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The Analysis of Hysteria Second Edition Understanding Conversion and Dissociation
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HAROLD MERSKEY
The Analysis of Hysteria Second Edition Understanding Conversion and Dissociation
©
The Royal College of Psychiatrists 1995, reprinted with amendements 1999
Gaskell is a registered trade mark of the Royal College of Psychiatrists, 17 Belgrave Square, London SW1X 8PG
All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers.
British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library. ISBN 0-902241-88-5
Distributed in North America by American Psychiatric Press, Inc. ISBN 0-88048-647-3 The views presented in this book do not necessarily reflect those of the Royal College of Psychiatrists, and the publishers are not responsible for any error of omission or fact. The Royal College of Psychiatrists is a registered charity (no. 228636).
Printed by Bell & Bain Ltd., Thornliebank, Glasgow Reprinted by RPM Reprographics, Chichester, West Sussex Cover photograph: Science Photo Library
To the memory of Harry and Sophie Merskey
v
Harold Merskey DM, FRCP, FRCP(C), FRCPsych, FAPA
Professor Emeritus of Psychiatry University of Western Ontario London, Canada London Psychiatric Hospital Ontario, Canada formerly Physician in Psychological Medicine The National Hospitals for Nervous Diseases Queen Square and Maida Vale London, England
Contents
Preface Acknowledgements Introduction
ix xiii xv
Part I. History and concepts 1 2 3 4 5 6 7
Some traditional concepts Early neurological analyses The turn of the century The contribution of Freud Combat hysteria Ernst Kretschmer Post-traumatic stress disorder
3 19 29 36 46 64 76
Part II. Motives and extremes 8 9 10
Malingering, self-damage and anorexia nervosa 91 Amnesia, pseudodementia and the Ganser syndrome: denial of illness 112 Compensation issues 125
Part III. Varied causes and symptoms 11 12 13 14
Organic brain disease Pain Somatisation disorder and somatisation Hypochondriasis vii
141 160 172 185
viii 15 16 17 18 19 20 21
Contents The diversity of hysterical complaints Epidemic or communicable hysteria Chronic fatigue syndromes Children Suggestion and hypnotic phenomena ‘Multiple personality disorder’ Dissociation, repression and false memories
200 231 245 257 263 272 309
Part IV. Individual dynamics and clinical subgroups 22 23 24
Personality traits Psychoses Psychoanalytic concepts
335 356 368
Part V. A perspective 25
The survival of hysteria
379
Appendices Appendix A. E. F. Dubois d’Amiens: Comparative table of the symptoms of hypochondriasis and hysteria Appendix B. Emil Kraepelin: Hysterical insanity Appendix C. Sir Charles Symonds: Hysteria Appendix D. J. F. C. Hecker: Epidemics of the Middle Ages
414
References Index
422 469
397 402 407
Preface
The subject of hysteria covers numerous phenomena and a wide range of ideas. Most of the latter have to do with the relationship between mind and body. Many focus on the way in which human beings adapt to emotional problems. However, it was not always so. For a very long time hysteria was regarded as a bodily disorder which produced physical or psychological changes, or both. Gradually, it was established that the psychological aspects were primary, and that the label (or its numerous synonyms) could best be used to denote a symptom, or symptoms, which corresponded to a patient’s ideas of an illness or a disability, and that the majority of such symptoms were best explained as the result of unresolved emotional conflicts. Even so, these fundamental concepts are far from covering everything that is, or has been, known as hysteria. In addition to the classical implications of a uterine disorder, or at least a female complaint, hysteria has come to mean more recently, a variety of symptoms affecting the body, occurring under stress, and not being related to physiological changes or organic disease. Some loss of the ability to use the muscles or to experience sensory change has been the most common pattern. Some psychoses have even been included under this heading. However, the concept extends much further from individuals to the way in which groups of people will respond to stress in their lives, and the way in which ideas of illness, or alterations in personality or behaviour, can be evoked by inappropriate suggestions. Thus the topic of hysteria ranges from pain and paralysis to alterations of awareness, mass responses and sometimes special beliefs. It should become evident as the discussion proceeds in this book how much the term embraces. It should also become equally clear that the label is often misapplied. ix
x
Preface
