and Mai provide an elegant review of hysteria and conversion symptoms. Physical symptoms that mimic neurological disorder were those generally implicit in the old notion of hysteria (fainting, paralysis, lump in throat, deafness, blindness, paresthesias, etc.) and constitute the essence of the somatoform group. They can be seen frequently as a ‘‘primary’’ syndrome (without other major comorbidities), and appear predictably in response to stressful events or ‘‘psychological’’ conflict. These symptoms have a long, distinguished tradition in psychopathology. In fact, the original construct of Briquet’s syndrome [12] was made up exclusively of pseudo-neurological symptoms until it was modified a century later by the St. Louis group to include many other physical symptoms and psychiatric comorbidities. While newer classifications simply count physical symptoms, research from our group shows that pseudo-neurological symptoms are highly unique and have predictive value [13, 14]. Thus, new nomenclatures ought to accord special weight to this dimension.

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Wakefield J.C. (1992) The concept of mental disorder: on the boundary between biological factors and social values. Am. Psychol. 47: 373–388. Shorter E. (1994) From the Mind into the Body: The Cultural Origin of Psychosomatic Symptoms. Free Press: New York, pp. 90–117. Morrison J., Herbstein J. (1998) Secondary affective disorder in women with somatization. Compr. Psychiatry 29: 433–440. Allen L.A., Gara M., Escobar J.I., Waitzkin H., Silver R.C. (2001) A debilitating syndrome in primary care. Psychosomatics 42: 63–67. Mayou R., Levenson J., Sharpe M. (2003) Somatoform disorders in DSM-V. Psychosomatics 44: 449–451. Escobar J.I., Gara M.A. (1999) DSM-IV somatoform disorders: do we need a new classification? Gen. Hosp. Psychiatry 21: 154–156. Regier D., Goldberg I., Taube C. (1978) The de facto mental health services system. Arch. Gen. Psychiatry 35: 685–693. DeGruy F. (1996) Mental health care in the primary care setting. In: Primary Care: America’s Health in a New Era, M.S. Donaldson, K.D. Yordy, K.N. Lohr, N.A. Vanselow (Eds). National Academy Press: Washington, D.C., pp. 285–311. Simon G., Gater R., Kisely S., Piccinelli M. (1996) Somatic symptoms of distress: an international primary care study. Psychosom. Med. 58: 481–488.

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Gureje O., Simon G., Ustun T., Goldberg D. (1997) Somatization in cross-cultural perspective: a World Health Organization study in primary care. Am. J. Psychiatry 154: 989–995. Araya R., Lewis G.H., Rojas G., Mann A.H. (2001) Patient knows best. Detection of common mental disorders in Santiago, Chile: cross sectional study. Br. Med. J. 322: 79–80. Briquet P. (1859) Traite Clinique et Therapeutique de l’Hysterie. Bailli`ere: Paris. Gara M., Cohen Silver R., Escobar J.I., Holman A., Waitzkin H. (1998) A hierarchical class’s analysis (HICLAS) of primary care patients with medically unexplained symptoms. Psychiatry Res. 81: 77–86. Interian A., Gara M., D`ıaz-Mart`ınez A.M., Warman M.J., Escobar J.I., Allen L.A., Manetti-Cusa J. (2004) The value of pseudoneurological symptoms for assessing psychopathology in primary care. Psychosom. Med. 66: 141–146.

1.3 Are Somatoform Disorders a Distinct Category? Gregory E. Simon1 Somatoform disorders occupy an important place in the history of psychiatric diagnosis and treatment. As reviewed by Merskey and Mai, the effort to understand hysterical or conversion symptoms stimulated much of Freud’s early thinking regarding defences, repression, and unconscious impulses. Studies of somatization disorder during the middle of the twentieth century served as models for modern psychiatric diagnosis. A review of recent epidemiologic and clinical research, however, reveals several arguments against the need for a separate somatoform category. First, the association between somatoform disorders and mood or anxiety disorders is strong enough to raise questions about the distinction between them. Unexplained somatic symptoms are highly correlated with mood and anxiety symptoms across a wide range of clinical and cultural settings [1, 2]. Hypochondriasis also shows strong cross-sectional and longitudinal associations with mood and anxiety symptoms [3]. Somatic distress is a nearly universal companion of psychiatric illness. Second, the boundary between ‘‘medically explained’’ and ‘‘medically unexplained’’ somatic symptoms (critical to the concept of somatoform disorders) appears less and less distinct. Both explained and unexplained somatic symptoms show a strong association with mood and anxiety disorders [4]. As discussed by Mersky and Mai, patients with so-called conversion symptoms often have unusually high rates of neurological illness. Anxiety and depression appear to increase reporting of somatic symptoms even among patients with well-defined chronic 1 Center for Health Studies, Group Health Cooperative, 1730 Minor Ave. #1600, Seattle, WA 98112, USA

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medical conditions [5]. Third, emerging evidence regarding management of somatoform disorders supports the effectiveness of treatments (cognitivebehavioural psychotherapy, antidepressant drugs) most often used in the management of mood and anxiety disorders. As discussed by Merskey and Mai, considerable evidence supports the effectiveness of cognitivebehavioural psychotherapy for the treatment of a range of somatoform disorders, including both unexplained somatic symptoms and hypochondriasis. Antidepressant drugs have proven effective in a range of pain syndromes and other conditions characterized by unexplained somatic symptoms [6]. The evidence reviewed above suggests that somatoform disorders could be re-absorbed into other parts of the ICD and DSM diagnostic schemes. Hypochondriasis might be considered a form of anxiety disorder. Conversion symptoms could be classified with other dissociative disorders. Many syndromes of unexplained somatic symptoms would become variants of depression or generalized anxiety. Body dysmorphic disorder could be classified with obsessive-compulsive anxiety. In such a re-classification, somatic symptoms would not be given any special status. While dissolution of the somatoform disorder category might be consistent with epidemiologic and clinical evidence, it would sacrifice much that is clinically or practically useful. The distinguishing feature of patients with somatoform disorders is the way they enter and interact with the health care system. Somatic symptoms and worries regarding undiagnosed medical illness prompt patients to seek care from primary care physicians and medical specialists rather than from psychiatrists or psychologists. Patients’ anxiety regarding undiagnosed medical illness can be contagious, leading physicians to pursue extensive and expensive diagnostic evaluations. Physicians often perceive patients with somatoform disorders to be difficult or frustrating. These practical issues distinguish somatoform disorders from the mood and anxiety disorders that typically present in mental health clinics. The current classification of somatoform disorders, however, is more influenced by history than by more recent epidemiologic or clinical research. An alternative classification might consider the major symptoms common to several of the somatoform disorders—heightened sensitivity to somatic distress, exaggerated fear of disease, and adoption of a withdrawn or disabled role. Heightened sensitivity to noxious sensations may manifest as pain complaints or as increased sensitivity to specific kinds of somatic distress (e.g., irritable bowel syndrome, fibromyalgia). As discussed above, the available evidence supports the effectiveness of both antidepressant pharmacotherapy and cognitive-behavioural psychotherapy [6, 7]. Disease fear and disease conviction are maladaptive cognitive processes amenable to both pharmacologic and psychotherapeutic treatment. Studies of hypochondriacal syndromes (including body dysmorphic disorder) support the use of selective serotonin reuptake inhibitors over tricyclic antidepressants. The cognitive and

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behavioural strategies found useful in the management of hypochondriacal syndromes closely resemble those proven useful in the management of anxiety disorders [8]. Moderate evidence supports the effectiveness of behavioural approaches in the management of illness behaviours [9]. Components of such an approach include reducing incentives for withdrawal, positively rewarding return to normal function, and developing specific plans for re-activation. Because patients typically present with a mixture of somatic, cognitive and behavioural difficulties, effective treatment must integrate a variety of active ingredients.

REFERENCES 1.

Kroenke K., Spitzer R.L., Williams J.B., Linzer M., Hahn S.R., deGruy F.V. III, Brody D. (1994) Physical symptoms in primary care: predictors of psychiatric disorders and functional impairment. Arch. Fam. Med. 3: 774–779. Simon G., Von Korff M., Piccinelli M., Fullerton C., Ormel J. (1999) An international study of the relation between somatic symptoms and depression. N. Engl. J. Med. 341: 1329–1335. Simon G., Gureje O., Fullerton C. (2001) Course of hypochondriasis in an international primary care study. Gen. Hosp. Psychiatry 23: 51–55. Simon G., Gater R., Kisely S., Piccinelli M. (1996) Somatic symptoms of distress: an international primary care study. Psychosom. Med. 58: 481–488. Ludman E.J., Katon W., Russo J., Von Korff M., Simon G., Ciechanowski P., Lin E., Bush T., Walker E., Young B. (2004) Depression and diabetes symptom burden. Gen. Hosp. Psychiatry 26: 430–436. O’Malley P., Jackson J., Santoro J., Tomkins G., Balden E., Kroenke K. (1999) Antidepressant therapy for unexplained symptoms and symptom syndromes. J. Fam. Pract. 48: 980–990. Kroenke K., Swindle R. (2000) Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother. Psychosom. 69: 205–215. Barsky A., Ahern D. (2004) Cognitive behavior therapy for hypochondriasis: a randomized, controlled trial. JAMA 291: 1464–1470. Donta S.T., Clauw D.J., Engel C.C. Jr, Guarino P., Peduzzi P., Williams D.A., Skinner J.S., Barkhuizen A., Taylor T., Kazis L.E., et al. (2003) Cognitive behavioral therapy and aerobic exercise for Gulf War veterans’ illness: a randomized controlled trial. JAMA 289: 1396–1404.

2. 3. 4. 5. 6. 7. 8. 9.

1.4 Somatoform Disorders: Deconstructing a Diagnosis Oye Gureje1 The review by Merskey and Mai reminds us of the complexity of the clinical entities known as ‘‘somatoform disorders’’. Largely defined on the basis 1

Department of Psychiatry, University of Ibadan, Nigeria

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of the absence of an objective explanatory model, the disorders pose both diagnostic and research difficulties. Making the diagnosis is a dilemma for the physician, who must proceed with the assumption that organic factors are either not present or, if present, are not sufficient explanations for the patient’s complaints, when indeed there can hardly be an absolute guarantee that this is the case. The epidemiologist is no less a victim of the same dilemma. Given the widespread nature of non-specific bodily symptoms in the community and the lack of specificity of any one symptom or group of symptoms, the challenge of defining a ‘‘case’’ on the basis of clusters of poorly connected symptoms is not inconsiderable [1, 2]. As noted by Jablensky, the current definition of somatoform disorders ‘‘ranks among the tallest and most complex conceptual edifices ever erected in medicine’’ [3]. The problem is partly to do with the fact that the basis and nature of the somatic complaints are unknown to the complainant, the patient, and that the doctor, from whom help is being sought, makes an inference about an aetiology that is located somewhere in the mind. A more fundamental conceptual difficulty underlying the complexity is the problem of viewing physical and psychological explanations as alternatives. The Cartesian mind-body dualism involved in the clinical conceptualization of somatoform disorders is clearly mistaken even though medicine has found no coherent way of dealing with the problem. Merskey and Mai have, rather boldly, divided somatoform disorders into two clusters, which they also suggest may bear more than an insignificant relationship to each other. Their conceptualization is interesting. However, current classifications present an array of heterogeneous group of diagnoses, with the common strand between them being complaints about the body. The validity of each runs far short of accepted criteria for reliability and validity [4]. Indeed, underlying the whole notion of a somatoform disorder is a lack of clarity about the extent to which one form is different from the other in regard to underlying biological correlates, such as pathophysiology and genetics. Still, progress has been made in trying to understand the phenomenon of medically unexplained symptoms. It is now clear that the claims that these symptoms serve as a defence against the awareness or expression of psychological distress, or that they are in some ways characteristic of psychologically unsophisticated people, or are more likely in developing countries, are now known to be incorrect. The largest cross-national study of somatoform disorders found that it was largely impossible to ascribe differences across sites to culture or socio-economic developmental stage [5]. Somatization was found in every culture in which it was sought, was common, often associated with depression or anxiety, but also occurred in the absence of either. Somatoform disorders were also associated with functional role impairment. There is nevertheless evidence that another cultural phenomenon may be related to the expression of somatic distress: the

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culture of patient-doctor interaction. When service was delivered in a rather impersonal manner and physicians had very little time to listen to patients’ presenting complaints, more patients reported somatic symptoms [6]. Management is the ultimate crux of the controversy, since patients who are suffering from symptoms, irrespective of how they were caused, will look to the physician for some relief. Indeed, as distinct from validity, the utility of the diagnoses ought to be judged on how effective treatment could be obtained by patients who are so diagnosed. Here, the picture is also less compelling. This is hardly surprising, given that the conditions to be treated are so poorly understood. Kirmayer et al. suggest that when the bodily quality and cultural meanings of their suffering are acknowledged, most patients with medically unexplained symptoms accept that stress and emotions affect their physical condition [7]. They are of the view that such an understanding provides an avenue for a therapeutic alliance between the clinician and the patient. However, and as noted by Sharpe and Mayou [8], most patients resist the suggestion that their symptoms have a psychogenic origin, thus making the basis for a collaborative management of their complaints rather tenuous. Their suggestion that we do away with the diagnostic rubrics under somatoform disorders may seem radical and probably unlikely to be accepted in the short term. However, the fundamentally flawed epistemological foundation on which the diagnoses are erected invites us to re-examine the suggestion. Still, dialogue is essential for deconstructing the symptoms that receive a label of somatoform disorder. Such dialogue requires that both doctors and patients go beyond assumptions underlying current diagnostic concepts and can only be achieved when the patient-doctor encounter is less constrained by time and economic considerations.

REFERENCES 1. 2. 3.

4. 5. 6.

Escobar J.I., Gara M.A. (1999) DSM-IV somatoform disorders: do we need a new classification? Gen. Hosp. Psychiatry 21: 154–156. Gureje O., Ustun T.B., Simon G.E. (1997) The syndrome of hypochondriasis: a cross-national study in primary care. Psychol. Med. 27: 1001–1010. Jablensky A. (1999) The concept of somatoform disorders: a comment on the mind-body problem in psychiatry. In: Somatoform Disorder: A Worldwide Perspective, Y. Ono, A. Janca, M. Asai, N. Sartorius (Eds). Springer-Verlag: Tokyo, pp. 3–10. Kendell R., Jablensky A. (2003) Distinguishing between the validity and utility of psychiatric diagnosis. Am. J. Psychiatry 160: 4–12. Gureje O., Simon G.E., Ustun T.B., Goldberg D.P. (1997) Somatization in crosscultural perspective: a World Health Organization study in primary care. Am. J. Psychiatry 154: 989–995. Gureje O. (2004) What can we learn from a cross-national study of somatic distress? J. Psychosom. Res. 56: 409–412.

34 7. 8.

SOMATOFORM DISORDERS Kirmayer L.J., Groleau D., Looper K.J., Dao M.D. (2004) Explaining medically unexplained symptoms. Can. J. Psychiatry 49: 663–672. Sharpe M., Mayou R. (2004) Somatoform disorders: a help or hindrance to good patient care? Br. J. Psychiatry 184: 465–467.

1.5 The Psychobiology of Somatization and Conversion Disorders C. Robert Cloninger1 and Mehmet Dokucu1 Somatization and conversion phenomena have always fascinated people because they require us to face the mysterious nature of human agency and self-aware consciousness [1]. Merskey and Mai present a classically dualistic approach to understanding personal agency and consciousness in patients with somatization and conversion disorders. They are concerned with the relative importance of processes involving ideas and intentional thinking versus involuntary hyperarousal of the autonomic nervous system. That is, they focus on differentiating the relative roles of nature versus nurture in aetiology, the soma versus the psyche in symptomatology, and immature patients versus wise authorities in treatment. As a result, the dilemmas they face about the aetiology, diagnosis, and treatment of these complex disorders are not fundamentally different from those of clinicians during the nineteenth century who also had a dualistic perspective, such as Charcot and Freud. Their scholarly historical perspective reveals the inadequacy of such dualistic thinking since antiquity. Fortunately, recent research about the psychobiology of human thought processes has begun to provide a more fundamental understanding of patients with somatization and conversion, based on a holistic perspective that does not try to separate mind from body artificially [1]. Dualistic thinking about agency and consciousness may be valid as an initial approximation, but it is ultimately inadequate because it oversimplifies the complex psychobiological processes that underlie development and treatment [1]. For example, the predisposition to autonomic hyperarousal can be assessed in patients by measuring temperament traits, such as harm avoidance in the Temperament and Character Inventory (TCI). The higher cognitive processes of mental self-government can be assessed in patients by measuring character traits, such as TCI self-directedness. Individuals with somatization disorder nearly always have both high scores on TCI harm avoidance (i.e., anxious, pessimistic, fearful, fatigable) and low scores on TCI self-directedness (i.e., irresponsible, aimless, and resourceless), indicating that they are both anxiety-prone and immature. Most, but not all, patients 1 Department of Psychiatry, Washington University School of Medicine, 660 S. Euclid, St. Louis, MO 63110, USA

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with somatization and conversion disorders have underlying personality disorders, as described in depth earlier in this book series [2]. In particular, patients with somatoform disorders often have mixed features of all three DSM-IV clusters of personality disorders, as seen in patients with borderline personality disorder [2, 3]. Likewise, the putative dichotomy between organic and psychogenic factors is a misleading distinction because biological, psychological, and social influences are inextricably intertwined throughout development and treatment. For example, individuals with somatization disorder usually have alexithymia, a disturbance of affect and cognition indicated by a reduced affective and fantasy life. They have difficulty in recognizing and describing their own emotions. They experience distress in terms of physical complaints and are often described as having hysterical or repressive personality traits. The tendency to repression can be reliably quantified by low scores on the first TCI self-transcendence subscale (i.e., self-forgetfulness or sensible versus repressive) or other scales that measure externally oriented thinking [1]. Such repressive personality traits are correlated with sensory numbing and slower consciousness of tactile stimulation [4], so these patients really do have reduced awareness of sensory inputs related to their sexuality. Differences between individuals in their awareness of agency and self-directedness are correlated with differences in the efficiency of activation of the prefrontal cortex and parietal cortex [5, 6], so these patients also really do have deficits in agency and self-directedness. Individual differences in harm avoidance are also correlated with individual differences in the modulation of startle, mismatch negativity, and the release of endogenous opioids in response to sustained noxious stimuli [1, 7], so these patients really do have heightened sensitivity to bodily pains. These predispositions are moderately heritable through interactions among many genetic and environmental factors. The effects of genes are strongly influenced by experience with soothing maternal care or by physical and sexual abuse [1, 2, 8]. As a result, the complexity of interactions between biological, psychological, and social influences needs to be recognized by clinicians in order to be able to approach assessment and treatment in a way that is realistic and also to be respectful of the patient’s capacity for growth in self-awareness and personal responsibility. Mersky and Mai are mistaken to suggest that the criteria for somatization in DSM-IV are less stringent than those in DSM-III or in the original criteria developed by Guze. Cloninger developed the DSM-IV criteria for somatization disorder based on extensive research with the prior criteria as well as research on the discrimination of somatoform disorders in the general population [9, 10]. While doing adoption studies of somatoform disorders, he and his colleagues discovered that symptom counts for traditional clinical groups of symptoms, such as number of bodily pains or irritable bowel symptoms, were more efficient for distinguishing groups of somatoform

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patients than were the symptoms counts recommended by Guze [11]. This discovery allowed the development of the DSM-IV criteria. The DSM-IV criteria are efficient because they allow clinicians to screen patients in a stepwise manner. First, a clinician assesses the number of bodily pains, then gastrointestinal problems, next conversion symptoms, and finally sexual symptoms. Patients must have a certain number of symptoms in each of these groups, otherwise they do not satisfy the criteria. As a result, questioning can stop at any step at which there are insufficient symptoms. This stepwise procedure was initially calibrated in a large clinical sample studied by Guze and his associates, and then was re-tested in field trials with psychiatric and other medical samples at independent sites. The field trials confirmed that the DSM-IV criteria reliably identified the same patients as did the earlier criteria [10]. The DSM-IV criteria identify the essential features of somatization disorder, which need to be explained psychobiologically. As long as clinicians are preoccupied with the false dichotomy between neurological and psychological disease, they are reluctant to think in terms of explicit inclusion criteria or essential features of a somatoform disorder. Even when the DSM-IV approach is properly applied, the system promotes categorical thinking rather than biopsychosocial understanding. Many patients go unclassified except for the residual category of undifferentiated somatoform disorder, as noted by Mersky and Mai. Such unvalidated residual categories expose the inadequacy of categorical thinking in general. Cognitive behaviour therapy must be adapted for effective application in patients with somatoform and/or personality disorders [12]. Special effort is required to establish a therapeutic alliance with patients who are often stigmatized and resistant to any suggestion that they are responsible for their symptoms [13]. Nevertheless, patients with somatization and conversion disorders can be helped to develop greater self-awareness, which is essential in order to reduce their vulnerability to future somatization and conversion. Techniques that are based on deception or direction by authority figures may produce transient benefits, but rob the patient of the opportunity for growth in self-awareness and can reduce trust in the integrity of care-takers. Psychotropic medications are often a useful adjunct to psychotherapy in somatoform disorders as they are in borderline personality disorder [14]. Selective serotonin reuptake inhibitors like fluoxetine, serotonin and norepinephrine reuptake inhibitors like venlafaxine, and mood stabilizers are often beneficial for all these conditions as they reduce impulsivity and emotional lability. However, transformation of personality with reduced vulnerability to somatization and conversion does require experience with mental exercises that increase the efficiency of brain circuits underlying self-awareness [1, 2]. A thorough discussion of treatment options in the treatment of somatoform disorders has recently been compiled for neurologists and psychiatrists [13].

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REFERENCES 1. 2. 3.

4. 5. 6. 7. 8.

9.

10. 11. 12.

13. 14.

Cloninger C.R. (2004) Feeling Good: The Science of Well Being. Oxford University Press: New York. Cloninger C.R. (2005) Antisocial personality disorder: a review. In: Personality Disorders, M. Maj, H.S. Akiskal, J.E. Mezzich, A. Okasha (Eds). Wiley: Chichester, pp. 125–129. Cloninger C.R. (2005) The role of personality in psychogenic movement disorders. In: Psychogenic Movement Disorders, M. Hallett, C.R. Cloninger, S. Fahn, J. Jankovic, A.E. Lang, S.C. Yudofsky (Eds). Lippincott Williams & Wilkins: New York, pp. 122–130. Shevrin H., Ghannam J.H., Libet B. (2002) A neural correlate of consciousness related to repression. Conscious. Cogn. 11: 334–341. Spence S.A., Crimlisk H.L., Cope H., Ron M.A., Grasby P.M. (2000) Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement. Lancet 355: 1243–1244. Gusnard D.A., Ollinger J.M., Shulman G.L., Cloninger C.R., Raichle M.E. (2001) Personality differences in functional brain imaging. Soc. Neurosci. Abstr. 27: 11. Zubieta J.K., Heitzeg M.M., Smith Y.R., Bueller J.A., Xu K., Xu Y., Koeppe R.A., Stohler C.S., Goldman D. (2003) COMT val158met genotype affects mu-opioid neurotransmitter responses to a pain stressor. Science 299: 1240–1243. Cloninger C.R. (2003) Completing the psychobiological architecture of human personality development: temperament, character, & coherence. In: Understanding Human Development: Dialogues with Lifespan Psychology, U.M. Staudinger, U.E.R. Lindenberger (Eds). Kluwer Academic Publishers: Boston, pp. 159–182. Cloninger C.R. (2001) The origins of DSM and ICD criteria for conversion and somatization disorders. In: Contemporary Approaches to the Study of Hysteria, P.W. Halligan, C. Bass, J.C. Marshall (Eds). Oxford University Press: Oxford, pp. 49–62. Cloninger C.R. (1996) Somatization disorder. In: DSM-IV Sourcebook, T.A. Widiger, A.J. Frances, H.A. Pincus, M.B. First, R. Ross, W. Davis (Eds). American Psychiatric Association: Washington, D.C., pp. 885–891. Cloninger C.R., Sigvardsson S., von Knorring A.L., Bohman M. (1984) An adoption study of somatoform disorders: II. Identification of two discrete somatoform disorders. Arch. Gen. Psychiatry 41: 863–871. Cloninger C.R. (2004) ‘‘Sickly’’: treatment of somatization disorder. In: Treatment Companion to the DSM-IV-TR Casebook, R.L. Spitzer, M.B. First, M. Gibbon, J.B.W. Williams (Eds). American Psychiatric Publishing: Washington, D.C., pp. 306–314. Hallett M., Cloninger C.R., Fahn S., Jankovic J., Lang A.E., Yudofsky S.C. (Eds). (2005) Psychogenic Movement Disorders. Lippincott Williams & Wilkins: New York. Oldham J.M., Gabbard G.O., Goin M.K., Gunderson J., Soloff P., Spiegel D., Stone M., Phillips K.A. (2001) Practice Guidelines for the Treatment of Patients with Borderline Personality Disorder. American Psychiatric Press: Washington, D.C.

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1.6 Patient or Process? Linda Gask1 As psychiatrists, we assert that we have expertise in diagnosing and managing people whom we have variously labelled as suffering from ‘‘hysteria’’, ‘‘somatization disorder’’, or more recently, ‘‘medically explained symptoms’’. We have spent many decades (even centuries) classifying and reclassifying symptoms, resulting in a section in both the DSM-IV and ICD-10 which, to many working in the field, still seems not particularly clinically useful. One of the problems that we face is that, in most health care systems in the world, psychiatrists actually see and treat very few people who meet these criteria. The majority of them present in primary care and general medical settings, which is not entirely surprising because of the conviction, possessed to varying degrees, that their problems are physical. It is partly because of this that the latest label ‘‘medically unexplained symptoms’’ has gained currency, as it seems to make sense to primary care workers who are deeply practical people, often highly suspicious of hypothetical psychological mechanisms. Some researchers in this field have even gone further, suggesting that the problem is not one of the ‘‘problem patient’’ who needs to be correctly categorized, but the ‘‘problem consultation’’ between doctor and patient. This is a challenging view that demands some examination. Ring and her colleagues in Liverpool [1] analysed qualitatively 36 patients selected consecutively from 21 general practices, in which doctors considered that patients’ symptoms were medically unexplained. They noted that it is widely assumed in the literature that patients with unexplained symptoms pressurize doctors for symptomatic intervention and that this explains the difficulty or dismay that general practitioners (GPs) feel in dealing with these patients and the high level of investigation and treatment that they provide. However, the GPs’ provision of symptomatic intervention could not be attributed to patients’ overt demands. All but two patients in this sample received somatic interventions. Most were prescribed drugs, a third were referred for investigations, and four were referred to hospital doctors. Nevertheless, none had requested investigation or specialist referral, and a few asked for prescriptions. Patients did, however, have striking ways of conveying the extent and intensity of their suffering and need for help and of constraining doctors’ attempts to help. They described their suffering with graphic words and metaphors, emphasized disabling effects of their symptoms, and cited friends and family as authority for their suffering or concern. The doctors’ feedback to this perceived emotional pressure was to respond somatically and prescribe symptomatically. In a companion paper, 1

School of Primary Care, University of Manchester, UK

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the same group [2] refuted the belief that patients in general practice who have medically unexplained symptoms do not often present their doctor with cues of emotional distress, thus enabling the doctor to engage in talk about feelings. All but two of the 36 patients studied presented opportunities for the doctor to talk about emotional topics, for example, by making references to their fears about serious disease and expressing worry and concern about symptoms. Perhaps these patients are different from those that are seen in hospital outpatient departments? Patients in UK general practice may be less likely to want to challenge their doctor and ask for referral or a second opinion, particularly if they are concerned to retain a relationship that may have been built over a long period of time. But, despite the limitations of this study, the small sample size, and difficulty in generalizing to other cultures or health care systems, it is certainly clear that doctors working in general medical settings the world over experience difficulties in their often protracted consultations with patients for whom they cannot find an organic cause for their symptoms. They perceive a lack of skills in managing these problems and they often do not feel that psychiatry has a great deal to offer. Most of these patients will not attend a psychiatric appointment. Even if they do, I think we need to be honest about our own level of interest and skills in managing such patients. If the mental health system is most concerned with treatment of psychosis, as is the case in many countries including my own, it is not unusual for psychiatric services to be unable (or unwilling) to offer appropriate support to the general physician or primary care worker. The psychological interventions described by Merskey and Mai require considerable investment in the psychological infrastructure of health care. But even that will not be enough, unless an attempt is also made to reach out those health care staff outside the mental health services. From my own experience, I know that patients with medically unexplained symptoms are more willing to see a mental health care worker in the primary care physician’s office than the mental health clinic. Primary care physicians need training in approaches to consultation that help them to engage patients with medically unexplained symptoms in meaningful dialogue. This has been my goal since I developed the model of reattribution with David Goldberg in the late 1980s [3]. We know that doctors can acquire new skills [4], and have some evidence that this can have an impact on patient outcome [5]. We are currently engaged in an exploratory randomized controlled trial of reattribution training in primary care. The model has been informed by the developments in understanding the patient perspective in this field over the last decade, particularly in primary care [6]. I would suggest that similar work, exploring both the patient’s view and the nature of the communication process itself, now urgently needs to be carried out in both general hospital and psychiatric settings. Such insights

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from qualitative research might help to shift the impasse that is so often apparent even in our own outpatient clinics.

REFERENCES 1. 2. 3. 4. 5. 6.

Ring A., Dowrick C., Humphris G., Salmon P. (2004) Do patients with unexplained physical symptoms pressurise general practitioners for somatic treatment? A qualitative study. Br. Med. J. 328: 1057. Salmon P., Dowrick C.F., Ring A., Humphris G.M. (2004) Voiced but unheard agendas: qualitative analysis of the psychosocial cues that patients with unexplained symptoms present to general practitioners. Br. J. Gen. Pract. 54: 171–176. Goldberg D., Gask L., O’Dowd T. (1989) The treatment of somatisation: teaching the skills of reattribution. J. Psychosom. Res. 33: 689–695. Kaaya S., Goldberg D., Gask L. (1992) Teaching the skills of ’reattribution’: a replicated study. Med. Educ. 26: 138–144. Morriss R., Gask L., Ronalds C., Downes-Grainger E., Thompson H., Goldberg D. (1999) Clinical and patient satisfaction outcome of a new treatment for somatised mental disorder taught to general practitioners. Br. J. Gen. Pract. 49: 263–267. Salmon P., Peters S., Stanley I. (1999) Patients’ perceptions of medical explanations for somatisation disorders: qualitative analysis. Br. Med. J. 318: 372–376.

1.7 Reading the Body? Leslie Swartz1 It has become commonplace to say that we live in a ‘‘body culture’’. Global saturation of the mass media has been associated with increasing emphasis on how bodies look and should look; the muscular, toned body is commonly displayed and is seen as a prescription for us all. Plastic surgery is marketed as a ‘‘solution’’ to body and social problems; television shows promoting plastic surgery are very popular. Excessive concern about the body is also widespread, and more widespread than many of us once believed. For example, symptoms associated with anorexia and bulimia nervosa are no longer viewed as disorders exclusive to white, middle-class women in western countries—high rates of these symptoms have been reported in Africa and Asia, for example, and there is concern about the psychopathological consequences of media images for how men attempt to control their bodies [1]. With the increasing emphasis on the body as a source of identity, there is also increasing concern with the extent to which our identities may 1 Department of Psychology, University of Stellenbosch, Private Bag X1, Matieland 7602, South Africa

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be separated from the limits of our bodies. Spare-part surgery has made the image of the cyborg (part human, part machine) both a reality and a preoccupation of a genre of popular films. The rise of the Internet and cyberspace has led to emphasis on multiple identities not linked to time, space and bodies in the conventional sense. Globalization, furthermore, is marked by an upsurge in mobility across the globe, and the large numbers of refugees and internally displaced people make us think about the ways in which we can live simultaneously in different times and places. Clashes of culture in Western countries lead some to think about whether it is possible to live physically in one place but emotionally and politically to inherit another world. The body, it seems, is everywhere and nowhere [2]. Against this background, the review by Merskey and Mai of somatization and conversion disorders presents us with a particular view of how psychiatry and related disciplines view the body. Merskey and Mai show that it is important for psychiatrists to understand the epidemiology of conversion and somatoform disorders, and to know about different ways in which the body can be seen to ‘‘speak’’ as part of psychopathological syndromes. To what extent, though, is it important for psychiatry to take account of the fact that, as Kleinman [3] has convincingly argued, speaking with the body is not only common, but also normative? It is clear that an observation like this is of great interest to students of culture, but to what extent is it, and should it be, of concern to mental health practitioners? Those of us who work with diverse populations in lower-income countries are confronted daily with different ways in which the body is used and understood by people from different social groups. A key factor in the way the body is used culturally relates precisely to the health systems available to people. As Merskey and Mai note, presentation of somatic symptoms in research tends to increase if those who are asking the questions are psychiatrists; where mental health care is not comprehensively available and tends to be accessed through physical health care systems, this may relate to increased use of the body as an idiom for psychological distress [4]. There is one sense in which understanding the context of the body as a cultural construction is relatively unimportant to psychiatry. There seems to be very little doubt that there are people across the world who use the body differently from how most people within their own cultures use it—we see some of these people as manifesting somatization or conversion disorders. It is important to recognize that these disorders are in need of evidence-based treatment and management, as Merskey and Mai suggest. But there is also an argument for taking a far broader view of the ways in which the body has meaning for all of us, and the ways in which patients will (consciously or otherwise) use their understanding of the body as a way of negotiating their path through healing systems, including those offered by psychiatry. A broader view of the body as a cultural and performative artefact may help us

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look beyond traditional diagnostic systems towards an understanding of the ways in which we may learn from the body more about the social bases of distress. Merskey and Mai note, for example, the suggestion by Kirmayer and his colleagues that high rates of unexplained physical symptoms amongst men who had migrated from Vietnam to Canada may relate to high rates of trauma in this group. The body is always an important site of both oppression (as in torture) and of resistance (as in hunger strikes) [5]. As the world seems more and more dangerous, and more and more beset by acts of inhumanity and naked aggression, it may be helpful for those of us interested in mental health on a global scale to pay more attention to what the body tells us [6]. An exclusive focus on the psychopathological phenomena of body-related disorders at the expense of a more general concern with the role of the body as a means of communication may, paradoxically, lead us to underestimate how important the languages of body may be to comprehensive mental health care.

REFERENCES 1.

Nasser M., Katzman M., Gordon R. (Eds) (2001) Eating Disorders and Cultural Transition. Brunner-Routledge: London. Helman C.G. (2000) Culture, Health and Illness, 4th ed. Churchill Livingstone: London. Kleinman A. (1991) Rethinking Psychiatry. Free Press: New York. Swartz L. (1998) Culture and Mental Health: A Southern African View. Oxford University Press: Cape Town. Scarry E. (1987) The Body in Pain: The Making and Unmaking of the World. Oxford University Press: Oxford. Swartz L. (2002) Dissociation and spirit possession in non-western countries: notes towards a common research agenda. In: Attachment, Trauma and Multiplicity: Working with Dissociative Identity Disorder, V. Sinason (Ed). Routledge: London, pp. 231–239.

2. 3. 4. 5. 6.

1.8 Somatization and Conversion Disorders: A Forgotten Public Health Agenda? Shekhar Saxena1 Somatization and conversion disorders have been interesting psychiatric phenomena from a clinical perspective for more than a century. They have 1

World Health Organization, CH-1211, Geneva, Switzerland

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attracted much attention from the conceptual, psychopathological and diagnostic viewpoints. However, little attention has been paid to their public health aspects. No disability or burden estimates for these disorders are available, very little research is available on the cost these disorders impose on individuals, families, societies, and on the health care systems, and almost no systematic information is available on their prevalence over time and regions of the world. Some possible reasons for this lack of attention can also be found in Mersky and Mai’s review. The phenomenon of somatization is well known and documented for many decades, but ‘‘the concept of somatization disorder remains controversial’’. The relatively recent formulation of diagnostic guidelines and criteria and the lack of consensus on these across cultures have acted as barriers for more focussed work on the natural course and disability associated with this disorder. The absence of a clear biological correlate and of any effective psychopharmacological drug for somatization has also dampened research interest in the industry. Lastly, but not insignificantly, the largest proportion of individuals with somatization disorder present themselves at the primary care level and remain there, hence this substantial problem often does not grip the attention of psychiatrists and psychiatric researchers as fully as it should. The World Health Organization (WHO) has conducted two international studies in the recent past that shed some light on issues around somatization disorders. The WHO International Study on Psychological Problems in General Health Care [1] screened more than 25,000 patients in 14 countries and assessed in detail nearly 5,500. Somatization was diagnosed in 2.7% of the patients and ranked as the sixth most prevalent disorder in this population. This rate of prevalence was however considered low by the investigators, and a much higher rate was detected using less restrictive criteria than those required under the ICD-10. There was a modest association with low education, though the frequency of unexplained somatic symptoms did not clearly vary according to geography or level of economic development [2]. Somatizing patients were at elevated risk for self-reported disease burden, negative perception of their health and comorbid depression, and generalized anxiety disorder. A common association with disability was also found. The study concluded that somatization is a common problem in primary care across cultures and is associated with significant problems and disability. The second study, the WHO International Study of Somatoform Disorders, investigated cross-cultural applicability and reliability of assessment of somatoform disorders in five centres representing distinct cultures. Fortytwo experts from 23 countries found the ICD-10 concept of somatoform disorders generally acceptable for use across cultures [3]. However, a number of culture-specific symptoms that do not appear in the ICD-10 were found to be common and important for diagnosis in particular cultures. It

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was found that aches and pains in different parts of the body represented cross-culturally the most frequent symptoms for these diagnoses [4]. Somatization and related disorders deserve more public health and research attention than has been given to them. Some of the specific issues that need to be focussed include cross-cultural aspects, comorbidity and natural course, associated disability, overall burden, socio-demographic correlates, and economic costs (including the cost of care and productivity losses). Research also needs to focus on ways in which the health systems can be strengthened to provide care for these disorders in the most cost-effective manner.

REFERENCES 1. 2. 3. 4.

Ustun T.B., Sartorius N. (1995) Mental Illness in General Health Care: An International Study. Wiley: Chichester. Gureje O., Simon G.E., Ustun T.B., Goldberg D.P. (1997) Somatization in crosscultural perspective: a World Health Organization study in primary care. Am. J. Psychiatry 154: 989–995. Janca A., Isaac M., Bennett L.A., Tacchini G. (1995) Somatoform disorders in different cultures—a mail questionnaire survey. Soc. Psychiatry Psychiatr. Epidemiol. 30: 44–48. Janca A., Isaac M. (1997) ICD-10 and DSM-IV symptoms of somatoform disorders in different cultures. Keio J. Med. 46: 128–131.

1.9 A Cognitive Account on Conversion and Somatization Disorders Karin Roelofs1 Merskey and Mai correctly argue that somatization and conversion disorders are controversial diagnostic entities that have been subject to intensive psychodynamic speculation for a long period of time. Accordingly, the authors convincingly dispel a number of psychodynamic misconceptions such as ‘‘la belle indiff´erence’’. At the same time, they still assume that at least a good part of the medically unexplained symptoms depend on ‘‘thoughts or embodied intentions’’. The present commentary will first discuss the question of intentionality and volition in somatization and conversion symptoms while laying out the basics of a cognitive theory that explains that the symptoms are not necessarily produced intentionally. Second, this commentary will discuss several predisposing, precipitating and perpetuating factors that may be related to the development of somatization and conversion symptoms. 1 Section of Clinical and Health Psychology, Leiden University, P.O. Box 9555, 2300RB Leiden, The Netherlands

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Conversion symptoms and other somatization symptoms can be ascribed to functional dissociations between the experience of volition and the control of thought and action. Modern cognitive theories of medically unexplained symptoms such as those of Oakley [1] and Brown [2] are based on hierarchical cognitive models of attentional control such as that of Norman and Shallice [3]. In their model, Norman and Shallice described a higherlevel executive control system, the supervisory attentional system (SAS), that, for the greater part, is based in the prefrontal cortex. It is conceived of as monitoring ongoing activity and modulating behaviour when established automatic routines are not sufficient, such as in novel situations. Automatic routines are in turn controlled by a hierarchical lower-level control process, involving a series of well-learned behavioural schemata or mental representations that can be activated by environmental and contextual stimuli through a decentralized and semi-autonomous process called ‘‘content scheduling’’ (for a more detailed outline, see [3]). On the basis of this model, Oakley [1] and Brown [2] developed cognitive theories of conversion and somatization that can explain that the symptoms are not produced intentionally and experienced as non-volitional. In these models, the experience of volition is associated with operation of the SAS, while the ultimate locus of cognitive and behavioural control occurs with the lower-level control system where schemata (or mental representations) underlying routine action are more automatically activated. When a patient with conversion paralysis, for example, deliberately attempts to move an affected limb and is engaging the SAS, the attempt will be unsuccessful because the locus of his/her deficit is the chronic activation and selection of symptom-related schemata or mental representations. That mental motor representations of paralysed limbs may indeed be impaired in patients with conversion paralysis was, for example, confirmed by reaction time studies investigating mental motor representations using mental hand rotation tasks [4]. According to these cognitive theories, conversion symptoms (and other somatization symptoms) arise when the chronic activation of such symptom-related representations stored in memory cause lower-level attentional selection process (content scheduling) to select inappropriate information. An important implication of these theories is that the symptoms are generated by psychological mechanisms but are not produced intentionally. Within these cognitive theories of somatization, several predisposing, precipitating and perpetuating factors can be differentiated. Throughout history, many factors have been raised that would make an individual vulnerable to developing conversion or other somatization symptoms, ranging from a weak mental constitution to a histrionic personality. However, only a few factors find empirical support. As far as personality traits are concerned, there is evidence from controlled studies that hypnotic

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suggestibility is related to conversion symptoms [5, 6]. Brown and Oakley [7] argued that individuals showing a high hypnotic susceptibility may be particularly prone to the automatic activation of cognitive and behavioural schemata/representations by internal and external events. In the second place, many patients with conversion disorder [8] and somatization disorder [9, 10] report a history of childhood sexual and physical abuse. In other trauma-related disorders, such as post-traumatic stress disorder, these types of childhood traumas have been associated with prolonged deregulations in physiological stress systems such as the hypothalamic–pituitary–adrenal (HPA) axis [11]. Similar mechanisms may explain the hyperactivity of the HPA axis in patients with somatization symptoms [12] referred to in Merskey and Mai’s review. Subsequently, several sources of information within the cognitive system can serve as a template for the development of the symptom. Merskey and Mai already mention that biological changes and organic conditions may be part of the antecedent stimuli that precipitate somatization, or that a pre-existing pathophysiological change may lower the threshold for the development of a somatic symptom. Besides these examples of direct exposure to physical states in the self (which can also occur during exposure to psychological trauma), I would like to point at other factors that may lead to symptom-related mental representations, such as indirect exposure to physical states in others, socio-cultural transmission of information about health and illness, and verbal suggestion (for a review see [2]). The storage of symptom-related mental representations alone is not sufficient to explain the development of somatization and conversion symptoms. Several behavioural and cognitive responses to the initial activation of a mental representation may contribute to the development of symptom chronicity. An important example of cognitive responses is self-focussed attention. There is good evidence that the direction of attention towards the self may lead to increased reports of subjective physical symptoms (e.g. [13]). There are also various behavioural responses, such as overactivity, underactivity, medical consulting, checking, and information and reassurance seeking, that may serve to perpetuate symptom focussing in patients with somatization or conversion disorder. In sum, hierarchical cognitive theories of somatization imply that the symptoms may be generated by various psychological mechanisms but are not produced intentionally.

REFERENCES 1.

Oakley D.A. (1999) Hypnosis and conversion hysteria: a unifying model. Cogn. Neuropsychiatry 4: 243–265.

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4. 5. 6. 7.

8. 9. 10.

11.

12. 13.

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Brown R.J. (2004) Psychological mechanisms of medically unexplained symptoms: an integrative conceptual model. Psychol. Bull. 130: 793–812. Norman D.A., Shallice T. (1986) Attention to action: willed and automatic control of behavior. In: Advances in Research and Theory, Consciousness and Self-regulation, Vol. 4, R.J. Davidson, G.E. Schwartz, D. Shapiro (Eds). Plenum Press: New York, pp. 1–18. Roelofs K., N¨aring G.W.B., Keijsers G.P.J., Hoogduin C.A.L., van Galen G.P., Maris E. (2001) Motor imagery in conversion paralysis. Cogn. Neuropsychiatry 6: 21–40. Kuyk J., Spinhoven P., van Dyck R. (1999) Hypnotic recall: a positive criterion in the differential diagnosis between epileptic and pseudoepileptic seizures. Epilepsia 40: 485–491. Roelofs K., Hoogduin C.A.L., Keijsers G.P.J., N¨aring G.W.B., Moene F.C., Sandijck P. (2002) Hypnotic susceptibility in patients with conversion disorder. J. Abnorm. Psychol. 111: 390–395. Brown R.J., Oakley D.A. (2004) An integrative cognitive model of hypnosis and high hypnotizability. In: The Highly Hypnotizable Person: Theoretical, Experimental and Clinical Issues, M. Heap, R.J. Brown, D.A. Oakley (Eds). Brunner-Routledge: London, pp. 152–186. Roelofs K., Keijsers G.P.J., Hoogduin C.A.L., N¨aring G.W.B., Moene F.C. (2002) Childhood abuse in patients with conversion disorder. Am. J. Psychiatry 159: 1908–1913. Kinzl J.F., Traweger C., Biebl W. (1995) Family background and sexual abuse associated with somatization. Psychother. Psychosom. 64: 82–87. Reilly J., Baker G.A., Rhodes J., Salmon P. (1999) The association of sexual and physical abuse with somatization: characteristics of patients presenting with irritable bowel syndrome and nonepileptic attack disorder. Psychol. Med. 29: 399–406. Bremner J.D., Southwick S.M., Charney D.S. (1999) The neurobiology of posttraumatic stress disorder: an integration of animal and human research. In: Posttraumatic Stress Disorder: A Comprehensive Text, P.A. Saigh, J.D. Bremner (Eds). Allan & Bacon: New York, pp. 103–143. Rief W., Shaw R., Fichter M. (1998) Elevated levels of physiological arousal and cortisol in patients with somatization syndrome. Psychosom. Med. 60: 198–203. Pennebaker J.W., Brittingham G.L. (1982) Environmental and sensory cues affecting the perception of physical symptoms. In: Advances in Environmental Psychology, Vol. 4, A. Baum, J. Singer (Eds). Erlbaum: Hillsdale, pp. 115–136.

1.10 Labelling the Unfathomable Bart Sheehan1 The murky borderlands between medicine and psychiatry have always been a challenge to the medical enterprise. The patients inhabiting this borderland often seem a threat. Clinicians feel unable to formulate biomedical 1

Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK

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explanations. The result is all too often a depressing and frustrating encounter for both the patient and the clinician (usually a doctor). Too often, a regression occurs to the default position of more tests with inevitable consequences; more referrals, more false hope, more expense, more heartsink. A quick run through the terminology used in this area, much of it used in Merskey and Mai’s review, illustrates the problems with understanding these presentations. Hysteria, hypochondriasis, somatization, Briquet’s syndrome, somatoform disorders, heartsink patients, medically unexplained symptoms, functional symptoms and syndromes—the terms accumulate. Names matter—a standard term is necessary to allow international communication and to allow people across medical specialities to quickly understand what is being discussed. No one is in doubt about the subject matter of a seminar on ‘‘Meningococcal meningitis’’. A seminar titled ‘‘Functional and medically unexplained symptoms’’ might attract a motley crew of the curious and the confused. What do we call these presentations? Even among experts in the field there is considerable doubt about what is included and what is not. In internal medicine, proven causes are often used to name the condition—bacterial meningitis, for example. In psychiatry, the residual home of patients and those interested in these presentations, proof of cause is usually conspicuously absent. Thus, in our diagnostic manuals, DSM and ICD, we diagnose by recognizing syndromes, that is, groups of symptoms occurring together with sufficient regularity to predict a particular outcome, for example, prognosis or treatment response. Views on cause change with time. The landmark decision to drop the term ‘‘hysteria’’ from DSM-III in 1980, and its replacement with ‘‘somatization’’, marks the symbolic change from an analytically dominated past, in which unconscious conflicts were held to have the power to generate symptoms, to a present in which it is acknowledged that we do not know the causes, and therefore use the more prosaic modern term somatization. Debates still rage about whether two prototypes, hypochondriasis and somatization, are the same or two different disorders. Even the current favourite terms, somatization and medically unexplained symptoms, can be held to be problematic, with their implication of psychological origin to symptoms. Terms matter in lots of ways. They can become pejorative over time. Nobody would use ‘‘cretin’’, ‘‘idiot’’ or ‘‘imbecile’’ now, but they started as respectable medical descriptors of syndromes with low IQ. Similarly, most patients will not thank us for calling them a hysteric. ‘‘Incompletely explained symptoms’’ may not trip off the tongue, but at least it is unlikely to offend. How far should we go? A basic assumption is that symptoms do not have an organic explanation—perhaps this term is a step too far in seeking to avoid offence. Individual disorders can crystallize the progression of thinking about these presentations. A good example of an ‘‘incompletely explained symptom’’

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is the fatigue of those with chronic fatigue syndrome. This condition has been widely debated from at least the nineteenth century. It has been given many names, including neurasthenia (a term which survives to this day in ICD-10), royal free disease, myalgic encephalomyelitis, post-viral fatigue syndrome, and chronic fatigue. The recent tendency to use myalgic encephalomyelitis and post-viral fatigue syndrome less frequently, and to use the descriptive term chronic fatigue more often, shows the previous tendency to name these conditions by attributing to them a cause which cannot be proven. Views on this disorder are held with remarkable ferocity. Like many of the so-called ‘‘functional disorders’’, impairment is considerable, comorbidity with other psychiatric conditions is common, while the best evidence for treatment efficacy comes from trials of cognitive behavioural approaches. Successful working with such patients requires a range of medical and psychological skills not found in most doctors. What is to be done? A practical approach, as outlined by Merskey and Mai, will involve acknowledgement of distress, legitimization of symptoms, trust, limiting of medical responses to symptoms, expectation of realistic improvement, and attempts to correct thinking styles (‘‘I know I need to rest more, the tiredness is telling me to go to bed’’) which may be manualized as in formal cognitive behavioural therapy, or integrated into common clinical practice. Research will help; an international consensus on what term to use to define the problem, which acknowledges the rarity of the pure prototype syndrome but delineates a troublesome level of distress, such as that seen worldwide in primary care [1], will be invaluable. Then we can pool data, achieve interdisciplinary and international understanding of what we mean, and design meaningful studies to address aetiology and, most important, treatment. The muddiness will clear; the medical enterprise will achieve this in the end. But we should not expect simple single explanations of these mysterious symptoms; indeed we may not need this. Better for now to adjust ourselves to dealing with our uncertainty and with the patients’ infinite need for reassurance.

REFERENCES 1.

Gureje O., Simon G.E., Ustun T.B., Goldberg D.P. (1997) Somatization in crosscultural perspective: a World Health Organization study in primary care. Am. J. Psychiatry 154: 989–995.

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1.11 Somatization and Conversion: An Ongoing Controversy Carsten Spitzer1 and Hans Jorgen Grabe1 ¨ In their comprehensive review, Merskey and Mai emphasize that the concepts of both somatization and conversion disorders remain controversial, and it is very likely that this debate will not cease in the near future. The controversy relates to issues of nosology, classification, epidemiology, pathogenesis, and treatment. For example, it is still a matter of intense debate whether conversion represents one form of somatization among others, or whether it is completely different from somatization and involves other mechanisms to translate psychosocial stress or conflicts into bodily symptoms [1]. The controversy is also reflected by some differences in the DSM-IV and the ICD-10: while the DSM-IV subsumes conversion disorders under the major heading of the somatoform disorders, the ICD-10 distinguishes between somatoform disorders on the one hand, and conversion and dissociative disorders on the other hand, merging the latter two into one category [2]. In order to understand the current controversy, it is essential to relate to the historical background of the concepts of somatization and conversion, as Merskey and Mai point out. When discussing the origins of these concepts within the framework of hysteria, it is important to mention the contributions of Pierre Janet [3]. He was among the first to elaborate on the construct of dissociation, currently defined as a ‘‘disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment’’. Janet argued that hysteria involves not only the body, but also the mind, with the core psychological feature of a retraction of the field of consciousness. Consequently, perceptions are not assimilated into normal consciousness, which results in the dissociative phenomena of amnesia for personally relevant information, identity disturbances or depersonalization. Although Janet assumed a hereditary diathesis for dissociation, he also emphasized that various psychosocial stressors and traumas finally trigger the hysterical symptoms. In the last two decades, the Janetian perspective on hysteria has been revived. Recent empirical research has confirmed a close association between dissociation, somatization and conversion, both on the level of symptoms and that of disorders [4–6]. With respect to the treatment, it is very important to diagnose and pay attention to the dissociative phenomena, because they can be assumed to be predictive of a) greater psychopathology at pretreatment, b) poorer treatment response and c) higher relapse rates [7]. 1 Department of Psychiatry and Psychotherapy, Ernst-Moritz-Arndt-University, Rostocker Chaussee 70, D-18437 Stralsund, Germany

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Furthermore, it has been demonstrated that traumatic experiences, particularly childhood maltreatment, play an important role in the pathogenesis and psychodynamics of somatization and conversion [4, 6, 8]. Therefore, it was proposed to conceptualize both somatization and conversion as traumarelated conditions and the corresponding disorders as post-traumatic stress spectrum disorders [9]. Indirect support for this proposal stems from studies demonstrating a) high comorbidity rates of the somatoform and conversion disorders with depression, anxiety, substance use and personality disorders [4, 10], and b) that the comorbidity pattern resembles the one reported for post-traumatic stress disorder. Definitely, we are in need of further research to clarify the association between trauma, post-traumatic stress, somatization, and conversion. However, it may be very helpful to adapt therapeutic strategies to meet the needs for traumatized patients with conversion and somatization disorders. Another controversial aspect relates to the epidemiology of conversion disorders. Merskey and Mai claim that ‘‘it is generally accepted that classical conversion disorders are now rare in developed countries’’. However, our clinical experience and epidemiological studies contradict this notion. For example, in the general population, the lifetime prevalence for conversion disorders is 0.6% [11], and in clinical samples, these patients are frequently found, for example, 10–58% of adults referred to epilepsy centres present with psychogenic, non-epileptic seizures as a specific type of conversion disorder [12]. In summary, the long-standing and fascinating debate on hysteria, somatization and conversion is far from being resolved. Patients still suffer (and probably will do so) from ‘‘medically incompletely explained symptoms’’. Thus, it remains a scientific and clinical challenge to refine our concepts about the mechanisms that underlie the transfer of psychological distress into bodily symptoms and to develop effective treatment options.

REFERENCES 1. 2. 3. 4. 5.

Taylor G.J. (2003) Somatization and conversion: distinct or overlapping constructs? J. Am. Acad. Psychoanal. Dyn. Psychiatry 31: 487–508. Spitzer C., Freyberger H.J., Kessler C. (1996) Hysteria, dissociation and conversion. A review of concepts, classification and diagnostic instruments. Psychiatr. Prax. 23: 63–68. van der Kolk B.A., van der Hart O. (1989) Pierre Janet and the breakdown of adaptation in psychological trauma. Am. J. Psychiatry 147: 1530–1540. Sar V., Akyuz G., Kundakci T., Kiziltan E., Dogan O. (2004) Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am. J. Psychiatry 161: 2271–2276. Spitzer C., Spelsberg B., Grabe H.J., Mundt B., Freyberger H.J. (1999) Dissociative experiences and psychopathology in conversion disorders. J. Psychosom. Res. 46: 291–294.

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6.

van der Kolk B.A., Pelcovitz D., Roth S., Mandel F.S., McFarlane A., Herman J.L. (1996) Dissociation, somatization, and affect dysregulation: the complexity of adaptation of trauma. Am. J. Psychiatry 153: 83–93. Michelson L., June K., Vives A., Testa S., Marchione N. (1998) The role of trauma and dissociation in cognitive-behavioral psychotherapy outcome and maintenance for panic disorder with agoraphobia. Behav. Res. Ther. 36: 1011–1050. Roelofs K., Keijsers G.P., Hoogduin K.A., Naring G.W., Moene F.C. (2002) Childhood abuse in patients with conversion disorder. Am. J. Psychiatry 159: 1908– 1913. Moreau C., Zisook S. (2002) Rationale for a posttraumatic stress spectrum disorder. Psychiatr. Clin. North Am. 25: 775–790. Tomasson K., Kent D., Coryell W. (1991) Somatization and conversion disorders: comorbidity and demographics at presentation. Acta Psychiatr. Scand. 84: 288–293. Faravelli C., Abrardi L., Bartolozzi D., Cecchi C., Cosci F., D’Adamo D., Lo Iacono B., Ravaldi C., Scarpato M.A., Truglia E., et al. (2004) The Sesto Fiorentino Study: background, methods and preliminary results. Psychother. Psychosom. 73: 216–225. Sirven J.I., Glosser D.S. (1998) Psychogenic non-epileptic seizures: theoretical and clinical considerations. Neuropsychiatry Neuropsychol. Behav. Neurol. 11: 225–235.

7. 8. 9. 10. 11.

12.

1.12 The Mind–Body Dualism and Conversion Disorders Carlo Faravelli1 and Massimo Lai1 Ancient medicine has been strongly influenced by the platonic dualism between mind and body, repeated during the seventeenth century with Descartes’ distinction between res cogitans and res extensa. Since then, and especially after the general acceptance of the anatomo–clinical method, medicine has always been embarrassed in evaluating the relationship between psyche and soma. In principle, following the Cartesian dualism, the study of the human mind should remain at the level of psychic symptoms. In organic medicine, the separation between mind and body is somehow acceptable, as organicism in itself represents a fairly autonomous system, able to explain most of the current pathology. The psychic component of the diseases is usually left apart, without an appreciable diminution of the explanatory power. Remaining at the level of the physical, no special epistemological paradigm is required, since those provided by the natural sciences are generally appropriate. The reverse is also true: the purely psychological theories of mind do not care about physical symptoms or, when they are obliged to do 1

Department of Neurological and Psychiatric Sciences, University of Florence, Italy

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so, like psychoanalysis, they simply get rid of the problem by invoking a ‘‘deus ex machina’’ named ‘‘energy’’. Psychiatry is in a different position: the present psychiatric classifications list an impressive number of somatic symptoms among the criteria required to make a diagnosis. In the DSM-IV, for instance, about half the symptoms taken into account for the diagnosis of psychiatric disorders are somatic. Yet, there is no acceptable theoretical framework that allows the inclusion of psychic and bodily aspects in a unitary vision. Basically, there are different positions to explain the physical symptoms in the context of mental disorders: a) the activation of the same areas of the brain produces both physical and psychic symptoms; b) mental activity stimulates centres that induce physical symptoms; c) the energy accumulated during the psychic processes is discharged via peripheral pathways; d) there is a language of the body, via which some messages are symbolized and transmitted through the body (partly a corollary of the preceding); and e) somatic symptoms induce mental reactions. It is worth noting that a precise historical course exists in this area, as in several cases the supposed psychogenetic origin of a somatic disorder has later been disconfirmed and replaced by a purely biological explanation. Few people remember that Freud described the psychodynamic mechanisms of epilepsy. In some of the most typical so-called psychosomatic illnesses, the progress of knowledge has discovered well-defined organic causes (the genetic origin of psoriasis, Helicobacter Pylori in gastric ulcer, to quote a couple of recent examples). It is illuminating to read a book of history of medicine: for those illnesses whose causes are still unknown, the hypotheses proposed often involve a psychosomatic pathogenesis. However, for those illnesses in which substantial aetiological factors have been later clarified, the psychosomatic interpretation sounds na¨ıve now, if not bizarre. Hysteria is perhaps the paradigm of the above difficulties. Charcot emphasized the affective nature of some neurological phenomena, trying to include hysteria among neurological diseases: hysteria as a congenital degeneration of the brain. However, he focused on the role of hypnosis, inducing the conception of psychological origin of hysteria in the young Freud. Psychoanalytical theories contributed to strengthening the psychogenic conception of symptoms. The lack of physiological evidence of structural nerve fibre disease in an arm paralysis was a sign of psychogenic and non-organic disease. Extensively, any symptom that could not be ascribed to a well-defined organic lesion was a confirmation of the mind-body dualism. The psychogenic origin of pseudo-neurological conversion symptoms is mainly inferred from the fact that they do not reflect the distribution of the motor and sensory pathways. However, current pathophysiological research has begun to provide mechanistic explanations for conversion symptoms, thus blurring the distinction between psychogenic and organic

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motor symptoms [1]. On the other hand, life events have also been associated with the onset of a variety of somatic illnesses. The fact that a given set of symptoms follows an emotional conflict does not warrant its psychological origin. The diathesis-stress model may well explain stress-related symptoms, both somatic and psychic [2]. The involvement of the hypothalamicpituitary-adrenal axis in stress, per se, could have consequences including psychosomatic disorders and cardiovascular, gastrointestinal and immune diseases [3]. Franz Joseph Gall’s phrenology was the first attempt to overtake the separation between psyche and soma in medicine. More recently, the unitary model has been reformulated in the book ‘‘The Descartes’ Error’’ by Damasio [4]. His view offers a good perspective for the understanding of mental disorders, including those without apparent organic explanation. What we commonly call the mind is a set of operations carried out by the brain [5]. The actions of the brain underlie not only relatively simple motor behaviours, such as walking or eating, but all the complex cognitive actions that we believe are quintessentially human, such as thinking, speaking, and creating works of art [5]. According to the unitary concept, the relationship between genetic and environmental processes is interactive, fluid, and cumulative in their ability to influence an individual’s developmental trajectory and alter subsequent behavioural outcomes [6]. Neuroplasticity can explain the modifications that environment can induce in the brain. The disorders that are grouped together with the anachronistic name ‘‘mental illnesses’’ may primarily be characterized by problems in synaptic communication, synaptic plasticity, and neural circuit function rather than by tissue damage, and then represent dysfunctions of the highest integrative functions of the brain, including cognition, emotional regulation, and executive functions [7]. Therefore, the distinction between mind and brain may no longer have a reason to exist.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Krem M.M. (2004) Motor conversion disorders reviewed from a neuropsychiatric perspective. J. Clin. Psychiatry 65: 783–790. Dersh J., Polatin P.B., Gatchel R.J. (2002) Chronic pain and psychopathology: research findings and theoretical considerations. Psychosom. Med. 64: 773–786. De La Torre B. (1994) Psychoendocrinologic mechanism of life stress. Stress Med. 10: 107–114. Damasio A. (1995) The Descartes’ Error. Emotion, Reason, and the Human Brain. Quill: New York. Kandel E.R., Schwartz J.H., Jessell T.M. (Eds). (2000) Principles of Neural Sciences, 4th ed. McGraw-Hill: New York. Fishbein D. (2000) The importance of neurobiological research to the prevention of psychopathology. Prev. Sci. 1: 89–106. Hyman S.E. (2002) Neuroscience, genetics, and the future of psychiatric diagnosis. Psychopathology 35: 139–144.

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1.13 Concepts of Medically Unexplained Symptoms in Relation to Mind-Body Dualism Athula Sumathipala1 Medically unexplained symptoms are a common problem all over the world in primary care, specialist clinics, and inpatient care. Symptoms can be transient or chronic. Patients are usually distressed, disabled, dissatisfied, heavily investigated, overuse health services, and incur health care costs disproportionate to their income. Therefore, this morbidity has implications for the patient, family, society, care providers and the health care system. However, its understanding is still limited. As Merskey and Mai point out in their timely review, the interpretation of these symptoms has vacillated between the mind and the body. Although this may be seen as a pendulum shifting to and from mind and body, the process has not meant a complete reversal each time. Return to the previous locus has been with some improvement in the understanding of the phenomenon. Early explanations focused on a disturbance of bodily organs, particularly the uterus, and consequently the unexplained symptoms were referred to as hysterical. Management included application of ointments to the labia and direct manipulation of the organ. After the Renaissance, increasing understanding of the anatomy led to the diseases of the nervous system being regarded as the origin of medically unexplained symptoms. However, the aetiology was still presumed to be physical and the treatment remained similar. By the end of the seventeenth century, psychological factors began to be considered important and there was a shift to ‘‘a disease in the mind’’. With this, came an improvement in the management of these patients by the physician’s interest in patient’s explanation, examination of the mental state, installation of hope and optimism. In the nineteenth century, there was a return to a predominantly physical explanation. However, because of the absence of observable anatomical abnormality in the brain or elsewhere, the concept of ‘‘functional’’ or ‘‘dynamic’’ lesion was developed, but the emphasis remained on physical interventions. By the end of the nineteenth century, emphasis returned again exclusively to a psychological origin. The treatment too became explicitly psychological, with an inevitable implication for some patients as well as physicians who may misinterpret the notion ‘‘psychological’’ as an imaginary condition. As correctly put across by Merskey and Mai, the concept of somatization disorder remains controversial. Current psychiatric systems for classifying disorders remain unsatisfactory for those patients with medically unexplained symptoms. Kanton et al. [1] reported that out of 100 patients referred 1

Institute of Psychiatry, Kings College, University of London, Denmark Hill, London SE5 8AF, UK

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to liaison psychiatrists with medically unexplained symptoms, only 6% met DSM criteria for somatization disorder and less than 30% had somatoform disorder. Thus, somatoform disorders do not describe the majority of patients presenting with unexplained symptoms who are referred to liaison psychiatrists. In another study in primary care, only 5% of patients who recently presented to their own general practitioner with unexplained symptoms met the criteria for somatization disorder [2]. An ‘abridged’ cut off score was proposed by Escobar et al. [3]—abridged somatization was defined by a cut off of four or more symptoms for males and six or more for females. Escobar et al. [4] estimated the prevalence of somatization disorder at 0.06–0.5% in primary care, but found that 20% of all attendees met criteria for an abridged somatization diagnosis. However, existing terms are unsatisfactory because they are used imprecisely, and may convey aetiological assumptions and/or have pejorative overtones [5]. Current thinking strongly resists the tendency of a na¨ıve conceptual separation of mind and body, and instead considers biological, psychological, and social aspects in such patients. There are many different models for understanding medically unexplained symptoms. However, there is a considerable overlap between these models—for example, between the psychodynamic model and the family systems model or between the learning model and the family systems model. The cognitive behavioural model appears as a pragmatic one, incorporating elements from the family systems, social learning and medical models.

REFERENCES 1. 2. 3.

4. 5.

Kanton W., Ries R.K., Kleinman A. (1984) A prospective DSM-III study of 100 consecutive somatization patients. Compr. Psychiatry 25: 305–314. Deighton C.M., Nicol A.R. (1985) Abnormal illness behaviour in young women in a primary care setting: is Briquet’s syndrome a useful category? Psychol. Med. 15: 515–520. Escobar J.I., Manu P., Matthews D., Lane T., Swartz M., Canino G. (1989) Medically unexplained physical symptoms, somatization disorder and abridged somatization: studies with the Diagnostic Interview Schedule. Psychiatr. Dev. 7: 235–245. Escobar J.I., Garam M., Silver R.C., Waitzkin H., Holman A., Compton W. (1998) Somatisation disorder in primary care. Br. J. Psychiatry 173: 262–266. Mayou R., Bass C., Sharpe M. (Eds). (1995) Treatment of Functional Somatic Symptoms. Oxford University Press: Oxford.

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1.14 A Challenge for Both Clinicians and Researchers Antonio Lobo1 Merskey and Mai’s timely and comprehensive review accurately describes not only the relevance but also the challenge of somatization disorders for both clinicians and researchers. Important conceptual questions remain about the validity of commonly used constructs and about the paradigms to approach the clinical phenomena, and new models have been suggested [1, 2]. The authors’ review begins by distinguishing ‘‘two groups of symptoms both phenomenologically and aetiologically’’, laying out the ground for differences between somatization and conversion disorders. However, controversies in the field are immediately apparent: both types are classified in the same group of somatoform disorders by the DSM-IV-TR; while the ICD10 classifies them separately, although included in a heterogeneous ‘‘overall group’’, the only common denominator being ‘‘their historical association with the concept of neurosis, and the association of a substantial (though not exactly known) proportion of these disorders with psychological causation’’. This is quite unsatisfactory, we believe. There is little doubt that both DSM and ICD represent advances in diagnostic practice. As McHugh and Slavney [3] have argued, ‘‘a reliable categorization is an important step in reasoning from initial construals about psychiatric conditions’’. However, they call attention about the precariousness of this advance based on ‘‘a negotiated terminology and diagnostic pathway’’ yet to be validated. In their four perspectives model, they recommend radically different approaches for different categories of disorders. Specifically, the ‘‘behaviour perspective’’ recommended for somatization and conversion disorders is radically different from the traditional ‘‘disease perspective’’ to be used in dementia or schizophrenia. The former are ‘‘behaviours, by definition, in that they are goal-directed activities; disorders, because the goals are deviant’’. In this particular case, ‘‘the goal of the behaviour is to persuade others to accept the patients’ beliefs in their sickness’’. Similarly, Goldberg et al. [4] classify somatization and conversion in the group of ‘‘abnormal illness behaviour’’. We agree with this approach. Dispositional features of the patient are taken into account in this ‘‘behaviour perspective’’. In fact, to understand the brain mechanisms that predispose to and contribute to maintaining these symptoms remains one of our greatest challenges [5]. However, according to the behavioural approach, psychosocial precipitating factors and the setting in which they develop are the crucial aspects in somatization and conversion disorders. This is one of 1

Department of Psychiatry, Hospital Cl`ınico Universitario, Planta 3, 50009 Zaragoza, Spain

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the main reasons to support the role of epidemiology and epidemiological methods in this field [6]. We have some data to support the idea that somatization ‘‘cuts across diagnostic categories’’. In a representative primary care sample in Spain, we found that the prevalence of somatizers (STs) was 9.4% (one-third of the cases) and most patients (68.7%) were diagnosed in the depression or anxiety DSMIV categories. Only 18.3% of STs fulfilled criteria for somatoform disorders, and two-thirds of these patients were chronic [7]. STs were three times more prevalent than psychologizers (PGs), but the ratio STs:PGs depended heavily on diagnostic categories. While most psychopathological scores were higher in PGs, both patient groups were similarly disturbed [8]. We supported the validity of Kirmayer and Robbins’ subclassification of somatizers (functional, hypochondriacal, and presenting somatization) in our Southern-European culture, but the overlap of the three clinical forms (42.7%) was more frequent than reported in North American studies [9]. Merskey and Mai adequately point out the difficulties in the conceptualization and diagnosis of conversion disorders. Ron [5] tends to confirm such difficulties and observes that the advent of non-invasive imaging and the better characterization of some neurological disorders have made it possible to diagnose as neurological hitherto ‘‘unexplained’’ symptoms. However, on the basis of clinical experience and follow-up studies, we agree with her claim that ‘‘there is still important evidence to suggest that for a core of symptoms the diagnosis of conversion disorder will remain valid’’. The principles of management in somatization disorders are well laid out by experts in the field, and Merskey and Mai review carefully the state of the art. We believe ‘‘antidepressant’’ medications might also have a role in the most severe cases of non-depressed, non-anxious somatizers, but the evidence for this is particularly weak at this point [2]. However, in consonance with the ‘‘behavioural approach’’, ‘‘rational treatments’’ should follow the identified psychosocial sources of the problem. To put it in McHugh and Slavney’s words, while the task in ‘‘diseases’’ would be the cure, a radically different approach, a ‘‘redirection of a way of life’’ is to be recommended in pathological ‘‘behaviours’’ [3]. This approach, specifically tailored for somatizers, has been successful in the hands of clinicians and researchers such as Goldberg et al. [4]. It is remarkable, though, that other types of psychotherapy have also proved to be of some value, particularly insight-oriented psychotherapy [10]. In respect to this, we believe that the conclusions of Frank and Frank [11] remain valid: ‘‘the shared moraleenhancing properties of all forms of psychotherapy contribute importantly to their favourable outcomes. The interaction between particular therapists and patients, determined by the personal qualities, values, and expectations of both, contributes more to outcome than does the therapeutic technique’’.

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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Mayou R., Levenson J., Sharpe M. (2003) Somatoform disorders in DSM-V. Psychosomatics 44: 449–451. Abbey S.E. (2005) Somatization and somatoform disorders. In: Textbook of Psychosomatic Medicine, J.L. Levenson (Ed). American Psychiatric Publishing: Washington, D.C., pp. 270–296. McHugh P.R., Slavney P.R. (1998) The Perspectives of Psychiatry. Johns Hopkins: Baltimore. Goldberg D., Benjamin S., Creed F. (1994) Psychiatry in Medical Practice. Routledge: London. Ron M. (2001) Explaining the unexplained: understanding hysteria. Brain 124: 1065–1066. Lobo A., Campos R. (1997) The contribution of epidemiology to psychosomatic medicine. Epidemiol. Psichiatr. Soc. 6: 40–47. Lobo A., Garcia-Campayo J., Campos R., Marcos G., Perez-Echeverria M.J. (1996) Somatisation in primary care in Spain: I. Estimates of prevalence and clinical characteristics. Br. J. Psychiatry 168: 344–348. Garcia-Campayo J., Campos R., Marcos G., Perez-Echeverria M.J., Lobo A. (1996) Somatisation in primary care in Spain: II. Differences between somatisers and psychologisers. Br. J. Psychiatry 168: 348–353. Garcia-Campayo J., Lobo A., Perez-Echeverria M.J., Campos R. (1998) Three forms of somatization presenting in primary care settings in Spain. J. Nerv. Ment. Dis. 186: 554–560. Guthrie E. (1995) Treatment of functional somatic symptoms: psychodynamic treatment. In: Treatment of Functional Somatic Symptoms, R. Mayou, C. Bass, M. Sharpe (Eds). Oxford University Press: Oxford, pp. 144–160. Frank J.D., Frank J.B. (1993) Persuasion and Healing. Johns Hopkins: Baltimore.

1.15 Somatization Disorders in the African Context Frank G. Njenga1 , Anna N. Nguithi1 and Rachel Kang’ethe1 In the early seventies, the standard teaching at the medical schools in parts of Africa was that hysteria was a common disorder of young women that responded rapidly to the forceful inhalation of ammonia (in cotton wool). The treatment was so painful to the patients that few dared come back after its administration. With each ‘‘diagnostic intervention’’, came a gleeful sense of achievement by the medical students (and sometimes their teachers), grounded on ignorance of the nature of the disorder, which was no better in some respects than that of the Greeks who hypothesized on the migration of the womb as the cause of the condition. 1

Upper Hill Medical Centre, Nairobi, Kenya

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Sadly, there is little evidence of an increase in the knowledge base (and practice) in some parts of Africa [1]. In our practice, it is still common to see patients who primarily present with ‘‘hysterical’’ symptoms. Many come to our care after prolonged, often expensive contact with colleagues in general medicine and neurology, where they present with medically unexplained symptoms of paralysis, blindness, seizures, cough and pains, and aches. Children and adolescents, for example, present interesting and sometimes challenging situations. Following reports of a death in an electrical fire accident in a rural village in Kenya, a 10-year old girl had a ‘‘fit’’ as she was hanging clothes on a line, claiming loudly to have experienced an electric shock, just like she had heard her parents say of the children from next door who had died. A 16-year old girl, fed up of seeing her parents fight, became ‘‘blind’’. A nine year old girl developed a backache which enabled her to miss school so that she could help her grandmother fetch firewood as the latter was unable to do so herself because of advanced osteoarthritis. Treatment of grandmother’s back got the girl better and back to school. Earlier authors from Africa, including Allan German [2], wrote about sub-clinical malnutrition of the African as a contributor to mental disorder (together with infections and infestations, and with anaemia, often due to worms). It is interesting that this line of early thinking resonates well with Merskey’s and Mai’s thoughts on the biological correlates of somatization disorder, which on the face of it would seem rather surprising, given a condition traditionally viewed purely as psychodynamic. Biological changes and organic conditions may be part of the antecedent stimuli that precipitate somatization. Further elaborating along these lines, one begins to put into focus a number of well-known facts about hysteria (as opposed to somatization). It is, for example, generally accepted that hysteria is more common in the developing world, and that its prevalence in the West has declined over the centuries. Additionally, there is some suggestion from Africa that it is declining in prevalence, for reasons that remain unclear. One could argue that hysteria is a mental disorder of poor sickly people that could potentially be eliminated by overall reduction in poverty. Another interesting, but unexplained, observation is that the condition has a good prognosis in the developing world, perhaps due to different aetiological factors at play. The economic and social costs of somatization are extremely high, particularly in a continent where the majority live on less than a dollar a day. In practice, therefore, there is greater urgency in Africa to diagnose and manage the disorder. Kiima [3] found that many primary care attendees in Nairobi received a diagnosis of ‘‘clinical malaria’’ in the absence of evidence to support that diagnosis (such as fever). This led to many repeat visits and expensive investigations. In the management of the few resources available to the developing world, proper and careful diagnosis and management of

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somatization disorder is imperative. However, the clinician must be careful. For example, HIV/AIDS, which has a prevalence of up to 35% in some parts of Africa, sometimes presents as hysteria, whereas in reality the clinical picture is a manifestation of the infection of the central nervous system. The clinician in areas with high HIV prevalence will therefore see some cases of ‘‘hysteria’’ due to this infection. The pressure for academic excellence in Africa is often great, and students sometimes succumb to somatization disorders under the weight of the demands of parents, who make subtle and sometimes not so subtle statements regarding their expectations of their children. For example, Kagwa [4] and Muhangi [5] studied the problems of mass hysteria in East Africa. They found that such epidemics commonly occurred in girls’ schools, under social or academic pressure. Other types of pressures also come into play. For example, hysterical fits occurring early morning before school only in girls (not their brothers) all came from a school where the sewage system to the girls toilet was blocked, meaning the girls had no toilet facilities all day. In another case, an entire group of school children who walked a particular path to school developed hysterical blindness after one of them was killed by a guard dog on the way to school ‘‘before their very eyes’’. They only recovered after an alternative path was found for them to get to school. In some cases, the mother (less commonly, the father) will loudly and dramatically explain a child’s symptoms to the doctor as the child watches with a combination of indifference and disbelief at what he is supposed to be suffering from. The key to the solution of this type of case lies in the answer to the question: ‘‘Do you also (mom) have any similar symptoms?’’ Usually the mother will confirm suffering the same symptoms, always with an onset earlier than that of the child. For as long as parents feel ashamed to admit to psychological symptoms, these conditions seem to persist. Njenga [6] describes the case of a five-year old girl whose fits of two months served the purpose of keeping her parents together as the family moved from place to place in search of a cure for her condition. As long as the child was ill, the family remained intact. Because somatization disorders are, by their very nature and definition, not life threatening, their significance as causes of morbidity and as a drain to the very limited resources in the developing world seems unimportant against such problems as AIDS, wars and malaria. The truth, however, is that the poorly resourced medical departments continue to pay heavily through increased utilization. Other additional costs arise from visits to traditional healers who, according to a recent study from Tanzania [7], have as their patients 48% with depression as opposed to 24% in primary care. The role of traditional healers in the management of somatization disorder is difficult to overstate. This is because they outnumber doctors by such

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large margins, and also because they live closer to the people. They are also more likely to be in touch with the fears and stresses of their people than the doctors. The encouraging experience in Kenya is that they are able and willing to work with doctors in identifying, for example, those seizure disorders due to ‘‘disease for hospital’’ and those best treated by traditional methods. In the former, the fits come ‘‘even when nobody is watching, lead to injury of the body, and are often accompanied by burns’’. The others have no such features and are often due to possession by evil spirits and curses. Simple educational contacts between the two groups of healers, if based on mutual respect for each other’s skills, can lead to a better outcome in the treatment of somatization disorders in Africa.

REFERENCES 1.

Othieno C.J., Okech V.C.A., Omondi J.A., Makanyengo M.A. (2001) How Kenyan physicians treat psychiatric disorders. East Afr. Med. J. 78: 204–207. German G.A. (1972) Aspects of clinical psychiatry in sub-Saharan Africa. Br. J. Psychiatry 121: 461–479. Kiima D.M. (1987) Prevalence rates of psychiatric morbidity among patients attending a primary health care facility (health centre) in a deprived community in Nairobi. Dissertation, University of Nairobi. Kagwa B.H. (1964) The problem of mass hysteria in East Africa. East Afr. Med. J. 41: 560–566. Muhangi J.R. (1973) A preliminary report on mass hysteria in an Ankole school in Uganda. East Afr. Med. J. 50: 304–309. Njenga F. (1991) Child psychiatry in Kenya. In: Mental Health in African and the Americas Today, S.O. Okpaku (Ed). Chrisolith Books: Nashville, pp. 257–274. Pierloot R.A., Ngoma M. (1988) Hysterical manifestations in Africa and Europe. A comparative study. Br. J. Psychiatry 152: 112–115.

2. 3. 4. 5. 6. 7.

1.16 Somatization and Conversion Disorders: An Arab Perspective Tarek A. Okasha1 Nearly 1000 years before Hippocrates used the term hysteria, ancient Egyptians, in the Kahun Papyrus (a papyrus for uterine diseases), described a series of morbid states, all attributed to the displacement of the uterus. They ascribed these morbid states to the ‘‘starvation’’ of the uterus by its upward displacement, with a consequent crowding of other organs leading to different bodily symptoms. As treatment, the genitalia were fumigated with 1

Institute of Psychiatry, Faculty of Medicine, Ain Shams University, Cairo, Egypt

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precious and sweet smelling substances to attract the womb, or evil tasting and foul smelling substances were injected or inhaled to repel the organ and drive it away from the upper part of the body where it was thought to have wandered. Most of these diseases are defined clearly enough to be recognizable today as hysterical disorders. It is interesting to know that the ancient Pharaonic Egyptian medicine did not recognize the specificity of mental disorders. They attributed all mental phenomena to disorders in the heart (Eber’s papyrus) or the uterus (Kahun papyrus). There was no psyche, only soma. Therefore, there was no stigma attached to mental illness [1, 2]. In 1990, the first 1000 patients presenting to the outpatient clinic of the Institute of Psychiatry of Ain Shams University in Cairo were screened to determine whether they fulfilled DSM-III-R criteria for either conversion or dissociative disorders [3], replicating a study undertaken at the same clinic 26 years earlier, where hysteria constituted 11.2% of the sample [4]. The newer study aimed to test the relevance of the diagnosis of ‘‘hysteria’’ (conversion and dissociative disorder). According to its results, many disorders that would formerly have been diagnosed as hysteria would now receive another diagnosis, mostly somatoform disorder. However, some cases still require the diagnostic label of hysteria to reflect the symptoms and the underlying mechanisms (stress, primary gain, secondary gain, and motor and sensory symptoms that are culturally and symbolically related to the stress). The prevalence of hysteria in that study (5%) is comparable with that of organic mental disorders (5.1%), personality disorders (4.9%), and anxiety disorders (7.9%), indicating that hysteria cannot be ignored as a diagnostic category. For Arabs, ‘‘pain’’ is the main indication of illness. It is usually attributed to a neighbouring organ, for example, headache, tightness of chest, and so on. Emotional and behavioural problems are not perceived as a mental illness. Sometimes they are explained in terms of delusional cultural beliefs, low level of endurance, or low level of patience. A number of writers have stressed the importance of viewing pain as a multi-dimensional experience with more similarity to emotional states than sensory processing. The Arabic language tends to be overemphatic and hyperbolic. It expresses emotively at the expense of rationality. Patients and relatives exaggerate their verbal reports of distress. Somatizers are usually young, more histrionic, and exposed to a multitude of stress factors. Okasha and Okasha argue that the higher prevalence of women among somatizers may be explained by the help-seeking behaviour of women. Expectations from housewives and mothers would attribute more respect to a somatic complaint than a psychological one [5]. While the former is frequently respected, the latter is frequently discarded as irrelevant. In another study, patients presenting to the outpatient psychiatric clinic of an Egyptian University Hospital were studied over a 4-month period.

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Out of 620 outpatients, somatoform disorders were present in 17.8%. Among those, 76.6% were diagnosed as undifferentiated somatoform. Other diagnoses included somatization disorder (9.5%), persistent pain disorder (8.7%), and hypochondriasis (5.4%). The most frequently reported symptoms were headache, pain in other parts of the body, autonomic symptoms, abdominal symptoms, and sensory complaints. Psychiatric comorbidity was 85–90%, where depression came first (58.7%), followed by anxiety (36.9%), and then anxiety/depression (6.5%) [6]. Okasha and Okasha studied 120 Egyptian patients (84 men and 36 women) with ages ranging between less than 20 and over 60 years. Symptom clusters involved central nervous system symptoms (90%), gastrointestinal symptoms (87.5%), pain and headache (80%), fatigue (90%), chest symptoms (82%), cardiovascular symptoms (72.5%), genito-urinary symptoms (52.5%), and muscular symptoms (52.5%). Diagnoses given to the 72 inpatients were as follows: depressive disorder (31.9%), schizophrenia (29.1%), anxiety and phobic disorder (13.8%), delusional disorder (12.5%), somatoform disorder (8.3%), and acute polymorphic psychotic disorder (7.1%). Among the 48 outpatients, 25% had depressive disorder, 25% had somatoform disorder, 25% had anxiety and phobic disorder, 18.7% had bipolar manic disorder, and 6.2% had neurasthenia [7]. In Bahrain, Haddad applied the General Health Questionnaire and the Bradford Somatic Inventory and showed psychiatric morbidity presenting with somatization in 19.4% of general hospital patients [8]. Fahmy investigated 100 somatizers and found 34% to suffer from depression, 30% from anxiety, 16% from adjustment disorders, 4% from somatoform disorders, and 2% from somatization. Women with somatization were significantly more illiterate, culturally deprived, and depressed [9]. There is increasing evidence that somatization as such is not necessarily a culturally bound phenomenon. What may be unique for every country is the clinical images of somatization and the challenges it puts on the existing mental health care facilities. The latter should be a prime area of input and concern, to the benefit of a considerable percentage of our psychiatric population [10].

REFERENCES 1. 2. 3. 4.

Okasha A., Okasha T. (2000) Notes on mental disorders in Pharaonic Egypt. Hist. Psychiatry 11: 413–424. Okasha A., Karam E. (1998) Mental health services and research in the Arab World. Acta Psychiatr. Scand. 98: 406–413. Okasha A., Aief El Dawla A., Assad T. (1993) Presentation of hysteria in a sample of Egyptian patients—an update. Neurol. Psychiatry Brain Res. 1: 155–159. Okasha A. (1967) Hysteria: its presentation and management in Egypt. Ain Shams Med. J. 18: 13–20.

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Okasha A., Okasha T. (1999) Somatoform disorders—an Arab perspective. In: Somatoform Disorders, A Worldwide Perspective, Y. Ono, A. Janca, M. Asai, N. Sartorius (Eds). Springer: Berlin, pp. 38–46. Soliman H. (1997) Comorbidity of somatoform disorder. Egypt. J. Psychiatry 20: 129–140. Okasha A., Okasha T. (1998) Somatoform disorders. An Arab perspective. Presented at the Conference on Somatoform Disorders, Tokyo, February 1998. Haddad M., Kamel C. (1996) Aspects of somatization in Bahraini patients. Egypt. J. Psychiatry 19: 61–67. Fahmy M. (1996) Somatic presentations of psychiatric illnesses in outpatient psychiatric clinic in Jeddah. Egypt. J. Psychiatry 19: 61–67. Okasha A. (2003) Somatoform disorders revisited. Acta Neuropsychiatr. 15: 161–166.

1.17 Much Theory, but Little Agreement Alberto Perales1 and H´ector Chue1 Magic precedes science. Human mind cannot tolerate uncertainty and, whenever truth is missing, it is replaced by hypothetical thinking, no matter how strange and far from reality this might be. Historically, scientific progress has been full of erratic proposals, as diagnostic classification in psychiatry proves. In their scholar review on somatization and conversion disorders, Merskey and Mai point out that ‘‘hysteria is not a specific clinical entity nowadays’’. As a concept, however, it was of great usefulness in the old psychiatric classification. We fear that, in spite of current advances in psychiatric nosology and classification, reliable and detailed clinical information is still too scanty to allow definite conclusions to be drawn. As scientists, we know that classifying diseases or disorders is a fundamental step for the discovery of the corresponding aetiologies, and we should make all possible efforts to better isolate the disorders in question in order to recognize them and differentiate them from other clinical entities. In Peru, the health care system is split in four different sectors that cover the health needs of 27 million people. The public sector covers 66.5%; social health insurance 27%; the private sector 4%; and the army sector 2.5%. According to the psychiatric statistics of public sector for 2004 provided by the Peruvian Ministry of Health, dissociative (conversion) disorders accounted for 0.01–0.05% of psychiatric visits and somatization disorders for 0.1%. These percentages increase drastically in the corresponding unspecified categories, ten times for dissociative (conversion) disorders and twice for somatoform disorder. The comparison by sex shows slightly higher 1

Universidad Nacional Mayor de San Marcos, Lima, Peru

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percentages in females than in males for dissociative (conversion) disorders, while the percentages for somatization disorders are similar. The social health insurance system reported a total of 19,748 psychiatric visits in 2004. Of these visits, 244 (1.2%) led to a diagnosis of F45 (somatoform disorder), of which none corresponded to F45.0 (somatization disorder). The army health sector reported 6,500 psychiatric visits in 2004. Of these visits, 70 led to a diagnosis of F44 dissociative (conversion) disorders (1.1%) and none to a diagnosis of F45.0 (somatization disorder). These data show the rarity of these diagnoses in psychiatric settings and the higher prevalence of unspecified diagnoses. This opens room to the suspicion that the criteria used to guide the diagnostic decisions in these disorders are not clearly defined or have little empirical support. This evidence claims for an urgent reassessment and clinical research in this area.

CHAPTER

2 Pain Disorder: A Review Steven A. King New York University School of Medicine, New York, USA

INTRODUCTION Of all the problems faced by physicians, pain is the most pervasive. Fifteen to 30% of adult Americans report having at least one episode of back pain during a 1-year period, and health care expenditures in the United States for individuals suffering from this form of pain alone is over $90 billion per year [1]. Ten percent of the population report having chronic pain [2]. Pain may be secondary to physical or psychological factors or a primary disorder. Though pain has traditionally been viewed as primarily a physical problem, current concepts of pain indicate that this view is outdated. The most commonly accepted definition of pain is that presented by the Committee on Taxonomy of the International Association for the Study of Pain: ‘‘An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage . . . . Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause’’ [3] (emphasis added). The Institute of Medicine Committee on Pain, Disability, and Chronic Illness Behaviour reported that ‘‘the experience of pain is more than a simple sensory process. It is a complex perception involving higher levels of the central nervous system, emotional states, and higher order mental processes’’ [4]. Research has indicated that, in many cases of acute pain and the majority of cases of chronic pain, both the mind and the body appear to play significant roles in both the development and maintenance of the pain. In order to reflect this, a new diagnostic category, pain disorder, was introduced in the DSM-IV [5].

Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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AETIOLOGY OF PAIN What causes pain remains something of a mystery. There is general agreement that peripheral injury leads to pain through a series of neurochemical processes that transmit the pain signal from the periphery to the central nervous system [6]. Though this model is acceptable for many cases of acute pain, it fails to adequately address most cases of chronic pain. Beginning with the introduction of the gate control theory of pain by Melzack and Wall in 1965 [7], where they postulated a gating mechanism in the dorsal horn that regulated transmission of pain and was influenced by both ascending and descending factors, there has been a growing focus on the role of central mechanisms in pain. More recently, Apkarian et al. [8] demonstrated that chronic back pain is accompanied by brain atrophy. The literature indicates that there is often little correlation between the level of pain and physical findings. In a study in which magnetic resonance imaging (MRI) of the lumbar spine was performed on asymptomatic subjects, Jensen et al. [9] found that 64% had at least one abnormal lumbar disk and 38% had two or more. Gore et al. [10] reported that there was no relationship between radiological findings and the severity of neck pain experienced. It is estimated that a clear physiologic aetiology cannot be identified for as many as 85% of patients with isolated low back pain [11].

DIAGNOSTIC CLASSIFICATION OF PAIN DSM-IV and Pain Despite its prevalence, pain has received relatively scant attention in the first three editions of the Diagnostic and Statistical Manual of Mental Disorders. In the second edition (DSM-II) [12], painful conditions caused by emotional factors were included under ‘‘psychophysiological disorders’’. A new diagnostic disorder specifically addressing pain, ‘‘psychogenic pain disorder’’, was introduced in the DSM-III [13]. The essential features of this diagnosis were the complaint of pain with evidence of psychological factors playing an aetiological role and either the absence of organic pathology to account for the pain or, if identifiable organic pathology was present, a degree of pain that was not consistent with the level of the physical findings. In the DSMIII-R [14], several changes were made in this diagnosis: the requirements that aetiological psychological factors be present and that the pain not be due to another mental disorder were eliminated, and instead of the pain itself being a criterion, ‘‘preoccupation with pain for at least six months’’ was required. In accordance with these changes, the disorder was renamed ‘‘somatoform pain disorder’’.