The diagnosis of hysteria has been called “A delusion and a snare” (Slater, 1965), concerning which Lewis (1975) observed that hysteria tends to outlive its obituarists. This survival of hysteria is marked nevertheless by frequent changes or adjustments of the label. In 1980 the American Psychiatric Association (APA) formally abandoned the diagnosis of hysterical neurosis which had been used since 1968 in the second edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM–II). A number of other changes have occurred since 1980, in DSM– III–R (APA, 1987), and DSM–IV (APA, 1994). There have also been alterations in the original system of the International Classification of the Diseases (ICD–9, WHO, 1977) and ICD–10 (WHO, 1992). We have seen a litany of diagnostic labels and modifications including hysterical neurosis, conversion symptoms, somatoform disorders, somatisation disorder, psychogenic pain, pain disorder (unqualified), dissociative disorders and dissociative [conversion] disorders. Hysterical personality has become histrionic personality. While the number of terms has grown some forms of hysteria have become remarkably rare in developed societies, except in neurological settings. Few psychiatrists currently see hysterical paralyses or ataxias but many consider that they see dissociative disorders in the form of multiple personality disorder, now defined as dissociative identity disorder in DSM–IV. Linked with this, there is an epidemic of artificially produced false memories. Whatever the diagnostic status of the illness, or the current rarity of forms such as paralyses and ataxias, the themes encompassed by the word ‘hysteria’ are of basic importance both to medicine and to our understanding of human behaviour. With or without the label hysteria, books and papers on the topic continue to appear in growing numbers. Somatoform disorders, hysterical responses to stress, and dissociative disorders are particularly busy fields for growth; and there is also a substantial recent literature on the historiography of hysteria. When the first edition of this book was published in 1979 its main purpose was to review, and, perhaps ambitiously, to illuminate the accumulated information on hysteria which was available from the widely scattered literature. In the course of the review an attempt was made to place hysteria in a perspective based on clinical practice and theoretical understanding. These aims remain the same in this second edition. The consideration of hysteria involves many interrelated topics such as symptoms, motives, personality, suggestion, psychodynamic theories, psychoses, organic
Preface
xi
causes, cultural influences, etc. The symptoms of hysteria, further, are enormously varied. To help cover these varied aspects new material has been added on a number of sub-topics including the history of hysteria and the meaning of the concept at different times, the occurrence of stress disorders and the effects of accidents, problems in the diagnosis of conversion disorder, the reductions in the number of cases where hysteria can legitimately be diagnosed, and current aspects of dissociative disorders. The growth of the latter has been such that it is bringing about a very hard look at the limitations of the concept of repression. To deal with these diverse matters the volume has been organised in the following way. Initially, the history of the concept has been reviewed, with particular reference to the 19th century when the basic ideas were established which we still use. This includes the contribution of Freud and his development of dynamic ideas to explain the origin of hysterical symptoms. The impact of the First World War and of other stresses upon our ideas of hysteria is then presented and discussed, since the overwhelming experiences of the First World War shaped the approach of neurologists and psychiatrists and other psychotherapists to the whole concept. The second and third portions of the book deal with the broad variety of hysterical symptoms and related disorders. These chapters culminate in discussions of a modern artefactual condition, “multiple personality disorder” and make an effort to come to grips with fundamental issues in the notion of dissociation, especially in chapter 21. Part IV then takes up the implications of the other sections with respect to personality traits and psychoses, and the later development of psychoanalytic concepts. The final chapter provides an overall perspective. I hope that this volume will serve several purposes. First, I hope it will provide a more full introduction to the topic than can be found in a long chapter in a textbook. At the same time, it presents revisions and corrections in the historical and traditional notions of hysteria, from the very earliest concepts (the ancient Egyptians) to the notion of dissociation which was most discussed in the first part of this century and the end of the 19th century. Next, I trust that it will provide a coherent and organised account of a large number of modern studies and observations which seem to me to have led to a more refined appraisal of what may be hysteria and what should no longer be considered to be hysteria. In this connection chapters 7 and 10–15 should be particularly relevant. The chapters on multiple personality disorder and dissociation (chapters 20 and 21) deal with some very vigorous current controversies, but ought to have a more fundamental
xii
Preface
impact, both on our understanding of how artificial syndromes can be created, and on the nature of the concept of dissociation. The latter topics have been among the most demanding and instructive to study and have important implications about the relationships between physicians, or other therapists, and patients. The four appendices are included for their interest and for the great skill with which three of them (Kraepelin, Symonds and Hecker) illuminate the topic. Lastly, some do not favour the word hysteria any more while the terms conversion and dissociation are now of questionable accuracy, and the word psychogenic is not acceptable for everyone. For those who seek another term, I suggest in chapter 11 and chapter 20 that the word doxogenic, meaning symptoms produced by thoughts, might serve well to describe the symptoms and problems related to hysterical seizures or “pseudoseizures” and to Multiple Personality Disorder respectively. The term could have a broader use for as much of the panoply of hysterical complaints as we fancy.
Harold Merskey London, Canada July 1995
Acknowledgements
The patients whose illnesses have encouraged me to explore this difficult but fascinating subject are the first objects of my thanks. Next, I wish to express appreciation to the people who successively taught me the management of hysterical patients, particularly, Dr Myre Sim; Dr R. W. Tibbetts; Major-General John M’Ghie, late R.A.M.C.; and the late Erwin Stengel. Professor Stengel especially urged me to work on the problems of pain and its psychological aspects, and this work led to a further developing interest in hysteria. When I came to the Queen Square and Maida Vale Hospitals the sympathetic interest and collaboration of my neurological colleagues gave me a major topic of inquiry in regard to hysteria and in this I was supported and substantially helped by my senior psychiatric colleague there, Dr R. T. C. Pratt, who also read the manuscript of my first draft and made helpful comments. So did Dr J. Aufreiter, Dr Michael Trimble and Dr Allan Walters. I particularly thank Dr Sim and Dr Walters for their detailed observations. Dr N. Geschwind helped me to revise the section dealing with denial of illness. Dr G. Low-Beer and Dr Peter Nathan translated parts of the German references. Dr Philip Evans translated the French of Dubois d’Amiens for Appendix A and Mrs Judith Plaister the Latin. Quotations of tables from Kretschmer (Chapter 6), Hawkings et al (Chapter 8), Sir Aubrey Lewis (Chapter 22) and Dr W. Linford Rees (Chapter 25) are reprinted with thanks to the authors and to the respective publishers, viz. Peter Owen Limited, Oxford University Press, The British Medical Journal and Churchill Livingstone. I am honoured by the permission of the late Sir Charles Symonds to include his address on hysteria as Appendix C. In the second edition I thank Drs G. A. Berrios and Hugh Freeman, together with Gaskell Press, for permission to quote extensively from a chapter on Shell-shock in the book ‘150 Years xiii
xiv
Acknowledgements
of British Psychiatry’. Parts of Chapter 21 have been taken from a manuscript prepared for Drs Berrios and Freeman for a historical volume which will be a sequel to the above work. Portions of Chapter 14 draw upon a chapter on Hysteria, in press in College Seminars on Adult Psychiatry (Gaskell). Thanks are also due to the British Journal of Psychiatry for permission to use the majority of the article on Multiple Personality Disorder (British Journal of Psychiatry, March 1992) in Chapter 20 and the Royal College of Psychiatrists and Alpha Academic and my co-author Christopher Alam, for permission to use substantial quotations and a line diagram from an article on The Development of the Hysterical Personality, in Chapter 22. Fellow members of the Scientific Advisory Board of the False Memory Syndrome Foundation, together with the Executive Director, Dr. Pamela Freyd, as well as several falsely accused parents and former accusers restored to better health, provided me with much information and encouragement for Chapters 20 and 21. Drs Emmanuel Persad and Peter Williamson read the first draft of the second edition and provided helpful comments, as did my wife Susan Merskey. Dr Paul Potter provided unfailing guidance on the classical Greek and Latin authors. Typing the drafts and organising material on a word processor was undertaken by Ms. J. Duncan, Ms. C. Hanas and Ms. G. Hudson who all also provided bibliographical assistance. I am further grateful to Ms. M. Why, MLS, and Ms. E. Spicer, MLS for their considerable help in tracing many references, and to Ralph Footring for the high standard of copy-editing.