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The literature revealed that the DSM-III and DSM-III-R pain disorder categories were rarely used for patients with pain. Several factors were identified as limiting the use of these diagnoses [15]: • It is often difficult to discern whether pain is in excess of that expected. • DSM-III-R offered no guidance as to the meaning of the term ‘‘preoccupation with pain’’. • The diagnoses were not applicable to the majority of patients with chronic pain and to the many patients with acute pain where both psychological factors and physical conditions are simultaneously involved in the development or maintenance of the pain. • These diagnoses perpetuated the dualistic view that there is a difference between pain of organic origin and pain of psychological origin, a view unsupported by research. • Neither DSM-III or DSM-III-R included a diagnostic category for acute pain. The DSM-IV diagnosis of pain disorder was developed in order to address these issues (Table 2.1). Rather than the preoccupation with pain, pain itself was made the primary factor. In addition, the diagnosis provided for more specification by creating two diagnostic sub-categories: pain disorder associated with psychological factors, where psychological factors are judged to have the major role in the onset, severity, exacerbation, or maintenance of the pain, and pain disorder associated with both psychological factors and a general medical condition, where both psychological factors and a general medical condition are judged to play roles in the pain. An additional category, pain disorder associated with a general medical condition, is also included, though it is noted that this is not considered a mental disorder. Pain has traditionally been sub-classified into acute and chronic. The most commonly used differentiating point between these two is temporal, with acute pain defined as that which is present for less than 6 months and chronic as that which is present for 6 months or longer. While this is helpful in differentiating between truly time-limited pain conditions, such as post-operative or other post-traumatic pain, and longer standing conditions, the dividing line between acute and chronic is less clear when applying these terms to chronic conditions with episodic exacerbations of pain, such as sickle cell disease, and in patients whose pain is related to a long-term terminal illness. The 6-month division is utilized in DSM-IV. Other definitions of acute and chronic have also been employed, most notably chronic pain as pain that lasts longer than would be expected. However, this definition is problematic, because it is usually based only on physical findings, while the influence of psychosocial factors that can play a

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SOMATOFORM DISORDERS DSM-IV diagnostic criteria for pain disorder

1. Pain in one or more anatomical sites is the predominant focus of the clinical presentation and is of sufficient severity to warrant clinical attention. 2. The pain causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. 3. Psychological factors are judged to have an important role in the onset, exacerbation, or maintenance of the pain. 4. The symptom or deficit is not intentionally produced or feigned (as in factitious disorder or malingering). 5. The pain is not better accounted for by a mood, anxiety, or psychotic disorder and does not meet the criteria for dyspareunia.

significant role in the development of chronic pain is either downplayed or ignored. Thus far, there have been limited studies that have applied DSM-IV criteria to patients with pain, but those that have indicated that the new category of pain disorder is a more clinically useful diagnosis. In their study of outpatients seen at a psychiatric pain clinic, Anooshian et al. [16] reported that 79% fit the diagnosis of pain disorder associated with both psychological factors and a general medical condition, and 9% the diagnosis of pain disorder associated with psychological factors. In a study of general medical and surgical inpatients evaluated by a psychiatric consultation-liaison service, King [17] found that 51% of the patients who reported having pain at the time of the initial evaluation fit the diagnostic criteria for pain disorder, while less than 2% fit the criteria for somatoform pain disorder. Aigner and Bach [18] reported that 66% of patients attending a multi-disciplinary pain clinic fulfilled the diagnostic criteria for DSM-IV pain disorder. Fifty of 59 patients who met the criteria were diagnosed with pain disorder associated with both psychological factors and a general medical condition.

Other Classification Systems The 10th edition of the International Classification of Mental and Behavioural Disorders (ICD-10) [19] offers the pain-related diagnosis of ‘‘persistent somatoform pain disorder’’, in which: ‘‘The predominant complaint is of persistent, severe, and distressing pain which cannot be explained fully by a physiological process or a physical disorder. The pain occurs in association with emotional conflict or psychosocial factors that are sufficient to allow the conclusion they are the main causative influences. The result is usually a marked increase in support and attention, either personal or medical’’. This diagnosis appears to be used infrequently, because of problems similar to that encountered in the utilization of the DSM-III and DSM-III-R pain diagnoses described earlier.

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The most comprehensive classification system is a five-axis schema proposed by the Task Force on Taxonomy of the International Association for the Study of Pain [3] (Table 2.2). It provides for comments on psychological factors on both the second axis, where psychiatric illness can be coded, and the fifth, where possible aetiologies include ‘‘physiological’’ and ‘‘psychological’’. It is important to note that the diagnosis of the psychiatric illness is based upon other classification systems of mental disorders such as the DSM. The validity of this classification system is difficult to determine, because it has rarely been employed in published research and appears to be used infrequently in clinical settings. Turk and Rudy [20] proposed the Multiaxial Assessment of Pain based on the West Haven-Yale Multidimensional Pain Inventory, a 52 question instrument that inquires about various aspects of the pain experience, including its effects on social and occupational functioning and on the patient’s family [21]. They identified three classes of patients whom they described as ‘‘dysfunctional’’, ‘‘interpersonally distressed’’, and ‘‘adaptive copers’’. As with the other classification systems noted above, there is scant literature establishing its validity. A diagnosis commonly applied to patients with pain is ‘‘chronic pain syndrome’’. Though there are varying views as to what constitutes this syndrome, the definition provided by Black [22] is the basis for most. He described the patient who suffers from ‘‘intractable, often multiple pain complaints, which are usually inappropriate to existing somatogenic problems; multiple physician contacts and many non-productive diagnostic procedures; excessive preoccupations with the problem of pain; [and] an altered behaviour pattern with some of the features of depression, anxiety, and neuroticism’’. This diagnosis is fraught with problems, most notably the fact that some of the factors described, such as the over-use of diagnostic procedures,

T A B L E 2.2 International Association for the Study of Pain classification system I. II. III. IV. V.

Anatomical region Organ system Temporal characteristics of pain; pattern of occurrence Patient’s statement of intensity; time since onset of pain Aetiology

Example: Chronic mechanical low back pain 533.X1 Axis I—Region: lower back 500 Axis II—System: musculoskeletal 30 Axis III—Temporal: continuous or nearly continuous, fluctuating severity 3 Axis IV—Intensity and time since onset: range from mild to severe and 1 month or less to 6 months or more X Axis V—Aetiology: trauma .01

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may be related as much to limitations in training and knowledge about pain among medical professionals as to patient behaviour.

ASSESSMENT OF PAIN Pain is a subjective complaint. Because there are no objective tests for measuring pain, the conclusion that the measurement of pain is inherently specious and not worth attempting is often drawn. Studies have shown that the failure of health care professionals to inquire about the presence and level of pain is one of the major causes of inadequate management of pain [23, 24]. Even the simple act of asking if the patient has pain may significantly improve its treatment. If nothing else is done with regard to pain, patients should at least be asked whether or not it is present. Once it is determined that pain is present, multiple instruments are available for assessing it. Three of the most commonly used instruments are the Visual Analog Scale, the Numeric Pain Intensity Scale, and the Descriptive Pain Intensity Scale [25]. The Visual Analog Scale usually consists of a 10-cm line with ‘‘no pain’’ marked at one end and ‘‘pain as bad as it could possible be’’ at the other. The patient is asked to mark off where on the line between these two points the severity of pain falls. In the Numeric Pain Intensity Scale, patients are usually asked to score their pain on a 0 to 10 scale, where 0 equals no pain and 10 equals the worst pain imaginable. The Descriptive Pain Intensity Scale asks the patient to rate pain as mild, moderate, severe, very severe, or worst possible. None of these instruments has been shown to be more reliable or accurate than any other. The choice as to which one to use should be based on which one health care professionals feel most comfortable in administering, so that they will use it frequently. For young children who are unable to use these instruments, a commonly employed tool is a facial expression scale where the children are shown pictures ranging from frowning to neutral or smiling faces and are asked to point to the one that best describes how they are feeling [26]. This instrument can also be employed for geriatric patients whose ability to communicate is impaired by medical conditions such as stroke or Parkinson’s disease [27]. All of the above are useful for following the level of pain in the individual patient. However, it should always be kept in mind that changes in scores on these scales do not necessarily represent an improvement or worsening of a physical condition, but may also reflect changes in coping with the pain and other psychosocial factors. It is also important to recognize that, because of the subjective nature of these instruments, they are of little value in comparing one patient’s pain with that of another patient. Attempts to

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use these instruments in this manner can result in poorer pain management, because the more severe pain reported by a patient may be discounted if a patient with a similar health problem reports milder or no pain. The McGill Pain Questionnaire (MPQ) [28] consists of 20 sets of words offering various descriptive factors regarding pain. Patients are asked to circle all the words in each set that they feel most accurately describe their pain. For example, one set includes the words ‘‘hot, burning, scalding, searing’’, another ‘‘annoying, troublesome, miserable, intense, unbearable’’. The major criticism of the MPQ is that, because of its reliance on vocabulary, the level of education and intelligence of the patient can influence the results. The MPQ also contains a pain drawing, where the patient is asked to mark where the pain is present, and questions about what alleviates and worsens the pain. The Brief Pain Inventory (BPI) consists of a series of questions on the pain, including its intensity and nature, and its impact on the patient’s functioning, mood and sleep [29]. Though not specifically designed for assessment of pain, the Short Form (SF-36) Health Status Survey has been employed in a number of studies to evaluate patients with pain [30]. This is a 36-question self-administered instrument that obtains information on several different aspects of the patient’s life, including activities, emotional issues, pain, social functioning, and general health perceptions. Instruments for evaluating patients for mental disorders are commonly used among patients with pain, usually to assess the possible role psychological factors play in the pain. Unfortunately, these often appear to be used in place of an evaluation by a mental health professional, in the mistaken belief that these tests provide essentially the same information. However, unless they are interpreted by a knowledgeable professional and used in conjunction with a formal evaluation, they may provide a false picture. The main reason for this is that, to a great degree, psychological testing instruments are standardized on a physically healthy population. When they are used for patients who have actual health problems, the results must be carefully interpreted to prevent over-inclusion of mental disorders. For example, the Beck Depression Inventory [31] and the Hamilton Rating Scale for Depression [32], two widely used screening instruments for depression, contain multiple questions on somatic complaints. Patients who score high on these questions alone would be considered depressed though this might not actually be so [33]. Attempts have been made to develop techniques for delineating between pain due to physical factors and that associated with psychological issues. For many years, it was believed that the Minnesota Multiphasic Personality Inventory (MMPI) could be employed for this purpose. It was initially reported that patients whose back pain did not have an organic aetiology were more likely to demonstrate a certain configuration on the MMPI, the so-called conversion V or neurotic triad, in which elevations on the

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hypochondriasis and hysteria scales were believed to reflect the patient’s concerns about his or her health [34]. A lower depression score suggested that the patient was indifferent to these concerns. Later studies found that this configuration reflects adjustment to chronic illness and can be found among patients with chronic health problems, whether or not there is identifiable organic pathology [35, 36]. With regard to pain assessment, the updated version of the MMPI (MMPI-2) has not appeared to provide a significant change from the earlier version. Waddell et al. [37] sought to determine if the results of the physical examination could be used to differentiate pain of physical and psychological origins. They described five signs that they believed indicated that low back pain was of non-organic origin: (a) tenderness that is superficial or nonanatomic in distribution; (b) pain brought on by movements that should not cause pain but are simulations of those that will; (c) the disappearance of positive physical findings when the patient is distracted; (d) regional disturbances involving weakness or sensory deficits that are non-anatomic in origin; and (e) over-reaction by the patient during the examination. However, the authors noted that these signs are subject to a range of interpretations on the part of the clinicians and may be invalid for certain connective tissue disorders. Subsequently, Main and Waddell [38] highlighted that these signs should be employed only with a high degree of caution and that they should be considered a psychological ‘‘yellow flag’’ to indicate that a comprehensive assessment of the role psychosocial factors may be playing in the pain should be undertaken.

DIFFERENTIAL DIAGNOSIS AND RELATIONSHIP TO OTHER MENTAL DISORDERS There are several DSM-IV mental disorders in addition to pain disorder where pain is a major complaint. Most prominent of these are somatization disorder, where four pain symptoms are one of the diagnostic criteria, and the sexual pain disorders, for example dyspareunia and vaginismus [39]. Patients suffering from conversion disorder may also complain of pain, but other criteria are necessary to make this diagnosis. Patients with factitious disorder and malingering may falsely complain of pain, though resultant medical treatments may result in the onset of true pain. Pain appears to be a common problem among patients suffering from other mental disorders, most significantly depressive and anxiety disorders. Delaplaine et al. [40] reported that 38% of patients admitted to a psychiatric hospital complained of pain. King et al. [41] found that, on interview, 87% of psychiatric inpatients reported having pain, with 58% of these patients stating that their pain was present for 2 years or longer. Chaturvedi [42] identified pain in 18% of patients attending a psychiatric clinic.

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Pain appears to be especially associated with depressive and anxiety disorders. In their multi-country study of persistent pain among primary care patients, Gureje et al. [43] found that 34% of patients with this problem had an ICD-10 anxiety or depressive disorder, compared to only 10% without pain. Though it is often conceived that the mental disorder is secondary to the pain, the relationship may be more complex. Research indicates that depressive disorders may be more common in the first-degree relatives of people with chronic pain, suggesting a possible environmental or genetic predisposition for developing pain [44, 45]. In their review of the literature, Blair et al. [46] found that, while an average of 37% of patients with chronic pain suffered from clinically significant depression, 65% of patients with depression had clinically significant pain. In a study of patients referred to neurology clinics, Williams et al. [47] reported that 16% of patients who had depression at the time of initial evaluation developed pain by a 12-month follow-up and 15% of those who initially only reported pain had depression by the end of the same period of follow-up. Furthermore, the authors found that those who suffered from both depression and pain had a worse overall health status and utilized health care services more frequently than those who only had one or the other of these problems. Ohayan and Schatzberg [48] reported that 40% of patients with major depressive disorders also suffered from chronic pain. Lin et al. [49], in their study of geriatric patients with arthritis, found that, if comorbid depression was treated, there was decreased pain and an improvement in functional status and overall quality of life. Simon et al. [50] found pain to be a common presenting symptom of depression and often the only symptom. Certain forms of acute pain appear to be frequently associated with other mental disorders. Beitman et al. [51, 52] observed that more than 30% of patients with chest pain and normal coronary arteries by cardiac catheterization met the criteria for panic disorder. Fleet et al. [53] reported that approximately 30% of patients with chest pain and normal angiograms fit the criteria for panic disorder. However, it was found that 98% of patients with panic disorder presenting to an emergency department for chest pain were not so diagnosed by treating physicians [54]. Post-traumatic stress disorder (PTSD) appears to be another anxiety disorder in which pain may be a common complaint. Beckham et al. [55] found that 80% of patients with combat-related PTSD suffered chronic pain. Sleep disorders are commonly encountered in patients with acute and chronic pain. Though the sleep problem is usually simply considered secondary to the pain, sleep disorders may in fact result in painful symptoms. Merskey et al. demonstrated that the symptoms of fibromyalgia could be induced by the disruption of stage 4 sleep [56].

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The stages of sleep that appear to be most likely to be disrupted during both acute and chronic pain are rapid eye movement (REM) and stages 3 and 4 sleep. It is interesting to note that, though both opioids and benzodiazepines are sedating medications and the benzodiazepines are commonly used as hypnotics to assist patients with insomnia, both classes of medications appear to disrupt these same stages of sleep, suggesting that their use in patients with pain may exacerbate rather than relieve their sleep disorders [57]. A number of psychological factors that may affect pain have been identified, in addition to those related to the existing DSM diagnostic categories. Keefe et al. [58] identified three major categories of psychological factors that appear to play a role in the onset and maintenance of persistent pain: (a) catastrophizing, which they defined as ‘‘a tendency to focus on pain and negatively evaluate one’s ability to deal with pain’’; (b) pain-related anxiety and fear of pain; and (c) helplessness. McCracken et al. [59] found that patients with chronic pain who successfully coped with it and accepted its presence had less pain, were less likely to be on disability, suffered less depression and anxiety, and had overall better functioning. A number of these concepts have been subsumed under the overall heading of illness behaviour [60, 61]. Criteria included in illness behaviour are: (a) pain perception; (b) decision making regarding whether to seek treatment and from whom to seek such treatment; (c) the meaning of the pain to the patient; (d) the manner in which the patient communicates about pain; and (e) the effect pain has on the patient’s functioning. Among the factors that have been reported to affect illness behaviour are cultural background, socio-economic status, psychological functioning, experiences, memory, and learning. Although most studies on these psychological factors affecting pain have focused on patients with chronic pain, evidence indicates that some of these factors can also play a major role in acute pain. In a pioneering study, Beecher [62] observed that soldiers severely wounded in battle often did not complain of pain or described pain of a level far below that which would be expected. He postulated that this might have reflected the relief felt by the soldiers, who realized that they would be removed from the battlefield and their lives would no longer be endangered. Stressful life events may contribute to the development of chronic pain [63]. A person’s knowledge of and expectations regarding a potentially painful insult to the body has also been demonstrated to alter patient response. It has been found that pre-operative psychological preparation of the patient can have a profound influence on post-surgical recovery, including the degree of pain experienced [64]. In countries such as the United States, where patients with chronic pain frequently enter workers compensation and disability systems or seek

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compensation through litigation, there is often concern about the possibility of malingering. Because pain is a subjective complaint, it is commonly believed that this problem is especially likely to be faked. Patients may exaggerate symptoms and the extent of disability to attain secondary gains, but such exaggerations usually occur after the presence of the illness that initiated the pain is established. Actual falsification of pain and injury appears to be infrequent. The Report of the Commission on the Evaluation of Pain [65] found that malingering was a rare problem in the Social Security Administration’s disability system. Furthermore, it considered it to be easily recognizable by most physicians. Leavitt and Sweet [66] similarly found malingering to be rare in individuals complaining of low back pain. Of all the pain-related diagnoses, fibromyalgia is one of the most controversial. Strong views have arisen on both sides of the issue as to whether it is a physical problem or whether its symptoms are simply the somatic representation of a mental disorder. Fibromyalgia is a clinical diagnosis for which there are no diagnostic tests. Though patients with any type of widespread pain are often diagnosed with this disorder, it is important to note that there are specific clinic criteria issued by the American College of Rheumatology [67]: (a) History of widespread pain. To be considered widespread, the pain must be present on both the left and right sides of the body and above and below the waist. In addition, there must be axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back pain). (b) Pain on palpation in at least 11 of 18 defined points throughout the body. The points must be painful and not merely tender to palpation. Though not required for the diagnosis of fibromyalgia, other common symptoms are fatigue, paresthesias, and sleep disturbances. Though the aetiology of fibromyalgia is unclear, it has been speculated that reductions in the bioavailability of serotonin and norepinephrine may play a major role in the development of this disorder [68].

MANAGEMENT OF PAIN Unfortunately, with regard to pain in general, there are limited studies indicating the best approach to the individual patient. To a great degree, much of the treatment of pain rests on anecdotal evidence. An obvious exception to this are medications, because in most industrialized countries it is required that they be shown to be efficacious and safe before marketed. However, even with regard to medications, there is a dearth of head-to-head studies comparing medications from different classes. Because of the limited studies on DSM-IV pain disorder, there do not seem to be any specific studies focusing on the treatment of the disorder.

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However, because it appears that a significant number of patients with pain suffer from this disorder and that most suffer from pain disorder associated with both psychological factors and a general medical condition, therapeutic modalities that have demonstrated efficacy for pain related to each probably are the optimal choice. The goal of treatment for acute pain is primarily to relieve the pain. Although medication management is the mainstay of the management of post-operative and other forms of acute pain and will usually be provided by surgeons, anesthesiologists, and other physicians directly involved in the care of the patient, psychologically based modalities can also be beneficial, though they are infrequently utilized. The Acute Pain Management Guideline Panel (23) highlighted the importance of employing cognitive and behaviourally based interventions such as relaxation, imagery, biofeedback, and education and instruction in the management of post-operative and other acute pain. In treating chronic pain, it is important to address functioning as well as the pain. The goal of treatment should be to manage the pain as opposed to curing it. In many cases, this requires refocusing the patient away from the pain. In essence, patients with chronic pain must wrest control of their lives back from the pain. Much of the benefit from the use of the psychologically based treatment modalities may relate more to their effect on the patient as a whole than to directly reducing the pain itself. In a meta-analysis of 109 studies of psychological treatments for pain, Malone and Strube [69] found that these therapies had a greater effect on mood and the number of subjective symptoms than on the frequency, intensity, and duration of pain. In approaching the patient with chronic pain, the psychiatrist faces a number of obstacles. Unfortunately, many patients with this problem tend to view referrals to psychiatrists and other mental health practitioners negatively. They fear that such referrals may indicate that their treating physicians do not believe that the pain is ‘‘real’’. Furthermore, many patients with this problem believe that the physicians, in making such referrals, are giving up and that acceptance of the referrals forces patients to acquiesce in this condition. As Blumer and Heilbronn [70] noted, ‘‘The chronic pain sufferer argues that he or she has no mental problem and needs no psychiatric intervention, that the only real problem is the pain and that the doctors better find out what is wrong where it hurts’’. To help these patients, psychiatrists must recognize and address these concerns. By the time they are referred to psychiatrists, patients with chronic pain often feel frustrated and abused by the health care system. In many cases, the specific form of therapy chosen may be less important than the therapist’s willingness to display empathy and understanding and to set realistic goals for treatment. Unfortunately, modern Western medicine has, to a great degree, emphasized therapies that are performed on patients—rather than

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recognized that for many problems it is what patients do for themselves, not what is done to them, that is the most effective. This is especially true for chronic pain. One of the obstacles that must frequently be overcome in cases of chronic pain is the common fear that the pain indicates the presence of a severe underlying condition that must be detected, and that an increase in activity will exacerbate rather than improve the pain. Patients who manage to avoid or conquer these concerns tend to do better than those who retain them [71].

Psychologically Based Modalities Psychologically based treatment approaches are considered to be a vital part of pain management programs. A wide variety of psychotherapies have been reported to be beneficial for pain, including many forms of individual, group, and family therapy. The most commonly used approaches fall into two major categories: (a) operant conditioning and (b) cognitive-behaviour therapies, including biofeedback, relaxation training, and hypnosis. Operant conditioning is based on the concept that certain operant or learned behaviours develop in response to environmental cues. Common examples among patients with pain include complaints of pain and reluctance to indulge in certain activities. The anticipated response to pain is often receipt of medication and being excused from work or normal daily tasks. The goal of operant conditioning is to reinforce the positive or ‘‘healthy’’ behaviours and to diminish the destructive behaviours that maintain the patient’s pain. Cognitive-behaviour therapy involves identifying and correcting the patient’s distorted attitudes, beliefs, and expectations. The goal of this therapy is, first, to make the patient more aware of factors that exacerbate and diminish the pain and, second, to cause the patient to therefore modify behaviour accordingly. A variety of therapeutic modalities may be used to achieve this. In biofeedback, electronic equipment is employed to measure certain physiological functions of which the patient is usually unaware and to convey this information to the patient. One example of such physiological parameters is muscle tension. The patient may be instructed in specific relaxation techniques or be encouraged to achieve certain goals involving the biofeedback equipment, such as lowering the pitch of a tone. A wide variety of relaxation techniques can be taught to patients. Among the most common methods is progressive muscle relaxation, in which the patient learns to relax different muscle groups by contracting and then relaxing each one [72]. Although hypnosis involves relaxation, its efficacy in the treatment of pain extends beyond this. Patients can be taught to reduce pain through hypnotic suggestions, such as forming a visual image of the pain and changing it or dissociating the painful part from the rest of the body. The benefits of hypnosis for acute pain are well documented but,

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unfortunately, support for its efficacy in chronic pain is based primarily on anecdotal evidence [73]. The application of each of these techniques to the management of pain has been studied to varying degrees, and controversy still remains concerning which approach is most efficacious. However, research suggests certain general guidelines regarding how each is best used. Through reviews of the literature, Turner and Chapman [74, 75] and Linton [76] found that operant conditioning is especially useful in decreasing patients’ medication use and increasing their activity levels. In contrast, cognitive-behaviour therapy was observed to be helpful in reducing pain complaints. Biofeedback was found to be of benefit in certain pain conditions, especially tension and migraine headaches, but was discovered overall to be inferior or at best equal to relaxation therapy, which appears to be efficacious in the treatment of a wide variety of both acute and chronic pain conditions. Each of these therapies may be employed when pain is the primary problem. However, when pain is the symptom of a mental disorder, that disorder should be addressed: appropriate treatment with psychotherapy and/or psychotropic medications must be initiated. Though the use of placebos is controversial, it appears that they can have a definite analgesic effect on a variety of painful conditions, including those in which there is an identifiable organic aetiology [77].

Pharmacological Management Multiple medications have been employed as analgesics. Among the most commonly used for chronic pain are the opioids, non-steroidal antiinflammatory drugs (NSAIDs) and acetaminophen, antidepressants, and anticonvulsants.

Opioid Analgesics Although opioid analgesics play a primary role in the management of acute pain and the pain associated with cancer, their prescription for patients with chronic non-cancer pain continues to be the subject of controversy [78, 79]. Though this class of medications can be safely and effectively utilized, there are fears that extended use may lead to abuse and dependence. The validity of these concerns is the subject of current debate. The number of chronic patients who will abuse or develop psychological dependence on opioids prescribed for pain remains unclear. One of the most cited references on the limited risk of the development of opioid abuse and addiction continues to be a letter published by Porter and Jick [80]. The authors reported that, of 11,882 patients who received at least one dose of an

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opioid analgesic during hospitalization, only four who did not have previous history of addiction developed this problem. However, no breakdown was provided as to the types of pain suffered by the patients described, and one might assume that many, if not most, of the patients suffered postoperative or other post-traumatic pain, or pain related to a terminal illness rather than chronic pain. In contrast, a study by Bouckoms et al. [81] of 59 patients with chronic pain and no detectable history of substance abuse or dependence disorder, who were followed for an average of 36 months, found that 27% abused these medication and 24% developed addiction. The authors were unable to identify any predictive factors for those who developed these problems. Hoffman et al. [82], in a study of 414 chronic pain patients, reported that 12.6% had current psychological dependence to opioid analgesics and 2.9% were in remission for this problem. Because most physicians receive scant training in the problems of drug abuse and dependence and their management, it often falls to psychiatrists to possess the appropriate knowledge. Unfortunately, there is a confusing mix of terms to describe these problems. Physical dependence reflects the withdrawal states that will occur if these medications are discontinued or their dosage markedly reduced without tapering. Tolerance refers to the requirement for increasing doses of an opioid over time in order to receive the same degree of analgesia [83]. Unfortunately, failure to understand these terms may result in unnecessary suffering. Patients who are under-treated for their pain and express desire for more effective pain management may be mislabelled as being drug dependent, a problem that has been termed pseudo-addiction [84]. In the case of mild to moderate post-operative and other acute pain, an NSAID or acetaminophen should be used. More severe acute pain should be treated with an opioid analgesic. Treatment for cancer-related and chronic non-cancer pain should begin with non-opioid analgesics, such as the NSAIDs, antidepressants, anticonvulsants, other non-opioids, and other forms of pain management. The World Health Organization Expert Committee [85] recommends a stepwise approach starting with non-opioid analgesics, with the addition of opioid analgesics if pain is not controlled. Even if the non-opioid analgesics are insufficient for pain relief, they should be continued after the introduction of an opioid. By providing analgesia by mechanisms different from the opioids, they may enable analgesia to be attained at a lower dosage of the opioid than would be required if it were used alone. Furthermore, it appears that both the NSAIDs and the tricyclic antidepressants may bolster the analgesic effects of opioids and allow for administration of a lower dosage that will result in a reduction in frequency and severity of opioid-related side effects. Traditionally, opioid analgesics have been viewed as being on a continuum from mild to strong, ranging from oxycodone, hydrocodone, codeine

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to methadone, morphine, and fentanyl. How valid this concept is remains open to question, as several of what are considered ‘‘milder opioids’’ are metabolized to ‘‘stronger’’ ones. For example, codeine is metabolized to morphine. To some degree, the concept of mild and strong is related to the fact that what are considered the milder ones are often prescribed in formulations that also contain non-opioids such as acetaminophen and aspirin which have dose ceilings, unlike the mu agonist opioids, the most commonly employed opioids. This appears to be why, in the United States, the Drug Enforcement Administration of the Department of Justice that regulates controlled substances, places opioids in combination with other drugs on a less restrictive schedule than the same medications used alone. Generally, when treatment with opioid analgesics is initiated for cancerrelated, terminal illness–related pain, and chronic non-cancer pain, it is recommended to try first what are considered to be the milder opioids, such as codeine, oxycodone, and hydrocodone. If these are insufficient, the stronger narcotics, including morphine, methadone, fentanyl, and hydromorphone, should be considered. All the opioids just discussed are mu opioid receptor agonists. The other basic class of opioid analgesics consists of the mixed agonist-antagonists and partial agonists, which bind at the kappa opioid receptors and block some of the mu receptors and bind at others. Although this second group of medications have often been employed, because of the belief that they may have less potential for abuse and psychological dependence than the mu receptor agonists, they do not appear to offer any marked benefit and they have the potential for creating additional problems. Patients who take a mixed agonist-antagonist after receiving pure agonists may go into withdrawal. The use of the mixed agonist-antagonists is therefore not generally recommended. Though it is beyond the scope of this chapter to describe all the opioids individually, there are several that bear special interest to psychiatrists because of their mechanisms of action, side effects, or popular beliefs regarding them. Though methadone is usually associated with the management of opioid addiction, it has been demonstrated to be an effective analgesic. Unlike other opioids, methadone appears to have a dual mode of action: like the other opioids, it binds to the mu receptors, but also is an N-methyl-D-aspartate (NMDA) receptor antagonist [86]. Because of its long half-life (16–24 h), methadone only needs to be taken once per day when used for management of opioid addiction. However, its analgesic effect is shorter and necessitates 6–8-h dosing when used for pain. Meperidine is a strong opioid analgesic that is used in a variety of pain settings. Its extended use (i.e., for more than 2–3 days) is contraindicated, because repeated dosing may result in the accumulation of the toxic

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metabolite normeperidine, a cerebral irritant that can cause problems ranging from marked anxiety to convulsions. The oral bioavailability of meperidine is also poor, necessitating the switch to an alternative analgesic when parenteral administration is no longer required. Also, alone among the opioid analgesics, meperidine can have a lethal interaction with monoamine oxidase inhibitors (MAOIs) [87] and increase the risk of post-operative delirium [88]. Tramadol is a unique medication that combines a weak mu opioid receptor agonism (1/6,000 the potency of morphine) with a weak inhibition of norepinephrine and serotonin (5-HT) reuptake. The analgesic effect of this medication appears to be primarily related to this latter effect rather than to its opioid actions.

Non-steroidal Anti-inflammatory Drugs All NSAIDs appear to exert their analgesic actions primarily through the inhibition of cyclooxygenase (COX), preventing the synthesis of prostaglandins. While this explains the anti-inflammatory actions of these medications, it is still unclear whether this is how they provide analgesia. The process of deciding which NSAID to use was substantially changed with the introduction of the selective COX-2 inhibitors. The use of these drugs is based on the concept that there are two major COX systems. The COX-1 system is primarily involved in what are often called the housekeeping chores, including protection of the stomach lining and renal and platelet function. The COX-2 system plays the major role in inflammation and, it is conjectured, in pain. At the time of this writing, there is one selective COX-2 inhibitor available in the United States: celecoxib. Rofecoxib and valdecoxib were removed from the market in the United States following concerns that they increased the risk for myocardial infarctions and strokes. Similar concerns have been raised about celecoxib and other COX-2 inhibitors in development [89]. Although the primary advantage of the COX-2 inhibitors has been considered to be a reduction in the gastrointestinal side effects compared to the older NSAIDs, the US Food and Drug Administration (FDA) only found sufficient evidence to allow rofecoxib to state this in its labelling. All NSAIDs, be they older non-specific COX-1 and COX-2 inhibitors or selective COX-2 inhibitors, are equally efficacious. Even before the problems associated with the use of the selective COX-2 inhibitors were identified, it was recommended that, unless there was a specific indication to utilize one of them, the older NSAIDs such as ibuprofen and naproxen should be used [90]. How acetaminophen exerts its analgesic effect is yet to be determined. There is evidence to suggest that it may have an anti-inflammatory effect [91].

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Antidepressants There is substantial literature supporting the use of antidepressants as analgesics. The analgesic effects of these medications were initially thought to be related to their antidepressant properties, with the relief resulting from an improvement in mood rather than any direct effect on the pain. However, substantial research indicates that those antidepressants that inhibit both serotonin and norepinephrine reuptake (SNRIs) have separate analgesic effects unrelated to the emotional state of the patient [92]. The antidepressants appear to be efficacious for a wide range of painful conditions, including neuropathic pain, tension and migraine headaches (for which the drugs are used prophylactically), fibromyalgia, osteoarthritis and rheumatoid arthritis, and irritable bowel syndrome [93–95]. The tricyclic antidepressants (TCAs) are considered to be first-line drugs for the treatment of pain related to neuropathies, including post-herpetic neuralgia and diabetic neuropathy [96]. Despite a commonly propagated myth that amitriptyline is the most analgesic of all the TCAs, it appears that all are equally analgesic. Thus, TCAs with more benign side effect profiles such as nortriptyline and desipramine can be used in place of amitriptyline. In 2004, duloxetine, an SNRI, became the first antidepressant approved by the US FDA for the treatment of any pain condition. It was approved for the treatment of peripheral diabetic neuropathic pain. Another SNRI, venlafaxine, has also been demonstrated to have analgesic properties, though it is not approved by the FDA as an analgesic [97]. How antidepressants exert their analgesic effect is unclear. The primary focus has been on their effects on serotonin and norepinephrine reuptake, and it appears that SNRIs provide significantly more analgesia than the selective serotonin reuptake inhibitors [98, 99]. Other mechanisms of action that have been suggested include enhanced endorphin secretion, the effect on sodium channels, anti-histaminic and anti-cholinergic effects, inhibition of substance P, a neuropeptide involved in pain transmission, and antagonism of NMDA receptors [92]. As in the treatment of depression, the recommended length of maintenance therapy with antidepressants for chronic pain varies from patient to patient. These medications carry a lower risk of side effects than other medications that are commonly used for chronic pain. Therefore, if a patient is doing well, these should be the last medications that are discontinued. Physicians should reassess the continuing need for an antidepressant every few months and should consider tapering and discontinuing the medication after the patient’s condition has stabilized.

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Anticonvulsants The analgesic effects of anticonvulsants for neuropathic pain have long been known. The older anticonvulsants—phenytoin, carbamazepine, and sodium valproate—were reported to provide effective pain relief, but their use was limited due to side effects [100, 101]. The only anticonvulsants that have been approved by the US FDA for the management of pain are carbamazepine for trigeminal neuralgia pain, gabapentin for post-herpetic neuralgia pain, pregabalin for post-herpetic neuralgia pain and diabetic peripheral neuropathic pain, and topiramate for migraine headache. How these medications exert their analgesic effects is still unclear. Research on the mechanism of action of gabapentin has focused on its blocking effects on calcium and sodium channels and on increasing GABA levels in the brain by bolstering its synthesis and release [102]. At this time, there is limited literature comparing the anticonvulsants and antidepressants as analgesics.

Benzodiazepines Though benzodiazepines are commonly prescribed to patients with both acute and chronic pain, primarily as aides for insomnia and as muscle relaxants [103], they do not appear to provide any direct analgesia, and for patients with chronic pain they are generally considered to be contraindicated. It has been noted that benzodiazepines may actually exacerbate pain rather than reduce it [104] and can interfere with the analgesic effects of opioids [105]. Because of the problems associated with benzodiazepine use, the sleep disorders associated with pain appear to be better treated with the nonbenzodiazepine hypnotics zolpidem, zaleplon, and zopiclone [106]. These medications have a significant advantage over benzodiazepines because of their more benign side effect profiles and, unlike the benzodiazepines, they do not appear to disrupt normal sleep architecture [107].

OTHER TREATMENT MODALITIES Among the other therapies found to be beneficial are various surgical interventions, nerve blocks, trigger point injections, acupuncture, physical therapy, and transcutaneous electrical nerve stimulation (TENS). The provision of each of these therapies requires clinicians with specific training and experience. As with the psychologically based modalities, support in the literature for the efficacy of each of these therapies is variable.

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The best recommendation is that, in the absence of a medical emergency, conservative therapies be tried before more invasive ones such as nerve blocks and surgery. Therapeutic interventions such as physical therapy, acupuncture, and TENS carry little risk of side effects or of worsening the patient’s pain. As the interest in pain has grown during the past quarter century, various forms of pain services, clinics, and treatment centres have been created. These vary from true multidisciplinary establishments to those offering single forms of treatment provided by one or more clinicians. Unfortunately, the type of therapy provided often is based less on what the patient needs than on what the clinician offers. Even when a truly multidisciplinary treatment team is present, the team may fail to recognize the differences between patients, and the clinicians may attempt a ‘‘one size fits all’’ treatment approach [108]. Patients appear to be much better served when a variety of modalities are available. Certainly the diagnosis of pain disorder associated with both psychological factors and a general medical condition would require that both be adequately managed. Because of the importance of improving the functioning of patients with chronic pain, the best multidisciplinary pain programs offer services that focus on this goal. Central to such programs are physical therapy, occupational therapy, and behaviourally oriented therapies. Although patients may prefer programs in which treatment is given to them, lasting improvement appears to depend on health care professionals’ teaching patients how to cope with and manage their pain and patients’ willingness to do this.

SUMMARY Both acute and chronic pain are major health problems. In an era when health care professionals rely increasingly on objective tests to evaluate patients and determine their levels of impairment, the lack of validity of these tests for measuring the subjective complaint of pain has limited appropriate treatment of this ubiquitous problem. Unfortunately, pain is still often categorized on the basis of the traditional dualistic view separating pain of physical and psychological origins, despite the fact that contemporary literature has shown this to be an outmoded model that also hinders rather than improves patient care. Though the currently available assessment instruments and classification systems need further refinement, they provide clinicians and researchers tools for assuring better care. As further knowledge about pain is attained, especially in regard to the nature of the relationship between physical and psychological factors, better methods for evaluating pain should become available.

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Consistent Evidence Pain disorder is common among patients with chronic pain. There are multiple treatments available for the treatment of pain.

Incomplete Evidence Though pain disorder does appear to be a distinct entity, there are still questions regarding its relationship to other mental disorders, especially depressive and anxiety disorders. Treatment approaches for both these disorders and pain disorder may be improved if common neurochemical mechanisms can be identified. The interaction between psychological factors and physical conditions in the development and maintenance of chronic pain also needs to be explored to a greater degree. Predictive factors that aid in determining patients at high risk for developing chronic pain after acute injury need to explored.

Areas Still Open to Research There are multiple areas that remain to be studied. Of most importance are further investigations into the aetiology of pain, especially with regard to determining the roles of central and peripheral factors and determining the best treatment approaches for the individual patient. Much more work needs to be done comparing the existing treatment options in addition to developing new ones. The limited research on the acute subtype of pain disorder makes this another significant area of research.

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SOMATOFORM DISORDERS King S.A. (1995) Antidepressants: a valuable adjunct for musculoskeletal pain. J. Musculoskeletal Med. 12: 51–57. Saper J.R. (1997) Diagnosis and symptomatic treatment of migraine. Headache 37(Suppl. 1): S1–S14. Sindrup S.H., Jensen T.S. (1999) Efficacy of pharmacological treatments of neuropathic pain: an update and effect related to mechanism of drug action. Pain 83: 389–400. Sindrup S.H., Bach F.W., Madsen C., Gram L.F., Jensen T.S. (2003) Venlafaxine versus imipramine in painful polyneuropathy. Neurology 60: 1284–1289. Ansari A. (2000) The efficacy of newer antidepressants in the treatment of chronic pain: a review of current literature. Harv. Rev. Psychiatry 7: 257–277. Smith A.J. (1998) The analgesic effects of selective serotonin reuptake inhibitors. J. Psychopharmacol. 12: 407–413. McQuay H., Carroll D., Jadad A.R., Wiffen P., Moore A. (1995) Anticonvulsant drugs for management of pain: a systematic review. Br. Med. J. 311: 1047–1052. Wiffen P., Collins S., McQuay H., Carroll D., Jadad A., Moore A.l. (2000): Anticonvulsant drugs for acute and chronic pain (Cochrane Review). The Cochrane Library, Issue 4. Update Software: Oxford. Ross E.L. (2000) The evolving role of antiepileptic drugs in treating neuropathic pain. Neurology 55(Suppl. 1): S41–S46. King S.A., Strain J.J. (1990) Benzodiazepine use by chronic pain patients. Clin. J. Pain 6: 143–147. Dellemijn P.L.I., Fields H.L. (1994) Do benzodiazepines have a role in chronic pain management? Pain 57: 137–152. Gear R.W., Miaskowki C., Heller P.H., Paul S.M., Gordon N.C., Levine J.D. (1997) Benzodiazepine mediated antagonism of opioid analgesia. Pain 71: 25–29. Wagner A.K., Zhang F., Soumerai S.B., Walker A.M., Gurwitz J.H., Glynn R.J., Ross-Degnan D. (2004) Benzodiazepine use and hip fractures in the elderly: who is at greatest risk. Arch. Intern. Med. 164: 1567–1572. Wagner J., Wagner M.L. (2000) Non-benzodiazepines for the treatment of insomnia. Sleep Med. Rev. 4: 551–581. Turk D.C. (1990) Customizing treatment for chronic pain patients: who, what, and why. Clin. J. Pain 6: 255–270.

Commentaries 2.1 The Major Paradigm Shift from the Biomedical Reductionist to the Biopsychosocial Approach to the Assessment and Treatment of Pain Robert J. Gatchel1 As appropriately noted by Steven King, today pain is still often categorized, unfortunately, on the basis of the traditional dualistic perspective separating pain of physical and psychological origins (i.e., the biomedical reductionist approach). However, this outdated, overly simplistic model not only is unsupported by current literature, but has traditionally hindered rather than improved the care of patients experiencing pain. Fortunately, there is now a more heuristic model of pain that is supported by a growing scientific literature—the biopsychosocial approach to pain—which has made important advances in the assessment and treatment of pain disorders [1, 2]. This biopsychosocial model appropriately conceptualizes pain as a complex and dynamic interaction among physiologic, psychologic, and social factors. Pain itself cannot be broken down into distinct, independent psychosocial or physical components, which was the approach of the biomedical reductionist perspective. Each individual experiences pain uniquely. The complexity of pain and various individual differences in pain expression are especially evident when it persists over time, as a range of psychological, social, and economic factors can interact with physical pathology to modulate a patient’s report of pain and physical disability. Although King highlights the positive changes in viewing pain as not only a physical phenomenon, he does not actually cite the large scientific literature supporting this biopsychosocial approach. Indeed, there is currently a revolution in developing a more comprehensive, biopsychosocial understanding of pain. In addition to the greater appreciation of psychosocial factors that contribute to the pain process, there is a current growing understanding of how physiological modulation of pain mechanisms occurs. Many of the issues raised by King in terms of the assessment and treatment of pain have been addressed by this new biopsychosocial paradigm. For example, Turk [3] had indicated that, within a biopsychosocial paradigm, pain problems need 1 Department of Psychology, College of Science University of Texas at Arlington, Arlington, TX 76019-0528, USA

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to be ‘‘viewed longitudinally as ongoing, multi-factorial processes in which there is a dynamic and reciprocal interplay among biological, psychological and social factors that shape the experience in response of patients’’. Thus, in order to comprehensively assess pain, clinicians must be certain to account for such potential interactions in prescribing the best treatment regimen, individualized for a particular patient with pain. For instance, a patient may present with chronic pain resulting from an earlier accident, which produced severe musculoskeletal injuries, such as bone fractures and ligament tears, that have not completely healed. Besides these physical injuries and resultant pain, the accident may have also led to the inability to work again. The patient might have therefore developed self-esteem problems because he or she is disabled and stigmatized by it. This may also have resulted in economic problems and stressors because of the sudden decrease in income. There are debts to be paid, causing a great deal of family stress, guilt, and turmoil. Thus, as one can see, there are potentially multiple levels of psychosocial issues that all need to be assessed before one can develop a comprehensive management program for a pain such as this. One will have to assess the patient not only individually but also in the context of his/her family, workplace, and other social situations. This, though, is not an example of an atypical chronic pain patient; it is more the norm than the exception. Fortunately, there are now comprehensive biopsychosocial evaluations methods that can be used in tailoring specific treatment programs to the needs of an individual patient [1]. Once biopsychosocial assessment takes place, there are now also effective biopsychosocial pain management methods available for patients. Developments and refinements will continue to occur as more is learned about biopsychosocial pain processes. For now, though, health care professionals have an armamentarium of techniques that can be used in this biopsychosocial treatment. Von Korff [4] introduced a step-care framework of pain treatment depending upon the amount of pain management needed. Step 1 is the lowest intensity of intervention, which consists of addressing a patient’s fear and avoidance beliefs about pain through education, information, and advice about the importance of returning to activities of daily living as soon as possible. It is applied usually to acute cases of pain of limited severity, and may be all that is necessary for a great number of patients with non-pathological pain. Step 2 refers to the need for increased intensity of intervention, and is reserved for patients who may continue to report pain 6–8 weeks following the onset of an episode and who demonstrate persistent limitations in activities of daily living. It represents ‘‘reactivation’’ treatment administered to patients who did not improve after the primary intervention at the acute stage. Interventions at this level might include a structured exercise program and additional cognitive-behavioural strategies to deal with patients’ fears and to help them resume their usual work and recreation

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activities. Finally, for those patients who fail to improve with either Step 1 or Step 2 interventions and who continue to experience significant disability and are at risk for becoming permanently disabled, Step 3 interventions might be required. Intervention at this step may be more costly and complex than Step 1 and 2 interventions, because it requires an interdisciplinary and intensive treatment approach. Fortunately, such interdisciplinary pain treatment programmes have been documented to be successful in the treatment of chronic pain patients [5–8]. Such interdisciplinary programmes are needed for chronic pain patients who have complex requirements. Although they represent a small minority of pain patients, there nevertheless are a significant number of patients who have failed to benefit from the combination of spontaneous healing and short-term, symptom-focused treatment. One variant of interdisciplinary chronic pain management programmes, functional restoration, has been extensively reviewed by Mayer and Polatin [9]. The above step-care framework provides a broad, overall approach to pain management. It also emphasizes the importance of matching treatment for each patient. Turk and Gatchel [10] have provided a comprehensive practitioner’s handbook of the major biopsychosocial approaches to pain management. The reader is referred to this work, as well as to Gatchel [1], for a more thorough review and understanding of the biopsychosocial assessment and treatment process for pain patients. This has indeed revolutionized the treatment of pain patients and has replaced the outmoded and ineffective traditional biomedical reductionistic approach to pain.

REFERENCES 1. 2. 3. 4. 5.

6. 7.

Gatchel R.J. (2005) Clinical Essentials of Pain Management. American Psychological Association: Washington, D.C. Turk D.C., Monarch E.S. (2002) Biopsychosocial perspective on chronic pain. In: Psychological Approaches to Pain Management: A Practitioner’s Handbook, 2nd ed., D.C. Turk, R.J. Gatchel (Eds). Guilford Press: New York. Turk D.C. (1999) Assessment of patients reporting pain: an integrated perspective. Lancet 353: 1784–1788. Von Korff M. (1999) Pain management in primary care: an individualized stepped-care approach. In: Psychosocial Factors in Pain: Critical Perspectives, R.J. Gatchel, D.C. Turk (Eds). Guilford Press: New York, pp. 301–316. Deschner M., Polatin P.B. (2000) Interdisciplinary programs: chronic pain management. In: Occupational Musculoskeletal Disorders: Function, Outcomes and Evidence, T.G. Mayer, R.J. Gatchel, P.B. Polatin (Eds). Lippincott, Williams & Wilkins: Philadelphia, pp. 629–637. Gatchel R.J. (1999). Perspectives on pain: a historical overview. In: Psychosocial Factors in Pain: Critical Perspectives, R.J. Gatchel, D.C. Turk (Eds). Guilford Press: New York, pp. 3–17. Okifuji A. (2003) Interdisciplinary pain management with pain patients: evidence for its effectiveness. Semin. Pain Manag. 1: 110–119.

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8.

Wright A.R., Gatchel R.J. (2002) Occupational musculoskeletal pain and disability. In: Psychological Approaches to Pain Management: A Practitioner’s Handbook, 2nd ed., D.C. Turk, R.J. Gatchel (Eds). Guilford Press: New York, pp. 349–364. Mayer T.G., Polatin P.B. (2000) Tertiary nonoperative interdisciplinary programs: the functional restoration variant of the outpatient chronic pain management program. In: Occupational Musculoskeletal Disorders: Function, Outcomes and Evidence, T.G. Mayer, R.J. Gatchel, P.B. Polatin (Eds). Lippincott, Williams & Wilkins: Philadelphia, pp. 639–649. Turk D.C., Gatchel R.J. (Eds). (2002) Psychological Approaches to Pain Management: A Practitioner’s Handbook, 2nd ed. Guilford Press: New York.

9.

10.

2.2 DSM and Pain: When (if Ever) Is Pain Truly a Psychiatric Disorder? Robert Boland1 Steven King’s paper shows how the idea of pain continues to vex psychiatry. A particular challenge is in deciding whether one should take a ‘‘wide’’ or ‘‘narrow’’ view of the diagnosis of pain disorder. As King describes, subsequent versions of the DSMs have continued to broaden the concept of what was originally called ‘‘psychogenic pain disorder’’. Driving this was the concern that the diagnosis of this disorder was rarely made in clinical settings [1]. This was largely due to the difficulty in determining whether a pain was physically or psychologically based, and the mind–body dualism implied in such a distinction. The DSM-IV attempted to address these inadequacies by broadening the definition of pain disorders. The most obvious change was the name itself, simplified to ‘‘pain disorder’’, with no adjectival implication of any particular aetiology. In defining the disorder, the criteria simply required that ‘‘psychological factors are judged to have an important role in the onset, severity, exacerbation, or maintenance of the pain’’. The DSM-IV also allowed the presence of a significant medical contribution to pain, by creating two categories: pain disorder associated with psychological factors and pain disorder associated with both psychological factors and a general medical condition. The first category is more akin to DSM-III and DSM-III-R, with no medical factors thought to be related to the pain. In the latter category, both psychological and general medical factors are thought to be significant. Though information is limited, it appears that the current diagnosis is more useful than the prior ones. As King shows, in many sites the disorder is diagnosed in many—often the majority—of pain patients. This greater utility likely results from the dropping of aetiological requirements for the 1

Department of Psychiatry and Human Behaviour, Brown University, Providence, RI 02906, USA

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diagnosis. The diagnosis does seem reasonable in that most pain patients do have both psychological and medical factors contributing to their pain. Pain itself is a combination of sensory and emotional factors. Viewed this way, virtually all pain can be considered psychological and somatic. However, the DSM-IV still leaves some dilemmas. A strict reading of the definition of the disorder still suggests a mind–body dichotomy. Implied in the diagnosis is that one can actually divide pain on the basis of the relative contribution of psychological and organic factors. In diagnosing pain disorder, the clinician must decide between not only two but three categories, as pain disorder associated with a general medical condition (in which psychological factors play no significant role) is included as a third, non-psychiatric disorder. Furthermore, the advantage of widening the diagnosis risks hurting its validity. Encompassing all pain patients with the diagnosis leaves no means to distinguish the cases of particular psychiatric concern [2]. There continues to be a lack of investigation to help clarify these issues. Research settings largely ignore the diagnosis in favour of other diagnostic schemas. The majority of articles examining DSM-IV-defined pain disorder are critical of it, noting the continued reliance on mind–body dualism [3]. Studies examining the utility of DSM-IV pain disorder have found little evidence to justify the sub-types proposed. In fact, available data infers the opposite. It appears that patients who are placed in either the psychological or psychological plus general medical sub-types of the disorder do not differ on such measures of pain as duration, intensity, or type, nor do they differ on measures of disability [4]. Other researches have questioned the sequestering of ‘‘pure’’ pain disorder from pain associated with other somatoform disorders [5]. It may be that psychiatry cannot have a pain disorder diagnosis that has both wide applicability and good validity. We may have to decide on which side we would rather err. We could give up psychological/somatic distinctions and broaden the diagnosis to encompass all pain patients. Alternately, we could include only those patients for whom we think their pain is a somatoform disorder. The remainder of pain patients would have either no psychiatric disorder or one that is secondary to the pain (e.g., an adjustment disorder, or mood disorder due to chronic pain). Such a system would leave only a minority of patients with a pain disorder that belongs among the somatoform disorders, but it may be that the disorder is rare. Such patients would still be important to identify, as they are likely to be misunderstood, mistreated, and misusers of medical resources. In the past, it was clear that the identification of such patients is difficult, but there are some potential guideposts (e.g., the work of Waddell, discussed in King’s review) that deserve further testing.

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Ultimately, the problem may be an unavoidable result of understanding pain within a categorical system. It may be that if psychiatrists are serious about nosology, we must incorporate the findings of pain research, most of which uses dimensional approaches to view pain disorders. Only then will we be able to adequately diagnose the myriad of presentations encountered by the psychiatrist who is interested in pain treatment.

REFERENCES 1.

King S.A., Strain J.J. (1996) Somatoform pain disorder. In: DSM-IV Sourcebook, Vol. 2, T.A. Widiger, A.J. Frances, H.A. Pincus, R. Ross, M.B. First, W.W. Davis (Eds). American Psychiatric Association: Washington, D.C., pp. 915–931. Streltzer J., Anooshian J. (2000) Effectiveness of a psychiatric pain clinic: reply. Psychosomatics 41: 283–284. Boland R. (2002) How could the validity of the DSM-IV pain disorder be improved in reference to the concept that it is supposed to identify? Curr. Pain Headache Rep. 6: 23–29. Aigner M., Bach M. (1999) Clinical utility of DSM-IV pain disorder. Compr. Psychiatry 40: 353–357. Hiller W., Heuser J., Fichter M.M. (2000) The DSM-IV nosology of chronic pain: a comparison of pain disorder and multiple somatization syndrome. Eur. J. Pain 4: 45–55.

2. 3. 4. 5.

2.3 Pain Disorder or Just Pain: Can We Escape Dualism? Robert G. Large1 and Tipu Aamir1 Pain, as Steven King rightly states in his review, is a major health care problem. The prevalence is high, and epidemiological studies show consistent findings from diverse countries. Medicine now recognizes pain as a fifth vital sign in acute settings. Despite the best efforts of psychiatry, our diagnostic terms for pain are not common currency in the interdisciplinary literature, which talks of ‘‘acute pain’’, ‘‘chronic pain’’, ‘‘persistent pain’’, or ‘‘intractable pain’’. Are our nonpsychiatric colleagues ignorant of the value of our terminology or is our terminology wanting? ‘‘Psychogenic pain disorder’’ and ‘‘somatoform pain disorder’’, as noted by King, were constrictive in application. The DSM-IV term ‘‘pain disorder’’ may have swung the pendulum too far. If the majority of patients with pain meet the criteria for this diagnosis, how does this help us understand them better or plan treatment? Boland [1] points out that the 1

The Auckland Regional Pain Service, Auckland District Health Board, Auckland, New Zealand

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DSM-IV still suggests a mind–body dichotomy, since one is asked to judge the relative contributions of physical and psychological factors. Most pain centres, in fact, will use the sub-category of pain disorder associated with both psychological factors and a general medical condition. ‘‘However, by making this diagnosis all-inclusive, there is a risk of rendering it useless’’. Aigner and Bach [2] found that there was no difference in pain duration, pain intensity, and disability between patients with psychological factors only and patients with both psychological factors and a general medical condition. They found that patients satisfying criteria for pain disorder also satisfied criteria for other somatoform disorders such as hypochondriasis, undifferentiated somatoform disorder, and somatization disorder. These findings seriously challenge the validity and utility of the ‘‘pain disorder’’ construct. Many diagnostic studies show very clearly that the majority of patients with persistent pain have both psychological issues and medical/physical issues contributing to their presentation [3–5]. Indeed, it seems more useful to identify the patients’ medical and psychiatric problems and deal with them specifically, than to spend time fussing about their ‘‘fit’’ with a ‘‘pain disorder’’ diagnosis. The DSV-IV is essentially dualistic in its structure, and forces the clinician into making dualistic decisions. However, perhaps it can be more usefully employed to note the multiple problems typically presented by the patient with pain. As King has emphasized, modern pain management depends upon the active engagement of the patient in self-management strategies. This task is difficult if the patient has limited personality resources and coping skills. Personality disorders have been somewhat neglected in the psychiatric literature on pain. Weisberg and Keefe [6] have suggested a diathesis-stress model in understanding the high prevalence of personality disorders in pain clinic populations. Sansone et al. [7], in a careful evaluation of borderline personality, found that 3 out of 17 primary care patients with pain had strong borderline traits. Borderline personality confers a handicap in coping with distress and is nowadays seen as a disorder of self-regulation. Recently, there has been a newfound interest in the concept of fear avoidance. Efforts are being made to measure this parameter, as it can be a predictive prognostic factor. A study by Buer and Linton [8] has shown that fear avoidance beliefs and catastrophizing bear important implications for the development of chronic pain. This is an important milestone in our understanding of the psychological catalysts in the development and progression of chronic pain. If we can measure these parameters following injury, early interventions could be planned, which might prevent the development of chronic pain [9]. As King has noted, earlier evaluations of multidimensional pain management programmes, incorporating operant conditioning and cognitivebehavioural principles, were promising. A more recent meta-analysis by

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Morley et al. [10] found that such programmes produce significant changes in pain experience, cognitive coping, appraisal, and behavioural expression of pain. Hypnosis, too, has been subjected to new scrutiny with the advent of imaging studies showing brain activity changes in response to hypnotic suggestion. There is now sufficient evidence, of sufficient quality, to conclude that hypnosis has demonstrable efficacy in the treatment of pain [11]. Modern pain management has become an interdisciplinary and collaborative endeavour between patients and clinicians. If we can escape the dualism of our diagnostic systems and attend to our patients’ multiple problems with a flexible use of treatments of all modalities, always with an eye on the evidence for efficacy (but, most importantly, always working to enhance our patients’ autonomy), perhaps we will be useful as doctors.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Boland R.J. (2002) How could the validity of the DSM-IV pain disorder be improved in reference to the concept that it is supposed to identify? Curr. Pain Headache Rep. 6: 23–29. Aigner M., Bach M. (1999) Clinical utility of DSM-IV pain disorder. Compr. Psychiatry 40: 353–357. Large R.G. (1986) DSM-III diagnoses in chronic pain: confusion or clarity. J. Nerv. Ment. Dis. 174: 295–303. Reich J., Tupin J.P., Abramowitz S.I. (1983) Psychiatric diagnosis of chronic pain patients. Am. J. Psychiatry 140: 1495–1498. Fishbain D.A., Goldberg M., Meagher B.R., Steele R., Rosomoff H. (1986) Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain 26: 181–197. Weisberg J.N., Keefe F.J. (1997) Personality disorders in the chronic pain population. Basic concepts, empirical findings, and clinical implications. Pain Forum 6: 1–9. Sansone R.A., Whitecar P., Meier B.P., Murry A. (2001) The prevalence of borderline personality among primary care patients with chronic pain. Gen. Hosp. Psychiatry 23: 193–197. Buer N., Linton S.J. (2002) Fear-avoidance beliefs and catastrophising: occurrence and risk factor in back pain and ADL in the general population. Pain 99: 485–491. Boersma K., Linton S.J. (2005) Screening to identify patients at risk: profiles of psychological risk factors for early intervention. Clin. J. Pain 21: 38–43. Morley S., Eccleston C., Williams A. (1999) Systematic review and meta-analysis of randomised controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 80: 1–13. Large R.G., Price D.D., Hawkins R. (2003) Hypnotic analgesia and its applications in pain management. In: Proceedings of the 10th World Congress on Pain, Progress in Pain Research and Management, Vol. 24, J.O. Dostrovsky, D.B. Carr, M. Koltzenburg (Eds). IASP Press: Seattle, pp. 839–851.

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2.4 The Mind–Body Dichotomy in the Modern World Hans Jorgen Grabe1 and Carsten Spitzer1 ¨ Steven King provides a comprehensive overview of the efforts that have been made to approach the phenomenon of pain, namely chronic pain. Most diagnostic concepts aim to balance between somatic causes and psychological factors that are assumed to cause the pain or, at least, to contribute to its onset or maintenance. In all, these concepts are reasonable, but several difficulties have not been solved yet. First, the interpretation of symptoms and the use of diagnostic criteria are heavily influenced by the educational and ‘‘psycho-philosophical’’ background of the investigator: is he a physician, is he committed to a ‘‘somatic-mechanical view’’ of the human body (and mind) and convinced of the fact that complex complaints will require complex diagnostic procedures and sophisticated somatic diagnoses? Or is he trained in psychology, psychotherapy or psychiatry, is he committed to an ‘‘everything is psychological view’’? Second, the prevalence of the disorder does not only depend on the subject interpretation but also on the criteria themselves. For example, we found a lifetime prevalence of somatoform pain disorder according to DSM-III-R criteria of 33.7% in the general population. Applying the strict distress and impairment criterion (DSM-IV) to the sample, the prevalence rate dropped to 12.3% [1]. Thus, huge differences may emerge from different diagnostic concepts, and in somatic medicine there are far more than two different concepts of chronic pain! This heterogeneity leads to the problem that most studies on epidemiology, treatment or psychobiological factors in pain are not comparable with each other. Third, as King points out, who will properly decide whether the perception of a symptom in the presence of an underlying physical problem is adequate and thereby ‘‘somatic’’ or inadequate and thereby ‘‘psychological’’? Or who will properly decide whether someone is ‘‘pre-occupied with pain for at least 6 months’’ or not? The DSM-IV aimed to circumvent some of the problems with DSM-III-R. Now, we have three types of pain disorders: (a) associated with psychological factors, where psychological factors are judged to have the main role in the onset, severity, exacerbation, or maintenance of the pain; (b) associated with both psychological factors and a general medical condition, where both psychological factors and a general medical condition are judged to play a role in the origin of the pain; (c) pain disorder associated with a general 1 Department of Psychiatry, Ernst-Moritz-Arndt-University of Greifswald, Rostocker Chaussee 70, 18437 Stralsund, Germany

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medical condition, not considered a mental disorder. In case of diagnostic troubles, the second option may be preferred, but the problem may start again. . . with the patient. The patient himself has a concept of how his body and his mind are connected and what might cause his pain. Thus, the patient himself selects a somatic pathway of diagnosis and treatment or a psychological/psychotherapeutic pathway. Thereby, the patient follows the educational pathways of the health professional or mental health professional and selects the type of diagnostic procedures, the type of diagnosis, and his treatment of choice. The referral of a pain patient by a physician who himself is committed to a ‘‘somatic-mechanical view’’ of the human body to a psychotherapist or psychiatrist may be a rare event: patients do not like this strange shift in thinking of their physician, and physicians are well aware of that. It might take a long (time and money consuming) explanation in order to get the patient to see a mental health professional. In sum, pain disorder does not represent only a ‘‘simple’’ diagnostic and therapeutic challenge. It is also a multi-professional, ‘‘psycho-philosophical’’, and cultural challenge. Health and mental health professionals should establish common diagnostic algorithms that include physical, cognitive, and psychosocial dimensions and are sufficiently operationalized, and use investigator-based as well as self-rating based information. This professional approach could help to overcome the over-simplified body–mind dichotomy that is shared by many people (professionals and patients) in modern societies.

REFERENCES 1.

Grabe H.J., Meyer C., Hapke U., Rumpf H.-J., Freyberger H.J., Dilling H., John U. (2003) The somatoform pain disorder in the community. Psychother. Psychosom. 72: 88–94.

2.5 Chronic Pain: Towards a Biopsychosocial Perspective Michael Bach1 and Martin Aigner2 Pain is one of the most common symptoms in health care, but despite this it is one of the least understood. With DSM-III, a psychiatric entity for chronic pain conditions was introduced, called the psychogenic pain disorder. 1 2

Department of Psychiatry, General Hospital, A-4400 Steyr, Austria Department of Psychiatry, University Hospital, School of Medicine, A-1090 Vienna, Austria

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Subsequently, this has been changed to somatoform pain disorder in DSM-III-R. These diagnostic terms have been established in the light of a dualistic view of pain, suggesting that psychogenic pain or somatoform pain may refer to something different from somatic pain. However, empirical research does not support this dualistic polarization of pain. In order to overcome these limitations, a more broadly defined diagnostic entity has been introduced in the DSM-IV, called pain disorder. The pejorative adjectives of ‘‘psychogenic’’ or ‘‘somatoform’’ pain disorder are now deleted. Instead, the dimension of psychosocial impairment due to pain has been emphasized, presenting a more holistic view of pain in terms of a biopsychosocial clinical perspective. Steven King’s comprehensive review of the concept of DSM-IV pain disorder illustrates the development of this new diagnostic category. As stated, pain disorder can be seen in line with the generally well-accepted definition of pain presented by the International Association for the Study of Pain (IASP). The IASP definition has several implications for a contemporary conceptualization of pain. First, pain has to be seen as a multidimensional phenomenon, including nociceptive as well as psychological aspects. In addition, pain is always a subjective experience of a (patho-)physiological condition, resembling to some extent some other inner feelings, such as hunger, thirst, or fatigue. However, it still remains unclear as to whether pain should be regarded as a psychological state with neurobiological correlates or, in contrast, as a neurobiological condition with mental representations. Facing these methodological issues, the IASP definition suggests a dimensional rather than a categorical view of pain, integrating both perspectives within the same definition. The dimensional approach of pain also supports the clinical experience that the vast majority of patients display (at least to some extent) both biological as well as psychosocial aspects of pain. Thus, pain of (exclusively) organic origin and pain of (exclusively) psychological origin may best be seen as two extreme and rare variants of the biopsychosocial spectrum. The concept of the DSM-IV pain disorder addresses this issue by the distinction of two diagnostic sub-categories: pain disorder associated with psychological factors (code 307.80), which appears as the re-formulation of ‘‘psychogenic’’ pain disorder, and the newly established pain disorder associated with both psychological factors and a general medical condition (code 307.89). A third category, pain disorder associated with a general medical condition, is added to identify pain conditions where psychological factors are judged to have only little influence on the onset, severity, exacerbation, or maintenance of the pain. This latter form of pain disorder is not considered a mental disorder. As stated by King, several studies have shown that a substantial proportion of chronic pain patients met the diagnostic criteria for the sub-category 307.89, with prevalence rates between 51 and 79%. Instead, only low prevalence rates could be found for the sub-category 307.80, which is

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consistent with previous findings for psychogenic pain [1, 2]. These findings add strong empirical weight to the conceptualization of a ‘‘psychosomatic’’ pain category, comprising both psychological and biological aspects of pain. On the other hand, it appears that these criteria lead to an over-diagnosis of DSM-IV pain disorder in chronic pain patients [3]. Caution should, therefore, be applied with regard to the potential stigmatization of pain patients by labelling their pain conditions in terms of a mental disorder. Looking closer to the diagnostic categories of pain disorder, the first two criteria, namely, the presence of pain in one or more anatomical sites as the predominant focus of the clinical presentation (criterion A) and the pain causing significant distress or impairment in social, occupational, or other important areas of functioning (criterion B), will be met by most pain patients seeking medical help for their problems. Thus, the only criterion supposed to discriminate between DSMIV pain disorder and other pain conditions will be criterion C: psychological factors are judged to have an important role in the onset, exacerbation, or maintenance of the pain. With regard to clinical decision making, the question of how this judgement should be made by different health professionals awaits further clarification, at least in those patients who display significant symptoms of depressive disorders or other mental disorders in addition to their pain conditions. Besides, as demonstrated in a study on chronic pain patients, the distinctive validity of the two sub-categories of pain disorder remains questionable with regard to pain duration, intensity, type and level of disability, somatoform and depressive symptom scores, and psychosocial aspects [4]. Finally, further validational studies are warranted to establish clear-cut boundaries or ‘‘points of rarity’’ [5] between the new pain disorder sub-category referring to both psychological factors and a general medical condition (code 307.89) and the classical diagnostic entity of ‘‘psychosomatic’’ disorders (code 316), which has now been reformulated in the DSM-IV as psychological factors affecting medical conditions. In sum, the broader conceptualization of pain in terms of a mental disorder underlines the impact of psychosocial factors in the development or maintenance of pain conditions, as well as the importance of psychologically based intervention modalities for the treatment of acute and chronic pain. To our view, one of the most important issues that emerge with the reconceptualization of pain disorder in DSM-IV is the consideration of distress or pain-related impairment in the psychiatric assessment and classification of pain [6, 7]. Accordingly, a number of studies in chronic pain patients report that treatments can be effective in improving the psychosocial functioning and quality of life without directly reducing the pain intensity. Among these, psychotherapeutic treatment approaches play a major role. In addition to the two main approaches of operant conditioning and cognitive-behaviour therapies as outlined by King, an increasing body of evidence now established hypnosis as an effective treatment for acute pain states [8].

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REFERENCES 1.

Reich J., Tupin J.P., Abramowitz S.I. (1983) Psychiatric diagnoses of chronic pain patients. Am. J. Psychiatry 140: 201–206. Fishbain D.A., Goldberg M., Meager B.R., Steele R., Rosomoff H. (1986) Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain 26: 181–197. Fishbain D.A. (1996) Where have two DSM revisions taken us for the diagnosis of pain disorder in chronic pain patients? Am. J. Psychiatry 153: 137. Aigner M., Bach M. (1999) Clinical utility of DSM-IV pain disorder. Compr. Psychiatry 40: 353–357. Kendell R.E., Brockington I.F. (1980) The identification of disease entities and the relationship between schizophrenic and affective psychoses. Br. J. Psychiatry 137: 324–331. Waddell G., Main C.J., Morris E., Dipaola M., Gray I.C. (1984) Chronic low back pain, psychological distress, and illness behaviour. Spine 9: 209–213. Slater M.A., Hall H.F., Atkinson J.H., Garfin S.R. (1991) Pain and impairment beliefs in chronic low back pain: validation of the Pain and Impairment Relationship Scale (PAIRS). Pain 44: 51–56. Montgomery G.H., Duhamel K.N., Redd W.H. (2000) A meta-analysis of hypnotically induced analgesia: how effective is hypnosis? Int. J. Clin. Exp. Hypn. 48: 138–153.

2. 3. 4. 5. 6. 7. 8.

2.6 Pain Disorder: Where’s the Utility? Lance M. McCracken1 Of all symptoms from which man can suffer, pain may be the one that is both the most compelling and the most defying of explanation and cure. The experience of pain typically includes the belief that something is wrong and asks the patient or the professional to do something to make it stop. In many cases, time and appropriate therapies provide good control of acute pain, and some recurrent or chronic pain, and many pain sufferers can live their lives quite well. In other cases, particularly with persistent pain, the notion that something is wrong can take on an overwhelming quality, and attempts to control it or make it stop can take on extreme forms. It is in these situations that pain occasions considerable suffering and life disruption and calls out loudly for a clinical response. Steven King clearly outlines some of the ways professionals have wrestled with trying to explain pain and judge when pain entails a disorder. In the past, when no physical cause was apparent or adequate, trying to make sense of pain meant finding a psychological cause. This is an easy step, appears 1

Pain Management Unit, Royal National Hospital for Rheumatic Diseases and University of Bath, UK

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simple, clean, and coherent, and can work quite well in some ways. It is nonetheless short-sighted and not an honest or compassionate response to the patient if done in a way that fails to legitimize the patient’s suffering or recognize that any pain experience is multifactorial in nature, whether those factors are readily observable or not. Fortunately, attempts to categorize pain disorders over time have moved from attempts at psychological explanation to an approach with greater potential utility, an approach that sees psychological influences as potentially exacerbating or maintaining and therefore calls for methods to manage these influences. As it stands, however, the current DSM approach may not serve clinical or research purposes as much as it might. Running parallel with approaches to pain that focused on the role of mental disorder have been approaches that focus on patient behaviour, learning, cognition, and emotion. The earlier of these emphasized the importance of overt ‘‘pain behaviour’’ and the variety of physical, social, and emotional influences in the patient’s environment that bore some maintaining influence on that behaviour [1]. On the basis of established principles of operant conditioning, this approach led to treatment methods involving physical exercise and manipulation of environmental influences on painrelated behaviour regardless of the patients’ experience of pain. These early behavioural treatment methods met success in inpatient programmes for chronic pain sufferers and were frequently adopted for acute or subacute pain circumstances. The operant behavioural approach to pain was soon subsumed by cognitive-behavioural approaches, beginning primarily in the 1980s [2]. Within these, the patient’s degree of pain, extent of suffering, and behaviour disruption were seen largely as products of cognitive influences such as attention, beliefs, and interpretations of pain. The added emphasis on cognitive responses led to pain-treatment methods for controlling attention and restructuring thoughts, as well as other cognitive and emotional selfmanagement strategies. Cognitive-behavioural approaches have tended to carry with them both a focus on behaviour change and, perhaps more significantly, a focus on controlling thoughts, pain sensations, and emotional responses, as means for enhancing patient functioning. Results of cognitive behaviourally based treatments for chronic pain have been quite positive, and they are arguably the most effective treatments for the problem [3]. There are developments within psychological treatments for a number of different disorders referred to as ‘‘third wave’’ cognitive-behavioural therapies [4]. These approaches share several features in common in that they (a) integrate the overt behavioural and environmental emphasis of the earlier operant approach with the cognitive emphasis of the cognitive-behavioural; (b) shift from a mechanistic to a contextual view of psychological events; (c) focus less on symptom elimination than on building positive behavioural

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repertoires; (d) place a greater emphasis on the nature of the therapeutic relationship; and (e) incorporate a mix of acceptance and control responses to psychological experiences rather than control alone. We have argued that these approaches are particularly applicable to pain-related suffering and disability, and accumulating data support this case [5]. Somewhere there is a line between where pain is simply present and where pain has become an occasion for significant problems in the pain sufferer’s life. That there are persons with ostensibly similar pain experiences on both sides of this line is psychologically interesting and requires explanation. In the absence of ways to take the pain away, helping to shift patients from the suffering side of that line to the functioning side is likely the most caring thing the professional can do. The ‘‘pain disorder’’ diagnoses that have come from the DSM approach ask the clinician to judge when psychological influences appear to be clinically important. To echo some of Steven King’s closing remarks, these diagnoses will have real utility when they help to improve our understanding of what those psychological influences are, how they operate, and how to manipulate them. This would seem to call for some greater integration of contemporary cognitive-behavioural approaches with approaches to diagnosis and classification.

REFERENCES 1. 2. 3. 4. 5.

Fordyce W.E. (1976) Behavioral Methods for Chronic Pain and Illness. CV Mosby: St. Louis. Turk D.C., Meichenbaum D., Genest M. (1983) Pain and Behavioral Medicine: A Cognitive-Behavioral Perspective. Guilford Press: New York. Morley S., Eccleston C., Williams A.C. (1999) Systematic review and meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 80: 1–13. Hayes S.C. (2004) Acceptance and commitment therapy, relational frame theory, and the third wave of behavioral and cognitive therapies. Behav. Ther. 35: 639–665. McCracken L.M. (2005) Contextual Cognitive-Behavioral Therapy for Chronic Pain. IASP Press: Seattle.

2.7 Patients Must Be at the Centre of Pain Management Joanna M. Zakrzewska1 Pain is an integral part of life and plays a crucial protective role that is often forgotten. At the same time, it is invisible, difficult to describe and 1 Clinical and Diagnostic Oral Sciences Dental Institute, Barts and London Queen Mary’s School of Medicine and Dentistry, Turner Street, London E1 2AD, UK

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quantify, and can cause great suffering. It is very appropriate that a chapter in this book is devoted to pain at a time when the US Congress announced a Decade of Pain Control and Research and the World Health Organization in 2004 held a meeting called the Global Day against Pain in order to increase the world’s awareness of pain. Much research has been done in the last two decades, but we still have little control over the suffering that pain brings. We have identified many of the processes that produce pain with our increasing knowledge of neurophysiology and gene-expressing profiling, but pain remains enigmatic. The pain experience, we know, is also affected by cultural, social, and psychological factors. The brain remains central to pain as it provides the ultimate interpretation and modulation, and functional magnetic resonance imaging is now capturing the numerous networks involved as it attempts to answer the following question: why does the same pain stimulus result in a different perception of pain for every individual? Aristotle classified pain as an emotion and the International Association for the Study of Pain has also defined it in those terms. It has therefore rightly been allocated a section in the DSM classification although, as Steven King points out, it is only the most recent version that has seen it being utilized clinically. In order to be able to say that pain has been relieved, some form of objective measure is needed. Yet, as King has illustrated, it remains very difficult to measure and map language onto pain. He also stresses that measures used in healthy individuals may not be applicable to those with mental health problems and points to a recent review that showed that 37% of patients with chronic pain had clinical depression and 65% of patients with depression reported significant pain. The gap between our understanding of pain and our ability to treat it has reduced, but it is still too wide, with one in every five people globally suffering from chronic pain. The widely accepted Oxford League table of analgesic efficacy, which shows a wide range of analgesics and their effectiveness in producing a 50% reduction in pain, has made a real difference to acute pain management [1]. McQuay et al. [2] have argued that ‘‘existing tools can do the job if doctors and nurses are educated both about dispelling the myths and misconceptions and about taking responsibility for providing good pain control. It is much easier to dispel myths when you have the evidence’’. On the other hand, chronic pain, and in particular neuropathic pain, remains poorly understood and managed. King has performed a comprehensive review of the literature and shown us that there is relatively little new—mainly a variation on the same theme with analgesics, anticonvulsants, and antidepressants remaining the main class of drugs that are used. Few surgical treatments or even complementary and alternative medicines provide long-term pain relief.

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What has been changing is the realization that chronic pain is a long-term condition that cannot be cured, that it does not necessarily signal ongoing destruction, and that acceptance is crucial if some measure of control is to be achieved. Evidence-based medicine has shown that cognitive behaviour therapy has an important role in improving quality of life [3] and that it should not be used as the last resort but alongside pharmacological therapy [4]. However, at the centre of pain management must lie the patient. Over the past 10 years, patients have shifted from being subservient to the clinician to evolving into a relationship of partnership where they take on more responsibility for management of their condition. Books such as Manage Your Pain reflect the need for the patient to engage in management of their suffering [5]. We have the evidence that these patients gain improved benefit from treatment and health care utilization decreases. For this to be effective, patients not only need knowledge but also be able to critically appraise it. There are now a wide range of resources available for the chronic pain patient, ranging from support groups to information leaflets to interactive internet sites, but their quality is extremely variable and they need a knowledge manager, that is, health care professional, to help. Thus, human contact and interaction between the physician and the patient remains a core function. Our knowledge of how the beliefs and values of patients, as told through the medium of narrative, affect the pain experience must continue to play as vital a role as our knowledge of neurons and genetic make-up. Only by keeping the patient at the heart of pain management can we hope to achieve more effective outcomes.

REFERENCES 1. 2. 3. 4. 5.

McQuay H., Moore A., Justins D. (1997) Treating acute pain in hospital. Br. Med. J. 314: 1531–1535. McQuay H.J., Moore R.A. (1998) An Evidence-Based Resource for Pain Relief. Oxford University Press: Oxford. Morley S., Eccleston C., Williams A. (1999) Systematic review and meta-analysis of randomized controlled trials of cognitive behaviour therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain 80: 1–13. Williams A.C. (2003) Cognitive behavioral treatment. In: Progress in Pain Research and Management, J.O. Dostrovsky, D.B. Carr, M. Koltzenburg (Eds). IASP Press: Seattle, pp. 825–837. Nicholas M., Molloy A., Tonkin L., Beeston L. (2003) Manage Your Pain. Souvenir Press: London.

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2.8 Chronic Pain: the Importance of a Comprehensive History Gerald M. Aronoff1 Steven King discusses the important topic of chronic pain and focuses his attention on the subgroup of patients with a diagnosis of pain disorder (DSM-IV). He traces the evolution of the current term from earlier DSM terms of psychophysiological disorders (DSM-II), psychogenic pain disorder (DSM-III), and somatoform pain disorder (DSM-III-R), and discusses the deficiencies that compromised the clinical utility of these terms. Benjamin Crue [1], neurosurgeon and founder of the City of Hope Pain Center in 1972, was one of the earlier modern pain pioneers to describe the concept of pain disorder long before the term (or its precursors) appeared in DSM. He introduced significant controversy into the assessment of chronic pain patients by suggesting that, for most patients with chronic pain, central factors more than peripheral factors were most important in understanding delayed recovery and dysfunctional pain behaviours. Over the years, in many communications with me, Crue indicated that, for all chronic pain patients, treatment needed to be psychotherapeutic. General medical audiences and neurosurgical audiences often misinterpreted this, and, therefore, as a concept it encountered violent opposition. Crue was not implying that all chronic pain needed to be managed by psychiatrists or psychologists but rather that all clinicians treating chronic pain patients needed to take a psychotherapeutic approach and develop an appreciation for the impact that chronic pain has on an individual’s life. Evaluators should not focus attention only on the back, extremity, or organ system. Some patients may just require reassurance, whereas others may need a more comprehensive evaluation by trained mental health professionals. Crue strongly confronted the Cartesian dualism that was the norm in the 1960s and 1970s. Steven King comments on the term chronic pain syndrome as a diagnosis and refers to a definition by Richard Black [2]. I need to emphasize that this term is no longer used as a diagnosis (and probably never should have been in the past). It is a descriptive term generally used to denote an individual with persistent pain and often subjective complaints in excess of objective findings, conditioned dysfunctional and maladaptive pain behaviours, self-limitations in activities of daily living, poor coping, and associated life disruption [3]. The term may be useful in distinguishing such a patient from a patient with persistent nociceptive pain and/or neuropathic pain without associated emotional pathology or life disruption. 1

Carolina Pain Associates, 1900 Randolph Road, Suite 606, Charlotte, NC 28207, USA

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I am dismayed that even today many clinicians still evaluate chronic pain with a biomedical rather than a biopsychosocial approach. More than 25 years of experience in the field now known as pain medicine has taught me that, for many patients with chronic pain syndromes, the pain complaint may be the patients’ way of saying (through a process of somatization) that their life hurts, although the process is manifested by a complaint of headache or back pain. Somatization is a common process occurring within a pain disorder [4]. Primary care specialists and other physician specialities underdiagnose it. Steven King refers to work done by Blumer and Heilbronn [5]. Blumer was one of my mentors as a resident, and one of his major contributions to chronic pain evaluation was his emphasis on the importance of taking a comprehensive developmental history. He expanded the concept of pain proneness described by Engel in the psychoanalytic literature [6]. The essence of Blumer’s position [7] was that certain individuals have a characteristic early developmental history notable for many unmet dependency needs, emotional neglect, physical and/or sexual abuse, and hyperresponsibility at an earlier age. Their psychosocial history reveals that the pattern may continue into adult life. If they become injured (at times insignificantly) or develop an illness (with symptoms at times far in excess of objective signs), often they fail to recover or have significantly delayed recovery. I believe that it is their way of saying ‘‘now it is my turn to be taken care of’’ [4]. Experiencing chronic pain is emotionally distressing. However, patients who have insight into their emotions, and know how to effectively cope with them, appear less likely to develop pain disorders. King discusses the evaluation of individuals with pain disorder and correctly emphasizes the difficulty in pain evaluation, given the subjective nature of pain itself. He also appropriately cautions clinicians without training in the interpretation of standardized psychological tests—such as the Minnesota Multiphasic Personality Inventory-2, the Beck Depression Inventory or the Hamilton Depression Scale, so often used to evaluate chronic pain patients—that these tests cannot reliably predict the extent to which pain is organically based. King is correct to emphasize the importance of using adjuvant analgesics in managing patients with pain disorder for whom medications are felt to be indicated. There is ample data to support many of the adjuvants, especially the heterocyclic antidepressants and multiple antiepileptic drugs that are currently being utilized off label in the management of chronic pain [8]. However, pharmacological management approaches are often unsuccessful in patients with chronic pain syndromes in the absence of a coordinated interdisciplinary treatment approach.

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REFERENCES 1. 2. 3.

Crue B.L. (1979) Chronic Pain. Spectrum Publications: New York. Black R.G. (1975) The chronic pain syndrome. Surg. Clin. North Am. 55: 999–1011. Aronoff G.M. (1999) Psychiatric aspects of nonmalignant chronic pain: a new nosology. In: Evaluation and Treatment of Chronic Pain, 3rd ed., G.M. Aronoff (Ed). Lippincott Williams & Wilkins: Baltimore, pp. 291–300. Aronoff G.M., Tota-Faucette M., Phillips L., Lawrence C.N. (2000) Are pain disorder and somatization disorder valid diagnostic entities? Curr. Rev. Pain 4: 309–312. Blumer D., Heilbronn M. (1987) Depression and chronic pain. In: Presentations of Depression, O.G. Cameron (Ed). Wiley: New York, pp. 215–235. Engel G. (1959) Psychogenic pain and the pain prone patient. Am. J. Med. 54: 899–918. Blumer D., Heilbronn M. (1982) Chronic pain as a variant of depressive disease. J. Nerv. Ment. Dis. 170: 381–406. Aronoff G.M. (2005) Handbook on Pharmacological Management of Chronic Pain. Wavecrest Publications: Charlotte.

4. 5. 6. 7. 8.

2.9 Psychological and Physiological Factors in Pain Disorder Morten Birket-Smith1 In his comprehensive review, Steven King illustrates the significance of health problems related to chronic pain, including individual suffering and major health expenses. Recently, it has been shown that 8.3% of the Danish population has pain lasting for 6 months or longer, and each year the pain population is growing by 0.3% [1]. In the general population, as well as in primary care and hospital settings, pain symptoms are more frequent than any other physical symptom, and are quite often medically unexplained [2]. Medically unexplained pain is often a symptom of mental disorders. Patients with depression or anxiety disorder initially seldom present mental discomfort, but rather physical symptoms, especially pain [3]. Though physical symptoms are important aspects of depression, the definition of a depressive episode in any of the current classification does not cover these aspects. On the other hand, it is not possible to have a DSM-IV or ICD-10 diagnosis of generalized anxiety disorder or agoraphobia without somatic symptoms. In somatoform disorders, the most commonly reported symptoms are musculoskeletal pain and headache, and, independent of referral symptom or somatoform diagnosis, almost all somatoform patients have pain complaints [4]. We found no differences in psychopathology between patients 1

Liaison Psychiatry, Bispebjerg University Hospital, DK-2400 Copenhagen NV, Denmark

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with somatoform pain disorder and other somatoform diagnoses, demonstrating the problems in the classification of somatoform pain. Though the DSM-IV has provided a clinical meaningful subdivision of pain disorder, the number of studies applying the diagnosis is still small compared to pain research in general. In current research, pain is often divided into four categories [5]. Nociceptive pain is the common, immediate reaction to a noxious stimulus, in which the signal is led to the brain without influencing the function of the nervous system. In inflammatory pain, a number of physiological changes leading to hypersensitivity occur in response to tissue damage, and the pain threshold is diminished by peripheral and central sensitization, including modulated gene expression and long-term potentiation of neurons of the dorsal horn in the spinal cord [6]. Neuropathic pain is a response to lesions to the peripheral nervous system, as in diabetic polyneuropathy, or to damage to the central nervous system, as in trauma, multiple sclerosis, and stroke, and may lead to sensitization and central pain. Functional pain is uncoupled from nociceptive input, and no damage to the nervous system can be detected. In somatoform pain and syndromes such as irritable bowel syndrome, chest pain, tension headache, and fibromyalgia, functional pain is a main feature [5]. In nociceptive pain, noxious stimuli are converted into electrical activity, conducted to the dorsal horn of the spinal cord, and transferred to neurons with projections to the brain. The transfer is by both single synaptic contacts and by interneurons, and is controlled by local circuits in the spinal cord, as well as by descending inhibitory and facilitatory pathways. The perception and transmission of pain is influenced by cognitive variables, such as attention, expectation, emotions, and changes in consciousness [7]. Individuals perceive pain less intensely when distracted, and a positive mood generally reduces pain perception and reporting, while negative emotional influence increases pain [8]. In normal situations, most inputs to the medulla fail to evoke an action potential [5]; in functional pain, central sensitization and other pain-enhancing mechanisms may be so prominent that subthreshold peripheral signals are transmitted to the brain and perceived as pain [9]. Patients with fibromyalgia exhibit functional pain with diminished pain thresholds and hyperalgesia inferring central sensitization [10, 11]. Furthermore, low levels of serotonin, dysfunction of the N-methyl-D-aspartate (NMDA) receptor, as well as an abnormal neuroendocrine response to stress have been demonstrated [12]. A functional polymorphism (S/S genotype) in the serotonin transporter promoter region is more frequent in fibromyalgia patients than in controls, indicating a genetic component [13]. In conclusion, research on different pain categories, especially functional pain, provides an explanation for the poor correlation between tissue damage, pain complaints, and pain-related behaviour, and illustrates the interaction between mental and physical factors in pain disorder.

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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Eriksson J., Jensen M.K., Sjøgren P., Ekholm O., Rasmussen N.K. (2003) Epidemiology of chronic non-malignant pain in Denmark. Pain 106: 221–228. Kroenke K., Price R.K. (1993) Symptoms in the community. Prevalence, classification, and psychiatric comorbidity. Arch. Intern. Med. 8: 2474–2480. Kroenke K., Spitzer R.L., Williams J.B., Linzer M., Hahn S.R., Defray F.V., Brody D. (1994) Physical symptoms in primary care: predictors of psychiatric disorders and functional impairment. Arch. Fam. Med. 7: 774–779. Birket-Smith M., Mortensen E.L. (2002) Pain in somatoform disorders: is somatoform pain disorder a valid diagnosis? Acta Psychiatr. Scand. 106: 103–108. Woolf C.J. (2004) Pain: moving from symptom control toward mechanismspecific management. Ann. Intern. Med. 140: 441–451. Sandkuhler J. (2000) Learning and memory in pain pathways. Pain 88: 113–118. ¨ Villemeure C., Bushnell M.C. (2002) Cognitive modulation of pain: how do attention and emotion influence pain processing? Pain 95: 195–199. Villemeure C., Slotnick B.M., Bushnell M.C. (2003) Effects of odors on pain perception: deciphering the roles of emotion and attention. Pain 106: 101–108. Price D.D. (2000) Psychological and neural mechanisms of the affective dimension of pain. Science 288: 1769–1772. Staud R., Vierck C.J., Cannon R.L., Mauderli A.P., Price D.D. (2001) Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain 91: 165–175. Gracely R.H., Petzke F., Wolf J.M., Clauw D.J. (2002) Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 46: 1333–1343. Meller S.T., Gebhart G.F. (1993) Nitric oxide and nociceptive processing in the spinal cord. Pain 52: 127–136. Offenbacker M., Bondy B., de Jonge S., Glatzeder K., Kruger M., Schoeps P., ¨ Ackenheil M. (1999) Possible association of fibromyalgia with a polymorphism in the serotonin transporter gene regulatory region. Arthritis Rheum. 42: 2482–2488.

2.10 Does the Somatoform Disorder Approach Broaden Our Perspective on Pain? Wolfgang Hiller1 and Paul Nilges1 Despite decades of intensive pain research, a surprisingly large number of questions relating to the diagnosis, aetiology, and treatment of chronic pain are still unanswered. Many mysteries continue to rank around this complex phenomenon. In the face of the immense number of people suffering from chronic pain conditions, it would be irresponsible not stepping up efforts to search for the causes and determinants of chronic pain, develop valid 1

Psychological Institute, University of Mainz, Staudingerweg 9, D-55099 Mainz, Germany

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diagnoses and diagnostic tools, and improve treatment methods. Steven King’s comprehensive review is clear in working out the limitations of our knowledge. Some aspects may complicate research and clinical management of chronic pain patients. The field is interdisciplinary by nature, with anaesthesiology, neurology and psychiatry as the major groups of somatic medicine involved. Essential contributions, however, come from psychology and cognitivebehavioural science. Almost all diagnostic methods to assess pain and associated features are psychometric. The psychological treatments, all aiming to change the patients’ perceptions, interpretations, and behaviours, are well developed. Their high standard as evidence-based treatments is documented through recent reviews of the Cochrane Collaboration [1, 2]. It will be important in future to investigate how psychological processes are associated with brain functioning. Modern neuroimaging techniques have already allowed new insights as to where and how pain signals are processed within the brain [3]. The subsumption of pain under the main chapter of somatoform disorders is a contentious issue. Somatoform symptoms are defined as ‘‘medically unexplained’’, but is often difficult or even impossible to decide whether or not a specified pain is due to medical disease or clear pathobiological mechanisms. Diagnostic uncertainty is common. Excessive diagnostic procedures, however, may lead to an overestimation of pathology. Hald et al. [4] demonstrated, in a large population sample of healthy and pain-free men between 17 and 25 years, that less than 5% had no demonstrable X-ray pathology of the spine. Why was the remaining majority free of complaints that would have corresponded to the somatic findings? On the other hand, there is evidence that the prevalence of post-surgery pain is frequently underestimated [5]. These examples demonstrate that the mechanisms leading to enduring and physically unclear pain are not yet understood. Pain symptoms are very typical and frequent in patients who suffer from multiple unclear symptoms in different regions of the body [6]. An obvious advantage of the somatoform disorder approach seems to lie in its broader perspective. Pain is not seen as an isolated symptom. It is rather considered under a common perspective with many other possible somatic symptoms, which may have a common origin or similar underlying mechanisms. There are good reasons to expect that research on somatoform disorders will enrich our knowledge about pain. It seems to be of significance to differentiate between disorders characterized by pain alone, and those with pain embedded into a larger number of different non-pain physical symptoms. For example, Hiller et al. [7] found that pain patients with additional multiple somatoform symptoms had higher levels of affective and sensoric pain sensations as well as more pain-related disabilities. They were also less successful during treatment to reduce their pain-related depression and anxiety.

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This confirms that general principles of symptom perception and evaluation might play a central role in these patients, rather than specific reactions typical only for pain. Cognitive-behavioural models of somatoform disorders try to describe how perceptions of bodily discomfort are developed and maintained. One valuable contribution is Barsky’s notion of somatosensory amplification [8], assuming that individuals may be predisposed to experience somatic and visceral sensations as intense, noxious, and disturbing. It is likely that such disposition enhances the development and maintenance of many pain complaints. Another example of relevant research is a study by Rief et al. [9] who identified a set of characteristic cognitions in patients with unclear somatic symptoms, such as the catastrophizing of physical perceptions (‘‘bodily complaints are always a sign of disease’’), a low tolerance of bodily discomfort (‘‘if something is wrong with my bodily sensations, it upsets me at once’’), or a negative attitude towards the body ( ‘‘I am physically rather weak and sensitive’’). Pain complaints may be accompanied by a large variety of illness behaviours. These may include persistent efforts to verify a positive medical diagnosis, the expression of symptoms in the presence of others, or the use of unnecessary medication in order to affirm the self-perception of being physically sick [10]. The types of illness behaviours found in patients with somatoform and pain disorders are almost identical. Such similarities of chronic pain and somatoform disorders will hopefully lead to more stringent research and clinical practice in the future.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.

Kisely S., Campbell L.A., Skerritt P. Psychological interventions for symptomatic management of non-specific chest pain in patients with normal coronary anatomy. The Cochrane Library, 2004. Ostelo R.W.J.G., van Tulder M.W., Vlaeyen J.W.S., Linton S.J., Morley S.J., Assendelft W.I.J. Behavioural treatment for chronic low back pain. The Cochrane Library, 2004. Peyron R., Laurent B., Garcia-Larrea L. (2000) Functional imaging of brain responses to pain. A review and meta-analysis. Neurophysiol. Clin. 30: 263–288. Hald H.J., Danz B., Schwab R., Burmeister K., B¨ahren W. (1995) Rontgenologisch ¨ nachweisbare Wirbels¨aulenver¨anderungen asymptomatischer junger m¨anner. Rofo 163: 4–8. Perkins F.M., Kehlet H. (2000) Chronic pain as an outcome of surgery. Anesthesiology 93: 1123–1133. Rief W., Hessel A., Braehler E. (2001) Somatization symptoms and hypochondriacal features in the general population. Psychosom. Med. 63: 595–602. Hiller W., Heuser J., Fichter M.M. (2000) The DSM-IV nosology of chronic pain: a comparison of pain disorder and multiple somatization syndrome. Eur. J. Pain 4: 45–55. Barsky A.J. (1992) Amplification, somatization, and the somatoform disorders. Psychosomatics 33: 28–34.

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Rief W., Hiller W., Margraf J. (1998) Cognitive aspects of hypochondriasis and the somatization syndrome. J. Abnorm. Psychol. 107: 587–595. Rief W., Ihle D., Pilger F. (2003) A new approach to assess illness behaviour. J. Psychosom. Res. 54: 405–414.

2.11 Diagnosis and Treatment of Pain: Consultation-Liaison Psychiatry Aspects Albert Diefenbacher1 Pain is a complex experience that involves both physical and mental components [1]. Though it is a common condition, it seems that physicians often feel uncomfortable in helping patients, especially those suffering from chronic pain. As King points out, this may lead to multiple physician contacts and many unproductive diagnostic procedures. Reasons for that may lie in the lack of adequate training with regard to pain issues during medical school and residency [2], and in the failure to pay adequate attention to the multifaceted aspects of communication between physicians and other staff and patients: up to 50% of patients are critical of the communication aspects of their hospital care [3]. In addition, there is noticeable overlap of pain states with psychiatric morbidity. This commentary will discuss issues of psychiatric service delivery in the treatment of pain syndromes under the perspective of consultation-liaison (C-L) psychiatry. Despite the well-known comorbidity of psychiatric disorders with pain syndromes, psychiatrists usually are called very late in the diagnostic and treatment process of pain patients. This is not a specific feature of pain patients, but a well-known phenomenon in C-L psychiatry. Obviously, somatic physicians use to apply their own specialist portfolio of knowledge first, and only call on additional psychiatric support once their usual armamentarium fails to succeed. This attitude may contribute to longer lengths of stay in hospitals of patients with somatic-psychic comorbidity [4, 5]. It has been argued that the most widely used form of co-operation between somatic physicians and psychiatrists, consultation psychiatry proper, does not lead to a sufficient number of referrals and often takes place late in the treatment process, as somatic physicians may not recognize the necessity and usefulness of an additional psychiatric perspective, and may discourage patients who think that a referral to a psychiatrist after other treatment efforts failed is equivalent to being abandoned and being declared as ‘‘being 1 Department of Psychiatry and Psychotherapy, Evangelisches Krankenhaus Koenigin Elisabeth Herzberge, Herzbergstrasse 79, D-10365 Berlin, Germany

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crazy’’ [6]. The model proposed to mend this problem is liaison psychiatry, a model in which a psychiatrist is part of the treatment team and therefore sees patients earlier. Since this takes place within a routine procedure, the problem of stigmatizing the patient is minimized [6]. Such an integrated approach seems especially useful in the treatment of patients suffering from pain. It can be organized under the umbrella of a multi-disciplinary pain clinic where patients undergo serial evaluation by multiple specialists [1]. The liaison psychiatrist may help detect psychiatric disorders as the basis for pain complaints in patients who otherwise would not be in contact with the mental health care system. As an expert in psychopharmacology, the C-L psychiatrist may complete a medication regime, for example, by using antidepressants as an adjunct medication to relief pain; or help in stopping the use of benzodiazepines, that may have led to dependency with ensuing dysphoric mood and sleep disorder that in turn aggravate the pain syndrome [7, 8]. As a specialist in substance use disorder, he may help in disentangling the sometimes intricate question of whether a patient has developed an addiction, and help clarify the problem of pseudo-addiction. He may also initiate psychotherapeutic techniques to help the patient develop cognitive-behavioural coping skills, either alone, or, even more effective, including the patient’s partner and family [2, 9]. As several studies have shown, multidisciplinary pain clinics that include psychological and cognitive treatments are effective for the treatment of chronic pain, especially in improving quality of life, which in turn is associated with lower levels of pain and better performance of daily activities. They lead to more patients returning to work or vocational rehabilitation, as compared to controls, and to decreased health care utilization [2, 10, 11].

REFERENCES 1. 2.

3. 4. 5. 6.

Turk D.C., Melzack R. (Eds). (1992) Handbook of Pain Assessment. Guilford Press: New York. Holmgren A., Wise M.G., Bouckoms A.J. (2002) Pain management. In: Textbook of Consultation-Liaison Psychiatry - Psychiatry in the Medically ill, 2nd ed., M.G. Wise, J.R. Rundell (Eds). American Psychiatric Publishing: Washington, D.C., pp. 989–1013. Royal College of Physicians and Royal College of Psychiatrists (2003) The Psychological Care of Medical Patients - A Practical Guide. Royal College of Psychiatrists: London. Diefenbacher A., Strain J.J. (2002) Consultation-liaison psychiatry—stability and change over a 10-year-period. Gen. Hosp. Psychiatry 24: 249–256. Huyse F.J., Herzog W., Lobo A., Lyons J.S., Slaets J.P.J., Fink P., Stiefel F., de Jonge P. (1997) Detection and treatment of mental disorders in general health care. Eur. Psychiatry 12(Suppl. 2): 70s–78s. Diefenbacher A. (2000) Consultation and liaison psychiatry. In: Contemporary Psychiatry, Vol. 1, F.A. Henn, N. Sartorius, H. Helmchen, H. Lauter (Eds). Springer: Berlin, pp. 253–267.

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Worz ¨ R. (2004) Psychiatrische Schmerzdiagnostik und Schmerztherapie. In: Psychiatrie in der Klinischen Medizin—Konsiliarpsychiatrie, -psychosomatik und -psychotherapie, V. Arolt, A. Diefenbacher (Eds). Darmstadt: Steinkopf, pp. 173–194. Diefenbacher A., Saupe R., Fegers S., Worz ¨ R. (1999) Psychiatrische Schmerzdiagnostik und -therapie Teil IV: Konsiliarpsychiatrie bei Schmerzpatienten. Nervenheilkunde 18: 139–142. Portenoy R.K., Cheville A.L. (2000) Chronic pain management. In: Psychiatric Care of the Medical Patient, 2nd ed., A. Stoudemire, B.S. Fogel, D.B. Greenberg (Eds). Oxford University Press: Oxford, pp. 199–225. Clark M.R., Chodynicki M.P. (2005) Pain. In: Textbook of Psychosomatic Medicine, J.L. Levenson (Ed). American Psychiatric Publishing: Washington, D.C., pp. 827–867. Radanov B.P. (2004) Therapeutic approaches to chronic pain and the role of the consultation-liaison psychiatrist. In: Consultation-Liaison Psychiatry in Germany, Austria and Switzerland, A. Diefenbacher (Ed). Karger: Basel, pp. 159–170.

2.12 Pain: Suffering, Semantics, and Sensitization Jeffrey Rome1 Pain is a pernicious, pervasive, and perplexing experience. It is practically synonymous with suffering and is ubiquitous in human existence, from the initial inspiration at birth to the agonal expiration at death. It is at once both a sensation and a psychological state. Pain has a wide array of attributes, which includes its physical characteristics, location, and duration, its emotional connotations, and its variable association with overt manifestations of illness or trauma. As David Morris muses in his treatise The Culture of Pain, ‘‘Pain comes in more spins and flavors than quarks’’ [1]. More than other somatic perceptions such as temperature, light touch, and proprioception, pain engenders affects and elicits cognitions. Diverse repertoires of behaviours develop in the presence of pain. These may be adaptive or maladaptive behavioural responses to pain, and when maladaptive, they can be a significant contributing factor to an individual’s diminished quality of life and level of functioning. These ‘‘pain behaviours’’ may be fostered by family and friends, are frequently entangled with bureaucracies and litigation, and suffused with remembrances of the past and premonitions of the future. Health care providers venture opinions about some of the myriad issues that affect patients in pain with speculations about how much pain is ‘‘expected’’ in a given clinical context, and about ‘‘secondary gain’’ and ‘‘malingering’’. The validity of these opinions is difficult to establish. The biopsychosocial complexity of pain, particularly chronic pain, is an important 1

Mayo Clinic, Rochester, MN, USA

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reason for differing approaches to the diagnosis and treatment of persons with chronic pain. In his thorough and balanced overview of pain disorders, Steven King traces the development of the taxonomy of pain-related conditions in several editions of the DSM. The evolution of the diagnostic categorization of pain disorders in the DSM mirrors the debate about the aetiology of pain complaints that do not follow the typical time course to resolution, or depart from the usual ratings of severity, or are described outside the anatomic boundaries of dermatomes or nerve root distributions. The changes over time in the DSM are more than semantic; they are substantive and convey the sense of a work in progress, in search of a principle that can unify the somatic and psychic components of the experience of pain into a seamless whole. A holistic and scientifically relevant conceptual model of pain must be based both on rapidly advancing knowledge of the neurobiology of nociception and on conventional wisdom that recognizes the centrality of psychological processes (i.e., affect, attention, and behaviour) in the experience of pain. Such a model must incorporate, on the one hand, the often ambiguous correlation between the level of subjective distress and pathophysiological findings and, on the other, the psychological make-up and social context of the person who is suffering. Stimulus-induced neuroplasticity may well be the binding agent that holds together these various components of a valid and inclusive biopsychosocial model of pain. Stimulus-induced neuroplasticity, in this context, refers to a complex array of changes which take place in the nervous system that alter the response characteristics of the neural networks generating the conscious experience of pain. Examples of neuroplastic changes that have been linked to pain include perturbations in the neurochemical mediators of nociception (i.e., substance P, neurokinins, calcitonin gene-related peptide, etc.), alterations in gene expression (i.e., c-fos, c-jun), changes in ion channels (Na+, K+, Ca++) and synapses, inflammation, dendritic arbourization, the recruitment of non-nociceptive fibres (allodynia), and neuronal apoptosis. The neuroplastic changes associated with pain develop over time and can be triggered by both noxious physical stimuli and traumatic psychological events [2]. The end result may be either sensitization or inhibition of neuronal responses to stimulation. Neuroplastic changes that take place in peripheral nerves, in the dorsal horn of the spinal cord, and in the medial and lateral pain systems of the brain are mechanisms by which traumatic life experiences can produce the diverse clinical features of chronic pain disorders that so often prove to be refractory to conventional medical treatment. In his discussion of the treatment of pain disorders, King differentiates acute from chronic pain conditions, an important distinction that can be difficult to make in practice. The differences between acute and chronic pain are so fundamental that these conditions have been labelled separately as eudynia

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and maldynia. The differences involve not only the time course and likelihood of resolution of the pain, but also the contribution of neuroplastic processes to the perception of pain, the burden of associated psychosocial comorbidities, and the responsiveness of the pain condition to anti-nociceptive treatment. The prevalence of chronic pain disorders, estimated to affect perhaps 80 million people in the United States alone, suggests that antinociceptive treatments, which generally are efficacious for acute pain, are insufficient to alleviate the suffering of most persons with chronic pain. There are obviously many reasons for this. Certainly, access to medical care and adherence to recommended treatment are important in this regard. But the focus of chronic pain treatment itself also can be the cause of poor outcomes. Treatment that exclusively targets the putative nociceptive generator (the body part that hurts) will overlook the psychosocial components of the pain disorder. These components are not only integral parts of the pain disorder itself, but also are quite amenable to treatment. Therapeutic interventions that are based on a biopsychosocial model hold much promise for assisting patients with chronic pain disorders by utilizing proven psychological and rehabilitative modalities of treatment in conjunction with evidence-based analgesic measures [3].

REFERENCES 1. 2. 3.

Morris D.B. (1991) The Culture of Pain. University of California Press: Berkeley. Rome H.P., Rome J.D. (2000) Limbically augmented pain syndrome (LAPS): kindling, corticolimbic sensitization, and the convergence of affective and sensory symptoms in chronic pain disorders. Pain Med. 1: 7–23. Flor H., Fydrich T., Turk D.C. (1992) Efficacy of multidisciplinary pain treatment centers: a meta-analytic review. Pain 49: 221–230.

2.13 Subjectivity and Communitas: Further Considerations on Pain Etzel Cardena ˜ 1 We are born with a cry and often die in pain. Its biological, psychological, sociocultural, and existential dimensions [1] deny the facile distinction between mental and bodily processes, as King’s comprehensive review points out. We can experience pain without tissue damage, and have damage without experiencing pain. Pain can increase or decrease depending on the 1 Department of Psychology and Anthropology, University of Texas-Pan American, Edinburg, TX 78539, USA

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meaning individuals and cultures assign to it, and whether we share that pain with someone else. Nonetheless, one of the limitations of much writing in this area has been a stress on proximal, biological variables while minimizing social and psychological ones. For instance, in a recent overview, Lewis mentions the ‘‘backdrop of circumstance and culture, memories, and mood’’ in pain, only to focus almost exclusively on its biology [2]. The neglect of this ‘‘backdrop’’ may condemn us to prioritize palliative remedies over long-term, cultural changes that may have a greater impact. This commentary focuses on the interrelated factors of social relationships, mood, and pain, and updates King’s discussion on the use of hypnosis for the treatment of pain. King presents compelling evidence that pain is closely related to depressive and anxiety disorders (e.g., 87% of psychiatric patients reported pain in one of his studies). As he mentions, although psychiatric disorders may be secondary to pain, the relationship is more complex (and bidirectional), but he does not address its sociocultural components. First, Western societies, especially the United States, have experienced an unravelling of their social fabric in the last few decades. At the ‘‘macro’’ level, sociologists have remarked on the ‘‘shallowness’’ of community in the United States and the extremes of its individualistic propensities [3]. At the ‘‘micro’’ level, about 50% of first marriages are expected to end in divorce, and it has been well established that the end of a relationship is one of the main triggers of depression [4]. There has also been considerable research showing that lack or loss of social support increases various types of pain [1, 5, 6], and has deleterious effects on the cardiovascular, endocrine, and immune systems [7, 8]. Thus, the very high and growing rates of pain may be mediated by the growing rates of social alienation and depression [9], through their direct and indirect effects on disease and illness. These relationships may account for a high amount of variance in the incidence of pain. As for hypnosis, recent meta-analyses and brain imaging studies have enhanced our understanding of its efficacy for pain, its modes of operation, and its effectiveness [10]. Hypnotic techniques are designed to enhance concentration and heighten responsiveness to suggestions to alter thoughts, feelings, behaviour, or physiology. Because pain involves all of these areas, it is not surprising that hypnosis has been found to attenuate pain, need for analgesics or sedation, nausea and vomiting, and length of hospital stay. It also enhances physiological stability and outcome after medical treatment, and induces a higher degree of satisfaction among patients, for half the price of the standard sedation procedure [11]. Although most research on hypnoanalgesia has focused on acute pain, a recent meta-analysis on its use for chronic pain found it to be clinically effective [12]. Hypnoanalgesia works because it changes the network of cognitions and emotions in which pain is inscribed, and also intensifies the therapeutic relationship. Although it may culminate in self-hypnosis, it typically begins with a caring ‘‘other’’ helping

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shape the subjectivity of the patient. Thus, both with regard to its aetiology and treatment, pain is as much a subjective and communal phenomenon, as a biological one. No matter what new drugs we devise, it is unlikely that we will have much impact on the ever-growing rates of pain until this ‘‘backdrop’’ of subjectivity and social support is taken as seriously as proximal, biological mechanisms. We need to de-emphasize a pill-popping culture and work on transforming people and communities into promoters of their own and others’ health.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Bakan D. (1971) Disease, Pain and Sacrifice: Toward a Psychology of Suffering. Beacon Press: New York. Lewis R. (2005) A sketch of the subjective. The Scientist S5: 1–6. Huntington S.P. (2004) Who Are We? The Challenges to America’s National Identity. Simon & Schuster: New York. Joiner T. (2002) Depression in its interpersonal context. In: Handbook of Depression, I.H. Gotlib, C.L. Hammen (Eds). Guilford Press: New York, pp. 295–313. Kolb L.C. (1954) The Painful Phantom: Psychology, Physiology and Treatment. Thomas Publisher: Springfield. Evers A.W.M., Kraaimaat F.W., Geene R. (2003) Pain coping and social support as predictors of long-term functional disability and pain in early rheumatoid arthritis. Behav. Res. Ther. 41: 1295–1310. Kiecolt-Glaser J. (2005) Marriage, stress, immunity, and wound healing: how relationships influence health. Presented at the 63rd Annual Meeting of the American Psychosomatic Society, Vancouver, March 2–5. Uchino B.N., Cacioppo J.T., Kiecolt-Glaser J. (1996) The relationship between social support and physiological processes: a review with emphasis on underlying mechanisms and implications for health. Psychol. Bull. 119: 488–531. Kessler R.C. (2002) Epidemiology of depression. In: Handbook of Depression, I.H. Gotlib, C.L. Hammen (Eds). Guilford Press: New York, pp. 23–42. Cardena ˜ E. (2004) Hypnosis for the relief and control of pain. www.psychologymatters.org/hypnosis pain.html Lang E.V., Rosen M.P. (2002) Cost analysis of adjunct hypnosis with sedation during outpatient interventional radiologic procedures. Radiology 222: 375–382. Patterson D.R., Jensen M.P. (2003) Hypnosis and clinical pain. Psychol. Bull. 129: 495–521.

2.14 The Relationship Between Pain and Anxiety Disorders Antonio Bulbena1 , Carlos Garcia Ribera1 and Lili Sperry1 Pain continues to generate and reclaim attention. This is in fact the main reason for its phylogenetic existence: pain is crucial for the conservation of 1

Institut d’Atenci´o Psiqui`atrica, Salut Mental i Toxicomanies, Hospital del Mar, Barcelona, Spain

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life and animal species. In medical practice, it remains a capital symptom involving multiple and interacting levels: somatic, cognitive, emotional, behavioural, and social. In some forms of pain (i.e., low back pain), course and outcome are considered dependent on non-somatic factors. But in any case, pain is a stressful and impairing symptom, often difficult to interpret and frequently neglected by family and even doctors, especially when it is chronic and when the expected organic correlation is lacking. The psychological and psychiatric assessment of a patient with pain is usually tackled too late and when the established dynamics and neurophysiological correlates are difficult to modify. The plasticity of the central nervous system may play a role in the persistence of some forms of pain. When pain is present for a long period of time and becomes chronic, neurobiological changes and adaptation phenomena take place, like the establishment of altered nociceptive pathways leading to the persistence of pain. Nociceptive pathways are modulated by psychological processes, which probably play an important role in amplifying pain symptomatology [1]. The goal of treatment in chronic pain should be to manage the pain and to avoid as much as possible, from the very beginning, isolation and withdrawal from daily activities, such as work and social life. Two factors seem essential in chronic pain: (a) to provide psycho-education about pain in order to promote adequate expectations and coping strategies and (b) to offer the most integrative treatment plan available to make the patient feel part of ‘‘the same team’’ with the physicians. It is in this sense that we agree with King’s statement that ‘‘the specific form of therapy chosen may be less important than the therapist’s willingness to display empathy and understanding and to set realistic goals for treatment’’. Anxiety has been recently brought back to the first line of the psychiatric aspects of pain. Despite the emphasis on depression in the literature, in the Midlife Development in the United States Survey (MIDUS) it was noteworthy that the associations between several pain conditions and anxiety disorders were generally stronger than those between the pain conditions and depression [2]. In chronic pain, the strongest associations were with panic disorder (OR = 4.27) and post-traumatic stress disorder (OR = 3.69) [3]. Among the new groups of pain sufferers, such as those with fibromyalgia, as many as one-third have a lifetime history of panic disorder [4]. A peculiar somatic feature, the joint laxity syndrome, a benign heritable collagen condition repeatedly found associated with panic and agoraphobic disorders, may shed light on the relationship between pain and anxiety. Twothirds of joint laxity patients attending a rheumatologic clinic were found to suffer from lifetime anxiety conditions [5]. A high prevalence of joint laxity was found among panic and agoraphobic patients. The same relationship between anxiety and joint laxity has been found in non-clinical samples [6].

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The relation between joint laxity and pain appears often in the childhood with so-called ‘‘growing pains’’, particularly after physical exercise, and consequent pain avoidance can lead to muscular deconditioning and a risk of developing chronic pain from an early age [7]. The association between anxiety (mainly panic disorder, agoraphobia, and social phobia) and the joint laxity syndrome paves the way for further research developments and a better understanding of the relationship between pain and anxiety.

REFERENCES 1. 2.

Eisendrath S.J. (1995) Psychiatric aspects of chronic pain. Neurology 45: S26. McWilliams L.A., Goodwin R.D., Cox B.J. (2004) Depression and anxiety associated with three pain conditions: results from a nationally representative sample. Pain 111: 77–83. McWilliams L.A., Cox B.J., Enns M.W. (2003) Mood and anxiety disorders associated with chronic pain: an examination in a nationally representative sample. Pain 106: 127–133. Malt E.A., Berle J.E., Olafsson S., Lund A., Ursin H. (2000) Fibromyalgia is associated with panic disorder and functional dyspepsia with mood disorders. A study of women with random sample population controls. J. Psychosom. Res. 49: 285–289. Bulbena A., Duro J.C., Porta M., Martin-Santos R., Mateo A., Molina L. (1993) Anxiety disorders in the joint hypermobility syndrome. Psychiatry Res. 46: 59–68. Bulbena A., Agullo A., Pailhez G., Martin-Santos R., Porta M., Guitart J., Gago J. (2004) Is joint hypermobility related to anxiety in a nonclinical population also? Psychosomatics 45: 432–437. Murray K.J., Woo P. (2001) Benign joint hypermobility in childhood. Rheumatology 40: 489–491.

3. 4.

5. 6. 7.

2.15 Gaps in Evidence Base of Pain Disorders Santosh K. Chaturvedi1 There are many issues related to the classification of pain, especially chronic pain, including whether to consider chronic pain as a symptom, a syndrome, a disorder or an illness behaviour. When chronic pain is considered a symptom, it is noted to be a common symptom of many physical conditions, involving literally any system of the body, and many psychiatric disorders, like depression, anxiety, somatoform, and dissociative disorders. 1

National Institute of Mental Health and Neurosciences, Bangalore, India

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Chronic pain as a syndrome has received a lot of attention recently, in terms of DSM-IV criteria for pain disorder and the comprehensive classification system proposed by the Task Force on Taxonomy of the International Association for the Study of Pain [1]. These diagnostic systems are multiaxial and attempt to cover major dimensions affected or involved. Chronic pain as a disorder has received lesser acceptability, due to the difficulties in establishing a clear-cut aetiopathogenesis, clinical features, course, and outcome. The validity of pain disorders as a clinical entity is not well established. The evidence base for the validity of these disorders needs to be addressed systematically. Pain therapists will need some more time to shelve the dualistic approach towards pain, that of being either physical or psychological. Like most symptoms, chronic pain can be physical, psychological, idiopathic [2], or both physical and psychological [3]. There can be emotional elaboration or psychological consequences of chronic pain, or neurophysiological or neuropathological changes related to psychogenic chronic pain. Chronic pain is also a behaviour pattern and manifests as different forms of abnormal illness behaviours [4, 5]. King’s review addresses an important relationship, that between sleep and chronic pain. Sleep-related features have not received much research or clinical attention, though in clinical practice one notes changes in pain symptoms in relation to sleep. Moderate or severe pain can disrupt sleep, and poor sleep can aggravate pain experience. The role of sleep hygiene and sleep medications in the management of pain disorders is yet to be examined systematically. King’s review has drawn attention towards fibromyalgia, which is undoubtedly a controversial pain-related diagnosis. In a recent study [6], 33% of chronic pain patients had 11 or more tender points and met diagnostic criteria for fibromyalgia. Chronic pain patients with multiple aches and pains need to be evaluated for fibromyalgia, for effective management. Chronic pain has not too often been considered as an outcome predictor. Given its vast prevalence in health care, chronic pain needs to be explored as such. What is the outcome of depressive disorder or ischaemic heart disease when chronic pain is one of the main symptoms? Is the outcome of depressive disorders worse or better? Does chronic pain remit earlier than depressive features or later or simultaneously in patients who have concomitant chronic pain and depression? The management of chronic pain by psychiatrists can have its own advantages and limitations. As discussed in King’s review, chronic pain is multifactorial and multidimensional, necessitating a multidisciplinary approach in the management. A multidisciplinary team using a multipronged approach perhaps manages chronic pain best. The goal of treatment should be to manage the pain as opposed to curing it. This may require refocusing the patient

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away from the pain. There are numerous randomized controlled trials on the effectiveness of different analgesics, antidepressants, adjuvants, and physical treatments for management of chronic pain, but the evidence base in support of multidisciplinary interventions is not clear. King concludes that there is evidence that pain disorder is common among patients with chronic pain and that there are multiple treatments available for the treatment of pain. However, the many gaps in the evidence base regarding this condition should also be acknowledged.

REFERENCES 1.

Merskey H., Bogduk N. (Eds). (1994) International Association for the Study of Pain Classification of Chronic Pain, 2nd ed. IASP Press: Seattle. Chaturvedi S.K. (1986) Chronic idiopathic pain disorder. J. Psychosom. Res. 30: 199–204. Chaturvedi S.K., Maguire P. (1998) Persistent somatization in cancer: a follow up study. J. Psychosom. Res. 45: 249–256. Pilowsky I. (1978) Pain as abnormal illness behaviour. J. Hum. Stress 4: 22–27. Chaturvedi S.K., Bhandari S.N. (1989) Somatization and illness behaviour. J. Psychosom. Res. 33: 147–153. Somashekar B.S., Chaturvedi S.K., Desai G., Faruq U. (2002) Fibromyalgic tender points in chronic pain patients. Indian J. Psychiatry 44: 68.

2. 3. 4. 5. 6.

2.16 Pain in General Practice Manuel Suarez Richards1 and Gustavo Alfredo Delucchi1 The history of attempts to understand, classify, and treat patients with poorly understood physical complaints ranges over a period of at least 2,000 years. As stated by Steven King, ‘‘pain is a subjective complaint’’ and therefore is a special situation to be understood in a particular way. In general practice, pain is a common presenting symptom, frequently not fully understood by the general practitioner. He has difficulties to get information and to measure the pain, which often leads him to refer the patient to the psychiatrist, because he thinks that the pain is not real. This warns us about the need to broaden our teaching in undergraduate programs at medical schools including everything a general practitioner must know about pain, the patient suffering from it, his family, and his environment. Pain has an important adaptive role, from the evolutionary point of view, because it alerts us that one part of our body is injured or has been injured. 1

Psychiatry Department, School of Medicine, 60 y 120 La Plata, University of La Plata, Argentina

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Chronic pain frequently outlasts the recognized pain stimulus, so that the pain becomes dissociated from many of the physiological evidences of nociception [1]. The patient with chronic pain commonly presents symptoms that are grossly disproportionate to the objective findings from the history, physical examination, and diagnostic tests. Psychiatric symptomatology may be prominent. The assessment of a patient presenting with pain of unknown cause should include an appropriate examination and investigation of possible physical causes. When these are negative, it should be remembered that not uncommonly physical illness presents with pain before it can be detected in other ways. There are distinctive characteristics between psychogenic pain and pain of largely physical origin. Psychogenic pain tends to be indefinite in nature, with no clear-cut onset; it is poorly localized and may vary with changes in patient’s mood; furthermore, it may be relieved by alcohol and psychotropic medication. A pre-morbid history of neurotic traits or mental illness is often present. In general practice, pain is a common presenting symptom of mood, anxiety, and conversion disorders. Depression frequently manifests with somatic complaints such as pain, fatigue, insomnia, and change of appetite. Patients with such non-specific symptoms are twice as likely as other medical outpatients to be suffering from depression. Back, neck, and head pain are the most frequent in general practice patients, but their relationship to depression is often not recognized even when several physical treatments have failed. Sleep disorders are frequent in patients with acute and chronic pain, and the drugs prescribed often do not work and the patients develop dependence to them, specially to narcotics and benzodiazepines [2], which enhance chronic pain problems [3]. Physicians readily acknowledge the co-occurrence of depression and pain, but may not recognize the degree of psychiatric distress that appears to be present in this group of patients. Such distress suggests that persons who have both depression and pain should receive more—not less, as we have found to be the case—mental health speciality care than depressed persons who do not have pain. Policy makers should carefully consider how to reduce potential barriers to mental health care for this vulnerable population.

REFERENCES 1. 2. 3.

Mailis A., Papagapiou M. (1993) Profile of patients admitted to the pain facility of a university-affiliated acute care hospital. Pain Clin. 6: 71–82. Ghodse H. (2003) Pain, anxiety and insomnia - a global perspective on the relieve of suffering. Br. J. Psychiatry 183: 15–21. Anooshian J., Streltzer J., Goebert D. (1999) Effectiveness of a psychiatric pain clinic. Psychosomatics 40: 226–232.

CHAPTER

3 Hypochondriasis: A Review Russell Noyes Jr. Psychiatry Research, Medical Education Building, Iowa City, IA 52242-1000, USA

INTRODUCTION Hypochondriasis is a preoccupation with fears of having, or the idea that one has, a serious disease, based on the person’s misinterpretation of bodily symptoms [1]. The disorder is prevalent in clinical populations, where it is a source of somatic distress and perceived ill health. It is also associated with increased utilization of, but dissatisfaction with, health services. Despite this, the diagnosis is rarely made by practitioners and is considered controversial by nosologists. The disorder has traditionally been neglected by researchers, but new interest has developed and important findings have begun to appear. Hypochondriasis involves illness behaviour that strains the doctor–patient relationship, yet this relationship holds the key to the success of treatment. For their part, physicians find patients with hypochondriasis a source of bewilderment and frustration. Trained in biomedical theory, their first concern is organic disease. Having ruled that out, they often fail to appreciate the distress of patients in whom ‘‘nothing is wrong’’ [2]. Yet, with the development of effective treatments, the attitudes towards such patients have begun to change.

History Hypochondria is a term used by Hippocrates to refer to a region below the cartilage of the ribs [3]. In the second century, Galen linked it to disturbances of the organs in this area as well as humours and animal spirits. The symptom picture remained ill defined and only gradually took on the characteristics recognized today. From earliest times, hypochondria was associated with melancholia, a temperamental disturbance related to an excess of black Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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bile. In his The Anatomy of Melancholy, Burton [4] described hypochondriacal melancholy in terms of vague physical symptoms, disturbances of mood, and fears. He said: ‘‘Some are afraid that they shall have every fearful disease they see others have, hear or read of, and dare not therefore hear or read of any such subject’’. In the seventeenth century, Sydenham described hypochondria in men as the counterpart of hysteria in women. Hypochondria became a fashionable disturbance in the eighteenth century. Cheyne, in The English Malady [5], observed that the English way of life and environment were responsible for the affliction. However, as notions of aetiology began to shift under the influence of Cartesian dualism, hypochondria was increasingly seen as a weakness and moral failing [6]. Falret [7] was perhaps the first to identify it as a mental disorder, one of the neuroses. As the neuroses emerged during the late nineteenth century, hypochondria found inclusion in neurasthenia, a category popularized by Beard. Presentday descriptions originated with Gillespie [8], who defined hypochondriasis as ‘‘a mental preoccupation with a real or suppositious physical or mental disorder’’.

Conceptualizations There are differing views about how hypochondriasis should be conceptualized. Some look upon it as a personality disturbance [9]. They view it as a lower-order factor of neuroticism [10] or, like Tyrer et al. [11], believe it constitutes a personality disorder. For them, its early onset and long-term stability in some patients fit this conception. Others see it as a variable dimension of psychopathology [12]. They note that illness worry and hypochondriasis fall on a continuum of severity and that hypochondriacal symptoms accompany many psychiatric disorders. For those who take a categorical approach, the issue of whether hypochondriasis is primary or secondary remains unsettled [13]. High rates of comorbidity have raised doubts about its independent status.

CLINICAL FEATURES Essential Features The core characteristics of hypochondriasis are shown in Table 3.1. The first is the fear of a serious disease that the patient believes is already present. Its feared consequences may include pain, suffering, disability, and death [14]. Patients find their minds filled with alarming thoughts and images concerning specific diseases. These diseases sometimes have a particular meaning (e.g., a loved one died of it).

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T A B L E 3.1 Essential and associated features of hypochondriasis Essential features Fear of disease Disease conviction Somatic symptoms Bodily preoccupation Reassurance-seeking Resistance to reassurance Associated features Fear of ageing and death Overvaluation of health and appearance Sense of vulnerability to illness and injury Low self-esteem Psychological symptoms

Disease conviction refers to a belief that the feared disease is present. This belief is based on misinterpretation of somatic symptoms. It is overvalued, meaning it is strongly held despite lack of evidence [15]. Starcevic [16] prefers the term suspicion, noting that hypochondriacal patients experience intolerable uncertainty about the disease in question. Although strongly held, the belief is not delusional. Somatic symptoms are a constant feature. These tend to be multiple and diffuse and pain is perhaps the most common [17]. When present, symptoms of existing medical conditions are more intense and distressing than seems warranted. Attention is also focused on bodily functions, minor abnormalities, and bodily sensations [1]. Patients often give a detailed account of their symptoms, yet are vague. They are more concerned with the meaning of symptoms than the distress that they cause. Bodily preoccupation is perhaps the most important characteristic. This takes the form of excessive interest in, and attention to, what is happening in the body. The preoccupation is of a hypervigilant quality and involves the meaning of symptoms [18]. It extends beyond the body to health- and illness-related concerns (e.g., diet, exercise, environmental exposures). Many have medical concerns that dominate their activities and conversation. Their self-absorption is accompanied by a withdrawal of interest in other people and pursuits. Reassurance-seeking is the chief behavioural manifestation. This may involve repeated checking of the body for evidence of any serious disease. Persons with hypochondriasis check their pulse, examine themselves in the mirror, look for lumps, and so on. They also search medical books or Internet sources for the meaning of symptoms. In addition, such persons repeatedly

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ask friends, family members, and physicians to reassure them. This may lead to repeated unnecessary examinations and tests, as well as visits to many doctors. Resistance to reassurance is a related feature. The diagnosis requires an adequate evaluation yielding no medical explanation for symptoms [1]. However, the communication of this result usually provides only temporary or incomplete relief.

Associated Features A variety of associated features have been observed. These include fears of ageing and death [19], which appear to be an integral part of hypochondriasis. The latter has been linked to hypochondriasis both psychodynamically and philosophically. Psychodynamically, the disorder has been seen as a defence against the fear of death, and philosophically it has been viewed as a failure to come to terms with the finiteness of existence [20]. Overvaluation of health and appearance is another related feature [19]. Hypochondriacal preoccupation may extend to eating natural foods, achieving peak fitness, and living a healthy lifestyle, all of which may be taken to extremes. In part, this may reflect an idealized conception of good health. Persons with hypochondriasis have low self-esteem and feel unworthy and unlovable [21]. As a consequence, they have negative expectations of encounters with physicians and others. They also have a sense of bodily vulnerability to illness [22]. Both of these features deal with fundamental aspects of the self that are viewed as deficient or undependable. Psychological symptoms are frequently observed in hypochondriacal persons. These include depression, anxiety, and obsessive–compulsive symptoms. Where such symptoms coexist, they may be linked to certain features of the hypochondriacal syndrome. Neuroticism is another associated feature.

Subtypes Hypochondriasis is a heterogeneous disorder, and subtypes may exist. Separate dimensions of disease phobia and disease conviction have consistently been identified; in some individuals fear predominates while in others conviction dominates the picture [23]. Patients with prominent disease phobia appear to have anxious features and greater insight. Those with disease conviction have more depressive features. They are preoccupied with somatic symptoms and are more convinced of having some serious disease [24]. Other patients may resemble those with obsessive–compulsive disorder [25].

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CLASSIFICATION Diagnostic Criteria In DSM-II, hypochondriasis was classified among the neuroses and defined as a condition ‘‘dominated by preoccupation with the body and with fears of presumed diseases of various organs’’ [26]. With DSM-III, it was moved to the somatoform disorders, and diagnostic criteria were provided [27]. In the subsequent revision (DSM-III-R), a duration of at least 6 months was added and patients with delusional beliefs were excluded [28]. Finally, with DSM-IV, the diagnosis was excluded if hypochondriacal concerns were better accounted for by certain mood, anxiety, or somatoform disorders [1]. The DSM-IV criteria are shown in Table 3.2. The ICD-10 criteria for hypochondriacal disorder, shown in Table 3.3, differ from the DSM-IV criteria in several respects. According to ICD-10, the diagnosis requires a persistent belief that the person has no more than two serious physical ailments, at least one of which is specifically named [29]. In addition, these criteria include body dysmorphic disorder, which the DSMIV criteria exclude. Illness behaviour is included in the criteria, which state that hypochondriacal concerns lead persons to seek medical investigation or treatment. Such patients may accept reassurance in the short term, but in the long run they are unlikely to respond. T A B L E 3.2 DSM-IV criteria for hypochondriasis A. Preoccupation with fear of having, or the idea that one has, a serious disease, based on the person’s misinterpretation of bodily symptoms. B. The preoccupation persists despite appropriate medical evaluation and reassurance. C. The belief in criterion A is not of delusional intensity (as in delusional disorder, somatic type) and is not restricted to a circumscribed concern about appearance (as in body dysmorphic disorder). D. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. E. The duration of the disturbance is at least 6 months. F. The preoccupation is not better accounted for by generalized anxiety disorder, obsessive–compulsive disorder, panic disorder, a major depressive episode, separation anxiety, or another somatoform disorder. Specify: With poor insight: if, for most of the time during the current episode, the person does not recognize that the concern about having a serious illness is excessive or unreasonable. Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Copyright 2000. American Psychiatric Association.

134 T A B L E 3.3

SOMATOFORM DISORDERS ICD-10 criteria for hypochondriacal disorder

A. Either of the following must be present: 1. A persistent belief, of at least 6 month’s duration, of the presence of a maximum of two serious physical diseases (of which at least one must be specifically named by the patient). 2. A persistent preoccupation with a presumed deformity or disfigurement (body dysmorphic disorder). B. Preoccupation with the belief and the symptoms causes persistent distress or interference with personal functioning in daily living, and leads the patient to seek medical treatment or investigations (or equivalent help from local healers). C. There is persistent refusal to accept medical reassurance that there is no physical cause for the symptoms or physical abnormality. (Short-term acceptance of such reassurance, i.e. for a few weeks during or immediately after investigations, does not exclude this diagnosis.) D. The symptoms do not occur only during any of the schizophrenic and related disorders or any of the mood (affective) disorders. Reproduced by permission of World Health Organization from ICD-10 Classification Manual of Mental and Behavioural Disorders. Diagnostic Criteria for Research.

The somatoform disorders grouping—to which hypochondriasis belongs—is controversial, and many question its inclusion in the classification. Critics see the somatoform disorders as ill-defined categories of questionable validity that are based more on illness behaviour than on clinical features. They also view them as creations of Western biomedicine that serve to devalue and marginalize patients who challenge the theoretical model upon which medical science is based [30]. For biomedicine, illness is a response to disease and the person who is ill without disease—as in hypochondriasis—remains an enigma. If the somatoform disorders were to be abandoned, some have proposed moving hypochondriasis to the anxiety or obsessive–compulsive spectrum disorders [31].

Validity of the Diagnosis A valid psychiatric diagnosis requires the demonstration of (a) a consistent clinical picture, (b) biological markers, (c) family aggregation, (d) distinctive course and outcome, and (e) a unique treatment response [32]. Evidence with respect to hypochondriasis is accumulating but research remains limited. In studies aimed at demonstrating validity, Barsky et al. [17] showed that, in medical outpatients, distinguishing characteristics of the disorder aggregated in some individuals and were less common in others. The same individuals had other features that gave hypochondriasis external validity. Using a structured interview for hypochondriasis, these investigators [33] observed

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a positive correlation between interview and physician ratings (concurrent validity). Hypochondriacal patients also had more ancillary features of hypochondriasis than did non-hypochondriacal patients (external validity). Finally, other clinical characteristics distinguished interview-positive from interview-negative patients, indicating a degree of discriminate validity. Using the same diagnostic interview, Noyes et al. [34] replicated these findings. Follow-up studies have shown a degree of diagnostic stability. In patients re-examined after 1 to 4 years, between one- and two-thirds continued to meet the criteria for hypochondriasis [35–38]. One small family study failed to support diagnostic validity. It found that hypochondriasis was no more frequent among the first-degree family members of hypochondriacal probands than among the family members of control probands [39]. However, somatization disorder was more common among the relatives of hypochondriacal probands, suggesting that hypochondriasis and somatization disorder might be differing aspects of a common underlying disturbance. Treatment studies have shown that hypochondriasis responds, but no efforts have been made to demonstrate a unique response to any treatment.

Assessment A variety of instruments have been developed to assess hypochondriasis. These have been reviewed by Speckens [40] and Stewart and Watt [41]. As shown in Table 3.4, they include self-rated questionnaires as well as structured interviews for diagnosis. The first to be developed and still the most widely administered is the Whiteley Index [42]. It contains 14 items based on observed characteristics of hypochondriacal psychiatric patients. The scale measures a single dimension, and is useful for the screening T A B L E 3.4 Instruments for the assessment of hypochondriasis Self-rated questionnaires Whiteley Index [42] Illness Worry Scale [44] Illness Behaviour Questionnaire [42] Illness Attitude Scales [43] Health Anxiety Questionnaire [45] Health Anxiety Inventory [46] Multidimensional Inventory of Hypochondriacal Traits [47] Structured interviews Structured Clinical Interview for DSM-IV [48] Structured Diagnostic Interview for Hypochondriasis [33] Composite International Diagnostic Interview [49]

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and assessing the level of hypochondriacal concerns. Physical illness may influence the response to some items and patients with anxiety disorders, especially panic, may score high. The Illness Attitude Scales, developed by Kellner [43], is another frequently used measure of fears, beliefs, and attitudes specific to hypochondriasis. Recently, Salkovskis et al. [46] developed the Health Anxiety Inventory. It contains 47 items, covering a range of hypochondriacal features rated on fourpoint scales of severity. In a series of studies, the scale discriminated between patients with high health anxiety and those with physical illness as well as anxiety disorders. A short (14-item) version appears to have psychometric properties comparable to those of the full scale. The instrument appears to assess the core features of hypochondriasis and addresses the weaknesses of previous scales. Several interviews are available to diagnose DSM and/or ICD hypochondriasis. One of these, the Structured Diagnostic Interview for Hypochondriasis (SDIH), was developed by Barsky et al. [33]. This interview focuses exclusively on hypochondriasis. It begins with a series of probe questions that, if answered affirmatively, trigger the complete interview. A modified version was recently published [50]. The Structured Clinical Interview for DSM-IV (SCID) and the Composite International Diagnostic Interview (CIDI) are comprehensive diagnostic instruments that contain somatoform disorder modules [48, 49]. The CIDI has been used in several epidemiologic surveys. The stem question for hypochondriasis is ‘‘In the past 12 months, have you had a period of six months or more when most of the time you worried about having a serious physical illness or deformity’’? A series of questions concerning this worry covers the criteria of hypochondriasis. Most inquire about aspects of medical care (i.e., in the past 12 months: several doctor visits, several diagnostic tests, dissatisfied with doctor’s examination, think doctor mistaken about diagnosis). At present, no gold standard for the diagnosis of hypochondriasis exists, because none of the available instruments has been adequately tested [41]. Available interviews differ. The CIDI is administered by lay interviewers and relies upon multiple medical care items, so that it is difficult to satisfy the full criteria. Of the instruments administered by psychiatric interviewers, the SDIH is limited to hypochondriasis and is perhaps most suitable for establishing the diagnosis in persons who have screened positive on a brief measure such as the Whiteley Index. None of these interviews takes into account independent medical evaluation.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of hypochondriasis must begin with organic disease that has not been detected. Some diseases in their early stages may cause

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vague symptoms; others, with insidious onset and atypical presentation, may generate illness concerns but few pathological signs or laboratory abnormalities. These might include neurological conditions, such as multiple sclerosis or myasthenia gravis; endocrine conditions, such as thyroid or parathyroid disorders; multi-system diseases such as systemic lupus erythematosus and occult malignancies [1]. Given such possibilities, a physical cause of symptoms merits continuing consideration even after work-up for such has been completed. Panic is an important psychiatric disorder to distinguish from hypochondriasis. This may be difficult, because patients with this disorder commonly have hypochondriacal features, and patients with hypochondriasis may have anxious or phobic features [51]. A diagnosis of hypochondriasis should not be made if illness concerns are better accounted for by panic disorder. Hypochondriacal patients tend to fear the long-term consequences of illness, whereas those with panic fear immediate catastrophic events; the former fear death and the latter dying [52]. In addition, hypochondriacal patients misinterpret a wide range of bodily sensations, whereas those with panic misinterpret symptoms of autonomic arousal. Obsessive–compulsive disorder must also be distinguished from hypochondriasis. Patients with obsessive–compulsive disorder often have intrusive thoughts about disease or contamination and rituals that involve checking or reassurance-seeking. They differ from patients with hypochondriasis in having other obsessions and compulsions. Obsessive–compulsive patients tend to regard their ideas as senseless and resist them, whereas those with hypochondriasis hold them with conviction [24]. In addition, patients with obsessive–compulsive disorder experience discrete, isolated thoughts, unlike the patient with hypochondriasis, whose thoughts about disease form an integrated whole. Hypochondriasis must also be differentiated from illness phobia, a subtype of specific phobia added to DSM-IV. Illness phobics fear developing a disease they do not yet have, whereas patients with hypochondriasis are preoccupied with a disease they believe is already present. Patients with illness phobia respond to external as well as internal threats [53]. For example, fear of a communicable disease may be triggered by exposure to infected persons. Illness phobics may, in contrast to those with hypochondriasis, have few or no somatic symptoms and recognize the unreasonable nature of their disturbance. Generalized anxiety disorder (GAD) is characterized by excessive worry about a number of areas. These may include worry about health, but other areas are involved as well. If worry is confined to illness, then a diagnosis of GAD should not be made. In addition, patients with GAD have general health worries, whereas those with hypochondriasis dwell upon specific serious diseases such as cancer [16].

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Hypochondriasis that develops during an episode of major depression and remits with treatment of the mood disorder should not receive a separate diagnosis [1]. In this instance, the hypochondriacal concerns may be better accounted for by the depressive disorder [54]. Thus, a patient with major depression might focus concern on the vegetative symptoms of depression and interpret these as irreversible loss of health. A diagnosis of hypochondriasis may be made if its features are not confined to an episode of depression and are not part of the clinical picture of depression. The differential diagnosis should also include somatization disorder. While both hypochondriasis and somatization disorder are characterized by somatic symptoms, several features distinguish them [55]. Patients with hypochondriasis tend to worry about the meaning of symptoms rather than the symptoms themselves. They are more concerned about specific serious illness than securing the gains of illness, as are patients with somatization disorder. Patients with hypochondriasis are as often men as women, while those with somatization disorder are predominantly women. Those with hypochondriasis are more likely to have obsessive–compulsive personality traits, and those with somatization disorder histrionic or borderline traits. Patients whose hypochondriacal beliefs are delusional should not receive a diagnosis of hypochondriasis [1]. Delusional beliefs may occur in patients with psychoses, and these patients usually have other psychotic manifestations. Delusions of disease are often the main or only manifestation of delusional disorder, somatic type. They usually have a bizarre or unrealistic quality not found in hypochondriasis.

EPIDEMIOLOGY Prevalence The prevalence of hypochondriasis in the general population has not been established. In fact, only recently have estimates for hypochondriasis and hypochondriacal concerns been sought [56]. When structured interviews such as the CIDI were used, almost no cases were identified [57]. For instance, Looper and Kirmayer [58] found that 6% responded affirmatively to the screening question for illness worry, but that only 0.2% met full criteria as elicited by this restrictive interview. Two studies that employed structured interviews, but focused exclusively on the somatoform disorders, obtained higher rates (4.5% and 7.7%) [59, 60]. In surveys by Looper and Kirmayer [58] and Noyes et al. [61], roughly half of the respondents with illness worry claimed to have the illness they worried about. In such persons, it may be difficult to distinguish normal worry from that which is excessive or unreasonable.

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The prevalence of hypochondriasis among primary care outpatients has been estimated in a number of studies shown in Table 3.5. Gureje et al. [62] observed that, if the criterion of failure to respond to reassurance was set aside, then 2.2% of patients qualified for the diagnosis of hypochondriasis and were as impaired as those who met full criteria. Using this adjusted rate and limiting prevalence estimates to those obtained with structured interviews, the range in eight studies was 2.2 to 9.4%. Hypochondriasis may be prevalent in medical speciality populations where many patients present with unexplained or functional disturbances. For instance, a survey of otolaryngology clinic patients found 13% to have the disorder [74]. Also, levels of hypochondriasis tend to be higher in patients with functional than with organic illness. For example, Gomborone et al. [75] observed higher hypochondriasis scores among patients with irritable bowel syndrome than among those with organic gastrointestinal disease. The prevalence of somatoform disorders in a psychiatric population (two-thirds inpatient) was examined by Altamura et al. [76]. They identified lifetime DSM-III-R hypochondriasis in 1.6%, or 2.5% when exclusionary rules were set aside.

Risk Factors Risk factors for unexplained somatic symptoms include female gender, older age, non-white race, less education, and lower income. With respect to hypochondriasis, few of these factors appear important, although the available data are inconsistent. Women do not appear to be at greater risk than men [77]. Persons with hypochondriasis and health worry tend to be older [56, 58, 60] and have more physical illness [35, 58, 61, 62]. Two studies found an association between hypochondriasis and less education [60, 67] and another found black persons disproportionately represented [66].

Boundaries and Comorbidity Overlap and boundaries between hypochondriasis and certain other disorders may determine its placement in future classifications. Because hypochondriacal concerns are common in patients with panic and other anxiety disorders, some have suggested that hypochondriasis be classified among these disorders [55]. As high as one-quarter of primary care patients with panic have hypochondriasis [51]. However, in many instances, hypochondriacal features are better accounted for by panic disorder [49]. Specific phobia, illness subtype—a new category in DSM-IV—will influence classification, but as yet there has been little study of the differentiation of this disorder from hypochondriasis [53].

685

191

217

van Hemert et al. [68]

El-Rufaie and Absood [69]

1,389

109 78

Kirmayer and Robbins [67]

Barsky et al. [66]

Beaber and Rodney [64] Palsson [65]

44

N

Primary care (United Arab Emirates)

General medical (Netherlands)

Family practice

General medical

Family practice General practice (Sweden)

Family practice

Population

Clinical Interview Schedule, ICD-9

Present State Examination, DSM-III-R

Structured Clinical Interview for DSM-III-R Illness Worry Scale ≥4

Whiteley Index ≥ 10 Whiteley Index ≥ 6

Illness Attitude Scales

Criteria

Studies examining the prevalence of hypochondriasis in primary care populations

Kellner et al. [63]

T A B L E 3.5

2.3

4.7

7.7

6.3

5.5 10.3

9.3

%

Sub-types of hypochondriasis identified Estimate based on structured interview and diagnostic criteria Patients with hypochondriacal worry distinguished from other forms of somatization Hypochondriasis more frequent among patients with unexplained symptoms Represents less than 10% of minor psychiatric disorders

2.0% of employees and 11.9% psychiatric outpatients are hypochondriacal

Comment

140 SOMATOFORM DISORDERS

1,000

175 5,447

1,456

1,559

Spitzer et al. [70]

Peveler et al. [71] Gureje et al. [62]

Escobar et al. [72]

Garcia-Campayo et al. [73]

Primary care (Spain)

Primary care

Primary care Primary care (crossnational)

Primary care

General medical

PRIME-MD, Primary Care Evaluation of Mental Disorders.

1,182

Noyes et al. [34]

Whiteley Index ≥ 6 Composite International Diagnostic Interview, ICD-10 Composite International Diagnostic Interview, DSM-IV Standardized Polyvalent Psychiatric Interview, DSM-III-R

Structured Clinical Interview for DSM-IV PRIME-MD, DSM-IV

Hypochondriasis associated with medically unexplained symptoms High degree of overlap with other forms of somatization

9.4

2.2% when failure of reassurance criteria set aside

14% often bothered by thought of serious undiagnosed disease

3.4

9.0 0.8

2.2

6.9

HYPOCHONDRIASIS: A REVIEW 141

142

SOMATOFORM DISORDERS

Because hypochondriasis resembles obsessive–compulsive disorder, some have suggested that it belongs to an obsessive–compulsive spectrum [25]. Two studies have found a higher rate of hypochondriasis in patients with obsessive–compulsive disorder (13% and 15%) than in controls (0%) [78, 79]. However, family studies have not found a clear increase in hypochondriasis among relatives of obsessive–compulsive probands [78]. More study of this issue is needed. Hypochondriacal patients in primary care settings have high levels of psychological as well as physical symptoms. Strong positive correlations have been observed between hypochondriacal concerns and depressive (r = 0.58), anxiety (r = 0.55), and somatic (r = 0.52) symptoms [17, 34]. Two studies examined the prevalence of psychiatric disorders among patients with hypochondriasis [80, 81]. Table 3.6 shows the results from these studies comparing hypochondriacal to non-hypochondriacal patients. The proportions of hypochondriacal and control patients with one or more comorbid disorders were 88% versus 51% in one study and 62% versus 30% in the other. Anxiety and depressive disorders accounted for most of the excess.

T A B L E 3.6

Comorbidity identified in patients with DSM-III-R hypochondriasis Barsky et al. [80]

Noyes et al. [81]

Hypochondriasis Controls (N = 42) (N = 76) % %

Hypochondriasis Controls (N = 50) (N = 50) % %

Major depression Dysthymic disorder Panic disorder Generalized anxiety Phobic disorders Obsessive–compulsive disorder Alcohol abuse/dependence Drug abuse/dependence Somatization disorder Any depressive disorder Any anxiety disorder Any substance disorder

p

p

43

18

0.005

38

16

0.005

45 17

9 3

0.0001 0.01

8 16

2 6

ns ns

71 43

28 21

0.0001 0.05

0 6

0 2

ns ns

10

2

0.05

0

0

ns

10

18

ns

14

12

ns

12

4

ns

8

10

ns

21

0

0.0001

7

0

—

55

20

0.0001

44

18

0.005

86

36

0.01

22

6

0.05

17

20

ns

20

18

ns

HYPOCHONDRIASIS: A REVIEW

143

Family and Twin Studies One family study compared the first-degree relatives of 19 patients with hypochondriasis and 24 patients without hypochondriasis from a general medicine clinic [39]. Interviews were done blindly using the SCID. Table 3.7 compares lifetime and current psychiatric diagnoses in the two groups of relatives. There were no significant differences except that somatization disorder was more frequent among the relatives of hypochondriasis probands. In addition, certain traits and attitudes, such as hostility, low agreeableness, and dissatisfaction with care, were more frequent among those relatives. Such traits and attitudes might serve to increase vulnerability to hypochondriasis or other somatoform disorders. A Swedish adoption study identified two distinct groups of somatizers, one resembling hypochondriasis and the other somatization disorder [82, 83]. ‘‘Asthenic somatizers’’ had a lower frequency and diversity of complaints but were more often disabled by fatigue, weakness, and minor illness. ‘‘Diversiform somatizers’’ had a higher frequency of brief sickness with a diversity of complaints, especially pain in the head, joints, and abdomen. Asthenic somatizers, who resembled hypochondriacs, were more often men T A B L E 3.7 Frequency of lifetime and current psychiatric diagnoses in interviewed first-degree relatives of probands with hypochondriasis and control probands Lifetime diagnosis

Current diagnosis

Hypochondriasis Control Hypochondriasis Control relatives relatives relatives relatives (N = 97) (N = 72) (N = 97) (N = 72) % % % % Major depressive disorder Dysthymia1 Alcohol abuse or dependence Drug abuse or dependence Panic disorder Agoraphobia Social phobia Specific phobia Generalized anxiety disorder1 Post-traumatic stress disorder Obsessive–compulsive disorder Somatization disorder Hypochondriasis Other somatoform disorders 1 2

Current diagnosis only. p ≤ 0.05.

31.9 4.2 30.6 9.7 9.7 4.2 11.1 8.3 9.7 11.1 1.4 12.5 6.9 2.8

34.0 1.0 29.9 8.2 10.3 4.1 6.2 9.3 3.1 8.2 1.0 3.12 8.2 2.0

11.3 4.2 4.2 0 5.6 4.2 5.6 8.5 9.7 2.8 1.4

8.2 1.0 6.2 2.1 7.2 3.1 2.1 5.2 3.1 1.0 1.0

12.5 6.9 2.8

3.12 8.2 2.0

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with little criminality in their biological relatives. Diversiform somatizers, who resembled those with somatization disorder, were more often women with criminality in their relatives. In his twin study of somatoform disorders, Torgersen [84] found little evidence of genetic transmission. Of the six probands with hypochondriasis, none had a co-twin with the same disorder. In a population-based twin study by Neale et al. [85], a small number of probands with an isolated fear of illness were identified. Tetrachoric correlations for this fear were the same for monozygotic and dizygotic twins (0.26 vs. 0.32). This disturbance appeared to aggregate within families because of shared environment.

Morbidity and Service Utilization Patients with hypochondriasis have impairment in physical functioning and work performance [33, 34]. They view their health as worse, are more physically disabled, and are more impaired in their occupational roles than patients without hypochondriasis [33]. They also use more medical services yet are less satisfied with them. The increased utilization involves the number of physician visits, laboratory tests, outpatient costs, and hospitalizations [86]. Patients with hypochondriasis are more likely to feel that their health problems have not been thoroughly evaluated and consult more physicians than non-hypochondriacal patients [34]. Hypochondriasis is associated with increased symptom reporting and impairment in both functional and organic diseases. For instance, hypochondriacal scores were associated with low quality of life and disability in patients with chronic fatigue, irritable bowel syndrome, and fibromyalgia [44]. One study found that hypochondriasis was the strongest predictor of pain due to osteoarthritis, and another found that high health anxiety was predictive of abdominal pain 12 months later [87, 88]. Similarly, hypochondriasis was among the predictors of disability associated with coronary artery disease [89]. Consistent with these observations, hypochondriasis is associated with increased reporting of medication side effects [90]. Hypochondriacal patients tend not to be recognized by primary care physicians. Indeed, the diagnosis is almost never made [34, 64]. Recognition apart from diagnosis is more frequent. For example, Gureje et al. [62] found that more hypochondriacal patients than non-hypochondriacal were identified as psychiatric cases (57% vs. 24%, p < 0.0001).

AETIOLOGY AND PATHOGENESIS Personality Hypochondriasis is related to the personality dimension of neuroticism or negative affectivity (reviewed in [10]). Persons with high neuroticism, one of

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the three major personality dimensions, tend to experience negative emotions and over-react to stress. They are also prone to find bodily sensations noxious and interpret them as signs of a serious illness [91]. Correlations of 0.4 to 0.5 between neuroticism and hypochondriacal concerns have been found in non-clinical samples [91, 92]. At this point, there is little evidence for the involvement of other major dimensions. Hypochondriasis is associated with personality disorders, but not any specific type. Barsky et al. [80] found that almost two-thirds of hypochondriacal patients gave evidence of having a personality disorder, compared to 17% of control patients. Although a variety of traits have been noted, the disorder most consistently mentioned has been obsessive–compulsive personality [93]. Certain personality traits may have more to do with troublesome patient– physician interaction [94]. Hypochondriacal patients have been described as being angry, resentful, and mistrustful. Such tendencies might reflect negative emotions within the domain of neuroticism or the negative pole of agreeableness, another personality dimension. They might also reflect masochistic traits observed in some patients [95].

Childhood Environment Childhood factors appear important in the development of hypochondriasis. Adverse childhood environment may involve traumatic events, and three studies have obtained reports of such events, including physical and sexual abuse, more frequently from patients with hypochondriasis than from nonhypochondriacal patients [96–98]. Although the findings from these studies were somewhat different, they are consistent with the literature linking childhood neglect and abuse to unexplained symptoms in adults [99]. Childhood experience with illness may contribute to hypochondriasis by creating a sense of physical vulnerability. Noyes et al. [98] obtained reports of extreme illness or injury before age 17 from one-third of hypochondriacal adults. Others have obtained similar reports from patients with hypochondriasis [96, 97] and somatization [99, 100]. Childhood exposure to serious illness or death of a family member or friend may also contribute to later hypochondriasis [98]. Parental attitudes towards illness may also contribute. Some somatizing patients recall parental attention and overprotection as well as special caretaking and rewards for ill health as children [101]. Parker and Lipscombe [102] found that more hypochondriacal patients claimed that their fathers had been overprotective and their mothers had been more sympathetic towards them when ill. Early adversity, traumatic events, solicitous attitudes, and parent modelling all suggest that hypochondriasis is a learned behaviour that in childhood may have been successful in eliciting care [103].

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Interpersonal and Social Factors According to the interpersonal model, hypochondriasis is a form of careeliciting behaviour that finds expression in physical complaints. Through somatic symptoms, patients with this disorder seek care and support from family members and physicians. Need for support arises from insecure attachment that developed during childhood [101]. In a test of this model, Noyes et al. [104] found that, in primary care patients, hypochondriacal concerns were associated with various forms of insecure attachment. These same concerns were positively correlated with interpersonal problems and negatively correlated with reassurance from, and satisfaction with, medical care. Social factors may also be important determinants of hypochondriasis. Worldwide, reporting of somatic symptoms is a common means of communicating distress. Somatic distress demands attention from family and community because it signals disability that could alter social roles. Not only does it elicit caretaking but also secures the sick role for those who have legitimate afflictions [105]. This social role, with its privileges and responsibilities, protects the society from the disruptive effects of illness and fosters return to health and social functioning of individual members. Persons who are socially isolated or lacking social support may be more prone to care-eliciting behaviour such as hypochondriasis [106]. Physicians play an important role in the development or prevention of hypochondriasis. They may contribute by ordering unnecessary tests, diagnosing undetected diseases, or treating injudiciously. They may also reinforce concerns simply by telling a patient with hypochondriasis that nothing is wrong. In doing so, they challenge and reject the patient, thereby contributing to suffering and alienation from the medical system [107]. Cultural attitudes may also encourage hypochondriacal concerns. The American lifestyle, with its emphasis on fitness and attractiveness, may foster preoccupation with health. Such preoccupation may cause people to see their distress in terms of physical illness. Also, reporting of somatic symptoms varies according to culture and ethnic origins. For example, there are cultural differences in pain threshold, pain tolerance, patterns of arousal, and behavioural response to pain [108].

Life Events Stressful life events may be related to increased reporting of physical symptoms and hypochondriacal concerns, although there have been few studies [58, 109]. Events related to illness and death may have a specific role. For instance, symptoms of hypochondriacal patients sometimes resemble those of family members who have been ill or died. Illness events may also cause hypochondriacal concerns, an example being ‘‘cardiac neurosis’’

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after a myocardial infarction. At least transient hypochondriasis may occur when acute illness occurs in response to life stress, when someone who is ill requires care, or when distressing but unexplained symptoms develop.

Cognitive and Perceptual Factors According to the cognitive perceptual model, hypochondriacal persons misinterpret bodily symptoms as serious disease and experience somatic sensations as intense, noxious, and disturbing [110]. This model suggests that faulty appraisal of innocuous sensations is the central defect. In fact, a number of studies have shown that attribution to pathological processes increases symptoms [111]. Such attribution may focus attention on symptoms and, in the process, amplify them. Misinterpretation of this sort may be based on cognitive schemas established through earlier experience with illness [35]. Somatosensory amplification is the tendency, just referred to, to experience bodily sensations as intense and disturbing. Using the Somatosensory Amplification Scale, Barsky and Wyshak [112] demonstrated a strong correlation (r = 0.56) between amplification and hypochondriasis in a patient sample. Hypochondriacal persons may have a constitutionally lowered threshold or tolerance for physical symptoms; or, they may have heightened attentional focus and increased physiological arousal. Evidence of abnormal physiological reactivity was found by Gramling et al. [113]. In their study, hypochondriacal women showed increased heart rate and decreased hand temperature during a cold pressor test compared to controls. These subjects terminated the cold pressor test more frequently and rated it more unpleasant than did controls. Additionally, there is evidence that the heightened body focus or preoccupation of hypochondriacal persons interferes with externally oriented tasks requiring attention [114].

COURSE AND OUTCOME Course Hypochondriasis may begin at any age and some patients recall worry about illness starting in childhood. The onset may be associated with stressful life events possibly involving illness. Some individuals react to physical illness by developing hypochondriacal concerns of short duration. Robbins and Kirmayer [35] observed that some family medicine patients became hypochondriacal a year after they had initially assessed them. At baseline, those who subsequently became hypochondriacal had higher levels of illness worry, were more

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likely to rate their health as poor, and had more unexplained symptoms than non-hypochondriacal patients. Ambiguous symptoms or illness events may have contributed to hypochondriacal concerns in those predisposed patients.

Outcome Follow-up studies show that, after their initial clinic visit, most patients with hypochondriasis improve [38]. Nevertheless, a substantial proportion continues to meet criteria for the disorder and many of the remainder have persisting symptoms. Among hypochondriacal general medicine patients, both Noyes et al. [37] and Barsky et al. [36] found that two-thirds continued to qualify for the diagnosis after 1 to 4 years and the remaining one-third had persisting symptoms. Despite their improvement, these patients continued to be more hypochondriacal, more impaired, and more symptomatic than comparison patients. It is likely that the hypochondriacal patients in these studies were initially assessed during more symptomatic periods. Their subsequent improvement may have represented natural fluctuation or the influence of physician contact [37]. Some patients said that they had responded to reassurance or symptomatic treatment; others claimed benefit from change in life circumstance [36]. In a few instances, serious medical illness appeared to relive hypochondriacal concerns by legitimizing symptoms. Studies indicate that greater initial severity and duration of hypochondriasis are associated with worse outcomes. Failure to remit was predicted in one or more studies by more severe hypochondriacal concerns and somatic symptoms, longer duration of hypochondriasis, more psychiatric comorbidity, poorer perception of health, and greater neuroticism [35–37].

Complications Little information is available concerning complications. Because some persons with hypochondriasis have increased medical contact, one might expect complications resulting from repeated, often unnecessary work-ups, procedures, and treatments. Such iatrogenic complications have been reported. On the other hand, actual physical illness is sometimes overlooked in patients whose health problems are viewed as psychiatric. There is almost no information concerning mortality. A prospective cohort study found that health worry was predictive of angina and sudden cardiac death after adjusting for known coronary risk factors [115]. Health worry was not well defined in this study, so the findings may not apply to hypochondriasis. Suicide is said to be rare in hypochondriasis, unless the latter is accompanied by severe depression, in which case the risk may be increased [43].

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MANAGEMENT AND TREATMENT The treatment of hypochondriasis has, until recently, been regarded with pessimism [116]. Patients with the disorder have traditionally been viewed as being poorly responsive to reassurance and resistant to the idea that their problem might be psychological. Recently, however, promising management strategies have been described and evidence-based psychological and pharmacological treatments have begun to emerge.

Management In order to effectively manage the patient with hypochondriasis, the physician must legitimize his or her symptoms, offer a plausible explanation, establish agreed-upon goals, and make a long-term commitment (see Table 3.8). Most patients are best managed by their primary physician. The aim of such management is to reassure the patient. To establish a trusting relationship, the physician should begin by reviewing the patient’s record, listening carefully to the history, and conducting a thorough physical examination. Statements to the effect that the patient’s symptoms are real and distressing are likely to be helpful. Acceptance of and respect for the patient are conveyed by genuine interest in him or her as an individual [117]. A trusting relationship requires sustained involvement, which may be achieved through regularly scheduled visits. Visits of this kind assure the patient of the physician’s continuing interest and provide for ongoing health monitoring. It is also a way of uncoupling access to the physician from symptom status [118]. The physician should approach evaluation and treatment cautiously, in order to minimize the patient’s anxiety and exposure to unnecessary procedures. New symptoms require thorough evaluation, but extensive testing should be avoided where possible, as it may lead to misinterpretation of results or complications. Testing of this sort can generate alarm and, when repeated, can suggest physician uncertainty.

T A B L E 3.8 Management strategies for patients with hypochondriasis 1. 2. 3. 4. 5. 6.

Legitimize the patient’s symptoms Base diagnostic evaluation on objective findings Provide a plausible explanation for symptoms Approach treatment of physical symptoms cautiously Establish a regular schedule of visits Establish a goal of improved functioning

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Treatment of physical symptoms, such as pain, should be conservative. Medications, even when prescribed for minor discomforts, can generate worry and cause alarming side effects. Also, medications for pain and other indications may have dependence potential. The goal of management should be improved coping with symptoms, not their removal. This is because symptoms often represent a solution, even if maladaptive, to underlying problems. Because initially most patients seek removal of symptoms, modified goals need to be agreed upon. This means less reliance on medical care and more on the patient’s own resources. The objective is improved functioning, a greater sense of control, and improved self-esteem. This may involve return to work and meaningful activities despite continuing distress. The hypochondriacal patient should receive an explanation for symptoms, one that does not involve serious disease [119]. A label of health anxiety or illness worry is perhaps preferable to the pejorative designation of hypochondriasis [120]. The cognitive perceptual model provides a framework for interpretation that may add legitimacy to symptoms [121]. A positive relationship with a hypochondriacal patient may be difficult to establish and maintain, yet is the key to successful treatment. The patient is often mistrustful and feels that his or her suffering has not been understood. According to Starcevic [116], treatment should be based on empathy, acceptance, understanding, and explanation.

Psychological Treatment In a preliminary trial, Warwick and Marks [122] successfully treated a group of hypochondriacal patients using behavioural techniques. They found that a combination of exposure to illness cues and prevention of reassurance yielded rapid results. They noted that reassurance-seeking was a prominent feature and that prevention of this anxiety-relieving ritual was important to the success of treatment. In a subsequent controlled trial, they assigned a small number of patients to cognitive behavioural therapy or a waiting list [123]. Cognitive procedures included identifying and challenging misinterpretation of symptoms, creating realistic interpretations, restructuring images, and modifying dysfunctional assumptions. Behavioural procedures included eliciting bodily sensations by focusing attention, graded exposure to illness situations, and prevention of checking and reassurance-seeking. The treatment proved effective. Three subsequent randomized trials for hypochondriasis have shown that cognitive behavioural therapies are superior to no therapy, with benefits sustained for up to 12 months [118, 124, 125]. However, one study found behavioural stress management, a non-specific intervention, as effective as

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cognitive therapy [124] and another found cognitive therapy and behavioural therapy, by themselves, equally effective [124]. These trials show that psychological treatment is effective, but leave important questions unanswered, such as: how acceptable is this treatment? Barsky et al. [118] reported that, of those primary care patients who were eligible, only 30% participated and that, of those who participated, only 62% attended all six weekly sessions. Another question is: how much better is cognitive behavioural treatment than non-specific therapist contact? The study showing benefit from stress management suggests that there may not be a difference. Finally, are cognitive behavioural interventions cost-effective? In order to maximize patient acceptance, psychological treatment should be available in the primary care clinic, and the primary care physician should remain involved. Also, to improve efficiency, some authors have advised using a group format [120]. Stern and Fernandez [126] showed that such treatment is feasible. Most patients referred to mental health professionals receive some form of psychotherapy, although such therapy has received little study. In a randomized trial, Fava et al. [127] assigned a small number of patients with hypochondriasis to exploratory therapy or a waiting list. The therapy produced significant improvement in illness behaviour and health care utilization that was maintained for 6 months. Exploratory therapy was developed by Kellner [128], who reported that two-thirds of his hypochondriacal patients benefited from the therapy. Additional randomized trials of this and other forms of psychotherapy (e.g., psychodynamic, interpersonal) are needed.

Pharmacological Treatment Secondary hypochondriasis responds to drug therapy for the primary disorder. For example, Noyes et al. [129] assessed hypochondriacal concerns in patients receiving pharmacological treatment for panic disorder and agoraphobia. At the completion of treatment, a significant reduction in concerns was observed among those whose anxiety symptoms had improved. Similarly, Kellner et al. [130] observed resolution of hypochondriacal features in patients with melancholic depression treated with imipramine. No randomized controlled trials of pharmacotherapy have been completed for hypochondriasis, but open label studies suggest that medication has promise. For example, Fallon et al. [131] reported that 10 of 16 patients with primary hypochondriasis very much improved after 12 weeks of fluoxetine. Others have reported similar results with fluvoxamine, nefazodone, and paroxetine [132–134]. Of the more than 50 hypochondriacal patients in these trials, two-thirds responded to a selective serotonin reuptake inhibitor (SSRI). Preliminary results from a controlled trial showed that eight of 10 patients responded to fluoxetine and three of six responded to placebo after 10 weeks.

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Since pain symptoms are frequent in hypochondriasis, pharmacological agents that are effective for pain may be of benefit. SSRIs do not appear helpful, but venlafaxine, which acts on serotonergic and noradrenergic neurotransmitters, has shown benefit in neuropathy and bupropion has proven effective for neuropathic pain. Anticonvulsants have also shown efficacy with this type of pain. In the hypochondriasis trials, drugs were relatively well tolerated and few dropped out on account of side effects. However, a high placebo response rate and difficulty in recruiting suitable patients are major obstacles for investigators undertaking controlled trials.

SUMMARY Consistent Evidence Hypochondriasis is a fascinating but troubling problem, one that we are only beginning to understand. A significant proportion of patients in primary care have hypochondriacal fears and beliefs. These patients are difficult to manage, in part because the medical community has a negative attitude towards them. But, beyond this, there is very little that is firmly established. Findings are based on small samples and inconsistent definition of cases under study. Nevertheless, exciting work is being done in this area, as evidenced by two recent volumes devoted to hypochondriasis and health anxiety [50, 135].

Incomplete Evidence The validity of hypochondriasis as a DSM category remains in some doubt and further examination of criteria is needed [136]. Refinement of these criteria is made difficult by the poor definition of what constitutes ‘‘serious disease’’ and ‘‘excessive worry’’. Many persons with illness worry have the disease they are worried about, but when is this unrealistic? The answer might involve medical evaluation, but should this be a part of the criteria? Probably not, since other psychiatric disorders are not defined in this manner. Failure to respond to reassurance should perhaps be dropped from the criteria for reasons mentioned earlier. In addition to work establishing core features, there is need for biological marker, family, follow-up, and treatment studies distinguishing persons with hypochondriasis from those with other psychiatric disorders, especially illness phobia and somatization disorder. Work is needed to examine thresholds for the diagnosis. Recent studies have suggested that, while worry about illness is common, DSM hypochondriasis is rare. The question of what constitutes clinically significant worry

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does not have a clear answer, and work is needed to examine a series of thresholds in the general population. The relationship between hypochondriasis and neuroticism or negative affectivity is well established. It is less clear whether other personality dimensions are related. However, since not all persons who score high on neuroticism are hypochondriacal, there must be other specific aetiologic factors, such as experience with illness. Genetic factors likely contribute to the vulnerability to hypochondriasis, and twin data may prove useful for examining relationships between genetic and environmental variables. Treatment studies have shown that cognitive behavioural treatment is better than no treatment for patients with hypochondriasis. They have not shown that this treatment is acceptable to most patients or that it is superior to non-specific contact with a health care professional. Also, other therapies need to be examined.

Areas Still Open to Research The boundaries of hypochondriasis need to be explored and criteria established that distinguish it from somatization disorder on the one hand and specific phobia of illness on the other. There is currently little evidence upon which separation of these disorders can be based. Hypochondriasis and somatization disorder may be variants of the same disturbances linked to contrasting personality styles—obsessive–compulsive in the former and histrionic or borderline in the latter. Further efforts are needed to identify features associated with fear of having an illness versus the belief that one has serious illness in clinical and general populations [30]. A research agenda for examining the distinction between hypochondriasis and specific phobia of illness has been outlined [53]. A related issue has to do with the distinction between primary and secondary hypochondriasis and possible subtypes of the disorder. Studies need to determine how best to separate the primary disorder from that better accounted for by another disorder. Hypochondriasis secondary to panic attacks may occur more often in women and at a younger age, suggesting that it differs in an important way from primary hypochondriasis. In addition, hypochondriasis is heterogeneous, and subtypes may be important to identify in future work. Research in this area is dependent upon reliable and valid measures. At present, it is hard to say that a gold standard for the diagnosis exists. Perhaps the closest is the Structured Clinical Interview for Hypochondriasis. However, this instrument focuses only on hypochondriasis and there is little information on the revised version for DSM-IV. The CIDI relies on questions about medical care and seems restrictive. A number of promising new selfreport measures have been developed. One of these, the Health Anxiety

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Inventory, is a multi-factorial assessment that appears to avoid the defects of earlier measures. Finally, there need to be studies of possible biological markers or correlates of hypochondriasis. Gramling et al. [113] demonstrated a number of physiological abnormalities in a small sample, but these must be replicated and extended. Neuropsychological testing is apt to show attentional deficits, but what else? Brain imaging studies may point to regions activated by fear or conviction concerning serious disease. This is an unexplored area. Work so far indicates that the traditional pessimism regarding treatment of hypochondriasis is no longer warranted. Now we must expand options, broaden their acceptance, and make effective treatments widely available for patients who, we should never forget, are truly suffering.

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Commentaries 3.1 Hypochondriasis: Future Directions in Classification and Aetiology Research Steven Taylor1 and Gordon J.G. Asmundson2 Russell Noyes has provided a scholarly overview of the current state of knowledge on hypochondriasis. His review provides an ideal foundation for considering important directions for future research. This commentary will examine three fundamental questions: how might we best delineate hypochondriacal phenotypes? Is there a better method than ICD-10 or DSM-IV-TR for classifying (diagnosing and grouping) hypochondriacal disorders? What are the promising approaches for investigating the underlying mechanisms? It is difficult to adequately investigate the aetiology of a disorder without an accurate description of its phenotype. The current classification systems—ICD-10 and DSM-IV-TR—assume that hypochondriasis is categorical (present vs. absent). Yet, research has consistently shown that hypochondriasis varies along a continuum of phenotypic severity, ranging from subclinical to full-blown hypochondriasis, with or without overvalued ideation [1]. Hypochondriacal phenomena may be actually composed of sets of dimensions, with each dimension corresponding to a distinct set of mechanisms. A dimension may be defined by an aggregate of causal factors that incrementally influence the risk of developing a particular feature of the disorder (e.g., the tendency to experience bodily sensations, or the tendency to worry about one’s health). Taxometric statistical methods [2] can be used to determine whether hypochondriasis is categorical or dimensional. This distinction has important implications for theory and research [3]. A categorical variable implies a different set of causes from a continuous variable. A categorical disorder presumably arises from a small set of causal factors (e.g., the presence vs. absence of traumatic, illness-related learning experiences). In comparison, dimensional variables are probably the result of a multitude of factors (for 1 Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, V6T 2A1, Canada 2 Faculty of Kinesiology and Health Studies, University of Regina, Saskatchewan, S4S 0A2, Canada

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example, numerous genetic factors, each making a small but important additive contribution to the risk of developing hypochondriacal phenomena). Dimensional approaches are consistent with current thinking about the role of genes in psychiatric disorders. Investigators are increasingly interested in identifying numerous genes that each make only tiny (e.g., 1–2%) contributions to phenotypic variance [4]. Thus, making the assumption that hypochondriacal phenomena are dimensional will focus research efforts differently from the assumption that the phenomena are grouped into one or more categorical entities. Classification systems serve several functions, one of which is to organize phenomena and thereby facilitate research into underlying mechanisms. Thus, a good classificatory system is important for understanding the aetiology of hypochondriasis. The current classification systems define and diagnose hypochondriasis on purely descriptive features. DSM-IV-TR, for example, considers hypochondriasis to be a somatoform disorder, because of the prominence of bodily complaints. Yet, hypochondriasis shares many symptom similarities with anxiety disorders, particularly panic disorder, generalized anxiety disorder, and obsessive–compulsive disorder (OCD), and with mood disorders [1]. Some theorists thus consider hypochondriasis to be an obsessive–compulsive spectrum disorder [5], while others suggest that it may actually be a mood disorder [6]. Thus, classification based on descriptive features (phenotypes) has been of limited value in understanding whether hypochondriasis should be grouped with somatoform disorders or with other disorders. One can look to biology for an alternative classificatory system. The most widely used system for classifying organisms is based on cladistics [7], which emphasizes the process of evolution. The merits of this approach for classifying psychopathology in general, and hypochondriasis in particular, remain to be investigated. There are several challenges in applying cladistics to the classification of psychopathology. However, one aspect of the cladistic approach that can be used is the emphasis on theory; that is, the theory of evolution. The fact that cladistics is the dominant school of biological classification suggests that classification of psychopathology eventually must incorporate theories into a psychiatric classification system [8]. A classificatory model of hypochondriasis (and related disorders) based on a diathesis-stress formulation is consistent with the theory-driven approach and evolutionary (genetic) emphasis of cladistics. According to a diathesisstress approach to classification, disorders would be grouped on the basis of the similarity of their diatheses. Two classes of diathesis are widely recognized in understanding psychopathology: genetic factors and environmental factors. The latter include learning experiences that may give rise to dysfunctional beliefs that some theorists have implicated in hypochondriasis [1].

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Ideally, disorders would be grouped together on the basis of the similarities of their diatheses; for example, the similarity of their molecular genetic profile and the similarity of disorder-promoting environmental events. Unfortunately, this information is currently lacking. In the absence of such information, findings from behavioural-genetic (twin) research can be used as a proxy, to evaluate the genetic and environmental similarity among disorders. As noted in Noyes’ review, the behavioural-genetic research to date in this area has either been based on very small samples or has failed to adequately assess all the components of hypochondriasis. We are currently conducting a twin study of fullblown and subclinical hypochondriasis, as part of the University of British Columbia Twin Project [9]. A goal of this research is to apply the multivariate methods fruitfully used by Kendler and colleagues [10] in the study of hypochondriasis. Kendler’s twin research suggests that some anxiety and mood disorders arise from a combination of (a) genetic factors that are specific to a given disorder, (b) genetic factors that are shared with one or more other disorders, (c) environmental factors that are specific to a given disorder, and (d) environmental factors that are shared with one or more other disorders. Similar research could be applied to hypochondriasis, to determine whether it shares genetic or environmental factors with other disorders. This would provide important information about the aetiology of hypochondriasis, and would also guide classification. If, for example, hypochondriasis shared a high degree of genetic and environmental variance with anxiety disorders, and lower levels of variance with somatoform disorders, then hypochondriasis would be more appropriately classified as an anxiety disorder rather than as a somatoform disorder. This would provide an empirically defined classification of which disorder falls within which spectrum. Unlike the DSMIV-TR and ICD-10 classification systems, the classification system proposed here is explicitly theory based, arising from the diathesis-stress perspective. An added advantage is that this approach does not assume that disorders are categorical, and is consistent with evidence suggesting that the various components of hypochondriasis may be dimensional. In conclusion, Russell Noyes commented on the limits of current classification systems for hypochondriasis and the need for future studies on the role of genetic and environmental factors in the disorder. We propose that the study of aetiology should guide efforts in classification. The merits of a diathesis-stress classificatory approach remain to be evaluated. However, methodologically sound twin studies will further our knowledge of the aetiology of hypochondriacal phenomena, and help us move away from a classificatory system based on superficial features (e.g., presenting symptoms) and towards an aetiology-based classification.

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3.2 Making Sense of Hypochondriasis Jonathan S. Abramowitz1 In his comprehensive literature review, Russell Noyes discusses the diagnostic and conceptual dilemmas that confront the study and treatment of hypochondriasis (HC). Early descriptions emphasized the phenomenology of the problem [1]. Behavioural psychology propagated this tradition by calling attention to the antecedents and consequences of attaining excessive medical reassurance [2]. Recent theorists have identified cognitive biases that play a role in the development and maintenance of HC [3]. But, in the meantime, the precision afforded by these functional and theory-driven approaches to phenomenology has been undermined by the growing enthusiasm for diagnostic criteria such as those of the DSM, which emphasize disorders composed of lists of signs and symptoms. The DSM’s medical model is a 1

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superficial observational approach that merely collects behaviours according to form or topography, as opposed to considering their function. Such an approach, inaugurated with the DSM-III operational criteria, made good sense in terms of resolving the major problem of DSM-II, namely diagnostic unreliability. Indeed, one way to enhance reliability is to generate a set of specific behaviours that can be identified as either present or absent. Provided that diagnosticians follow the procedures, such a system is guaranteed to improve inter-rater agreement compared with a system that asks merely for global judgements about vague global constructs. However, the emphasis on improving diagnostic reliability has stifled, rather than aided, progress in understanding and treating HC. Empirical research and clinical observations of the underlying psychological mechanisms and emotional experiences in HC patients now suggest that HC is essentially an anxiety disorder (i.e., ‘‘health anxiety’’) with phenomenology that is quite similar to that of other anxiety disorders (e.g., obsessive–compulsive disorder, OCD). All involve identifiable anxiety-evoking stimuli (e.g., body sensations, social situations), which elicit escape/avoidance responses to reduce anxiety (e.g., checking, passive avoidance) [4, 5]. Moreover, all respond well to exposure-based cognitive-behavioural therapy. Yet, as Noyes points out, the attempt to define HC on the basis of its overt topography led to its being moved from the ‘‘neuroses’’ (anxiety states) in DSM-II to the somatoform (bodily-focused) disorders in DSM-III and DSM-IV. As a result of this (mis)classification (within a questionable diagnostic category), the field has only recently begun to develop therapies and apply the relevant research paradigms to understanding HC. If patients with HC are not really suffering from serious physical illnesses—if they are only misinterpreting innocuous bodily sensations as threatening—why don’t they realize this and stop their over-utilization of medical resources? The answer is that patients with HC fall prey to physiological, cognitive, and behavioural mechanisms, associated with the experience of anxiety, that maintain anxious thinking and behaviour. Thus, HC can be conceptualized as a problem in which misinterpretations of innocuous bodily sensations and thoughts of illnesses lead to pathological health anxiety, the consequences of which serve to maintain the misinterpretations and complete a vicious cycle. Worrying about one’s health leads to increased autonomic activity (i.e., the fight-flight response), which includes normal and harmless sensations such as fluttering heart, hot flash, or dizziness, that may be unexpected and uncomfortable. Not surprisingly, individuals with HC often misinterpret such symptoms as indicating the presence of illnesses. Thus, at the very point that they are getting anxious over their health, additional threatening ‘‘symptoms’’ appear. The result is further anxiety, increased autonomic

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symptoms, and an upward spiral leading to urges to seek evaluation for a suspected ‘‘medical problem’’. Biases in how people with HC think about health-related information include selective attention, in which patients attend closely to information that could confirm the presence of sickness, and discount information suggestive of good health (e.g., ‘‘the doctor is just trying to pacify me’’) [6]. This explains the urge to get second opinions when doctors conclude there is no sign of illness. Body vigilance, another cognitive bias, is the tendency to pay excessive attention to normally occurring bodily sensations. This leads to noticing an endless array of seemingly unexplained symptoms (which most people simply ignore) that may be misinterpreted as illness related [7]. Acting to prevent harm is a natural tendency when one perceives threat. However, if the perception of threat is based on a misinterpretation, then such safety-seeking behaviour prevents the persons from noticing that their fear was groundless in the first place. The most noticeable example of safety-seeking in HC is seeking reassurance from a doctor; for example, ‘‘hearing Dr. Jones say that I do not have lung disease is the only way I can stop worrying about it.’’ Not only does reassurance trick the patient into believing that he narrowly escaped disaster (i.e., ‘‘I didn’t die because I went to the doctor’’), it may further increase distress if the patient receives different information from different sources, or worse, inconsistent information from the same source on different occasions. Thus, from a phenomenological perspective, HC doesn’t actually persist despite medical reassurance, as DSM suggests, but because of such reassurance. Anxiety-motivated behaviours such as repeated body checking (e.g., of blood pressure) also preserve hypochondriacal thinking. First, such behaviour leads to ‘‘discovering’’ and misinterpreting what is ostensibly harmless internal ‘‘body noise’’ (e.g., normal changes in blood pressure). Second, repetitive body checking can exacerbate bodily perturbations, such as an increase in blood pressure in anticipation of measuring this vital sign. The treatment implications of this conceptualization of HC are clear. Therapy must correct patients’ misinterpretations of their benign bodily sensations and prevent any responses that interfere with the self-correction of mistaken beliefs. To do this, the patients must be helped to identify and challenge their mistaken interpretations, and helped to resist their urge to seek reassurance from doctors or other medical sources. The procedures for accomplishing these goals fall under the umbrella of cognitive-behavioural therapy, which, as Noyes correctly points out, is the treatment of choice for HC. In our clinical experience, patients embrace a thoughtfully presented cognitive-behavioural model of their problem, because it begins with validating that they are indeed experiencing real body sensations. Moreover, it leads to an understanding of the problem on an individual level, rather than labelling it as a ‘‘personality disorder’’ or ‘‘attention-seeking’’. Finally, there

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is evidence that patients perceive treatment based on this model as highly acceptable and likely to be helpful [8].

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.

Gillespie R. (1928) Hypochondria: it’s definition, nosology, and psychopathology. Guy’s Hosp. Rep. 8: 408–460. Dollard J., Miller N.E. (1950) Personality and Psychotherapy: An Analysis in Terms of Learning, Thinking, and Culture. McGraw-Hill: New York. Warwick H., Salkovskis P. (1990) Hypochondriasis. Behav. Res. Ther. 28: 105–117. Abramowitz J., Deacon B., Valenteiner D. (In press) The Short Health Anxiety Inventory in an Undergraduate Sample: Implications for a Cognitive-Behavioral Model of Hypochondriasis. Submitted for publication. Abramowitz J., Schwartz S., Whiteside S. (2002) A contemporary conceptual model of hypochondriasis. Mayo Clin. Proc. 77: 1323–1330. Owens K., Asmundson G., Hadjistavropoulos T., Owens T. (2004) Attentional bias toward illness threat in individuals with elevated health anxiety. Cogn. Ther. Res. 28: 57–66. Schmidt N., Lerew D., Trakowski J. (1997) Body vigilance in panic disorder: evaluating attention to bodily perturbations. J. Consult. Clin. Psychol. 65: 214–220. Walker J., Vincent N., Furer P., Cox B., Kjernisted K. (1999) Treatment preference in hypochondriasis. J. Behav. Ther. Exp. Psychiatry 30: 251–258.