Introduction
“The disorders which are the subject of the following Observations have been treated of by authors, under the names of Flatulent, Spasmodic, Hypochondriac, or Hysteric. Of late, they have also got the name of NERVOUS; which appellation having been commonly given to many symptoms seemingly different, and very obscure in their nature, has often made it to be said, that physicians have bestowed the character of nervous, on all those disorders whose nature and causes they were ignorant of. To wipe off this reproach, and, at the same time, to throw some light on nervous, hypochondriac, and hysteric complaints, is the design of the following observations;” (Robert Whytt, 1767, p. iii)
It is customary for books on hysteria to commence with a reference to the fact that the term is derived from the Greek word hysteron, meaning uterus, and that the diagnosis dates back to ancient Greek medicine, according to which a variety of symptoms was attributed to a wandering of the womb through the body. This historical approach is still helpful today because it allows us to see how certain basic ideas about physical symptoms and emotional causes have developed and been formulated according to the scientific language of successive generations. Many of the problems of hysteria which remain are the same, but in different guise, as those which troubled physicians of the past. Among such past items, Soranus of Ephesus (Temkin, 1956, p. 9) and Galen (Siegel, 1976, pp. 187–8), who were both active in the second century denied that the womb could wander. In the 17th century Jorden (1603) argued in a case of alleged witchcraft that the symptoms of the supposed victim were due to the state of the uterus (Hunter & MacAlpine, 1963; MacDonald, 1991). In the nineteenth century Landouzy (1846), according to the most up-to-date criteria of his time, reported on the state of the ovaries and uterus in affected xv
xvi
Introduction
persons and denied Sydenham’s (1697) view that hysteria in women and hypochondria in men were the same condition. Throughout the nineteenth century, others considered that hysteria was a dysfunction of the brain which produced multiple symptoms in various parts of the body e.g. Georget (1821, v. 2, pp. 261–2 & 265–86) and Brachet (1847, p. 204), a point of view shared and advanced by Briquet (Mai & Merskey, 1980). In Josef Breuer’s student days in the second half of the nineteenth century hysteria had become “A so called general neurosis” without definite localization in the nervous system (Hirschmuller, 1989). If psychological complaints also occurred it was called a psychosis – a very different use of the latter word from that of today. Today we can find good papers (e.g. Lerner, 1974) concerned to show that the hysterical personality is not inherently feminine, gently qualified by Chodoff (1982) who agrees that the hysterical personality is a caricature and then goes on to point out that there can be no caricature without an underlying normality. We also have the suggestion (Merskey & Merskey, 1993) that “The suffocation of the Mother” i.e. globus hystericus, reflects the recognition of the ancients that anxiety was more common in women than in men, and gave rise to dyspnoea plus sensations of choking or difficulty in swallowing. Part of the fascination of the subject derives from the manner in which certain somatic symptoms, not only of women, have been attributed through the ages to various emotional and physical causes. This fascination is enhanced both by the way in which the diagnostic skills of the neurologist are often needed to delineate the symptoms, and by the satisfying notion of unconscious conflict which we owe to Freud and which has played such a prominent part in twentieth-century thought. Yet medical and psychiatric problems persist in relation not only to individual cases but also in regard to major aspects of the concept of hysteria. Some (e.g. Slater, 1965) have rejected the diagnosis of hysteria whilst accepting the idea of hysterical symptoms. The hysterical personality which is a common psychiatric diagnosis is by no means regularly associated with hysterical symptoms, and organic disease, especially cerebral disease, appears to be an important contributory cause in a number of patients. Hysteria has also been involved in the problems of pain. Now, most strikingly, the enormous rise in the numbers of reported cases of multiple personality disorder (MPD) has given rise to much scepticism. There is thus good reason still to be interested in the problem of hysteria even though classical conversion symptoms are no longer common in Western society except in certain settings such as neurological departments.