3.3 Hypochondriasis: An Endless Source of Controversies? Vladan Starcevic1 Noyes’ review elegantly summarizes hypochondriasis and points to the salient issues about this condition. Although much progress has been made in terms of our understanding and treatment of hypochondriasis, this is probably a unique disorder, in that everything about it—from its very name to treatment approaches—seems to be shrouded in controversy. Of all these controversies, there is space here to select and discuss just a few. Accordingly, this commentary will focus on conceptual, nosological, and treatment issues. Although hypochondriasis is an official psychiatric diagnosis, many do not use it as such, and refer to it as a behavioural style, an aspect of personality or even a defence mechanism. Some are reluctant to use the term, because it carries negative connotations. Others find the diagnostic criteria too narrow and hence rarely applicable in clinical practice. All of this may help explain why the diagnosis of hypochondriasis is relatively rarely made, 1 Department of Psychological Medicine, University of Sydney and Nepean Hospital, P.O. Box 63, Penrith, NSW 2751, Australia

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as mentioned by Noyes, despite various hypochondriacal features being commonly encountered in general and patient population. It is imperative for psychiatry to be clear about the definition and meaning of hypochondriasis as a diagnosis, lest the concept loses clinical relevance. A part of this task is to modify the existing diagnostic criteria. For example, Noyes and others [1] have argued that a failure to respond to medical reassurance should no longer be a diagnostic criterion for hypochondriasis. A related issue is that of the boundaries of hypochondriasis. How far should the term be ‘‘stretched’’? Although hypochondriacal manifestations seem to be distributed on a dimension of severity, ranging from mildly increased health concerns to a delusional condition, the term ‘‘hypochondriasis’’ should be reserved only for those cases that qualify for the corresponding DSM or ICD diagnosis. That would avoid the confusion of applying the term to heterogeneous forms of psychopathology. Other terms (e.g., ‘‘transiently increased health anxiety’’ and ‘‘increased health anxiety due to panic disorder’’) may be used for those presentations that fall outside the diagnostic concept of hypochondriasis, and any reference to the term ‘‘hypochondriasis’’ in these contexts should best be avoided. That would also obviate the need for terms such as ‘‘transient’’ and ‘‘secondary’’ hypochondriasis. There are also some disagreements as to what should be emphasized in the diagnostic concept of hypochondriasis. Is hypochondriasis primarily a fear or a suspicion that one already has a particular disease? Is it both? Or, is the essence of hypochondriasis in hypervigilance about one’s own body and bodily preoccupation? Attempts to create subtypes of hypochondriasis on the basis of what component may be more prominent have not been particularly fruitful, and hypochondriasis appears to be a unitary concept (albeit with several interrelated dimensions) more than a loose constellation of the purportedly distinct subtypes. Should hypochondriasis be renamed ‘‘health anxiety disorder’’ and classified among the anxiety disorders? The answer should be a negative one. Hypochondriasis appears to be a wider concept, which certainly includes health anxiety, but cannot entirely be subsumed under it. Likewise, despite similarities with obsessive–compulsive disorder, hypochondriasis is in many ways significantly different from the latter, and there is very little support for the notion that hypochondriasis may be one of the ‘‘obsessive–compulsive spectrum disorders’’. Hypochondriacal features seem to be a part of several personality disorders, but conceptualizing hypochondriasis itself as a personality disorder would imply that any condition with a relatively early onset and chronic course might in fact be a personality disorder. Whether hypochondriasis is to remain classified among the somatoform disorders may crucially depend on what will happen with the group of somatoform disorders. Although there is dissatisfaction with the conceptualization of somatoform disorders [2], no clear and superior alternative to

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the somatoform concept has emerged. The classification of hypochondriasis among the somatoform disorders is not optimal, but at least hypochondriasis shares with other members of that group the occurrence of physical symptoms for which no ‘‘organic’’ explanation can be found. Over the last decade, several controlled studies have demonstrated the efficacy of cognitive-behavioural therapy (CBT) for hypochondriasis. But, as Noyes points out, CBT does not seem acceptable to the majority of patients with hypochondriasis, and it is not clear whether CBT is more effective than non-specific therapeutic contacts. This raises further questions. Is CBT suitable only for certain patients, perhaps those with a form of hypochondriasis that resembles an anxiety disorder, with prominent illnessrelated fears and avoidance and the corresponding cognitions? How should CBT be modified to become more appealing to a larger number of patients? Should there be some changes in the way CBT is administered? Would a move towards a more intense and a more prolonged form of CBT make it more effective? What treatments may work for the more ‘‘prototypical’’ hypochondriacal patients? That is, for patients who cling ‘‘stubbornly’’ to their symptoms, who continue to believe that they have a dreadful disease, and who continue to seek reassurance even when reassurance has been withheld in the context of therapy? Finding optimal treatment for such patients is still an unexplored territory, although there is no shortage of ideas as to what may be suitable (e.g., ‘‘cognitive-educational treatment’’ [3] and ‘‘explanatory therapy’’ [4]). Many of these treatment strategies contain non-specific and/or overlapping elements, such as building trust, improving communication, using explanation, and reassuring carefully. Perhaps these elements can be combined with some CBT techniques to improve outcomes. There is an urgent need to elucidate those treatment ‘‘ingredients’’ that make the greatest contribution to the improvement of most patients with hypochondriasis.

REFERENCES 1. 2. 3. 4.

Starcevic V. (2001) Clinical features and diagnosis of hypochondriasis. In: Hypochondriasis: New Perspectives on an Ancient Malady, V. Starcevic, D.R. Lipsitt (Eds). Oxford University Press: New York, pp. 21–60. Rief W., Sharpe M. (2004) Somatoform disorders—new approaches to classification, conceptualization, and treatment. J. Psychosom. Res. 56: 387–390. Barsky A.J., Geringer E., Wool C.A. (1988) A cognitive-educational treatment for hypochondriasis. Gen. Hosp. Psychiatry 10: 322–327. Fava G.A., Grandi S., Rafanelli C., Fabbri S., Cazzaro M. (2000) Explanatory therapy in hypochondriasis. J. Clin. Psychiatry 61: 317–322.

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3.4 Hypochondriasis: Defining Boundaries, Exploring Risk Factors and Immunology Eamonn Ferguson1 Russell Noyes provides an authoritative and comprehensive review of the current scientific literature with respect to hypochondriasis, succinctly highlighting the gaps in our current understanding and identifying a number of key research issues for the future. A number of these issues (classification, risk factors and biomarkers) form the focus of this commentary. In the general literature on mental disorders, two main boundary issues have been identified: the issue of the boundary between normality and disorder and that of the boundary between different disorders [1]. Both issues are highlighted by Noyes in relation to hypochondriasis, as is the idea that there may be subtypes of the disorder. The first boundary issue (normality vs. disorder) specifically concerns the question of whether a condition is best viewed as categorical or dimensional. A set of statistical procedures, referred to as taxometrics, have been developed to address this boundary question [2–4] and applied to a variety of other disorders [5, 6]. Taxometric procedures are specifically designed to assess whether or not data are taxonic, in that individuals form non-arbitrary groups, or are dimensional, with individuals differing in a quantitative manner along a continuum [1–4]. These techniques are seen as an improvement over other techniques such as cluster analysis and may be applied to a wide variety of markers (self-report questionnaires, interviews, behavioural data) [3], a number of which are available for hypochondriasis. Application of taxometrics to the question of normality or disorder may be applied hierarchically to identify subtypes [1]. For example, if hypochondriasis data were initially found to be taxonic (using the Whiteley Index items or subscales), each taxon could be further explored for subtypes. Different markers (e.g., indices of anxiety, insight and depression) could be used to see if there are two subtypes of hypochondriasis—based primarily around either disease phobia or disease conviction—as suggested by Noyes. However, large sample sizes and careful consideration of sampling will be required to conduct these types of analyses [2–4]. Caution has been expressed about applying taxometrics directly to the second boundary issue (different disorders). However, procedures for how to start to tackle this question have been suggested [1]. Recently, the related technique of latent class analysis has been applied to the second boundary issue in hypochondriasis [7]. 1

School of Psychology, University of Nottingham, Nottingham, NG7 2RD, UK

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One important principle for applying taxometric procedures is whether the taxometric question is scientifically worth asking for a specific disorder [3]. Noyes’s review highlights that these boundary questions are important for research and clinical practice with hypochondriasis (see also [3, 8]). Within cognitive-behavioural models of hypochondriasis, the anxiety associated with stress may be misinterpreted as a ‘‘sign’’ of disease and act to trigger the disorder [9, 10]. Noyes points out that there are few studies exploring the role of stress in hypochondriasis. Furthermore, most of these studies have not explored the role of cognitive appraisals and coping [11, 12]. Where this has been done, there is evidence that increased levels of health anxiety are associated with a tendency to perceive the re-occurrence of life events and disease as more controllable [11]. This tendency may be problematic if it generalizes to events (both health and non-health related) that are not controllable (e.g., multiple sclerosis), as anxiety and depression may increase as a sense of helplessness develops. Therefore, more work exploring the relationship between event appraisals and hypochondriasis is needed. Noyes points to the fact that while neuroticism (N) is the most consistent personality correlate of hypochondriasis and may be a risk factor [13], not all those with hypochondriasis score high on N. This leaves the possibility that other personality factors (i.e., conscientiousness) may interact with N to increase the risk of hypochondriasis [14] or have non-linear effects for other personality domains [15]. Noyes argues that more research is needed to explore biological correlates of hypochondriasis. One fruitful line of enquiry would be to explore potential immunological correlates, of which the pro-inflammatory cytokines interleukin-1 and -6 are potential candidates. These relate to the non-specific symptoms of the sickness response [16, 17] of the type reported by those with hypochondriasis, and are related to fatigue in other medically unexplained syndromes [16].

REFERENCES 1. 2. 3. 4. 5.

Ruscio J., Ruscio A.M. (2004) Clarifying boundary issues in psychopathology; the role of taxometrics in a comprehensive program of structural research. J. Abnorm. Psychol. 113: 24–38. Waller N.G., Meehl P.E. (1998) Multivariate Taxometric Procedures: Distinguishing Types from Continua. Sage: London. Ruscio J., Ruscio A.M. (2004) A nontechnical introduction to the taxometric method. Understanding Stat. 3: 151–194. Meehl P.E. (1999) Clarifications about taxometric method. Appl. Prev. Psychol. 8: 165–174. Ruscio A.M., Ruscio J. (2002) The latent structure of analogue depression: should the Beck Depression Inventory be used to classify groups? Psychol. Assess. 14: 135–145.

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SOMATOFORM DISORDERS Marcus D.K., John S.L., Edens J.F. (2004) A taxometric analysis of psychopathic personality. J. Abnorm. Psychol. 113: 626–635. Fink P., Ornbol E., Toft T., Sparle K.C., Frostholm L., Olesen F. (2004) A new, empirically established hypochondriasis diagnosis. Am. J. Psychiatry 161: 1680–1691. Hiller W., Rief W., Fichter M.M. (2002) Dimensional and categorical approaches to hypochondriasis. Psychol. Med. 32: 707–718. Warwick H.M., Salkovskis P.M. (1990) Hypochondriasis. Behav. Res. Ther. 28: 105–117. Noyes R., Watson D.B., Carney C.P., Letuchy E.M., Peloso P.M., Black D.W., Doebbeling B.N. (2004) Risk factors for hypochondriacal concerns in a sample of military veterans. J. Psychosom. Res. 57: 529–539. Ferguson E., Swairbrick R., Clare S., Bignell C.J., Anderson C. (2000) Hypochondriacal concerns, somatosensory amplification and primary and secondary appraisals. Br. J. Med. Psychol. 73: 355–369. Ferguson E., Cox T. (1997) The functional dimensions of coping scale; theory, reliability and validity. Br. J. Health Psychol. 2: 109–129. Ferguson E. (2004) Personality as a predictor of hypochondriacal concerns: results from two longitudinal studies. J. Psychosom. Res. 56: 307–312. Williams P.G. (2004) The psychopathology of self-assessed health: a cognitive approach to health anxiety and hypochondriasis. Cogn. Ther. Res. 28: 629–644. Ferguson E. (2001) Intellect and somatic health: associations with hypochondriacal concerns, threat appraisals and fainting. Psychother. Psychosom. 70: 319–327. Vollmer-Conna U., Fazou C., Cameron B., Li C., Brennan C., Luck L., Davenport T., Wakefield D., Hickie I., Lloyd A. (2004) Production of pro-inflammatory cytokines correlates with symptoms of acute sickness behaviour in humans. Psychol. Med. 34: 1289–1297. Ferguson E., Cassaday H. (2002) Theoretical accounts of Gulf War syndrome: from environmental toxins to psychoneuroimmunology and neurodegeneration. Behav. Neurol. 13: 133–147.

3.5 Hypochondriasis, Health Anxiety, and Cognitive-Behavioural Therapy Patricia Furer1 and John R. Walker1 Hypochondriasis may be viewed as the tip of the iceberg of a much broader problem: health anxiety. As Russell Noyes points out in his review, it is only in recent years that researchers have turned their attention to the assessment and treatment of hypochondriasis. A great deal of work remains to be done to improve our understanding of this disorder and its relationship with other disorders in the anxiety, mood, and somatoform areas. Our knowledge of developmental factors and the aetiology of hypochondriasis is also very limited. The DSM-IV and ICD-10 definitions are quite complex. As Noyes suggests, estimates of the prevalence in the community depend to a great 1 Department of Clinical Health Psychology and Anxiety Disorders Program, University of Manitoba, M5-St. Boniface General Hospital, 409 Tache Ave., Winnipeg, MB, Canada

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extent on the definition that is applied. When the definition is applied very restrictively, very few cases are identified. When the definition is applied more broadly, many more cases are identified and the problem is quite common in the community and in primary care. Russell Noyes highlights an important study that demonstrates that individuals meeting all diagnostic criteria for hypochondriasis and those meeting an abridged definition (that did not include the criterion of failure to respond to medical reassurance) were similar in level of disability [1]. This finding that some individuals with persistent worries about health concerns do respond to medical reassurance fits well with our experience in treating this problem. However, the effects of reassurance are often temporary and worry arises again with the emergence of new or renewed symptoms. When hypochondriasis is viewed as a dimensional concept, health anxiety is even more common in the community. Rief et al. [2] asked about health worries in their study of somatic symptoms in over 2000 residents of Germany. One item asked ‘‘Are you afraid or convinced that you have a serious disease, but doctors do not find a sufficient explanation?’’. Eleven percent of females and 8% of males answered yes to this question, with a higher rate of endorsement by those 46 years and older. This suggests that many different health concerns and worries are very common in community samples. Hypochondriasis has been historically viewed as resistant to treatment. However, this perspective has changed over the last 20 years, as several treatment approaches, including pharmacological and psychosocial treatments, have been found to be effective. Our research suggests that individuals seeking help for health anxiety and hypochondriasis are particularly receptive to psychosocial treatments [3]. Various forms of cognitive-behavioural therapy (CBT) have been the most thoroughly evaluated treatments to date and the results have been very encouraging. Recent research has demonstrated considerable success in reducing worries about health, time spent checking bodily symptoms and obtaining reassurance from others, and avoidance of health-related situations. Some studies have found that health-services utilization decreases after CBT. These changes with treatment have been maintained over 3–12 month follow-up periods after the end of treatment. As Noyes indicates, both individual and group CBT treatments appear to be viable options. Preliminary findings suggest that CBT administered via bibliotherapy may also be effective with this population [4]. In our treatment for hypochondriasis and health anxiety, we emphasize approaching illness- and death-related situations in a gradual, systematic way; reduction of bodily checking and reassurance-seeking; acceptance of the reality of death; enhancing life satisfaction through goal-directed activities; and cognitive reappraisal. We are currently completing a randomized trial comparing group CBT for hypochondriasis to a waiting-list control condition [5]. Our pre-post effect sizes with group treatment are comparable

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to those reported by Taylor and Asmundson [6] in their meta-analytic comparison of psychosocial and pharmacological treatments for health anxiety. What emerges from these studies is that interventions emphasizing either cognitive or behavioural components of treatment are effective in reducing hypochondriasis and health anxiety. Researchers are interested in establishing which components of treatment and what doses of these components are most important in producing and maintaining behaviour change. A greater understanding of these issues could help in the development of treatments that are briefer, less costly, and easier to disseminate outside of research settings. A greater availability of effective treatments would reduce the distress and disability associated with the variety of common psychiatric disorders in which health anxiety is prominent. More effective management may also reduce the high health utilization of health services associated with these problems.

REFERENCES 1. 2. 3. 4. 5.

6.

Gureje O., Ustun T.B., Simon G.E. (1997) The syndrome of hypochondriasis: a cross-national study in primary care. Psychol. Med. 27: 1001–1010. Rief W., Hessel A., Braehler E. (2001) Somatization symptoms and hypochondriacal features in the general population. Psychosom. Med. 63: 595–602. Walker J.R., Vincent N., Furer P., Cox B.J., Kjernisted K. (1999) Treatment preference in hypochondriasis. J. Behav. Ther. Exp. Psychiatry 30: 251–258. Jones F. (2002) The role of bibliotherapy in health anxiety: an experimental study. Br. J. Commun. Nurs. 7: 498–503. Furer P., Walker J.R., Torgrud L., Lionberg C., Vincent N. (2004) Cognitive behavioral group treatment for hypochondriasis: a randomized trial. Presented at the Meeting of the Association for the Advancement of Behavior Therapy, New Orleans, November 18–21. Taylor S., Asmundson G.J.G. (2004) Treating Health Anxiety: A Cognitive-Behavioral Approach. Guilford Press: New York.

3.6 Progress with Hypochondriasis Theo K. Bouman1 Russell Noyes’ overview provides us with detailed state-of the-art information on the conceptualization, assessment, and treatment of a disorder that has long discouraged both clinicians and researchers. 1 Department of Clinical and Developmental Psychology, University of Groningen, Grote Kruisstraat 2/1, 9712 TS Groningen, The Netherlands

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An important issue raised by Noyes is the nature of hypochondriasis: should it be considered a nosological entity, a category, or a dimensional phenomenon? Several predominantly questionnaire studies starting in the early 1970s have indicated the presence of various constituting components, such as health anxiety, disease conviction, illness behaviour, and somatosensory amplification. Interestingly, these components can be found in many other mental disorders as well. Health anxiety, for example, may be a prominent feature in panic disorder; abnormal illness behaviour features in somatization disorder; disease conviction in delusional disorders, and somatosensory amplification in pain disorder. Although considering hypochondriasis as a psychopathological category may be helpful for communication purposes, it could, however, hinder scientific knowledge, since it draws the scientific emphasis away from the phenomenology of a disorder towards the issues of consensus between researchers. Recently, some authors have focused on so-called transdiagnostic processes [1], cutting across diagnostic boundaries whilst presenting specific manifestations within a specific symptom constellation. These processes may be of a time-limited nature, as in Axis I disorders, but may also be more structural, as in personality characteristics and Axis II disorders. Disease conviction is an example of a rigid and overvalued belief system that is also a prominent feature of obsessive–compulsive disorder and obsessive–compulsive personality traits. In the case of hypochondriasis, the specific content of this belief system focuses on health and bodily symptoms. A transdiagnostic perspective on hypochondriasis would allow for a better understanding of its overlap and similarities with other disorders, and may shed a different light on issues related to comorbidity. Moreover, questions such as hypochondriasis being an Axis I or Axis II disorder may become less relevant within the framework of a transdiagnostic approach. Another crucial issue refers to the nature of the physical symptoms that constitute the hypochondriacal picture. Noyes points to the importance of ruling out known organic diseases and to the various causes of physical symptoms, such as panic disorder. Although many clinicians argue that symptoms of hypochondriacal patients are unexplained or even non-existent, this is not necessarily the case. Some of our patients, for example, were diagnosed with a medically known heart disease, but were unable to accept this diagnosis. Rather, they were negatively preoccupied with their cardiac symptoms, to which they attributed a far too catastrophical meaning. Their health anxiety and ensuing behaviours resulted from a misunderstanding of and mistrust with the cardiologist’s opinion. Excessive fear and preoccupations, therefore, are the main elements of hypochondriasis, rather than the nature of the bodily symptoms. This emphasis on preoccupation has serious implications for both assessment and treatment, since paradoxically the cause and nature of bodily symptoms are the least of our concern.

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Over the years, psychological treatments of hypochondriasis have seen an increased sophistication, theoretical underpinning, and empirical evidence. This is particularly true within the cognitive-behavioural frame of reference [2]. Recently, a number of specific treatment strategies have been devised and empirically tested for each of the components mentioned above, such as cognitive therapy, behaviour therapy, and attentional training [3]. However, drop-out rates vary over studies, long-term follow-ups are lacking, and many patients refuse to be referred to a psychologist or a psychiatrist in the first place. Therefore, despite their optimistic conclusions, outcome studies may paint a too positive picture. An efficient treatment approach should involve a stepped care model. As a first step, dedicated psychoeducation has great potential as a secondary prevention tool, and also a motivator to engage patients in ‘‘real’’ therapy [4]. When hypochondriacal patients know more about their disorder and about ways to change this, they are likely to benefit more from formal treatment. It has been repeatedly documented, as Noyes rightly point out, that the relationship between hypochondriacal patient and caregiver is far from optimal. For that reason more emphasis should be given to the actors involved in the treatment, that is, we should study the patients’ perspective, the therapists’ perspective, and their mutual relation. Patients obviously differ in their acceptance of a biopsychosocial vision of hypochondriasis, one that combines physical symptoms with psychological processes and with environmental (social) factors. If a hypochondriacal patient strongly adheres to a single medical approach, referral to a psychologist may not occur. On the other hand, caregivers themselves should become more aware of their own responses to hypochondriacal patients, since frustration, mistrust, anger, and similar negative emotions and beliefs are a serious obstacle to a constructive therapeutic relationship [5]. In a recent experimental study, we found a higher level of these negative reactions to emerge in a consultation with somatizing patients than with non-somatizing patients [6]. These considerations pave the way for a greater emphasis on interactional—in addition to intraindividual—models in the understanding of hypochondriasis and related disorders. Russell Noyes is one of the great contributors to this approach.

REFERENCES 1. 2. 3.

Harvey A., Watkins E., Mansell W., Shafran R. (2004) Cognitive Behavioural Processes Across Psychological Disorders: A Transdiagnostic Approach to Research and Treatment. Oxford University Press: Oxford. Taylor S., Asmundson G. (2004) Treating Health Anxiety. A Cognitive Behavioral Approach. Guilford Press: New York. Cavanagh M.J. (2004) Attention training: towards a new effective treatment for hypochondriasis. Presented at the Conference of the European Association of Behavioural and Cognitive Therapies, Manchester, September 9.

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Bouman T.K. (2002) A community-based psychoeducational group approach to hypochondriasis. Psychother. Psychosom. 7: 326–332. Starcevic V. (2002) Overcoming therapeutic pessimism in hypochondriasis. Am. J. Psychother. 56: 167–177. Wilgen C.P., van Koning M., Bouman T.K. Health care professionals’ initial responses to the somatizing patient. Paper in preparation.

5. 6.

3.7 The Clinical Spectrum of Hypochondriacal Fears and Beliefs Giovanni A. Fava1 and Stefania Fabbri1 Any undue concern about bodily function is often labelled as hypochondriacal. As a result, hypochondriasis may be seen primarily as an amplification of somatic sensations or not substantially different from health anxiety. Russell Noyes provides a clear description of its distinctive features and its related fears and beliefs, such as disease conviction and bodily preoccupations. Whether such fears are only components or dimensions of hypochondriacal disorder [1] or warrant specific phenomenological differentiation [2] is a research and clinical issue that has not received adequate attention. The Diagnostic Criteria for Psychosomatic Research (DCPR) have introduced three syndromic variations of hypochondriasis [3]. One is health anxiety, a generic worry about illness that readily responds to appropriate medical reassurance. The other is disease phobia, a persistent, unfounded fear of suffering from a specific disease. There are three main clinical characteristics of disease phobia. One is the specificity and longitudinal stability of the fear (e.g., patients who are afraid of suffering from heart disease are unlikely to ‘‘transfer’’ their fear to other organ systems). The other key characteristic is a tendency to manifest itself through episodic attacks rather than constant, chronic worries. In this sense, the relationship of disease phobia to hypochondriasis is similar to that of panic disorder and generalized anxiety disorder. Another syndrome is thanatophobia, characterized by attacks with sense of impending death and the conviction of dying soon, even though there is no objective medical reason for such fear. Marked and persistent fear and avoidance of news that reminds of death (e.g., funerals, obituary notices) is an important associated feature. Thanatophobia, disease phobia, and hypochondriasis may coexist in the same patient, but may also be differentiated. In one investigation where both DSM and DCPR criteria were used in functional gastrointestinal disorders [4], DSM-IV hypochondriasis was diagnosed in 7% of patients, whereas disease phobia occurred in 12%, health 1

Department of Psychology, University of Bologna, Viale Berti Pichat 5, 40127 Bologna, Italy

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anxiety in 12%, and thanatophobia in 2% of cases. This may suggest that the DSM-IV diagnosis of hypochondriasis represents the more severe end of a spectrum that encompasses several forms of hypochondriacal fears and beliefs. A more precise phenomenological description may pave the way for more specific treatment approaches. For instance, patients with disease phobia may be more likely to respond to exposure to illness cues and prevention of reassurance than those with hypochondriasis. As outlined by Noyes, several randomized controlled trials have suggested that hypochondriasis is a treatable disorder. However, treatment strategies ranged from very simple approaches (explanatory therapy) to complex mixtures of cognitive and behavioural techniques. Explanatory therapy is a short-term therapy developed by Kellner [5], mostly derived from findings of studies concerned with patients with functional somatic symptoms. It consists of providing accurate information, reassurance, clarification, and repetition. Further research should disclose the actual components of the mechanism of change in hypochondriacal patients, by comparing simple and complex treatment strategies in patients whose hypochondriacal fears and beliefs have been outlined in their main variants. The health costs and unwarranted use of medical facilities of hypochondriacal patients are often underscored. However, an issue that is frequently neglected is that hypochondriacal patients are less likely to take precautions against health hazards (e.g., refraining from smoking, eating habits). They may be so distressed by their belief of having an undiagnosed and neglected disease that behaviours that may yield benefits in the distant future appear to them irrelevant. This finding, which has been supported by several investigations [2], has considerable implications for health promotion.

REFERENCES 1. 2. 3. 4. 5.

Pilowsky I. (1967) Dimensions of hypochondriasis. Br. J. Psychiatry 113: 89–93. Fava G.A., Grandi S. (1991) Differential diagnosis of hypochondriacal fears and beliefs. Psychother. Psychosom. 55: 114–119. Fava G.A., Freyberger H.J., Bech P., Christodoulou G., Sensky T., Theorell T., Wise T.N. (1995) Diagnostic criteria for use in psychosomatic research. Psychother. Psychosom. 63: 1–8. Porcelli P., de Carne M., Fava G.A. (2000) Assessing somatization in functional gastrointestinal disorders. Psychother. Psychosom. 69: 198–204. Kellner R. (1979) Psychotherapeutic strategies in the treatment of psychophysiological disorders. Psychother. Psychosom. 32: 91–100.

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3.8 A Nosological Nightmare Geoffrey G. Lloyd1 To a psychiatric nosologist, all other problems of classification pale into insignificance compared with the difficulty of constructing a valid definition of hypochondriasis. This is now conventionally grouped with the somatoform disorders, a motley collection of conditions not all of which have a solid foundation in terms of their stability over time and their response to treatment. Russell Noyes has provided a comprehensive and very helpful guide to these difficulties, which is based on his considerable research experience. The two commonly used classification systems, DSM-IV and ICD-10, are reviewed with reference to their differences. ICD-10 includes body dysmorphic disorder with hypochondriasis, but DSM-IV classifies this separately. Another important distinction is the exclusion of delusional beliefs from DSM-IV. Both systems make it clear that the diagnosis should not be made if the preoccupation with disease can be explained by other disorders. ICD-10 excludes schizophrenia and affective disorders, while DSM-IV requires, in addition, the exclusion of generalized anxiety, panic disorder, obsessive–compulsive disorder, and other somatoform disorders. It would be expected therefore that the DSM-IV criteria are stricter and that their application would lead to a lower prevalence and more homogeneous samples. Prevalence studies of hypochondriasis have yielded widely differing results, the differences between studies being up to 10-fold. This greatly reduces the clinical usefulness of the concept and suggests that different surveys have used such widely differing criteria that comparisons are difficult if not misleading. Is hypochondriasis a useful concept for the clinician? Russell Noyes sits on the fence on this dilemma but others have been less restrained. Sharpe and Mayou [1] are among the most outspoken critics of the concept. Indeed, they have criticized the entire classification of somatoform disorders, of which hypochondriasis constitutes a subgroup. They believe that somatoform disorders have a number of practical limitations, including their unacceptability to patients, their lack of validity or reliability, the risk of underdiagnosing depression and anxiety, and their limited implications for treatment. There is also a problem concerning the aetiology of these conditions. The implication is that they are psychologically determined, but the evidence for this is not convincing. Their causes remain poorly understood and are likely to be multifactorial, involving minor physiological changes as well as psychological and social factors. Sharpe and Mayou [1] believe that many 1

Royal Free Hospital, London NW3 2QG, UK

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specific diagnostic categories of the somatoform group could be re-classified elsewhere and propose that hypochondriasis be grouped with the anxiety disorders. A debate has also been conducted over the term ‘‘functional somatic syndrome’’ [2], which has sometimes been used as an alternative to somatoform disorder. Clinicians from different specialities see patients with different symptoms. Gastroenterologists see patients with irritable bowel syndrome or non-ulcer dyspepsia. Neurologists see patients with tension headaches. Cardiologists see patients with non-cardiac chest pain. Rheumatologists are consulted because of fibromyalgia, and infectious disease specialists see patients with chronic fatigue. Wessely et al. [3] have argued that these patients have much in common. Their symptoms overlap and they all have a tendency to elevated levels of anxiety and depression. The prognosis is also broadly similar. Outcome is generally poor for those referred to secondary or tertiary care services, and response to conventional medical intervention is disappointing. They favour a single functional somatic syndrome. White [2], on the other hand, has argued for splitting these conditions and studying them separately if their aetiology is to be understood. He believes that the different syndromes have different aetiological factors and respond differently to treatment; these differences would be diluted and overlooked if all syndromes were lumped together. Noyes reviews the usual sources of evidence used to establish the validity of a psychiatric diagnosis, including genetic studies, the stability of the diagnosis over time, personality factors, and response to treatment. He admits that on these criteria hypochondriasis does not do well and its status as a diagnostic category is in doubt. It is not even clear whether it should be regarded as a distinct illness or as a personality disorder. Further research to determine whether a valid diagnostic category can be defined must start with reliable and valid measures, so that comparisons between different outcome and treatment studies can be made with a greater degree of confidence than has been the case previously. At present, hypochondriasis seems to be defined more by what it is not than by any consistent symptoms or patterns of behaviour. It should only be used when physical illness and other psychiatric disorders have been excluded. Nevertheless, like hysteria, hypochondriasis is not going to disappear. It may have its name changed, but clinicians will continue to find it a useful diagnostic category for a puzzling group of patients who consume an enormous amount of medical time and resources. Russell Noyes’ review has made a useful contribution to this confusing area of psychiatric classification, not by providing answers but by clearly outlining the problems and indicating where further research is needed.

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REFERENCES 1.

Sharpe M., Mayou R. (2004) Somatoform disorders: a help or a hindrance to good patient care? Br. J. Psychiatry 184: 465–467. Wessely S., White P.D. (2004) There is only one functional somatic syndrome. Br. J. Psychiatry 185: 95–96. Wessely S., Nimnuan C., Sharpe M. (1999) Functional somatic syndromes: one or many? Lancet 354: 936–939.

2. 3.

3.9 Hypochondriacal Syndromes: Where Did They Go? Driss Moussaoui1 Hypochondriasis has already been described by Hippocrates, and probably always existed, though with a different meaning from the one we have nowadays: a systematic pejorative assessment of one’s health status. The interesting explanation had then to do with the hypochondrium, where the liver is located, when black bile was thought to be responsible for the occurrence of melancholia, its fumes ascending to the brain darkening all perceptions of the patient. This biological explanation of melancholia and its anatomical link to the liver and black bile in the hypochondrium is an interesting one. Ancient Greek doctors seem to have had the premonition of the link between depression and hypochondriasis, or at least hypochondriacal syndromes. In my clinical experience in Morocco, I have witnessed a steady and progressive decrease of hypochondriacal syndromes in patients over the past three and a half decades. It was extremely frequent in psychiatric patients, the ‘‘neurotic’’ ones, to present all kinds of somatic complaints. Some doctors called it the ‘‘chronic koulchisis’’, a word coined from the words ‘‘koulou chai’’ which means everything in Arabic. Every single part of the body was said to be aching. Some young doctors pushed the patients to describe more than 30 locations of painful or unpleasant sensations. This presentation is now rarely seen in psychiatric settings, and even in primary care. If the hypochondriacal syndromes almost disappeared, at least from the patients seen by psychiatrists, the question is to know where they went. Part of the answer lies in the big effort made to improve the teaching on how to diagnose and to treat depression to undergraduates and in continuing medical education courses to general practitioners and to non-psychiatrist 1

Ibn Rushd University Psychiatric Center, Casablanca, Morocco

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specialists. One of the best indicators of the efficacy of such training is that for the past decade, while the pharmaceutical market progressed yearly 2 to 4%, the progression of the antidepressants reached 18 to 20%. At the same time, the benzodiazepine market declined significantly. The information of the general public also plays an important role in this shift. For example, the word depression in Arabic (‘‘Iktiaab’’), which is relatively new to the public, is more and more spontaneously used by patients to describe the way they feel about their symptoms. Another explanation is more cultural. Most of the Moroccans, 35 years ago, were illiterate, and interpreted systematically their depressive symptoms as a consequence of a somatic disease. Very few psychiatrists were available, less than 10 in 1979 for the entire country, and the expectation of a patient going to a doctor and presenting him with somatic complaints, was to take all kinds of lab tests, and to receive prescriptions of vitamins and tonics. On the other hand, the recognition of psychological symptoms of depression, such as sadness and anhedonia, was culturally hardly acceptable. They were identified by the family and the friends as signs of laziness and unhappiness with others. This does not mean that most depressed patients are now aware of their psychiatric disorder, and come with their diagnosis in hand, asking for an antidepressant prescription. Many psychiatric patients, and depressed ones are no exception, still ask for help from traditional healers before thinking of general practitioners. The behaviour then is the one of many hypochondriacal people in the world: looking for the doctor who will find the right treatment for the right diagnosis. My other personal experience was with Maghrebian workers who were migrants in France, and the picture was completely different, with severe hypochondriasis occurring after job accident or incident, when the possibility of obtaining a financial compensation was there. Small trauma occurring in workplaces led in some individuals to physical complaints, handicapping totally any professional reintegration. Patients were then completely focussed on the administrative and sometimes judicial processes, neglecting the medical help provided. The treating teams had the unpleasant feeling of non-cooperation of the patient, with a bad outcome, whatever the time and efforts invested. The hypochondriacal syndrome can be found in many mental disorders, including schizophrenia. But depression and anxiety disorders represent, by far, the best theoretical and pragmatic frameworks for the ‘‘unexplained somatic complaints’’, although they do not explain all cases of somatic complaints and health worry [1]. On the one hand, depression lowers the threshold of pain in patients suffering from this disorder, not to mention the anti-pain pharmacological activity of antidepressants. On the other, panic disorder is linked to hypochondriasis [2].

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This is why the use of antidepressants, especially the serotonin reuptake inhibitors, is one of the best pharmacological responses to the hypochondriacal syndrome, along with an appropriate psychological approach, depending on the personality and environment of the patient.

REFERENCES 1.

Creed F., Barsky A. (2004) A systematic review of the epidemiology of somatisation disorder and hypochondriasis. J. Psychosom. Res. 56: 391–408. Noyes R. Jr., Woodman C.L., Bodkin J.A., Yagla S.J. (2004) Hypochondriacal concerns in panic disorder and major depressive disorder: a comparison. Int. J. Psychiatry Med. 34: 143–154.

2.

3.10 Dimensional versus Categorical Approach to Obsessions, Delusions, and Hypochondriasis Joseph Zohar1

It is not always easy to differentiate delusions from obsessions and obsessions from hypochondriasis. An example is the case of obsessive–compulsive disorder (OCD) with poor insight [1]. On the basis of mental status examination alone, it would not be possible to differentiate obsessions with poor insight from delusions. The only way to differentiate the poor insight obsessions from delusions is by taking careful history [2]. If we find that in the past there was insight, this suggests that it is more likely to be an obsession than a delusion. In cases of pathological jealousy, it might even become more complicated, as we tend to diagnose this as a delusional disorder, although in some cases it could actually be an obsession. The issue of making the right diagnosis (i.e., differentiating obsessions with poor insight from delusions) is not just an academic exercise, since if we diagnose an obsession, then the treatment will be with an antiobsessive medication, while if we diagnose a delusion, then the treatment will be with an antipsychotic. Intuitively, it seems that obsessions with poor insight would probably benefit more from a combination of antiobsessive and antipsychotic medications. Although very little research has been done in this regard, a study by Eisen et al. [3] looked into this question, and the main finding was that there was no difference in the response between patients with poor insight and those with egodystonic obsessions. However, a more recent study by Ravi-Kishore 1

Division of Psychiatry, Chaim Sheba Medical Center, Tel-Hashomer, 52621 Israel

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et al. [4] found that patients with poor insight tended to respond less to antiobsessive medication. The issue of insight is often raised in hypochondriasis, as a way to differentiate it from OCD [5]. However, this is not always straightforward. Actually, the dimension of obsessionality and compulsivity is in the heart of hypochondriasis. Hypochondriasis is described as a preoccupation with fear of having or the idea that one has a serious disease, and the compulsive component is actually represented by the repeated examinations and tests that the patients go through as part of the disorder. Along this line of thought, at least some patients with hypochondriasis might be diagnosed as part of the obsessive–compulsive spectrum. Indeed, Hollander [6] includes hypochondriasis in this spectrum, and advocates active pursuit of obsessive–compulsive symptoms and OCD among relatives of patients with hypochondriasis as a way to explore this possibility in a given patient. At least in a subset of the obsessive–compulsive spectrum, namely body dysmorphic disorder (or dysmorphophobia), the differences between somatic concern, somatic delusion, and hypochondriasis become blurred. Many of these patients have convictions (i.e., the disorder is not egodystonic anymore), and they develop extensive ritualistic activity, ranging from spending hours looking in a mirror to repeated clinical examinations. For those patients, until a biological marker (which will help us to classify them appropriately) is found, we need to rely on careful clinical evaluation with a special emphasis on the history of the symptoms. However, along with our current clinical efforts to explore whether this is delusion, obsession, somatic delusion or hypochondriasis, we need, at least theoretically, to revisit the continuum hypothesis; that is, to re-examine whether we are dealing with a continuum ranging from egodystonic (like a classical case of OCD) to hypochondriasis (where the belief might be shaken—although not for very long) and up to somatic delusion, which might represent the severe end of the spectrum.

REFERENCES 1. 2. 3. 4. 5. 6.

American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, 4th ed. American Psychiatric Association: Washington, D.C. Montgomery S., Zohar J. (1999) Obsessive Compulsive Disorder. Dunitz: London. Eisen J.L., Rasmussen S.A., Phillips K.A., Price L.H., Davidson J., Lydiard R.B., Ninan P., Piggott T. (2001) Insight and treatment outcome in obsessive-compulsive disorder. Compr. Psychiatry 42: 494–497. Ravi-Kishore V., Samar R., Janardhan-Reddy Y.C., Chandrasekhar D.R., Thennarasu K. (2004) Clinical characteristics and treatment response in poor and good insight obsessive-compulsive disorder. Eur. Psychiatry 19: 202–208. Barsky A.J. (1992) Hypochondriasis and obsessive-compulsive disorder. Psychiatr. Clin. North Am. 15: 791–801. Hollander E. (1993) Obsessive-Compulsive Related Disorders. American Psychiatric Press: Washington, D.C.

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3.11 The Nosographic Complexity of Hypochondriasis and the Ambiguity of the Body H´ector P´erez-Rincon ´ 1 Every era has had its own way to express hypochondriasis. According to Oury [1], ‘‘The history of medicine may be deciphered through hypochondriacal accounts’’. On the other hand, in each era, medicine has had to reconceptualize hypochondriasis. Russell Noyes’ review should be considered, therefore, as the current equivalent to the ‘‘mise au point savante’’ which Jean-Louis Brachet [2] and Fr´ederic Dubois D’Amiens [3] carried out at their time. Nevertheless, the new nosographic paradigm should not lead us to forget the semiological and psychopathological traditions of classic psychiatry. As Kuhn pointed out [4], ‘‘paradigm changes’’ in scientific revolutions do not completely erase the previous paradigm, which may even return in time in a different guise. Psychiatry is not an exception to this law. For instance, it would be useful to re-propose the classic dichotomy between a merely psychical hypochondria sine materia and a hypochondria cum materia resulting from ‘‘real abnormal perceptions’’. In this context, the hypochondriacal experience was linked to the concept of c´enesthopathie, a theoretical and clinical notion from French psychiatry, which is of great heuristic interest but has never been accepted by Anglo-Saxon psychiatry. Another classic distinction was established according to the degree of verisimilitude of hypochondriacal complaints. On the one hand there would be a hypochondria minor, organized around a neurotic structure, and on the other a hypochondria major, where the clearly absurd nature of the complaints reaches the level of a true delusional system. The best example of the latter would be the d´elire hypocondriaque described by Jules Cotard [5]. In a hypochondriacal condition, the ‘‘silent appearance of a normal body is broken down’’ [6]. ‘‘Such a state underlies the ambiguous value of a body going beyond the condition of being a body and having a body, and falls in a contradiction where the body is at the same time the very Self and a part from the outside world in the perception each one has from his body. Similarly, the body supports my existence and at the same time is a burden and a weight which I have to bear’’ [7]. Marcel Proust [8] pointed out such an ambiguity as follows: ‘‘It is in sickness when we realize we do not live by ourselves, but chained to a Self from a different realm from which we are separated by abysms, which does not knows us and cannot understand us: our body’’. In a way, the ‘‘real’’ somatic patient and a hypochondriacal one may be distinguished in that the former suffers from an exogenous transformation in 1 Instituto Nacional de Psiquiatr´ıa Ram´on de la Fuente, Calzada M´exico-Xochimilco 101, San Lorenzo Huipulco, Tlalpan 14370, M´exico

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his body, which he incorporates in a personal way and which he overcomes by adapting himself to it. In contrast, for a hypochondriacal patient, the body, insofar it stands for his world, is experienced as transformed and alien. The ambiguous character of the body, placed between the limits of the Self and the outside world, the realm of language and communication, is pointed out once again. Here is how the Mexican poetess Veronica Volkov [9] expresses it: ´ ‘‘Only in skin do we exist/faint atmosphere between the visceral night/and the other night’’. Thus, hypochondriasis becomes a communication system. For Maurel [10], it is always a two-character drama, whereas, for Jean-Louis Place [11], in hypochondriasis there is a ‘‘coming together of a feeling, an individual dynamic and a discourse’’. This is why hypochondriasis should also be studied through an approach that takes into account the relationships between the ability (or disability) to express emotions verbally [12] and the somatic use of language to communicate psychological suffering. The specular concepts of alexithymia and somatothymia [13] may be highly useful tools to understand the nature of hypochondriasis, to explain its clinical expression and to build a new conceptualization.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Oury J. (1993) Hypocondrie. In: L’Apport Freudien, P. Kaufmann (Ed). Bordas: Paris, pp. 155–162. Brachet J.-L. (1844) Trait´e Complet de l’Hypochondrie. Bailli`ere et Savy: Paris. Dubois d’Amiens E.F. (1933) Histoire Philosophique de l’Hypocondrie et de l’Hyst´erie. Librairie de Deville Cavellin: Paris. Kuhn T.S. (1962) The Structure of Scientific Revolutions. University of Chicago Press: Chicago. Cotard J. (1999) On nihilistic delusion. In: Anthology of French Language Psychiatric Texts, F.-R. Cousin, J. Garrab´e, D. Morozov (Eds). Institut Synth´elabo: Le PlessisRobinson, pp. 288–317. Jaspers K. (1913) Allgemeine Psychopathologie. Springer: Berlin. Follin S., Azoulay J. (1961) Hypochondria. In : Les Alt´erations de la Conscience de Soi. Encyclop´edie M´edico-Chirurgical, Psychiatrie, 37125 A 10. Edition Techniques: Paris, pp. 8–14. Proust M. (1954) Le Cˆot´e de Guermantes I. Gallimard: Paris. Volkov V. (1979) Litoral de Tinta. Universidad Nacional Autonoma de M´exico: ´ M´exico. Maurel H. (1975) Actualit´e de l’Hypocondrie. Masson: Paris. Place J.-C. (1984) Contribution a` l’histoire de l’hypocondrie. Th`ese, University of Paris. P´erez-Rincon ´ H. (1997) Alexithymia considered as a survival of an archaic structure of language. Importance of Bruno Snell’s theories. New Trends Exp. Clin. Psychiatry 13: 159–160. Stoudemire A. (1991) Somatothymia, Parts I and II. Psychosomatics 32: 365–381.

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3.12 Hypochondriasis: Is There a Promising Treatment? Tewfik K. Daradkeh1 Hippocrates used the term hypochondrium in the fourth century B.C. to refer to the anatomic area below the ribs. Later, the term hypochondriasis emerged to refer to the ill effects upon the psyche and soma of humours or fluids that emanate from the hypochondrium and cause disease. The key feature of hypochondriasis is an abnormal concern that one is developing or has a serious illness. These persons may not claim particular symptoms, but are often preoccupied with health and avoiding germs. They may focus excessively on minor bodily signs and are most troubled by their tendency to believe that these signs imply development of a severe condition. In spite of their concerns about having illnesses undiagnosed by physicians, these patients do not tend to show typical anxiety nor do they seem to have poor health despite excessive use of health remedies. They seem to overinterpret bodily signs and are not relieved by reassurances that they are healthy. Patients with hypochondriasis believe good health is defined as a relatively symptom-free state. Onset of hypochondriasis can occur in people of any age, and is associated with dissatisfaction with medical care, doctor shopping, and deteriorating interpersonal relationships. Hypochondriasis can occur as an independent disorder (primary hypochondriasis) or as part of another underlying psychiatric disorder (e.g., depression, anxiety disorder). However, high rates of comorbidity have raised doubts about its independent status. The narrow ICD-10 and DSM-IV definition of hypochondriasis makes it rarely used, yet does not prevent extensive diagnosis overlap. On the basis of scientific evidence, a new empirically established hypochondriasis diagnosis was proposed to allow better diagnostic performance and permit categorization of the disorder into mild and severe forms [1]. This approach requires rumination about illness and at least one of five symptom clusters in order to make the diagnosis. Hypochondriasis has been a neglected subject, and in the past there has been considerable pessimism over its treatment. Doctors have regarded these as ‘‘ill-worried’’, ‘‘difficult to treat’’, or people who ‘‘have nothing wrong’’, and patients have not been satisfied with the care they have received. Russell Noyes has superbly reviewed the scientific evidence concerning the validity, aetiology, and the new emerging promising treatment of the disorder. Noyes et al. [2] studied the interpersonal model of hypochondriasis, which regards the condition as a care-eliciting behaviour. By communicating their 1 Department of Neuroscience, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan

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anxiety and distress over physical symptoms to other people, patients with hypochondriasis hope to obtain care and concern. The study showed that hypochondriacal people are insecurely attached to other people. They, therefore, are likely to feel insecure in the physician–patient relationship, which can lead to problems with health care satisfaction. Many of these patients see physicians as unskilled and uncaring, and feel their relationship with the physician suffer because of poor communication. Physicians need to be more aware of hypochondriasis to improve physician–patient relationship. Noyes et al. [3] presented some evidence that childhood adversity such as physical and sexual abuse, becoming seriously ill as a child, or having parents who are neglectful or overly attentive during a child’s illness, can contribute to hypochondriasis in adulthood. The treatment of hypochondriasis has traditionally been difficult. Where it is secondary to another condition, it usually resolves with treatment of the primary disorder. For example, hypochondriasis that is secondary to depression will usually resolve when the depression is successfully treated. Recognition and early diagnosis are important. Reassurance, combined with a serious appraisal of symptoms and an explanation of psychological factors, may then be effective. It is not enough simply to tell the patient that there is nothing wrong. It is important to acknowledge the patient’s distress and provide an alternative model, introducing psychological factors. A dismissive attitude that ‘‘it is all in your head’’ is counterproductive. Management regimes based on regular, brief appointments with one key doctor, and avoiding admissions to hospital are useful. They have been found to greatly improve physical functioning and cut costs for investigations and hospital admissions by one-third. Various drug treatments and talking therapies are beginning to be evaluated with controlled trials. Even in chronic cases, about 50% of patients improve with treatment. Until recently, no specific treatment has been clearly demonstrated to be effective. In a randomized clinical trial, patients receiving cognitivebehavioural therapy had significantly lower levels of hypochondriacal symptoms, beliefs, attitudes, and health-related anxiety than controls [4]. They also had less impairment of social role functioning. However, hypochondriacal somatic symptoms did not improve significantly. Case reports suggest that tricyclic antidepressants are helpful. There is better evidence for the efficacy of selective serotonin reuptake inhibitors. Preliminary results from a controlled trial indicate a better response to fluoxetine than placebo, although the placebo effect is large. In conclusion, hypochondriasis is common and can cause considerable distress, iatrogenic illness, and costs to health services. Diagnosis is often delayed, which exacerbates the condition. Greater awareness and the expansion of liaison psychiatry should correct this. There is growing evidence for the efficacy of treatments, particularly for cognitive-behavioural therapy and

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selective serotonin reuptake inhibitors. Finally, it seems that the traditional pessimism regarding treatment of hypochondriasis is no longer warranted and, as Noyes points out, now we must expand options, broaden their acceptance, and make effective treatment widely available for patients who, we should never forget, are truly suffering.

REFERENCES 1. 2. 3. 4.

Fink P., Ombol E., Sparle K.C., Frostholm L., Olesen F. (2004) A new, empirically established hypochondriasis diagnosis. Am. J. Psychiatry 161: 1680–1691. Noyes R., Stuart S., Langbehn D.R., Happel R.L., Longley S.L., Muller B.A., Yagla S.J. (2003) Test of an interpersonal model on hypochondriasis. Psychosom. Med. 65: 292–300. Noyes R., Stuart S., Langbehn D.R., Happel R.L., Longley S.L., Yagla S.J. (2002) Childhood antecedents of hypochondriasis. Psychosomatics 43: 282–289. Barsky A.J., Ahem D.K. (2004) Cognitive behavior therapy for hypochondriasis: a randomized controlled trial. JAMA 291: 1464–1470.

CHAPTER

4 Body Dysmorphic Disorder: A Review Giulio Perugi1,2 and Franco Frare3 1

Department of Psychiatry, University of Pisa, Via Roma 67, 56100 Pisa, Italy 2 Institute of Behavioural Science G. De Lisio, Carrara-Pisa, Italy 3 Adults Mental Health Unit, Pistoia, Italy

INTRODUCTION Body dysmorphic disorder (BDD) is a relatively common and often impairing mental disorder, characterized by a persistent preoccupation with an imagined anomaly in appearance (such as ‘‘large’’ nose, ‘‘excessive’’ sweating, or facial ‘‘scarring’’). Even if a slight physical defect is present, the subject’s concern about this is markedly exaggerated. The preoccupation can be very pervasive. It typically causes significant and often severe distress, impaired functioning, social withdrawal, repeated attempts to correct the imagined defect, and may even lead to suicide. The preoccupation cannot be accounted for better by any other mental disorder, such as anorexia nervosa or gender identity disorder [1]. BDD has long been described in European and Japanese literature under a variety of names, the most common being ‘‘dysmorphophobia’’, a term coined by the Italian physician Enrico Morselli in his original description more than 100 years ago [2]. At the turn of the last century, other European authors, such as Janet [3] and Kraepelin [4], described the syndrome and considered it as a variant of obsessive neurosis. Janet regarded the ‘‘obsession de la honte de corps’’ (obsession with the shame of the body) as a relatively common, but often overlooked, disorder, and emphasized the extreme shame that BDD patients experience, often leading to severe social withdrawal. Psychoanalytical literature contains a classical case of BDD: the ‘‘hypochondriacal paranoia’’ experienced by the Wolf Man [5]. Other terms used to describe BDD include ‘‘beauty hypochondria’’ (Schonheitshhyponcondrie), ¨ Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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‘‘dermatological hypochondriasis’’, ‘‘one who is worried about being ugly’’ (H¨asslichkeitskummer). Most authors emphasize the ‘‘tormenting’’ ego¨ dystonic character of body dysmorphic concerns and the way they typically ‘‘dominate’’ the patient’s life, so that ‘‘nothing else has significance anymore’’ [6–8]. Other authors focus on the impairment of insight and classify the syndrome as a monosymptomatic hypochondriacal psychosis, along with the delusion of parasitosis and the olfactory reference syndrome (the delusional belief that one emits an offensive body odour) [9–11]. For a long time, however, BDD has been often interpreted as a non-specific symptom of several mental disorders, such as schizophrenia, mood disorders, personality disorders, organic mental disorders, and substance-related disorders [12–14]. Only recently has it been recognized as a specific syndrome and as an autonomous diagnostic category [9, 15, 16]. Despite its presence in the European literature, BDD was not included in diagnostic systems until the publication of the DSM-III [17] and the ICD-10 [18]. The DSM-III mentioned dysmorphophobia as an example of atypical somatoform disorder (because of its focus on somatic concerns) without providing any diagnostic criteria. The DSM-III-R [19] introduced the label BDD and continued to classify the condition as a somatoform disorder, but introduced a distinction according to the degree of impairment of insight: if such impairment was absent, then the condition was regarded as a delusional disorder. This distinction, however, was not supported by the growing evidence [20–22] that BDD is a unitary disorder, of which delusional dysmorphophobia is a more severe form. In recognition of this evidence, the DSM-IV [1] allowed patients with delusional BDD to receive a diagnosis of both BDD and delusional disorder. The ICD-10 classifies non-delusional BDD as a variant of hypochondriacal disorder. Delusional BDD is instead classified as a variant of delusional syndrome. Differently from the DSM-IV, the ICD-10 does not allow to use both the above diagnoses in patients with delusional body dysmorphic syndrome.

EPIDEMIOLOGY BDD appears not to be a rare disorder in the general population. Most studies reported rates ranging from 0.7 to 2.2% [23–26]. Studies amongst college student populations reported rates of 4.0–5.3% [27, 28]. As expected, BDD seems to be quite prevalent amongst patients seeking cosmetic surgery and dermatological treatment. In a study carried out in a dermatological setting, 8.8% of patients seeking treatment for acne screened positive for BDD [29], and another study found a prevalence of 12% among dermatological patients [30]. Rates among cosmetic surgery patients may be even higher, with reports of 6–20% [31–35].

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Furthermore, BDD shows up rather frequently amongst subjects seen in clinical settings for other psychiatric disorders, such as depressive and anxiety disorders. Rates of 14–42% are reported in subjects with atypical major depression [36–38]. In one such study, BDD was more common than most other major psychiatric disorders, including obsessive–compulsive disorder (OCD), generalized anxiety disorder, social anxiety, and substance use disorders [38]. The prevalence of BDD among patients with non-atypical major depression was found to be significantly lower (5%) [36]. Fairly high rates of BDD (11–13%) are also reported among patients with social anxiety disorder [39, 40]. BDD may show up frequently among patients with OCD (8–37%), and this is one of the factors that led some authors to hypothesize a spectrum relationship between these disorders [40–44]. BDD often remains unrecognized in medical settings, because of patients’ shame and reluctance to reveal their concerns and the fact that clinicians only rarely inquire specifically about these concerns [42, 45]. In a study amongst general outpatients, the disorder was missed by the clinician in every case, despite the fact that body dysmorphic symptoms were one of the reasons for seeking treatment in more than half of the patients [46, 47]. With regard to gender distribution, available studies have yielded contrasting results. The largest published series reports an almost equal incidence of the disorder across genders, with 51% of patients being men [48]. Other studies have shown a preponderance of men [41, 49] or women [50–52]. Differences in referral patterns, inclusion/exclusion criteria, and severity of illness may account for these discrepancies. Two studies have examined possible gender-related differences in clinical features of BDD. One study [48] found that females were more likely than males to focus on their hips and weight; to be concerned about defects in their skin, camouflaging these with make-up; and to have comorbid bulimia nervosa. On the other hand, men were more likely to be preoccupied with body-building and the size of their genitals; to be concerned about hair loss, using a hat for camouflaging; and to have alcohol-related disorders. The other study [50] found that women were more likely to focus on their breasts and legs, constantly checking their appearance in mirrors and dressing to camouflage perceived defects, and to have concomitant bulimia, generalized anxiety disorder, and panic disorder. On the other hand, men were more likely to focus on their genitals, height, and excessive body hair, and to suffer from lifetime comorbid bipolar disorder. Available data from clinical and retrospective studies have indicated that BDD generally begins during adolescence, with a mean age at onset of 16–17 years, and has a chronic, unremitting course, with symptoms persisting for years, even decades, sometimes worsening over time [8, 48, 53]. A vast majority of the BDD patients studied had never been married (71–89%), and a rather high percentage (38–53%) were unemployed [8, 48, 53].

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Many years (ranging from 9 to 16) would seem usually to pass before the patient is referred for psychiatric treatment [48, 53]. In many cases, the presence of BDD may even pass unnoticed if the patient is not specifically questioned, because of feelings of shame on the part of the patient or diminished insight into his or her concerns. A comparison between psychiatric outpatients diagnosed using an unstructured clinical interview and others diagnosed using a structured interview, the Structured Clinical Interview for DSM-IV (SCID), showed that no patient had been diagnosed with BDD in the first sample, whereas 3.2% patients had been diagnosed in the second sample [47]. It has been estimated that less than 10% of BDD patients receive adequate treatment. A retrospective follow-up chart review study of patients previously treated for BDD indicates that a substantial percentage attained partial remission (with a reduction in the number, frequency, and intensity of body dysmorphic concerns and associated compulsive behaviours), but only a minority were able to achieve and maintain full remission [54].

CLINICAL FEATURES Subjects with BDD are concerned that some part or area of their body or aspect of their appearance is unattractive, ugly, deformed, misshapen, or ‘‘not right’’, when the perceived flaw is actually minimal or non-existent. Some patients actually describe themselves as hideous, repulsive, and monstrous. Patients are concerned about their perceived physical defects, which they cannot tolerate, and they are fearful of being rejected or judged negatively by other people because of these supposed defects. On the other hand, such patients tend not to fear or shun any ugliness or deformity they may note in others. Generally, a BDD subject’s concerns are totally unremitting despite any external reassurance. Clear indications of an attractive appearance, such as being courted or receiving compliments about his or her good looks, have no beneficial effect. Preoccupations about physical defects may involve a subject’s overall appearance (simply because there are concerns about too many body areas to be specific), the general size and shape of the body, or single body parts such as the skin, nose, eyes, hair, eyebrows, ears, mouth, teeth, breasts, buttocks, or genitals. Features that may differentiate body dysmorphic concerns from normal ones are, apart from excessive worry about a non-existent or minimal defect, the number and intensity of such preoccupations and the vague way in which they are expressed by patients. Most frequently, preoccupations involve the skin or the face, either taken as a whole or because of specific areas such as the nose, eyes, or ears. However, any area of the body or physical feature may become involved

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in BDD preoccupations, and patients may focus their concern on either single or multiple aspects of their body image. About one-third of patients tend to be concerned about many different body areas simultaneously, and body dysmorphic concerns generally shift from one body part to another over time [42, 53]. Patients with BDD generally think about their perceived defects for a large part of their waking hours (3–8 h a day, according to Phillips [45]). BDD thoughts are generally difficult to resist or control and are very distressing, often being described as intensely painful, tormenting, or devastating: even early descriptions of the disorder referred to the ‘‘tormenting’’ character of body dysmorphic concerns and the ‘‘miserable’’ quality of the patient’s existence [2, 6, 7]. BDD preoccupations are often described as obsessive in character. However, in comparison with the obsessive thoughts typically found in OCD, dysmorphic concerns are characterized by a less-defined ego-dystonic character, with patients showing varying levels of adherence to and insight into their concerns. Before treatment, most patients have a reduced level of insight and may often be fully delusional. According to one study [22], more than half of the BDD patients were delusional for a significant length of time. Delusional subjects did not differ significantly from other BDD patients with regard to most demographic and clinical features. It would seem that insight may shift over time in many patients, with body dysmorphic concerns varying in character over a continuum, ranging from obsessive preoccupations, to overvalued ideas, to full delusional thoughts. Clinical experience would suggest in fact that stress and social exposure may cause some patients to have less insight. In addition to concerns about their appearance, most patients also tend to fear specifically that others may take particular notice of their supposed defect, focus on it during social or public occasions and stare at it, talk about it, or mock it. These ideas, too, may range over a continuum from obsession to delusion, in different patients and over time. BDD patients have been found to be remarkably rejection-sensitive, and have a reduced self-esteem, with prominent feelings of unworthiness, defectiveness, embarrassment, and shame [47, 55]. An often strongly held belief is that the only way to improve self-esteem is to improve the way the individual looks. Some authors have suggested that the main cognitive feature of BDD is an excessive preoccupation with looking defective and unattractive, coupled with the belief that the perceived defect reveals a personal inadequacy [56]. An alternative view is that a BDD patient’s excessive preoccupation with appearance is related more to an internal aversion towards his or her own appearance than to a concern about being evaluated by others [57]. Nearly all patients with BDD (more than 90%) show repetitive, timeconsuming, and compulsive behaviours related to their concerns [22, 53].

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Their intent is generally to examine, hide, improve, correct, or seek reassurance about their perceived defect. The most common behaviour is to check the perceived flaw in appearance in mirrors for several hours a day. Some patients may expand their checking to include many other reflecting surfaces, such as compact discs, windows, shop glasses, spoons, faucets, and any number of other reflecting surfaces. Sometimes, they may seek out special lighting conditions, or repeatedly photograph themselves. On the contrary, other patients may avoid all reflecting surfaces because of what they perceive to be their monstrous reflection. Individuals with BDD often compare their appearance with that of others, compulsively seek reassurance about the perceived flaw (generally from relatives or close friends), or attempt to convince others of their ugliness. Reassurance-seeking compulsive behaviours may be especially tormenting for both patients and close relatives, since positive verbal feedback about appearance has little beneficial effect. BDD patients are usually very worried also about being observed by or speaking with persons outside their circle of family and close friends, fearing that their defect may be noticed. As a result, another very common compulsive behaviour is excessive grooming and/or trying to camouflage their perceived flaw with several, sometimes bizarre, methods, involving their hair, a wig, make-up, their hands or body position, or articles of clothing or accessories such as a hat, scarf or sunglasses, or even a mask or hood. BDD patients may also engage in other compulsive behaviours, such as dieting, excessive exercising, using anabolic steroids, touching or measuring the body part, comparing their appearance with those of people on TV or in movies, buying excessive amounts of beauty products, changing clothes repeatedly, or meticulously hoarding and reading books and magazines concerning physical appearance and shape, as well as all possible information about their particular perceived defect. Another very common feature is the persistent search for a medical ‘‘cure’’ for their defect: most patients eventually seek corrective treatment for their perceived defects, such as cosmetic surgery [49], or dental [42], orthopaedic, dermatological [58], or other medical treatments. A majority of patients seen in a psychiatric setting have already received some such treatment, most frequently dermatological treatment and/or surgery [22, 59]. Patients’ concerns are usually quite resistant to any positive comments or reassurance regarding their appearance which they might receive from consulted physicians, and this can result in patients going ‘‘doctor shopping’’ or hounding the professional with repeated and excessive visits until they are granted the treatment they crave. The medical literature notes that BDD patients request extensive work-ups, consult numerous physicians, and pressure them to prescribe and perform unsuitable and ineffective treatments and interventions [58]. Surgery and non-psychiatric medical treatments, however, generally have poor results: patients have wholly unrealistic and

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often vague expectations about the results of treatments, which usually leave them unsatisfied. Body dysmorphic concerns usually do not remit and may actually worsen: either the patient begins to worry about the results of the treatment, or remains just as dissatisfied with his or her appearance because of a new or remaining perceived defect or because another body part has become the new focus of concern [16, 48, 49, 58, 59]. This may often prompt the patient to seek a ‘‘better’’ surgeon or physician, and thus multiple procedures may be undergone in the search for a physical solution to a psychiatric problem. In some cases, the patient may become suicidal or behave violently towards the treating physician [8]. Some patients may even perform, to their own considerable risk, ‘‘do-it-yourself’’ surgery [35, 47]. One-third of all patients with BDD tend to show aggressive behaviour [53]. Differently from other mental disorders, BDD aggressiveness is generally restricted to subjects living in close contact with the patient and is closely related to body dysmorphic ideas. Patients may either seek to pressure or punish relatives whom they see as being insensitive because they don’t ‘‘understand’’ or ‘‘help’’ them to undergo a corrective treatment for their defect, or they may direct violence towards objects in their own homes as a result of their pent-up anger and frustration over their appearance. Another common behaviour in BDD patients is skin picking. It has been estimated that one-third of all subjects with this disorder pick at their skin with instruments such as needles, tweezers, or razor blades, in order to improve their appearance [60]. Because some patients may engage in skin picking for hours at a time every day, it may cause noticeable skin lesions (and in extreme cases, more severe health problems), which may worsen the patients’ concerns over their appearance, thus creating a vicious cycle. Muscle dysmorphia, in which a patient is preoccupied with the belief that he or she has too small a frame or is inadequately muscled, is a recently recognized syndrome, which, according to several authors, may represent a form of BDD and is much more common in men than in women [61–64]. This syndrome is associated with compulsive behaviours remarkably similar to those of typical BDD, such as camouflaging, mirror checking, reassurance seeking, as well as compulsive working out, excessive attention to diet, use of steroids, and with a general impairment of social and occupational functioning. Available data indicate that muscle dysmorphia may be rather common amongst amateur competitive body builders (53.6%), and those with muscle dysmorphia are likely also to have BDD preoccupations focused on body areas other than those associated with muscularity (33%) [62]. People with muscle dysmorphia are more likely than normal weightlifters to have body dissatisfaction, anabolic steroid use, subjective distress, and social-occupational dysfunctioning [63]. Because of BDD symptoms, patients typically experience severe subjective distress, neglect their academic or job performance and social activities, and

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have a poor quality of life. DeMarco et al. [65] found that BDD outpatients had markedly higher levels of perceived stress, with scores significantly higher than those of population norms and most clinical samples. Perceived stress scores were significantly correlated with BDD symptom severity. Phillips [66] reported that BDD outpatients’ quality of life scores were worse than those of the general population and of patients with depression, diabetes, or a recent myocardial infarction. The more severe the BDD symptoms and delusion, the poorer the mental health-related quality of life. Functional disability is a severe problem in patients with BDD, because they commonly avoid situations that may expose or exacerbate the perceived defect, or they experience severe distress, anxiety, and reduced interpersonal functioning in everyday social situations, such as shopping, dining in a restaurant, or going to the gym or the beach. Some patients have difficulty entering a clothes shop because they are afraid of their reflection or of having to remove camouflaging clothes. They may completely shun non-structured social interactions (such as going to a party or a club or dating) and sexual relationships or they may leave home only at night in order to avoid meeting people. In many cases, avoidance of social interactions may worsen and generalize and patients may become housebound for long periods. According to a case series, 89.6% of BDD patients avoided the usual social activities and 51.7% showed an impairment in their academic or job performance because of their symptoms [53]. Another study found similar rates of social impairment and an even greater prevalence (80%) of job/academic impairment; furthermore, one-third of BDD patients had been housebound for at least 1 week, and nearly half had been hospitalized for psychiatric treatment [48]. Many BDD patients may also experience suicidal ideation or make suicidal attempts. In a clinical sample [53], nearly half (45%) of BDD patients reported suicidal ideation. Phillips et al. [22] reported similar rates of suicidal ideation, as well as 30% of their sample having undertaken suicidal attempts because of BDD symptoms.

COMORBIDITY, DIFFERENTIAL DIAGNOSIS, AND RELATIONSHIP WITH OTHER MENTAL DISORDERS Most patients with BDD seen in psychiatric settings have at least one more mental disorder, with a mean of more than two lifetime comorbid Axis I disorders [48, 53]. A greater number of comorbid disorders is associated with greater functional impairment and morbidity [47]. The most common Axis I mental disorders appear to be major depression, OCD, social phobia, and substance use disorders [53, 67]. Social phobia has usually begun before the onset of BDD, whereas depression and substance use disorders typically develop after onset of BDD [48].

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Lifetime rates of comorbid mental disorders in the largest clinical series to date are 80% for major depression, 36% for social phobia, 30% for OCD, and 36% for substance use disorders. Another frequent comorbidity is with delusional disorders (27%), almost entirely attributable to the presence of delusional BDD [48]. Another large case series showed similar results, with major depression being found in 41% of patients, bipolar disorder in 31%, OCD in 41%, social phobia in 12%, and bulimia nervosa in 17% [53]. Other studies reported lower rates of comorbid mood disorders (26%), social phobia (16%), and OCD (6%) [52]. These discrepancies might be explained at least partially by differences in treatment setting, referral sources, or other factors. BDD is still classified as a somatoform disorder, due to the predominant feature of preoccupation with somatic complaints. However, it has been argued that, because of the very low comorbidity and lack of relevant clinical similarities with other somatoform disorders (except hypochondriasis), BDD is inappropriately classified in that general category. Similarities with hypochondriasis have been noted regarding exaggerated beliefs about the body, thoughts concerning the body provoking anxiety, and attempts to alleviate symptoms by reassurance seeking and body checking [56]. Epidemiological, clinical, and treatment studies have suggested a possible link of BDD with other mental disorders, such as mood disorders, OCD, social phobia, eating disorders, and delusional disorders. However, the paucity of studies making extensive comparisons between BDD and other disorders limits definitive conclusions about these relationships. It is most likely that the aetiology and pathophysiology of BDD and related disorders are multifactorial and complex, involving the interaction of multiple genetic (most likely multiple genes with small, additive effects), developmental, ethological, psychological, and psychosocial factors. It is also likely that BDD and related disorders are heterogeneous syndromes, which might be the clinical expression of several different pathophysiological paths, and that, amongst various pathogenetic factors, some will eventually be found to be peculiar to specific disorders and others to overlap.

Mood Disorders BDD has been postulated to be a symptom of depression [68] or to be related to depression [22]. BDD and mood disorders, both unipolar and bipolar, are highly comorbid [48, 53], and BDD subjects are at a significantly increased risk of suicidal behaviours. Both BDD and depression are characterized by low self-esteem, rejection sensitivity, and feelings of unworthiness [45, 55]. However, BDD and depression have some remarkable differences. Depressed patients typically neglect their appearance, rather than focusing on it. They may dislike their appearance, but they are unlikely to focus selectively on that

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aspect of themselves or to spend hours every day performing appearancerelated behaviours, such as mirror checking, grooming, camouflaging, or reassurance seeking. Moreover, BDD tends to have an earlier age of onset than depression and to run a chronic course, and is not clearly shown to have a greater frequency in women. Furthermore, currently available evidence suggests that the onset of BDD often precedes that of major depression, indicating that BDD is not simply a symptom of depression [48]. BDD seems to be responsive to serotonin reuptake inhibitors (SRIs), but not to other classes of antidepressants or to electroconvulsive therapy (ECT) [69, 70]. BDD has been reported to be the most common comorbid disorder in subjects with atypical depression [38]. This condition shares some clinical and treatment response features of BDD, such as increased rejection sensitivity and preferential response to SRIs. It has been hypothesized that BDD may in fact be an affective spectrum disorder [71, 72]. Treatment, comorbidity, and family history data are compatible with this hypothesis. However, while some elements suggest that BDD and depression may share some steps in the aetiological chain, the whole pattern of similarities and differences between these disorders indicates that BDD is neither a symptom nor a clinical variant of depression nor even closely related to it (despite having an association with atypical depression).

Obsessive–compulsive Disorder BDD has long been recognized as having some important similarities to OCD. Morselli [2] noted the ‘‘obsessional preoccupations’’ and ‘‘compulsive behaviours’’ that characterize these patients. Subsequently, Janet [3] classified the body dysmorphic syndrome as a subtype of ‘‘obsessive neurosis’’. Stekel [7] described the syndrome as ‘‘compulsive ideas. . . concerning the body’’ and noted the ‘‘obsessive’’ character of thoughts. More recently, several authors [24, 71, 73, 74] have proposed that BDD may belong to the ‘‘obsessive–compulsive spectrum’’, a group of disorders that share several features with OCD, including symptoms, sex ratio, course, comorbidity, familial loading, and treatment response to selective serotonin reuptake inhibitors (SSRIs). BDD shows some similarities to OCD: preoccupations that are often described as obsessional and persistent, and recurrent thoughts that are distressing, anxiety-producing, and difficult to resist or control [41, 53], although BDD concerns are accompanied by shame, embarrassment, humiliation, low self-esteem, rejection sensitivity, and referential thinking, which is not usually the case with OCD [45]. Most patients with BDD show repetitive behaviours, such as mirror checking, requests for reassurance, and skin picking, which resemble OCD compulsions. It should be noted, however, that the focus of concern differs between the disorders: physical appearance in BDD versus

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fears of contamination or other harm in OCD. Furthermore, it seems that BDD rituals are less likely to decrease anxiety [75]. Dysmorphophobic patients have been reported to have higher scores on the Leyton Obsessional Inventory than healthy controls [12], and two neuropsychological studies found that BDD patients have deficits similar to those reported for OCD [76, 77]. Other clinical similarities between BDD and OCD include the similar prevalence in both sexes, the onset during adolescence, and the chronic course [8]. BDD, like OCD, appears to respond to SRIs and to exposure and response prevention, although it has been suggested that BDD’s response to SRIs may differ from that of OCD [70] and BDD may not respond as well as OCD to behavioural therapy without a cognitive component [78]. There are also some indications of a joint familial loading for BDD and OCD. A controlled family study [24] investigated the frequency of OCD spectrum disorders (BDD, hypochondriasis, eating disorders, pathological grooming, and impulse control disorders) in probands with OCD and their first-degree relatives. BDD, hypochondriasis, and pathological grooming occurred more frequently in relatives of probands with OCD, whether or not those probands had received the same diagnosis. Some important differences between BDD and OCD have been reported. It would seem that beliefs concerning appearance that underlie BDD preoccupations generally involve poorer insight than that observed in OCD obsessions. BDD preoccupations frequently lose their ego-dystonic character, become more similar to overvalued ideas than obsessions, and may develop into full-blown delusional thinking [71]. Body dysmorphic concerns are experienced as being more natural than intrusive and are accepted and felt with a significant degree of conviction rather than being regarded as senseless. Consequently, resistance is often lacking. According to Phillips et al. [22], more than half of a case series of 100 BDD patients appeared to have been delusional for a significant period of time and a majority of patients had also had ideas or delusions of reference. An investigation into patients who had participated in a DSM-IV field trial for OCD showed that, in subjects with comorbid BDD, insight was significantly more impaired in connection with body dysmorphic preoccupations than with OCD symptoms [44]. In a comparative study, McKay et al. [79] reported that BDD patients were similar to OCD patients in terms of obsession and compulsiveness as well as depression and anxiety, but had higher levels of overvalued ideas. Saxena et al. [80] compared the clinical characteristics, symptom severity, and treatment response of 11 BDD and 96 OCD patients: they found that BDD was associated with greater severity of depressive and anxiety symptoms than OCD, but responded similarly to intensive, multi-modal treatment. Phillips et al. [81] compared three groups of patients with OCD (n = 53), BDD (n = 53), and both disorders (n = 33): they found no significant differences in terms of sex ratio and in most demographic, course or impairment variables.

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Illness severity and lifetime frequency of most associated mental disorders in probands and first-degree relatives were similar in the three groups. However, subjects with BDD were less likely to be married and more likely to have a worsening course of the illness and to have had suicidal ideation or behaviour. They also showed an earlier onset of major depression and higher lifetime rates of major depression, social phobia, and psychotic disorders, as well as a higher rate of substance abuse in first-degree relatives. Another study [82] compared the demographic characteristics, clinical features, and psychiatric comorbidity of 34 patients with BDD, 79 with OCD, and 24 with BDD-OCD. Subjects with BDD and BDD-OCD were significantly younger and experienced the onset of their disorder at a significantly younger age than subjects with OCD. The two BDD groups were also less likely to be married and more likely to be unemployed, and had achieved a lower level of education than OCD subjects, even when allowing for age. The three groups were significantly different in the presence of comorbid bulimia and alcohol-related and substance use disorders, with BDD-OCD patients showing the highest rate and OCD the lowest. BDD-OCD patients had more comorbid bipolar II disorder and social phobia than the other two groups. Patients with BDD and BDD-OCD were similar with regard to the presence of repetitive BDD-related behaviours, such as mirror checking or camouflaging, and showed a similar pattern of localization of the supposed physical defects. The only significant difference concerned localization in the face, which was more frequent in the BDD group. Another study [83] compared insight in BDD versus OCD patients. Subjects with BDD showed a significantly poorer global insight. They also showed a significantly poorer insight regarding the following components: conviction that the belief was accurate, perception of others’ opinions of the belief, explanation for differing views, willingness to consider the belief possibly wrong, and recognition that the belief had a psychiatric/psychological cause. In the BDD group, but not in the OCD one, poorer insight was associated with more severe symptoms of the disorder. In summary, available data do not contradict the concept of BDD as an OCD spectrum disorder. However, they also suggest that BDD should not be viewed as a simple clinical variant of OCD.

Social Anxiety Disorder BDD and social anxiety disorder have a similar early age at onset, sex ratio, chronic course, response to SSRIs and cognitive-behavioural therapy (CBT), and are both related to the fear of negative social evaluation. Feelings of shame, embarrassment and humiliation, low self-esteem, rejection sensitivity, as well as referential thinking may be found in both disorders. Avoidance of, or significant distress in, situations where the patients may be exposed

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to the judgement of others is another common feature. BDD also appears to be associated frequently with social anxiety disorder in clinical samples [48, 52, 53], and the Japanese literature considers BDD to be a form of social phobia [84, 85]. Some authors [86] actually viewed dysmorphophobia as a social phobia, as evidenced by high anxiety in social situations, avoidance of social situations, and fear of criticism and adverse comments about physical appearance. A neuropsychological study suggests that BDD patients and socially anxious subjects may share similar impairments in the processing of emotional verbal information, being more vulnerable than normal controls to distraction by emotional cues in general and by words related to their current concerns in particular [87]. However, patients with social anxiety disorder usually lack the extensive concern-related, time-consuming compulsive rituals that are so common in BDD subjects. Moreover, social anxiety symptoms are generally prompted by an external cue, such as actual or imagined exposure to social judgement, whereas BDD concerns are persistent, recurring, pervasive thoughts with an obsessional character and reduced or absent insight. It therefore appears likely that while BDD and social anxiety disorder may probably share some common pathophysiological factors, the former disorder is not a simple clinical variant of the latter.

Eating Disorders Recently, attention has been focused on the overlap of BDD with eating disorders. One striking similarity involves the primary feature of body image distortion in these disorders. Both BDD and eating disorders may be defined as the presence of excessive concerns about physical appearance in addition to body image dissatisfaction and distortion [56]. Additional similarities include a similar age at onset, overemphasis on appearance in connection with relationships and self-worth, avoidance of places, activities, and manners of dress that provoke self-consciousness about appearance, and performance of repetitive behaviours aimed at examining, hiding, improving, or correcting a perceived defect, such as mirror checking, body measuring, camouflaging, excessive exercise or dieting, and searching for beauty remedies [55]. Rosen and Ramirez [55] compared women with eating disorders and BDD in terms of body image and psychological adjustment and found that they were equally low in self-esteem and showed an equally severe body image disturbance. As in BDD, thought patterns of patients with eating disorders have been described as both overvalued ideas and delusions [88, 89]. Owing to similarities between BDD and eating disorders regarding cognitive, behavioural, and affective features, it has been proposed that these disorders be viewed as variants of a body image disorder [90].

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Differences between eating disorders and BDD can be identified in terms of location and type of body concern, in that BDD patients are preoccupied with specific body parts, whereas those with eating disorders are primarily concerned with their weight and overall body size (although this distinction is not always applicable). Moreover, BDD patients have been found to report more avoidance of activities due to self-consciousness about appearance and more negative self-evaluation due to appearance [55]. A major difficulty in viewing BDD and eating disorders as variants of a body image disorder involves gender differences in prevalence rates: while BDD is as common in men as in women, it is widely recognized that prevalence of eating disorders is much higher amongst women. Furthermore, both family history and treatment response do not strongly support the hypothesis that these disorders are closely related [42].

Delusional Disorder Clinical research has shown that both delusional and non-delusional forms of BDD do exist, causing a clinically important controversy about whether they are the same or different disorders. Some authors believe that the distinction is impossible from a phenomenological point of view and body dysmorphic beliefs are better classified as overvalued ideas [91]. Other authors, drawing from clinical and empirical evidence, suggest that the delusional and non-delusional variants may actually represent a single disorder, with body dysmorphic beliefs existing on a spectrum of insight ranging from obsessive preoccupations to delusional beliefs [20–22]. In acknowledgement of this possibility, DSM-IV currently allows delusional BDD to be double-coded as both BDD and delusional disorder, somatic type. This model is supported by the observation that, in some cases, the degree of certainty about the perceived defect changes over time, sometimes fluctuating between nondelusional and delusional thinking [71]. This fluctuation can be triggered by social interaction or stress and can make it difficult to categorize a patient’s preoccupation definitely as being either delusional or non-delusional. In addition, a comparison of individuals diagnosed with non-delusional and delusional BDD [22, 92] revealed that the groups did not differ significantly in terms of most variables measured, including demographics, phenomenology, course, comorbidity, family history, and treatment response. Both groups showed a favourable response to SRIs but not to antipsychotics alone, and the response to SRIs was sometimes associated with a significant increase in insight. However, higher scores for symptomatology and greater impairment of functioning were found in delusional subjects, indicating that the delusional variant may be a more severe form of the disorder. A range of current insight was found amongst the patients studied: they were described as having either good insight, fair insight, poor insight, or being currently

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delusional [93]. Finally, the old diagnostic tradition of regarding the body dysmorphic syndrome as a gateway to, or prodromal stage of, schizophrenia has been completely discredited: while BDD patients may develop functional disability deriving from distressing and pervasive thoughts about perceived defects, social avoidance and time-consuming compulsive behaviours, symptoms of the negative series are totally lacking, and most clinical and treatment response features appear to be completely different.

PERSONALITY, BODY IMAGE, AND NEUROPSYCHOLOGICAL PATTERN Clinical information about pre-morbid clinical features of BDD patients suggests a variable pattern of obsessive–compulsive, schizoid, narcissistic and self-critical, and avoidant-sensitive-insecure personality features, even in those cases where no specific personality disorder can be diagnosed [8]. Patients may be described by themselves and by their relatives as having been shy, perfectionist, austere children and adolescents who had few close friends and limited sexual experience, and rarely took part in group school or peer activities. Their drive towards perfection had been focused usually on self-betterment in terms of personal features or abilities concerning culture, appearance, or health, rather than on achieving success in group activities involving school, job, or sport. Personality disorders appear to be very frequent in BDD, with reported rates ranging from 57 to 100%: the most common personality disorders appear to be the avoidant, dependent, obsessive–compulsive, and paranoid [52, 94, 95]. Preliminary empirical reports indicate that BDD patients do not have deficits in general sensory processing, but that, quite to the contrary, they seem to have a super-normal discriminatory ability, with a reduced capacity for filtering out irrelevant stimuli and with a visual attention bias [75, 77]. According to one report, BDD patients assess facial proportions more accurately than controls or cosmetic surgery patients [96]. Another study found that BDD patients had a more accurate perception of nose size and shape than a control group [97]. However, a neuropsychological study found that, subjects with BDD overfocused on minor and irrelevant stimuli, suggesting that their beliefs about physical defects might arise from overfocusing on isolated details of their appearance [77]. Another report found that, in comparison with normal controls, BDD patients were more likely to focus their attention on an internal impression or feeling (rather than their external reflection in the mirror) and on specific aspects of their appearance [75]. In a study making a comparison between BDD, OCD, and normal subjects, individuals with BDD were less accurate than the normal subjects,

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but not than those in the OCD group, in identifying facial expressions of emotion, and they were more likely than the subjects in both other groups to wrongly identify emotional expressions as anger [98]. Another report by the same group suggested that BDD patients are more vulnerable than normal controls to distraction by emotional cues in general and by words related to their current body concerns in particular, in a way similar to socially anxious patients [87]. Another study suggested that BDD patients may also harbour an unrealistic ideal or requirement with regard to how they believe they should look, and that they may be more concerned with failure to achieve their own aesthetic standards than the perceived ideals of others [99].

AETIOLOGY AND BIOLOGICAL CORRELATES Little information is available so far with regard to the aetiology and pathophysiology of BDD. It seems likely, however, that the aetiology of this disorder is multifactorial, with biological, psychological, and sociocultural factors all playing a role. Biological theories of BDD focus on serotonin dysregulation and on neurological disturbances. Results from neuropsychological studies indicate that the pathogenesis of BDD might involve executive dysfunction, as well as impaired processing of facial images and emotional information [87, 98], which could involve frontostriatal and temporo-parieto-occipital pathology [77, 100]. A case report of a patient developing BDD after an inflammatory brain process in the frontotemporal region [101] would appear to confirm these suggestions, as would a magnetic resonance imaging study of regional brain volumes, indicating the presence of greater caudate left asymmetry in BDD patients compared with healthy controls [102]. Some authors have hypothesized that BDD may involve a dysfunction of the orbitofrontal or the orbitofrontal-amygdalar axis, similar to that in OCD [102], or a dysfunction in the temporal, parietal, or occipital lobes, which are involved in neurological disorders associated with disturbed body image [103]. It has also been proposed that BDD may result from a temporal lobe disturbance that produces a sensation of swelling throughout the body, so that the subject actually feels that the body has become distorted and views it as such [26]. Indirect evidence, based on the efficacy of treatment with SRIs, would suggest a pathophysiological role for the serotoninergic system. This has been supported by a case report of BDD occurring after chronic abuse of an antagonist of the serotonin system, ciproeptadine [104], and by a report of acute exacerbation of BDD after tryptophan depletion [105]. Cognitive-behavioural models of BDD have proposed a mixture of cultural factors, biological predispositions, psychological vulnerabilities, and

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early childhood experience [90]. Cultural attitudes emphasizing the importance of beauty and physical attractiveness, comparison with others or with an idealized standard, and social feedback are believed to play a role in the development and maintenance of BDD. Some authors have proposed developmental models of BDD, including biological factors predisposing towards fear of rejection and a drive for symmetry and perfection, and psychological vulnerabilities, such as low self-esteem and shyness, which may enhance self-consciousness [90]. It has also been suggested that the risk of developing BDD may be increased when critical events or traumatic incidents occur that involve the subject’s physical appearance. The most common example of this arises when a subject has been teased about his or her appearance [26] or when repeated criticism regarding appearance has been received from family members. Clinical evidence from case reports and small case series has suggested that an acute precipitating factor, such as a chance remark about the body part of concern, or a comment on appearance, may trigger the onset of symptoms [8, 90]. It has also been hypothesized that inharmonious family backgrounds or unfavourable childhood experiences producing enduring feelings of being unloved, insecure, and rejected might be risk factors for BDD [8]. A case series reports that a history of frequent teasing was present in 58% of BDD patients and a comment on appearance was mentioned as a trigger of symptoms in 19.5% of the group [48]. In a study that used the Parental Bonding Instrument, BDD patients reported parental care scores which were poorer than the published norms [78, 106]. Additional critical events reported by patients include physical and sexual abuse or assault, sexual harassment, public failure in athletics or dance, or physical injury or illness [107], although it is important to recognize the possibility that a patient’s recall of such events may be biased by negative affectivity. A psychoanalytical view of the development of BDD proposes that the disorder arises from an individual’s unconscious displacement of sexual or emotional conflict or feelings of guilt or poor self-image. It has also been suggested that the chosen body part is symbolic of yet another body part [26]. A major difficulty with this developmental model is the complete lack of empirical support [90].

TREATMENT During the last decade, a growing body of evidence has suggested that BDD may be treated effectively with two types of intervention: pharmacotherapy with SRIs and CBT. On the other hand, pharmacological treatment with medications other than SRIs, insight-oriented or supportive psychotherapy, and ECT have appeared generally to be ineffective in treating BDD [42, 108].

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Pharmacotherapy Initially, several case reports and small case series reported the satisfactory response of BDD to SRIs (clomipramine or an SSRI), while other medications appeared to be ineffective [8, 73, 109]. Subsequently, two large retrospective studies investigated extensively the effects of SRIs in BDD. The first reported data on 50 patients, which showed that 35 trials with SRIs had resulted in an overall improvement, whereas 18 trials with tricyclic antidepressants had led to no improvement [110]. A larger retrospective case series of 130 patients (who had received a total of 316 medications) found that 42% of 65 trials with an SRI had resulted in improvement, compared with 30% of 23 trials with monoamine oxidase inhibitors (MAOIs), 15% of 48 trials with tricyclics, 3% of trials with antipsychotics, 6% of trials with mood stabilizers or other medications, and 0% of trials with ECT [111]. The same author also reported a prospective case series of 45 patients, in whom 70% of 61 SRI trials resulted in improvement [111]. The author suggested that the higher response rate in the prospective case series was probably due to the higher doses and longer treatment trials used. More recently, a chart review of 90 patients who had been treated for up to 8 years indicated that 63.2% (55 out of 87 adequate SRI trials) had shown an improvement in BDD symptoms. Similar response rates were obtained with each type of SRI. Discontinuation of an effective SRI resulted in relapse in 83.8% (31/37) of cases. Response rates to selective SRI augmentation were: clomipramine, 44.4% (4/9) of trials; buspirone, 33.3% (12/36); lithium, 20.0% (1/5); methylphenidate, 16.7% (1/6), and antipsychotics, 15.4% (2/13) [54]. In a 10-week open-label fluvoxamine study, 10 (67%) of 15 patients responded (mean dose = 208.3 ± 63.4 mg/day); 6 patients (40.0%) were rated very much improved on the Clinical Global Impression (CGI), and 4 (26.7%) much improved. Significant improvement tended to occur after 10 weeks of treatment [112]. Another 16-week, open-label study of fluvoxamine found that 19 (63%) of 30 patients responded (mean dose = 238.3 ± 85.8 mg/day; mean time to response = 6.1 ± 3.7 weeks); 10 patients (33.3%) were rated very much improved on the CGI and 9 (30.0%) much improved [69]. Delusional and non-delusional subjects showed a similar improvement in BDD symptoms. In addition, insight improved significantly in both delusional and non-delusional subjects [93]. A more recent, 12-week, open-label study [113] investigated the efficacy of citalopram in 15 BDD patients (mean dose = 51.3 ± 16.9 mg/day; mean time to response = 4.6 ± 2.6 weeks). Eleven (73.3%) patients were deemed responders, with 6 (40.0%) patients being rated very much improved on the CGI and 4 (26.7%) much improved. Psychosocial functioning and mental health-related quality of life also improved significantly.