Introduction
xvii
Sydenham (1697) regarded hysteria as the most common of all chronic diseases. With Freud it became the starting point for a revolutionary series of ideas about the mind. The personality characteristics with which it has been linked are a perennial topic of interest, both inside and outside medicine. Efforts continue to describe them and to explain the symptoms and their causes. In actual clinical practice it still presents vexing problems, although one might think that so much has been written about it that its management, at least, should be thoroughly understood. Understanding such a condition would seem to involve not merely matters of technical skill, and theoretical explanation, but also the response of the doctor to the patients. It used to be said of syphilis that he who knew that disease knew the whole of medicine. As Boyd (1947) put it: ‘Of all diseases it is the most subtle. It is a master of disguise. There is no symptom which it cannot cause, no syndrome for which it may not be responsible.’ With the great decline in the incidence of syphilis no other illness has come forward to take the place of such a master of simulation. It would be unpardonable, especially in connection with hysteria, to exaggerate and to suggest that it can fit such a role. Yet hysteria does have some of the characteristics which were attributed to syphilis. It is at least true that it can mimic a large variety of physical symptoms. Any symptom of organic disturbance which the mind can impose on the body may serve an hysterical function. That is to say that any physical symptom which can be produced consciously may also develop as the result of an unconscious mechanism, whether that symptom be a paralysis, a fit, or a loss of sensation. Moreover, any psychological symptom, such as the complaint of depression or anxiety, can be the result of a similar mechanism. For these reasons alone hysterical symptoms are important in the practice of medicine in general, even if some of them like ataxias and paralyses are now rather rare. For these reasons too they are of great interest within the field of psychiatry, whether they occur in the many psychologically ill people who are seen by their general practitioners or whether they come the way of specialists. Yet these considerations indicate only part of the importance of the phenomena of hysteria. The psychodynamic mechanisms of defence which operate in hysteria, the cultural influences which it expresses and even the organic illnesses which may provoke it, provide rich material for the better understanding of man and his emotions. Although often seen by doctors as a nuisance, patients with hysteria contribute a plentiful source for the proper study of mankind, as well as a diagnostic or therapeutic challenge.
xviii
Introduction
Throughout the book, one assumption is made which might be challenged and is not discussed except at this point and in the final chapter; that is the view that physical complaints caused by psychological processes, and not thought to be produced by any physiological or pathological mechanisms, are a proper subject for treatment by doctors. Occasional authors (e.g. Szasz, 1961) hold that, once diagnosed, such symptoms should no longer be treated by doctors as such. Most doctors, however, find themselves unable to take this view, not least because conversion symptoms are often deeply intertwined with problems of physical illness; and even when that is not the case the diagnostic process inevitably leads to a relationship in which the most effective help comes from doctors and their associates. To reject patients to whom this applies on the grounds that either the problems are not ‘medical’ or that they are in some sense deceivers either of themselves or others, is an immature professional response.
1
Part I. History and concepts
2
History and concepts
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3
1
Some traditional concepts
“Plus ça change, plus c’est la même chose.” (Alphonse Karr, Les Guêpes, 1849)
Although it is often said that the symptoms which have been grouped under the term hysteria were recognised by the Greeks and attributed to the wandering womb, there is reason to qualify this notion. Not all the Greek medical writers believed in it and some of the seemingly wild flights of fancy which would have the womb cause choking need qualification. To begin with the earlier discussions, some historians of medicine have suggested that certain ancient Egyptian medical papyri referred to hysteria (Sigerist, 1951; Veith, 1965). The papyri were held to enumerate a series of morbid states attributable to displacement of the uterus. The notion of these events was said to have been handed on through the Greeks and developed into the description of a variety of bodily ailments ascribed under one term or another to emotional disturbance, especially in women, emerging in the late 19th and early 20th centuries as a diagnosis of somatic and other complaints attributable to conflicts in the patient’s unconscious mind. It is the aim of this book to examine the nature of the diagnosis mainly since the 19th century, its evolution and partial dissolution, and its relations among other matters to hypochondriacal complaints, to the hysterical personality, and to organic brain disease. I hope it will be shown, as the quotation opening the chapter suggests, that there is a common unchanging element in the several patterns of behaviour which are regarded as hysterical, even though some of the earlier concepts have been misinterpreted. At the same time it is intended to demonstrate that the concept can usefully be divided into several parts. 3
4
History and concepts
The reliability of some of the earlier suggestions is in serious dispute. To return to the Egyptians, Veith (1965, p. 3) remarks that: “certain behavioural disorders were associated with the generative organs, and specifically with aberrations in the position of the womb. This was so firmly established that no other explanation for the symptoms was so much as suggested.” (Her italics)
An evaluation of the best available translations of the Egyptian sources – the Ebers and Kahun papyri which are approximately 3550 and 3900 years old – casts great doubt on this view. In particular, when these texts blame the uterus for a symptom at a distance, it is never said to be mobile, and when it is said to be out of its place (usually by prolapse) symptoms at a distance are not described. Thus there is no warrant for the fanciful view that the ancient Egyptians believed that a variety of bodily complaints were due to an animate womb (Merskey & Potter, 1989). The Greek sources start, essentially, with the Hippocratic collection, some 68 works gathered under the name of the physician who is believed to have been their principal author and who lived from about 460 to 370 BCE. Among these volumes few sections dealing with hysteria have been translated into English, but the French version (Littré, 1839–61) described several phenomena which could be diagnosed as ‘hysterical’. These include a type of fit in which the patient wakes if the skin of the abdomen is pinched (Potter, 1988, vol. 5, para. 35). Headache is also attributed to the uterus (Littré, 1846, ‘Epidemics’, vol. 5, para. 68). It was also said that ‘hysterical suffocation’ (hysterike pnix) occurred with other symptoms in patients with fever (‘Epidemics’, vol. 5, para. 96) and that spasms without accompanying fever occurred readily in women with hysterical symptoms (‘Coan Prenotions’, vol. 5, para. 343). If the womb caused suffocation, fumigation with evil-smelling substances was recommended (‘Nature of Women’, vol. 7, para. 26); a lamp wick might be lit and extinguished to provide smoke under the nostrils and an aromatic pessary applied (‘Nature of Women’, vol. 7, para. 3). This material seems to be the origin of the idea that the womb could move around the body, block the channels of respiration and cause ‘suffocation’ as well as have some effect on the throat. Unpleasant substances were applied above to drive the womb down, and fragrant ones below to attract the womb into its correct position. It is not apparent, however, that the womb was thought to rise above the diaphragm, but when situated nearer to the
Some traditional concepts
5