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With regard to controlled trials, a 16-week, double-blind crossover study of 40 patients (29 of which were randomized) found that clomipramine was more effective than desipramine [114]. At the end of the first phase of the study, 65% of patients had responded to clomipramine and 35% to desipramine. Clomipramine was superior to desipramine in improving obsessive body appearance concerns, repetitive behaviours, functional disability, and overall symptom severity. The presence of delusional BDD did not affect response to treatments. Another double-blind, placebo-controlled parallel-group study [115] found that 12-week fluoxetine treatment was significantly more effective than placebo in 67 BDD patients, with a response rate of 18 (53%) out of 34 subjects to fluoxetine and 6 (18%) out of 33 to placebo. The BDD symptoms of delusional patients were as likely as those of non-delusional patients to respond to fluoxetine and no delusional patients responded to placebo. In the sample as a whole, treatment response was independent of the duration and severity of BDD and the presence of major depression, obsessive–compulsive disorder, or a personality disorder. Fluoxetine treatment [116] in this sample was also associated with significantly greater improvement in the baseline impaired psychosocial functioning of BDD patients and with an improvement in mental health-related quality of life which approached significance. A decrease in the severity of BDD symptoms was correlated significantly with an improvement in functioning and quality of life. Response to medication usually results in a reduction of intensity of appearance concerns, decreased time spent preoccupied with the perceived defect, reduced distress, a decrease in performance of compulsive behaviours, and improved insight, as well as an improvement in functioning. Evidence from clinical studies and drug trials indicates that delusional BDD patients respond to SRIs [21, 22, 69, 114]. There have been some reports of the antipsychotic pimozide being effective in treating monosymptomatic hypochondriacal psychosis, including delusional BDD [10]. However, these reports have not been confirmed by larger case series [22], and available data would suggest that monotherapy with antipsychotics is not effective in delusional BDD. On the other hand, the addition of an atypical antipsychotic, such as risperidone, has been suggested as an augmentation therapy in delusional BDD [70]. Other possible augmentation strategies might be to add clomipramine to SSRIs, or to augment with lithium or a stimulant if the patient has severe depressive symptoms. Switching to another SRI or venlafaxine might prove useful if the patient has not responded to an SRI [70]. An open-label study of 13 patients who had not responded or had responded only partially to an SRI found that buspirone augmentation (mean dose = 48.3 ± 14.7 mg/day; mean time to response = 6.4 ± 1.7 weeks) was effective, although only in a minority of cases: 6 patients (46%) improved; 3 patients who had decreased the dose or discontinued buspirone experienced an increase in symptom

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severity, and BDD symptoms improved once again in the subject who resumed the previous dose. Several patients improved further with higher doses (70–90 mg/day) [117]. Clinical experience and chart reviews suggest that all SRIs may be effective for BDD [22, 42, 54, 73, 108, 110]. Relatively high SRI doses (analogous to those used for OCD and social anxiety disorder) are often necessary to treat BDD effectively, and treatment must be maintained for at least 10–12 weeks in order to determine efficacy, with long-term treatment often being required. Clinical experience and chart reviews also suggest that the efficacy of SRIs in BDD is usually sustained over time and that discontinuation of an effective SRI treatment will, in most cases, lead to relapse [54]. In conclusion, data from pharmacological treatment studies would suggest that SRIs are effective in the treatment of BDD, but more placebo-controlled treatment trials are needed to confirm these findings.

Cognitive-behavioural Therapy Although only a few controlled studies are available, encouraging results have been reported with various forms of behavioural and cognitive therapy for patients with BDD. Early case reports and multiple case studies have indicated a successful outcome with exposure therapy [118, 119], systematic desensitization [120], audio-visual self-confrontation [121], and cognitive plus behavioural techniques [122–126]. The most common treatment strategies include exposure (e.g., exposure of the perceived defect in social situations or exposure of the patient to the sight of his or her own body) with response prevention (e.g., helping patients to avoid compulsive behaviours by having them remove or cover mirrors, limit grooming time, stop using make-up, reduce the frequency of weighing, refrain from inspecting skin, and stop asking for feedback) [56, 90, 127, 128]. Cognitive restructuring is also a frequent component of treatment for BDD and involves primarily the identification of dysfunctional thoughts (such as the belief that an objective, rigid standard of beauty exists and that the self-worth of human beings must be evaluated on the sole basis of their appearance), which are then challenged through the evaluation of evidence and by encouraging the patient to interrupt negative self-statements of body dissatisfaction with more objective, neutral, sensory self-descriptions that are free of emotionally loaded self-criticism [56, 57, 90, 119]. Other techniques that have received attention in literature include skills training, psychoeducation, and reverse role-play (a role-play technique that requires patients to research and debate beliefs that are contrary to their own overvalued ideas) [56, 57, 90, 123, 125, 129]. Studies using these techniques have found these approaches to be effective for a majority of patients, with an improvement in BDD symptoms as well

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as in associated features such as depression, low self-esteem, avoidance, and anxiety. In a report on 5 patients, 4 improved through these techniques in 90-min sessions held 1 to 5 days per week, with the total number of sessions ranging from 12 to 48 [128]. In another open case series of 13 patients treated with group CBT, BDD symptoms improved significantly in twelve 90-min group sessions [129]. Another study of 10 patients who participated in an intensive behavioural therapy programme and then either took part in a 6-month maintenance programme or served as controls found that improvement was maintained for up to 2 years in both groups but that those patients participating in the maintenance group were more effective at managing limited symptom return [127, 130]. Two studies have used a waiting-list patient group as control. In a study of eight weekly 2-h sessions of group CBT, cognitive techniques associated with exposure and response prevention were effective with 27 (77%) of 35 women, with patients in the CBT group improving significantly more than those in the waiting-list control group [51]; however, these patients appeared to have relatively mild BDD, and some subjects may have been suffering from an eating disorder instead of BDD. Another pilot controlled study of 19 patients, randomly allocated to CBT or to a waiting-list control group, found a significantly greater improvement in BDD symptoms and in depressed mood in the former group [57]. It is unclear whether behavioural techniques alone are effective in treating BDD, with some studies suggesting that they are [127] and others indicating that cognitive restructuring is an essential component of treatment [78]. Furthermore, data on CBT, although promising, are from clinical open series and studies using a waiting-list control design, which does not check for therapist attention and other non-specific treatment factors. These studies often appear to involve a subgroup of patients who are less severely disturbed than those seen in clinical and pharmacological treatment studies; it is still uncertain whether CBT alone is effective with BDD patients who are severely depressed, suicidal, and delusional.

SUMMARY Consistent Evidence BDD appears to be quite prevalent in some clinical populations, such as patients seeking cosmetic surgery or dermatological treatment, and among subjects with other psychiatric disorders, such as depressive and anxiety disorders. BDD usually begins during adolescence, with a chronic, unremitting course, with symptoms persisting for years, even decades, sometimes worsening over time. Some patients have a reduced level of insight and may often

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be fully delusional with regard to their body dysmorphic concerns. Many BDD patients repeatedly search for and eventually receive non-psychiatric treatment, such as cosmetic surgery, or dental, orthopaedic, dermatological, or other medical treatments. These treatments often have poor results, and body dysmorphic concerns usually do not remit, with, at least in some cases, an actual worsening of the situation. Since, typically, because of their symptoms, BDD patients experience subjective distress, they often neglect their academic or job performance and social activities and experience severely impaired interpersonal functioning. Many BDD patients also report suicidal ideation or perform actual suicidal attempts. Historically, BDD has been deemed either to belong to the obsessive– compulsive spectrum or to be a form of somatic psychotic disorder. Available evidence, ranging from important clinical similarities to treatment outcome, does not contradict these views. However, this same evidence, including important differences in insight, would also suggest that BDD should not be viewed as a simple clinical variant of OCD. Clinical research has shown that both delusional and non-delusional forms of the syndrome do exist and that they do not differ significantly in several respects, including response to treatment, with the delusional variant, however, involving more severe symptoms and more impaired functioning. A growing body of evidence, derived from case reports, retrospective and prospective case series, chart reviews and open studies, and also a limited number of controlled studies, indicates that BDD may be treated effectively with two types of intervention: pharmacotherapy (with SRIs) and CBT. Other forms of treatment, such as medication with drugs other than SRIs, insight-oriented and supportive psychotherapy, and ECT appear generally to be ineffective. Delusional and non-delusional forms of BDD show a similar response to SRIs, with regard to symptoms, insight, functioning, and quality of life; the delusional score often improves with SRI treatment. CBT techniques most commonly reported as having been effective include exposure with response prevention, systematic desensitization, audio-visual self-confrontation, cognitive restructuring, skills training, and reverse role-play.

Incomplete Evidence BDD has been known and described intermittently in medical literature for more than a century under a variety of names and diagnostic categories. Current diagnostic classification as a somatoform and/or delusional disorder, according to the degree of insight, is under debate. Insight may shift over time in many patients, and delusional and non-delusional variants of BDD may actually be a single disorder, with body dysmorphic beliefs existing on a spectrum ranging from obsessive preoccupations to delusional beliefs.

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Long-term follow-up studies are necessary in order to explore the diagnostic stability of the syndrome. BDD is currently classified as a somatoform disorder due to the predominant feature of preoccupation with somatic complaints. It has been argued that, because of the very low comorbidity and lack of relevant clinical similarities to other somatoform disorders (except hypochondriasis), BDD is classified inappropriately in that general category. Epidemiological, clinical, and treatment studies suggest a possible link between BDD and other mental disorders, such as mood disorders, OCD, social phobia, eating disorders, and delusional disorders. The paucity of studies comparing BDD with other disorders limits definitive conclusions about these relationships. Furthermore, as long as the aetiopathogenesis of BDD is unknown, the exact nature of its relationship with other mental disorders will remain uncertain. While SRIs and CBT appear to represent effective treatment strategies for most BDD patients, further evidence from controlled studies is still needed to confirm these suggestions, and many topics of interest regarding optimal clinical management still require investigation. Information from prospective observations and naturalistic treatment studies about predictors of response, long-term course, and outcome of treated subjects should be gathered. It is unclear whether CBT and SRI monotherapies are likely to be equally effective amongst the majority of BDD patients or whether they are best applied to different subgroups of subjects (CBT studies seem to involve lessdisturbed patients than those seen in clinical and pharmacological treatment studies). It is also unclear which response predictors are most relevant to which treatment and what may be the indications for and possible additional benefit of the combination of SRIs with CBT. Additional information is needed regarding the optimal treatment length and the usefulness of longterm maintenance with both treatment strategies. It is also unclear whether behavioural techniques alone are effective in treating BDD or whether cognitive restructuring is a necessary component of treatment.

Areas Still Open to Research Although BDD appears not to be a rare disorder in the general population, epidemiological data are still lacking. For instance, available clinical and epidemiological studies have yielded contrasting results with regard to gender distribution and other demographic variables. Another area of interest is the development of effective diagnostic tools and clinical strategies to minimize under-recognition and under-treatment of BDD in clinical populations where it has been shown to be frequent. Several clinical aspects of BDD deserve further study. Some BDD patients seem to show aggressive behaviour that is largely restricted to subjects living

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in close proximity to them. It is not well established whether such behaviour should be considered as part of the body dysmorphic syndrome or whether it is related to other factors such as comorbidity. Muscle dysmorphia, in which a patient is preoccupied with the belief that he or she is too small of frame and inadequate in muscularity, is a recently recognized syndrome that may represent a form of BDD. In BDD, alterations of body image perception, sensory processing and/or cognitive patterns with regard to self-evaluation and referential thinking require further investigation. Preliminary empirical reports would seem to indicate that BDD patients, far from lacking in the area of general sensory processing, seem on the contrary to have a super-normal discriminatory ability with regard to facial proportions, but with a reduced capacity for filtering out irrelevant stimuli. This visual attention bias seems to be related to unrealistic internal ideals and expectations. BDD patients may also have an impaired ability to identify and discriminate between different facial expressions of emotion and they may suffer from an increased vulnerability to distraction by concern-related emotional cues. Biological, developmental, psychological, and sociocultural factors that would seem to be involved in the pathogenesis of BDD and that may deserve further investigation are: (a) the dysregulation of the serotonin system; (b) neurological disturbances leading to body image distortion and impaired processing of facial images and emotional information; (c) the biopsychological predisposition towards low self-esteem, shyness, and fear of rejection; (d) rigidly held beliefs about appearance and an increased drive for symmetry and perfection; (e) cultural attitudes emphasizing the importance of beauty and physical attractiveness; and (f) negative social feedback and critical events regarding appearance and social standing. Although medications other than SRIs appear to be generally ineffective if used as the main treatment in BDD, there is some preliminary suggestion that venlafaxine, buspirone, pimozide, lithium, methylphenidate, and atypical antipsychotics may be useful in augmenting SRIs. This has to be confirmed by further research. Prospective observations and naturalistic studies concerning course stability, predictors of treatment response, and long-term outcome of treated subjects represent areas that are almost unexplored. The questions of optimal treatment length and the effectiveness of long-term maintenance of treatment require additional study. Preliminary evidence would suggest that the greater efficacy of SRIs compared with other medications tends to persist over time and that the discontinuation of an effective SRI treatment will lead to relapse in most cases. Improvement of BDD symptoms as a result of CBT can be sustained over time, but participation in a long-term maintenance program is more likely to reduce the likelihood of symptom return.

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Commentaries 4.1 The Complexity of Body Dysmorphic Disorder Vilma Gabbay1 and Rachel G. Klein1 This comprehensive and thoughtful review of body dysmorphic disorder (BDD) clearly demonstrates the challenge the condition poses for diagnosis and treatment. The epidemiological and clinical data summarized document that BDD is not uncommon, is chronic, and is highly comorbid with other disorders, especially major depression disorder (MDD), obsessive–compulsive disorder (OCD), and social phobia. In addition, the very high prevalence of personality disorders in individuals with BDD attests to the complexity of its associated dysfunctions. Current evidence suggests that BDD has an early onset, likely to be in adolescence in many instances. Clinical similarity between adolescent and adult BDD documents that adolescent BDD, in a significant proportion, represents an early expression of adult BDD [1]. In adolescence, the differential diagnosis of BDD may be complicated by the normative prevalence of excessive concerns about minutiae of appearance in this age group. Unfortunately, in spite of the importance of detecting the disorder early, BDD in adolescence has attracted only minimal research and clinical attention; the disorder has gone almost unmentioned in the adolescent literature. Specific inquiry about possible BDD symptoms is almost never pursued in clinical pediatric psychiatric and other medical settings. Strikingly, systematic diagnostic interviews such as the Diagnostic Interview Schedule for Children Parent Version (DISC-IV) [2] and the Schedule for Affective Disorders and Schizophrenia for School-Age Children—Present and Lifetime (K-SADS-PL) [3], widely used in clinical research, do not include an assessment of BDD. This omission reflects the general failure to consider the presence of BDD in adolescence, and highlights the need for increased awareness in the medical community. The hope is that early identification and treatment of BDD may alter the chronic course of BDD. This possibility is fostered by the review’s clinical observation that relatively milder cases of BDD may respond to behavioural interventions. 1 New York University School of Medicine, Child Study Center, 577 First Avenue, New York, NY 10016, USA

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Patients almost never present with a main complaint of BDD, and comorbidity seems to be the rule. The overlapping clinical features of BDD with other disorders may account for why this relatively common and impairing disorder goes unrecognized. At the same time, high comorbidity creates a dilemma for classification. Could it be that BDD is heterogeneous, and that in some patients it is a complication of another disorder, that is, MDD? Such a clinical pattern is known to exist. For example, some patients may develop obsessive–compulsive symptoms in the context of an MDD episode, but these remit when the mood disorder is treated successfully. Although possible, this pattern is not the rule, since the onset of BDD often precedes that of MDD. In the past, symptoms of BDD were attributed to other psychiatric disorders, and it is only recently that BDD has been recognized as a specific disorder. Yet, controversy remains regarding the specific categorical classification of the disorder and the disorder’s ‘‘possible link to other mental disorders such as mood disorders, OCD, social phobia, eating disorders, and delusional disorders’’. Perugi and Frare pointedly note clinical distinctions between OCD and BDD, that is, the absence of ego-dystonic symptoms in BDD. In addition, we believe that a clinical distinction between BDD and social phobia is worth noting. Patients with BDD may avoid various social situations due to concerns about their perceived body defect, but this concern remains even when others are not present. In social phobia, the person’s anxiety about the opinion of others is relieved by removing themselves from public scrutiny. Unlike individuals with social phobia, those with BDD have no escape from their torment. BDD is a complex disorder and its expression depends on multi-factorial mechanisms such as environmental, psychosocial, biological, and genetic pathways. Perugi and Frare appropriately caution against allocating causal significance to childhood events recalled by patients with multiple psychiatric disorders, only one of which is BDD. The overlapping clinical presentation of BDD with other related disorders has led to several aetiological theories regarding the neurobiology of the disorder. Theories implicate serotonin dysregulation and abnormal activity of brain regions that are also found in OCD and MDD. However, a recent small neuroimaging study in BDD using single photon emission computed tomography (SPECT) did not confirm the types of abnormalities reported in OCD or MDD [4]. Immune system dysregulation may also be a factor in BDD. A putative subgroup of children with OCD and pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) display symptom onset and/or exacerbations that are temporally linked to streptococcal infections [5]. With respect to BDD, several case reports have noted a new onset or exacerbation of BDD following an inflammatory illness, suggesting

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that the clinical overlap of BDD with OCD may involve common biological pathways [6, 7]. As raised by Perugi and Frare, ‘‘It is likely that BDD and related disorders are heterogeneous syndromes which might be the clinical expression of several different pathophysiological paths and that, amongst various pathogenetic factors, some will eventually be found to be peculiar to specific disorders and others to overlap’’. Additionally, the limited comparison studies across disorders (clearly summarized in the review) have yielded conflicting results from which no scientific conclusions can be derived. As in all psychiatric disorders, findings are complicated by our inability to distinguish between state or trait dysfunctions.

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4.2 Preoccupation with Appearance: Limitations of Our Understanding and Treatment Jon E. Grant1 Most people are dissatisfied with some aspect of their appearance. In fact, more than half of all women and nearly half of all men in the United States 1 Department of Psychiatry and Human Behavior, Brown Medical School and Butler Hospital, 345 Blackstone Blvd., Providence, RI 02906, USA

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are dissatisfied with the way they look [1]. Although some concern about appearance seems to be normative, the scientific literature has grappled with how to understand and treat people whose preoccupations with appearance are excessive, cause significant personal distress, and result in functional impairment. Perugi and Frare provide a thorough overview of what is known about body dysmorphic disorder (BDD), its relationship to other psychiatric disorders, treatment options, and the limitations of our current knowledge. Having provided this background, the review raises several important, and as yet unanswered, questions concerning BDD: (a) what is the most meaningful way to understand BDD—somatoform disorder, affective spectrum disorder, obsessive–compulsive spectrum disorder, or delusional body image as seen in eating disorders? (b) what are the most effective treatments for BDD? and (c) where should future BDD research focus its energy? Perugi and Frare eloquently describe the nosological debates surrounding BDD. Their review highlights the similarities and important differences that BDD has to depression, social anxiety, obsessive–compulsive disorder (OCD), eating disorders, and delusional disorders. They caution, however, that there is a ‘‘paucity of studies making extensive comparisons between BDD and other disorders’’, and therefore our current knowledge of BDD’s relationship to other disorders may in fact shed little light on how to categorize this disorder. While highlighting the numerous descriptive studies of BDD, the authors recognize the paucity of research on aetiopathophysiology and treatment. This imbalance should make readers impatient about the current state of research in this area. Patients I treat with BDD are severely disabled and distressed. They do not care if BDD is included as a somatoform disorder, an affective spectrum disorder, or an obsessive–compulsive spectrum disorder. They want to understand what caused the disorder and they want effective treatment. As the authors remind us, however, ‘‘optimal clinical management still requires investigation’’. Although there are numerous case studies, open-label studies and chart reviews in the literature, only two double-blind pharmacological studies and two controlled psychotherapy studies have been published. Treatment decisions for patients with BDD, therefore, rely upon only four published studies with small, fairly homogeneous samples. Thus, our knowledge of effective treatments for BDD is simply too limited. Perhaps BDD is particularly difficult to treat because either our model for how we understand the disorder is flawed or we may in fact be treating multiple, related disorders with different pathophysiologies. The treatment studies that have been performed have, for the most part, used the hypothesis that BDD should be treated as one treats OCD—using high doses of serotonin reuptake inhibitors (SRIs) for long periods of time and cognitive-behavioural therapy. The problem with these treatment options is that there is little data to support their use, and the OCD model may not be an ideal fit for

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BDD. Furthermore, we recently completed a study wherein we found a strong association between BDD and substance use disorders [2]. The study found that approximately 49% of BDD patients have a lifetime substance use disorder. The elevated rate of substance use disorders in BDD may complicate how we understand BDD’s relationship to other disorders, and it highlights the difficulty in treating these patients. Perugi and Frare’s review should make us wonder whether the focus on aetiopathogenesis may not provide a greater wealth of information about treating these patients than studies of the relationship of BDD to other disorders. In response to the current limitations of our knowledge, the authors provide a useful and challenging agenda for future research. They recommend that several key areas should be examined: sensory processing and cognitive patterns, neurochemical dysregulation of the serotonin system, biopsychological predispositions, long-term follow-up studies, and more controlled studies. I would add that greater awareness of imaging techniques, genetic studies, treatment studies with comorbid conditions, and dose-ranging studies to examine the idea of higher dose SRIs may also be worthwhile. Perhaps with a clear focus for the next stage of BDD research, we will not only answer the diagnostic dilemma of this disorder but also provide clear treatment options for the people who suffer from it.

REFERENCES 1.

Pope H.G., Phillips K.A., Olivardia R. (2002) The Adonis Complex: How to Identify, Treat, and Prevent Body Obsession in Men and Boys. The Free Press: New York. Grant J.E., Menard W., Pagano M., Fay C., Phillips K.A. (2005) Substance use disorders in individuals with body dysmorphic disorder. J. Clin. Psychiatry 66: 309–316.

2.

4.3 Translational and Evolutionary Models of Body Dysmorphic Disorder Dan J. Stein1 Given that body dysmorphic disorder has only recently become the focus of systematic research, it is perhaps not surprising that our theories of its pathogenesis are partial at best. An increasing focus of research in the cognitive-affective neuroscience of psychiatric disorders is the development of translational and evolutionary animal models [1]. Laboratory models provide data on which to base clinical experiments, and clinical data in 1

University of Cape Town, South Africa

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turn provides hypotheses to test in molecular or behavioural experiments in different paradigms and species. In the case of anxiety disorders, a translational approach has proven particularly fertile [2, 3]. Basic science research on the neurocircuitry of fear processing has informed functional brain imaging studies of clinical subjects. Conversely, observations such as the responsiveness of anxiety disorders to selective serotonin reuptake inhibitors has encouraged increased attention to the role of the serotonergic system in laboratory studies of the molecular neurobiology of anxiety. It is notable that obsessive–compulsive disorder appears to have a rather different neurocircuitry from that of other anxiety disorders [4], suggesting that perhaps it should be classified differently. Whereas translational models focus on proximate mechanisms, evolutionary models focus on distal mechanisms—the way in which evolutionary history has created vulnerability to particular kinds of pathology. Evolutionary approaches to a range of psychiatric disorders, including mood and anxiety disorders, are becoming increasingly sophisticated [5, 6]. It has been suggested that anxiety disorders represent different kinds of ‘‘false alarm’’; ordinarily, such alarms enhance survival, but at times their threshold may be pathologically lowered [7]. In the case of body dysmorphic disorder, there is unfortunately no obvious animal or evolutionary model. This provides a considerable barrier for developing a sophisticated approach to delineating the relevant cognitive-affective neuroscience. Nevertheless, the growing literature on the importance of symmetry in determining what is attractive, both in animals and humans, may be particularly pertinent [8]. Although much of this literature is phenomenological in scope, there is every reason to also assess the relevant underlying psychobiology. Indeed, there is also a growing literature on the functional brain imaging of the assessment of facial attractiveness in humans [9, 10]. It might be speculated that body dysmorphic disorder represents an exaggeration of an evolutionarily conserved mechanism for assessing symmetry as part of judgements about attractiveness. Although cases of body dysmorphic disorder by proxy have been described, it is clear that, in the typical case, this exaggeration concerns self-asymmetry rather than asymmetry in others. This is consistent with the phenomenological overlap between body dysmorphic disorder and social anxiety (particularly in the East); there is heightened awareness of and criticism about self-presentation [11]. The idea that patients with body dysmorphic disorder are more prone to observe asymmetry is perhaps also consistent with evidence of superior perceptual abilities and increased aesthetics training in these patients [12]. As cognitive-affective neuroscience extends into the complex arena of social cognition [13], we can expect that the proximal and distal mechanisms involved in assessment of attractiveness, as well as its psychopathology—as exemplified by body dysmorphic disorder—will be increasingly

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well delineated. These might involve areas, such as the medial orbitofrontal cortex, that process stimulus-reward values [10], as well as areas that process body perception [14]. Ultimately, it can be hoped that the specific neurocircuitry involved in these processes will prove to be normalized by particular medications and psychotherapeutic interventions.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Stein D.J. (2003) Cognitive-Affective Neuroscience of Mood and Anxiety Disorders. Martin Dunitz: London. Gorman J.M., Kent J.M., Sullivan G.M., Coplan J.D. (2000) Neuroanatomical hypothesis of panic disorder, revised. Am. J. Psychiatry 157: 493–505. Le Doux J. (1998) Fear and the brain: where have we been, and where are we going? Biol. Psychiatry 44: 1229–1238. Stein D.J., Goodman W.K., Rauch S.L. (2000) The cognitive-affective neuroscience of obsessive-compulsive disorder. Curr. Psychiatry Rep. 2: 341–346. Nesse R.M. (2000) Is depression an adaptation? Arch. Gen. Psychiatry 57: 14–20. McGuire M.T., Marks I., Nesse R.M., Troisi A. (1992) Evolutionary biology: a basic science for psychiatry? Acta Psychiatr. Scand. 86: 89–96. Stein D.J., Bouwer C. (1997) A neuro-evolutionary approach to the anxiety disorders. J. Anxiety Disord. 11: 409–429. Thornhill R., Gangestad S.W. (1999) Facial attractiveness. Trends Cogn. Sci. 3: 452–460. Aharon I., Etcoff N., Ariely D., Chabris C.F., O’Connor E., Breiter H.C. (2001) Beautiful faces have variable reward value: fMRI and behavioral evidence. Neuron 32: 537–551. O’Doherty J., Winston J., Critchley H., Perrett D., Burt D.M., Dolan R.J. (2003) Beauty in a smile: the role of medial orbitofrontal cortex in facial attractiveness. Neuropsychologia 41: 147–155. Stein D.J., Matsunaga H. (2001) Cross-cultural aspects of social anxiety disorder. Psychiatr. Clin. North Am. 24(4): 773–782. Veale D., Ennis M., Lambrou C. (2002) Possible association of body dysmorphic disorder with an occupation or education in art and design. Am. J. Psychiatry 159: 1788–1790. Adolphs R. (2001) The neurobiology of social cognition. Curr. Opin. Neurobiol. 11: 231–239. Carey P., Seedat S., Warwick J., van Heerden B., Stein D.J. (2004) SPECT imaging of body dysmorphic disorder. J. Neuropsychiatry Clin. Neurosci. 16: 357–359.

4.4 Our Evolving Understanding of Body Dysmorphic Disorder Nancy J. Keuthen1 and Antje Bohne2 Perugi and Frare articulately convey to the reader the challenges that yet abound in the conceptualization and treatment of body dysmorphic disorder 1 2

Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA University of Muenster, Germany

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(BDD). As a relative newcomer to the diagnostic nomenclature, conceptual modellers still struggle to define the boundaries of BDD in comparison to kindred illnesses such as eating disorders and obsessive–compulsive disorder (OCD), among others. To wit, is there validity in the distinction between body dissatisfaction that is primarily weight-related versus body dissatisfaction focussed on other body aspects? Not surprisingly, some consider primary weight-related body image concerns as compatible with a BDD diagnosis. And, conversely, exaggerated non-weight-related body image concerns in eating-disordered patients have also been conceptualized as an indicator of greater eating disorder severity rather than a comorbid BDD diagnosis [1]. In contrast, Grant et al. [2] have endorsed the distinction made in DSM-IV between the two diagnostic entities, given their data that anorexia patients with and without BDD significantly differ on several illness-related variables. Clearly, further research is needed. For example, it would be of theoretical interest to examine those neuropsychological and information processing variables recently identified to be of relevance in BDD in matched BDD and eating-disordered patients with body dissatisfaction. Similarly, neuroimaging techniques can be used to compare both groups to see if critical differences exist. On another note, the question of meaningful subtypes of BDD remains unanswered. Do BDD patients differ as a function of their main focus of concern (e.g., muscle dysmorphia in males or concerns about hip size or skin condition in females), or their predominant safety behaviours (e.g., mirror checking vs. mirror avoidance)? Clinical heterogeneity also extends to level of insight (ranging from obsessional to delusional thinking) and existing comorbid conditions (e.g., OCD, eating disorders or personality disorders). In addition, there are sufferers with a mild defect versus no defect in physical appearance. Should we treat BDD symptoms without accommodation for these differences? Or do the former distinctions have direct treatment implications for cognitive-behavioural or pharmacological interventions? While scientific evidence and discussion of heterogeneity in OCD and other obsessive-compulsive spectrum disorders (e.g., in trichotillomania; see [3]) is increasing, there has been a paucity of this research in BDD, which might partially explain poor treatment outcome. Additionally, better delineation of aetiologic variables also remains a pivotal issue, with multi-causality, as emphasized by the authors, likely the case. Sociocultural factors, such as an emphasis on the importance of physical attractiveness, seem to be one possible source of exaggerated body concerns. A cross-cultural comparison [4] consistently revealed that significantly more American than German students were concerned about and preoccupied with their physical appearance. Earlier findings also indicated that Americans place significantly greater value on physical attractiveness than do Germans [5]. Further evidence for the hypothesis that more extreme

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body shape ideals predispose to body image concerns comes from a recent study. In a sample of male body builders and athletes training for triathlons, extreme body size ideals were related to greater muscularity-related concerns and decreased satisfaction [6]. Furthermore, greater discrepancies occurred between subjective ratings of ideal and perceived body size for the largersized participants. Another potential aetiological factor, as mentioned by Perugi and Frare, is self-reported histories of frequent teasing. The authors correctly mention that negative affectivity may bias patients’ retrospective recollections. In addition, an exaggerated sensitivity to critical remarks, as well as delusionality (when present), might be additional factors in BDD sufferers that influence perception and bias self-reports. These problems aside, there have been numerous reports associating teasing with the development of body image concerns, though most have focused on weight-related body image concerns. Also, in contrast to research on weight-related body image concerns (e.g., [7]), there have been no studies addressing the predictors of non-weight-related body image concerns that have not been biased by retrospective data. Further examination of the role of specific sociocultural influences, including idealized body shape standards, family environment, and peer relatedness, requires the design of prospective studies to eliminate the potential bias of negative affectivity and other variables involved in retrospective recollection.

REFERENCES 1. 2. 3.

4. 5. 6.

7.

Gupta M.A., Johnson A.M. (2000) Nonweight-related body image concerns among female eating-disordered patients and nonclinical controls: some preliminary observations. Int. J. Eat. Disord. 27: 304–309. Grant J.E., Kim S.W., Eckert E.D. (2002) Body dysmorphic disorder in patients with anorexia nervosa: prevalence, clinical features, and delusionality of body image. Int. J. Eat. Disord. 32: 291–300. Keuthen N.J., Bohne A., Himle M., Woods D.W. Advances in the conceptualization and treatment of body-focused repetitive behaviors. In: Progress in Obsessive-Compulsive Disorder Research, B.E. Ling (Ed). Nova Science: Hauppauge (in press). Bohne A., Keuthen N.J., Wilhelm S., Deckersbach T., Jenike M.A. (2002) Prevalence of symptoms of body dysmorphic disorder and its correlates: a cross-cultural comparison. Psychosomatics 43: 486–490. Buss D.M., Angleitner A. (1989) Mate selection preferences in Germany and the United States. Pers. Individ. Diff. 10: 1269–1280. Petersen I., Gerlach A.L., Rist F. (2004) Influence of a regular work-out session on ideal and perceived body image and body satisfaction in male bodybuilders and tri-athletes. Presented at the 34th Congress of the European Association for Behavioural and Cognitive Therapies, Manchester, September 11. Vander Wal J.S., Thelen M.H. (2000) Predictors of body image dissatisfaction in elementary-age school girls. Eat. Behav. 1: 105–122.

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4.5 Is Body Dysmorphic Disorder a Culturally Determined Expression of a Body Image Disorder? David H. Gleaves1 and Suman Ambwani1 Elsewhere [1] we argued that body dysmorphic disorder (BDD) was perhaps best conceptualized as a body image disorder, a categorization shared with the eating disorders. This conceptualization is one of several discussed by Perugi and Frare, and we would argue that it is still tenable and worthy of further study, particularly from a cultural perspective. More specifically, our position (shared by several other researchers) is that bodily preoccupation is a global phenomenon; the specific target of the preoccupation varies as a function of cultural values. Such a conceptualization is consistent with the gender differences associated with eating disorders (primarily in women) and muscle dysmorphia (primarily in men) because of the different cultural standards. Both are based, to some degree, on the cultural ideal of attractiveness (or desirable physical characteristics) that vary for men versus women. This model predicts that there is a core similarity (perceived bodily defect) across different cultures, but that the specifics will differ depending on an individual’s culture. Indeed, cross-cultural examinations of BDD have suggested not only some similarities but also interesting differences. For instance, Holt et al. [2] described a Chinese-American first-generation immigrant woman with BDD. The client’s presenting problem was her alleged ugliness, in particular, her wide face, protruding upper lip, and large nose. The client professed her desire to appear more ‘‘Caucasianlooking’’, stating that ‘‘[they] have all the economic power’’. In another study, exploring BDD among female college students in Turkey, Cansever et al. [3] described one woman preoccupied with her small breast, but because of a possible ‘‘breast-feeding deficiency’’, not physical unattractiveness. Another culturally determined manifestation of BDD was witnessed in two women who focused on their narrow bone structure because of concerns about problems giving birth. These cases and the conceptualization we are describing make it obvious that it is important to study not only what the areas of preoccupation are but also the nature of the alleged defect. Even within the same society (e.g., the United States), different subcultures (i.e., different racial-ethnic groups) may put emphasis on different aspects of appearance as being attractive [4]. Furthermore, as the above cases illustrate, attractiveness may have little or nothing to do with the preoccupation. Thus, as Holt et al. [2] argued (in the context of therapy), it is important to ‘‘probe the personal 1

Department of Psychology, Texas A&M University, College Station, TX 77843-4235, USA

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and ethnopsychological meanings of the symptoms relative to the patient’s cultural context’’. The same should apply to research. This conceptualization also raises questions about some alleged culturebound syndromes. For example, Suzuki et al. [5] recently examined the Japanese subtypes of taijin kyofusho, the fear of embarrassing others, currently identified as a culturally bound syndrome in the DSM-IV. They reported that taijin kyofusho is categorized in the Japanese diagnostic system in four subtypes, one of which is shubo-kyofu, the phobia of a deformed body, which meets DSM-IV criteria for BDD. Thus, they argued, taijin kyofusho may not be as culturally specific as previously understood. Moreover, this suggests that, although BDD may be labelled differently, it presents a similar clinical picture among Japanese clients. Furthermore, the debate over the ‘‘culture-boundedness’’ of eating disorders [6] suggests that these disorders may be types of body image spectrum disorders specific to Western cultures. The Chinese-American client’s desire to appear more Caucasian, the Japanese cultural fear of offending others with one’s physical appearance, and the Turkish client’s preoccupation with breast size, all seem to suggest that the values of the culture dictate the meaning of the physical preoccupation. Phillips [2] has argued that, although culture may influence the nuances of BDD (e.g., a focus on eyelids among Asians versus the relative unimportance of the same among non-Asians), in general BDD appears to be more similar than different across cultures. These data imply that, although bodily preoccupation is a global phenomenon, the specific idiom of distress varies as a function of cultural values [2]. Thus, it seems that we live in a ‘‘BDD culture’’, one in which the meaning behind body dislike is partially determined by the individual, and partially by the culture [7].

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Cororve M.B., Gleaves D.H. (2001) Body dysmorphic disorder: a review of conceptualizations, assessment, and treatment strategies. Clin. Psychol. Rev. 21: 949–970. Holt D.J., Phillips K.A., Shapiro E.R., Becker A.E. (2003) ‘‘My face is my fate’’: biological and psychosocial approaches to the treatment of a woman with obsessions and delusions. Harv. Rev. Psychiatry 11: 142–154. ¨ Donmez Cansever A., Uzun O., E., Oz¸sahin A. (2003) The prevalence and clinical ¨ features of body dysmorphic disorder in college students: a study in a Turkish sample. Compr. Psychiatry 44: 60–64. Miller K.J., Gleaves D.H., Hirsch T.G., Green B.A., Snow A.C., Corbett C.C. (2000) Comparisons of body image dimensions by race/ethnicity and gender in a university population. Int. J. Eat. Disord. 27: 310–316. Suzuki K., Takei N., Kawai M., Minabe Y., Mori N. (2003) Is Taijin Kyofusho a culture-bound syndrome? Am. J. Psychiatry 160: 1358. Keel P.K., Klump K.L. (2003) Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology. Psychol. Bull. 129: 747–769. Parker R. (2003) Body hatred. Br. J. Psychother. 19: 447–464.

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4.6 Body Dysmorphic Disorder: Awareness Needed Don E. Jefferys1 Body dysmorphic disorder (BDD) is a pathological disturbance in body image, the defining feature being preoccupation with imagined defects or a markedly exaggerated concern over a slight physical defect leading to significant distress. Historically, this disturbance was described as dysmorphophobia, a name given, in 1886, by the Italian physician Morselli. Several decades later, Pierre Janet observed that this syndrome, which he labelled ‘‘obsession de la honte de corps’’ (obsession with shame of the body), was indeed ‘‘common, invariably overlooked and evoked extreme shame’’. Janet’s observations unfortunately remain valid today, in that the illness is common but continues to be under-recognized. Perugi and Frare’s review is authoritative and timely. It summarizes the results of scientific studies in BDD at a time when community awareness of BDD is rapidly increasing, perhaps triggered by the publication of ‘‘The Broken Mirror’’ by Katharine Phillips [1]. My observations suggest that community awareness is increasing at a rate faster than is occurring in clinical settings. BDD is not a rare illness; epidemiological evidence is supportive of this. Its failure to be diagnosed depends on a reluctance to reveal symptoms by the patient and the failure by the clinician to ask specific questions concerning body image. My clinical experience suggests that two other factors also inhibit diagnosis: some people have difficulty describing their symptoms, while others do not view their symptoms as pathological, particularly in cases of muscle dysmorphia. Asking the question ‘‘Is there any part of your body you consider ugly or needs change?’’ often enables the sufferers to openly discuss their appearance concerns. Today, BDD is classified as a somatoform disorder in DSM-IV-TR and a variant of hypochondriasis in ICD-10. Both Morselli and Janet, however, recognized that those who experience BDD have similarities with obsessive–compulsive disorder (OCD). Perugi and Frare highlight that BDD may belong to a group of disorders termed ‘‘the obsessive–compulsive spectrum disorders (OCSDs)’’. BDD certainly shares similarities with OCD in terms of comorbidity, familial history, and treatment response to serotonin reuptake inhibitors. Clinical presentations are also similar, as both are characterized by intrusive thoughts and compulsive behaviours. Further evidence comes from a recent morphometric magnetic resonance imaging study of BDD subjects [2]. In this study, an abnormal asymmetry of the caudate nucleus and 1 Department of Psychiatry, University of Melbourne, Austin Hospital and Repatriation Medical Centre, Heidelberg, Victoria, Australia

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an increase in total white matter volume was shown. The authors considered the findings consistent with the conceptualization of BDD as an OCSD. Functional neuroimaging studies have consistently shown abnormalities in the caudate nucleus in OCD [3]. Perugi and Frare also emphasize that there are indeed differences between BDD and OCD, perhaps the most significant being the presence of delusions. Research shows that half of those with BDD are delusional for a significant period, the level of delusions varying over time. The presence of delusions in BDD has led to a differential classification of BDD in DSM-IV-TR; in ICD-10, BDD with delusions is defined as a variant of a delusional syndrome. When delusions are present, BDD is more severe, impairment is greater, and the risk of suicide elevated, a factor that needs to be assessed in these patients. Perugi and Frare suggest that, considering the findings to date, BDD should not be considered a simple clinical variant of OCD, a position emphasized by their recent findings that BDD is also closely related to social phobia, mood, eating, and impulse control disorders. The challenge clearly remains: where does BDD belong in the psychiatric landscape? This uncertainty may be a factor in the failure to recognize this illness more frequently. The efficacy of serotonin reuptake inhibitors in the treatment of BDD with or without delusions is highlighted by Perugi and Frare, a high dose being the norm, with treatment gains measured by reduction in symptoms and impairment. To date, most pharmacological studies have been limited in time; my clinical experience suggests that a significant clinical improvement also occurs well outside the period of time used in clinical trials. Patience by the clinician and the sufferer, l have found, often has the most favourable outcome. Perugi and Frare highlight that discontinuation of pharmacotherapy often sees a return of symptoms, and hence pharmacotherapy ought to be viewed as long-term. However, discontinuation has not been assessed after long-term use. Limited studies suggest that cognitive-behavioural therapy (CBT) is effective in BDD; most such studies have simultaneously used pharmacotherapy. It has not yet been demonstrated that, as in OCD, CBT alone is efficacious in BDD. Perugi and Frare’s review shows that our knowledge about BDD has expanded. Yet, as they acknowledge, much research remains to be done about an illness that continues to be under-diagnosed and, for most, significantly compromises life. Awareness is the answer, particularly in clinical settings.

REFERENCES 1. 2.

Phillips K.A. (1996) The Broken Mirror: Understanding and Treating Body Dysmorphic Disorder. Oxford University Press: New York. Rauch S.L., Phillips K.A., Segal E., Makris N., Shin L.M., Whalen P.J., Jenike M.A., Caviness V.S., Kennedy D.N. (2003) A preliminary morphometric magnetic

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resonance imaging study of regional brain volumes in body dysmorphic disorder. Psychiatry Res. Neuroimaging 122: 13–19. Rauch S.L., Baxter L.R. (1998) Neuroimaging of OCD and related disorders. In: Obsessive-Compulsive Disorders: Practical Management, M.A. Jenike, L. Baer, W.E. Minichiello (Eds). Mosby: Boston, pp. 289–317.

3.

4.7 Recent Findings in Body Dysmorphic Disorder and Future Directions Sabine Wilhelm1 and Ulrike Buhlmann1 Most of us are dissatisfied with certain aspects of our appearance. However, individuals with body dysmorphic disorder (BDD) are so distressed about their looks that their appearance concerns interfere with their daily life. Perugi and Frare’s comprehensive review of the current BDD research illustrates that the disorder only entered the diagnostic nomenclature in 1987 [1] and researchers only recently began to investigate it (e.g., [2]). This is surprising given that BDD appears to be relatively common and has a major impact on everyday functioning and quality of life (e.g., [3]). Perugi and Frare point out that epidemiological data about the prevalence of BDD in the general population is still very limited. Large-scale community-based epidemiological survey studies need to be conducted to more accurately assess the prevalence of BDD and its comorbidity. While several models for BDD development and maintenance have been introduced (e.g., [3, 4]), they still lack empirical support. Prospective epidemiological studies are therefore needed to identify biological (including genetic), psychological, and sociocultural factors contributing to the development and maintenance of BDD and their impact on its onset and course. Several treatment studies suggest the efficacy of specific pharmacological and psychosocial interventions for patients with BDD. However, the studies conducted so far have typically been very small and have frequently lacked (active) control groups. Future treatment studies will need to determine the efficacy of treatments for BDD in larger samples and will also have to elucidate the mechanisms underlying change in BDD. So far, only one structural and no functional neuroimaging studies have been conducted in BDD. Future research should focus on neuroimaging to investigate the pathophysiology of BDD as well as to explicate the relationship between neuroimaging measures (regional cerebral metabolic rate) and treatment response. Such studies have been performed in patients with mood disorders and obsessive–compulsive disorder (OCD), and have significantly improved our understanding of the pathophysiology and mechanisms 1

Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

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associated with clinical improvement in these disorders (e.g., [5]). Future studies will also need to determine the effects of integrated combination treatments, including cognitive-behavioural therapy (CBT) and concurrent medication. Research will also need to focus on the prediction and prevention of relapse. Perugi and Frare mention muscle dysmorphia as one subgroup of BDD. Future studies will need to address treatment effectiveness in subgroups of BDD patients, severely delusional patients, as well as in racial/ethnic minorities. Modular treatments that allow clinicians to flexibly target specific symptoms and problem areas may be particularly useful and should be developed for this purpose. For example, to develop a treatment module for delusional BDD, researchers could utilize the clinical literature on specific treatment strategies for psychotic disorders (e.g., [6]). Future CBT treatment development efforts should also be guided by cognitive-behavioural models of BDD [7] and should directly address the information processing biases found in BDD, such as selective attention to details, or the misinterpretation of emotional expressions [8, 9]. While the few treatment studies that have been conducted for BDD suggest that CBT and selective serotonin reuptake inhibitors (SSRIs) are efficacious, little is known about how well these treatments work in realworld settings. Thus, treatments need to be disseminated to providers in the community and services research is needed. Moreover, given that BDD is a frequently under-recognized and under-diagnosed disorder, the identification of individuals with BDD needs to be improved and effective programmes targeting high-risk populations need to be developed. Given that BDD usually develops during adolescence or early adulthood, it may be fruitful to develop intervention programmes that could be implemented in high schools or colleges. Similar to body image intervention programmes in eating disorders (e.g., [10, 11]), these prevention programmes could focus on factors such as psychoeducation, culturally influenced beauty norms, and dysfunctional thoughts and beliefs about one’s appearance.

REFERENCES 1. 2. 3. 4. 5.

American Psychiatric Association (1987) Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. American Psychiatric Association: Washington, D.C. Phillips K.A., McElroy S.L., Keck P.E., Pope H.G., Hudson J.I. (1993) Body dysmorphic disorder: 30 cases of imagined ugliness. Am. J. Psychiatry 150: 302–308. Phillips K.A. (1991) Body dysmorphic disorder: the distress of imagined ugliness. Am. J. Psychiatry 148: 1138–1149. Neziroglu F., Roberts M.A., Yaryura-Tobias J.A. (2004) A behavioral model for body dysmorphic disorder. Psychiatr. Ann. 34: 915–920. Baxter L.R., Schwartz J.M., Bergman K.S., Szuba M.P., Guze B.H., Mazziotta J.C., Alazraki A., Selin C.E., Ferng H.K., Munford P., et al. (1992) Caudate glucose

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metabolic rate changes with both drug and behavior therapy for obsessivecompulsive disorder. Arch. Gen. Psychiatry 49: 681–689. Chadwick P., Birchwood M.J., Trower P. (1996) Cognitive Therapy for Delusions, Voices and Paranoia. Wiley: New York. Wilhelm S. (2003) New cognitive interventions for body dysmorphic disorder. Presented at the 156th Annual Meeting of the American Psychiatric Association, San Francisco, May 17–22. Buhlmann U., McNally R.J., Wilhelm S., Florin I. (2002) Selective processing of emotional information in body dysmorphic disorder. J. Anxiety Disord. 16: 289–298. Buhlmann U., McNally R.J., Etcoff N.L., Tuschen-Caffier B., Wilhelm S. (2004) Emotion recognition deficits in body dysmorphic disorder. J. Psychiatr. Res. 38: 201–206. Rodin J., Silberstein L., Striegel-Moore R.H. (1984) Women and weight: a normative discontent. Nebr. Symp. Motiv. 32: 267–307. Matusek J.A., Wendt S.J., Wiseman C.V. (2004) Dissonance thin-ideal and didactic healthy behavior eating disorder prevention programs: results from a controlled trial. Int. J. Eat. Disord. 36: 376–388.

4.8 Body Dysmorphic Disorder: Some Issues Concerning Classification and Treatment Fugen Neziroglu1 Body dysmorphic disorder (BDD) is a very serious, debilitating mental disorder. It is still under-diagnosed, because most patients seek dermatological and cosmetic surgery rather than psychiatric treatment. It is excluded in structured interview scales. Patients are secretive about their symptoms, and professionals do not ask the proper questions to elicit symptoms. Although catchment studies are lacking, there is some research to suggest that the prevalence rate may range from 0.7 to 13%. Since 1991, there has been some growing awareness of the disorder, although the paucity of research studies in the area indicates that our knowledge is still very limited. For this reason, Perugi and Frare’s comprehensive review of the current literature is extremely useful and necessary to bring awareness to clinicians worldwide. This commentary will focus primarily on the issues raised by Perugi and Frare as to BDD’s classification and the difficulties encountered with treatment. As Perugi and Frare point out, it is unclear whether BDD is a somatoform disorder, a delusional disorder, a form of social anxiety, an obsessive–compulsive disorder (OCD), or a personality disorder. Neziroglu and Yaryura-Tobias [1, 2] have argued that BDD fits more within the OCD 1

Bio-Behavioral Institute, 935 Northern Blvd., Great Neck, NY 11021, USA

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spectrum and that more similarities than dissimilarities exist between BDD and OCD. One important distinguishing factor is the higher overvalued ideas found in BDD as compared to OCD [3]. Higher overvalued ideas have been found to lead to poorer treatment outcome [4], which might explain why BDD is harder to treat than OCD. Moreover, the number of Axis II personality disorders in BDD is greater than for OCD [5]. We know that the existence of comorbid personality disorders make treatment especially difficult. Furthermore, other factors that may distinguish BDD from OCD are abuse history [6], lower self-esteem [7], and somatosensorial and perceptual distortions [8, 9]. Three aetiological theories have been proposed for BDD: the neurobiological, the aesthetic self, and the two-factor theory based on classical and operant conditioning. The neurobiological theory has been based primarily on findings from OCD. The primary basis is a serotonergic deficit hypothesis, with treatment geared towards correcting this deficit via selective serotonin reuptake inhibitors [10, 11]. The aesthetic self-model, proposed by Veale [12], discusses how individuals with BDD perceive themselves as an aesthetic object and then respond to others accordingly. This model recommends the usage of imagery and techniques to turn attention away from the self to the environment. It also emphasizes challenging values of appearance and reducing the importance of appearance in defining the self. Within this treatment model, experiments are designed to test the efficacy of safety behaviours, such as mirror gazing. The two-factor theory, proposed by Neziroglu [13] and later expanded upon [14], presumes a biological disposition to acquiring BDD. It is through classical conditioning that the particular body part gets conditioned to a negative mood, and through operant conditioning the negative mood is removed when an avoidance behaviour (e.g., checking, camouflaging, etc.) is performed. It is suggested that patients with BDD are initially positively or intermittently reinforced for their appearance. Early reinforcement history and social learning, through modelling and vicarious learning, instill in a child a self-value based on body image beliefs about the importance of being considered attractive. Classical conditioning occurs when a person is teased, or abused, in regard to some aspect of his body and this negative event elicits a negative emotional reaction. Thereafter, the ridiculed body part becomes conditioned to negative emotions. Later, BDD is maintained via operant conditioning; specifically, negative reinforcement, whereby the negative emotions are reduced through avoidance behaviours. The latter two models, although conceptualized differently, borrow several similar treatment strategies from each other. Neziroglu and KhemlaniPatel [15] present all the cognitive-behavioural treatment research conducted to date, including the utilization of purely cognitive approaches [16] and

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cognitive versus behavioural approach [17]. Additional research is necessary to test each component of the theories and the efficacy of subsequent treatment strategies.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Neziroglu F., Yaryura-Tobias J.A. (1993) Body dysmorphic disorder: phenomenology and case descriptions. Behav. Psychother. 21: 27–36. Neziroglu F., Yaryura-Tobias J.A. (1997) A review of cognitive behavioral and pharmacological treatment of body dysmorphic disorder. Behav. Modif. 21: 324–340. McKay D., Neziroglu F., Yaryura-Tobias J.A. (1997) Comparison of clinical characteristics in obsessive-compulsive disorder and body dysmorphic disorder. J. Anxiety Disord. 11: 447–454. Neziroglu F., Stevens K.P., McKay D., Yaryura-Tobias J.A. (2001) Predictive validity of the overvalued ideas scale: outcome in obsessive compulsive and body dysmorphic disorders. Behav. Res. Ther. 39: 745–756. Neziroglu F., McKay D., Todaro J., Yaryura-Tobias J.A. (1996) Effect of cognitive behavior therapy on persons with body dysmorphic disorder and comorbid Axis II diagnoses. Behav. Ther. 27: 67–77. Neziroglu F., Khemlani S., Roberts M., Yaryura-Tobias J.A. Prevalence of abuse history in body dysmorphic disorder. Submitted for publication. Phillips K.A., Pinto A., Jain S. (2004) Self-esteem in body dysmorphic disorder. Body Image 1: 385–390. Yaryura-Tobias J.A., Neziroglu F., Chang R., Lee S., Pinto A., Donohue L. (2002) Computerized perceptual analysis of patients with body dysmorphic disorder. CNS Spectr. 7: 444–446. Yaryura-Tobias Y.A., Neziroglu F., Torres-Gallegos M. (2002) Neuroanatomical correlates and somatosensorial disturbances in body dimorphic disorder. CNS Spectr. 7: 432–434. Phillips K.A. (2004) Treating body dysmorphic disorder using medication. Psychiatr. Ann. 34: 945–953. Hollander E., Liebowitz M.R., Winchel R., Klumker A., Klein D.F. (1989) Treatment of body dysmorphic disorder with serotonin reuptake blockers. Am. J. Psychiatry 146: 768–770. Veale D. (2004) Advances in a cognitive behavioral model of body dysmorphic disorder. Body Image 1: 113–125. Neziroglu F. (2004) How to apply cognitive and behavior therapy for BDD. Presented at the American Psychological Association Meeting, New York, May 1–6. Neziroglu F., Roberts M., Yaryura-Tobias J.A. (2004) A behavioral model for body dysmorphic disorder. Psychiatr. Ann. 34: 915–920. Neziroglu F., Khemlani-Patel S. (2003) Therapeutic approaches to body dysmorphic disorder. Brief Treat. Crisis Interven. 3: 307–322. Geremia G.M., Neziroglu F. (2001) Cognitive therapy in the treatment of body dysmorphic disorder. Clin. Psychol. Psychother. 8: 243–251. Khemlani S., Neziroglu F. Cognitive and behavioral therapy for body dysmorphic disorder. Submitted for publication.

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4.9 Body Dysmorphic Disorder: The Antithesis of Narcissus Andrew A. Nierenberg1 Narcissus fell in love with his own image. Those with body dysmorphic disorder (BDD), in contrast, hate their image, are obsessed with their perceived ugliness, and find themselves locked in a repetitive cycle of trying to correct, ignore, or avoid their ugly parts. Some controversy exists about whether BDD warrants its own diagnostic label or whether it can fit under the rubric of existing diagnostic categories, such as somatoform or obsessive–compulsive disorders. Perugi and Frare provide a compelling overview of BDD, in that they show that the disorder is highly prevalent, causes substantial distress and dysfunction, and is usually under-recognized. They leave little doubt that BDD meets the requirements of a ‘‘legitimate’’ disorder with face validity (pun intended). Furthermore, they describe how BDD differs from obsessive–compulsive disorder not only in content of obsessive and dysregulated worries and concerns, but also in associated behaviours and the consequences of those behaviours. They point out that more work is needed to clarify the pathophysiology of BDD. Functional neuroimaging of patients with BDD who look at images of their perceived defects might further clarify not only the neurocircuitry of the disorder, but also if those brain areas that are activated are consistent with the neurophysiology of fear, anxiety, disgust, or reinforcing masochistic pleasure. Since the behaviours associated with BDD are repetitive even in the face of adverse consequences, why are the behaviours reinforcing? What are the salient characteristics that stimulate reward pathways? What is the fundamental defect that leads to the disorder? Perhaps provocative functional neuroimaging studies of unaffected first-degree family members would clarify premorbid relevant abnormal neuronal circuitry. These unaffected relatives could be shown pictures of themselves (or their least favourite body part), and the areas of their brain that are activated can be compared to an appropriate control group. This can complement the neurophysiological studies that implicate the fronto-parietal and temporo-parieto-occipital neurocircuits. In the near future, genetic epidemiological studies that use whole-genome scans could also clarify potential causes. Current studies of BDD tend to ignore that fact (and the old joke) that the large majority of adults were once children [1]. Using the Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS), retrospective and systematic assessment of 1 Depression and Bipolar Programs, Massachusetts General Hospital, Harvard Medical School, 50 Staniford Street, Boston, MA 02114, USA

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childhood psychiatric disorders, and the progression of those disorders, could further clarify precursors of BDD and describe how the disorder develops. Similarly, longitudinal case–control studies of high-risk offspring (the children of adult probands afflicted with BDD) could also be informative. Preliminary familial studies strongly suggest that first-degree relatives of probands with BDD have a higher risk of not only BDD but also abnormal grooming conditions [2]. Animal models of normal and abnormal grooming behaviours may further illuminate the pathophysiology of BDD [3].

REFERENCES 1. 2.

3.

Smoller J.W. (1986) The etiology and treatment of childhood. In: Oral Sadism and the Vegetarian Personality, G.C. Ellenbogen (Ed). Ballentine: New York, pp. 3–13. Bienvenu O.J., Samuels J.F., Riddle M.A., Hoehn-Saric R., Liang K.Y., Cullen B.A., Grados M.A., Nestadt G. (2000) The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol. Psychiatry 48: 287–293. Greer J.M., Capecchi M.R. (2002) Hoxb8 is required for normal grooming behavior in mice. Neuron 33: 23–34.

4.10 Playing the Devil’s Advocate: Is the Concept of Delusional Disorder, Somatic Type, Condemned to Extinction? Leonardo F. Fontenelle1 , Mauro V. Mendlowicz1 and Marcio Versiani1 We believe that Perugi and Frare’s comprehensive review of the state-of-art knowledge on body dysmorphic disorder (BDD) has raised several relevant points concerning key clinical and diagnostic issues. There is no doubt that BDD is often a severe disorder that can reach life-threatening proportions, displaying high levels of suicidality [1], and serious, sometimes bizarre, selfinjurious behaviours [2, 3]. Nevertheless, we feel that there is not sufficient scientific evidence as of now to support the existence of a delusional subtype of BDD that would encompass the concept of delusional disorder, somatic type (DDST). In one of the most often quoted and provocative articles on this subject, Phillips et al. [4] compared 48 patients with non-delusional BDD with 52 patients with delusional BDD (or, according to some authors, DDST). The two groups did not differ significantly in terms of most variables examined, including demographics, phenomenology, course, associated features, 1 Anxiety and Depression Research Program, Institute of Psychiatry, Federal University of Rio de Janeiro, 88 Lopes Trov˜ao St., Icaraˆı, Niter´oi, RJ 24220-071, Brazil

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comorbidity pattern, and treatment response. However, delusional subjects had higher total scores in the modified Yale-Brown Obsessive Compulsive Scale, suggesting that the delusional variant of BDD (or DDST) may be a more severe form of the non-delusional BDD. As pointed out by Perugi and Frare, this impression was further reinforced by the findings of two double-blind, placebo-controlled treatment studies showing that the treatment of BDD with clomipramine [5] and fluoxetine [6] was effective regardless of whether the patients had insight or held their dysmorphic misperception with delusional intensity. Currently, the DSM-IV allows ‘‘delusional’’ BDD to be double-coded, that is, individuals with dysmorphic delusions may be diagnosed with both BDD and DDST. However, given the increasing acceptance of a dimensional perspective, it is conceivable that future editions of the DSM may even recommend the exclusion of the diagnosis of DDST whenever isolated dysmorphic delusions are present, arguing that the latter should be considered no more than a symptom of BDD. But is there enough empirical evidence to support such a bold diagnostic shift? Is the concept of DDST condemned to extinction in favour of that of delusional BDD? We are not so sure about this point and will list a few reasons for our disbelief. First, the concept of DDST encompasses not only individuals with dysmorphic delusions but also those suffering from delusions of infestation (Ekbom syndrome), of body odour or halitosis (olfactory reference syndrome), of abnormal dental conditions (phantom bite syndrome), and of infectious diseases [7]. The regular reporting of such cases highlights the descriptive utility of the concept of DDST. Second, it has already been suggested that the diagnosis of BDD (and its delusional form) should be moved from the somatoform disorders section of the DSM-IV to a new section of the future DSM-V that would be entitled ‘‘obsessive–compulsive spectrum disorders’’ [8]. Although there have been previous attempts to incorporate some of these delusional entities into the socalled obsessive–compulsive spectrum (for example, the olfactory reference syndrome [9]), most of these categories seem to fit rather forcibly into this putative construct. Third, although several research groups [4–6] could not find any significant clinical and therapeutic difference between delusional and nondelusional forms of BDD and concluded that the concept of BDD might therefore incorporate that of DDST, their studies could be challenged on the basis that they have employed controversial concepts of ‘‘delusion’’. In the study by Phillips et al. [4], for instance, subjects were considered delusional if they were or had ever been for a ‘‘significant period of time’’ completely (or ‘‘100%’’) convinced that their view of their supposed defect was accurate and undistorted. Likewise, Phillips and coworkers [6] employed the Brown Assessment of Beliefs Scale (BABS), which assesses both dimensionally

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and categorically the appealing construct of delusionality, but is nevertheless restricted to the ‘‘past week’’. However, as pointed out by Munro [7], delusional disorders are not episodic illnesses. Long-term follow-up studies suggested that the diagnosis of delusional disorder should be reserved to patients with delusions persisting for at least 6 months [10]. Therefore, the definitions adopted by Phillips et al. [4, 6] may have led to the inclusion in their studies not only of patients with genuine DDST (chronic or persistently delusional patients) but also of individuals with BDD exhibiting an episodic or fluctuating ‘‘delusional’’ course. These inclusion criteria may have conceivably blunted putative differences between BDD and DDST. Fourth, Mullen [11] argued that the identification of delusions should not be based only on the presence of extreme or absolute conviction. Reports of non-psychotic beliefs (such as those found in BDD) eventually developing into a full delusional system and leading to the establishment of a diagnosis of a delusional disorder (or any other psychosis) frequently rely on changes in the levels of conviction expressed by the subject. This emphasis on the level of conviction ignores the other elements that comprise the delusion construct and that are referred to in the various commonly accepted definitions of a delusion, including that adopted by the DSM-IV. Two types of studies are urgently needed in order to substantiate our judgement regarding the existence of the DDST with dysmorphic delusions. As Perugi and Frare have noted, prospective, long-term studies of BDD will unveil how the level of insight of patients with BDD fluctuates and which factors lead to such variations. Moreover, comparisons between the demographic, clinical, biological, and therapeutic characteristics of patients with BDD, with their ‘‘episodic’’ lack of insight, and those of patients with DDST, with their chronic dysmorphic delusions, need to be performed in order to delineate diagnostic boundaries between these two disorders.

REFERENCES 1. 2. 3. 4.

Phillips K.A., McElroy S.L., Keck P.E. Jr., Pope H.G. Jr., Hudson J.I. (1993) Body dysmorphic disorder: 30 cases of imagined ugliness. Am. J. Psychiatry 150: 302–308. O’Sullivan R.L., Phillips K.A., Keuthen N.J., Wilhelm S. (1999) Near-fatal skin picking from delusional body dysmorphic disorder responsive to fluvoxamine. Psychosomatics 40: 79–81. Fontenelle L.F., Mendlowicz M.V., Mussi T.C., Marques C., Versiani M. (2002) The man with the purple nostrils: a case of rhinotrichotillomania secondary to body dysmorphic disorder. Acta Psychiatr. Scand. 106: 464–466. Phillips K.A., McElroy S.L., Keck P.E. Jr., Hudson J.I., Pope H.G. Jr. (1994) A comparison of delusional and nondelusional body dysmorphic disorder in 100 cases. Psychopharmacol. Bull. 30: 179–186.

244 5.

6. 7. 8.

9. 10. 11.

SOMATOFORM DISORDERS Hollander E., Allen A., Kwon J., Aronowitz B., Schmeidler J., Wong C., Simeon D. (1999) Clomipramine vs desipramine crossover trial in body dysmorphic disorder: selective efficacy of a serotonin reuptake inhibitor in imagined ugliness. Arch. Gen. Psychiatry 56: 1033–1039. Phillips K.A., Albertini R.S., Rasmussen S.A. (2002) A randomized placebocontrolled trial of fluoxetine in body dysmorphic disorder. Arch. Gen. Psychiatry 59: 381–388. Munro A. (1999) Delusional Disorder: Paranoia and Related Illnesses. Cambridge University Press: Cambridge. Phillips K.A., Price L.H., Greenberg B.D., Rasmussen S.A. (2003) Should the DSM diagnostic grouping be changed? In: Advancing DSM: Dilemmas in Psychiatric Diagnosis, K.A. Phillips, M.B. First, H.A. Pincus (Eds). American Psychiatric Press: Washington, pp. 57–84. Stein D.J., Le Roux L., Bouwer C., Van Heerden B. (1998) Is olfactory reference syndrome an obsessive-compulsive spectrum disorder? Two cases and a discussion. J. Neuropsychiatry Clin. Neurosci. 10: 96–99. Opjordsmoen S. (1993) The duration criteria of delusional disorder in modern classification. Psychopathology 26: 85–89. Mullen R. (2003) Delusions: the continuum versus category debate. Aust. N. Zeal. J. Psychiatry 37: 505–511.

4.11 Advancing the Understanding of Body Dysmorphic Disorder Eric Hollander1 and Bernardo Dell’Osso1 Over the last decade, body dysmorphic disorder (BDD), ‘‘the distress of imagined ugliness’’ [1], has received increasing empirical attention in terms of its phenomenology and treatment response. The disorder has a rich tradition in European psychiatry, yet it first entered the official psychiatric nomenclature as a separate disorder in DSM-III-R in 1987. It induces a significant impairment in social and occupational functioning and its course is often complicated by the occurrence of secondary depressive symptoms, suicidal ideation, and suicide attempts [2, 3]. One issue that deserves attention in managing BDD patients is the notable clinical heterogeneity of the disorder. In fact, although the main psychopathologic outline of BDD is well established, it is true that within the BDD population it is possible to find patients who markedly differ from each other not only in terms of severity of illness but also in terms of specific clinical dimensions. The degree of insight, for example, the presence of psychotic features and the common coexistence with a wide range of other psychiatric symptoms represent some aspects of the great variability that patients with BDD demonstrate. 1

Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA

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Over the last two decades, the comorbidity model in psychiatry has led to more successful choices of specific pharmacotherapies for various psychiatric disorders, and also has more recently led to the evolution of the spectrum concept. Applied to several psychiatric conditions, such as BDD, the spectrum model has allowed a further and more specific dissection and psychopathological characterization of various mental disorders, highlighting specific profiles in discrete psychiatric conditions as well as underscoring common features amongst different disorders. BDD seems to represent an emblematic case in which the spectrum dimensional model has allowed us to highlight the complex relationship and the reciprocal influence between the disorders classified as somatoform in DSM-IV and several other psychiatric conditions. Perugi and Frare’s comprehensive analysis of BDD phenomenology illustrates clearly these aspects of diversity and overlap between dysmorphophobia and the other psychiatric disorders that have been historically viewed as related to BDD. The preoccupation on specific parts of the body represents one of the core phenomenological features that determine the inclusion of BDD in the somatoform disorders in the DSM-IV. However, the obsessive nature of this preoccupation as well as the repetitive, time-consuming and compulsive behaviours related to this concern suggest a close relationship with obsessive–compulsive disorder (OCD). BDD has high rates of family history and comorbidity with OCD, which also support its conceptualization in the obsessive–compulsive spectrum (risk aversive/harm avoidant) [4]. However, BDD, as Perugi and Frare argue, should not be viewed as a simple variant of OCD, since it might fall in a broader affective spectrum of disorders. In our experience, moreover, the relationship between BDD and social anxiety disorder is also close, suggesting the inclusion of BDD in a social anxiety spectrum within body image disorders [5]. The uncertainty about where BDD belongs reveals the inadequacy of current categorical classification models for some mental disorders, and supports the utility of dimensional models. In fact, the capacity to detect and recognize common psychopathological features between BDD and other psychiatric conditions does not represent a pure nosographic issue, since it presupposes and implies several important consequences in terms of pharmacological choice. It should not be surprising, in fact, given the strong relationship with obsessive–compulsive spectrum disorders, that patients with BDD have a preferential pharmacological response to agents also found to be helpful for OCD. Preliminary neuroimaging studies demonstrate increased metabolic activity in limbic regions such as the anterior cingulate gyrus in both OCD and BDD patients, and these patients have been shown to have a robust response to serotonin reuptake inhibitors (SRIs) [6]. Confirming this hypothesis, we found, in a crossover trial in BDD patients [7], a greater efficacy of clomipramine in comparison with desipramine, and we also noted

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that even BDD patients with a delusional conviction had a good response to anti-obsessional treatments. Previously, a similar result had been reported in a study conducted by our group using the SRI fluvoxamine [8]. As Perugi and Frare point out, in spite of the growing body of research on this topic, SRIs and cognitive-behavioural therapy are the only interventions whose efficacy is documented in BDD. This restricted therapeutic range for such a heterogeneous and complex disorder suggests the need for further pharmacological trials in order to advance current intervention strategies. Neuroimaging and genetic studies are expected to produce further information on the aetiopathogenetic mechanisms in BDD, allowing to develop a more rational and valid pharmacotherapy for such a distressing and impairing illness. Currently, a successful approach to BDD patients needs to take into account the great clinical variety in terms of subthreshold psychopathology and relationship with other mental disorders. Improvement in comorbid symptoms, such as depression, anxiety, or obsessive–compulsive features, may also lead to a reduction in the core symptomatology of the disorder.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

8.

Phillips K.A. (1991) Body dysmorphic disorder: the distress of imagined ugliness. Am. J. Psychiatry 148: 1138–1149. American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders, 4th ed., text revision. American Psychiatric Association: Washington, D.C. Phillips K.A., Hollander E. (1996) Body dysmorphic disorder. In: DSM-IV Sourcebook, Vol. 2, T.A. Widiger, A.J. Frances, H.A. Pincus, R. Ross, M.B. First, W.W. Davis (Eds). American Psychiatric Press: Washington, D.C., pp. 949–960. Hollander E., Cohen L.J., Simeon D. (1993) Obsessive-compulsive spectrum disorders: body dysmorphic disorder. Psychiatr. Ann. 23: 59–364. Hollander E., Aronowitz B.R. (1999) Comorbid social anxiety and body dysmorphic disorder: managing the complicated patient. J. Clin. Psychiatry 60: 27–31. Hollander E., Liebowitz M.R., Winchel R., Klumker A., Klein D.F. (1989) Treatment of body dysmorphic disorder with serotonin reuptake blockers. Am. J. Psychiatry 146: 768–770. Hollander E., Allen A., Kwon J., Aronowitz B., Schmeidler J., Wong C., Simeon D. (1999) Clomipramine vs desipramine crossover trial in BDD: selective efficacy of a serotonin reuptake inhibitor in imagined ugliness. Arch. Gen. Psychiatry 56: 1033–1039. Hollander E., Cohen L., Simeon D., Rosen J., DeCaria C., Stein D.J. (1994) Fluvoxamine treatment of body dysmorphic disorder. J. Clin. Psychopharmacol. 14: 75–77.

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4.12 Is Body Dysmorphic Disorder More than a DSM Construct? Michel Botbol1 In this very well documented paper, Perugi and Frare adopt the conceptualization of body dysmorphic disorder (BDD) proposed by the DSM-IV along the line initiated by the DSM-III-R. They clearly support the idea that BDD is an autonomous disorder rather than a symptom of various disorders. Nevertheless, in clinical practice, we find very different patterns: behind the common excessive preoccupation concerning an imaginary physical defect, we face schematically two contrasting clinical and therapeutic situations [1]: (a) a neurotic situation in which the preoccupation has all the characteristics of an obsessive–compulsive disorder or another anxiety disorder; (b) a psychotic situation in which the preoccupation has all the characteristics of a delusional disorder. If we accept that, in a clinical setting, what counts for case management and for treatment is not only the symptomatology but also the structural organization underlying the disorder, these two situations are not only different but actually opposite, and this opposition has important therapeutic and prognostic consequences. For example, in an adolescent with body dysmorphic symptoms, the psychiatrist’s first concern is to find out whether this symptom is a temporary manifestation of an adolescence crisis, the sign of an obsessive–compulsive disorder with somatic contents, the first stage of a schizophrenic process (‘‘le signe du miroir’’), or the sign of a delusional non-schizophrenic disorder of somatic type (rare at this age). It is only after discarding these diagnoses that a clinician may be led to conclude that he is facing an autonomous disorder, the specific BDD entity. In their paper, Perugi and Frare bring many arguments against this classical clinical process, for example, arguments stating that, from an epidemiological and therapeutic point of view, there is no evidence that delusional BDD is different from non-delusional BDD. They then justify the fact that, unlike the DSM-III-R, the DSM-IV does not mention the non-delusional quality of the body dysmorphic preoccupation in the first criterion defining the disorder. Nevertheless, delusional body preoccupations still exist in the DSM-IV, but only in other chapters, namely, persistent delusional disorders of somatic type, including very heterogeneous delusional thought contents, and schizophrenia, where body preoccupation is only one of many heterogeneous symptoms. A psychiatrist considering a delusional dysmorphophobia as a category by itself has then, in DSM-IV, the choice between at least three diagnostic 1

Clinic Dupr´e, BP 101, 92333 Sceaux, France

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options: BDD, persistent delusional disorder of somatic type, and both categories. As the existing criteria in the DSM-IV do not easily allow the psychiatrist to select between these three options, his choice will depend on the rank he gives in the overall clinical description to the body excessive preoccupation symptom, on his representation of these diagnostic categories, on his overall appraisal of the psychic organization underlying the disorder, and on his evaluation of the clinical context. If we add to that the fact that an excessive body preoccupation can be, in some cases, better explained by other disorders (like eating disorders) or that, as we said before, it can be seen as the symptom of a broader disorder (like obsessive–compulsive disorder without insight or schizophrenia), the conclusion is that all truly delusional cases are likely to be excluded from the BDD category, as well as those cases in which the psychiatrist considers preoccupations with no insight as delusional because he does not know precisely where to put the cut-off between delusion and lack of insight. In other words: (a) what really counts is the context of a dysmorphophobia, not its specificities; (b) the evaluation of the context depends upon the rank the clinician gives to the dysmorphophobia symptom in the overall description of the patient’s condition; (c) this ranking process relies in part on the clinician’s subjective judgement. This part of the diagnostic task can be fulfilled only by going beyond the descriptive observable criteria offered by the DSM-IV and on the basis of the psychiatrist’s global appraisal of the patient psychic organization and the psychotic or non-psychotic context of the patient’s condition. We could say that, in its attempt to gain more objectivity in the definition of BDD, the DSM-IV brings back to the diagnostic process much of the subjectivity it tries to avoid, leaving the clinician alone with his own representations of the differences between BDD and other disorders, and with his own subjective evaluation of the patient’s psychic functioning and of the clinical context. The above process favours the inclusion of psychotic-like BDD cases under other delusional categories. This probably explains why many DSM-IV-based studies [2] do not find any significant effect of antipsychotic drugs despite the fact that clinical practice and several case reports [3] find these medications useful in delusional dysmorphophobia. BDD seems, therefore, to be an example of the limitations of current classification systems, which, behind the false security given by their supposed empirical and atheoretical qualities, leave us with ‘‘half a science’’ [4]. To overcome these limitations, it would be necessary to approach more scientifically the subjective impression of the psychiatrist in his diagnostic process. Reference to psychodynamic entities such as neurosis or psychosis could be of much help in this process, because they help the clinician to identify the psychic organization underlying the objective symptoms of

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the disorders. Of course, these entities require an interpretation from the clinician’s viewpoint, but this interpretation is based on a theoretical frame that makes them less subjective than a complete absence of frame. Since, as the example of BDD shows us, subjective impression exerts an inevitable influence on the diagnostic process, we think that this theoretical frame could be seen as a progress in the difficult task of labelling a disorder in a rational way. This does not imply that one has to agree upon the psychoanalytic ‘‘etiologic’’ conceptions of BDD, reported by Perugi and Frare in their paper. As they point out, there is no evidence of their validity, not only in systematic studies but also in psychoanalytically informed case reports [5]. In other words, we could conclude that, because of the light they put on the psychic organization underlying BDD symptoms, psychodynamic references could be of much help in the diagnostic process, in spite of the lack of any evidence of their validity from the aetiologic viewpoint.

REFERENCES 1.

Ferreri M., Godefroy M., Nuss P., Ferreri F. (2002) Dysmorphophobie, peur de dysmorphie, dysmorphoesth´esie. Encyclop´edie M´edico Chirurgicale, Psychiatrie, 37–146 A10, Elsevier: Paris. Phillips K.A., McElroy S.L., Dwight M.M., Eisen J.L., Rasmussen S.A. (2001) Delusionality and response to open-label fluvoxamine in body dysmorphic disorder. J. Clin. Psychiatry 62: 87–91. Filteau M.J., Pourcher E., Baruch P., Bouchard R.H., Vincent P. (1992) La dysmorphophobie (trouble dysmorphique physique). Rev. Can. Psychiatrie 37: 503–509. Strauss J. Personhood and agency: Kraepelin revisited. Psychopathology (in press). Guedeney C., Weisbrot C. (1995) L’histoire de l’hypochondrie. In: L’Hypochondrie, A. Fine, G. Pragier, M. Aisenstein (Eds). Presses Universitaires de France: Paris, pp. 29–49.

2. 3. 4. 5.

4.13 Body Dysmorphic Disorder and Obsessive–Compulsive Disorder: More Similarities than Differences Euripedes C. Miguel1 , Albina R. Torres2 and Ygor A. Ferr˜ao3 The current concept of obsessive–compulsive spectrum disorders (OCSD) includes disorders related to obsessive–compulsive disorder (OCD) based on 1

Department of Psychiatry, University of S˜ao Paulo Medical School, S˜ao Paulo, Brazil Discipline of Psychiatry, Botucatu Medical School, State University of S˜ao Paulo, Brazil 3 Institute of Psychiatry and Mental Health of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil 2

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clinical features, putative common aetiological mechanisms, family loading, and treatment response. Along with Tourette’s syndrome, body dysmorphic disorder (BDD) is one of the OCSD having the strongest evidence of a close relationship to OCD. As pointed out by Perugi and Frare, BDD and OCD share similar intrusive and distressing thoughts, repetitive and time-consuming behaviours aiming to achieve some sort of relief, similar age at onset and chronic course, shame and embarrassment, low self-esteem, and impairment in global functioning. High levels of comorbidity with depression and other anxiety disorders, under-recognition and delay in seeking and receiving appropriate treatment (which, by the way, is strikingly similar) are also seen in both disorders. A particularly interesting characteristic of these two conditions is the irrational search for perfection and symmetry, which in the case of BDD is focused on personal appearance. The content of the preoccupations, which in BDD are solely esthetical, tends to be multiple and to change over time, as in OCD. The aggressive behaviours towards close family members described in BDD patients are also quite common in OCD sufferers, when they are not able to avoid stressful stimuli or perform their rituals. The predominance of attention to internal impressions rather than to real perceptions also occurs in both conditions. BDD sufferers seem to disregard what they see in the mirror in the same way OCD patients disregard the locked door or their clean hands (a distorted body image perception?). There are probably common environmental factors that, interacting with genetic factors, play a role in the aetiology of both BDD and OCD. Several studies have suggested a possible relationship between streptococcus infection, rheumatic fever, BDD, and OCD. These studies reported a higher prevalence of BDD in association with OCD in rheumatic fever with and without its neurological complication (Sydenham’s chorea), both in active and non-active phases. Furthermore, familial aggregation of OCSD, including BDD, has been described in studies involving relatives of rheumatic fever cases [1]. Using a genetic standpoint, several disorders have been more frequently observed among relatives of OCD probands compared to controls. This is the case of BDD and several other OCSD. The differently expressed phenotypes could reflect the interaction of the same genetic vulnerability factors with different environmental factors, consistent with the concept of clinical heterogeneity. Given the fact that OCD is a very heterogeneous disorder, BDD can be related to some forms of OCD and not to others. In this respect, there are some data suggesting an association between BDD and early onset and tic-related OCD [1]. Since recent genetic studies have been unsuccessful in identifying the most likely mode of transmission of these disorders, the hypothesis that several genes produce a cumulative effect, mentioned by Perugi and Frare, seems

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plausible. Therefore, from a quantitative point of view, we could speculate that different loadings of susceptibility genes predispose to different manifestations of OCSD. For instance, there could be several thresholds that, when reached, increase the risk for a specific phenotype, such as OCD or OCD + BDD, or OCD + BDD + other OCSD. The most important difference in the psychopathology of BDD and OCD is the degree of insight, typically poorer in the former disorder. However, insight is not considered an all-or-nothing phenomenon anymore, but a dimensional one. It seems reasonable to suppose that insight can also vary in the same patient according to the content of the obsessions, with somatic obsessions usually showing a poorer level of insight compared to the other types, a clinical hypothesis that warrants specific studies. An unanswered question is what mechanisms mediate the transformation of ‘‘ego-dystonic’’ obsessional doubts and fears into ‘‘ego-syntonic’’ overvalued ideas, when the patient stops fighting against the idea and starts to defend it (and vice versa). Can BDD or OCD sufferers with ‘‘poor insight’’ ever be called delusional? According to Jaspers’ definition, they cannot, as delusions are not psychologically understandable and involve a complete and long-lasting transformation in the way the individual sees the outside world and relates to it. Overvalued ideas are psychologically understandable, emotionally overwhelming, leading the individual to try to solve his/her ‘‘problem’’ and convince the others about its veracity. In conclusion, our current ‘‘appearance-driven’’ classification systems make us lose the global picture of the psychiatric conditions, and create the highly artificial phenomenon of ‘‘comorbidity’’. It does not seem reasonable to oversplit diagnoses based on minor content differences (obsessional or overvalued idea of having a thin arm, a fat hip, a big nose, or even a foul smell, a skin cancer, or permanently dirty hands). This seems to be the case of ‘‘muscular dysmorphia’’, which clinically is just a BDD with a more specific preoccupation, quite understandable in times of overvaluation of physical fitness. A broader conceptual diagnostic view of our multifaceted patients may allow an earlier diagnosis and a more adequate treatment, and help minimize their long-lasting suffering.

REFERENCE 1.

Miguel E.C., Leckman J.F., Rauch S., do Rosario-Campos M.C., Hounie A.G., Mercadante M.T., Chacon P., Pauls D.L. (2005) Obsessive-compulsive disorder phenotypes: implications for genetic studies. Mol. Psychiatry 10: 258–275.

CHAPTER

5 Chronic Fatigue and Neurasthenia: A Review Michael C. Sharpe1 and Simon Wessely2 1

School of Molecular and Clinical Medicine, University of Edinburgh, and Royal Edinburgh Hospital, Edinburgh, UK 2 Institute of Psychiatry, King’s College, London, UK

INTRODUCTION This chapter reviews current knowledge about chronic fatigue syndrome (CFS) and neurasthenia. The central feature of these syndromes is severe chronic disabling fatigue, typically exacerbated by exertion and unexplained by any other medical condition. The diagnosis of neurasthenia has fallen out of fashion in most Western medical cultures, but remains an important one in many other cultures, most particularly in the Far East. CFS, along with many other similar syndromes defined by somatic symptoms, such as fibromyalgia, is a condition whose home both in medicine (as a functional syndrome) and in psychiatry (as a somatoform disorder) remains somewhat precarious. These functional disorders [1] are, however, of central concern to psychosomatic medicine in its broadest meaning.

GENERAL ISSUES A Discrete Disorder? Although CFS is often regarded as a discrete condition, much as neurasthenia used to be, the severity of the symptoms of fatigue is continuously distributed in the general population [2] and the case definition can also be regarded as simply defining cut-off points on these continua. Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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Organic or Psychogenic? Is CFS an ‘‘organic’’ or a ‘‘psychogenic’’ disorder? This is an issue that arouses intense passions nowadays [3]. This is nothing new, however, since very similar disputes, passions, and polemics surrounded neurasthenia at the end of the nineteenth century [4]. The extreme organic position argues that CFS will be eventually found to be as firmly based in disease pathology as any other medical condition. Attempts to establish a conventional pathology (e.g., chronic infection) have however not yet succeeded. An extreme psychogenic view would be that CFS is a ‘‘pseudo-disease’’, not in fact rooted in biology, but rather representing a social construction based on psychological amplification of a normal somatic sensation of fatigue. Neither of these extreme positions is sustained by the evidence or helpful for patients. In clinical practice, an extreme organic position encourages patients to engage in an often endless search for a doctor who will find the pathology and prescribe the right medication, whilst they adapt themselves to having a chronic disease. The extreme psychological view ignores the demonstrable physiological disturbances associated with the condition and, if perceived as dismissive and rejecting, can paradoxically encourage the patients in a defensive entrenchment of the belief that they really do have a disease [5]. An aetiologically neutral and integrated perspective that recognizes CFS as real and that acknowledges the likely contribution of biological, psychological, and social factors is almost certainly the best basis for effective clinical practice [6].

Medical or Psychiatric Diagnosis? Parallel with the debate about aetiology is the argument about whether CFS is most appropriately regarded as ‘‘medical’’ or as ‘‘psychiatric’’. For the same symptoms, the medical diagnosis may be CFS and the psychiatric diagnosis may be an affective, anxiety or somatoform disorder. It can be argued that neither of these diagnoses alone is adequate. The proper use of the DSM-IV axes allows the patient to be given both a medical (Axis III) and a psychiatric (Axis I) diagnosis: the final diagnosis may, for example, be CFS/generalized anxiety disorder. However, we ideally need a classification that avoids two diagnoses being given for the same symptoms. This is a task for the authors of the forthcoming DSM-V [7].

THE SYNDROME History CFS is certainly not a new illness. The description of neurasthenia from over 100 years ago sounds remarkably similar [8]. The term CFS was coined in

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1988 to describe a condition characterized by chronic disabling fatigue, with a large number of other somatic symptoms and strict psychiatric exclusions [9]. The authors of this early definition anticipated that a specific disease cause, possibly infectious, would be found, but this has never been established. The term CFS subsumed a multitude of previous terms used to describe patients with similar symptoms. These include chronic Epstein–Barr virus infection, myalgic encephalomyelitis and post-viral fatigue syndrome, as well as neurasthenia (which remains a specific diagnosis in ICD-10). Patient advocacy groups have been very vocal and politically active in arguing that CFS is an inadequate description of their illness and that terms such as myalgic encephalomyelitis or encephalopathy or chronic fatigue and immune deficiency syndrome (CFIDS), which emphasize a medical pathology, are more appropriate. However, the concept of CFS does have the important advantage of being operationally defined and providing a basis for replicable scientific research.

Definition A number of operational diagnostic criteria for CFS have been published. The first [9] that were in practice were found to be excessively cumbersome and restrictive. It was found that requiring multiple somatic symptoms as well as fatigue and using strict psychiatric exclusions made the condition very rare. Consequently, simpler and less exclusive case definitions were published [10, 11]. The most recent criteria, based on an international consensus, have been published in 1994 [12] (Table 5.1). Recommendations for their application have been recently further refined [13]. Whilst the different definitions have been a source of confusion and dispute, it should be remembered that all have been constructed by committees to aid research. Clinical practice should therefore not necessarily be tightly bound by them. The ICD-10 criteria for neurasthenia are summarized in Table 5.2.

Clinical Features The clinical presentation of the individuals who meet the criteria for CFS is heterogeneous, although the core symptoms of fatigue exacerbated by exercise, subjective cognitive impairment, and disrupted and unrefreshing sleep are almost universally described, and some degree of widespread pain is common. Patients often report marked fluctuations in fatigue that occur from week to week and even from day to day. Most patients are not so disabled that they cannot attend an outpatient consultation, although some describe difficulty in walking or can only attend with the aid of wheelchairs

256 T A B L E 5.1 et al. [12])

SOMATOFORM DISORDERS Diagnostic criteria for chronic fatigue syndrome (adapted from Fukuda

Inclusion criteria 1. Clinically evaluated, medically unexplained fatigue of at least 6 months duration that is: – of new onset (not life long) – not a result of ongoing exertion – not substantially alleviated by rest – associated with a substantial reduction in previous level of activities 2. The occurrence of 4 or more of the following symptoms: Subjective memory impairment, sore throat, tender lymph nodes, muscle pain, joint pain, headache, unrefreshing sleep, post-exertional malaise lasting more than 24 h. Exclusion criteria Active, unresolved or suspected medical disease; psychotic, melancholic or bipolar depression (but not uncomplicated major depression); psychotic disorders; dementia; anorexia or bulimia nervosa; alcohol or other substance misuse; severe obesity.

T A B L E 5.2

ICD-10 diagnostic criteria for neurasthenia

(a) Either persistent and distressing feelings of exhaustion after minor mental effort, or persistent and distressing feelings of fatigue after minor physical effort. (b) Accompanied by one or more of the following symptoms: muscular aches or pains, dizziness, tension headache, sleep disturbance, inability to relax, and irritability. (c) Inability to recover through rest, relaxation, or enjoyment. (d) Duration exceeds 3 months. (e) Does not occur in the presence of organic mental disorders, affective disorders, or panic or generalized anxiety disorder.

and other appliances. Other patients remain bed bound and unable to visit a clinic: they represent an important and neglected group. The symptom of fatigue is subjective, and there is a poor correlation between this feeling and objectively measured performance [14]. If patients with CFS are asked to perform exercise tests, they may not show the expected decrement, but rather report greater effort and increased fatigue, both at the time of the test and over the following days. Similarly, standard neuropsychological testing is usually normal, although often accompanied by complaint of greater effort [15]. There is some evidence that more complex cognitive tests do reveal deficits, although these usually appear less severe than those expected from the patient’s subjective complaints and are hard to distinguish from those associated with depression [16].

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In summary, the core clinical features of CFS are physical and mental fatigue exacerbated by physical and mental effort. These are subjective phenomena, often less evident on objective testing. While some may interpret this observation as evidence of exaggeration of disability, it can also be interpreted as indicating the essentially subjective and sensory nature of this condition.

Primary or Secondary CFS is diagnosed when the patient has no evidence of another medical condition. This makes it easy to define the symptoms as ‘‘medically unexplained’’. However, similar symptoms are often found in patients with other medical diagnoses. For example, symptoms of CFS have been identified in disease-free cancer patients [17] and in patients with multiple sclerosis [18]. The terms ‘‘primary’’ (occurring in the absence of another condition) and ‘‘secondary’’ (accompanying a medical condition) have been used to describe these findings. The terminology is however confusing and arguably more a matter of differential diagnosis than of comorbidity (see below). It is best avoided.

Association with Other Functional Somatic Syndromes Studies that have assessed the comorbidity of CFS with other functional somatic syndromes have found high rates of migraine, irritable bowel syndrome, pelvic pain, and temporo-mandibular joint pain. These syndromes, like CFS, are associated with high lifetime rates of comorbid mood and anxiety disorders [19]. There are other similarities between CFS and these disorders, including a female predominance, association with childhood abuse, and treatment response patterns. This observation raises the possibility that all these functional syndromes have more in common than previously thought by the specialists who diagnose each [1, 20]. It has been further suggested that these syndromes, along with mood and anxiety disorders, share a common psychological and/or central nervous system pathophysiology [21].

Association with Psychiatric Disorders In clinical practice, many but not all patients with CFS can be given a psychiatric diagnosis. Most will meet the criteria for a depressive or an anxiety disorder. The others are likely to meet DSM-IV criteria for a somatoform disorder or merit an ICD-10 diagnosis of neurasthenia [22]. The more somatic symptoms the patient has, the more likely is a diagnosis of depression or anxiety [23]. Precise prevalence rates of psychiatric disorders do however depend on the nature of the patient population studied and the diagnostic

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criteria used. Several factors may influence the estimates obtained. First, compared to a community sample, patients attending clinics are likely to be more disabled and distressed and therefore to have more depression and anxiety. Second, some symptoms (such as fatigue, sleep disturbance, and poor concentration) overlap with those of depression and anxiety, and the observed prevalence of psychiatric disorders will depend on whether all symptoms are counted towards a diagnosis of psychiatric disorder, or those regarded as related to CFS are excluded. Third, it has been argued that atypical presentations of depression [24] and anxiety [25] are common in these groups, adding further unreliability to estimates of prevalence. Fatigue is strongly associated with depression. The international World Health Organization (WHO) study of more then 5,000 primary care patients in a number of countries [26] found that 67% of cases of CFS (defined from survey data) also had an ICD-10 depressive syndrome [27]. Studies of clinic attenders with CFS have reported that more than 25% have a current DSM major depression diagnosis, and 50–75% a lifetime diagnosis [28]. Some features of CFS, such as chronic pain, are also strongly associated with depression in the general population [29]. One study reported generalized anxiety disorder in as many as half of clinic patients with CFS when the hierarchical rules that subsume it under major depression were suspended [30]. Panic disorder is especially common in patients with medically unexplained symptoms: a prevalence of 13% was reported in one study of CFS [31]. Panic should be suspected when symptoms are markedly episodic. Post-traumatic stress disorder has been reported to have higher than general population prevalence in patients with CFS [32] and is associated with a report of previous abuse (see below). Some CFS patients will meet criteria for hypochondriasis, because of persistent anxious concern about the nature of their illness. Others may meet the criteria for somatization disorder, because of a long history of multiple symptoms. The majority of patients with CFS who do not meet the criteria for anxiety or depression will fit the undemanding criteria for a diagnosis of undifferentiated somatoform disorder, but this is largely replacing one set of ignorance with another and does not advance the cause very far. The association of CFS with psychiatric disorders appears not to be explained simply by overlapping symptoms, as it remains high even when fatigue is excluded from the diagnostic criteria for major depression [33, 34]. The occurrence of depression or anxiety disorders in patients with CFS cannot be attributed entirely to referral bias, as the rate is still elevated, although less so, in community cases. Neither does it appear that depression can be explained entirely as a reaction to disability, as it has been found to be more common than in patients with other chronic disabling medical conditions, such as rheumatoid arthritis [35]. In these studies, the absolute rates of

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psychiatric disorder vary, according to the vagaries of interviews, methods, and criteria, but what does not vary is the finding that rates are about two times higher in CFS patients than in those with other disabling medical conditions. However, many patients with CFS do not have depressive and anxiety syndromes, even after detailed assessment [34]. The relationship with somatoform disorders is controversial, both theoretically and in the ‘‘real world’’. All disorders whose diagnostic criteria include a long symptom checklist but lack definitive ‘‘external’’ diagnostic features (biochemical, pathological or radiological) are certain to overlap. Ninety-five percent of those seen in a UK CFS clinic also fulfilled the criteria for neurasthenia [36], even if none of the patients had ever heard of the term, while 70% of those attending an Austrian clinic with the diagnosis of neurasthenia also fulfilled the criteria for ICD-10 undifferentiated somatoform disorder [37]. Whether this will get us very far is not clear: there is a danger of using one unexplained syndrome (e.g., CFS) to explain another (ICD-10 somatoform disorder), or vice versa. It has been proposed that depression, anxiety and CFS have shared risk factors. These may include both genetic factors [38] and adverse experiences such as abuse and victimization [39]. The lack of acceptance by others of the suffering associated with these medically ambiguous conditions may also contribute to emotional distress [40].