hypochondrium and the liver, as in pregnancy, it might have affected respiration. Examination of references to aromatic substances and unpleasant fumigations as treatment does not provide uniform support for the ‘carrot and stick’ theory of uterine therapy (Merskey & Merskey, 1993). Moreover, other theories were put forward, such as the idea that hysteria tended to occur in virgins and in widows, and that marriage or pregnancy was a cure (‘Diseases of Women’, vol. 8, bk. 1, paras 7, 127–128). Recent authors have expressed scepticism about the more farfetched ideas in the Hippocratic collection. King (1993) pointed out that the Littré translations introduced headings and labels to organise the concept of hysteria or hysterical suffocation in French, an organisation not necessarily present in the original material. Micale (1989a) remarked about hysteria that indeed the Littré 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 palpitation, dizziness, vomiting and sweating”. There is no clear reference to globus hystericus or hyperaesthesia. In a very thorough discussion of the Hippocratic texts King also demonstrates that the phrase ‘suffocation of the womb’ is probably an inferior translation and that the original Greek hysterike pnix is better taken to mean stifling, with an implication of heat as well as difficulty in breathing. She concludes that although in some cases this notion applies to the woman suffocating or stifling, the notion more often refers to the womb itself, which would have natural influences upon female physiology. Hysterical essentially meant suffering from the womb and had no particular psychological importance. From these limited beginnings other classical authors developed concepts of hysteria of a mythical type. In a famous passage, Plato (c. 428– c. 347 BCE) said: “the so called womb or matrix of women. The animal within them is desirous of procreating children and when remaining unfruitful long beyond its proper time, gets discontented and angry and wandering in every direction through the body, closes up the passages of the breath, and, by obstructing respiration, drives them to extremity, causing all varieties of disease.” (Jowett, 1953)
This extract from the Timaeus (91b–c) comes from a dialogue or discussion and is not necessarily meant to be definitive. It is preceded by an item which is less frequently mentioned, where,
6
History and concepts
in likening sexual desire to an animal, Plato first mentions “in men the organ of generation becoming rebellious and masterful like an animal disobedient to reason”. Only then does he go on to make the same analogy for women. However, this particular idea seems to have taken on a literary life of its own and, for example, was adopted by Aretaeus of Cappadocia who, living about 500 years after Plato, wrote similarly about the varied movements of the womb (be it only within the abdomen) and said, “on the whole, the womb is like an animal within an animal” (Adams, 1856). Aretaeus also held that in consequence of the upward movement of the uterus the intestines might be violently compressed, the result being choking and a form of epilepsy, but not convulsions. Also, because the liver, diaphragm, lungs and heart were quickly squeezed into a narrow space, the patient experienced loss of breathing and speech. Soranus of Ephesus, who practised from 98 to 138 CE and was a near contemporary of Galen, denied that the womb was an animal but recognised hysterical suffocation (hysterike pnix), with a connotation of “Obstructed respiration together with aphonia and a seizure of the senses caused by some condition of the uterus.” Both he and Galen thought that it was a silly idea to suggest that the womb could move around the body (Temkin, 1956, pp. 8–9, 149). Despite the scepticism of prominent medical authors, the idea of the mobile uterus persisted quite strongly. In the medieval period Paul of Aegina (625 to 690 CE) (Adams, 1844, Vol. I, p. 633) wrote an extensive compendium of the views of the ancients and described uterine suffocation, or hysterical convulsion, as “a rising up of the uterus, affecting sympathetically the most important parts, as the carotid arteries, the heart, the membranes of the brain”. This would lead to attacks of weakness, fear, deep sleep, loss of the senses and of speech as well as contraction of the limbs, among other symptoms. Improvement occurred with gradual relaxation of the uterus. We have rather scanty information about the medieval period overall, but Green (1985, pp. 170–171) traced ancient theories of female physiology and disease through the early Middle Ages. It appears that Galen’s ideas, which were opposed to the wandering womb, were adopted by writers at the medical school of Salerno, but by contrast several authors have noted a formulaic Christian exorcism of the ‘wandering womb’. This is found in the blank space of a lateninth-century medical manuscript in which a priest commanded the womb to cease tormenting an afflicted woman:
Some traditional concepts
7