EPIDEMIOLOGY Fatigue is common, but CFS as currently defined is relatively rare. A large survey of 90,000 residents in Wichita, Kansas, which used rigorous assessment and exclusion criteria, found that whilst 6% of the population had fatigue of more than 1 month duration, only 235 per 100,000 (or 0.2%) had CFS [41]. It should, however, be noted that the application of current diagnostic criteria [12] excluded large numbers of patients, mainly because of diagnoses of rheumatoid arthritis and psychiatric disorder. Few modern epidemiological studies have looked specifically at neurasthenia. In an Australian national sample that did include neurasthenia, prolonged and excessive fatigue had a population prevalence of 13%, but with substantial comorbidity. ‘‘Pure’’ neurasthenia was reported in 0.5% [42]. It was slightly commoner in the Zurich studies of Jules Angst, but again comorbidity with depression and anxiety was conspicuous [43]. CFS is more common in women: the sex ratio has been reported to be about four to one [41]. The most common age of onset for CFS is between 30 and 50 years. The syndrome is also diagnosed, although controversially, in children. A recent epidemiological study from the United Kingdom found a prevalence of CFS

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of only 0.002% in 5–15-year olds [44]; another in the United States found it to be equally uncommon [45]. In the original nineteenth century formulation, neurasthenia was described as an illness associated with higher socio-economic status, of high achievers and ‘‘captains of industry’’. Likewise, when myalgic encephalomyelitis first became popular in the 1980s, it was labelled by the media as ‘‘yuppie flu’’. With the passage of time, neurasthenia descended the social scale, until it became one of the commonest diagnoses in very disadvantaged groups, such as New York garment workers. For CFS and its cousin fibromyalgia, new epidemiological studies have confirmed a higher prevalence in persons of lower socio-economic status and in those who have received less education [46, 47]. CFS is associated with substantial self-reported loss of function and substantial work disability [48]. Unemployment in patients with CFS attending specialist services in the United States was as high as 50% [49]. It is often noted that the diagnosis of CFS is almost entirely restricted to Western nations, whereas the symptoms of fatigue and pain are universal. It is unclear to what extent this reflects differing epidemiology or simply different diagnostic practice. The WHO Collaborative Study of Psychological Problems in General Health Care, conducted in 14 countries, reported wide variations in the prevalence of persistent pain (including both medically explained and medically unexplained) and fatigue [50, 51]. If we move from symptoms and research criteria to actual labels, the cultural variation is enormous. CFS, for example, is clearly a very big issue in the English-speaking world, Scandinavia, and Holland, but mysteriously is not talked about in most other countries. One can find the occasional paper from Italy, Spain, and Germany, but these usually reflect the interests of one or two clinicians. CFS seems to be ignored in the Francophone world, as indeed is neurasthenia. The same clinical territory is instead claimed by ‘‘spasmophilia’’, a concept virtually unknown to the rest of the world [52]. The obvious question is whether disorders such as CFS can be found in the Francophone world, but are ignored (as some argue). One paediatrician returning to practice in France after a period of working in England was astonished by the absence of any cases of severe CFS in French children, whereas they had formed a demanding part of his practice in London [53]. He argued that it would be inconceivable that children with the level of disability that he had witnessed in England (confined to bed or wheelchairs and unable to undertake any form of education) could have been overlooked in France, if they existed. Our hypothesis is that fatigue syndromes are universal, but that culture is important in understanding the transition from symptoms to disability. Where there is considerable concern around concepts such as immune dysfunction, viral persistence, and environmental toxicity (irrespective of

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the true prevalence of all of these factors), there may be a greater likelihood of symptom persistence and severe disability. Finally, the vicissitudes of the diagnosis of neurasthenia in China are such that this topic deserves a separate text of its own. Arthur Kleinman will be forever associated with his studies of neurasthenia in Chinese society, suggesting that it was a culturally sanctioned expression of distress, akin to depression, where more ‘‘psychological’’ forms of distress would be less acceptable and seen perhaps as a political gesture [54]. Sing Lee has argued that even this complex formulation does not do justice to Chinese concepts of health and illness, and in particular mind and body [55].

PROGNOSIS The prognosis for patients with CFS is variable. The condition typically has a chronic but fluctuating course. Prospective studies in the general population report that about half of CFS patients have partial or complete remission at 2–3 years [56]. Poor outcome in CFS is predicted by longer illness duration, more severe symptoms, older age, depression, and lack of social support [57], and also by a strong belief in physical causes [58]. Severely disabled patients attending specialist clinics have a particularly poor prognosis [59].

ETIOLOGY The precise aetiology of CFS remains unknown. A wide range of factors have been proposed, but none unequivocally established. The available evidence may be summarized as suggesting that a combination of environmental factors and individual vulnerability initiates a series of social, psychological, and biological processes that lead to the development of CFS (Table 5.3). These factors will be discussed under the headings of predisposing, precipitating and perpetuating factors. It is worth noting that, with notable exceptions, most research in this area is based on small case–control studies (typically 10–20 patients per case and control group) with insufficient power to control for confounding variables, thereby limiting our ability to draw strong causal inferences about any of the findings reported below.

Predisposing Factors Biological Factors There is modest evidence from family and twin studies for genetic factors playing a part in predisposing individuals to CFS. A small study found that

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T A B L E 5.3 Possible aetiological factors to consider in a formulation of chronic fatigue syndrome Predisposing Biological

Genetics

Precipitating Acute disease or injury

Psychological Personality

Perceived stress

Social

Life events

Lack of support

Perpetuating Neuroendocrine changes Deconditioning Sleep disorder Depression Fixed disease attribution Catastrophizing Low self-efficacy Avoidance of activity Information Lack of legitimacy of illness Social or work stress Occupational and financial factors

individuals with a family member with CFS are more likely to also have the condition [60]. In a study of 146 female–female twins, one of whom had CFS, the concordance was 55% in monozygotic and 20% in dizygotic twins [61], suggesting moderate heritability and also the importance of environmental factors.

Psychological and Social Factors A predisposing personality type is often commented on by clinicians, but has been little studied. The clinical observation that CFS patients lead abnormally active lives prior to becoming ill has received limited empirical support [62]. Childhood and adult neglect, abuse, and maltreatment have been reported by some, but not all studies, to be more common in CFS than in medical comparison groups [39]. Low social status and lower levels of education seem to be risk factors (see above).

Precipitating Factors Biological Factors There is good evidence that infection can precipitate CFS, whilst the historical literature on neurasthenia frequently reported post-infective onset, the main culprits being influenza and typhoid fever. Modern epidemiological research has failed to confirm the association with influenza [63], and typhoid fever has yet to be studied. Instead, prospective studies have found that the specific infections associated with the

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subsequent development of CFS include Epstein–Barr virus infection [64], Q fever [65], viral meningitis [66], and viral hepatitis [67]. The aetiological mechanisms to explain these associations remain unclear, but may include both immunological factors and an acute reduction in activity [64] (see perpetuating factors below). The role of physical injury in the aetiology of CFS has been controversial, in part because of the implications for legal liability and compensation. In general, traumatic explanations of CFS are not very common, as compared, for example, to infective triggers [68].

Psychological and Social Factors Clinical experience indicated that patients often report the onset of CFS as occurring during or after a stressful period in their lives. The evidence for life stress or life events being a precipitant of CFS is however both limited and retrospective [69]. One of the best studies so far examined 64 cases and a similar number of matched controls. An excess of severe life events and difficulties was found in the CFS cases for the year prior to onset. More specifically, a certain type of life events called dilemmas (defined as events when the person had to choose between two equally undesirable responses to circumstances) was found in one-third of CFS cases and none of the controls [70].

Perpetuating Factors Biological Factors There has been much interest in the potential role of ongoing infection and associated immunological factors, not least because many of the symptoms of CFS remind sufferers of those of viral infections. It was previously thought that chronic Epstein–Barr virus infection was a cause of CFS, but that hypothesis has been rejected, to be replaced by much sounder evidence that this infection has a particular propensity to trigger CFS [64]. There have been numerous reports of chronic infection with other agents in CFS, but no compelling evidence has been presented. Immunological factors, especially cytokines, have also been much investigated in CFS, not only because of the possible triggering effect of infection, but also because administration of immune active agents, such as interferons, is recognized as a cause of fatigue and myalgia [71], and because similar symptoms in conditions like hepatitis C have been associated to changes in measured cytokines [72]. A variety of immune changes have been reported in patients with CFS. Chief amongst these are lowered natural killer cell activity and a modest

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immune activation, but the results have been difficult to replicate and bring together [73]. Once again, the direction of causality is unclear—are these, for example, secondary to the modest hypocortisolaemia that is frequently reported? The hypothesis that CFS is associated with immune activation therefore remains tantalizing, but unproven. The bulk of evidence indicates that there are no proven pathologic or biochemical abnormalities of muscle or muscle metabolism, either at rest or with exercise, other than those associated with deconditioning. Deconditioning describes the physiological changes that lead to the loss of tolerance of activity after prolonged rest (as a result of pain, for example). It has been found in many but not all patients with CFS [74, 75]. Deconditioning offers a potential biological explanation for exercise-induced fatigue and worsening or persistent muscle pain in patients with CFS, and also provides a rationale for treatment using graded activity (see below). Patients with CFS typically complain of unrefreshing and broken sleep, a symptom that has been objectively confirmed using polysomnography. Abnormalities in sleep have been claimed to be of major aetiological importance, but their significance remains unclear [76]. A core finding in CFS is that patients report greater cognitive effort and more cognitive impairment than is detectable on objective assessment. Or, to put it another way, CFS is a disorder of effort perception, both physical and mental. Patients require additional central resources to produce the same amount of mental work, as neuroimaging is starting to demonstrate [77], and consistently underestimate their performance relative to normal performance [78]. This has been repeatedly shown not just in neuropsychological studies, but also in studies of exercise tolerance (see [79]). Abnormal perception of sleep has also been found in CFS [80]. The source of these abnormal perceptions is unclear, and will require a careful investigation. Is it a primary central information processing abnormality? Alternatively, is it the consequence of avoidance of demanding tasks? Irrespective of the cause, one consequence should be a shift away from unrewarding attempts to show static structural lesions in the central nervous system to studies of what is actually impaired in CFS—the dynamics of physical and mental effort. One of the best-supported biological abnormalities reported to be associated with CFS is a change in neuroendocrine stress hormones. A repeated observation has been a tendency to low blood cortisol and a poor cortisol response to stress [81]. This finding differs from what would be expected in depression (in which blood cortisol is typically elevated) but is similar to that reported in other stress-induced and anxiety states. It is unclear whether this is a primary abnormality or merely a consequence of inactivity or sleep disruption, but recent evidence is starting to suggest that the changes are multifactorial, and might be a consequence of illness. They seem to be reversed by behavioural interventions (see [82]).

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Failure to maintain blood pressure when assuming erect posture (orthostatic intolerance) and particularly a pattern in which the heart rate increases abnormally (postural orthostatic tachycardia syndrome) have been reported in CFS [83]. This finding has been interpreted as indicating abnormal autonomic nervous system function. However, postural hypotension occurs after prolonged inactivity [84], and its specificity to CFS remains unclear. The brains of patients with CFS are probably structurally normal, although minor abnormalities have been reported in a minority of patients [85]. A small magnetic resonance imaging study suggested a deficiency of brain choline in patients with CFS compared with healthy controls [86]. The use of functional brain imaging has great potential to elucidate the biology of syndromes such as CFS in which the source of fatigue is felt to be central rather than peripheral. An early single photon emission computed tomography (SPECT) study [87] and a positron emission tomography (PET) study [88] reported reduced brain stem perfusion in patients with CFS. However, another study found fewer differences when CFS was compared with depressed patients, reminding us of the need for careful control for variables such as depression [89]. There is evidence of more widespread cerebral activation in CFS patients than controls when performing a fatiguing cognitive task [90]. Although tantalizing, these functional brain imaging findings must be regarded as preliminary. Furthermore, evidence of changes in brain activation or brain reorganization should not be taken to mean that the symptoms are necessarily based in fixed neurological pathology; behavioural rehabilitation and drug therapy can potentially reverse such changes [91].

Psychological and Social Factors Although the cause of CFS is unknown, many patients, and especially those seen in specialist clinics, strongly attribute their symptoms to a physical disease [92]. A systematic review of prognostic studies in CFS found that such strong attributions predicted a poorer outcome [58]. The mechanism of this effect is unclear. It may be because such an attribution favours focusing attention on symptoms, more passive coping, and greater inactivity [93], or alternatively, it may lead to non-participation in potentially effective psychological and behavioural treatment (see below). Catastrophizing is a tendency to make excessively negative predictions about symptoms, for example, ‘‘If I do more, my pain or fatigue will keep getting worse and worse’’. Catastrophizing has been observed in patients with CFS [94] and is associated with increased symptom vigilance and avoidance of activity, and more severe disability. Furthermore, a reduction in the belief that activity is damaging is associated with recovery during rehabilitative therapy [95], suggesting that it may be a critical psychological target for effective rehabilitation.

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Self-efficacy is the belief that one can do something, despite symptoms. It has been found to be low and this has been associated with more severe disability in patients with CFS [96]. Achieving an increase in self-efficacy is another potential target for treatment that aims to improve function. Patients cope with their symptoms in different ways. The way a patient copes will also be influenced by his illness beliefs [97]. Of particular interest is coping by avoiding any activity that it is feared will exacerbate symptoms. This ‘‘fear-avoidance’’ phenomenon is well established in chronic pain patients [98] and has also been observed in CFS [99] and in fibromyalgia [100]. Objective assessment also confirms that patients with CFS show reduced overall activity, with most patients oscillating between activity and rest, and a quarter being more pervasively inactive. This reduced activity produces deconditioning, and increasing activity is a treatment task. Another potentially important coping behaviour is the focusing of attention on symptoms, so-called symptom focusing or symptom vigilance [101]. This behaviour is, not surprisingly, associated with catastrophizing beliefs and greater perceived symptom intensity. It offers another target for treatment. Patients’ beliefs about their illness and associated coping behaviour will be influenced by the information received from others. A striking social aspect of CFS is the high level of activity of patient support and advocacy organizations, mainly over the Internet [102]. Studies from the United Kingdom have reported that patients who are members of a support group have a poorer outcome, despite similar illness duration and disability [103], and a poorer response to rehabilitation [104]. It is unknown whether this reflects self-selection into such groups or the effect of the group on patients’ beliefs, coping, and willingness to engage in rehabilitation. Other factors include the experience of repeated questioning of the legitimacy of one’s illness by doctors and others, which probably serves to drive some patients to join advocacy organizations [3,105]. Perhaps unsurprisingly, in fibromyalgia, the acquisition of a disability pension is also associated with a worse prognosis [106].

Summary In summary, there is some suggestive evidence that patients are predisposed to develop CFS by some combination of genetic factors, previous experience, and possibly lack of social support. Many patients with CFS give a history of preceding infection. Others can identify no precipitant. Most research has been into factors associated with established illness, so-called perpetuating factors, as these are both clearly more accessible to study and more relevant to treatment of established cases. A large number of biological factors have been investigated, with interest initially being directed at peripheral nerves and muscles and subsequently focusing on the central nervous system and its neuroendocrine and autonomic

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outputs. There have also been some tantalizing findings suggesting but not yet establishing the role of immune factors. The physiological effects of inactivity seem to be important. There is substantial evidence for the importance of psychological and behavioural factors, especially the fear of exacerbating symptoms and the associated avoidance of activity. Social factors are harder to study, but often of striking importance clinically.

Models of CFS The above findings can be amalgamated into models. There are three main models corresponding to biological, psychological, and social perspectives, although in reality all three are probably relevant. It is well known that the immune and central nervous system interact and also have reciprocal relationships with sleep and activity. It is therefore possible to construct a tentative biological model in which these interact to perpetuate the illness [107]. There seems to be evidence for the role of infection triggering CFS and perhaps some neuroendocrine mechanisms acting to perpetuate illness. Whatever the biological aspects of CFS, cognitive-behavioural models assume that the symptoms and disability are perpetuated, at least in part, by psychological, behavioural, and social factors. Biological factors are assumed to be either only partially responsible for the illness or largely reversible [108]. The cognitive-behavioural models for chronic pain and CFS have much in common [98]. Both emphasize the importance of fear of symptoms leading to focusing on the symptoms, helplessness, and avoidance of activity. This model provides the rationale for behavioural and cognitive-behavioural approaches to rehabilitation (see below). The third model emphasizes the role of social factors in shaping the illness. A fight for the legitimacy of the syndrome as a chronic medical condition is central [109]. Patient advocacy has been strongly hostile to psychological and psychiatric involvement, probably because it is seen as undermining legitimacy. The social model proposes that patient organizations, whilst providing valuable social support, can also shape patients’ illness beliefs, medical care, and disability payment seeking in ways that are not conducive to recovery [110].

DIAGNOSTIC EVALUATION Effective management of patients with possible CFS and/or neurasthenia requires first that alternative medical and psychiatric diagnoses are considered and second that the patient receives a comprehensive assessment upon which to collaboratively plan management.

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Identifying Medical and Psychiatric Conditions Medical Differential Diagnosis The medical differential diagnosis for CFS and linked conditions is a long one, as many diseases present with pain and/or fatigue [111]. A physical examination must therefore be performed in every case to determine any alternative medical diagnoses. As with many chronic diseases, particularly rheumatologic conditions, time is often the principal arbiter as the conditions evolve clinically. For symptoms in general, 75% of patients presenting to primary care improve within 2–4 weeks [112]. Thus, it makes sense to rely on an initial 4–6 week wait to clarify whether the symptoms will be persistent [113]. For persistent symptoms, most of the common medical diseases can be diagnosed from a standard history, physical examination, and basic laboratory studies. When symptoms exceed 4–6 weeks, basic investigations are appropriate. The following have been found to be adequate as screening tests: thyroid-stimulating hormone, erythrocyte sedimentation rate (sensitive for any condition with systemic inflammation), complete blood count, and basic chemistries. Withdrawal of some medications (particularly statins) is also appropriate. Special investigations should only be carried out if clearly indicated by history or examination. Immunological and virological tests are generally unhelpful as routine investigations and remain research tools. Sleep studies can be useful in excluding other diagnoses, especially when the fatigue is characterized by sleepiness: these include sleep apnoea, narcolepsy, nocturnal myoclonus, and periodic leg movements during sleep. Once symptoms become chronic (>3 months) and remain unexplained, the general approach is to avoid excessive testing, establish regular follow-up, screen for depressive and anxiety disorders, and focus on symptoms management. Those concerned about missing a serious medical diagnosis can be reassured that in most cases the primary care physician’s initial judgement in this regard is likely to be accurate [114]. However, there is some evidence that CFS may be over-diagnosed by primary care physicians [115], and psychiatrists should feel able to request second medical opinions.

Psychiatric Differential Diagnosis The under-diagnosis of psychiatric disorders is particularly common [116], probably reflecting a focus of the initial medical assessment on somatic symptoms and a tendency to disregard mood changes as simply being a consequence of these. The most important psychiatric diagnoses to consider are depressive and anxiety disorders, because of their frequency and their

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implications for treatment. Depression may be ‘‘masked’’ and require expert assessment. Panic attacks with agoraphobia may cause intermittent severe fatigue and disability. Somatoform disorders are common, but have fewer implications for management. A diagnosis of somatization disorder indicates a poorer prognosis and hypochondriasis indicates special attention to repeated reassurance seeking, which may perpetuate fears of undiagnosed disease [117].

Assessment of the Illness Other than making diagnoses, the aims of the assessment are: (a) to establish a collaborative relationship with the patient, (b) to elicit the patient’s own understanding of his illness and how he copes with it, and (c) to identify current family and social factors such as employment and litigation that may complicate management. It is important to inquire fully about the patient’s understanding of his illness (e.g., ‘‘what do you think is wrong with you?’’ or ‘‘what do you think the cause is?’’). Patients may be fearful that their symptoms indicate a severe, as yet undiagnosed, disease or that exertion will cause a long-term worsening of their condition. A formulation (see Table 5.3) that identifies potential predisposing, precipitating and perpetuating factors is valuable both in providing an individualized explanation to the patient and for targeting interventions.

MANAGEMENT Agreeing on a Diagnosis, Formulation and Management Plan Forming a Therapeutic Relationship with the Patient The patient will have often seen many other doctors and will have experienced problematic interactions with them [105]. Other doctors may have offered overly biomedical or overly psychological explanations, or even dismissed the patient completely.

How to Explain Psychiatric Involvement Psychiatrists’ involvement in management may be interpreted by the patient as indicating that their condition is considered to be ‘‘all in their head’’. It is often best to begin with a somatic assessment and only then to introduce discussion of psychological factors. This is best done in a non-blaming and normalizing way. For example: ‘‘You have clearly had a terrible time made

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worse by not being believed. It is entirely understandable that this has got you down’’. It is generally unhelpful to force a psychiatric diagnosis on an unwilling patient. It is also important to explain how treatments commonly associated with psychiatry (particularly antidepressant medication and cognitive-behavioural therapy, CBT) do not necessarily imply that the person is mentally ill. Rather, they can be explained as ways of normalizing brain and bodily function in conditions that are exacerbated by stress.

Giving the Diagnosis It is important to give the patient a positive diagnosis supplemented with an aetiological formulation. There is some controversy about whether giving patients a diagnosis of CFS is helpful or harmful [118]. There are those who feel that a diagnosis enables patients to both conceptualize their illness and communicate about it with others [119]. Others are concerned about the potentially harmful effect of a diagnosis, arguing that it medicalizes and pathologizes symptoms in a way that can exacerbate social and occupational disability [120]. The particular label of myalgic encephalomyelitis, used in the United Kingdom as a popular term for CFS, carries with it the connotation of an organic inflammatory disease of the central nervous system, as well as numerous other cultural ‘‘tropes’’. In a large study using the General Practice Research DataBase, it was found that patients with the label of myalgic encephalomyelitis seemed to do worse than those with the label of fibromyalgia or post-infective fatigue syndromes [121]. In our clinical experience, what matters less is the label, and more what information is given after the act of diagnosis. A positive diagnosis linked to an explanation of the potential reversibility of symptoms and a management plan to achieve this is an essential starting point for effective management.

Offering an Explanation This should ideally be scientifically accurate, acceptable to the patient, and congruent with the management plan. It can be explained that, whilst the specific causes of CFS or fibromyalgia remain unknown, a combination of vulnerability and environmental stress involving the brain and the endocrine system are most likely. One such explanation is that the illness is a disorder of brain function rather than structure; that is, a ‘‘functional’’ nervous disorder [122].

The Management Plan This should be explained to the patients as following from the formulation, focusing on illness perpetuating factors and consisting of elements aiming to

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(a) relieve symptoms such as depression, pain, and sleep disturbance with agents such as antidepressants, (b) assist the patients efforts at coping by stabilizing activity and retraining the body to function effectively (graded exercise, CBT), and (c) assist the patients in managing the social and financial aspects of their illness and where possible remaining in or returning to employment (problem solving).

General Measures Providing Advice on Symptom Management One of the most important interventions the clinician can make is to encourage and guide the person in the active self-management of his illness. Such advice will include the importance of being realistic about what one is able to accomplish, without giving up hope for improvement in the future. It should include information on the pros and cons of self-medication, particularly with analgesics, and might also require a discussion of the potential benefits and risks of iatrogenic harm from seeking treatment from other practitioners, conventional and alternative. The overall aim is to encourage the patients to feel that there are things that they can do to manage the condition themselves, to accept the reality of their illness while still planning positively for the future, and to be cautious about seeking potentially harmful and expensive treatments.

Managing Activity and Avoidance Once activity is stabilized and large fluctuations between excessive rest and unsustainable activity reduced, gradual increases in activity can be advised. It is critical, however, to distinguish between carefully graded increases carried out in collaboration with the patient and a ‘‘forced’’ or over-ambitious exercise regimen.

Managing Occupational and Social Factors Patients who continue working may be over-stressed by the effort of doing this. Those who have left work may have become inactive and demoralized and may not wish to return to the same job. These situations require a problem-solving approach to consider how to manage work demands, achieve a graded return to work, or plan an alternative career. Ongoing litigation is potentially a complicating factor, because it reinforces (and may reward) the patient for remaining symptomatic and disabled. A large trial in Canada that randomized patients either to litigation or to no fault

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compensation for whiplash injury found that symptoms lasted longer in the former group [123].

Pharmacological Therapies Antidepressants Antidepressant drug treatment is indicated by the fact that (a) many patients with CFS have depressive and anxiety syndromes and (b) these agents reduce pain and improve sleep, even in the absence of depression. However, the evidence that antidepressants lead to an overall improvement in CFS is mixed [124]. Tricyclic antidepressants (TCAs) are probably more effective than selective serotonin reuptake inhibitors (SSRIs) for relieving pain [125] and for inducing sleep. Small doses (e.g., 25–50 mg/day of amitriptyline) are often adequate for these purposes. SSRIs are generally better tolerated than TCAs. However, the very few available clinical trials have not been very encouraging for the treatment of CFS [126]. Venlafaxine, a dual serotonin and norepinephrine reuptake inhibitor (SNRI), is useful for pain and has been reported as showing initial promise in CFS [127]. Moclobemide, a reversible inhibitor of monoamine oxidase A, has been reported to be of no benefit in fibromyalgia, but of some value in increasing energy in CFS [128].

Other Pharmacological Agents Analgesics, including opiates, are occasionally used for pain in CFS and related conditions, especially fibromyalgia. However, there are no trials of their use, and a major concern about the development of dependence. As with opiates, great caution is required with benzodiazepines, because of the risk of dependence in patients with chronic conditions. TCAs are probably preferable to treat insomnia, and the chronic use of benzodiazepines should be reserved for cases with intractable anxiety. Given the finding of low serum cortisol, it is not surprising that corticosteroids have been tried. Hydrocortisone was reported to produce some benefit in CFS, but was not recommended because of the long-term risks of adrenal suppression [129]. Fludrocortisone has been used in CFS patients with orthostatic hypotension, but has been found to be of no value [130]. Amphetamines have been tried in CFS with some evidence of short-term efficacy [131], but are not widely used because of the risk of dependence and are not recommended.

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Numerous other agents have also been tried in CFS. These include central nervous agents such as galanthamine, vitamins such as B12, alternative approaches such as homeopathy, antiviral agents including acyclovir, immunological therapies such as immunoglobulins, and many others. None can yet be recommended [132].

Summary It is wise to exercise caution when prescribing in CFS. The mainstay of therapy continues to be antidepressant drugs, which may be helpful for mood, pain, and sleep, but have limited effect on overall outcome. TCAs are preferred for night sedation and pain, but greater tolerability may mean that an SSRI or an SNRI is preferable as first-line treatment. In current clinical practice, patients often receive low doses of antidepressants, but higher doses may be required to achieve a therapeutic response in some patients. The increased interest in pharmacological treatment of functional syndromes in the past few years will likely expand treatment options, and there are several new medications that show promise, including duloxetine, milnacipran, and pregabalin. However, the available evidence suggests that drug therapy has a limited role in the management of these conditions.

Specialist Non-Pharmacological Treatments If the patient does not respond to or requires more active treatment than the general and pharmacological management described above, referral for specialist non-pharmacological therapy should be considered. For most patients, a rehabilitative outpatient programme based on appropriately managed increases in activity, either as graded exercise therapy or as CBT, is indicated. Some patients may require inpatient multidisciplinary rehabilitation, but at present there is inadequate evidence of its efficacy [133].

Graded Exercise Therapy This is a structured progressive exercise programme administered and carefully monitored by an exercise therapist. It may be given in individual or group form, but the evidence is best for individually administered treatment [134]. Graded exercise therapy follows the basic principles of exercise prescription for healthy individuals, adapted to the patient’s current capacity. The initial exercise intensity and duration are determined on an individual basis, and may be done using heart rate monitoring. Most patients can begin at an intensity of 40% of their maximum aerobic capacity, which approximately

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equates to 50% of their estimated individual heart rate reserve added to their resting heart rate (e.g., if the maximum heart rate is 180 beats per minute (bpm) and the resting heart rate is 80 bpm, the heart rate reserve is 100 bpm and the exercise target heart rate is 80 + (0.5 × 100) = 130 bpm). This heart rate should not be exceeded; if it does, the patients should stop exercising for one or two minutes and then resume. Patients who are very disabled, or who have extremely low exercise tolerance, may be better to begin with two weeks of stretching alone without aerobic activity, and then to adopt alternate day aerobic exercise, before building up frequency, duration, and then intensity. The important principle is to calculate exercise capacity conservatively to start with, as well as ensuring agreement to try what is proposed. At each clinic visit, joint planning of the following one or two weeks’ exercise prescription is completed. The initial aim is to establish a regular pattern of exercise (usually walking), with exercise 5 days per week. Home exercise sessions should initially last between 5 and 15 minutes, depending on ability and exercise tolerance. The duration is increased by 1 or 2 minutes per week up to a maximum 30 minutes per homework session. Then the intensity of exercise can be increased to a target heart rate of 60% and then 70% of their heart rate reserve added to their resting heart rate. Patients will respond differently: some will take a lot longer to adapt to each new level, whereas others will have to be held back, particularly those who have been active sports participants in the past. Those patients who are inclined to over-exert themselves in an attempt to speed up the recovery process should be monitored carefully, as this can be a contributing factor in non-recovery or relapse. Graded exercise therapy has been found in a systematic review to be of benefit in both CFS and fibromyalgia. In fibromyalgia, four high-quality aerobic training studies reported significantly greater improvements in pain with exercise than with comparison treatments [135], whilst in CFS, four highquality trials all found benefits over comparison treatments in symptoms and disability [136]. There were, however, substantial numbers of dropouts in one study. Of particular interest is a trial of brief simple education about the physiology and rationale of exercise that found it to be as effective as CBT [137]. The Australian immunologist Andrew Lloyd reviewed all the evidence in an editorial entitled ‘‘To exercise or not to exercise in chronic fatigue syndrome? No longer a question’’ [138]. However, if we were to judge only by patient confidence in the intervention and anecdotal evidence of possible ill effects from apparently hasty and amateurish programmes, we would have to conclude that it remains very much a question.

Cognitive-Behavioural Therapy (CBT) There are a variety of types of CBT. Here we refer to a collaborative psychologically informed type of rehabilitation that aims to achieve both graded

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increases in activity and changes in unhelpful beliefs and concerns about symptoms. It may also include problem solving for life and occupational dilemmas. It can be given in an individual or group form, although there is more evidence for the efficacy of individual therapy [139]. The procedure includes: (a) non-judgmentally eliciting the patients’ own illness model, appraisal of situation, and the ways to cope; (b) introducing the possibility of alternatives; (c) helping the patient choose which beliefs and coping behaviours are most helpful by conducting behavioural experiments. The key question for the behavioural experiment is: ‘‘Is it possible for me to make changes in my behaviour that will allow me to achieve my goals?’’ The patient is encouraged to think of the illness as ‘‘real but reversible by his or her own efforts’’ rather than (as many patients do) as a fixed unalterable disease. Their ability to make changes is a test of these alternative hypotheses. The aim of behavioural change is to increase activity and to achieve specific goals. Problem solving is used to address relevant occupational and interpersonal difficulties. A typical therapy takes place over 14 sessions. The duration of each session is initially 90 minutes, then 50 minutes. The first four sessions are weekly; the subsequent ones bi-weekly over 5 months. In CFS, individually administered CBT has been found to be effective in two systematic reviews, with approximately two-thirds of patients showing significant improvement. Three high-quality trials (total 164 patients) found improvement in both symptoms and disability and concluded that CBT appears to be an effective and acceptable treatment for adult outpatients with CFS [132, 140]. However, CBT remains a skilled treatment that not everyone is qualified to deliver: Dutch general practitioners were unable to perform it for CFS patients [141].

Patients Who Do Not Respond to Treatment Most patients respond to some degree to rehabilitative therapies, but many will only achieve partial improvement and some will fail to improve at all. In such cases, the management is the same as that for other chronic conditions: to maximize functioning and quality of life while minimizing the risk of iatrogenic harm. While it is desirable that all patients should have a trial of rehabilitative treatment, a balance has to be struck between heroic efforts at therapy and acceptance of chronic illness. Many physicians are reluctant to accept chronic disability in these patients, perhaps because they do not regard these conditions as true diseases. Pushing patients beyond their capabilities may only demoralize them, or cause them to retreat further into invalidism. For such patients, regular follow-up from a single physician is often the best treatment.

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SUMMARY Consistent Evidence CFS is not a new condition. Both CFS and neurasthenia can be reliably diagnosed using well-defined epidemiological criteria. The core symptom in CFS is excessive mental and physical fatigue, made worse by minor mental or physical activity, and not readily relieved by rest. Sleep is rarely normal. There are substantial overlaps between CFS and neurasthenia: virtually everyone who fulfils criteria for the former will fulfil criteria for the latter. There is considerable overlap between CFS, neurasthenia, and other unexplained syndromes such as fibromyalgia. In the English-speaking world, CFS is often called myalgic encephalomyelitis. There is overlap between CFS, neurasthenia, and common psychiatric disorders, mainly depression and anxiety. Such comorbidity is more pronounced in specialist centres. CFS affects all age groups, but is very uncommon before puberty. It is commoner in females, especially in specialist settings. Contrary to popular belief, neither CFS nor neurasthenia is commoner in upper social classes. CFS can be triggered by external stressors such as certain viral infections and/or life events. Some viral infections, most particularly Epstein–Barr virus infection, are more likely to trigger CFS than others. Vulnerability to these triggers is increased by a previous history of emotional disorders. Patients seen in specialist settings in Western cultures with the label of CFS or its equivalents are often resistant to psychological labels and/or explanations. Prolonged rest is not the treatment of choice for CFS.

Incomplete Evidence Although both CFS and neurasthenia can be reliably diagnosed, their nosological status is uncertain. The origin of the profound physical and mental fatigue in CFS is fundamentally unknown, but it is more likely to reflect central rather than peripheral processes. It is unlikely that there is a primary neuromuscular origin to symptoms: observed abnormalities in the peripheral muscles are more likely to be secondary rather than primary. There is some evidence that particular personality types, such as perfectionism, increase the risk of CFS, but this is not established beyond doubt. Early deprivation/abuse is often reported in clinical populations, but whether this is a genuine risk factor or the result of selection or recall bias remains unclear.

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There is increasing evidence of dysfunction of the hypothalamic-pituitaryadrenal axis in CFS: it is unknown how or if this is related to ill health, or is a consequence. The changes are not those seen in classic major depression. There is increasing evidence of mild immune activation in CFS: it is uncertain if this is a primary abnormality, or related to neuroendocrine changes. Orthostatic intolerance is reported in CFS populations, but it is unclear whether this is secondary, and how it relates to anxiety disorders. Whilst some form of graded activity programme is the best current treatment, it is unclear how, when, and in what form this should be managed. The role, if any, of antidepressant therapy remains unclear. The prognosis of CFS in specialist settings is poor, but it is unclear how much this reflects selection bias as opposed to the true natural history. There is clear genetic predisposition, but what genes are involved, what is the nature of the genetic vulnerability, and how this relates to genetic vulnerability to depression or anxiety is unknown. The cultural epidemiology of CFS and neurasthenia remains uncertain, but fatigue is universal. Why are there cultural variations, and what significance do they have?

Areas Still Open to Research The issues still open to research are many. Among them: how some viral infections, such as Epstein–Barr virus infection, have a particular propensity to trigger CFS; the origin of the sex differences observed in epidemiological studies; the precise nature and role of sleep disturbance; the mechanism of fatigue; how rehabilitative treatment works; how or if CFS can be prevented.

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Commentaries 5.1 From Neurasthenia to Chronic Fatigue Syndrome: A Journey, Not a Destination Kurt Kroenke1 The practical approach to truth espoused by the late nineteenth century pragmatism school of philosophy was succinctly summarized when James wrote: ‘‘You can say either that ‘it is useful because it is true’ or that ‘it is true because it is useful’. Both these phrases mean exactly the same thing’’. In fact, this was presaged by Schiller, who said ‘‘the true is that which works’’. Likewise, the century-long journey from neurasthenia to chronic fatigue syndrome (CFS) is more a work-in-progress than a finished product. While the symptoms remain relatively constant, the disease labels, cultural framing, purported mechanisms, and management have evolved in a complex rather than linear fashion. Sharpe and Wessely eloquently delineate the consensus as well as the current controversies surrounding CFS. From this, I extract five themes that, though not comprehensive, constitute several salient messages. Definitions of CFS are heuristic rather than ultimate truths. As the authors acknowledge, operational criteria for CFS were created to allow researchers to study similar groups of patients. Even so, there have been numerous difficulties. Requiring multiple symptom criteria (e.g., upper respiratory, pain, cognitive, sleep) may in fact over-select for depressive, anxiety, and somatoform disorders. On the other hand, excluding psychiatric disorders or common medical conditions may create an artificial distinction between primary and secondary chronic fatigue. The simple triad of unrelenting fatigue, persistence more than 3–6 months, and disability is more prevalent yet has similar characteristics to more rigorously defined CFS [1]. Other challenges regarding the construct of CFS include its overlap with other functional somatic syndromes [2] and its substantial cultural variability in presentation, labelling, and disability. Associations may be causal, consequential, coincidental, or co-descendant. Though there is an increased prevalence of depression in patients with CFS, depression may either be a cause or a consequence of the chronic, disabling 1

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fatigue. Two of the more commonly cited antecedents of CFS—viral infection and stress—are nearly ubiquitous in the general population. Therefore, the development of persistent fatigue in a small proportion of individuals is just as likely to be a coincidental finding as it is to be a derivative outcome. Finally, fatigue, depression, cognitive difficulties, and pain may ‘‘co-descend’’ from a common pathway (e.g., sleep disturbance, immune dysregulation). Likewise, the directional relationship between objective findings, such as hypocortisolaemia, postural hypotension, deconditioning, neuroimaging changes, and immune abnormalities, is unclear. While the authors nicely illustrate predisposing, precipitating and perpetuating factors, the latter are probably the most promising targets for intervention. Mind-body dualism must be relentlessly opposed. The ‘‘either-or’’ approach to physical and psychological causes remains a major impediment. While the authors ardently articulate an integrated approach that respects both the biological and psychosocial aspects of the illness, some members of the scientific and patient community continue to turn a deaf ear towards psychosocial mechanisms. Indeed, for many chronic conditions, a ‘‘web of causation’’ is more explanatory than a single aetiological factor. While half a dozen major risk factors contribute to the development of coronary artery disease (CAD), these risk factors collectively only explain half of the variance in CAD incidence. No factor is necessary, each may contribute, and many ‘‘causes’’ of atherosclerosis remain unknown. The interaction between mental and medical disorders is increasingly appreciated. Depression and cardiovascular disease is a prime example where the relationship is bidirectional in terms of disease incidence, prognosis, and treatment. There is no diagnostic test for CFS. Even the simple laboratory testing recommended by the authors typically has a low yield but is inexpensive and reassuring. More costly work-ups in specialized fatigue clinics (e.g., immune function, cardiopulmonary testing, neuropsychological batteries) may require large out-of-pocket expenses for the patient and still not guide treatment in an evidence-based manner. Sleep studies may be warranted for the selected CFS patient with excessive daytime somnolence, obesity, abnormal snoring, or other risks or signs of potential sleep apnoea. However, sleep testing is quite expensive and the treatment for patients who test positive is not always easy to tolerate. Thus, routine sleep studies are not advised. Effective treatments require patient collaboration. The two treatments for which there is the strongest body of evidence are cognitive-behavioural therapy (CBT) and graded exercise, not only for CFS but also for fibromyalgia and other functional somatic syndromes [3–6]. However, both CBT and exercise require active collaboration on the part of the patient and a sustained commitment to behavioural changes. Non-adherence and treatment drop-out are particularly common, even among volunteers in closely supervised clinical trials. More passive treatments, like taking a pill, have an adjunctive role in

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symptom management though even here the impact is typically symptom reduction rather than eradication or cure. Antidepressants are most likely to benefit mood symptoms (depression and anxiety) and, possibly, pain, whereas their impact on isolated fatigue is uncertain. Thus, the management of CFS is more like that for diabetes than an acute infection; the patient must partner with the clinician in adhering to prescribed medications, life-style modifications (diet and exercise), and self-management strategies. Finally, the availability of trained professionals to deliver CBT as well as appropriate reimbursement are necessary for a wider uptake, as well as further testing of less complex interventions, such as self-efficacy training [7] and problem-solving therapy, that have improved outcomes for other symptoms.

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debate and controversy. Neurasthenia was established at the end of the nineteenth century, when psychiatry had consolidated its position within academic medicine, and many psychiatrists turned their attention to socalled neurotic disorders which appeared to be linked to stressors within the new industrialized societies. New diagnostic categories such as agoraphobia and traumatic neurosis were defined at the time. Neurasthenia was used for patients, originally mainly from higher social classes, who felt ‘‘weak’’ and not capable of fulfilling the expected societal roles without having a conventional medical disorder as an explanation for their weakness. A century later, the diagnostic category of chronic fatigue syndrome (CFS) was termed, again at a time of societal changes. Historians suggest that 1989 marks the end of the post-war era and the beginning of a new historical period in Western industrialized societies [1]. This coincides remarkably with the establishment of the term CFS as a medical diagnosis. It may be too early to take a historical view of what happened less than 20 years ago and analyse systematically the similarity of processes that may have given rise to the diagnostic concepts of neurasthenia and CFS. Yet, comparing the literature on neurasthenia and CFS reveals a striking difference: whilst aspects of industrialization, urbanization, and economic processes were extensively discussed as possible factors leading to neurasthenia in the nineteenth century [2], societal changes are now rarely considered as important factors for the emergence of CFS and related medical concepts. The comprehensive and clear review of Sharpe and Wessely reveals little, if any, research on how CFS might be seen as determined by more fundamental processes within the modern or postmodern culture. It is difficult to say whether this gap in research is due to specific aspects of the diagnosis of CFS or rather reflects a more general problem of a weak link between psychiatry and the relevant fields of social sciences. As intriguing as the historical analysis is the international comparison. The review reports that CFS is a common diagnosis in some countries, but more or less unheard of in others. Systematic comparative research would be interesting and should go beyond identifying how frequently operationalized diagnostic criteria are met in different populations. Patients’ experience and presentation of symptoms is likely to be influenced by social expectations and cultural factors that also impact on the role of medicine in the given society and diagnostic patterns. In other words, the diagnostic concept of CFS is likely to be embedded in a cultural context, and an isolated epidemiological perspective of differences of symptom rates may fail to capture this. Comparative research should probably consider what diagnoses are used to describe similar forms of distress in different countries. An example is the diagnosis of ‘‘low blood pressure’’, which was commonly used in Germany—although less frequently in recent times—for patients feeling weak, tired, and unable to perform as they themselves or other people

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expected. The diagnosis has the advantage of being undoubtedly recognized as a physical disorder requiring specific medication. This may have been in line with the expectation of many patients and their explanatory model of the symptoms, leading to higher treatment satisfaction. Sharpe and Wessely avoid positioning chronic fatigue as a primary or secondary phenomenon. Yet, it may indeed be an important distinction as to whether fatigue occurs as a consequence of other symptoms, or is the primary problem for the distress of the patient. It has been argued [3] that the incapacity to fulfil a societal role, i.e., the feeling ‘‘I do not have the capacity to do what I want to or is expected’’, is a primary characteristic of CFS, while in other physical and psychiatric disorders such subjective incapacity can occur as a consequence of other symptoms that define the disorder. Yet, primary incapacity is not a concept that would easily fit into the realm of Western medicine, so that patients express their distress in terms of more conventional symptoms and insist on the disorder being a medical illness. Subsequently, CFS and neurasthenia pose a special challenge to medicine, as their nature is distinct from other medical disorders, which would explain why doctors and patients often struggle to find a common basis to understand and treat the problem. Sharpe and Wessely suggest doctors should provide an ‘‘etiological formulation’’. This sounds reasonable, but is difficult to do when (a) medical science has not provided sufficient evidence for an aetiological model, and (b) many patients only accept the explanation of a physical illness, an attitude that goes along with a poorer prognosis. The explanatory model of the patients and their frequent insistence on physical causes for the fatigue has been identified as an obstacle to successful treatment. An alternative approach is to view it as a central feature of the disorder itself [4]. This might be a way to understand better the common features with other disorders characterized by unexplained medical symptoms. The review outlines that CFS overlaps with symptoms of other functional disorders, but does not draw conclusions as to whether this opens up new ways to study and possibly treat the group of similar disorders. In any case, patients expect an explanation for their problems from the doctor, and the explanation provided may influence the motivation to accept a prescribed treatment. Sharpe and Wessely refrain from suggesting that the doctor’s explanation should be worded along the lines of the patient’s expectation, increasing the probability that the patient will follow medical advice. One wonders whether graded exercise therapy follows this approach. That exercise may help to overcome inactivity and fatigue appears common sense. Yet, the challenge is to persuade patients to engage in exercise, and there are different ways to present the idea to the patient. If patients are asked to exercise and become active because they are not as ill as they make other people believe, they are likely to refuse. Within graded exercise therapy,

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however, patients are asked to do exercise because of the illness, which is thus implicitly and explicitly accepted by the doctor. The crucial element of the intervention might be the acceptance of the distress of the patient and the provision of an explanation that enables patients to do something that is different from and incompatible with their own coping strategy, i.e., refraining from activity to avoid further fatigue. This strategy is at the heart of some solution-oriented therapies and has been suggested to be effective in sleep deprivation therapy [5]. More than other disorders, CFS tends to raise the question among clinicians as to whether it really exists. For various reasons, many clinicians doubt that CFS is a disorder in its own right and not just a consequence of obvious or hidden psychiatric disorders. The review clarifies that CFS is indeed rare. As an isolated disorder without any comorbidity it is even rarer, but can be diagnosed in a small group of patients. Following constructivism, diagnoses are constructs to explain the phenomena clinicians face. The criterion for a diagnosis is not whether it does or does not exist in reality, but whether it is useful. A useful construct should help researchers to find ways to understand the distress of the patients and clinicians to treat them effectively. Given the low rate of full long-term recovery and the ongoing struggle between many self-help groups of patients and medical doctors, one might wonder as to whether the diagnostic concepts of neurasthenia and CFS have passed this test. Arguably, the jury is still out on this, and medicine may have to find new approaches to cope with the traditional challenge of patients who feel weak and tired, but do not fit into the established categories of other medical disorders.

REFERENCES 1. 2. 3. 4. 5.

Levy C. (2002) Three Post-War Eras in Comparison: Western Europe 1918-1945-1989. Palgrave: Basingstoke. Gijswijt-Hofstra M., Porter R. (Eds) (2001) Cultures of Neurasthenia. From Beard to the First World War. Rodopi: Amsterdam. Henningsen P., Priebe S. (1999) Modern disorder of vitality: the struggle for legitimate incapacity. J. Psychosom. Res. 46: 209–214. Henningsen P., Priebe S. (2003) New environmental illnesses: what are their characteristics? Psychother. Psychosom. 72: 231–234. Priebe S., Haug H.J. (1992) Interactional pattern in sleep deprivation therapy: an empirical study. J. Nerv. Ment. Dis. 180: 59–60.

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5.3 Disease, Sickness or Illness: Which One Is Chronic Fatigue Syndrome and/or Neurasthenia? Bedirhan Ustun1 Whatever name is given—chronic fatigue syndrome (CFS), neurasthenia, neuro-endocrine-immune dysfunction syndrome, or any other label such as fibromyalgia, myalgic encephalopathy (ME), Gulf War syndrome, or yuppie flu—the nosological status of this group of conditions has remained controversial over the last century [1–3]. Persons who suffer from this condition see themselves ‘‘sick’’: they perceive a change in their energy levels, tire easily, suffer from activity limitation and restrict their participation in daily life at home, work, or social and private leisure activities. Doctors and other health professionals from different disciplines may not agree on this ‘‘disease’’ status. Society as a whole may have varying arrangements for this ‘‘illness’’ about provision of treatment and benefits: many pension systems do not accept this as a form of chronic disability. Unfortunately, the assessment, diagnosis, classification and treatment of these conditions have suffered from lack of precision and objective measures, and from arbitrary definitions. In no other condition has there been such a direct polarization between providers and consumers, which we should pay serious attention to, because it may end up in a potential iatrogenesis, producing undue suffering. The scholarly review by Sharpe and Wessely presents us with a lucid synopsis of the current state of affairs from different dimensions. ‘‘The symptom of fatigue is subjective’’ and the available objective measures to assess this symptom do not pick up the details reported by the person. The vexing issue of comorbidity with depression, anxiety, and other somatic illness may confound diagnosis, treatment, as well as research. ‘‘Pure’’ neurasthenia as described by narrow research criteria has low prevalence rates in epidemiological surveys. Francophone medicine is ignorant of this condition, whereas in China the word ‘‘depression’’ does not exist and shenjing shuairuo, or neurasthenia, has been made famous by Arthur Kleinman [4] as the Chinese version of depressive disorder. Conceiving CFS as a ‘‘functional’’ disorder, the authors conclude with a multidimensional model of aetiology and assessment involving biological, psychological, and social factors. It is noteworthy that their views are compatible with the model of the International Classification of Functioning, Disability and Health [5] in that the body functions regarding energy, sleep, and sensation of pain may be accompanied by psychological functions and 1

World Health Organization, Geneva, Switzerland

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may result in activity limitations in interaction with social and environmental factors [6]. Regarding management of these conditions, wide-spectrum antidepressants that are generally effective in mood and anxiety disorders are unsurprisingly effective here too [7]. Graded exercise [8] and cognitive-behavioural therapy [9] can assist the self-management of the illness by the person her/himself. It is noteworthy that in a recent meta-analytical review the pooled placebo response was 19.6% for CFS interventions, lower than predicted and lower than in some other medical or mental conditions, perhaps linked to patient expectations [10]. Disappointed by the inability of medical science to explain their conditions, many patients turn to alternative medicine, such as acupuncture, aromatherapy, ayurvedic medicine, balneotherapy, homeopathy, osteopathy, reiki, yoga, and various diets. The relevance and effectiveness of these interventions should also be evaluated in future studies, and useful elements could be incorporated into management schemes. The ‘‘ill-defined’’ nature of this group of disorders tests the sharpness of our diagnostic system too. CFS and neurasthenia form a group of complex conditions that may best be categorized as a syndrome (i.e., a collection of signs and symptoms that are taken as a whole under the appropriate conditions). The World Health Organization (WHO) receives more than 5,000 applications each year calling for nosological clarification of these conditions. ME has been formally classified by the WHO as a neurological disorder since 1969 and remains classified in the current ICD as a neurological disorder (G93.3). The fact that neurasthenia is also referred to in the ICD chapter of mental and behavioural disorders as F48.0 is a useful distinction that may be the basis for reliable subcategorization. However, many consumers have found it ‘‘stigmatizing’’ to be classified within other mental disorders. It is somehow paradoxical to see this issue as a stigma, as many other mental disorders are also conceived as brain disorders and have viral theories for their aetiology, such as schizophrenia, autism, depression, and eating disorders. The authors’ proposal for adapting Fukuda et al.’s diagnostic criteria is a sensible one. The inclusion of sore throat and lymph node pain would definitely increase the diagnostic specificity and reduce the heterogeneity of populations [11]. However, autonomic manifestations (neurally mediated hypotension, light headedness) and neuroendocrine manifestations (e.g., recurrent feelings of feverishness and cold extremities) may need to be explored for their possible addition. The medically unexplained component should also be operationalized: for example, ‘‘those with fatigue for at least 2 months and no alternative diagnosis received on the basis of a detailed history, physical examination, and a battery of laboratory tests (complete blood count, sedimentation rate, chemistry panel, chest X-ray, thyroid-stimulating hormone, thyroxine, anti-nuclear antibodies, urinalysis,

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immunoglobulins, and Epstein–Barr virus, toxoplasma and cytomegalovirus serologies)’’. For future research, we should take into account that fatigue is distributed as a continuous variable in the community and is closely associated with psychological morbidity. We do need better measures for objectification of fatigue, incorporating better assessment of basal metabolism rate as well as reserve aerobic and anaerobic capacity of the individual. The subjective nature of the complaint could be overcome and taken out of the eye-of-thebeholder with future scientific assessments. The ICD revision process will review the evidence in a systematic fashion and guide the users accordingly. This type of operational evidence-based criteria will definitely be better than arbitrary phenomenological definitions by committees and pave the way for better treatment of sufferers. They will also help reduce the disparaging manner in which these patients are perceived and treated by physicians, family, and the general public.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Abbey S.E., Garfinkel P.E. (1991) Neurasthenia and chronic fatigue syndrome: the role of culture in the making of a diagnosis. Am. J. Psychiatry 148: 1638–1646. Anonymous (1996). Frustrating survey of chronic fatigue. Lancet 348: 971. Jason L.A., Taylor R.R., Stepanek Z., Plioplys S. (2001) Attitudes regarding chronic fatigue syndrome: the importance of a name. J. Health Psychol. 6: 61–71. Kleinman A. (2004) Culture and depression. N. Engl. J. Med. 351: 951–953. World Health Organization (2001) International Classification of Functioning, Disability and Health. World Health Organization: Geneva. Nijs J., Vaes P., McGregor N., Van Hoof E., De Meirleir K. (2003) Psychometric properties of the Dutch Chronic Fatigue Syndrome—Activities and Participation Questionnaire (CFS-APQ). Phys. Ther. 83: 444–454. Spath M., Welzel D., Farber L. (2000) Treatment of chronic fatigue syndrome with 5-HT3 receptor antagonists—preliminary results. Scand. J. Rheumatol. 113(Suppl.): 72–77. Edmonds M., McGuire H., Price J. (2004) Exercise therapy for chronic fatigue syndrome. Cochrane Database Syst. Rev. (3). Price J.R., Couper J. (1998) Cognitive behaviour therapy for chronic fatigue syndrome in adults. Cochrane Database Syst. Rev. (4). Cho H.J., Hotopf M., Wessely S. (2005) The placebo response in the treatment of chronic fatigue syndrome: a systematic review and meta-analysis. Psychosom. Med. 67: 301–313. Kennedy G., Abbot N.C., Spence V., Underwood C., Belch J.J. (2004) The specificity of the CDC-1994 criteria for chronic fatigue syndrome: comparison of health status in three groups of patients who fulfill the criteria. Ann. Epidemiol. 14: 95–100.

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5.4 Constructing Chronic Fatigue: Empiricism, Psychiatry, and Sociocultural Contexts Ren´ee R. Taylor1 Since its controversial re-emergence at the end of the twentieth century, chronic fatigue syndrome (CFS) has continued to exist as one of the most perplexing diagnostic conundrums within the field of psychiatry. With circumspection, the timely and erudite review by Sharpe and Wessely exposes some of the most vexing and complex questions facing contemporary understanding of this and other similar syndromes. Is CFS a discrete disorder or an exaggerated form of a group of symptoms that are commonly experienced and ubiquitous to the human condition? Is its cause organic or psychogenic? Is it fundamentally a medical or a psychiatric diagnosis? From the authors’ perspective, the dauntingly uncomfortable answer to all of these questions is: ‘‘both’’. The less conspicuous question is: what forces act to discourage an attitude of ongoing striving for a more complex, biopsychosocial understanding of this and other syndromes of unknown aetiology? Why does human cognition tend to want to reduce our understanding of the syndrome to the level of either-or? Sharpe and Wessely then raise the question of how CFS is best managed and treated. They summarize the issues at stake by reviewing three of the existing models of CFS: (a) a biological model in which the central nervous system and the immune system interact and are influenced by sleep and activity levels; (b) a cognitive-behavioural model in which social factors and feelings of helplessness, somatic anxiety, and symptom focusing lead to activity avoidance and increased impairment; and (c) a social model in which symptoms and impairments are sustained and prolonged by membership in self-help groups, negative interactions with medical providers, and disability payment seeking. Beyond any conceptual utility they might offer, these models, in isolation of one another, are not helpful for science or for practice. The uncomfortable observation that is introduced is that there is empirical support for all three of these models. The most likely conclusion is that numerous variables converge uniquely to initiate and sustain this syndrome in each individual. Rehabilitation programs that correct faulty beliefs that CFS is irreversible and encourage re-engagement in activity and other occupations appear to have greatest empirical support. The authors conclude that a stance of ‘‘etiological neutrality’’, that legitimizes CFS as a real syndrome and acknowledges the contribution of biological, psychological, and social variables, is the best way to approach the 1 Department of Occupational Therapy, College of Applied Health Sciences, University of Illinois at Chicago, 1919 W. Taylor St., Chicago, Illinois 60612, USA

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dilemma in clinical practice. From a scientific perspective, a more complex biopsychosocial understanding of this syndrome is desperately needed. As both a researcher and practitioner, my perspective is that, with each new clinical discovery and empirical finding, the fog on the lens of CFS only becomes heavier. What is clear is that the syndrome is characterized by an enormous level of complexity. For scientists, there is tremendous amount of work ahead to disentangle the various contributions of genetics, neuroimmunology, neuroendocrinology, psychology, and social and behavioural factors. From a psychological perspective, the predisposing, precipitating, and perpetuating emotional and behavioural variables that, in part, contribute to the development and course of CFS are no different from those that have been associated with numerous widely acknowledged chronic illnesses. The likelihood that CFS involves both body and mind is no less true for the individual with this syndrome than it is for the person who, after a period of prolonged life stress and corresponding changes in activity levels and sleep, becomes more vulnerable to an upper respiratory infection [1]. Similarly, like other chronic illnesses, CFS fluctuates in terms of its symptom picture, perceived intensity, and resulting impairment. As with other chronic illnesses, psychological, behavioural, and social variables do, to differing degrees, contribute to this variation between and within individuals. Despite lay knowledge of the influence of stress on immune function and support from years of evidence within the field of psychoneuroimmunology, these observations have been much more difficult to digest as they pertain to individuals with CFS. Why the heated controversy? As acknowledged by Sharpe and Wessely, the difference, perhaps, is that there are no consistent laboratory, radiological, or other structural abnormalities that support the medical legitimacy of this syndrome. Sharpe and Wessely keenly highlight both the universality of fatigue syndromes and the wide variation in diagnostic labels, conceptualizations of fatigue, and daily life manifestations and consequences across cultures. Neurasthenia, which in Western countries has been described as a historical ancestor of CFS, remains an active ICD-10 diagnostic category that is mainly utilized in Australia and in other Far Eastern countries. Variation in language and specific diagnostic labels aside, the entity known most commonly as CFS is most frequently acknowledged in the United Kingdom, Scandinavia, and Holland, but is not nearly as commonly recognized in countries such as France, Italy, Spain, Germany, India, and the Middle East. Sharpe and Wessely aptly observe that cultures that devote more attention to issues involving public health, immunology, and environmental toxicity are those in which CFS symptoms and associated impairments are most often observed. The final but perhaps most serious issue raised by the review involves the fate of CFS as a unique diagnostic entity. The authors highlight recurring

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observations that the same symptoms tend to invite different diagnoses depending upon the professional discipline consulted. Within a medical context, the diagnosis of CFS is often given and symptoms are described as part of a functional syndrome. Within a psychiatric context, the same patient may be given a diagnosis of a somatoform disorder, depressive disorder, or anxiety disorder. With neurasthenia, the historical result of this diagnostic inconsistency was that the syndrome was eventually regarded as non-existent for nearly a century. Without a home in either discipline, CFS may be vulnerable to the same fate. Complicating this dilemma are recent efforts to emphasize commonalities between symptoms of CFS and those of conditions such as fibromyalgia, irritable bowel syndrome, temporo-mandibular joint dysfunction, somatic anxiety, and somatic depression. Though some empirical evidence points to the possibility that these syndromes may share a common psychological or central nervous system pathophysiology [2], other studies have produced contradictory evidence [3, 4]. Some scientists are working vigorously to identify nuanced differences in the symptoms and manifestations of CFS, so that distinct subgroups can be identified and research can then trace genetic and constitutional vulnerabilities with more accuracy and consistency [5]. Perhaps the most significant issue at stake is not whether these syndromes share commonalities, but instead the implications of any given scientific approach to the study of these syndromes. The most enduring question raised by Sharpe and Wessely’s review is: will science and practice best be served by reductionism or by focusing on nuanced interpersonal and intrapersonal differences? Only time and continued research that takes advantage of the more advanced biotechnologies being offered today will best answer this question.

REFERENCES 1. 2. 3. 4. 5.

Kasl S.V., Evans A.S., Niederman J.C. (1979) Psychosocial risk factors in the development of infectious mononucleosis. Psychosom. Med. 41: 445–466. Barsky A.J., Borus J.F. (1999) Functional somatic syndromes. Ann. Intern. Med. 130: 910–921. Robbins J.M., Kirmayer L.J., Hemami S.M. (1997) Latent variable models of functional somatic distress. J. Nerv. Ment. Dis. 185: 606–615. Taylor R.R., Jason L.A., Schoeny M. (2001) Latent variable models of functional somatic distress in a community-based sample. J. Ment. Health 10: 335–349. Jason L.A., Corradi K., Torres-Harding S., Taylor R.R., King C. (2005) Chronic fatigue syndrome: the need for subtypes. Neuropsychol. Rev. 15: 29–58.

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5.5 Chronic Fatigue Syndrome as a Paradigm for Psychosomatic Medicine James L. Levenson1 In another era, William Osler said: ‘‘He who knows syphilis knows medicine’’. As Sharpe and Wessely illustrate in their review of chronic fatigue syndrome (CFS), one could well now claim: ‘‘He or she who knows CFS knows psychosomatic medicine’’. The theories and arguments over its nature, classification, causation, diagnosis, and treatment, as well as the methodological difficulties in its study, are a microcosm of the controversies that have swirled around psychosomatic medicine since its infancy, and here I mean psychosomatic medicine to widely encompass psychiatric disorders in the medically ill, functional disorders, unexplained medical symptoms, and the somatoform disorders. Indeed, one might go further and claim: ‘‘He or she who knows CFS knows psychiatry and medicine’’, for there is much widely relevant wisdom to be gained in understanding CFS (including accepting what we do not understand). Is the aetiology of CFS fundamentally psychogenic or is it somatic? While many physicians endorse the biopsychosocial model, similar debates have raged on for years, around one disease after another, including psychiatric disorders (e.g., obsessive–compulsive disorder), somatic disorders (e.g., peptic ulcer), and functional disorders (e.g., migraine). While elucidating causal factors represents real progress, posing the pathology question as ‘‘either/or’’ leads to reductionism. The conclusive attribution of peptic ulcer aetiology to Helicobacter pylori infection or non-steroid anti-inflammatory drugs does not account for the fact that only a small portion of individuals with either of these somatic factors develops ulcers, overlooking the research demonstrating that psychological factors are independent risk factors for peptic ulcer [1] (albeit not as potent as believed by early psychosomatic investigators). The psychosomatic approach to the aetiology of disease is exemplified when Sharpe and Wessely state that ‘‘a combination of environmental factors and individual vulnerability initiates a series of social, psychological and biological processes that leads to the development of CFS’’. Should CFS be considered a categorical diagnosis or is fatigue dimensional, extending from normal fatigue to full-blown CFS? This question is a fundamental one for (though not unique to) psychiatry, and is centre stage in the philosophical and empirical critiques of DSM and ICD, relevant to many Axis I and probably all Axis II disorders [2]. What is the relationship between CFS and depression or anxiety? As with other functional disorders and medically unexplained somatic symptoms, 1 Department of Psychiatry, Virginia Commonwealth University School of Medicine, Box 980268, Richmond, VA 23298-0268, USA

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the amount of depression or anxiety present in patients with CFS is generally proportional to the number of physical symptoms [3]. The problem of how to interpret ‘‘vegetative’’ symptoms of depression like insomnia and fatigue in a patient with CFS (should they be counted toward a diagnosis of depression, or of CFS, or of both?) is a universal problem in the diagnosis of depression in the medically ill [4]. As with so many chronic physical illnesses, it is difficult in CFS to determine whether depression, if present, is a reaction to the demoralizing effects of chronic fatigue, a manifestation of CFS, or a distinct but commonly comorbid illness. Analogous issues arise in examining depression in patients with coronary artery disease, and it is also worth noting that shared social and other non-specific risk factors can underlie some of these comorbidities. Low socio-economic status and low education are risk factors for coronary disease, depression, and CFS alike, and stressful life events may precede onset of any of them as well. How generalizable are the research findings in CFS? As with most studies in psychosomatic medicine, most of the research conducted in CFS has been at tertiary care academic medical centres. As Sharpe and Wessely note, patients with CFS coming to clinics are more likely to have psychopathology than cases of CFS in a community sample. This kind of referral bias is a common barrier to generalizability [5]. For example, high rates of childhood sexual abuse have been found in patients with irritable bowel syndrome seen by specialists [6] but not in population-based studies [7]. Thus, one must consider whether psychopathology, histories of childhood trauma, or other psychological factors identified in CFS patients studied at specialized centres might be non-specific findings, influencing when, where, and how individuals seek care [8]. Other problems of generalizability noted by Sharpe and Wessely include uncertainty whether CFS in children is the same as in adults, and the overly pessimistic views of prognosis derived from disproportionate exposure to the worst cases, a common problem throughout medical education and practice (e.g., alcohol dependence, sickle cell anaemia). Although CFS is a relatively young concept, one can see in its history the recapitulation of many of the classic mistakes that have occurred in psychosomatic medicine. These include mistaking triggers as causes (e.g., Epstein–Barr virus infection), over-interpreting endocrine or immune changes of ambiguous significance and causal direction (e.g., reduced cortisol response to stress), mistaking consequences as causes (e.g., postural hypotension), and searching fruitlessly for specific explanatory lesions (e.g., in the central nervous system). But one also sees the wisdom of psychosomatic medicine re-emergent in the field of CFS study, in rejection of reductionistic explanations, and in understanding the role of abnormal cognition, selfperception, and illness behaviour in many patients with CFS. Many aspects of the sick role in CFS closely resemble those in chronic pain, including catastrophizing and fear-avoidance coping [9].

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Finally, the sensible treatment plan outlined by Sharpe and Wessely—relief of symptoms, promotion of active coping ‘‘by stabilizing activity and retraining the body to function effectively’’, and helping patients to manage the social and financial aspects of their illness—is equally applicable not only to other functional disorders, but any disease for which there is no cure.

REFERENCES 1.

Levenstein S. (2000) The very model of a modern etiology: a biopsychosocial view of peptic ulcer. Psychosom. Med. 62: 176–185. Phillips K.A., First M.B., Pincus H.A. (Eds) (2003) Advancing DSM: Dilemmas in Psychiatric Diagnosis. American Psychiatric Association: Washington, D.C. Kroenke K., Spitzer R.L., Williams J.B., Linzer M., Hahn S.R., deGruy F.V. III, Brody D. (1994) Physical symptoms in primary care. Predictors of psychiatric disorders and functional impairment. Arch. Fam. Med. 3: 774–779. Rodin G.M., Nolan R.P., Katz M.R. (2005) Depression. In: The American Psychiatric Publishing Textbook of Psychosomatic Medicine, J.L. Levenson (Ed). American Psychiatric Publishing: Washington, D.C., pp. 193–218. Levenson J.L., Colenda C., Larson D.B., Bareta J. (1990) Methodology in consultation-liaison research: a classification of biases. Psychosomatics 31: 367–376. Drossman D.A., Talley N.J., Leserman J., Olden K.W., Barreiro M.A. (1995) Sexual and physical abuse and gastrointestinal illness. Review and recommendations. Ann. Intern. Med. 123: 782–794. Talley N.J., Boyce P.M., Jones M. (1998) Is the association between irritable bowel syndrome and abuse explained by neuroticism? A population-based study. Gut 42: 47–53. Katon W., Sullivan M., Walker E. (2001) Medical symptoms without identified pathology: relationship to psychiatric disorders, childhood and adult trauma, and personality traits. Ann. Intern. Med. 134: 917–925. Clark M.R., Chodynicki M.P. (2005) Pain. In: The American Psychiatric Publishing Textbook of Psychosomatic Medicine, J.L. Levenson (Ed). American Psychiatric Publishing: Washington, D.C., pp. 827–870.

2. 3. 4. 5. 6. 7. 8. 9.

5.6 Beyond Fashion Gordon Parker1 While Sharpe and Wessely have neurasthenia in the title, they rapidly abandon its consideration. This appears appropriate. The explanatory models imputed at the time of its introduction (i.e., ‘‘lack of nerve strength’’ and ‘‘exhaustion of the nervous system’’) were manifestly non-specific, reflecting the lack of knowledge at that time. Such ineffability had advantages in 1

University of New South Wales and Black Dog Institute, Sydney, Australia

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effectively subsuming numerous physical and psychological states without ad hominem connotations. For example, its rapid adoption and adaptation as shenjing shuairuo in China reflected the Chinese epistemology of illness (i.e., disease being caused by an imbalance of vital organs), respected the ubiquity of physical symptom presentations and provided a non-stigmatizing diagnosis. Its preservation in ICD-10 hopefully only reflects such secondary advantages to those who might otherwise be stigmatized in some cultures, since its diagnostic guidelines lack any intrinsic redeeming features. Turning to chronic fatigue syndrome (CFS), the inherent problems are only in part different. While ‘‘neurasthenia’’ imputed a weakness of the nerves, which allowed both physical and psychological explanations for a potpourri of perturbed domains, CFS circumscribes a ‘‘domain’’ where fatigue is the central complaint. This was not inappropriate initially to advance aetiological research, but we now need to consider why it failed. Let us consider pain and breathlessness, as respective symptom and domain analogies. Both can be ‘‘normal’’ (e.g., pain from holding a burning match too long; dyspnoea from exerting too strenuously) or reflect underlying pathological processes, and have physical and/or psychological determinants. They are generally viewed, however, as merely providing first-level clinical judgements, inviting refined assessment. For instance, the description of the pain, its site, and other characteristics may offer a presumptive diagnosis. Further clinical assessment and investigation may allow a more definitive diagnosis. For example, does the dyspnoeic individual have pneumonia, asthma, emphysema, or a pulmonary embolus? Only when we refine the diagnosis to some level of specificity can aetiology and treatment be estimated with any precision. Such a process has not occurred for CFS, reflecting the ineffability of the concept and the strategic approaches adopted. Imagine if we similarly allowed a heterogeneous ‘‘chronic pain syndrome’’ category, operationally defined (say) by having ‘‘physical or mental pain lasting six months’’. Further imagine then assembling a thousand individuals who met inclusion criteria and seeking to validly assess the relevant contribution of broad psychological and physical factors, or specific aetiological factors (e.g., Epstein–Barr virus). We might expect a general tendency for chronic pain syndrome sufferers (compared to a pristine pain-free group) to report more stress and a range of psychological symptoms, and to have greater disability, but whether these were antecedents or consequences of pain would remain problematic. If we pursued the relevance of a narrow aetiological factor (e.g., prolapsed lumbar disc), its suggested group relevance would be strongly influenced by sample characteristics, while its identification as the definitive cause of one individual’s pain might well escape identification. I suggest then that, despite considerable honest and laborious research that has been undertaken into CFS, our understanding is limited as a consequence of a primary ‘‘model failure’’. When categorical definition

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allows intrinsic heterogeneity, there is an immediate risk of its intrinsic nonspecificity generating non-specific aetiological and treatment findings. If the heterogeneous category is then dimensionalized, any subsumed subtypes are diffused along a continuum (e.g., severity) that may be quite independent of cause and treatment response. Sharpe and Wessely inform us that the severity of CFS symptoms ‘‘is continually distributed in the general population’’ and that ‘‘case definition can also be regarded as simply defining cut-off points on these continua’’. Simple, yes. Meaningful, unlikely. A similar situation holds for the concept of ‘‘major depression’’, another pseudo-entity [1]. While its constituent disorders have quite varying psychosocial and biological causes, their specificity (e.g., childhood sexual abuse, sub-cortical dementia) will be principally dictated by sample selection. As noted [1], research seeking to identify biological markers of ‘‘major depression’’ has produced desultory information, while there is increasing recognition that a diagnosis of ‘‘major depression’’ is associated with equivalent response rates to quite differing treatments in randomized controlled trials. Just as a diagnosis of ‘‘major depression’’ provides only an estimate of clinical depression and invites second-level delineation of the depressive subtype, such intrinsic and application limitations hold for CFS. It could be argued that, by abandoning overly diffuse generic diagnoses, we risk leaving many individuals ‘‘undiagnosed’’. The obverse risk is to provide a ‘‘pseudo-profound’’ diagnosis or a false diagnosis—for reification over time. The consequences of not offering a diagnosis of CFS are worth considering. For some, it may encourage relentless pursuit of a fine-focussed diagnosis via unnecessary investigations but, for others, it may lead to a more definitive, explicit and satisfactory diagnosis—or for a diagnosis ‘‘postponed’’ but inviting review and reinvestigation. Would we be worse off adopting such an approach? Sharpe and Wessely have overviewed an extremely broad domain with reciprocal breadth and tenacity. Their treatment model is impressively pluralistic, albeit non-specific. They effectively encourage the clinician to form a therapeutic relationship with the patient, to try a range of specific and non-specific treatments, and to adopt a stance that allows the patients to retain their respect and dignity. Their model resembles many current models for pain management and, for the individual whose condition resists all diagnostic attempts, this is clearly appropriate. However, it strikes me that the field is more likely to advance by abandoning pseudo-diagnoses such as CFS and neurasthenia. We should not wait for them to fall out of fashion. The current paradigm failure argues for them to be pushed.

REFERENCE 1.

Parker G. (2005) Beyond major depression. Psychol. Med. 35: 467–474.

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5.7 Chronic Fatigue and Disembodied DSM Sing Lee1 and Arthur Kleinman2 Chronic fatigue syndrome (CFS) has demonstrated an overall fate that is not substantively different from that of its historical ally neurasthenia. This fate consists of initial fascination, cultural popularization, inconclusive research results, marginalized disease status and, in all likelihood, a quiet burial in the years to come. If there is any difference at all, it would be the rapidity with which the condition dies out in response to professional and social forces that dictate whether an illness should be considered real or legitimate. These forces include, among others, the hegemony of the psychocentric DSM classification and the pharmaceutical authentication of disease categories [1, 2]. Although Sharpe and Wessely suggest that the diagnosis of neurasthenia remains an important one in the Far East, the diagnosis has rapidly fallen out of favour in urban China [2]. Today, neurasthenia is rarely, if ever, diagnosed by Chinese psychiatrists, who consider it merely a misdiagnosed depression. A clinician who continues to make the diagnosis may be considered not having made a thorough psychiatric evaluation and not being in touch with international standards of practice. Moreover, in all likelihood, he would be unwelcome by pharmaceuticals, that provide a large share of funding for psychiatric research in the country. Indeed, the most recent national system of classification of mental disorders (CCMD-3) in China stipulates that neurasthenia should only be considered after all possible depressive and anxiety disorders are excluded [3]. This means that neurasthenia, once the single most common psychiatric diagnosis made throughout China, has become a somatoform disorder (though the latter category does not exist in the Chinese classification). We find this change in diagnostic practice among Chinese psychiatrists striking for at least two reasons. First, Chinese psychiatrists previously responded vehemently to Arthur Kleinman’s study of patients with neurasthenia in Hunan [4]. They pointed out that Kleinman overdiagnosed depression by using a culturally inappropriate ‘‘American’’ system (DSM-III). Second, in accordance with traditional Chinese medical epistemology, Chinese psychiatrists have long believed that both somatic and psychological symptoms represent core elements of neurasthenia and other neurotic disorders. Until recently, they did not adopt the epistemology that psychological symptoms such as depressed or anxious mood are the core of mental 1 2

Department of Psychiatry, Chinese University of Hong Kong, Hong Kong Department of Anthropology, Harvard University, Boston, MA, USA

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disorders, whereas somatic symptoms should be marginalized as peripheral, or deleted altogether [3]. We recapitulate the Chinese scenario of neurasthenia because of its implications for understanding the relationships between depressive/anxiety disorders and CFS or other functional somatic disorders. The question of how the DSM system has come to disconnect the body from the mind involves a complex political economy that will not be discussed here [2]. But we can look at a number of facts to appreciate that there is something deeply wrong with the DSM schema even though most people keep quiet about it. First, epidemiological studies have amply demonstrated a high level of comorbidity between mental disorders and chronic pain and other somatic syndromes. They also show that psychological distress and somatic distress are positively correlated. Second, somatic symptoms represent by far the most common mode of clinical presentation among people with depressive and anxiety disorders worldwide [5]. Third, experienced clinicians (many do not truly follow the DSM in practice) invariably attest to the intertwined nature of psychological and somatic distress among their patients. By listening closely to patients’ bodily voices, they may find such categories as ‘‘depressive episode without somatic features’’ a professional joke. This is because a depressed patient who does not exhibit any somatic distress does not really exist outside of the DSM. Fourth, although we are not pharmacologists by training, it seems obvious to us that the main neurotransmitters that underlie depressive and other mental disorders do not recognize the mind and the body as separable entities. To the best of our knowledge, for example, no depressed mood-specific or fatigue-specific serotonin receptors have ever been identified. Finally, even the most specific psychopharmacological agents uniformly bring about improvement of psychological and somatic distress at the same time. Human experience is a variable amalgam of biology and psychosocial reality. What characterizes both the biological and psychosocial worlds is diversity, not homogeneity [6, 7]. For this reason, a classification of human distress that over-privileges either the mind or the body as core will necessarily be problematic. Diagnoses such as CFS will always involve subgroups of patients that overlap with depression or anxiety disorders as well as others that will fall under the grotesque label of undifferentiated somatoform disorder [1]. To the extent that the issue is epistemological, empirical research will not provide the final answer. As in the case of CFS, research will typically produce a plethora of mixed aetiological, treatment, and prognostic data that lead us to conclude, within the DSM framework, that a particular somatic syndrome is not a real entity. Interestingly, few researchers have doubted the disease validity of ‘‘legitimate’’ disorders such as depression or anxiety disorders even though they exhibit considerable heterogeneity and overlap at all levels of research. For example, some patients with depression

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have clear psychological aetiology and respond well to antidepressants, but there are others who cannot be diagnosed as depression but respond well to antidepressants, or who fit the DSM criteria perfectly but prove totally resistant to the combination of the best medications. The marginalization of bodily forms of distress has deep-seated impacts on the contemporary development of psychiatry in the West and, increasingly, in non-Western parts of the world. For example, it delegitimizes functional somatic syndromes and results in a dearth of research on illnesses that do not fall under the familiar ‘‘anxiety’’ and ‘‘depressive’’ categories. This is unfortunate because, if similarly vigorous treatment research like that on depression had been applied to functional somatic syndromes, many more people with such afflictions might have been helped. The evidence seems persuasive that we should ‘‘bring the body back to the DSM’’. But to do this is to reverse complex political and economic factors that create and sustain the DSM. Our guess is that this will not happen until a substantial redistribution of power takes place in international psychiatry. By leaving out a large body of information about chronic fatigue and other somatic syndromes in the developing world, Sharpe and Wessely’s review may yet be another demonstration of research that marginalizes most human beings and overgeneralizes from the contemporary West.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Lee S. (1994) The vicissitudes of neurasthenia in Chinese societies: where will it go from the ICD-10? Transcult. Psychiatr. Res. Rev. 31: 153–172. Lee S. (1999) Diagnosis postponed: shenjing shuairuo and the transformation of psychiatry in post-Mao China. Cult. Med. Psychiatry 23: 349–380. Lee S. (2001) From unity to diversity: the classification of mental disorders in 21st century China. Psychiatr. Clin. North Am. 24: 421–431. Kleinman A. (1986) Social Origins of Distress and Disease: Depression, Neurasthenia, and Pain in Modern China. Yale University Press: New Haven. Kirmayer L. (1998) Culture and somatization: clinical, epidemiological, and ethnographic perspectives. Psychosom. Med. 60: 420–430. Kleinman A. (1999) Experience and its moral modes: culture, human conditions and disorder. Tanner lectures. In: The Tanner Lectures on Human Values, Vol. 20, G.B. Peterson (Ed). University of Utah: Salt Lake City, pp. 357–420. Kleinman A. (2004) Culture and depression. N. Engl. J. Med. 351: 951–953.

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5.8 Problems of Definition, Aetiological Approaches and Issues of Management in Chronic Fatiguing Disorders Anne Farmer1 and Tom Fowler2 As Sharpe and Wessely clearly show, problems of terminology bedevil the field of chronic fatiguing disorders. While sufferers talk of myalgic encephalitis, the Royal Colleges of Physicians, General Practitioners and Psychiatrists [1] differentiate ‘‘chronic fatigue’’ and ‘‘chronic fatigue syndrome’’ (CFS) according to whether the subject fulfils either the Oxford definition [2] or the Centers for Disease Control (CDC) consensus operational definition [3] or not. These operational definitions for CFS are all somewhat different from each other in terms of both inclusion and exclusion criteria, and consequently define different groups of individuals as ‘‘cases’’ of disorder. Further complications are the substantial overlap of chronic fatigue symptoms with irritable bowel syndrome and fibromyalgia as well as with psychiatric disorders such as depression, anxiety, and somatoform disorders. Another diagnostic problem for the clinician is that complaints are largely subjective. There are numerous symptoms, but sufferers presenting to their doctors have no signs, abnormal chemistry, virology, immunology, X-rays, and so on. Consequently, it is not surprising that chronic fatigue sufferers and their doctors may fail to communicate well with one another. These definitional problems produce a knock-on effect when attempting to describe the epidemiology of chronic fatiguing disorders. While fatigue is one of the commonest symptoms, and complaints of ‘‘being tired all the time’’ are one of the most frequent presentations in primary care [1], prevalence rates of CFS are quite low, ranging from 0.2 to 1.29% in the United Kingdom [1, 4]. This discrepancy is mainly due to the narrowness of the definition of CFS. For instance, the CDC definition has so many exclusion criteria that it can only be applied somewhat rarely. This leaves a large number of individuals who have prolonged and disabling fatigue in a ‘‘not CFS’’ chronic fatigue category. As we have pointed out elsewhere [5], there are major issues regarding the definition of a disorder when the ‘‘rag bag’’ or ‘‘not elsewhere specified’’ category has a higher prevalence than that of the operationally defined disorder itself. Consequently, epidemiological studies need to include a broad range of symptoms and disability in their definitions of ‘‘caseness’’ so that the proper outcome studies can be undertaken and the criteria included in the operational definition adjusted accordingly.

1 2

Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, London, UK Division of Psychological Medicine, Cardiff Medical School, Heath Park, Cardiff, Wales, UK

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This is particularly relevant for fatigue disorders in children and young people. Although rare in children under 10, chronic fatigue is one of the commonest causes of prolonged absence from school, and can have a major impact not only on educational attainment but also on psychosocial development at a critical time. The Royal College of Paediatrics and Child Health (RCPCH) has recently defined chronic fatigue in young people as ‘‘generalised fatigue persisting after routine tests and investigations have failed to find an obvious underlying cause’’ [6]. Although this resolves the issue of fatigue duration in this young age group, there remains the problem of how to define ‘‘failure to find an obvious cause’’. Basic screening tests such as full blood counts, urea and electrolytes, liver function tests, and thyroid function tests are almost always within a normal range in those suffering from chronic fatigue of whatever age. However, glandular fever, which is common in young people, is frequently associated with post-viral fatigue, which may last for several months, and evidence of persisting infection may not be present. It is not clear whether such cases would be included or excluded from the RCPCH definition of CFS. Similarly, it is unclear whether individuals who have had a ‘‘known’’ medical cause for fatigue but whose symptoms and disability appear disproportionate to what is usually the case are to be categorized. With regard to aetiology, Sharpe and Wessely highlight a number of important technological developments that may help with the problems of disease definition as outlined above. In particular, genetic studies can provide a ‘‘bottom up’’ aetiological approach, by starting with estimations of the proportion of variance contributed to by genetic and environmental risk factors using twin and family study methods. Various twin studies [7–10] have used different definitions of chronic fatigue in different age ranges and have found that between a quarter (26%) [10] and a half (54%) [7] of the variance in liability to develop disabling fatigue for a week or more is contributed by genes, but a substantial proportion of the variance is also attributed to shared and non-shared environmental factors [11]. Twin studies have also shown that the genetic risk factors for chronic fatigue are mainly specific to fatigue and not shared with other psychiatric syndromes, providing evidence that prolonged chronic fatigue is not merely an atypical presentation of depression [11]. Further studies using linkage and association methods are required to elucidate candidate genes and their interplay with environmental risk factors. Sharpe and Wessely emphasize the extreme health problems and disability faced by the most severely ill. Before the establishment of specialized clinics, it was often the case that those suffering from chronic fatigue ‘‘did the rounds’’ of other medical and psychiatric services where their assessment and treatment from sometimes sceptical clinicians may have been less than satisfactory. This may have contributed to the entrenched attitudes found in some of the more severely handicapped CFS patients. Clinics specializing in

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the assessment and management of chronic fatigue have been slowly established around the United Kingdom over the past 10 years. This development goes some way to ensuring that new sufferers can be referred directly, and diagnosed and treated at an earlier stage in their illness. Prompt assessment and ready access to the combination of cognitive-behavioural psychotherapy and graded exercise approaches carefully described in Sharpe and Wessely’s review will hopefully ensure that fewer patients develop severe intractable symptoms or acquire the intransigent attitudes associated with poor outcome.

REFERENCES 1.

2. 3.

4. 5. 6. 7. 8. 9. 10. 11.

Royal Colleges of Physicians, Psychiatrists and General Practitioners (1996) Chronic Fatigue Syndrome. Report of a Joint Working Group of the Royal Colleges of Physicians, Psychiatrists and General Practitioners. Royal College of Physicians Publications Unit: London. Sharpe M.C., Archard L.C., Banatvala J.E., Borysiewicz L.K., Clare A.W., David A., Edwards R.H., Hawton K.E., Lambert H.P., Lane R.J. (1991) A report on chronic fatigue syndrome: guidelines for research. J. R. Soc. Med. 84: 118–121. Fukuda K., Straus S.E., Hickie I., Sharpe M.C., Dobbins J.G., Komaroff A., International Chronic Fatigue Syndrome Study Group (1994) The chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann. Intern. Med. 121: 953–959. Farmer A., Fowler T., Scourfield J., Thapar A. (2004) Prevalence of chronic disabling fatigue in children and adolescents. Br. J. Psychiatry 184: 477–481. Farmer A.E., Wessely S., Castle D., McGuffin P. (1992) Methodological issues in using a polydiagnostic approach to define psychotic illness. Br. J. Psychiatry 161: 824–831. Royal College of Paediatrics and Child Health (2005) Guidelines on Chronic Fatigue Syndrome. http://www.rcpch.ac.uk/news/index.html. Farmer A., Scourfield J., Martin N., Cardno A., McGuffin P. (1999) Is disabling fatigue in childhood influenced by genes? Psychol. Med. 29: 279–282. Hickie I., Kirk K., Martin N. (1999) Unique genetic and environmental determinants of prolonged fatigue: a twin study. Psychol. Med. 29: 259–268. Buchwald D., Herrell R., Ashton S., Belcourt M., Schmaling K., Sullivan P., Neale M., Goldberg J. (2001) A twin study of chronic fatigue. Psychosom. Med. 63: 936–943. Sullivan P.F., Kovalenko P., York T.P., Prescott C.A., Kendler K.S. (2003) Fatigue in a community sample of twins. Psychol. Med. 33: 263–281. Fowler T.A., Rice F., Scourfield J., Thapar A., Farmer A. Relationship of disabling fatigue and depression in children: a genetic study. Submitted for publication.

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5.9 Chronic Fatigue Syndrome: Time to Concentrate on Fatigue, Not Chronicity Petros Skapinakis1 and Venetsanos Mavreas1 Research interest on chronic fatigue and related syndromes is still growing even though more than 3,000 articles have been already indexed in Medline. Sharpe and Wessely offer us a comprehensive and timely overview of the most important aspects of diagnosis, aetiology, and management of these conditions. In this commentary, we will discuss some issues concerning diagnosis and classification, the association between psychiatric disorders and chronic fatigue, and natural history and prognosis. Finally, we will comment on the cross-cultural perspective of chronic fatigue syndrome (CFS). Sharpe and Wessely point out that the categorical view of CFS is not supported by research evidence. The core symptom of fatigue is very common in the general population, and there seems to be a continuum of fatigue symptoms of varying severity and duration [1]. There is no doubt that diagnostic criteria are useful both for research and clinical practice. However, one should not forget that they impose arbitrary cut-offs when in reality these do not exist. The example of major depression is quite relevant here. Various studies have shown that depressive symptomatology not meeting criteria for DSM-IV or ICD-10 major depression (sub-threshold syndrome) is almost as disabling as the full syndrome and has a great likelihood to lead to a full syndrome in the future [2]. Current diagnostic criteria for chronic fatigue and related syndromes adopt a categorical and narrow view of these syndromes, implying that the more severe forms of fatigue are qualitatively different (i.e., more ‘‘organic’’) from the less severe ‘‘psychosocial’’ forms of tiredness. A consequence of this narrow view is the requirement for several physical complaints for a diagnosis of CFS in the 1994 definition of the Centers for Disease Control. First, one should note that some of these symptoms (such as tender lymph nodes) require a medical examination and therefore cannot be assessed in large epidemiological surveys of unselected patients. Second, the remaining are common symptoms of various forms of pain, sleep problems or cognitive dysfunction, which are present in a wide variety of medical and psychiatric diseases. Overlap with other conditions, especially with psychiatric disorders, is therefore inevitable. The aim of including accessory symptoms in the definition of CFS was to select subjects with a greater likelihood of severe, and thus more ‘‘organic’’ fatigue. However, this was not achieved. In our own analysis of chronic fatigue syndromes in international primary care, we examined the effect of adding more somatic symptoms in the definition of chronic fatigue. We found that as we added more somatic 1

Department of Psychiatry, University of Ioannina, School of Medicine, Ioannina 45110, Greece

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symptoms the association with psychiatric disorders increased from 53 to 81% [3]. This was not surprising. The association between psychiatric disorders and multiple somatic symptoms is well documented in the literature [4]. In our view, future revisions of the definition of CFS should concentrate on defining better the core symptom of severe fatigue and eliminate the multiple symptoms so as to reduce the association with depression or anxiety disorders. There is no doubt that the association between CFS and depression or other psychiatric disorders is the most controversial issue surrounding this condition. The possible alternative explanations for this association are: (a) CFS is ‘‘caused’’ by depression (the ‘‘causal hypothesis’’); (b) depression is secondary to a disabling illness of unknown aetiology (the ‘‘reverse causality’’ hypothesis); (c) depression and CFS share common risk factors that confound the association between them (the ‘‘common etiology’’ hypothesis); and (d) the association is caused by the overlapping criteria in the definitions (the ‘‘overlapping hypothesis’’). It is worth noting that these explanations are not mutually exclusive and may all explain a small part of the reported strong association. Clarification of this issue requires longitudinal studies. We carried out such a study using data from the World Health Organization collaborative study of psychological problems in general health care [5]. This data set gave us the opportunity to study the relation between chronic fatigue and depression in unselected primary care patients, thus avoiding the inherent selection bias of studies from CFS specialist centres. We found that cases of depression at baseline were more likely to develop a new episode of chronic fatigue at follow-up. This supported the ‘‘causal’’ hypothesis. However, when we looked at cases of chronic fatigue at baseline we found that these were also more likely to develop a new episode of depression at follow-up. This supported the ‘‘reverse causality’’ hypothesis. How can one explain these apparently contradictory findings? We proposed a vicious cycle model (depression leads to fatigue leads to depression), according to which depression and CFS could be independent risk factors for each other. The level of physical activity or exercise could be the potential intervening variable that links the two conditions. Sharpe and Wessely suggest that physical deconditioning offers a potential biological explanation for exerciseinduced fatigue. On the other hand, it is well known that depression is associated with reduced energy and physical activity [6]. In addition, effective treatments for both chronic fatigue and depression include elements of graded exercise [7, 8]. Future longitudinal studies should aim to investigate the temporal association of depression and CFS in unselected patients, after having taken into account the level of physical activity as a confounding or intervening variable. We would like to stress the importance of studying unselected patients with idiopathic chronic fatigue/CFS to investigate natural history or prognosis.

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Otherwise the results may reflect the selective nature of tertiary centres rather than the condition. In particular, community or primary care patients with a diagnosis of CFS are needed. In our own study in primary care, subjects meeting criteria for idiopathic chronic fatigue had a generally very good prognosis, with less than 20% having a persistent disorder. The severity of fatigue at baseline seems to be the most important predictor. Most of the studies with unselected patients do not support the idea that CFS is a condition that is bound to be chronic and unremitting [9]. Sharpe and Wessely point out that the diagnosis of CFS is almost entirely restricted to specific Western nations, while the symptoms of fatigue and pain are universal. We previously reported wide variations in the prevalence of medically unexplained fatigue among 14 countries of different economic development. In addition, we found an association between a higher economic development and the prevalence of fatigue [10]. Is CFS a culture-bound syndrome? A general definition of a culture-bound syndrome is that of a condition that occurs in many cultural settings, but which is only elaborated as an illness in one or a few. Sharpe and Wessely’s description of the lack of diagnosis outside the English-speaking world and some other countries seems to support this idea. We can also confirm that severe CFS is absent in Greece as is the case in France. Apart from the French diagnosis of ‘‘spasmophilia’’, it seems that in Germany, Greece, and perhaps other European countries, many of the patients who would have got the diagnosis of CFS in the United Kingdom are considered to have ‘‘low blood pressure’’. This is a popular unofficial diagnosis for unexplained fatigue in primary care in these countries [11]. Whether the specific diagnostic label of CFS, as used in the United Kingdom and elsewhere, is leading to greater disability is an interesting but as yet unanswered hypothesis.

REFERENCES 1. 2. 3.

4. 5.

Pawlikowska T., Chalder T., Hirsch S.R., Wallace P., Wright D.J., Wessely S.C. (1994) Population based study of fatigue and psychological distress. Br. Med. J. 308: 763–766. Broadhead W.E., Blazer D.G., George L.K., Tse C.K. (1990) Depression, disability days, and days lost from work in a prospective epidemiological survey. JAMA 264: 2524–2528. Skapinakis P., Lewis G., Mavreas V. (2003) Unexplained fatigue syndromes in a multinational primary care sample: specificity of definition and prevalence and distinctiveness from depression and generalized anxiety. Am. J. Psychiatry 160: 785–787. Simon G.E., VonKorff M. (1991) Somatization and psychiatric disorder in the NIMH epidemiologic catchment area study. Am. J. Psychiatry 148: 1494–1500. Skapinakis P., Lewis G., Mavreas V. (2004) Temporal relations between unexplained fatigue and depression: longitudinal data from an international study in primary care. Psychosom. Med. 66: 330–335.

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Strawbridge W.J., Deleger S., Roberts R.E., Kaplan G.A. (2002) Physical activity reduces the risk of subsequent depression for older adults. Am. J. Epidemiol. 156: 328–334. Fulcher K.Y., White P.D. (1997) Randomised controlled trial of graded exercise in patients with the chronic fatigue syndrome. Br. Med. J. 314: 1647–1652. Lawlor D.A., Hopker S.W. (2001) The effectiveness of exercise as an intervention in the management of depression: systematic review and meta-regression analysis of randomised controlled trials. Br. Med. J. 322: 763–767. Cairns R., Hotopf M. (2005) A systematic review describing the prognosis of chronic fatigue syndrome. Occup. Med. 55: 20–31. Skapinakis P., Lewis G., Mavreas V. (2003) Cross-cultural differences in the epidemiology of unexplained fatigue syndromes in primary care. Br. J. Psychiatry 182: 205–209. Tonkin A. (2004) Low blood pressure and low energy: (how) are they related? J. Hypertens. 22: 671–673.

5.10 Chronic Fatigue Syndrome: A Real Disease, A Real Problem Jonathan R. Price1 Chronic fatigue syndrome (CFS) is one of the most challenging medical problems for doctors to manage and for patients to experience. Sharpe and Wessely are to be commended for their thorough and balanced approach in their review of current evidence. CFS sits within a vexatious group of disorders, known variably as ‘‘functional’’, ‘‘psychosomatic’’, and ‘‘somatoform’’. These disorders present major problems, not least because of the apparent complexity of their aetiology, and associated difficulties in engaging many patients. Sharpe and Wessely do not shirk from wholeheartedly embracing the biopsychosocial perspective, in which a person’s social and psychological context, in addition to relevant biological factors, is a key factor in their illness and recovery [1]. The adoption of this perspective triggers, for some, the question of whether CFS is a ‘‘medical’’ or a ‘‘psychiatric’’ condition. This question is unnecessarily polarizing. Psychiatrists are excited by the burgeoning evidence for the relevance of psychological interventions in the management of a wide range of disorders, many of which are ‘‘physical’’, and all of which are legitimate illnesses like CFS that cause real disability and distress. CFS is obviously a disease, with unmistakable associated distress and disability. As a psychiatrist, I do not doubt this. I regard depression as an important disease of the nervous system, just as I regard diabetes mellitus as an important disease of the endocrine system. Depression may be ‘‘all 1

University of Oxford Department of Psychiatry, Warneford Hospital, Oxford, UK

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in the mind’’, but it is a true disease. Why, therefore, does the suggestion that the aetiology of CFS involves potent psychological factors arouse such passions, among many patients and some doctors? Isn’t it good news that, according to the cognitive-behavioural model, biological factors are only partly responsible for the illness, or largely reversible [2]? For many CFS patients, this is not the case. The suggestion that psychological factors are relevant or, indeed, pivotal, is seen as questioning the legitimacy of the illness, not taking their problems seriously, or dismissing their experience and expertise [3]. Doctor and patient are potentially placed at odds, in a situation that has been likened to a political arena, where facts and beliefs are opposed and confused [4]. Similar responses are seen in other common problems with which biomedicine struggles to provide clear aetiological or therapeutic answers, such as low back pain [5]. The common reluctance of patients to accept an integrated, biopsychosocial model of aetiology and, thereby, of treatment is a problem for both patients and doctors. Sharpe and Wessely try hard to embrace concerns about the biopsychosocial approach. And so they should. Meaningful and effective engagement with CFS sufferers, their carers, and their support and advocacy organizations is pivotal to successful treatment. Fifty, or even twenty, years ago, the doctor’s ‘‘expert’’ view would inevitably have triumphed over that of the patient’s. By 2005, the balance of power has shifted as governments have endorsed the validity and centrality of the patient’s view, and embedded patient power within the delivery and management of health care. Simultaneously, the Internet has given ready access to medical evidence of all kinds. The patient is also an expert now, and a powerful one. How should the doctor respond? Help the patient make his own decision, rather than dominate or coerce. Assist the patient to understand the evidence. Be frank about uncertainty—most patients will appreciate candour. Encourage the patient to have an open mind, rather than close down therapeutic possibilities. Encourage an experimental approach—discuss and facilitate therapeutic  n of 1 trials. Finally, be positive about the prospects for improvement. As Sharpe and Wessely state, presenting a positive diagnosis, with an aetiological formulation that addresses biological, psychological and social factors, and a management plan that clearly relates to that formulation, is ‘‘an essential starting point for effective management’’. The key message is that CFS is not a fixed, unalterable disease, lying outside the patient’s control. Rather, CFS is a real disease that is reversible by the patient’s own efforts, alongside those of professionals. Self-care, appropriately informed and supported, is the focus here. Relatively simple interventions may be effective, if they have a clear rationale that is well communicated to patients [6]. Recent decades have seen an increased public interest in ‘‘stress’’ and its consequences. Simultaneously, medicine has been criticized for being too

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biomedical and neglecting ‘‘the whole person’’. It therefore seems surprising that many CFS patients are reluctant to embrace a more holistic, biopsychosocial, approach to their management. We need the help of sociologists and anthropologists to try to understand this paradox, which is at the core of many problems that biomedicine struggles to understand. But biomedicine itself may come to our rescue. Functional neuroimaging promises to visualize the currently invisible and, thereby, to explain the inexplicable. As psychiatry becomes more biological, we will be able to demonstrate the ‘‘organic’’ basis of what has hitherto been ‘‘functional’’. Apparent abnormalities in brain function in CFS patients are already being reported [7], and we look forward to the endorsement of the role of the brain in this problematic disorder.

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White P. (Ed) (2005) Biopsychosocial Medicine. Oxford University Press: Oxford. Surawy C., Hackmann A., Hawton K.E., Sharpe M. (1995) Chronic fatigue syndrome: a cognitive approach. Behav. Res. Ther. 33: 535–544. ˚ Asbring P., N¨arv¨anen A.L. (2002) Women’s experiences of stigma in relation to chronic fatigue syndrome and fibromyalgia. Qual. Health Res. 12: 148–160. Banks J., Prior L. (2001) Doing things with illness. The micro politics of the CFS clinic. Soc. Sci. Med. 52: 11–23. Johansson E.E., Hamberg K., Lindgren G., Westman G. (1996) ‘‘I’ve been crying my way’’—qualitative analysis of a group of female patients’ consultation experiences. Fam. Pract. 13: 498–503. Powell P., Bentall R.P., Nye F.J., Edwards R.H.T. (2001) Randomised controlled trial of patient education to encourage graded exercise in chronic fatigue syndrome. Br. Med. J. 322: 387–390. DeLange F.P., Kalkman J.S., Bleijenberg G., Hagoort P., van der Werf S.P., van der Meer J.W., Toni I. (2004) Neural correlates of the chronic fatigue syndrome—an fMRI study. Brain 127: 1948–1957.

3. 4. 5. 6. 7.

5.11 The Specificity of Chronic Fatigue, Neurasthenia, and Somatoform Disorders Winfried Rief1 In the area of functional somatic syndromes, various diagnoses and corresponding classification criteria exist, such as chronic fatigue syndrome (CFS), neurasthenia, irritable bowel syndrome, fibromyalgia, somatization disorder, and polysymptomatic somatization syndrome. In this commentary, I 1

University of Marburg, Clinical Psychology and Psychotherapy, Marburg, Germany

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will use the terms functional somatic syndrome, somatoform symptoms, and polysymptomatic somatization syndrome interchangeably. I will comment on the issue of whether all of these terms and syndromes describe specific disorders, or whether they are members of one and the same category. For most of the ‘‘functional’’ syndromes, the diagnostic criteria do not only include the core symptom (e.g., fatigue) but also other somatic complaints. For CFS, these are, for example, muscle pain, joint pain, and headache, while for neurasthenia they are muscle aches or pains, dizziness, or tension headache. This implies that CFS and neurasthenia are by definition not monosymptomatic, but include various other somatic complaints. The nature of these other complaints implies a high prevalence in the general population, and difficulties in describing their origin [1, 2]. This is one of the reasons why the existing classification approaches to neurasthenia, CFS, and polysymptomatic somatization syndrome [3–5] do not allow any differentiation between these syndromes. Consequently, Wessely and others found that 80% of patients who fulfil the criteria for one of the functional somatic syndromes (e.g., CFS, irritable bowel syndrome, fibromyalgia) also fulfil the criteria of other functional syndromes [6, 7]. In other words, the focus on one of the somatic symptoms (as is done in terms such as CFS or irritable bowel syndrome) is frequently not warranted. Since single physical symptoms do not seem to be the characteristic feature of these syndromes, the question arises as to what the typical features of these syndromes are. Cognitive and behavioural aspects typical for these patients have been described. They tend to over-interpret the relevance of physical perceptions, focus their attention on bodily processes, and frequently have a self-concept of being weak and having a bad constitution. These cognitive features have been found for polysymptomatic somatization disorders [8], and also for CFS [9] and other functional somatic syndromes. They represent one of the features discriminating patients with multiple somatic complaints from patients with other mental and psychosomatic disorders [8]. In terms of the behavioural characteristics of these syndromes, increased and abnormal illness behaviour has been suggested [10]. However, illness behaviour seems to be less specific than illness cognitions are, since many patients with depression or panic show comparable illness behaviour to patients with polysymptomatic somatization syndromes [11]. In a recent study, it was shown that somatization, depression, and panic all contribute to illness behaviour, but these contributions are independent and additive [12]. Moreover, subfeatures of illness behaviour show some specificity: while depression contributes significantly to ‘‘illness expression’’ and aspects of disability, somatization is more closely related to ‘‘seeking medical treatment’’. One general result of the studies on illness behaviour was the high individuality, with low intercorrelations between different aspects of illness behaviour.

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Since the functional syndromes mentioned above can only be poorly differentiated from each other, the question arises whether they should be classified as a separate category, or whether they are mere by-products of other mental disorders. Fatigue and exhaustion is typical not only for depression but also for most chronic conditions in medicine. The same is true for symptoms such as abdominal pain, headache, or dizziness. However, while it is argued that there is no evidence to differentiate CFS, neurasthenia, or polysymptomatic somatization disorder, we favour the opinion to discriminate these syndromes from other mental and psychosomatic disorders [13]. As outlined before, the patients can be discriminated from depressive or panic patients in terms of cognitive and behavioural features. Moreover, there is some evidence for different psychobiological aspects in somatization syndrome versus depression [14]. And finally, the age at onset and the course of the disorders differ between polysymptomatic somatization syndromes and depression, panic, and other psychiatric disorders. To conclude, there is currently no evidence to differentiate the various syndromes in patients with multiple physically unexplained symptoms. On the basis of current diagnostic criteria, the various syndromes overlap substantially and do not allow any sensible differentiation. However, it makes sense to differentiate these syndromes from other mental and psychosomatic disorders, as their course and outcome, as well as behavioural, perceptual, and cognitive features suggest that they should be considered as a separate category. Therefore, the existing classification approaches to polysymptomatic somatization syndromes should be modified to reflect the new findings concerning these common and costly conditions. The above conclusion has significant implications for the management and treatment of these patients. Currently, many of them are treated only for the physical symptom characterizing the syndrome (e.g., fatigue in CFS, abdominal complaints in irritable bowel syndrome). In reality, most of these patients have a history of multiple somatic complaints. Therefore, the treatment approaches should not focus on single symptoms, but on the perception of bodily processes in general.

REFERENCES 1. 2. 3.

Kroenke K., Mangelsdorff D. (1989) Common symptoms in ambulatory care: incidence, evaluation, therapy and outcome. Am. J. Med. 86: 262–266. Rief W., Hessel A., Braehler E. (2001) Somatization symptoms and hypochondriacal features in the general population. Psychosom. Med. 63: 595–602. Escobar J.I., Rubio-Stipec M., Canino G., Karno M. (1989) Somatic symptoms index (SSI): a new and abridged somatization construct—Prevalence and epidemiological correlates in two large community samples. J. Nerv. Ment. Dis. 177: 140–146.

316 4.

5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

SOMATOFORM DISORDERS Kroenke K., Spitzer R.L., deGruy F.V., Hahn S.R., Linzer M., Williams J.B.W., Brody D., Davies M. (1997) Multisomatoform disorder. An alternative to undifferentiated somatoform disorder for the somatizing patient in primary care. Arch. Gen. Psychiatry 54: 352–358. Rief W., Hiller W. (1999) Toward empirically based criteria for somatoform disorders. J. Psychosom. Res. 46: 507–518. Wessely S., Nimnuan C., Sharpe M. (1999) Functional somatic syndromes—one or many? Lancet 354: 936–939. Nimnuan C., Rabe-Hesketh S., Wessely S., Hotopf M. (2001) How many functional somatic syndromes? J. Psychosom. Res. 51: 549–557. Rief W., Hiller W., Margraf J. (1998) Cognitive aspects in hypochondriasis and the somatization syndrome. J. Abnorm. Psychol. 107: 587–595. Petrie K., Moss-Morris R., Weinman J. (1995) The impact of catastrophic beliefs on functioning in chronic fatigue syndrome. J. Psychosom. Res. 39: 31–37. Pilowsky I. (1997) Abnormal Illness Behaviour. Wiley: Chichester. Rief W., Ihle D., Pilger F. (2003) A new approach to assess illness behaviour. J. Psychosom. Res. 54: 405–414. Rief W., Nanke A., Klaiberg A., Br¨ahler E. Specific effects of depression, panic, and somatic symptoms on illness behavior. Psychosom. Med. (in press). Hiller W., Rief W. (2005) Why DSM-III was right to introduce the concept of somatoform disorders. Psychosomatics 46: 105–108. Rief W., Barsky A.J. Psychobiological perspectives on somatoform disorders. Psychoneuroendocrinology (in press).

5.12 Chronic Fatigue in Developing Countries Vikram Patel1 Fatigue is one of the commonest complaints in medicine and, as the authoritative and comprehensive review by Sharpe and Wessely demonstrates, it presents an excellent example of the confluence of psychological, social, and biological models for understanding health complaints. There is a great deal of uncertainty regarding the specific category of chronic fatigue syndromes: as with most non-psychotic syndromes, changing definitions of disorders and the blurred boundaries between disorders are likely to be the primary explanation for the varying findings of different studies. The key message of Sharpe and Wessely’s review is that, while chronic fatigue is a common complaint in primary care and in community settings, the prevalence of chronic fatigue as a syndrome varies according to the diagnostic criteria used. Exhaustive research on the aetiology of the syndrome and the complaint suggests that psychosocial factors are the most consistent, and strongest, risk factors. In particular, common mental disorders, adverse life events, other somatoform 1

London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK

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disorders, specific types of illness models, and social factors such as disability claims seem to have the strongest associations with the syndrome. In this commentary, I focus on the issue of fatigue in developing countries. Perhaps the best known fatigue-related condition in non-Western societies is neurasthenia. Although neurasthenia is almost exclusively diagnosed in East Asia, there appears to be little research describing its risk factors. It is possible that much of the evidence base on this syndrome is in Chinese and thus not covered in English language reviews. It seems apparent, though, that fatigue, the defining symptom of neurasthenia, is a culturally sanctioned expression of distress, not only of psychological distress such as depression but also of social unease. Apart from neurasthenia, however, it appears that there is very limited published evidence on chronic fatigue in developing countries. Indeed, the only reference to developing countries in Sharpe and Wessely’s review is the World Health Organization’s multinational study of common mental disorders in general health care published in 1995 [1]. Although not a study focusing on fatigue, it did generate estimates of the prevalence of the complaint in primary or general health care settings. Its most notable finding was the considerable variation in the prevalence of the complaint between different countries. The importance of the aetiology of fatigue in developing countries is underscored by the fact that the epidemiological pattern of the burden of disease is very different. It is not surprising, then, that fatigue is typically viewed as a complaint associated with chronic nutritional and infectious diseases. In a survey of women’s health in India, nearly a quarter complained of feeling weak or tired, more than half of whom had experienced these complaints for more than 6 months [2]. Half the women with this complaint had sought health care. The complaint of fatigue was attributed to nutritional deficiencies, particularly anaemia, which is common in women on account of menstrual blood loss and poorer nutrition, child-bearing and multiple pregnancies [3]. As a consequence, physicians are likely to prescribe iron, vitamins, tonics, and a variety of other nutritional supplements to treat the symptom presumptively. Indeed, such preparations account for the most common category of medications dispensed in Asia [4]. But, is this approach evidence-based? Our recent community study in India sheds light on the prevalence and risk factors for the complaint of chronic fatigue in women [5]. More than 1 in 10 women reported the complaint of fatigue of at least 6 months duration. The socio-economic risk factors independently associated with chronic fatigue were older age and indicators reflecting socio-economic deprivation, that is, low education, being in debt, and having experienced hunger in the recent past. Gender disadvantage is a major social determinant of health in developing countries [6]; our study demonstrates the strong association of this factor with chronic fatigue, in particular, widowhood, oppressive

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restrictions on women’s lives, lack of a trusting relationship with a spouse, and marital violence. Excess physical work and gendered disadvantages in access to food are perhaps the most likely explanation for the association of fatigue with low body mass index. Mental health factors, notably the comorbidity with other physical complaints, and symptoms of depression and anxiety, had the strongest associations with chronic fatigue. There was no association between haemoglobin levels or frank anaemia with the complaint, suggesting that the common practice of prescribing iron or vitamins to women with this complaint is likely only to help through a placebo effect. Sharpe and Wessely rightly say that cultural factors play a major role in the experience of fatigue, and the way patients explain the association of fatigue with other health and social factors. In South Asia, for example, sexual complaints in men (e.g., the involuntary passage of seminal fluid) and women (vaginal discharge) often co-occur with the complaint of fatigue. Typically, one symptom is seen to be caused by the other (most often, the sexual complaint is primary) and both are strongly associated with psychological and social distress [7]. Thus, the evidence base, thin as it is at present, suggests that, despite widely varying cultural beliefs and epidemiological profile of disease burden in developing countries, the risk factors of the complaint of chronic fatigue are very similar to that of developed countries, with the key difference being the nature of the social adversities and the types of illness models that might predispose or precipitate the complaint. This evidence needs to be disseminated to primary and general health care practitioners who are the front-line in the clinical management of somatic complaints; the assessment of psychological health and social difficulties and the avoidance of unnecessary, expensive, nutritional supplements must be emphasized.

REFERENCES 1. 2. 3. 4. 5. 6.

Skapinakis P., Lewis G., Mavreas V. (2003) Cross-cultural differences in the epidemiology of unexplained fatigue syndromes in primary care. Br. J. Psychiatry 182: 205–209. Bhatia J.C., Cleland J. (1995) Self-reported symptoms of gynecological morbidity and their treatment in South India. Stud. Fam. Plann. 26: 203–216. Lennartsson J., Bengtsson C., Hallberg L., Tibblin E. (1979) Characteristics of anaemic women. The population study of women in Goteborg 1968–1969. Scand. J. Haematol. 22: 17–24. Dineshkumar B., Raghuram T.C., Radhaiah G., Krishnaswamy K. (1995) Profile of drug use in urban and rural India. Pharmacoeconomics 7: 332–346. Patel V., Kirkwood B.R., Weiss H., Pednekar S., Fernandes J., Pereira B., Upadhye M., Mabey D. Chronic fatigue in developing countries: a population based survey of women in India. Br. Med. J. (in press). Shiva M. (1992) Women and health. In: State of India’s Health, A. Mukhopadhyay (Ed). Voluntary Health Association of India: New Delhi, pp. 265–302.

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Patel V., Pednekar S., Weiss H., Rodrigues M., Barros P., Nayak B., Tanksale V., West B., Nevrekar P., Kirkwood B., et al. Why do women complain of vaginal discharge? A population survey of infectious and psychosocial risk factors in a South Asian community. Int. J. Epidemiol. (in press).

5.13 Functional Somatic Syndromes: Many Names for the Same Thing? Marco Antonio Brasil1 , Jos´e Carlos Appolin´ario2 and Sandra Fortes3 As Christopher Bass [1] observed, the so-called functional illness inhabits a borderland between psychiatry and medicine, and is often overlooked by both. The failure of psychiatrists to develop a satisfactory classification of this subject matter, or even to agree on the principles on which that classification should be based, has proved to be a barrier to useful research in this field. Since the seminal work of Balint [2], we know that a significant percentage of general practice patients have no organic disease, although they commonly bring somatic complaints to their doctors, who cannot ignore them, even when they want to. These somatic symptoms have long been considered as ‘‘communicative acts’’ [3, 4] and ‘‘coded messages’’ [5], since these patients, having difficulties in various areas of their lives, express their suffering through ‘‘bodily terms’’, in a process named somatization. Balint [2] points out that these patients will go on and on, changing symptoms and doctors till one of their complaints is recognized as valid by one of these doctors and treated. The doctor often needs to diagnose these complaints, giving psychopathological names to them. This ‘‘battery’’ of terms hardly conceals their uselessness. The patient’s most urgent need is for a name to be given to his suffering; only secondarily does he demand treatment. Citing Andr´e Maurois, ‘‘Nommer le d´emon, c’est d´ej`a l’exorciser’’. The importance of cultural factors has been shown by Sharpe and Wessely, in their comprehensive and authoritative review, as well as by others. Kleinman [6] pointed out, in his study of mental health in China, that many patients called by Chinese psychiatrists ‘‘neurasthenics’’ fulfilled the criteria for major depressive disorder. However, all the patients had sought help for somatic symptoms such as headache, dizziness, and chest pains. Only 9% mentioned depression as one of their main complaints. Many other investigators in India, Pakistan, Nigeria, Mexico, Porto Rico, and Saudi Arabia (see [7]) have reported in transcultural studies that somatization of 1 2 3

Department of Psychiatry, School of Medicine, Federal University of Rio de Janeiro, Brazil Medical Sciences School, University of the State of Rio de Janeiro, Brazil Institute of Psychiatry, Federal University of Rio de Janeiro, Brazil

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psychological distress is present to a much greater degree in non-European cultures. In Brazil, authors such as Brasil [7] and, more recently, Fortes [8] and Tofoli [9] have studied these patients who presented multiple and non´ specific symptoms with no physical cause. The symptoms consisted of multiple, non-specific and varied complaints, usually associated with situations such as domestic conflicts, violence, and housing problems. Although these patients seek medical attention, their symptoms are rather an expression of being upset, anger, frustration, or sadness at the chronic stress of their environment, as well as being a temporary escape from it, and a way of getting sympathy and help from other people. The disruption of family life, unemployment, discrimination, overcrowded housing, violent neighbourhood are all part of this wider context. One cannot understand them only at the micro-level; one also needs to examine the sociocultural, political, and economic status of these people and the sense of having no hope, no help, and no control over their own lives. Hardly any of them could be diagnosed as a ‘‘pure’’ case of one of the functional somatic disorders subtypes described by Manu [10]. These patients have to be dealt with through a multidimensional approach. As Kirmayer and Robbins [11] suggested, we might shift our attention from efforts to identify and characterize disorders to an attempt to better understand the underlying pathological processes that may result in functional somatic distress. In the contemporary practice of psychiatry, ‘‘diagnosis’’ has to go beyond the mere naming of a referral condition to encompass all the many significant factors necessary for a full understanding of the condition. If we do not adopt a multidimensional approach, we may only be giving new names to an old problem, which is clinically useless. We must not forget that more important than dividing up the functional somatic syndromes is trying to find out if there could be a common mechanism that underlies them. Remembering Henry Maudsley’s words: ‘‘As it is not Nature which makes division, but man who imposes his conditions on it, the prudent inquirer will not make too much of them’’ [12].

REFERENCES 1. 2. 3. 4. 5.

Bass C.M., Cawley R.H. (1990) Somatization, Physical Symptoms and Psychological Illness. Blackwell: Oxford. Balint M. (1956) The Doctor, his Patient and the Illness. Pitman: London. Kirmayer L.J. (1984) Culture, affect, and somatization. Part I. Transcult. Psychiatry Res. Rev. 21: 159–188. Kirmayer L.J. (1984) Culture, affect, and somatization. Part II. Transcult. Psychiatry Res. Rev. 21: 237–262. Racy J. (1980) Somatization in Saudi women: a therapeutic challenge. Br. J. Psychiatry 137: 212–216.

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9. 10. 11. 12.

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Kleinman A.M. (1986) Social Origins of Distress and Disease: Depression, Neurasthenia, and Pain in Modern China. Yale University: New Haven. Brasil M.A. (1995) Pacientes com queixas difusas, Um estudo nosologico de ´ pacientes com queixas multiplas e vagas. Doctorate thesis, Federal University ´ of Rio de Janeiro. Fortes S. (2004) Transtornos mentais na aten¸ca˜ o prim´aria: suas formas de apresenta¸ca˜ o, perfil nosologico e fatores associados em unidades do programa de ´ saude da fam´ılia do munic´ıpio de Petropolis/Rio de Janeiro/Brasil. Doctorate ´ ´ thesis, University of the State of Rio de Janeiro. Tofoli L.F.F. (2004) Investiga¸ca˜ o categorical e dimensional sobre sintomas f´ısicos e s´ındromes somatoformes na popula¸ca˜ o geral. Doctorate thesis, University of S˜ao Paulo. Manu P. (1998) Functional Somatic Syndromes. Cambridge University Press: Cambridge. Kirmayer L., Robbins J.M. (Eds) (1991) Current Concepts of Somatization— Research and Clinical Perspectives. American Psychiatric Press: Washington, D.C. Maudsley H. (1895) The Pathology of Mind. MacMillan: London.

5.14 Recent Developments in Chronic Fatigue Syndrome Ruud C.W. Vermeulen1 Promising developments in research on chronic fatigue syndrome (CFS) were published in the literature and presented at meetings in the last 2 years. They provide new insights into the diagnosis and pathogenesis of the syndrome. Up to now, no objective tests have been available to measure the presence of CFS and the severity of its symptoms. This lack of objective tests makes the diagnosis and outcome of intervention studies disputable. New developments in testing of cytokines, oxidative stress, heart rate variability, and gene expression response to stress and exercise in these patients open new opportunities for objective criteria [1–6]. Several studies have explored the activity of the immune system in CFS. It was found that the increase of pro-inflammatory cytokines in the periphery of the body results in their increase in the brain and vice versa [7]. It has been suggested that the peripheral system is chronically stimulated by a low-grade infection by mycoplasma or other agents [8]. Inescapable stress induces activity in the central pro-inflammatory cytokines in animals and possibly in subjects with burn-out [7]. The result is sickness response: an urge to go to bed, loss of fluid and electrolytes, irritability, sleep disturbance, pain in muscles and joints, cognitive impairment, and post-exertional malaise. Proton magnetic resonance spectroscopy (1H-MRS) showed in CFS patients an abnormal phospholipid metabolism in the cell membranes of the occipital 1

CFS and Pain Research Center Amsterdam, Waalstraat 25-31, 1078 BR Amsterdam, The Netherlands

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cortex, with release of choline [9, 10] likely due to oxidative stress [10]. Okada et al. [11] reported a bilateral reduction in grey matter volume in the prefrontal cortex in CFS patients. The volume reduction in the right prefrontal cortex paralleled the severity of the fatigue. This may explain the full recovery rate of only 5% in CFS patients [12]. Differences in the gene expression between CFS patients and healthy controls were reported by Gow et al. [13]. Their iterative group analysis indicated ‘‘a shift of immune response with consequential suppression of natural killer cells and αT-cell receptors, increased cell-membrane prostaglandinendoperoxide synthase activity with downstream changes in oxygen transport and macrophage activation with phagocytosis of apoptotic neutrophils’’. These studies are all pointing at an immune disturbance in the brain, causing symptoms of ‘‘sickness’’, but only after elucidation of the biochemical processes involved, will we be able to develop a causal therapy for CFS. We should realize that since the signal of fatigue is not the disease [14], it should not be the target of the therapy. Apparently, chronic fatigue and CFS are developing into a new discipline of medicine, and we hope that appropriate medication will become available within the next 10 years.

REFERENCES 1. 2. 3. 4.

5.

6. 7. 8.

Gaab J., Rohleder N., Heitz V., Engert V., Schad T., Schurmeyer T.H., Ehlert U. (2005) Stress-induced changes in LPS-induced pro-inflammatory cytokine production in chronic fatigue syndrome. Psychoneuroendocrinology 30: 188–198. Gaab J., Rohleder N., Heitz V., Schad T., Engert V., Schurmeyer T.H., Ehlert U. (2003) Enhanced glucocorticoid sensitivity in patients with chronic fatigue syndrome. Acta Neuropsychiatr. 15: 184–191. Jammes Y., Steinberg J.G., Mambrini O., Bregeon F., Delliaux S. (2005) Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. J. Intern. Med. 257: 299–310. VanNess J.M., Snell C.R., Stevens S.R., Gibbons R., Keller B. (2004) Impaired aerobic metabolism 24-hours post exercise in chronic fatigue syndrome. Presented at the 7th International Conference on Chronic Fatigue Syndrome and Fibromyalgia, Madison, October 8–10. Kikuchi H., Yoshiuchi K., Cook D.B., Ohashi K., Yamamoto Y., Natelson B.H. (2005) Nonlinear analysis of heart rate variability before and after exercise in chronic fatigue syndrome. Presented at the International Conference on Fatigue Science, Koruizawa, February 9–11. Whistler T., Jones J.F., Unger E.R., Vernon S.D. (2005) Exercise responsive genes measured in peripheral blood of women with chronic fatigue syndrome and matched control subjects. BMC Physiol. 5:5. Maier S.F. (2003) Bi-directional immune-brain communication: implications for understanding stress, pain, cognition. Brain Behav. Immunol. 17: 69–85. Nicolson G. L., Gan R., Haier J. (2003) Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients: association with signs and symptoms. APMIS 111: 557–566.

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Puri B.K., Counsell S.J., Zaman R., Main J., Collins A.G., Hajnal J.V., Davey N.J. (2002) Relative increase in choline in the occipital cortex in chronic fatigue syndrome. Acta Psychiatr. Scand. 106: 224–226. Chaudhuri A., Behan P.O. (2004) In vivo magnetic resonance spectroscopy in chronic fatigue syndrome. Prostaglandins Leukotr. Essent. Fatty Acids 71: 181–183. Okada T., Tanaka M., Kuratsune H., Watanabe Y., Sadato N. (2004) Mechanisms underlying fatigue: a voxel-based morphometric study of chronic fatigue syndrome. BMC Neurol. 4: 14. Cairns R., Hotopf M. (2005) A systematic review describing the prognosis of chronic fatigue syndrome. Occup. Med. 55: 20–31. Gow J.W., Cannon C., Behan W.M.H., Herzyk P., Riboldi-Tunnicliffe G., Behan P.O., Chaudhuri, A. (2005) Whole-genome (33,000 genes) affymetrix DNA microarray analysis of gene expression in chronic fatigue syndrome. Presented at the International Conference on Fatigue Science, Koruizawa, February 9–11. Damasio A. (2003) Looking for Spinoza. Joy, Sorrow and the Feeling Brain. Harcourt: New York.

5.15 Does Neurasthenia Really Exist in this Century? Edmond Chiu1 The controversy over the existence of neurasthenia as a clinical syndrome is exemplified by the fact that it has been removed from the DSM-IV classification, while the ICD-10 continues to include it. Does this syndrome really exist? If so, what is it? The construct of neurasthenia has not been up to now the subject of vigorous phenomenological research backed by good-quality psychometric analysis. In recognition of this lack, the World Psychiatric Association (WPA) undertook the first step in the journey to clearly delineate the syndrome. A technical report, which was the outcome of a consensus meeting held under the auspices of the WPA, was approved by the WPA General Assembly at the World Congress of Psychiatry in 2002. This technical report [1] identified five clinical domains central to the syndrome: the cognitive, the emotional, the somatic, the energy, and the sleep ones. The predisposing personality factors, belief systems, explanatory models, social factors, and comorbidity related to neurasthenia were also summarized. Issues requiring clarification were highlighted. With this consensus technical report, the WPA hopes that research will proceed to test the diagnostic validity of this syndrome and establish a psychometrically rigorous measurement of its content. Chan et al. [2] have developed the Neurasthenia Scale, which has satisfactory psychometric properties. Further research into this instrument to 1

Academic Unit for Psychiatry and Old Age, University of Melbourne, Australia

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establish its usefulness in other populations will be helpful to advance the study of the syndrome. Several questions remain open: (a) what are the primary clinical characteristics of the syndrome? (b) What is the relationship between this syndrome and other closely related emotional/somatic conditions (such as anxiety and depressive disorders)? (c) What clinical markers may distinguish neurasthenia from other mood or somatic conditions? (d) Does the syndrome manifest differently within different ethnic or social groups? If so, what are the possible explanations? (e) Can neurasthenia be appropriately classified in a categorical system, or is a dimensional approach more appropriate? The rejection of neurasthenia by the DSM-IV is unfortunate, as it closes the door to vigorous research. The reopening of this door will allow some progress towards answering the question: does neurasthenia really exist?

REFERENCES 1. 2.

World Psychiatric Association (2002) Neurasthenia—A Technical Report from the World Psychiatric Association Group of Experts. www.wpanet.org/institutional/ consensus.html. Chan C.K.Y., Wong K.C., Liu Z. (2001). The Neurasthenia Scale: a psychometric analysis of neurasthenia and its relationship with depression, anxiety and stress. Presented at the Third Pan-Asia-Pacific Conference on Mental Health, Beijing, October 12–15.

CHAPTER

6 Factitious Physical Disorders: A Review Stuart J. Eisendrath1 and John Q. Young1 1

Langley Porter Psychiatric Institute, 401 Parnassus Avenue, San Francisco, CA 94143-0984, USA

INTRODUCTION Patients with factitious disorders present special challenges to the clinician and the health care system. By definition, these patients wilfully produce the signs and symptoms of disease. Often, significant efforts have been made by the health care team to uncover the cause of the patient’s initial complaints. Frustration and discouragement may accompany the physician’s inability to identify a cause. When the diagnostic inquiries lead to the possibility of fabrication or exaggeration by the patient, the physician–patient relationship faces a severe challenge. As Nadelson noted, ‘‘. . . mimicry of disease violates the boundary of the patient role’’[1]. The physician and health care team may feel betrayed and misled by the factitious disorder patient, leading to a desire to punish or dismiss the patient. Moreover, the team may feel resentment over the significant energy and time invested in the patient’s care, and anger about the diagnostic tests and consultations consumed, often at great cost to the institution and society. In addition, the team may experience guilt regarding the morbidity and disability, sometimes permanent, which may result from the interventions eventually shown to be unnecessary. As a result, the patient is commonly discharged without any attempt at psychiatric intervention. This generally leads to the patient re-engaging in the same pattern of care with a different set of health care providers. The patient continues to receive unnecessary diagnostic and treatment interventions with the attendant risks and complications. The burden and cost of inappropriate care is shifted from one system to another. However, this negative outcome Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

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for the patient and his or her family, the health care team, and the system can often be averted when the behaviour of the patient is understood in terms of its underlying motivations, and appropriate interventions are made. This chapter will focus on individuals who create factitious physical disorders.

HISTORICAL BACKGROUND In 1838, Gavin first described ‘‘feigned and factitious diseases’’ in a book published by the University of Edinburgh [2]. A century later, Asher [3] brought increased attention to this disorder. He described a set of patients with severe, chronic factitial behaviour—patients who ‘‘wandered’’ from one clinic or hospital to another, continuously fabricating illness in order to receive medical attention. These patients often had minimal, if any, social support, and adopted ‘‘patienthood’’ as an occupation. He classified these disorders according to the organ system chosen by the patient for ‘‘disease falsification’’. Asher labelled this behaviour Munchausen’s syndrome. Asher borrowed the term ‘‘Munchausen’’ from a book by Rudolph Erich Raspe, a children’s author in the late eighteenth century. Raspe wrote stories about a fictional character, Baron Munchausen, who always lied, albeit harmlessly. He depicted the Baron as preoccupied with tales of his own heroic military conquests and miraculous escapes from foreign dungeons [4]. Thus, Asher ‘‘continued the notion of a truth-bending Munchausen when he ‘respectfully dedicated the syndrome of [medical deception] to him’ ’’ [1]. Asher’s use of the rather pejorative label may well represent some of the typical resentment that caregivers often develop when faced with factitious patients. But the ‘‘unusual vitriol’’ with which Asher and others at the time characterized the ‘‘peregrinating problem patients’’ may also reflect the context in which this diagnosis first emerged. Asher wrote his paper just a few years after Britain’s National Health Service (NHS) had been established. The NHS offered free health care to millions of Britons dislocated by the war. Physicians saw this new national system as a threat to their more lucrative private practices. Physicians feared that this dramatic expansion of access would overwhelm them with thousands of ‘‘dole’’ patients. Thus, these social and economic changes brought ‘‘needy patients’’ in contact with ‘‘frustrated doctors’’. This interaction gave birth to the pejoratively regarded Munchausen patient. With the advent of managed care and the consumer movement, one might argue that the current American health care system structures a similar conflict between ‘‘demanding’’ patients empowered by the consumer movement with ‘‘embattled’’ physicians frustrated by increased restrictions

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and less time with patients. These forces may also add to the intense reactions that physicians have to factitious patients [5]. Since Asher’s article, research and clinical observation has better characterized these factitious disorders. We now know that Munchausen’s syndrome represents a minority of factitious disorders.

CONTEMPORARY CLASSIFICATION As stated above, factitious disorders arise when a patient consciously creates illness. In other words, the patient engages in the wilful production of the signs and symptoms of disease. Usually, the patient’s primary goal is to receive medical or surgical care to satisfy some psychological need. In addition, external incentives for the behaviour, such as economic gain or possession of pain medication, must not exist. These patients are often of great interest to physicians, because their behaviour typically causes physicians and nurses to participate unwittingly in their psychological disorder. The DSM-IV criteria for factitious disorders are given in Table 6.1. As indicated in this table, the factitious illness that is produced can be either physical or psychological in nature. Factitious disorders may best be considered one type of abnormal illnessaffirming behaviour [7]. In addition to factitious disorders, this broader category of abnormal illness-affirming behaviour includes malingering, conversion, somatization and body dysmorphic disorders, hypochondriasis, and pain disorder with psychological factors. Factitial behaviour occurs when individuals either create or amplify clinical signs or symptoms to appear T A B L E 6.1 DSM-IV diagnostic criteria for factitious disorders (American Psychiatric Association [6]) 1. Intentional production or feigning of physical or psychological signs or symptoms. 2. The motivation for the behaviour is to assume the sick role. 3. External incentives for the behaviour (such as economic gain, avoiding legal responsibility, or improving physical well-being, as in malingering) are absent. Code based on type: 300.16 With predominantly psychological signs and symptoms 300.19 With predominantly physical signs and symptoms 300.19 With combined psychological and physical signs and symptoms 300.19 Factitious disorder NOS: This category includes disorders with factitious symptoms that do not meet criteria for a specific factitious disorder. An example is factitious disorder by proxy: the intentional production or feigning of physical or psychological signs or symptoms in another person who is under the individual’s care for the purpose of indirectly assuming the sick role.

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more ill than they otherwise would, given their actual level of biomedical disease. In contrast to self-mutilating patients, who usually admit to producing their injury and do not aim their behaviours at obtaining medical care, factitious disorder patients typically conceal the origin of their disorder and specifically seek care. In contrast to malingering patients, factitious disorder patients produce illness primarily to achieve a psychological benefit; external incentives play only a secondary role. Finally, in contrast to patients with conversion disorder, who produce the symptoms unconsciously, these patients produce the symptoms consciously. Table 6.2 compares factitious disorders to other abnormal illness behaviours in terms of the goals of the behaviour, the extent to which the behaviour is conscious or not, and the readiness to accept high risk or painful procedures. We will explore these distinctions further in the section on diagnosis. Finally, it is important to recognize that factitious behaviours fall on a spectrum that ranges from normal adaptive functioning to severe disability. All human beings experience dependency needs, or the need to be taken care of by others, as a normal developmental interaction. Some individuals will amplify their own somatic symptoms or level of distress in order to fulfil this psychological need. For example, a young child who experiences the entry of a new sibling into the family may elaborate somatic symptoms as a means

T A B L E 6.2

Distinguishing features of abnormal illness-affirming behaviours

Disorder Malingering

Factitious disorder

Conversion disorder Somatization disorder Body dysmorphic disorder Hypochondriasis Pain disorder with psychological factors

Sign and symptom production Conscious

Motivation Conscious

Primary goal

Painful or high risk procedures

Secondary or Avoided external gain, such as money, pain medication, shelter Conscious Unconscious Primary gain, such Accepted as receiving readily or attention, the even demanded sick role Unconscious Unconscious Primary gain, such Accepted as receiving attention, the sick role

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of refocusing parental attention. An adult may exaggerate his or her distress due to work demands in order to obtain support and sympathy from a friend or spouse. Factitious behaviours become a disorder only when they interfere with normal functioning [8].

CLINICAL FINDINGS Factitious physical disorders can take many forms, limited only by human imagination. Patients with this disorder have feigned the signs and symptoms of almost all disease states. Table 6.3 illustrates the all-encompassing breadth of the various feigned disorders. This table also highlights the most common manifestations. The various means by which fever has been simulated shows the ingenuity often involved: holding a thermometer near a light bulb, ingesting a hot liquid prior to temperature measurement, rapidly contracting and relaxing of the anal sphincter in order to produce friction heat (thereby elevating rectal thermometer readings), and injection of bacteria. Similarly, numerous infectious states such as septicemia, abscesses, cellulitis, urinary and gastrointestinal tract infections, and slow healing ulcers have been created. Patients have also induced abnormalities such as hypokalemia, anaemia, hyperamylasuria, and hypoglycemia. Moreover, patients have simulated a wide range of other conditions, including coronary artery disease [10], ventricular tachycardia and acute coronary syndrome [11, 12], acquired immunodeficiency syndrome (AIDS) [13], cancer [14], systemic lupus erythematosus [15], limb edema/reflex sympathetic dystrophy [16], Cushing’s syndrome [17], shoulder-hand syndrome [18], psoriasis-like dermatitis [19], and aplastic anaemia [20]. Table 6.4 further illustrates the ingenuity, skill, and cleverness often involved in causing these disorders. Individuals with factitious disorders are generally considered to produce signs and symptoms on three possible levels [22]. First, patients may provide the physician with a fictitious history. For example, such patients may claim to have migraine headaches, human immunodeficiency virus (HIV) infection, cancer, seizures, or familial colonic polyposis when in fact they do not. These factitious histories are not without consequences. Accordingly, the presumed HIV patient may receive anti-retroviral therapy and the presumed polyposis patient may undergo a colonoscopy. Second, a factitious disorder patient may simulate disease. For example, a patient may add drops of blood or a geologic (i.e., non-physiologic) stone to urine to simulate hematuria or renal stones. Finally and often most seriously, a patient may actually create a pathophysiological state by, for example, injecting bacteria to create an infection, epinephrine to create coronary vasospasm-induced ischaemia or insulin to create hypoglycemia. All of these factitious production levels,

330 T A B L E 6.3 et al. [9])

SOMATOFORM DISORDERS Examples of factitious physical disorders (adapted from Feldman

Acromegaly Acute respiratory distress Alcohol dependence *Anaemia Bartter’s syndrome *Bleeding Blepharokeratoconjunctivitis (chronic) Breast cancer Burns Cervicofacial sub-cutaneous emphysema Cheilitis *Connective tissue diseases Cushing’s syndrome Deafblindness Dermatoses Diabetes mellitus *Diarrhoea Diphenhydramine poisoning Diplopia *Dizziness Epidermolysis bullosa simplex *Fever Gastrointestinal bleeding Gingival injury Hemoptysis Human immunodeficiency virus (HIV) disease Hypercortisoluria Hypertensive crisis Hypocalcemia *Hypoglycemia

*Impaired wound healing *Infectious diseases (various) Intra-alveolar pulmonary siderophages Lymphedema Malaria Malignancy Maxillofacial injuries Methemoglobinemia Mutilation of the hand Nasal ulceration Necrotizing fasciitis Orbital emphysema *Pain Periodontal injury Persistent discharge from arthroscopic portals Pheochromocytoma Psoriasis-like dermatitis Pulmonary talcosis Purpura Quadriplegia *Rash Rectorrhagia Reflex sympathetic dystrophy Renal colic *Seizure Sickle cell acute painful episodes Thrombocytopenia Urinary calculi Vaginal bleeding *Vomiting

An asterisk designates the most common types.

but especially the latter category, can lead to disability, morbidity, and even death. As noted above, Munchausen’s syndrome represents the best known variant of factitious disorder. In addition to its severe and chronic course, this condition has three classical features: pseudologia fantastica; peregrination; and sociopathic tendencies. The first feature, pseudologia fantastica, refers to the patient’s propensity to embellish his or her history with fantastically exaggerated tales about his or her educational, societal, or military credentials, past exploits, and social or political connections. The second feature, peregrination, means ‘‘wandering’’. These patients in the past have been described as ‘‘hospital hoboes’’ because they moved from one clinic or hospital to another

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T A B L E 6.4 Examples of methods used to cause factitious disorders (adapted from Eisendrath [21]) Manifestation or disorder simulated Hypoglycemia Hyperthyroidism Cushing’s syndrome Pheochromocytoma Hypokalemia Bleeding diathesis Anaemia Hemoptysis Human immunodeficiency virus (HIV) disease Mydriasis Diarrhoea Vomiting Urinary calculi Goodpasture’s syndrome Hematuria

Bacteriuria

Example of a cause Administration of insulin or ingestion of oral hypoglycemics Ingestion of thyroid hormone Ingestion of steroids and/or addition of glucocorticoid to urine Self-injection of metaraminol or epinephrine Laxative abuse, induced vomiting, diuretic abuse Sodium warfarin ingestion Self-administered phlebotomy Addition of blood, self-induced trauma Fictitious history Self-administered homatropine eye drops Excess ingestion of castor oil or laxatives Ipecac abuse Materials added to urine, stones added to urethra Adding blood to urine, false history Contamination with external blood or meat; sodium warfarin ingestion; addition of providone-iodine to urine, causing false positive dipstick result Urine contamination in vivo or in vitro with, for example, faeces

once the health care staff became suspicious about the patient’s role in the illness. The third feature, sociopathic tendencies, captures these patients’ use of lying, impostorship, aliases, and other forms of manipulation in order to gratify their needs. With Munchausen’s syndrome, the individual pursues an unceasing lifestyle of patienthood. It is important to note, however, that the majority of factitious disorder patients do not fit the criteria for Munchausen’s syndrome. Reich and Gottfried [23] and Kapfhammer [24] reported that the proportion of factitious disorder patients who have the more severe variant (i.e., Munchausen’s syndrome) may be as small as 10%. In contrast, up to 90% of factitious disorder patients have stable homes, families, and jobs. This differentiation is important for several reasons. Failure to appreciate this heterogeneity may result in underdiagnosis of cases that are less severe and chronic than the Munchausen’s syndrome, but nonetheless pathologic and disabling if not treated appropriately. In addition, the treatment for the two types

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of factitious disorder is different. Munchausen’s syndrome patients are refractory to psychiatric interventions to which other factitious disorder patients may readily respond. With Munchausen’s syndrome patients, the main intervention is to try to avoid the potential harm of invasive medical procedures and the massive expenses incurred.

EPIDEMIOLOGY Well-established incidence and prevalence data for factitious physical disorders do not exist. Clearly, there is a broad spectrum of severity, which ranges from the patient who temporarily feigns illness such as migraine headaches or low back pain to the patient who injects insulin to mimic an insulinoma or epinephrine to cause acute coronary syndrome. The data that does exist comes from retrospective chart reviews of patients treated on a given clinical service. Clinical services studied in the literature vary, and include psychiatric consultation, neurosurgery, neurology, endocrinology, HIV, haematology, and general medicine units. A few studies report the prevalence of all factitious disorders in a given cohort. For example, after reviewing the charts of over 1,200 patients referred to a psychiatric consultation service, Sutherland and Rodin [25] found that 0.8% had a factitious physical disorder. But most of the studies have a much narrower focus, and use chart reviews to determine the prevalence of a specific factitious disorder, such as fever or bleeding disorders, that are of concern to that service, such as a general medicine or haematology unit, respectively. These studies of specific cohorts have suggested a higher incidence, which some have used to argue that the occurrence of factitious disorder may be greater than expected by most physicians. In Aduan’s study of fevers of unknown origin at the US National Institutes of Health, 9.6% of the cases were identified as factitious [26]. Knockaert et al. [27] reported that, in a general hospital setting, 3.5% of cases of fevers of unknown origin were factitious, a rate of frequency higher than that of drug-related fevers. Similarly, in a Canadian study, Gault et al. [28] noted that approximately 3% of kidney stones submitted by patients were artefactual. Reich and Hanno [29] reported that 0.6% of a series of renal colic patients had factitious etiologies. Table 6.5 summarizes the studies that have investigated prevalence of factitious physical disorders in various settings. In reviewing the epidemiology of the disorder, it is important to distinguish between the more severe variant, that is, Munchausen’s syndrome, and the more common, but less severe variants. Typically, at least 50% of Munchausen’s syndrome patients are male, whereas non-Munchausen patients are predominantly female, with estimates ranging from 72 to 95% [23, 26, 40, 41]. Munchausen patients tend to be of lower than average socio-economic

Setting

Neurosurgery inpatients at a London Hospital over 8 years Chua and Tertiary referral centre in Friedenberg [31] rural Wisconsin Kapfhammer et al. [32] German university hospital over 4 years Kapfhammer et al. [32] German university hospital over 18 years Reich and Hanno [29] Two Philadelphia-area hospitals Ballas [33] Centre for haematologic research in Philadelphia Bauer and Boegner [34] Neurology service at a Berlin university hospital over 1 year Churchill et al. [35] Speciality HIV unit in central London over 5 years Knockaert et al. [27] General medical service at a Belgian university hospital during the 1980s

Papadopoulos and Bell [30]

Study Neurosurgical emergency Superwarfarin poisoning Pseudo-neurologic signs Miscellaneous ailments Renal colic Sickle cell painful episodes Neurologic syndromes HIV infection Fever of unknown origin

11 169 15,000 2,000 NA 1,538 706 199

Illness

18,893

Size of study population

3.5

1.7

0.3

0.9

0.6

0.62

5.3

18.2

0.032

(continued overleaf )

7

12

5

NA

12

93

9

2

6

Number Prevalence of cases (%)

T A B L E 6.5 Prevalence of factitious physical disorders in various settings (adapted from Feldman et al. [9])

FACTITIOUS PHYSICAL DISORDERS: A REVIEW 333

Bunim et al. [39]

Rumans and Vosti [38]

Aduan et al. [26]

Mohammed et al. [37]

Gault et al. [28]

Sutherland and Rodin [25]

Fishbain et al. [36]

Study

T A B L E 6.5 (continued)

Pain and rehabilitation centre 2,860 in Florida Psychiatric consultation 1,288 service at a large teaching hospital in Toronto over 3 years General hospital in Canada 3,300 kidney stones from 72 patients Australian casualty 713 department ‘‘black books’’ of ‘‘problem patients’’ National Institute of Allergy 343 and Infectious Diseases Stanford University Medical 506 Center over 10 years Adult and child patients at 200 National Institutes of Health

Setting

Size of study population

Fever of unknown origin

Fever of unknown origin

Fever of unknown origin

13

11

32

21

6.5

2.2

9.3

2.9

2.7 (of stones factitious)

∼9

Kidney stones

Miscellaneous ailments

0.8

0.14

10

4

Number Prevalence of cases (%)

Miscellaneous ailments, mostly self-induced infection and trauma

Chronic pain

Illness

334 SOMATOFORM DISORDERS

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status and to appear socially isolated, whereas patients with the less severe variants tend to have stable social and economic support systems and an average or above average educational achievement. For example, Krahn et al. [40] report that over 70% of their (mostly non-Munchausen) cohort identified via chart review had obtained an educational level of high school or greater and over 19% had obtained a college degree or higher. The onset of the disorder usually occurs during the third and fourth decades of life and the diagnosis in the fourth and fifth decades. Often, however, precursors of factitious disorders (e.g., illness amplification, false stories) may be seen in the childhood histories of these patients. These patients typically have a long history of using somatic complaints to secure their emotional needs, generally with minimal biomedical disease to support the symptoms [41]. In addition, factitious disorder patients often have had traumatic childhood illnesses that produced some benefit. For example, the illness may have generated increased caretaker concern (in the form of medical care) that the child did not experience in the family environment. And a relatively high percentage of these patients have health-related jobs that, in part, provide them with the background necessary to engage in the cunning simulations described above. Table 6.6 summarizes the demographic characteristics of factitious disorder patients from four representative studies. A wide spectrum of comorbid psychiatric diagnoses exist in factitious disorder patients. Serious personality pathology tends to characterize Munchausen’s syndrome patients, with a preponderance of borderline features, sociopathic features, or both [43]. In contrast, the non-Munchausen factitious disorder patients may have personality disturbance, often borderline, but less severe. These patients often have concurrent Axis I disorders (e.g., major depression, anxiety or adjustment disorders and substance abuse). The relatively higher ratio of Axis I to Axis II disturbance makes the non-Munchausen factitious patients more amenable to treatment [44]. T A B L E 6.6 Demographic characteristics of factitious disorder patients from selected studies (all retrospective chart reviews)

Study Carney and Brown [42] Reich and Gottfried [23] Eisendrath and McNiel [41] Krahn et al. [40]

Sample size 42 91 20 93

Setting Academic medical center Academic medical center Civil litigation Academic medical center

Sex (% F)

Age at diagnosis (years)

% with healthrelated jobs

76

34

68

95

33

50

95

43

60

72

34

47

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Factitious disorder may be under-reported for a number of reasons. First, under-recognition of the disorder may contribute to under-reporting. Physicians may not suspect these disorders very readily, primarily because most physicians do not expect their patients to deceive them. Moreover, enough ambiguity exists in the diagnosis or exclusion of physical disorders to allow both for successful fabrication and reluctance on the part of physicians to rule out a physiologic etiology. These and other challenges may contribute to the fact that it often takes 6 to 10 years before a condition is identified as factitious in origin [23]. This delay supports the notion that significant under-recognition may exist. Second, even when factitious disorder has been recognized, other factors may lead to under-reporting. Failure to document the diagnosis, once established, may occur for many reasons. In many cases, once a consultant makes the diagnosis, the primary physician is quite surprised and may even refuse to accept the diagnosis despite compelling evidence. Other reasons for failing to document the diagnosis include lack of familiarity by the medical or surgical team with psychiatric nomenclature and the differences between factitious, malingering, and somatoform disorders. This unfamiliarity, combined with the mixed presentation of the patients and the remaining medical uncertainty, may lead to non-specific diagnoses such as ‘‘abdominal pain, resolved’’. In some instances, physicians may avoid making a factitious diagnosis because of fears of angering the patient. Furthermore, physicians may be reluctant to make a psychiatric diagnosis of factitious disorder because this may jeopardize insurance coverage for the episode under the US system of diminished benefits for mental illness as compared to medical illness. These factors, combined with the methodological limitations of the prevalence studies, make it very difficult to have confidence in our present estimates.

SOCIAL AND ECONOMIC COSTS Given the limited epidemiologic data and even more sparse social cost studies, the social and economic costs of factitious disorders are not known at the aggregate level. Clearly, though, factitious disorders impose substantial direct (i.e., medical) and indirect (i.e., lost productivity, etc.) costs on society. The case histories give us anecdotal evidence of significant direct medical costs. Two case histories documented over $1 million in medical costs [20, 45]. The case histories also reveal substantial impairments to the patient’s health and function due to unnecessary medical and surgical interventions and associated complications. These impairments result in reduced productivity at work and decreased capacity to sustain social commitments such as parenting and caregiving, sometimes on a permanent basis, as is the case with, for example, the loss of an eye or limb or even death. Some data does exist for the direct costs associated with somatization disorder. Ford [46] estimated

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that the direct costs to society may reach $20 billion annually. It is difficult to predict how the costs associated with factitious disorders would compare to somatization disorder, but even a small fraction would be substantial.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS As the prior sections make clear, the diagnosis of factitious physical disorders presents significant challenges to the physician. The diagnostic inquiry and, more generally, the physician–patient relationship are predicated on the assumption that the patient presents a truthful history and desires relief from the physical complaint or disorder. Patients with factitious disorders seek care, but notably different assumptions guide their behaviour. The operating assumptions of the physician and patient conflict and, therefore, confound diagnosis. There are, however, a number of indicators of factitious disorder, which facilitate recognition. In general, the course of the illness is atypical and does not follow the natural history of the presumed biomedical disease process on a repeated basis. For example, the wound infection fails to respond to appropriate antibiotics or the skin graft inexplicably does not take time after time. Another indicator is a history of unexplained or inconsistent medical findings or non-physiological physical signs. Fevers without a concomitant appropriate increase in pulse rate represent one example. Also, there may be physical evidence of a factitious cause of symptoms (e.g., a syringe or surreptitious medication) that is discovered during the course of treatment. Finally, there may be direct observation of the patient factitiously producing illness. In addition to these indicators, there are features associated with factitious disorders that do not establish the diagnosis but do raise the clinician’s suspicion. The patient may accurately and repeatedly predict clinical deterioration. The patient may request or eagerly agree to invasive medical procedures such as surgery. The patient’s history may include a previous diagnosis of factitious disorder or, more commonly, numerous prior poor outcomes or failures to respond to medical intervention. Multiple physicians may have been consulted and they may have been unable to explain the course of the individual’s illness. Additional clues include the patients appearing socially isolated, with few friends or family members visiting them in the hospital despite their often critical medical problems, or the patient’s failure to respond to appropriate medical treatment. When these findings occur in someone who has either worked in or is related to someone who has worked in the health field, the caregivers should have a high index of suspicion for a factitious disorder. Obtaining collateral information from family members, prior physicians, and hospitals is crucial. Table 6.7 summarizes the indicators and associated features.

338 T A B L E 6.7

SOMATOFORM DISORDERS Clues to the diagnosis of factitious physical disorders

Indicators Direct observation Non-physiologic physical signs Physical evidence Atypical course contradicting natural history of disease

Associated features Patient predicts worsening Patient invites or welcomes invasive procedures Previous diagnosis of factitious disorder Numerous prior poor outcomes Worked in a health-related occupation Female, 20s to 40s (except Munchausen, which is male) Multiple physicians have been consulted and unable to explain the course of the illness

Other historical factors Symptom model Recent loss Multiple somatic complaints Childhood loss Childhood illness Psychiatric illness

There are also a number of other historical factors that commonly occur in patients with factitious disorders, knowledge of which can help with diagnosis. Table 6.7 lists these factors as well. The patient may have a preexisting model that informs his or her symptoms. Often, psychologically generated symptoms are based on a prototype, such as a close friend or relative who had similar symptoms. The patient may have experienced a recent psychological loss that correlates with onset of the symptom. As mentioned earlier, these patients often have a history of multiple somatic complaints that were unexplained or out of proportion to the biomedical disease present. The experience of significant childhood loss, such as death of a parent, or of childhood illness that required hospitalization or surgery, has also been associated with somatic complaints as an adult [41]. The differential diagnosis for factitious disorder is quite broad. Rare medical diseases that might explain an unusual clinical picture need to be considered. The physician should also assess the possibility of other forms of abnormal illness-affirming behaviour [7, 47]. Patients with factitious disorders consciously produce signs or symptoms, but generally do so for unconscious motivations, similar to phobic patients, who consciously avoid a phobic object, but do not know why. In contrast, malingering patients consciously produce signs or symptoms, but know that they are doing so to achieve an external gain. And patients with somatoform disorders, such as conversion disorder, somatization disorder, or hypochondriasis, produce their illness-affirming behaviour without knowing that they are doing so or their motivation for doing so. Table 6.2 summarizes these major distinctions between the various types of abnormal illness-affirming behaviour.

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It is important to note that the type of abnormal illness-affirming behaviour may shift over the course of a patient’s life. A prior diagnosis of one type does not preclude another at a later time. Symptom production may shift between conscious and unconscious awareness, and motivation may shift between primary and secondary gain. For example, case reviews have demonstrated how behaviour may shift from somatization to factitious to malingering when patients are followed longitudinally [41]. The high comorbidity of the related somatoform disorders with factitious disorders is further evidence of the overlap and fluidity that exist between them [48, 49]. In distinguishing factitious disorders from somatoform disorders, the conscious production of symptoms must be established. Conscious production can be established from behaviours such as a direct admission, direct observation of fabrication, atypical course, non-physiologic responses, physical evidence, or change in symptomatic behaviour when the patient believes he or she is not being observed [50, 51]. In the absence of such direct evidence, conscious production or intentionality is inferred after a long process of diagnostic and treatment interventions that have failed to find any physiologic explanation for the symptoms. In distinguishing factitious disorders from malingering, the patient’s primary motivation must be ascertained. In factitious disorders, this centres on obtaining the sick role. With a malingering patient, the secondary gain will be evident to an outside observer once the patient’s individual circumstances become clear and the material rewards the illness would bring are appreciated. The secondary gains may include monetary awards in litigation, disability or worker’s compensation benefits, relief from a noxious situation such as prison or military duty, or obtaining narcotics. The malingering patients will generally not endure significant secondary loss, such as invasive medical procedures or permanent disability, in order to obtain what they desire. Patients who malinger are more likely to give a fictitious history or simulate a disease but not to create a pathophysiologic state [52]. Factitious disorder patients differ markedly from malingering patients and act in a counter-intuitive fashion. Unlike patients with malingering, there is no observable goal to the production of symptoms except attaining the sick role. The only motivation an outside observer could reasonably infer is some psychological gain such as satisfying dependency needs. Such patients will endure significant secondary loss, including somatic dysfunction (e.g., loss of a limb or other chronic condition resulting from the disorder) and loss of self-esteem enhancing career, financial self-support, or prestige. For these patients, the secondary loss (e.g., loss of a limb) is greater than the secondary gain (e.g., disability) but the primary gain (permanent sick role with dependency gratifications) outweighs the secondary loss [12].

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Thus, the need to remain in the sick role is so strong that these secondary losses are accepted. However, the secondary costs are often so high that they make the physician assume that the disorder could not have been self-induced. This assumption can lead to substantial delays in diagnosis. In one example, a nurse blinded herself by staring at the sun with atropine-dilated eyes after her husband recovered from a serious automobile accident [52]. She became permanently disabled, and the etiology of her condition remained confusing until the idea of a factitious disorder was entertained and eventually admitted to by the patient.

THEORIES OF ETIOLOGY Research into the neurobiology of factitious disorders has been limited. Abnormalities found by neuroimaging, neuropsychological testing, and electroencephalogram in individual patients and small case series are nonspecific. These abnormalities include frontal temporal cortical atrophy on brain imaging or impairments in conceptual organization, judgement, and management of complex information on neuropsychological testing [53]. While case histories have shown multi-generational occurrence within a given family, there have been no genetic studies to date. Most theories employ psychological models to explain the etiology of the disorder. These models utilize psychodynamic, behavioural, and cognitive perspectives. We will briefly describe each of these perspectives. While we present these perspectives as distinct theories, simultaneous use of all three perspectives often leads to a better appreciation of the causative factors than exclusive reliance on one. Several major psychodynamic themes frequently occur in factitious disorder patients [8, 54]. One theme understands the disorder itself as an attempt by the patients to gain mastery or control that has heretofore eluded them. An adult who was traumatized by a medical illness in childhood may create a factitious illness that he or she can control entirely, unlike the illness he or she experienced in childhood. In such cases, the physician caring for the patient is often more worried about the illness than the patient. Masochism constitutes a second common theme. Some patients feel a compulsion to suffer in an atonement for various forbidden feelings, such as anger or sexual excitement. A third frequent theme centres on dependency gratification. Many factitious disorder patients experienced significant deprivation in childhood that left them with unfulfilled cravings for attention and care. These patients then seek to gratify these dependency needs by creating illness to obtain the ‘‘attention and care’’ of the medical system. A fourth theme arises in patients who were physically or sexually abused as children. These patients attempt to master their trauma by reenacting

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the abuse with physicians who unknowingly step into the symbolic role of abuser. Fifth, some factitious disorder patients’ deceit serves as an expression of rage towards the symbolic parental figure, as patients exult in outwitting the physician, manifesting ‘‘duping delight’’. A sixth common theme is that the factitious behaviour serves as a defence against a loss that has occurred or was threatened. Finally, Spivak [55] noted that the factitious disorder patient may be attempting to prevent psychosis by using the behaviour as an external structure to organize the self. Theories of etiology also employ behavioural perspectives. The behavioural literature explains factitious disorder as a function of past social learning and current positive and negative reinforcement [56, 57]. The patients may have learned at a critical juncture that illness brings certain benefits, either through their own experience or witnessing the experience of a family member. The experience of the sick role brings reinforcements that are positive, such as nurturance, sympathy, and attention. The experience also brings negative reinforcements (increasing the likelihood of repeating the factitious behaviour), such as relief from responsibilities or the expectations of others. These reinforcements stand as a powerful incentive to repeat the behaviour when the rewards are needed or desired. Finally, cognitive perspectives focus on the role that cognition, affective bias, and maladaptive information processing play in the etiology and maintenance of factitious disorder. In this view, some patients may have perceptual deficits that lead them to misinterpret normal physiologic phenomena as a sign of serious illness. This distortion generates anxiety and a need for reassurance. Patients with factitious disorder may exaggerate or create symptoms in order to obtain tests and medical advice that will reassure them of their health. Of the three perspectives, the cognitive approach has the least emphasis in the literature on factitious disorders and has been developed much more for the related somatoform disorders.

MANAGEMENT Early Approaches The treatment of factitious physical disorders has developed significantly over the past decades. Shortly after Asher identified the Munchausen’s syndrome in the early 1950s, other physicians began to frequently report cases of the disorder. Many physicians began to develop the idea of a ‘‘blacklist’’ to allow hospital emergency rooms to identify and exclude these patients. Because of problems with confidentiality, ethics, and the possibility of real disease, blacklists never emerged as a major tool in managing factitious disorders.

342

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Pharmacological Management Some psychiatrists began treating factitious disorder patients with various medications. Fras and Coughlin [58] described a positive response to phenothiazine by a factitious disorder patient in whom they had noted the onset of psychotic thought. As a consequence of this observation, they advocated judicious utilization of neuroleptic medication. Prior and Gordon [59] reported the effective use of pimozide after observing that the individual’s factitious disorder resembled hypochondriacal delusions. Earle and Folks [44] suggested that affective disorders may play a role in the genesis of some factitious disorders, and Merrin et al. [60] noted the onset of a factitious episode following a loss or separation: antidepressants may be extremely effective in these patients. In fact, the presence of a disorder such as major depression improves the likelihood of response to treatment. Unfortunately, the literature on pharmacological treatments does not extend beyond the occasional case report and does not provide much evidence for the direct treatment of factitious disorders with pharmacological agents.

Non-punitive Confrontation For most patients, psychological interventions are necessary. Hollender and Hersh [61] developed a noteworthy strategy of non-punitive confrontation in which the psychiatrist and primary physician approach the patient together. Joint confrontation prevents the psychiatrist from being seen as a prosecutor by the patient. In this approach, the primary physician would reveal the diagnosis of factitious disorder to the patient and the findings that led to this conclusion. Following this, the physician might say: ‘‘We know that you must have been feeling great distress to have used this way of coping’’. The psychiatrist would then interpret the patient’s factitious behaviour as a cry for help. Finally, psychiatric treatment would be offered to provide the patient a more adaptive way of coping with his or her stressors. Building on this approach, other physicians have recommended ‘‘closing the circle’’ around the patient with vigorous confrontation and transfer of the patient into intensive psychiatric treatment [62]. Some patients have benefited from intensive psychoanalytically oriented psychotherapy [63, 64]. These therapies often use the factitious physical symptoms as metaphorical communications from the patient, with less emphasis on detecting the origin of the symptom [65]. Although Hollender and Hersh’s [61] approach has some merit, clinical experience has suggested that it is not effective for many patients. Even if presented with incontrovertible evidence, most patients will not admit to the factitious nature of their disorder. For example, in one of the larger case series reported, Reich and Gottfried [23] noted that less than onesixth of the patients admitted the factitious etiology following confrontation,

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and only a small fraction of those patients appeared to have benefited from the confrontation in long-term follow-up. A recent retrospective case review of 93 patients with factitious disorder [40] replicated these findings: 76% of patients were confronted and only 17% acknowledged their role. Many patients will experience the confrontation as humiliating and seek care from a different clinic or hospital.

Non-confrontational Strategies Given the limited effectiveness of the confrontational approach, several physicians have developed alternate strategies that emphasize face-saving over confrontation. These strategies encourage the patient to relinquish the factitious symptom, but allow the patient to do so without having to admit to the fabrication. For example, Klonoff et al. [66] advocated a behavioural approach. Once convinced that a patient’s seizures were factitious, her staff trained the patient in biofeedback as a face-saving technique to allow him or her to gain control over the seizures. The staff also positively reinforced healthy behaviour. Similarly, Solyom and Solyom [67] used a behavioural approach in treating factitious paraplegia. Rather than arguing with the patient about the origins of the paraplegia, the physicians accepted the symptom as needing treatment. After removing positive reinforcements for the factitious behaviour, they prescribed faradic massages to stimulate movement in the paralysed limbs. These massages were painful. They also informed the patient that they would increase the duration of the massage if the initial ‘‘dose’’ was not sufficient. The patient responded dramatically to these efforts by walking soon after the beginning of treatment. In a unique systems-based approach, Schwartz et al. [68] reversed the usual reinforcements of hospitalization. In this case, a patient with factitious disorder had required repeated hospitalizations. Attention, in the form of hospitalizations, had become contingent on the presence of illness, thus promoting illness behaviour. The team sought to de-link illness from attention by developing an intervention in which the patient was permanently admitted to the hospital and then granted passes to leave the hospital, when feeling better, instead of repeatedly discharging the patient. This technique resulted in markedly reduced hospital stays for the patient in the follow-up period. The patient had less need for illness behaviour with the guarantee of a permanent bed. However, many hospitals today may not possess the administrative and financial flexibility required by this particular nonconfrontational intervention. Nonetheless, less dramatic variants may be possible, such as non-contingent medical care in the outpatient setting. In this approach, the patients are scheduled for regular, for example monthly, appointments with their physician, regardless of whether they are ill or not,

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so that illness does not need to be feigned in order to obtain the attention and care of the physician [69]. Eisendrath [70] suggested other non-confrontational approaches, including inexact interpretations, therapeutic double binds, and face-saving techniques. Inexact interpretations are partially correct but incomplete. The interpretation to the patient captures much of the psychodynamics of the patient’s disorder, but does not identify the factitious nature of the disorder. For example, one female patient was guilt ridden as a consequence of childhood sexual abuse. She developed abdominal pain without an identifiable organic etiology whenever her romantic relationships turned sexual. During an inpatient evaluation of the pain, a psychiatric consultation was obtained. While the evaluation was under way, her current boyfriend asked her to marry him. That night she developed unexplained septicemia, as she had on two prior hospitalizations. The psychiatric consultant suggested to her that she might feel a need to punish herself when good things, like the engagement, happened in her life. The patient readily agreed with the interpretation and two days later revealed that, because of her guilty feelings, she had injected a foreign substance intravenously after her boyfriend proposed. She then entered outpatient psychotherapy that was successful in helping her to tolerate intimate relationships with less guilt. Non-confrontational approaches include a technique called the ‘‘therapeutic double bind’’. Similar to the other non-confrontational techniques, the physician does not confront the patient directly with the diagnosis of a factitious etiology. Instead, the team offers the patient another medical intervention, such as a new medication or minor procedure (e.g., a split-thickness graft for a wound that has not healed). The therapeutic offer includes a bind, however. In the process of discussing the intervention, the team informs the patient that the differential diagnosis for the condition now includes a factitious etiology. Moreover, the team indicates that if the medical technique does not prove effective, the physicians will conclude that the disorder is factitious. The patient then faces a choice of relinquishing the factitious disorder without ever admitting to it or persisting in the factitial behaviour and facing a confrontation. Many patients, given this choice, will choose to heal following the procedure or new medication rather than be labelled factitious. Hypnosis and biofeedback are two additional face-saving techniques available to the psychiatric consultant. Learning hypnosis to improve blood flow and tissue oxygenation may be helpful for patients with wounds that do not heal. Biofeedback to reduce muscle spasm, increase blood flow, and increase relaxation can similarly be effective techniques to use with patients. Many patients will accept these procedures much more readily than overt psychotherapy and then, once engaged in the procedure, will develop a willingness to discuss significant psychological issues.

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All of the face-saving techniques create opportunities for the patient to relinquish the factitious symptom without having to endure the humiliation of public acknowledgement of the etiology of the disorder. The expectations appropriate for these techniques must be kept in mind: the goal is not personality reconstruction, but symptomatic improvement. While effective in many circumstances, these non-confrontational techniques do have limitations. These approaches are not practical in emergent situations. Some patients may create a life-threatening disorder that demands authoritative intervention. In these cases, there is insufficient time for the non-confrontational approaches. For example, one woman with an aplastic anaemia was being seen in psychiatric consultation for evaluation of depression and a possible factitious etiology for her anaemia [20]. During the early stages of the evaluation, a friend of the patient revealed information that indicated the cause of the patient’s disorder: self-administration of chemotherapy drugs. The patient’s white blood cell and platelet counts had been suppressed to life-threateningly low levels. Because of the urgency of her medical situation, and fearing that she might still be taking the drugs while in the hospital, the haematologist and psychiatrist confronted her, and a room search was carried out with her permission. There was no time to try a non-confrontational approach without endangering her life.

Systems Interventions and Ethical Considerations The above discussion has focused on various approaches to treating the factitious disorder patient. But these interventions occur in a broader system of care. The therapeutic approaches must also address the system that treats the patient. Optimal management requires collaboration between different disciplines. Once this diagnosis is made or even suspected by the primary medical team, psychiatric consultation is appropriate. The psychiatric consultant can help the team determine whether the patient’s history and presentation is consistent with a factitious disorder. And once a firm diagnosis of factitious disorder has been made, the psychiatrist plays a key role in the caregiving system. It is not uncommon for the medical and nursing staff to react with anger and a sense of betrayal towards factitious disorder patients [71]. The patient gains the attention of the caregivers by assuming the sick role, a role sanctioned by society for people who suffer from disease and want to recover. The diagnosis of factitious disorder reveals that the patient has violated this contract. The patient, not the disease, is now regarded as an antagonist [72]. It is important for the staff members to explore and ventilate their natural feelings of anger towards the patient. The psychiatrist can play a critical role by facilitating a group meeting in which these feelings can be expressed. If these feelings are not acknowledged, normalized, and contained, it is possible that the staff will act out their feelings in some other way (e.g.,

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through premature discharge or through inappropriate medical decisions). The psychiatrist can also educate physicians and nurses about the concept of factitious disorders. This often allows the staff to view the patient with less anger and more appropriately as having a serious psychiatric disorder. In addition, the psychiatric consultation, through staff meetings and other communications, can help establish clear intra-staff communication. Clear communication within the staff becomes even more essential when treating factitious disorder patients, because these patients tend to split staff into opposing factions. Table 6.8 lists management guidelines that psychiatric consultants often help the primary team develop. Finally, staff meetings are a useful context for considering the ethical issues raised by factitious disorder cases, including those that directly impinge on treatment. Table 6.9 highlights these questions. These questions and others have been considered at length by several authors [73, 74]. In general, physicians are responsible for upholding the obligations of the patient–doctor relationship, even though the patient does not. There are, however, no simple answers to these questions; a full discussion of these issues in a staff meeting is often extremely helpful, particularly when the hospital ethicist and attorney can participate in the discussion and treatment planning. T A B L E 6.8

Management guidelines for the entire staff

One primary physician to direct all care and consultations for the patient Invasive tests or procedures should only be done after positive signs indicate these are necessary Regular visits with the patient, so the patient does not need to invent new symptoms to see the primary physician Encouragement of self-management Positive reinforcement of healthy behaviours Treatment of comorbid conditions such as depression T A B L E 6.9

Common ethical questions raised by factitious disorder cases

1. Are investigations to discern the true cause of a patient’s illness an invasion of privacy when they include room searches without the patient’s consent? 2. Is it appropriate for the discovering physician to communicate the factitious disorder diagnosis to the referring physician if the patient does not authorize the release of information? 3. Does the patient have the usual rights of a patient–doctor relationship, or has the patient abrogated them by his or her duplicity? 4. Should patients with factitious disorders be regarded as suicidal and thus be considered for involuntary psychiatric hospitalization? 5. Should factitious disorder patients be regarded as autonomous individuals who are responsible for their behaviour and thus be candidates for criminal prosecution for committing fraud?

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SUMMARY Consistent Evidence Multiple case series have provided consistent evidence regarding the demographic characteristics of patients presenting with factitious disorders, especially with respect to age of onset (usually third and fourth decades of life), gender (predominantly female with the non-Munchausen variant, predominantly male with Munchausen), and prior history of health-related occupation. These studies have also identified heterogeneity of the disorder, with the peregrination, pseudologia fantastica, and sociopathy of Munchausen at the severe, but less common end of the spectrum. Common indicators facilitating recognitions, such as atypical course (not following the natural history of the presumed biomedical disease process), have been identified.

Incomplete Evidence Much of what is presently known about factitious disorder is incomplete and drawn from retrospective chart reviews and case histories. Prospective studies are needed to further define the epidemiology and core features of this illness. The evidence for treatment is similarly limited. No randomized trials have been undertaken to date. For example, comparing confrontational versus non-confrontational or behavioural versus other interventions would greatly expand our knowledge of what constitutes effective treatment. In order to design prospective trials, innovative approaches would need to be developed. For example, utilizing a high-risk population, such as that which might be found in a wound-healing clinic, might yield a significant sample of factitious disorder patients who might then be randomized to different approaches. Such an approach is not straightforward, however, since by their nature factitious disorder patients do not typically admit the self-induced nature of their disorders, so that the need for informed consent would provide one obstacle to successful studies.

Areas Still Open to Research The boundaries of this disorder need to be better defined. Multiple nosological issues exist. For example, the disorder, as presently defined, requires the conscious production of illness. But the distinction between conscious and non-conscious often remains difficult to establish with confidence, both in theory and clinical practice. Indeed, patients may fluctuate in the volitional component of their illness over time. Similarly, the distinction between

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primary and secondary gain, though clear in semantics, can be clinically elusive. In general, to what extent are these features best viewed as categorical or dimensional? What are reliable and valid methods for making these clinical distinctions? Clarifying these issues will help distinguish this illness from malingering that requires secondary gain, on the one hand, and other somatoform disorders that require unconscious symptom production, on the other hand. Research is also needed to better ascertain the boundary between factitious disorder and personality disorders, obsessive–compulsive disorder (OCD), or eating and other disorders. For example, how do we understand the relationship of OCD to factitious disorder in the patient who has a slow to heal ulcer due to compulsive ‘‘picking’’ that the patient conceals? In factitial behaviour associated with distorted body image, the boundaries with body dysmorphic disorder and eating disorders can become blurred. Factitious disorders offer unusual challenges for physicians. They represent fascinating aspects of human behaviour that must be carefully identified so that specific treatment strategies may be developed. The treatment approaches often must be innovative to be effective with this population. Because these conditions embody marked aberrations from the usual doctor–patient relationship, they call for physicians to be highly aware of their own reactions. Psychiatrists play a central role in helping other physicians understand these conditions and in developing creative treatment plans.

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Commentaries 6.1 Wilful Deception as Illness Behaviour Christopher Bass1 Most discussions on factitious physical disorders begin with a description of Asher’s ‘‘classic’’ paper of 1951, published in the Lancet [1]. In this paper, Asher coined the term ‘‘Munchausen’s syndrome’’ to describe a group of nomadic fabricators of illness, usually men who travelled to different hospitals and persuaded doctors to carry out procedures and investigations. I regard Asher’s article as one of the most misleading papers published in the field of general hospital psychiatry in the last 50 years. Why is this? I have taught medical students for many years, and the term ‘‘Munchausen’s syndrome’’ conjures up an image of a sociopathic male wanderer fabricating illnesses and tricking doctors. This stereotype differs from the clinical reality, which is that two-thirds of patients who fabricate symptoms are nurses or health care workers who, more often than not, reside within a short distance of the hospital where they enact their deceptions. Most psychiatrists in the United Kingdom have welcomed the fact that the term ‘‘Munchausen’s syndrome’’ has recently been replaced by the word ‘‘factitious disorder’’, especially in the related factitious or induced illness in children. In the United Kingdom, the term Munchausen’s syndrome by proxy has been dropped, possibly as a result of recent publicity attracted by the acquittal of three women convicted of smothering their children. My main argument with the DSM-IV and the ICD-10 is that they assume that their users have the capacity to determine whether (a) symptoms are produced consciously or unconsciously and (b) the motivation to produce the symptoms is primarily internal (psychological benefit) or external (e.g., financial gain). These arguments about the reliability of a diagnosis of factitious disorder have been rehearsed elsewhere, often by psychologists who are not constrained by the medicalization of behaviour forced on psychiatrists by diagnostic glossaries. For example, Cunnien [2] asserted that questions of intentionality and motivation are likely to evade any objective assessment, and he called 1

John Radcliffe Hospital, Oxford OX3 9DU, UK

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into question the validity and reliability of the diagnostic criteria used in psychiatric glossaries. He also pointed out that much of the clinical information about these patients was based on single case reports from deceptive patients, and was therefore likely to be unreliable. He argued that the pitfall of diagnosing factitious disorder by DSM-IV was as follows: the clinician must determine conscious symptoms, based on unconscious motives, in an uncooperative patient. Other psychologists [3] have also highlighted the seemingly intractable difficulties in unravelling the motivational drive of deceptive individuals on the basis of the artificial dichotomization ‘‘to be or not to be a patient’’. Most individuals are unlikely to know their motivations, as in the patient with factitious disorder who, following a recent interview with myself, asked: ‘‘Is it possible that I could have been doing this [fabricating blood sugar levels] and not be aware of why I did it’’? Thus, the specific motivations for ‘‘factitious presentation’’ may never be knowable. If this is the case, then to differentiate between factitious disorder and malingering is futile. Furthermore, the theory that intrapsychic phenomena alone would account for a complex set of interpersonal behaviours is not a sufficient explanation. In DSM-IV, there is a requirement for ‘‘evidence of an intrapsychic need to maintain the sick role’’ in factitious disorder, whereas malingering is assumed to be motivated by external incentives, many of which have clear biological benefit, for example, avoiding prison. As a consequence, clinicians tend to lean towards signing a label of malingering as opposed to factitious disorder or hysteria if obvious gains or incentives are apparent to them. But this latter criterion is dependent, to a large extent, on the judgement, training, and reaction of the clinicians. For example, if a patient with fabricated skin lesions carries out this behaviour to remain an invalid, so that her husband will not leave her, is this an external incentive? If so, then this woman is malingering and should not be characterized as having a factitious skin disorder [4]. We have proposed elsewhere that there is a need for a paradigm shift away from the implicit determinism of the biomedical model and towards the proposition that human beings, in most everyday situations (including many aspects of their illness), possess a sense of control and influence over their actions (as opposed to behaviour); that is, they can choose between different courses of action [5]. This capacity is the necessary basis for morality, personal responsibility, democracy, and justice. Considered as a volitional act, rather than a psychiatric disorder, illness deception (ranging from mild symptom magnification to frank and protracted feigning or malingering) is meaningfully conceptualized within a socio-legal or human model that recognizes the capacity of free will and the potential for pursuing benefits associated with the sick role.

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Western medicine has become increasingly dominated (and preoccupied) with symptom-based illnesses and a more tolerant attitude towards illness deception. By blurring this distinction between wilful deception and medical disorder, illness behaviours could be explained in terms of an ever-expanding list of psychopathologies and a growing recognition of psychosocial disorders. However, a medical account alone has difficulty in explaining the threefold increase in claims to incapacity benefits since 1970 in the United Kingdom and other countries despite improvements in most other indices of health. This threefold increase mirrors a similar increase in the number of psychiatric ‘‘syndromes’’ listed in DSM since 1968. Aside from the question of reliable base rates and problems with assessment, the major problem of non-medical accounts of illness deception has been the belief by many in medicine (and in society) that (a) illness behaviours have a medical cause; (b) all patients in describing their impairments and disabilities do so accurately; and (c) illness deception is not common. This ‘‘medical bias’’ has effectively ensured that today most discussions and explanatory models are couched in psychiatric or psychological terms, with little or no reference to the normal moral capacity of many of these persons to exercise choice and determine (at least to some extent) their actions.

REFERENCES 1. 2.

Asher R. (1951) Munchausen’s syndrome. Lancet i: 339–341. Cunnien A.J. (1997) Psychiatric and medical syndromes associated with deception. In: Clinical Assessment of Malingering and Deception, R. Rogers (Ed). Guilford: New York, pp. 23–46. Rogers R., Bagby R., Rector N. (1989) Diagnostic legitimacy of factitious disorder with psychological symptoms. Am. J. Psychiatry 146: 1312–1314. Kalivar J. (1996) Malingering versus factitious disorder. Am. J. Psychiatry 153: 1108. Halligan P., Bass C., Oakley D. (2003) Wilful deception as illness behaviour. In: Contemporary Approaches to the Study of Hysteria, P. Halligan, C. Bass, D. Oakley (Eds). Oxford University Press: Oxford, pp. 3–28.

3. 4. 5.

6.2 Factitious Disorders: Diagnosis or Misbehaviour? Charles V. Ford1 Eisendrath and Young provide a comprehensive and well-balanced summary of contemporary views of factitious disorders. They note that these 1

University of Alabama at Birmingham, 1700 7th Avenue South, Birmingham, AL 35294, USA

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‘‘patients’’ are remarkably resourceful in their simulation of a wide variety of diseases, that factitious disease behaviour is essentially always associated with personality disorder, and that success in treating these persons is extremely limited. This commentary will, to the contrary, be provocative and possibly politically incorrect. I propose that it is a mistake to view factitious symptoms as a ‘‘diagnosis’’ (either a disease or disorder). Instead, it should be regarded as one of a number of syndromes that reflect misbehaviour by personality disordered individuals. There is even a question as to whether these perpetrators of surreptitiously self-induced disease should be regarded as ‘‘patients’’ [1]. The support for this contention is presented below. The key issue with factitious disease behaviour is deceit. All of these patients surreptitiously manufacture their signs/symptoms and tell lies in a variety of ways to mislead physicians, friends, and relatives as to the true nature of their illnesses. In the extreme form of factitious disease behaviour, Munchausen’s syndrome, surreptitious disease simulation is accompanied by the use of aliases, travel from hospital to hospital, and pseudologia fantastica. Through the process of pseudologia fantastica, these persons create an entire identity for themselves by falsely reporting grandiose accomplishments. Examples include the report of having played in the National Football League, or being the fianc´e of an ambassador. At times, the stories dramatically report victimization. Irrespective of the extremes of deceit employed by perpetrators of factitious illness behaviour, they all live a lie. A minority of these persons may have some underlying cerebral dysfunction, but the majority do not and therefore they must be considered responsible for their perfidy. I have previously detailed that lying is a symptomatic feature commonly found in all the DSM-IV-TR cluster B personality disorders [2]. Most factitious disease perpetrators have been described as having either antisocial or borderline personality disorders. Narcissistic features have also been described as characteristic of many of these persons [3]. All factitious disorder perpetrators demonstrate sentinel features of cluster B personality disorders in that they lack empathy for others, use and exploit others for their personal needs, and appear to experience little or no remorse for their behaviour. Their behaviours appear to be egosyntonic, and the distress they create is to others rather than themselves. Relatives and friends who discover that they have been tricked, and their emotions manipulated and abused, are often severely damaged [4], yet factitious disorder patients rarely, if ever, express any remorse. They typically refuse to acknowledge their disease simulation and usually refuse any type of psychologic treatment. Instead, when exposed, they perpetrate their behaviours by changing physicians and/or location where they seek medical care. Attention-seeking behaviour, one of the criteria for histrionic personality disorder, is characteristic of the factitious disorder patient. These patients

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are rarely quiet unnoticed patients at the back of the ward; rather, they become the health care team’s focus of attention. Symptomatic presentation is usually dramatic, and personal styles, including the patient’s false stories, are engaging. These patients also frequently display splitting behaviours (playing health care providers off against each other), which demands that ward personnel remain involved with them. One means by which factitious disorder patients can remain the focus of dramatic attention, and potentially reap secondary awards, is by pursuing malpractice litigation against one or more of their physicians. This serves to change their dramatic venue from that of being a star patient in a medical setting to that of being the star (the injured victim) on the equally dramatic stage of the courtroom [5, 6]. Unfortunately, this transformation from hospital to courtroom is not rare. I have personally seen a number of such cases and they have also been reported by other authors [7–10]. When one has been deceived, exploited, and possibly the object of a lawsuit, the response of anger is not counter-transference; it is an appropriate emotion. I would therefore disagree with the statement made by Eisendrath and Young that the physician should not become angry with the patient but instead with the disease. Factitious disease is misbehaviour by a personality disorder and therefore the person is the ‘‘disease’’. It is important, however, to keep in mind that, irrespective of the justification of anger, one must not, inappropriately, act out on that anger. Ethical and legal principles must continue to be exercised by the physician even when the patient does not play by the rules [8, 11]. The question must be posed as to how reconceptualization of factitious disorder as misbehaviour of a personality disordered person might change the way that we respond to these patients. The answers to this question in my opinion are that: (a) if the factitious behaviour is construed as misbehaviour (it may be fraud when third-party payers are involved) with subsequent penalties (e.g., financial and legal), then the behaviour may become more egodystonic and the perpetrator might be more motivated to change, and (b) improved treatment modalities for more severe personality disorders are currently being developed. For example, dialectic behavioural therapy is proving to be a useful intervention for medical patients with borderline personality disorder [12]. Through this treatment, patients are confronted with their behaviour, its effects upon others, and the counterproductive results of their behaviour. A number of psychodynamic formulations have been proposed as the underlying motivation for factitious disease behaviour. Viewing this behaviour as symptomatic of a personality disorder does not invalidate these theories nor does the presence of psychodynamic factors mitigate individual responsibility for behaviour. I have proposed that exacerbations of factitious disease behaviour are frequently precipitated by loss or separation and

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represent efforts by the patient to defend against anxiety by obtaining a sense of power and superiority by fooling others and simultaneously having dependency needs met [13]. This formulation is consistent with the phenomenology of many personality disorders. In summary, there may be legal, ethical, financial, and therapeutic advantages to reconceptualize factitious disorder as the (mis)behaviour of an undifferentiated cluster B personality disorder. The personality disorder should be considered the primary diagnosis, not the secondary diagnosis, and the focus for interventions.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Ford C.V., Zaner R.M. (1987) Response to the article ‘‘Ethical and management considerations in factitious illness: one and the same’’, by John Z. Sadler. Gen. Hosp. Psychiatry 9: 37–39. Ford C.V. (1996) Lies! Lies!! Lies!!! The Psychology of Deceit. American Psychiatric Publishing: Washington. Ehlers W., Plassmann R. (1994) Diagnosis of narcissistic self-esteem regulation in patients with factitious illness (Munchausen syndrome). Psychother. Psychosom. 62: 69–77. Feldman M.D., Ford C.V. (1994) Patient or Pretender: Inside the Strange World of Factitious Disorders. Wiley: New York. Ford C.V. (1996) The spectrum of simulated disease. Presented at the Baltic Sea Conference on Treatment in Psychosomatics, Riga, September 20. Ford C.V. (2005) Deception syndromes: factitious disorders and malingering. In: Textbook of Psychosomatic Medicine, J.L. Levenson (Ed). American Psychiatric Publishing: Washington, pp. 297–309. Eisendrath S.J. (1996) When Munchausen becomes malingering: factitious disorders that penetrate the legal system. Bull. Am. Acad. Psychiatry Law 24: 471–481. Ford C.V. (1996) Ethical and legal issues in factitious disorders: an overview. In: The Spectrum of Factitious Disorders, M.D. Feldman, S.J. Eisendrath (Eds). American Psychiatric Press: Washington, pp. 51–66. Ford C.V. (1986) The somatizing disorders. Psychosomatics 27: 327–337. Janofsky J.S. (1994) The Munchausen syndrome in civil forensic psychiatry. Bull. Am. Acad. Psychiatry Law 22: 489–497. Lipsitt D.R. (1986) The factitious patient who sues. Am. J. Psychiatry 143: 1482. Ford C.V., Abernethy V. (1981) Factitious illness: a multidisciplinary consideration of ethical issues. Gen. Hosp. Psychiatry 3: 329–336. Huffman J.C., Stern T.A., Harley A., Lundy M., Nancy A. (2003) The use of DBT skills in the treatment of difficult patients in the general hospital. Psychosomatics 44: 421–429.

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6.3 Factitious Disorder and Malingering: The Doctor’s Dilemma Stephen M. Lawrie1 and Michael C. Sharpe1 Where did the idea of factitious disorder come from? Eisendrath and Young trace the origins of the concept to some early work in Edinburgh and to the development of the national health system in the United Kingdom. Has this British contribution been a useful one? The key feature of factitious disorders is the wilful production of the signs and symptoms of disease with the aim of obtaining medical care. The critical judgements required by the clinician are: (a) to determine that the symptoms do not reflect disease; (b) to distinguish between conscious and unconscious willing, and thereby to distinguish factitious from somatoform disorders; and (c) to discern that the motivation for the behaviour is to assume the ‘‘sick role’’ and be cared for, rather than money or release from responsibility, which would be malingering. Whilst the first judgement can arguably be made reliably, the second cannot. Teasing apart unconscious ‘‘hysterical’’ behaviour from deliberate deception is notoriously difficult, if not impossible in practice. How then can divining the motivation for such behaviour be any easier? Many more or less equally potent factors may be operating. Factition (or malingering) can therefore arguably only be convincingly diagnosed when the perpetrator openly admits it and provides an explanation, or when careful surveillance yields evidence that he was deliberately creating symptoms and signs and then seeking care. But even these are imperfect guides to the diagnosis. One might ask: how reliable or insightful is a witness who ‘‘confesses’’ in this way? And even when apparent lying about symptoms, signs, and disability is observed, the variability of somatoform complaints and unconscious motivation remain alternative explanations that cannot be readily discounted. To make matters worse, as Eisendrath and Young point out, patients can shift from one category to another as the years go by. And worse still, seeking help from health care professionals in a bizarre or unusual fashion can itself reflect, or at least be associated with, brain disease [1]. So the dilemma is that, whilst all doctors have seen cases of patients who have clearly lied about their symptoms or manufactured signs and disability, we have great difficulty in constructing a workable operational definition of factitious disorder. Perhaps the task is hopeless and diagnostic criteria requiring that a clinician discerns a patient’s true motivation are irretrievably flawed and inherently subjective. Maybe we do better to restrict our diagnosis to a description of what we 1 Division of Psychiatry, School of Molecular and Clinical Medicine, University of Edinburgh, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF, UK

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can reliable see—signs or disability that is disproportionate to identifiable biological abnormalities. Rather than offer a firm diagnosis, perhaps the clinician should restrict himself to describing the patient’s behaviour and making it clear that his judgement on the multiple inner psychological benefits and external material incentives is merely an opinion. Eisendrath and Young helpfully describe such behaviour, and usefully suggest that the patients’ willingness to accept painful or high-risk procedures may be another form of evidence for informing this opinion and for distinguishing the malingerer from the ‘‘hysteric’’. They arguably go too far when they suggest that feigned or fabricated illness can be reliably inferred after a long process of diagnostic and therapeutic interventions have failed to find any physiologic explanation for the symptoms. And we are even more sceptical that being ‘‘female, 20–40s’’ should raise the index of suspicion; many wives would argue that their husbands take to bed when ill with almost no provocation! The fact of clinical life is that doctors expect patients to be honest with them and just cannot function if they do not trust their patients. In consequence, the doctor’s judgement that the patient is not giving him a true account is difficult, often delayed, and heavily weighted with moral judgement. The lengths that some patients go to in a bid to convince their doctors that they have disease when they do not are startling, even to time-served physicians. Eisendrath and Young’s account of the factors influencing the reluctance or difficulty in making the diagnosis of factitious disorder is therefore useful. And intriguingly, it is possible that we doctors share unmet dependency needs with such patients, indicating that our diagnoses should be tempered by the self-awareness that such a realization demands. The rarity and sheer variety of these disorders makes it difficult for any physician to acquire much clinical expertise, let alone the opportunity to enrol such patients in clinical studies and treatment trials. Together with the diagnostic difficulties, it is not surprising that cognitive perspectives have been much less well developed for factitious disorders than for somatoform disorders. Skilled psychiatric management should include educating and helping medical staff to support the patients, rather than merely judging and blaming them. Regardless of whether or not ‘‘non-punitive confrontation’’ is the best way of describing this approach, reframing the patients’ behaviour as a cry for some sort of help does seem to be a useful way to proceed. The therapeutic ‘‘double-bind’’, hypnosis and biofeedback are well-described procedures that allow everyone to save face. In one of the very few treatment trials we are aware of, Shapiro and Teasell [2] found that suggesting a full recovery constituted proof of an organic aetiology was very effective in acute cases but much less so in longer lasting problems. As can be seen, however, from the title of their paper, they got round the differential diagnostic issue by ignoring it.

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In summary, this is an aspect of medical practice that forces doctors to reflect on their social role: are they the patients’ advocates or their judges [3]? We conclude that effective medical practice in this area depends as much, if not more, on the doctors’ insight into their own motivation than it does on their ability to discern the motivation of their patients.

REFERENCES 1.

Lawrie S.M., Goodwin G., Masterton G. (1993) Munchausen’s syndrome and organic brain disorder. Br. J. Psychiatry 162: 545–549. Shapiro A.P., Teasell R.W. (2004) Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders. Br. J. Psychiatry 185: 140–146. Sharpe M. (2003) Distinguishing malingering from psychiatric disorders. In: Malingering and Illness Deception, P.W. Halligan, C. Bass, D.A. Oakley (Eds). Oxford University Press: Oxford, pp. 156–170.

2. 3.

6.4 Factitious Physical Disorders: The Challenges of Efficient Recognition and Effective Intervention Lois E. Krahn1 Most psychiatrists can vividly recall the details concerning the stories, behaviours, and consequences of the few patients with factitious physical disorder that they have encountered. Because of their limited experience, physicians feel ill-prepared to work with these patients. Having a comprehensive discussion of the origins, approach, and management options in the medical literature becomes essential. Eisendrath and Young’s paper provides an enormously interesting and valuable review. From my perspective, despite efforts to collect data, the prevalence of factitious physical disorders will remain unknown. Indeed, the prevalence in a community-dwelling population is expected to be so low as to be impossible to determine without a prohibitively expensive research project. Furthermore, because patients actively strive to be recognized as medically ill while routinely denying that they are consciously portraying themselves sick, epidemiological tools like surveys are unlikely to be useful. The prevalence of this disorder will be highest in renowned medical centres that specialize in evaluations of medically refractory conditions. 1

Mayo Clinic College of Medicine, 13400 E. Shea Blvd., Scottsdale, AZ 85259, USA

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Over the years, these institutions have provided a beacon for the patients with factitious physical complaints as well as for their local physicians. However, conducting an epidemiological study is challenging even in these settings. Findings are also difficult to generalize to other institutions. The patients currently diagnosed with factitious physical disorder are typically those with the more severe form of the disorder. The cardinal criterion of factitious physical disorder, the patient’s efforts to appear ill in order to be cared for as a patient, is reached after extensive diagnostic testing on the part of the treatment team. The likelihood of recognizing more severely ill patients has contributed to the ongoing fascination with the more rare Munchausen’s variant of this disease spectrum. This preoccupation with a subtype of factitious physical disorder, while probably unavoidable, is unfortunate. The patients with more subtle symptomatology, for example, exaggerating their medical history, are eclipsed. Nonetheless, a patient, for example, portraying herself as suffering from cancer can consume precious health care resources and eventually be at risk because of invasive tests. The prevalence of patients who seek to receive medical attention by misrepresenting or exaggerating their medical history is really unknown. These patients are less likely to have antisocial personality disorder than their Munchausen counterparts. While largely unstudied, they are suspected to have high rates of borderline, histrionic, or narcissistic character structure. These patients are also at risk for coexisting Axis I psychiatric disorders such as prescription drug abuse, complex chronic pain syndromes, and bulimia. The process of identifying factitious physical disorder as a primary diagnosis in the midst of these overlapping conditions is truly daunting. Moreover, patients who depict themselves as ill without causing themselves physical harm can mimic malingering. The task of confirming the patient’s conscious efforts to appear ill is getting more intricate in the United States. Federal legislation has led to a medical environment where the patient determines whether a new physician can talk to family members, contact previous health care providers, or review medical records. Patients have access to their personal medical records, meaning that they can review all documented speculation concerning psychological factors at play in their illness. They can request that ‘‘errors’’ in these clinical notes be corrected, although after review these requests do not need to be accommodated. An addendum can be added to the record recording the patient’s disagreement without revising the medical documents in question. Mindful of these developments, physicians need to carefully reflect on how to approach the patients suspected of factitious disorder. Data indicate that patients with factitious physical disorder, even when presented with convincing evidence of their conscious role in remaining ill, will seldom

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confess [1]. In more uncertain situations, confronting the patient or even communicating one’s suspicions in the medical record is now very difficult. Fortunately, the observant psychiatrist can effectively treat the patient without a definitive diagnosis. With a therapeutic alliance in place, the psychiatrist can explore the aetiology of the patient’s dependency needs or drive to distort his image to simulate that of a person suffering from illness. This probing holds the most promise in assisting the patient in reframing his emotional pain and receiving health care that addresses his deeper yearnings. Years ago, Stuart Eisendrath started to promote ‘‘non-punitive confrontation’’ [2]. He urged physicians to refrain from the temptation to proclaim that they were not being duped. Patients, by definition already conscious of this component of their psychiatric disorder, would feel humiliated and misunderstood. Effort needs to be directed towards gaining an understanding into the patient’s unconscious processes and responding to these needs in other ways. This approach will lead to more knowledge into the aetiology, risk factors, and effective interventions for these distressed patients. Physicians need to generate a broad differential diagnosis for patients with mysterious illnesses. However, as much as possible, even when feeling misled and angry, physicians need to blend both understanding and compassion as they guide patients towards self-understanding that could eventually lead to symptom resolution. Physicians must affirm their responsibility to care for the patients even when they deviate from health-promoting behaviours. Having a team approach provides a setting for discussion and support without leaving the individual physician feeling unduly exposed to tension stemming from the patient’s psychopathology. Ethical conflicts, summarized in Eisendrath and Young’s table, are inherent with these patients, perhaps which is why they prove to be so memorable. Despite the considerable barriers to efficient recognition and effective management of factitious physical disorders, more discussion of the relevant issues is essential. In the absence of first-hand experience, physicians need a medical literature to refer to for assistance for their infrequent and delicate interactions with these patients. Characterizing the underlying psychodynamic, behavioural, and cognitive underpinnings will, over time, add to the menu of effective therapeutic interventions.

REFERENCES 1. 2.

Krahn L.E., Hongzhe L., O’Connor M.K. (2003) Patients who strive to be ill: factitious disorder with physical symptoms. Am. J. Psychiatry 160: 1163–1168. Eisendrath S.J. (1989) Factitious physical disorders: treatment without confrontation. Psychosomatics 30: 383–387.

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6.5 Some Aspects of Factitious Physical Disorders by Proxy Christopher Cordess1 Factitious disorders defy—and, indeed, pervert—the usual assumptions about the doctor–patient relationship, leading, as Eisendrath and Young describe, to feelings of betrayal and often hostility. It is in the proxy version of factitious disorders—in which physical disorders are simulated or created in others, invariably dependent others and usually a child—that the extraordinariness and horror of these behaviours especially impact on health workers. In the comments that follow on, I will refer to the prototypic mother–child relationship for convenience. It is recognized, however, that the perpetrator may be the father in an estimated 10% of cases and that, where nurses are the offenders, male nurses appear to be as represented as female nurses, although detailed epidemiologic data are not available. The behaviour involves a spectrum from mere (understandable) exaggeration of perceived illness in order to gain attention via simulation (as in anxious mothers) to frank and alarming production of illness (e.g., apnoea attacks by smothering, or enforced ingestion of toxic substances, e.g., excessive common salt, or parental medication). We may assume that much of the behaviour at the less dangerous end of the spectrum remains unrecognized, but the more serious behaviours thrust themselves eventually into medical awareness, often involving severe induced illness and permanent morbidity (e.g., renal failure and the need for transplantation after salt poisoning). Of course, it is not uncommon that a child dies, but the motivation is not primarily homicidal. Death, so to say, is incidental, the consequence of high-risk behaviours gone ‘‘wrong’’, with the child as the mere cipher, the dehumanized appendage of the mother’s own overweaning (and seeming ruthless) dependency needs. But what needs? Some writers have emphasized the failure to distinguish the child as a separate individual—and this makes clinical sense in understanding this behaviour in phenomenological terms as an extension of self-directed factitious behaviour that the mother will often have caused prior to having a child. By extension of this, the pregnancies of these mothers are increasingly recognized to be factitiously abnormal. The diagnostic sub-categories of persons exhibiting this behaviour do not help us very much, but fall broadly within those described for factitious disorder—with possibly greater severity of pathology within the sociopathic, borderline, and histrionic dimensions. Affective disorder is less significant and invariably secondary to the Axis II disorder. There are elements of ‘‘perversion’’, but no single diagnostic term, in this author’s view, does this unfathomable, yet frequently stereotypic behaviour (across cases), full justice. 1

University of Sheffield, UK

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Family and personal histories of illness, illness behaviour, and excessive consultation are common, as are health-related occupations. The capacity for expression of emotional life and especially of emotional distress is limited. Significantly, the subject is often lonely, isolated, living in straightened material circumstances, with at least one dependent child if not more. The appeal of the comforts of a comprehensively caring, kindly, and ‘‘mothering’’ (at least in fantasy) health care system must, indeed, seem alluring. Preliminary studies of ‘‘attachment’’ status of perpetrators have shown disorganized and insecure attachment, which is predictable, but possibly helps in adding to the complicated jigsaw of attempted understanding. I shall now allow myself some more personal reactions to my years of assessing many, and treating a few, of these cases. One’s reaction—and that generally of health care workers—may be described as first a tendency towards collusion, with the plight of the mother and child; then of disbelief, when the reality dawns; then of a wish for rejection of the perpetrator. It is at this point that psychiatric or psychotherapeutic intervention can help staff and others concerned into a position of helpfulness and damage limitation—for both parties—rather than the merely punitive. This sequence has been well described more generally as the ‘‘counter-transference’’ aroused by the psychopath. We may wish to invoke the concept of massive projection (or evacuation), by the mother, of feelings, anxieties, indeed a whole confusion of mental events into the health worker. Certainly, one’s feelings in the presence of such mothers can be a bleak confusion like no other in my experience. For sure, she will maintain that she is a mother who loves her child—and there may be evidence that this is credible for much of the time—and that she could not possibly harm her own child. Such is the intensity of the mental pathology that she will often begin to persuade the open-minded clinician that it is he/she who is ‘‘sick’’ or perverse to even entertain the idea of such behaviour—against overwhelming evidence. One can invoke the explanatory concepts of ‘‘splitting’’, or of ‘‘dissociation’’, of knowledge of actions and of feelings—often separately to try to understand the mental set of such perpetrators. However, such ‘‘explanations’’ have the disadvantage of actually adding little, whilst purporting to explain all. In crude experiential terms—after a professional career as a forensic psychiatrist—this is still the ‘‘maddest’’ behaviour that I have ever tried and failed to understand and, of course, it masquerades as precisely its opposite—as cool, calm, caring rationality personified. ‘‘What does she think she’s doing’’? is the naive, unanswered question that ricochets around one’s head—as she breaks, perhaps, the fundamental taboo in the animal kingdom by systematically and painfully, over time, harming her offspring. In the light of the disbelief that this behaviour sometimes engenders in clinicians, it is not surprising that it has become a battleground, too, within affected families, and more recently in the media—where polarized positions are taken, even

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to the point of denying the existence of any such behaviour or ‘‘condition’’ at all. Some media coverage has been downright irresponsible—with views formed not from evidence, but from the wild feelings that this behaviour provokes. One of the more thoughtful examples of ‘‘denial’’ is a book with the telling title ‘‘Disordered mother or disordered diagnosis: Munchausen by proxy syndrome’’ [1]. The book is dedicated ‘‘to those who have been wrongly accused of criminal abuse and neglect because they suffered from a non-existent disorder’’. Significantly, the authors are philosophers and cultural critics and not clinicians. I have seen my role in consultation with individuals, families, clinical teams, and in relation to family and criminal court proceedings to try to provide a thinking presence, weighing probabilities and possibilities, and trying, despite the immense pressure from multiple parties to join one ‘‘faction’’ or another, to hang on to one’s usual independent thinking capacities. This seems to be the only way the clinician can help a frequently dire situation. Finally, I should refer to some of the ethical and management issues in the proxy cases, which obviously contrast significantly with those of selfinduced factitious illness. All are agreed that the first consideration must be the paramountcy of the interests and safety of the child. First steps will be emergency protection measures, the calling of a child protection conference, and, if indicated, the finding of a place of safety. This greatly influences our likely answers to ‘‘the common ethical questions’’ posed by Eisendrath and Young for their cases. In brief, I would say: (a) it is justified that investigations invade privacy (e.g., covert video surveillance); (b) the usual rules of sharing information and confidentiality are changed, in so far as the child’s welfare is concerned; (c) the patients cannot expect the doctor–patient relationship to continue to offer the same rights, but they can expect to be treated with respect; (d) of course, voluntary acceptance of the need for treatment is to be aimed at, but in my experience—at least at the initial stages—without some ulterior motive, is very rare. I have only recommended involuntary hospitalization when the subject has been found guilty at criminal trial. Invariably, in such cases, there is a personality disorder that potentially may be treated. But enforced treatment is controversial in these cases. I have taken the view that, in the light of our very poor understanding of this condition, these subjects deserve an attempt at treatment—which invariably means psychological and long-term psychotherapeutic intervention. It has seemed too nihilistic to argue for a penal disposal for an often very young mother, with years of likely, future fecundity (and more damaged babies?) ahead of her. Anecdotally, I know of several such cases who have been able to parent their children later. If there is realistic hope that the perpetrating mother may be able to responsibly care for the child she has damaged in the future, then therapeutic intervention in a mother and baby unit is the treatment of choice.

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One such example is the Cassel Hospital in London, in which prolonged, say more than a year long, admission of mother and child with intensive psychotherapy has allowed mother and baby to return home. The subject should be regarded as an autonomous individual and thus liable to criminal prosecution. There may then be a case for mitigation—for example, diminished responsibility in the case of homicide, in those jurisdictions where it applies. I harbour a belief that there is a more general human and clinical lesson to be learned from our inability to come to grips with an understanding of the ‘‘causes’’ of the proxy versions of factitious disorders: that our conventional psychiatric and psychodynamic modes of thinking are inadequate to the task of unravelling what is, no doubt, a multi-determined state and behaviour. Perhaps we need a Kuhnian ‘‘paradigm shift’’—there is just more going on here than we can presently conceive—and that’s a challenge.

REFERENCE 1.

Eminson M., Postlethwaite R.J. (2002) Munchausen Syndrome by Proxy Abuse; A Practical Approach. Butterworth Heinemann: Oxford.

6.6 Inventing Illness: The Deviant Patient Don R. Lipsitt1 ‘‘The impact of the fantasy life of one person on another is always strong—the creations of the artist, the power of the lover, the deeds of the criminal, and the symptoms of the neurotic hold the imagination through the fantasies thus roused’’ [1]. Thus did John Rickman, a British psychoanalyst, alert the general practitioner to problems likely to be encountered in general office practice. He called attention to the patient who seeks simultaneous satisfaction for incompatible present needs as well as ‘‘unfulfilled and unconscious desires of the remote past’’. In trying to meet the neurotic on the ground of his own unfulfilled passions, his anxieties and guilt, Rickman warned that ‘‘the physician shoulders a heavy task’’. Nowhere is this task better illustrated than in the patient with factitious illness. Unfortunately, the fantasies aroused in the physician confronted with a patient who feigns disease seldom benefit the patient. When informed by the psychiatrist consultant that his factitious patient was ‘‘fascinating’’, a 1

Harvard Medical School, 15 Griggs Road, Brookline, Massachusetts 02446-4701, USA

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surgeon’s response was ‘‘To you maybe, but to me she’s a pain in the ass’’. Colourful accounts of rogues, thieves, impostors, and con artists make for engaging reading, but the same level of curiosity and entertainment is not enjoyed by all physicians encountering the dissembling patient. We are fortunate that psychiatrists like Eisendrath and Young, reflecting the profession’s interest in all aspects of atypical behaviour, remain intrigued by this mysterious and challenging condition. Their comprehensively informative review highlights the eccentricities of patients who deceive, the pitfalls of diagnosis, the uncertainties of treatment, and the dysfunctions of the patient–doctor relationship. Medical deception has been recorded for centuries, but only came to prominence with Asher’s caricature of the Munchausen’s syndrome [2] and Spiro’s [3] more formal classification and its inclusion in psychiatric nomenclature. It is, indeed, difficult to comprehend why one would intentionally wish to be ill. The hundreds of anecdotal reports in the literature seem intent on warning doctors and hospitals of potential victimization more than clarifying aetiology or pathogenesis. Explanations to date are largely conjectural, since few confabulating patients remain in collaborative alliance with health professionals long enough to reveal reliable developmental histories. Because aetiological speculation invokes unconscious and complex motives to explain ‘‘unexplainable’’ behaviour, psychodynamic and psychoanalytic insights may have the most to offer as aids to comprehending this most puzzling broad spectrum of illnesses [4]. Lying is a part of every individual’s behavioural repertoire. Emerging from the child’s capacity for play-acting, fantasy, and story-telling, the adult carries forth the defensive uses of fibbing, ‘‘white lies’’, and integrityprotecting ‘‘stories’’, often elaborated to disguise personal secrets. All pass through phases of belief in Santa Claus, the Tooth Fairy, and other fictitious characters. Of virtually universal interest and experience is the ‘‘doctor game’’ of childhood, in which unconscious conflicts around sexual interest, aggressiveness, sadism and masochism, and victimization are played out in an ‘‘acceptable medical setting’’ [4]. Do these experiences lie dormant, waiting to be resurrected in individuals whose identity and self-esteem are vulnerable to the stresses of adult life? When these vulnerabilities involve children, as in the unique form of child abuse identified by Meadow [5] as Munchausen-by-proxy, the physician carries the special burden of not only recognition and treatment but also the need for protective measures to rescue the child from his parent. As Eisendrath and Young state, treatment approaches have been modified greatly since the days of ‘‘blacklists’’ and ‘‘rogues’ galleries’’. Nonetheless, recommended interventions have been almost as elusive and varied as the

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presentations of factitia. Indeed, physicians, out of frustration and hopelessness, sometimes rally to the temptation to creatively match wits with the fraudulent patient, an exercise that more often than not meets with futile results and may even perpetuate the ‘‘game’’. The ethics of diagnosing and managing patients who deceive invites rampant controversy. Apart from the perennial dictum to ‘‘do no harm’’, questions revolve around how far one might legitimately go in preventing factitious disordered patients from harming themselves. Since these patients often engage in quasi-suicidal behaviour, would it not be appropriate to secure or divulge information even without customary consent? Finally, the ‘‘cost’’ of factitious illness is great and not easily measured, not only in dollars but also in time spent, aggravation roused, attention ‘‘stolen’’ from other patients, materials wasted, and suffering unabated. As noted by Eisendrath and Young, even dollar expenditures are difficult to assess. Nonetheless, assuming one factitious patient per hospital per year devoting energy to ‘‘snookering’’ medical practitioners, at a cost of $1,000 to $10,000 per encounter, the annual expense to health services would be between $4 million and $40 million (in 1983 value) [6]. With the advancement of medical technology and the constantly escalating health care costs, opportunities exist for the innovative fraudulent patient to impose ever greater demands on the entire health care system while repeatedly jeopardizing his or her own well-being. The need for more and better understanding of the deceptive patient’s motives, improved recognition of the varieties of factitious disorder, and more specific and effective treatments is apparent. Until these goals are achieved, it is well to heed Rickman’s advice to general practitioners that ‘‘. . . whatever the patient’s demands may be, he will be helped best if the physician can preserve an attitude of detachment without coldness, and friendliness without prejudice for or against the wayward impulses at work’’ [1]. Psychiatrists will continue to provide essential education, consultation, and therapeutic advice.

REFERENCES 1. 2. 3. 4. 5. 6.

Rickman J. (1939) The general practitioner and psycho-analysis. In: Selected Contributions to Psycho-Analysis by John Rickman, M.D. (1957), W.C.M. Scott (Ed). Basic Books: New York, pp. 61–67. Asher R. (1951) Munchausen’s syndrome. Lancet i: 339–341. Spiro H.R. (1968) Chronic factitious illness. Munchausen’s syndrome. Arch. Gen. Psychiatry 18: 569–574. Nadelson T. (1979) The Munchausen spectrum: borderline character features. Gen. Hosp. Psychiatry 1: 11–17. Meadow R. (1982) Munchausen syndrome by proxy. Arch. Dis. Child 57: 92–98. Lipsitt D.R. (1983) The Munchausen mystery. Psychol. Today 17: 78–79.

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6.7 Characterizing Factitious Physical Symptoms David G. Folks1 Most clinicians will at some point in their career encounter a case of factitious disorder. These somatizing states are essentially characterized by the voluntary production of signs, symptoms, or disease for no apparent goal other than to assume the role of a patient. Munchausen syndrome, the more extreme form of factitious disorder, includes a triad of features involving simulation of disease, pathological lying, and wandering. However, most cases of factitious disorder will involve socially conforming women who are intelligent and well educated, and employed individuals who have a stable home life. Eisendrath [1] has previously outlined the nature of factitious disorder with respect to three levels of enactment: a fictitious history, simulation of disease, and, the most extreme, factitious presentation resulting in the actual creation of a pathophysiological state, for example, the ingestion of a chemotherapeutic agent and the subsequent development of aplastic anaemia. The available literature provides little information about the incidence of factitious disorders. However, these disorders appear to be far more common than generally believed, perhaps because of the progress in medical technology and the popular medical journalism that is readily available to the lay public. The paucity of systematic studies and the disproportionate number of case reports on Munchausen syndrome have resulted in contradictory data on the more typical cases of factitious disorder. Eisendrath and Young correctly emphasize that most cases, perhaps 90%, involve individuals who have ‘‘stable homes, families, and jobs’’. Indeed, the recognition and treatment of less severe cases are critical, as they too may be just as ‘‘pathologic and disabling’’ as is the Munchausen variant. The aetiology of factitious disorders remains a difficult subject of study. Any attempt to understand these disorders requires careful consideration of any development disturbance, personal history, and current life stressors, and an appreciation of psychodynamic mechanisms. These generally revolve around mastery, masochism, and dependency [2]. Commonly involved are the desire to be the centre of attention and interest; a grudge against a health system, somehow satisfied by frustrating and deceiving the staff; a desire for drugs; a desire to escape the police; and a desire to obtain free room and board while tolerating the consequences of various therapeutic investigations, treatments, and procedures. 1 University of Nebraska College of Medicine, Omaha, NB, USA and Maine General Medical Center, Augusta, ME, USA

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Many patients will meet diagnostic criteria for borderline personality disorder and/or have a history of trauma or abuse, particularly as a child. One can often obtain a history of childhood emotional insecurity; excluding or rejecting parents; and broken homes leading to foster home placement or adoption, and subsequent delinquency, antisocial behaviour, or failure in psychosexual development. The possible enactment of past or present developmental disturbances within the medical setting should also be considered. In essence, it seems as if these patients, through their illness, also may primarily seek to compensate for developmental traumas and secondarily escape from stressful life situations. Psychodynamic explanations suggest that the factitiously disordered patients experience satisfaction from manipulating as many aspects of their own medical and surgical care as possible (mastery), receive strong sexual gratification from diagnostic and therapeutic procedures (masochism), and enjoy warm and personal but ambivalent care inherent to the doctor–patient relationship (dependency), culminating in the excitement of the hospital experience. These features are associated with a poor consolidated sense of self and difficulty regarding emotional experiences as real. The diagnostic and differential diagnostic approach to factitious disorder with physical symptoms requires consideration of a multi-axial format, as outlined in DSM-IV. Factitious illness is not real or genuine, or natural. Thus, physical symptoms are under voluntary control and are produced to deceive the clinician, although the manifestation of symptoms may take on a rather compulsive quality. The original presentations reported by Asher included abdominal, haematologic, neurologic, and self-medicating types, especially insulin, thyroid, vitamins, diuretics, and laxatives. As medicine has evolved, the types of presentations have changed, as patients have become better educated on medical syndromes. Clinical presentations may involve physical or psychological symptoms or both. Factitious disorder with physical symptoms is the most common subtype. A dramatic presentation, with a history of multiple hospitalizations and, of course, the primary goal of assuming the patient role are the pertinent diagnostic features. As a diagnosis of inclusion, not exclusion, factitious disorder requires a high index of suspicion and clinical perseverance. As Eisendrath and Young note, collateral information from medical records and family members is crucial to the diagnostic evaluation. In addition, the possibility that a true disease exists and accounts for the presentation, malingering, pseudo-malingering, conversion disorder, and hypochondriasis are the leading differential diagnoses. Personality disorder is often, if not always, diagnosed as a coexisting condition. Borderline personality disorder is the most common type of personality disorder observed. Understanding the relationship between factitious disorder and personality traits is helpful to the treatment planning

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process. Clinicians must appreciate that the need to remain in the sick role is paramount for the patient, and secondary losses are accepted in order to achieve this goal. The clinical management of factitious disorder with physical symptoms requires a consideration of the psychosocial factors, both current and past, a therapeutic alliance with the treating clinicians, the facilitation of any social support, regular appointments, and a patient–clinician dialogue that examines any new symptoms or signs that may emerge over time. As previously noted, the significance of personality features, as well as substance use and self-destructive risk, must be determined and addressed. Psychiatric consultation should be requested for all patients, and, if confrontation is advisable, the primary physician, as opposed to the psychiatric consultant, should confront the patient in a non-punitive manner [3]. Patients are usually less difficult to confront than might be expected, and do not show the intense anger, impulsivity, or instability of interpersonal relationships that is commonly reported with the more extreme cases of Munchausen syndrome [4]. Confrontation is not necessary for all cases, and rapport building and non-invasive approaches with support may suffice. A psychotherapeutic approach that validates the patient’s subjective experience may lead to reduced factitious behaviour. Family members can be especially therapeutic in providing history and assisting the clinician in maintaining acceptable limits on illness behaviour. Treatable psychiatric disturbances, such as depression, anxiety, psychosis, or conversion symptoms, must be evaluated and effectively treated. Ethical and legal issues are best considered on a case-by-case basis. Hospital ethicists and attorneys are quite helpful in this regard. The prognosis for factitious disorder has generally been considered to be poor at best. However, careful exclusion of malingerers, patients with severe borderline features, and wandering patients with Munchausen syndrome, and the chronic medically ill, can result in a group potentially amenable to treatment. The prognosis is better for patients with coexisting psychiatric disturbances than for those merely with a personality disorder. Reich et al. [4] observed that, once the diagnosis is established, even some of the more severe cases can respond favourably to a combined general medical and psychiatric approach. Finally, the possibility of coexisting physical disease or intercurrent illness should be appreciated in all diagnostic or therapeutic endeavours.

REFERENCES 1. 2.

Eisendrath S.J. (1984) Factitious illness: a clarification. Psychosomatics 25: 110–117. Folks D.G., Freeman A.M. (1985) Munchausen syndrome and other factitious illness. Psychiatr. Clin. North Am. 8: 263–278.

372 3. 4.

SOMATOFORM DISORDERS Hollender M.D., Hersh S.R. (1970) Impossible consultation made possible. Arch. Gen. Psychiatry 23: 343–345. Reich J.D., Gottfried L.A. (1997) Factitious disorders in a teaching hospital. Ann. Intern. Med. 99: 240–247.

6.8 Moral Constraints, Regret, and Remorse in Treating Patients with Factitious Disorder Ovidio A. De Leon ´ 1 It is difficult to imagine an illness that challenges the ethical behaviour of physicians more profoundly than the condition we term factitious disorder. It is important to bear in mind that the physician is presented with a case that defies his diagnostic skills. The clinical manifestations lack internal coherence, deductive connexions, causal relations, or discursive regularity. The physician resists the notion that the rational constraints imposed by medical theories make clinical reality more opaque instead of more transparent, when confronted with symptoms, signs, and laboratory findings that are not logically linked to his/her medical discourse. The impetus behind medicine’s obsession for classification and understanding causality undoubtedly derives from therapeutic need. As a consequence, incomplete information, omission of details, forgotten dates may impulse the overzealous physician to look for collateral information and verification, which can result in breach of confidentiality, one of the most important ethical aspects of doctor–patient relationship. Similarly, when suspiciousness arise that illness is self-induced and patient is deceptive, unauthorized room searches, concealed videotaping, and surreptitious diagnostic testing are contemplated. While authors persuaded by the rights-and-duties systems of ethics contend that these interventions are appropriate when there is a high risk of surgical procedures and diagnostic interventions, or even death [1], others coming from the virtue-ethics approach feel that doctors need to establish trustworthiness, and assume a non-judgemental compassionate role even in the face of patient abuse [2]. Also, the factitious patient may appear lucid and rational but, after his deception is discovered, and the imminent risk of serious health consequences or death is evident, mental competence becomes questionable. Many clinicians feel ethically compelled to take the patient to court for involuntary commitment proceedings [3]. Eisendrath and Young provide us with a superb overview of this condition. They appropriately deal first with epidemiological studies. Incidence 1 University of Illinois at Chicago Department of Psychiatry, 912 S. Wood Street, Chicago, IL 60612, USA

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and prevalence studies, due to the methodological problems well synthesized by the authors, fail to reveal any consistent causal association. The most interesting association revealed is that a high percentage of patients presenting the disorder come from health-related jobs. The retrospective chart review methodology weakens this inference, and there is no support for the notion that, by increasing the ‘‘exposure’’ to this purported causal agent, the risk of disease from that agent also rises. This evidence could come from studies demonstrating an increased prevalence of factitious disorder in health-related professions when compared with the general population. The theories of aetiology advanced in the literature are also problematic. The best we can come up with is that case studies seem to indicate that these hypotheses make sense. A higher standard requiring that the mechanism and the role of the supposed causal factor on that mechanism be well documented in the literature dealing with this disorder is not met. Not to mention that heterogeneity stubbornly conspires against a unified understanding of the illness. Factitious disorder confronts physicians with their fallibility, and not infrequently with their clinical errors when unnecessary, and even dangerous procedures are performed. Gorovitz and MacIntyre [4] dealt with the issue of medical fallibility, and in their view an understanding of this problem cannot be reached without acknowledging the role that ‘‘particulars’’ and non-universal forms of generalization play in medicine. These authors propose that unavoidable errors may arise either from scientific ignorance or from incomplete knowledge of the ‘‘particulars’’ due to the ‘‘mysteries of individual diversity’’. These concepts are hardly more applicable to a condition other than factitious disorder by virtue of its heterogeneity. The diagnosis can only be reached when isolated events are looked at as a whole. The impact of the imperfect knowledge of the ‘‘particulars’’, not only in medical practice but also in the community at large, is illustrated by the case of Beverly Allitt [5], a nurse deemed to be suffering from Munchausen’s syndrome and found guilty of the death of four children and the injuries of nine others in a hospital ward in England. She was presenting herself with self-inflicted injuries in the emergency room, and eventually diagnosed as Munchausen, and yet she was in charge of severely sick babies in the same hospital. The evidence concerning her diagnosis would not be allowed because the diagnosis could only be proven in a court of law, if what she said every time she went into the emergency room was found not to be true, not an easy task from the medico-legal point of view. It is precisely the expectation that ‘‘particulars’’ can be fully spelled out and connected with sweeping statements of predictive value what interferes with the best possible judgement that the medical and legal professions alike can exercise. Cases of factitious disorder put radical constraints on the moral agent in terms of choice. We cannot forget that the physician perceives himself as a

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victim as well. Faced with the situation of having subjected the patient to a dangerous and unnecessary procedure, resulting sometimes in iatrogenic injury, the physician may choose to remain emotionally appalled by the serious consequences of his/her act, or to alleviate his/her own suffering, taking consolation in the fact that there were no possibilities of predicting this outcome in advance due to the misleading behaviour of the patient. The choice is between remorse and regret. From the point of view of the patient’s welfare, it matters a lot which emotional option the physician endures and goes through, as it remains within the physician’s moral power to heal the emotional wounds created by these unfortunate situations in his/her own self as well as the patient’s. In the less extreme situations, when the diagnosis of factitious disorder is timely contemplated, the constraints on moral behaviour are no less severe. In these demanding situations, it would be na¨ıve to believe that one of the conflicting ‘‘oughts’’ must and can be totally rejected. As only one can be acted upon, others must certainly be rejected. The agent can act on one in preference to others because a moral reason has been found. But, in factitious disorder, finding a moral reason for preference does not cancel other ‘‘oughts’’, and it is impossible to be convinced that the rejected ‘‘oughts’’ did not actually apply. In other words, the possibility of abstaining from making a choice is non-existent as is the possibility of making a choice not contaminated with regret or remorse. The various therapeutic interventions described by Eisendrath and Young not only attempt to help these patients in a compassionate way but also try to do so in an ethically responsible manner, and they correctly acknowledge that there are no simple answers to these questions. This does not, however, mean that there are no viable solutions to the problem; only that its resolution requires the inclusion of physicians’ emotional responses and our rational capacities as well.

REFERENCES 1. 2. 3. 4. 5.

Wise M.G. (1990) Commentary on ‘‘the ethics of surreptitious diagnostics’’. J. Clin. Ethics 1: 121–122. Braithwaite S.S., Eatherton J.K., Ellos W.J., Emanuele M.A., Morrisey M., Sizemore G.W. (1990) The ethics of surreptitious diagnosis for factitious hypoglycemia. J. Clin. Ethics 1: 116–121. McFarland B.H., Resnick M., Bloom J.D. (1983) Ensuring continuity of care for a Munchausen patient through a public guardian. Hosp. Commun. Psychiatry 34: 65–67. Gorovitz S., MacIntyre A. (1976) Toward a theory of medical fallibility. J. Med. Philos. 1: 51–71. Hunt J., Goldring J. (1997) The case of Beverly Allitt. Med. Sci. Law 37: 189–197.

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6.9 Fact, Fiction, Factitious, or Fractious Disorders Dinesh Bhugra1 Factitious physical disorders, Eisendrath and Young argue, are a wilful presentation by patients with certain signs and symptoms of disease. The fabrication or exaggeration and perceived ‘‘wilful’’ nature of these symptoms indicate a possibility that the patients have brought this upon themselves and maybe deserve it. There is an indication in some circles that the health care professionals feel betrayed (because perhaps the patient is not only misbehaving but also not behaving as a patient should, thereby violating the boundaries of the patient role) and frustrated. Eisendrath and Young, in their paper, raise important nosological concerns. In particular, they raise the point that Munchausen’s syndrome constitutes only a minor part of the overall factitious disorders. In view of the recent debate in the Courts of Law in the United Kingdom about the existence of Munchausen-by-proxy, the clinicians, nosologists and phenomenologists do need to revisit this syndrome. The true prevalence of factitious disorders may never be known in its entirety for several reasons. It is possible that some individuals may have symptoms but never reach the clinicians because they may gain whatever they need to from their family, kinship, and folk sector. The existence of comorbid psychiatric conditions raises the question of which is the primary clinical condition: my contention is that factitious disorder is perhaps a secondary response to an unresolved and untreated psychiatric condition. The distinction between disease and illness initially described by Eisenberg [1] and then by Kleinman [2] is a useful way of looking at factitious disorders. Disease is malfunctioning psychological or physical processes and is what doctors are interested in. Illness is the patient’s perception of disease and is what the patient and his carers are interested in. My contention is that, in sociocentric societies and cultures, the emphasis on illness is likely to be greater. It is also likely that the reason hysteria has virtually disappeared from industrialized societies has to do with economic and social factors. It is conceivable that factitious disorders presenting in Western societies are a variation of hysteria. This needs to be investigated further. As Eisendrath and Youth observe, factitious disorders may be underreported for a number of reasons: under-recognition, ambiguous diagnosis, and insurance problems. They propose that Asher’s diagnosis of factitious disorders was a reflection of socialized medicine in the United Kingdom. Physical and psychological investigations of factitious disorders can be 1

Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK

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cumbersome, multiple, and prolonged. Physical, psychological, and social investigations may all give clues but, in isolation, not necessarily the diagnosis. Biopsychosocial investigations in the context of the culture may enable the clinician to reach accurate diagnosis. Managing factitious disorder must also include biopsychosocial interventions. The health care systems will indicate where the treatment takes place and what kind of treatment is offered. As Eisendrath and Youth indicate, the type of illness behaviour may change in the course of a patient’s life. A prior diagnosis of one type does not preclude another at a later date. Their suggestion that malingering needs to be differentiated from factitious disorders is a useful one. However, the management strategies in the use of pharmacological agents indicates that underlying neurotransmitter abnormalities (indeed if they are as such) may be primary and the presentation of core symptoms may be coloured by social and cultural influences, which are likely to respond to psychological intervention. The secondary nature of factitious disorders, the shifting of symptoms from one variety to another, and the common aetiological and perpetuating factors for a number of conditions indicate that there should be a bringing together of these conditions rather than splitting them into several varieties.

REFERENCES 1.

Eisenberg L. (1977) Disease and illness: distinction between professor and popular ideas of sickness. Cult. Med. Psychiatry 1: 9–23. Kleinman A. (1980) Patients and their Healers in the Context of Culture. University of California Press: Berkeley.

2.

6.10 Factitious Physical Disorders: A Strategy of Survival for Medically Trained Traumatized Borderlines? Ramon Florenzano1 This most thorough review about the characteristics of factitious disorders allows us to reflect about current classificatory systems and their culturally bound characteristics. The authors posit a clear cut, perhaps too neat distinction between several diagnoses: malingering, factitious disorders, and a third array of conditions (conversion, somatization, body dysmorphic, pain disorders, and hypochondriasis), all of them involving the body. The key distinction made by the 1

Universidad del Desarrollo, Avda La Plaza 70, Santiago de Chile, Chile

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authors is based on the production of signs and symptoms, as well as the patient’s motivation. In malingering, both are conscious; in factitious disorder, the production is conscious but the motivation unconscious; in the varied final group, both are unconscious. This distinction we find a little bit too neat: real life is more complex. These patients have very complex and, to us, puzzling intentions, which create the common clinical impression that they behave in an almost psychotic fashion. However, if we take a culture sensitive approach, we can see that there is a method in their madness: they like and want to stay in the medical world as long as possible. Krahn et al. have demonstrated that factitious disorders appear more frequently among health professionals, and especially nurses [1]. Many cases have been described of patients that peregrinate from one hospital to another, concealing the fact that they are creating their condition by sometimes quite sophisticated maneouvers. The authors also emphasize that most cases present severe personality disorders, making again a distinction between Munchausen patients, with borderline or sociopathic tendencies, and non-Munchausen patients, with less severe personality pathology. Many of the cases described in the literature attest to the fact that reflective functioning, or the capacity to auto-evaluate one’s behaviour, is impaired in this condition. The pseudo-cardiological cases (‘‘cardiopathia fantastica’’) [2] or the neurosurgical patients who reopened the complex flaps that closed their cranial defects, all share a need to go back to the hospital [3], and to be taken into consideration by the medical establishment. In many cases, there is no gross attempt to obtain secondary gain through long licenses or invalidity definitions, but a more specific interest in being taken into consideration by the medical system. In Chile, Fasani and Durcudoy [4] described a male patient who returned to the neurology service over and again with memory problems that seemed initially a nominal aphasia: he had difficulties in naming objects, but he demonstrated that he knew their use. After extensive studies, he received the diagnosis of depressive pseudo-dementia, and was referred to the psychiatric service. The fact was clear that he had a most deprived childhood, with a very chaotic family environment. The only way to receive some attention was to become sick, and that he did throughout his disease. Psychological testing revealed a borderline personality structure with severe problems in reality testing. In summary, factitious disorder is a complex condition, that shares with other pictures that seem to be receiving progressive focus in the medical literature the characteristic of presenting traumatic events in childhood or later on. The disorder seems to be more frequent among health professionals and to reflect the need to call the attention of the health system. We agree with

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Scheper-Hughes [5] that it may be ‘‘a weapon of the weak’’, representing a strategy of survival to function within the medico-social realm.

REFERENCES 1.

Krahn L.E., Hongzhe L., O’Connor M.K. (2003) Patients who strive to be ill: factitious disorder with physical symptoms. Am. J. Psychiatry 160: 1163–1168. Chen T.O. (1999) Munchausen syndrome. J. Int. Med. 245: 555–556. Lad S.P., Jobe K.W., Polley J., Byme R.W. (2004) Munchausen’s syndrome in neurosurgery: report of two cases and review of the literature. Neurosurgery 55: 1436. Fasani R., Durcudoy M.P. (2004) Two Case Reports of Factitious Disorder. Grand Rounds, Hospital del Salvador. Scheper-Hughes N. (2002) Disease or deception: Munchausen by proxy as a weapon of the weak. Anthropol. Med. 9: 153.

2. 3. 4. 5.

6.11 Factitious Physical Disorders and Malingering: The Hazardous Link Sa¨ıda Douki1 , Sara Benzineb1 and Fathy Nacef1 Factitious physical disorders (FPDs) are among the most challenging and troublesome mental disorders. Despite their apparent rarity (no more than 0.8% in a clinical population), they could be considered a public health concern, given their high potential severity and the substantial costs imposed on society. Indeed, feigning or provoking illness can result in significant morbidity, disability, or even mortality, through the production of actual medical conditions or the implementation of unnecessary tests or treatments. One of our patients suffering from an haemorrhagic subtype of FPD was admitted in an intensive care unit with an haemoglobinemia at 2 grams! This 25-year-old male nurse was used to withdraw daily a high quantity of blood by means of syringes. In Tunisia, FPDs are very uncommon in psychiatric settings. A recent study [1] reported only four cases that were followed up in a mental hospital for many years. All these patients were women. The onset of the disorder was in early adulthood. The diagnosis of Munchausen’s syndrome was established after 5 years on average. The four patients had in common the following risk factors: an early contact with the medical environment through a serious personal or parental disease resulting in extensive medical treatment; an experience of family problems in childhood (deaths, disease, 1

Service de Psychiatrie, Hospital Razi, La Manousa, 2010 Tunisia

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separation) and instable parental relationships; social isolation; and major stressors before the beginning of the disorder (in particular, the death of a close relative). FPDs are also of great interest for the psychiatrist because they raise crucial questions in the clinical, nosological, aetiological, ethical, and therapeutical fields, which are partly related to their postulated link with malingering. Indeed, the landmark publications by Gavin [2] and Asher [3] underlined the similarities between these two illness-affirming behaviours. Among the eight motivations of FPDs listed by Gavin [2], seven would fit the criteria for malingering in the contemporary classifications. Eisendrath and Young acknowledge that the boundaries between malingering and factitious disorder may be permeable. Similarly, according to Elwynn and Ikbal [4], FPDs must be distinguished from the somatoform illnesses and malingering, but may actually fall on a continuum between these conditions. It is of crucial importance to better characterize the various forms of FPD in order to exclude the possible contamination by malingering. This issue has critical ethical and therapeutical implications. Individuals with FPDs are regarded as violating the three ‘‘rules of being a patient’’: to provide a true history, to experience symptoms resulting from accident, injury, or chance, and to hold the desire to recover and cooperate with physicians towards that end. Violation of his role by the patient generates a risk of transgression of his duties by the therapist. Practices like blacklists or inspecting patient’s belongings without permission illustrate the possible drift from the fundamentals of our ethics and should be discouraged. We have to keep in mind that the patient with FPD is entitled to the same rights to privacy and confidentiality of information as any other patient. Moreover, the underlying assumption of a ‘‘medical deception’’ threatens the doctor–patient relationship and the whole management. Accordingly, these patients often generate feelings of anger, frustration, or bewilderment in the physician, whereas they share a desperate need for attention, condolence, and empathy! As noted by Feldman [5], perhaps no phenomenon in medical practice is as daunting to caregivers: ‘‘It seems flatly counterintuitive that anyone would batter, bleed, or even blind himself in the quest for illusory emotional gratification’’. Most of us cannot imagine why a person would wish to become sick. Why would someone be willing to endure pain and multiple hospital stays, remain isolated from family, and risk a permanent disability? For this reason, and also because their behaviour involves the deliberate deceit of others, these patients have had few advocates among members of consumer, family, or professional organizations. Moreover, some authorities feel that therapy should not be attempted with patients who have FPD unless they show a good-faith desire for therapy.

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The voice of a factitious disorder patient reported by Feldman [5] is strongly instructive: ‘‘I want physicians to realize that my goal was not to deceive them but rather to gain hospitalization. Within this context, physicians were, simply put, a conduit. When I finally gained insight, motivation, and a consistent relationship with a single caring doctor, I soon ended my deceptions because my need to be sick lessened dramatically’’. Maybe the right answer to these patients’ lack of enduring and stable relationships is there: a ‘‘single doctor’’? Indeed, most clinicians advocate a non-confrontational strategy reframing the factitious manifestations as a ‘‘cry for help’’. This chapter is of crucial interest to break the silence on FPDs, unveil the masked suspicion, and sensitize all the physicians about the unconscious psychodynamics, the suffering, and the risks threatening the ethics and the therapeutical alliance and relationship.

REFERENCES 1. 2. 3. 4. 5.

Ben Moussa N. (2001) Les pathomimies: approche clinique et th´erapeutique (`a propos de quatre cas). Th`ese, University of Tunis. Gavin H. (1838) On Feigned and Factitious Diseases. University Press: Edinburgh. Asher R. (1951) Munchausen’s syndrome. Lancet i: 339–341. Todd S.E., Ikbal M. (2004) Factitious Disorders. eMedicine.com, Inc. Feldman M.D. (1998) Breaking the silence of factitious disorder. South. Med. J. 91: 1.

Index Notes: page numbers in italics refer to tables; abbreviations used in the index are: BDD = body dysmorphic disorder; CFS = chronic fatigue syndrome; OCD = obsessive-compulsive disorder

acetaminophen 81, 82, 83 acupuncture 85, 86 adolescents BDD 222, 236 CFS 259 somatization disorder 60, 61 advocacy organizations 266, 267, 312 aesthetic self model 238 Africa hypochondriasis 181–2 somatization disorder 2, 59–62 agency-consciousness relation 34–5 see also mind-body dualism aggressive behaviour, BDD 197, 213–4, 250 AIDS see HIV/AIDS alcohol abuse 142, 143 alexithymia 35, 186 alternative medicine 292 amitriptyline 84, 272 amphetamines 272 analgesia, hypnosis 122–3 analgesics 80–5, 108, 111, 272 anticonvulsants hypochondriasis 152 pain management 81, 85, 111, 152 antidepressants BDD 208–10 categorical classification and 245–6 comorbid affective disorders 200 future research 213, 214, 236 long-term use 234 OCD and 201, 225–6 CFS 272, 273, 277, 287

conversion disorder 58 factitious disorders 342 hypochondriasis 151, 152, 182–3, 188 pain management 81, 84, 111 somatization disorder 36, 58 somatoform disorders as distinct category 30–1 antipsychotics BDD 208, 209, 214 factitious disorders 342 antisocial personality disorder 355, 361 anxiety disorders CFS 257, 259, 268–9, 297, 302–5, 308, 309, 314, 315 evolutionary models 227 factitious disorders 335 hypochondriasis clinical features 132 cognitive-behavioural therapy 169 comorbidity 142, 142, 143 diagnostic classification 134, 139, 162, 163, 165, 168–9, 180 differential diagnosis 137, 183–4 future research 153, 162, 163 pharmacotherapy 151 subtypes 132 joint laxity syndrome 124–5 pain disorder 74, 75, 122, 123–5, 128 somatization disorder 10, 27–8, 51, 64 somatoform disorders as distinct category 29–30 translational models 227 see also obsessive-compulsive disorder

Somatoform Disorders. Edited by Mario Maj, Hagop S. Akiskal, Juan E. Mezzich and Ahmed Okasha  2005 John Wiley & Sons, Ltd

382 appearance preoccupation see body dysmorphic disorder, preoccupation with appearance Arab perspective 62–4 Asher R. 326, 352 attachment factitious disorders by proxy 364 hypochondriasis 146, 188 somatization 11–2, 24 attention-seeking behaviour 355–6 attentional control system 45 autonomic nervous system, hyperarousal 1, 27, 34 Bahrain 64 beauty hypochondria 191 see also body dysmorphic disorder Beck Depression Inventory 73 behaviour, illness see illness behaviour behaviour problems, Arab perspective 63 behavioural models factitious disorders 340, 341 hypochondriasis 165, 166–7 somatization/conversion disorders 57–8 behavioural therapy BDD 210, 211 conversion disorder 17 factitious disorders 343 hypochondriasis 150, 151, 173, 176 pain disorder 106 somatization disorder 15–6 somatoform disorders as distinct category 31 belle indiff´erence 5 benzodiazepines 76, 85, 128, 272 biofeedback factitious disorders 344–5, 359 pain management 79, 80 biological correlates BDD 206, 214, 233–4, 238, 240 CFS 268, 292, 321–22 hypochondriasis 154, 171 somatization/conversion disorders 12–4, 35, 46, 53–4 biological model CFS 267, 294, 292 factitious disorders 340 biomedical approach, pain 93, 111 biopsychosocial approach

INDEX CFS 262 262–7, 276, 277, 286, 291, 311–2, 313, 314, 320 hypochondriasis 176 pain 93–5, 102–4, 111, 119–23 bipolar disorder, BDD and 199 blood pressure CFS 264–5, 286, 310 somatization disorder 13 body dysmorphic disorder (BDD) 191–2 adolescents 222, 236 aesthetic self model 238 aetiology 206–7, 213, 223–4, 226, 229–30, 231–2, 238–9, 240–1, 249, 250–1 awareness of 233–4, 235, 237 biological correlates 206, 214, 233–4, 238, 240 as a body image disorder 203–4, 231–2 clinical features 194–8 aggressive behaviour 197, 213–4, 250 compulsive behaviours 195–6, 197, 200–1 health care utilization 196–7 see also preoccupation with appearance below clinical heterogeneity 244 cognitive-behavioural models 206–7 course 193–4 cultural factors 207, 214, 229–30, 231–2 diagnostic classification 192, 212–3, 225, 233–4, 237–8, 242, 245–6, 247–9 epidemiology 192–4, 211–2, 213, 235, 240–1 evolutionary models 226–8 factitious disorders and 348, 376–7 family studies 201, 240–1 future research 213–4, 226, 235–6, 240–1, 246 genetic factors 240–1, 250–1 history 191–2, 235 hypochondriasis and 133, 134, 184, 191–2 immune system dysregulation 223–4 insight 195, 201, 202, 204–5, 251 intervention programmes 236 neuropsychological pattern 205–6, 214, 223, 227–8

INDEX other mental disorders and 198–205, 212, 213 depression 193, 198, 199–200, 223 limitations of understanding 225–6 OCD see obsessive-compulsive disorder social anxiety disorder 198, 199, 202–3, 223, 245 spectrum dimensional model 245–6 weight-related concerns 204, 229, 230 pathogenesis 206–7, 213, 214, 223–4, 226, 240–1, 250–1 personality features 205 preoccupation with appearance 194–5 aesthetic self model 238 aetiology 207, 229–30, 231–2 depression and 199–200 eating disorders and 203–4, 229 evolutionary model 227 limitations of understanding 224–6 neuropsychological pattern 205, 214, 227–8 OCD and 201, 249–50 two-factor theory 238 visual attention bias 205, 214 weight-related concerns 204, 229, 230 serotonin system 206, 214, 223, 238 social costs 198 as a somatoform disorder 199, 213, 225, 242 streptococcal infections 223, 250 subtypes 229 delusional 192, 204, 209, 212, 236, 241–3, 247 muscle dysmorphia 197, 252 treatment effectiveness 236 translational models 226–8 treatment 207–11, 212, 213 aetiological theory implications 238–9 future research 214, 235–6, 246 limitations of understanding 225–6 long-term pharmacotherapy 234 subthreshold psychopathology and 246 two-factor theory 238 body image disorder, BDD as 203–4, 231–2 body, the ambiguity in hypochondriasis 185–6

383 culture of 40–2 see also mind-body dualism borderline personality disorder factitious disorders 355, 361, 370, 377 pain 99 somatization disorder 35, 36 brain function see cerebral function Brief Pain Inventory (BPI) 73 Briquet’s syndrome 3, 13, 28 Brodie B. 3 buspirone 208, 209–10, 214 carbamazepine 85 Cartesian mind-body dualism see mind-body dualism catastrophizing CFS 265, 266 pain and 99, 116 celecoxib 83 c´enesthopathie 185 cerebral function BDD 206, 214, 233–4, 240 CFS 265, 276, 321–2 factitious disorders 340 hypochondriasis 154 pain transmission/perception 113, 120 somatization/conversion disorders 12–3, 35, 45, 46, 54 see also neuropsychological pattern childhood abuse BDD 207 CFS 262 factitious disorders 340–1, 344 hypochondriasis 24, 145 somatization disorder 24, 35, 46, 51 childhood factors BDD 207, 214, 230, 238, 240–1 factitious disorders 335, 338, 340–1, 344, 367, 370, 377 hypochondriasis 145 see also childhood abuse children BDD 222, 236 CFS 259, 260, 306–4 factitious disorders by proxy 363–6 pain assessment 72 somatization disorder 60, 61 China, neurasthenia 261, 291, 300, 302, 317, 319 chronic fatigue and immune deficiency syndrome (CFIDS) 255

384 chronic fatigue syndrome (CFS) 253 advocacy organizations 266, 267, 312 aetiology 262–7, 262, 276 biopsychosocial 262, 262–7, 276, 277, 286, 291, 311–2, 313, 314, 320 definitional problems 306 developing countries 317 directional relationship of findings 286 environmental factors 306 genetic factors 262, 261, 277, 306 neutral stance on 266–7, 294 organic 254, 288, 294, 297, 313 psychogenic 254, 288, 294, 297 as a discrete disorder 253, 294, 299–301 autonomy of patients 312 as a pseudo-diagnosis 300–1 biological model 267, 294 clinical features 255 cognitive-behavioural model 267, 286, 294, 292, 314 cultural factors 260, 277, 295, 310–11, 318, 319–20 definitions 49, 255–6, 285, 305–6, 308, 309, 313–5 developing countries 304, 316–8, 319 diagnosis categorical or dimensional 297, 308 consumer-provider polarization 288, 311–2 cultural factors 307–8 definitional problems 285, 305–6 differential 268–9, 314–5 evaluation for 267–9, 286–7, 292, 321–2 fashionability 300–2 Fukuda et al.’s criteria 255–6, 255, 292 medical 254, 268, 292, 294, 296 mind-body disconnect in DSM schema 303–4 multi-dimensional approach 320 psychiatric 254, 268–9, 294, 296 WHO classification 292 epidemiology 259–61, 288, 293, 305–6, 317–8 functional disability 260, 291 future research 277, 293, 309 generalizability of findings 298

INDEX genetic factors 261, 262, 277, 304 history 254–5 illness assessment 269 immunological factors 263–4, 267, 276, 286, 295, 321–2 ineffability of the concept 299–300 legitimacy 312 management 269–75, 277 accepting the biopsychosocial approach 313 alternative medicine 292 applicability 299 benefits of ready access 307 models of CFS 294 need for positive message 310 nutritional supplements 317, 318 patient collaboration 271, 286 placebo response 292 polysymptomatic somatization syndrome 315 mental disorders and 257–9, 297 differential diagnosis 268–9 discriminating CFS from 315 explanations for association 309 somatic symptoms of CFS 308, 309 vicious cycle model 309 mind-body dualism 286, 303–4 neurasthenia 259, 276, 285–7, 315–3 other functional somatic syndromes 257, 296, 303–4, 314–5 paradigm for psychosomatic medicine 297–8 patient-doctor interactions 269, 311–2 primary 257 prognosis 261, 277, 309 research subject selection 309, 310 secondary 257 social model 267, 294–5 other somatoform disorders and 258, 259, 269 chronic pain syndrome 71, 110 citalopram 208 cladistics 162 clomipramine 208, 209 codeine 81, 82 cognitions CFS 266, 314 pain perception 113, 116, 119 cognitive-behavioural models BDD 206–7 CFS 267, 286, 294, 314

INDEX hypochondriasis 165, 166–7, 171 somatoform disorders 116 cognitive-behavioural therapy BDD 210–1, 212, 213, 214, 225–6, 235–6, 238–9 CFS 49, 274–5 factitious disorders 344–5, 359 hypochondriasis 150, 151, 153, 166–7, 169, 173, 176–7 pain management 79–80, 99–100, 104, 106–7, 109, 118, 122–3 somatization disorder 14, 15–6, 36 somatoform disorders as distinct category 30, 31 cognitive function, CFS 264 cognitive models factitious disorders 340, 341 somatization/conversion disorders 44–6, 54 cognitive perceptual model, hypochondriasis 147 cognitive restructuring, BDD 210, 211 cognitive therapy BDD 210, 211 hypochondriasis 150, 173, 176 communication body as a means of 40–2, 185–6, 319 intra-staff, factitious disorders 346 see also patient-doctor interactions Composite International Diagnostic Interview (CIDI) 135, 136, 141, 153 compulsive behaviours, BDD 195–6, 197, 200–1 see also obsessive-compulsive disorder conditioning, BDD 238 consciousness-agency relation 34–5 see also mind-body dualism consultation-liaison (C-L) psychiatry 117–8 conversion disorder Arab perspective 62–4 biological correlates 12, 13–4, 35, 46, 53–4 childhood abuse 24, 46, 51 cognitive theories 44–6, 54 comorbidity 26–8, 35, 36, 51 diagnostic classification 4–6, 50–1, 57–8, 65–6 dissociation 6, 17, 50–1 epidemiology 7–8, 51, 63, 65–6 factitious disorders 328, 338–9, 376–7

385 genetic factors 13–4, 35 historical background 1–4, 50–1 hypochondriasis 24–5 management 16–7, 36, 58 medication induced 15 mind-body dualism 27, 34–6, 52–4 pain 4–5, 74, 128 Peru 65–6 prognosis 8 pseudo-neurological symptoms 28 psychobiology 34–6 public health aspects 42–4 or somatic presentation of mental disorder 26–8 somatization disorder and 24–5, 50–1, 57 somatoform disorders as distinct category 29–30 coping behaviour, CFS 266 corticosteroids, CFS 272 cortisol CFS 264, 272, 286 somatization disorder 13 cosmetic surgery 196–7 COX inhibitors 83 cultural factors 32–3 BDD 207, 214, 229–30, 231–2 CFS 260, 277, 295, 310, 318, 319–20 factitious disorders 375–7 hypochondriasis 146, 182 pain 122 reading the body 40–2 somatization disorder 9–10, 42, 43–4 see also Africa; Arab perspective culture-bound syndromes 232, 310–1 cyclooxygenase (COX) inhibitors 83 cytokines 171, 263, 321 deconditioning 264, 286, 309 d´elire hypocondriaque 185 delusions BDD 199, 201, 204–5 clinical features 195 delusional disorder, somatic type 204, 241–3 as DSM construct 247, 248 evidence base 212 history 192 treatment 208, 209, 236 factitious disorders 342 hypochondriasis 138, 183, 184

386 depression BDD 193, 198, 199–200, 223 CFS 257–9, 265, 268–9, 286, 297, 303–5, 308–9, 314, 315 Egypt 64 factitious disorders 335, 342 hypochondriasis 132, 138, 142–3, 148, 151, 181–3 illness behaviour 314 major as a pseudo-entity 301 diagnostic cut-offs 308 pain disorder 74, 75, 112, 122, 126, 128 somatization disorder 10, 24, 27–8, 51, 64 somatoform disorders as distinct category 29–30 dermatological hypochondriasis 192 see also body dysmorphic disorder Descriptive Pain Intensity Scale 72–3 desipramine 84, 209 developing countries 60–1 CFS 305, 316–8, 317 conversion disorder 8 see also Africa; China Diagnostic Criteria for Psychosomatic Research (DCPR) 177–8 diathesis-stress model hypochondriasis 162–3 somatization disorder 54 disease-illness distinction 375 disease phobia 177–8 see also illness phobia dissociative disorders 6, 17, 50–1 Egypt 63 Peru 65–6 doctor-patient interactions see patient-doctor interactions doxogenic disorders 6 doxomorphic disorders 6 drug abuse/dependence hypochondriasis 142, 143 opioids 80–1, 82, 128 drug tolerance, opioids 81 drug treatments see pharmacotherapy DSM-II, hypochondriasis 133, 165 DSM-III BDD 192 changing terminology 48 hypochondriasis 133, 165 pain disorder 68, 69, 96, 102

INDEX somatization disorder 6, 35 DSM-III-R BDD 192 hypochondriasis 133 pain disorder 68, 69, 96, 101, 103 DSM-IV BDD 192, 204, 242, 247–9 CFS 254, 303–5 conversion disorder 57 delusional disorder, somatic type 204, 242 factitious disorders 327, 327, 352–3 hypochondriasis 133, 133, 152–3, 178 illness phobia 137, 139 mind-body disconnect 303–5 neurasthenia 323, 324 pain disorder 67, 68–70, 70, 96–9, 101–2, 103–4, 106, 107 phenomenological emphasis 26 somatization disorder 6–7, 10, 35–6, 57 DSM-IV-TR hypochondriasis 161, 162 personality disorders 355 DSM-V, obsessive-compulsive spectrum disorders 242 duloxetine 84, 273 dysmorphophobia see body dysmorphic disorder dysthymic disorder 142, 143 eating disorders 199, 203–4, 229, 232, 348 economic costs factitious disorders 336–7, 368, 378 hypochondriasis 144 somatization disorder 11–2, 60–1 education levels CFS 260, 262 factitious disorders 335 Egypt 2, 62–4 emotions Arab perspective 63 pain perception 113 environmental factors BDD 207, 214, 230, 238 CFS 306 hypochondriasis 145, 162–3, 176 mind-body dualism and 54 somatization disorder 13–4, 35 epidemic hysteria 8 see also mass hysteria

INDEX Epstein-Barr virus infection 263 ethics, factitious disorders 346, 346, 362, 365–6, 368, 372–4, 379 evolution, hypochondriasis and 162 evolutionary models, BDD 226–8 exercise see physical exercise explanatory therapy, hypochondriasis 127, 178 exposure therapy, BDD 210 factitious disorders 325–6 aetiology 340–1, 353–4, 356–7, 367, 369–70, 373 as survival strategy 376–8, 380 behavioural models 340, 341 by proxy 363–6 clinical findings 329–32, 330, 331, 358, 370 cognitive models 340, 341 comorbidity 335, 370–1, 375 cultural factors 375–7 deceitful behaviour knowability of motivations 352–4, 358–60 lying 367 personality disorders 354–7 diagnosis 337–8, 370 cultural factors and 376–7 differential 74, 328, 338–40, 348, 362 knowability of motivations 352–3, 358–60 medical fallibility 373 nosological issues 375 proxy version 363–4 US legislation and 361–2 diagnostic classification 327–9, 347–8, 352–3 disease-illness distinction 375 economic costs 336–7, 368, 378 epidemiology 332–6, 360–1, 369, 372–3, 375, 378–9 future research 347–8 historical background 326–7 illness behaviour 352–4, 376 legal issues 356, 361–2, 373, 375 malingering 328, 338, 339, 348, 353, 358–60, 376–7, 378–80 management 341–6 biofeedback 344–5, 359 biopsychosocial interventions 376 blacklists 341

387 doctors’ motivation and 360 ethics 346, 362, 365–6, 368, 372–4, 379 face-saving techniques 344–5, 359 future research 347 guidelines 346 hypnosis 344–5, 359 non-confrontational strategies 343–5, 359 non-punitive confrontation 342–3, 359, 362, 371 pharmacotherapy 342 physician’s moral agency 373–4 proxy version 365–6 psychiatrist’s role 345–6, 348, 359, 362, 364, 365, 371 psychotherapy 342–3, 365–6, 371 staff education 345–6, 359, 364 systems interventions 345–6 therapeutic alliance 362, 371 therapeutic double bind 344, 359 methods used to cause 329–30, 331, 369 moral agency of physicians 373–4 moral capacity of patients 353–4 neurobiological models 340 other somatoform disorders and 328, 338–9, 348, 376–7 patient-carer relationship 325, 326–7, 337, 345–6, 348, 356, 359, 363, 364–5, 366–7, 371, 373–4, 375, 379–80 personality disorders 335, 354–7, 361, 370–1, 377 prognosis 371 psychodynamic mechanisms 340–1, 356–7, 367, 369, 370 psychological models 340–1, 356–7, 367, 369, 370 rise in incapacity benefit claims 354 secondary nature 375–6 social costs 336–7, 368, 378 under-reporting 336, 375–6 fear avoidance 99, 266 fentanyl 82 fibromyalgia 75, 77, 113, 126 management 272, 274, 287 fluoxetine BDD 209 hypochondriasis 151, 188 somatization disorder 36

388 fluvoxamine BDD 208 hypochondriasis 151 Freud S. 3, 53 functional disability BDD 198, 205, 209 chronic fatigue syndrome 260, 291 functional pain 113 functional somatic syndromes 180, 319–20 relation between CFS and other 257, 295–7, 303–4, 313–5 see also somatoform disorders gabapentin 85 Galen 2, 129 gender-related differences see sex differences general practice and practitioners (GPs) hypochondriasis 140–1, 144, 162, 181–2 medically unexplained symptoms 38–9 pain 127–8 reattribution training 39 generalized anxiety disorder (GAD) CFS 258 hypochondriasis 137, 142, 143, 162 genetic factors BDD 240–1, 250–1 CFS 262, 262, 277, 306 hypochondriasis 144, 153, 162–3 mind-body dualism and 54 somatization disorder 13–4, 35 globalization, culture of the body 40, 41 graded exercise therapy 273–4, 286 Hamilton Rating Scale for Depression 73 harmful dysfunction analysis 26 health anxiety 172–4, 175, 177–8 health anxiety disorder 168–9 Health Anxiety Inventory 135, 136, 153–4 health care utilization BDD 196–7, 212 factitious disorders 326–7, 336–7, 368, 378 hypochondriasis 144 somatization disorder 11–2, 24, 60–1

INDEX somatoform disorders as distinct category 30 health systems, culture of the body 41 Hippocrates 1–2, 129, 181 history-taking, somatization disorder 14–5 histrionic personality disorder 355–6, 361 HIV/AIDS 61 factitious 329, 333 Hoover test 4 hydrocodone 81, 82 hydromorphine 82 hypnosis conversion disorder 15 factitious disorders 344–5, 359 pain management 79–80, 100, 104, 122–3 hypnotic suggestibility 45–6 hypnotics 76, 85, 128 hypochondriasis 129 aetiology 144–7, 153 future research 161–3 treatment implications 166–7 ambiguity of the body 185–6 as a category 161, 170–1, 175, 183–4 as dimensional phenomenon 161–2, 170–1, 175–6, 183–4 assessment 135–6, 153–4 BDD 133, 134, 184, 191–2 behavioural mechanisms 165 biological correlates 154, 171 care-eliciting behaviour 145, 146, 187 CFS 258, 269 childhood abuse 24, 145 childhood environment 145 clinical features 130–2, 131 clinical spectrum of fears/beliefs 177–8, 184 cognitive-behavioural models 165, 166–7, 171 cognitive perceptual model 147 comorbidity 132, 139, 142, 142 complications 148 conceptualizations 130, 164–6, 185–6 conversion disorder 24–5 course 147–8 cultural factors 146, 182 diagnostic classification 133–4, 139, 152–3, 167–9 anxiety disorders 134, 139, 162, 163, 165, 168–9

INDEX as somatoform disorder 134, 163, 165, 168–9, 179–80 boundaries 139, 142, 152–3, 168, 170–1 debates 179–80 future research 161–3, 180 limitations 164–5 taxometrics 170–1 diagnostic validity 134–5, 180 differential diagnosis 136–8, 183–4, 338–9 disease phobia and 177–8 economic costs 144 Egypt 64 epidemiology 64, 138–44, 173–4 family studies 143–4, 143 health anxiety 173–4, 175, 177–8 health care utilization 144 history 129–30, 181, 185–6 importance of terminology 48 insight 184 interpersonal factors 146, 187 management 149–52, 153, 154, 187–9 cognitive-behavioural therapy 150, 151, 153, 166, 169, 173, 176–7, 189 explanatory therapy 127, 178 pharmacotherapy 151–2, 182–3, 189 prototypical patients 169 somatoform disorders as distinct category 30–1 medical education and 181–2 Morocco 181–2 outcomes 148 pathogenesis 144–7 patient-doctor interactions 145, 146, 149, 150, 176, 188 personality factors 144–5, 153, 171–2 phenomenological emphasis 164–5, 178 physiological mechanisms 165–6 precautions against health hazards 178 risk factors 139, 171–2 social costs 144 social factors 146, 176 somatization disorder 7, 12, 24–5, 135, 138, 142, 143, 153 somatoform disorders as distinct category 30–1, 134 stressful life events 146–7, 171 subtypes 132, 153, 168, 170 syndromic variations 177–8

389 thanatophobia 177–8 transdiagnostic processes 175 twin studies 144, 153, 163 hypothalamic-pituitary-adrenal (HPA) axis 46, 54, 277 hysteria 1–4 African context 59–60, 61 biological correlates 12–3 diagnosis 4–6 Egypt 2, 62–3 epidemic 8 epidemiology 7–8 factitious disorders 375 genetic factors 13–4 importance of terminology 48 Janetian perspective 50–1 mind-body dualism 53 or HIV/AIDS 61 pseudo-neurological symptoms 28, 53 somatic presentation of mental disorder 28 ICD-10 BDD 192 CFS 291, 293 conversion disorder 57 factitious disorders 352 hypochondriasis 133, 134, 161 neurasthenia 292, 300 pain disorder 70 somatization disorder 7, 43–4, 57 identity, body as source of 40–1 Illness Attitude Scales 135, 136, 140 illness behaviour chronic fatigue syndrome 314 factitious disorders 352–4, 376 hypochondriasis 129, 133 pain 76, 116, 119, 126 see also sick role illness-disease distinction 375 illness phobia 137, 139 see also disease phobia illness worry 24, 152–3 immunological factors BDD 223–4 CFS 263–4, 267, 276, 286, 295, 321–2 incompletely explained symptoms 48 infections BDD 223, 250 CFS 262–4, 267, 277, 286 factitious 329, 333 inflammatory pain 113

390 insight BDD 195, 201, 202, 204–5, 251 hypochondriasis 184 OCD 183, 202, 251 intentions, embodied 1, 27, 34, 44, 45, 46 International Association for the Study of Pain (IASP) 71, 71, 103 International Classification of Functioning, Disability and Health 291 International Study of Psychological Problems in General Health Care 43, 260 International Study of Somatoform Disorders 43–4 Janet P. 50–1, 191, 200, 233 Japan, culture-bound syndromes 232 joint laxity syndrome 124–5 Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS) 240–1 Kleinman A. 261, 291, 302, 319 legal issues, factitious disorders 356, 361–2, 373, 375 life stress see stressful life events Lipowski Z.J. 4 lithium, BDD 208, 209, 214 Littr´e E. 2 McGill Pain Questionnaire (MPQ) 73 major depression as a pseudo-entity 301 diagnostic cut-offs 306 malingering factitious disorders 328, 338, 339, 348, 353, 358–60, 376–7, 378–80 Morocco 182 pain 74, 76–7 malnutrition, subclinical 60 mass hysteria 61 see also epidemic hysteria massage, conversion disorder 15 media images, body culture 40 medically unexplained symptoms cognitive theories 45–6 diagnosing somatoform disorders 6, 7, 9, 23, 32–3

INDEX GP consultations 38–9 importance of terminology 48 mind-body dualism 55–6 pain as somatoform disorder 115–6 reattribution training 39–40 medication see pharmacotherapy melancholia 129–30, 181 mental representations conversion disorders 45, 46 hypochondriasis 147 meperidine 82–3 methadone 82 methylphenidate 208, 214 mind-body dualism CFS 286 DSM schema 303–4 pain 96, 97, 98–100, 101–2, 126 somatization disorder 27, 32, 34–6, 52–4, 55–6 Minnesota Multiphasic Personality Inventory (MMPI) 73–4 moclobemide 272 monoamine oxidase inhibitors (MAOIs) 208, 272 moral agency of physicians 373–4 moral capacity of patients 353–4 Morocco 181–2 morphine 82 Multiaxial Assessment of Pain 71 Munchausen’s syndrome clinical features 330–2, 369 comorbidity 335 deception as illness behaviour 352 epidemiology 332, 335, 361, 369 historical background 326–7 medical fallibility and 373 nosological issues 375 personality disorder 355, 361, 377 see also factitious disorders, by proxy muscle dysmorphia 197, 214, 236, 252 myalgic encephalomyelitis 255, 270 see also chronic fatigue syndrome narcissism BDD 240 factitious disorders 355, 361 nefazodone 151 nerve blocks 85, 86 neurasthenia 253, 255 aetiology 263, 317 as fashionable diagnosis 299, 301–2 CFS and 259, 276, 285–7, 313–5

INDEX China 261, 291, 300, 302, 317, 319 diagnostic evaluation 267–9, 295 diagnostic validity 323–2 epidemiology 259–61, 288–91, 293 future research 323, 324 ICD-10 diagnostic criteria 258, 292, 300 Neurasthenia Scale 323 neurobiology see cerebral function neuroendocrine stress hormones 13, 264 neuropathic pain 113 neuroplasticity 54 pain 120–1, 124 neuropsychological pattern, BDD 205–6, 214, 223, 227–8 neuroticism, hypochondriasis 144–5, 153, 171 neurotransmitters mind-body dualism 303 pain 113, 120 nociceptive pain 113, 120–1 nomenclature issues see terminology issues non-steroidal anti-inflammatory drugs (NSAIDs) 81, 83 nortriptyline 84 Numeric Pain Intensity Scale 72–3 nutrition 60 nutritional supplements, CFS 317, 318 obsessive-compulsive disorder (OCD) BDD 200–2 awareness of 233–4 clinical features 195 immune system dysregulation 223–4 lifetime rates 199 similarities/differences 212, 238, 240, 242, 245–6, 249–52 differentiating delusions from 183 factitious disorders 348 hypochondriasis clinical features 132 comorbidity 142, 142, 143 diagnostic classification 134, 162, 169 differential diagnosis 137, 183–4 future research 153 obsessive-compulsive spectrum disorders (OCSDs) 200–2, 212, 233–4, 238, 242, 245–6, 249–52 occupational demands, CFS 271

391 operant therapy, pain 79, 80, 99–100, 106 opioids abuse 80–1 CFS 272 for pain management 80–3 sleep disorders, pain and 76, 128 oxidative stress, CFS 321–2 oxycodone 81, 82 pain and pain disorder 67 acute-chronic sub-classification 69–70, 120–1 aetiology 68 Arab perspective 63 as outcome predictor 126 assessment 72–4 biomedical approach 93, 111 biopsychosocial approach 93–5, 111 Crue’s approach 110 developmental history 111 in general practice 128 biopsychosocial approach 93–5, 102–4, 111, 119–23 categories of pain 113 CFS 272 conversion disorder and 4–5, 74 diagnostic classification 67, 68–72, 96–100, 101–4, 105–7, 120, 125–6 differential diagnosis 74–7 Egypt 64 epidemiology 64, 101, 103–4 evidence base gaps 125–7 functional pain 113 in general practice 127–8 illness behaviours 76, 116, 119, 126 inflammatory pain 113 joint laxity syndrome 124–5 management 77–86 biomedical approach 93 biopsychosocial approach 93–5, 104, 121, 122–3 consultation-liaison psychiatry 117–8 diagnostic dualism and 99–100 evidence base gaps 126–7 hypnosis 79–80, 100, 104, 122–3 hypochondriasis and 152 inter-disciplinary programmes 86, 95, 100, 111, 117–8, 126–7 patient-centredness 107–9 step-care framework 94–5

392 pain and pain disorder (continued ) utility of diagnosis 106–7 mind-body dualism 96, 97, 98–100, 101–2, 126 neuropathic pain 113 neuroplasticity 120–1, 124 nociceptive pain 113, 120–1 other mental disorders and 4–5, 74–7, 112–3, 122, 123–5, 126, 128 prevalence 67 psychological factors 76–7 sleep and 75–6, 85, 126, 128 subsumption under somatoform disorders 114–6 suffering and 119–21 validity as clinical entity 126 panic disorder CFS 258, 269, 314, 315 hypochondriasis 137, 139, 142, 143, 153, 162 pain 75, 124 parental care BDD 207 factitious disorders by proxy 363–6 hypochondriasis 145 paroxetine 151 patient advocacy organizations 266, 267, 312 patient-doctor interactions 15, 33, 36 CFS 269, 311–2 consultation-liaison psychiatry 117–8 factitious disorders 325, 337, 346, 348, 356, 359, 362, 366–7, 371, 373–4, 379–80 GP consultations 38–9 hypochondriasis 145, 146, 149, 150, 176, 188 reattribution training 39–40 persistent pain disorder 64 persistent somatoform pain disorder 70 personality disorders 35, 36, 51 BDD 205, 238 factitious disorders 335, 354–7, 361, 370–1 hypochondriasis 130, 145, 168 pain 99 personality traits BDD 205 CFS 262, 262, 276 hypochondriasis 138, 144–5, 153, 171–2

INDEX pain and 99, 116 somatization disorder 45–6, 138 Peru, somatization disorder 65–6 pharmacotherapy BDD 207, 208–10, 212, 213, 214, 225–6, 234, 235–6, 245–6 CFS 272–3, 277, 287 factitious disorders 342 hypochondriasis 151–2, 182–3, 188 pain management 80–5, 108, 111, 118 somatization disorder 14, 15, 36 somatoform disorders as distinct category 30 phenothiazines 342 phenytoin 15 phobic disorders CFS 269 hypochondriasis 137, 139, 142, 143, 151 see also social anxiety disorder/social phobia physical deconditioning, CFS 264, 286, 309 physical exercise CFS 273–4, 287, 309 somatization disorder 15 physician-patient interactions see patient-doctor interactions physiotherapy, conversion disorder 15 pimozide body dysmorphic disorder 209, 214 factitious disorders 342 polysymptomatic somatization syndrome 314–5 post-traumatic stress spectrum disorders 46, 51 CFS and 258 hypochondriasis and 143 pain and 75, 124 post-viral fatigue syndrome see chronic fatigue syndrome postural hypotension 265, 286 pregabalin 85, 273 primary care CFS 268, 309–10, 317 factitious disorders 345–6, 346 hypochondriasis 139–42, 140–1, 144, 151, 181–2 pain 127–8 somatization disorder 23–4, 28, 38–40, 43 pseudo-addiction 81 pseudo-neurological symptoms 28, 53

INDEX pseudologia fantastica 330 psychogenic pain disorder 68, 98, 102, 103 psychotherapy BDD 207, 210–1, 212, 213, 214, 225–6, 235–6, 238–9 CFS 49, 274–5, 287 conversion disorder 58 factitious disorders 342–3, 365–6, 371 hypochondriasis 150–1, 153, 166–7, 169, 174, 176–7, 178, 188 pain management 79–80, 99–100, 104, 106–7, 109, 118, 122–3 somatization disorder 14, 15–6, 30, 36, 58 public health, somatization/conversion disorders 42–4 quality of life, BDD 198, 209 reattribution training 39–40 relaxation training conversion disorder 15 pain management 79, 80 repetitive use syndromes 5 Reynolds J.R. 3 rheumatic fever 250 risperidone 209 rofecoxib 83 Royal College of Paediatrics and Child Health (RCPCH) 306–8 schemata conversion disorders 45, 46 hypochondriasis 147 schizophrenia 205 seizures, non-epileptic 51, 61, 62 selective serotonin reuptake inhibitors (SSRIs) BDD 208–10 categorical classification and 246 comorbid affective disorders 200 future research 213, 214, 236 long-term use 234 OCD and 201, 225–6 CFS 272, 273 hypochondriasis 151–2, 182–3, 188 somatization disorder 36 self-awareness 34–5, 36 self-efficacy, CFS 266 self-focused attention 46

393 self-help groups 266, 267, 312 serotonin and noradrenaline reuptake inhibitors (SNRIs) BDD 209, 214 CFS 272, 273 hypochondriasis 152 pain 84, 152 somatization disorder 36 serotonin system, BDD 206, 214, 223, 238 service utilization see health care utilization sex differences BDD 193, 197 CFS 259, 277, 317–8 conversion disorder 13–4, 65–6 factitious disorders 332, 363 hypochondriasis 138, 139, 143–4 somatization disorder 9–10, 13–4, 24, 42, 63, 65–6 sexual pain disorders 74 Short Form (SF-36) Health Status Survey 73 shubo-kyofu 232 sick role factitious disorders 339–40, 341, 353, 358 hypochondriasis 146 see also illness behaviour skin picking, BDD 197 sleep CFS 264, 267, 268, 272, 273, 277, 286– pain disorder 75–6, 85, 126, 128 social anxiety disorder/social phobia 193 BDD 198, 199, 202–3, 223, 245 social costs BDD 198 factitious disorders 336–7, 368, 378 hypochondriasis 144 somatization disorder 11–2, 60–1 social factors BDD 207, 214, 229–30, 238 conversion disorder 57–8 hypochondriasis 146, 176 somatization disorder 13–4, 35, 57–8 see also biopsychosocial approach; socio-economic status social model, CFS 267, 294–5 social phobia see social anxiety disorder/social phobia

394 sociocentric societies, factitious disorders 375–6 socio-economic status CFS 260, 262, 317, 320 factitious disorders 332, 335 neurasthenia 259–60 somatization CFS 314–5, 319–20 use of term 3–4, 7, 23, 47–9 Somatization Amplification Scale 147 somatization disorder African context 59–62 Arab perspective 62–4 biological correlates 12–4, 35, 42, 46, 53–4 CFS 258, 269 childhood abuse 24, 35, 46, 51 cognitive theories 44–6 comorbid disorders 10, 24, 26–8, 35, 36, 51, 64, 142 conversion disorder and 24–5, 50–1, 57 cultural factors 9–10, 42 diagnostic classification 6–7 behaviour perspective 57–8 cultural factors 43–4 DSM-III criteria 6, 35 DSM-IV criteria 6–7, 10, 35–6, 57 ICD-10 criteria 7, 43–4, 57 Janetian perspective on hysteria 50 medically unexplained symptoms 6, 7, 9, 23, 32–3 overlapping clinical forms 58 Peruvian experience 65–6 phenomenological attributes 26–7 trauma-related conditions and 51 dissociation 6, 50–1 economic costs 11–2, 60–1 epidemiology 8–11, 43, 51, 63–4, 65–6 factitious disorders 338–9 genetic factors 13–4, 35 historical background 1–4, 6, 23, 50–1 hypochondriasis 7, 12, 24–5, 135, 138, 142, 143, 153 management 14–6, 36, 58 mind-body dualism 27, 32, 34–6, 55–6 pain disorder 74 patient-doctor interactions 15, 33, 36 GP consultations 38–9 reattribution training 39–40 Peru 65–6

INDEX population studies to conceptualize 23, 24 primary care studies to conceptualize 23–4 psychobiology 34–6 public health aspects 42–4 sex differences 9–10, 13–4, 24, 42 social costs 11–2, 60–1 or somatic presentation of mental disorder 26–8 symptom dichotomy agency-consciousness relation 34 cognitive theories and 44, 45 involuntary/automatic symptoms 1, 27, 34 somatic presentation of mental disorder 27, 28 thoughts/embodied intentions 1, 27, 34, 44, 45, 46 terminology 7, 23 importance of 27–8, 47–9 pseudo-neurological symptoms and 28 somatoform disorders as distinct category 29–31, 134, 179–80, 311, 319–20 BDD as 199, 213, 225, 242 cognitive-behavioural models 116 deconstruction of diagnosis 31–3 hypochondriasis as 134, 163, 165, 168–9, 179–80 pain complaints in 4–5, 74, 112–3, 128 pain disorder as 114–6 see also body dysmorphic disorder; chronic fatigue syndrome; conversion disorder; factitious disorders; hypochondriasis; pain and pain disorder; somatization disorder somatoform pain disorder 68, 98, 103 somatosensory amplification 116, 147, 177 somatothymia 186 spasmophilia 260 spinal cord, pain transmission 113, 120 Stekel W. 3–4 stimulus-induced neuroplasticity 120–1 streptococcal infections 223, 250 stress biological markers in CFS 264, 321–2 BDD 198

INDEX

395

stress hormones CFS 264 somatization disorder 13 stress management, hypochondriasis 150, 151 stressful life events CFS 263 hypochondriasis 146–7, 171 pain and 76 see also traumatic experiences Structured Clinical Interview for DSM-IV (SCID) 135, 136, 141, 153 substance abuse BDD 198, 199, 226 factitious disorders 335 hypochondriasis 142, 143 opioids 80–1 somatization disorder 51 suicide BDD 198 hypochondriasis 148 supervisory attentional system (SAS) 45 support groups 266, 267, 312 supportive techniques 33 somatization disorder 15, 16 surgery, BDD 196–7 Sydenham T. 2–3 symptom vigilance, CFS 266

therapeutic double bind 344, 359 topiramate 85 traditional healers 61–2 tramadol 83 transcutaneous electrical nerve stimulation (TENS) 85, 86 transdiagnostic processes 176 translational models, BDD 226–8 traumatic experiences BDD 207 CFS 262 factitious disorders 335, 340–1, 344 hypochondriasis 24, 145 somatization disorder 24, 35, 46, 51 see also stressful life events tricyclic antidepressants BDD 208, 209 CFS 272, 273 hypochondriasis 188 pain management 81, 84 tryptophan 13

taijin kyofusho 232 taxometrics 170–1 taxonic data 170 Temperament and Character Inventory (TCI) 34–5 terminology issues CFS 255, 256–7, 270, 305–6 functional somatic syndrome 180, 319–20 hypochondriasis 167–8, 180 pain and pain disorder 98–9, 110 somatization/conversion disorders 6, 7, 23, 47–9 thanatophobia 177–8 therapeutic alliance 33, 36 CFS 269 factitious disorders 362 hypochondriasis 176 see also patient-doctor interactions

valdecoxib 83 venlafaxine BDD 209, 214 CFS 272 hypochondriasis 152 pain 84 somatization disorder 36 viral infections, CFS 263, 277, 286 Visual Analog Scale 72–3

undifferentiated somatization disorder CFS 258, 259 DSM-IV criteria 10 Egypt 64 psychobiology 36

West Haven-Yale Multi-dimensional Pain Inventory 71 Whiteley Index 135–6, 135, 140, 141 womb movement, hysteria 2, 59, 62–3 work demands, CFS 271 World Health Organization (WHO) 43–4

396 World Health Organization (WHO) (continued ) CFS 257–8, 292, 317 International Study of Psychological Problems in General Health Care 43, 260

INDEX International Study of Somatoform Disorders 43–4 pain management 81 zaleplon 85 zolpidem 85 zopiclone 85