“not to harm this maid-servant of God ... nor to hold onto her head, neck, throat, chest, ears, teeth, eyes, nostrils, shoulders, arms, hands, heart, stomach, liver, spleen, kidneys, back, sides, joints, navel, viscera, bladder, thighs, shins, ankles, feet or toes, but to quietly remain in the place which God delegated to you, so that this hand-maiden of God ... might be cured.” (Bernfeld, 1929; Zilboorg & Henry, 1941; Green, 1985)
By this time we can see medical notions mingled with religious and supernatural beliefs. The implications of this in the late Middle Ages and early Renaissance period in Europe have been of interest to many authors who recognised the connection between alleged witchcraft, demonic possession, and hysterical symptoms. In 1602 during a famous trial it was claimed that a 14-year-old girl, Mary Glover, had been bewitched by “an old Charewoman”, Elizabeth Jackson, and as a result had “fallen into fittes ... so fearful that all that were about her supposed she would dye”. She became speechless and blind, “her neck and throat did swell extremely depriving her of speeche” and later her arm and whole side were deprived of feeling and movement (Bradwell, 1603). All these symptoms commenced after a quarrel with Elizabeth Jackson and got worse in her presence, and Miss Jackson was tried for witchcraft. The doctor for the defence, Edward Jorden, held that Mary Glover’s symptoms were due to natural causes rather than the result of diabolical influences and witchcraft. He lost the case and Elizabeth Jackson was convicted of witchcraft and imprisoned for a year. After his evidence was rejected, Jorden went away and wrote his classic treatise A Breife Discourse of a Disease Called the Suffocation of the Mother, which includes a useful clinical description of hysteria and a statement that hysteria was often due to perturbations of the mind. His actual words were: “the easie passage which [the wombe] has to [the braine, heart and liver] by the Vaines, Arteries, and Nerves ... it is an affect of the Mother or wombe wherein the principal parts of the body by consent do suffer diversly according to the diversitie of the causes and disease wherewith the matrix is offended.” (Jorden 1603, pp. 1, 5)
At this point we see a naturalistic explanation being preferred to a supernatural one, and not only for medicolegal reasons. Jorden’s idea is that somehow the womb influences the mind or other bodily functions but not by mobility. This is indicated by his reference to access via the veins, arteries and nerves and by his phrase “wherein the principal parts of the body by consent do suffer diversly”.
8
History and concepts
Hunter & MacAlpine (1963) pointed out that Jorden was treating as natural an illness liable to be attributed to witchcraft. He used the ancient doctrine of ‘sympathy’, or “communitie and consent”, to suggest the womb affected other organs and while the affliction was often blamed on “the perturbations of the minde”, the concept was apparently unified through the idea that the uterus, at some distance, was influencing the situation. Harvey (1651, p. 542), deeply immersed in studies of reproduction and gynaecology, also believed that: “the uterus is a most important organ, and brings the whole body to sympathize with it. No one of the least experience can be ignorant what grievous symptoms arise when the uterus either rises up or falls down, or is in any way put out of place, or is seized with spasm – how dreadful, then, are the mental aberrations, the delirium, the melancholy, the paroxysms of frenzy, as if the affected person were under the dominion of spells, and all arising from unnatural states of the uterus.”
In one patient who “for more than ten years laboured under furor uterinus and melancholy”, a prolapse of the uterus allowed its “overheat” to be “moderated by the contact of the external air” and on returning the uterus to its proper situation she lived in good health. He reports a similar event in another woman (p. 543). He also describes two cases of pseudocyesis (pp. 528–529). Harvey clearly saw the uterus as having an effect on the body, at least in part through the brain. A distinct departure in concepts concerning symptoms can be traced to the 17th century. Wright (1980) remarked on the fact that Descartes explained strange aversions by past experience. For example, a cat might have jumped into a baby’s cradle, thus causing a dislike of cats without the adult “retaining any memory of it afterwards”. Attraction could also be explained this way. Descartes attributed an interest of his own in cross-eyed women to his love as a young child for a nurse who had this defect. He found incidentally that the recollection of the memory in analysis cured him. Robert Boyle (1664), as Wright observes, had a clear notion of the operation of external stimuli – and hence ideas – in the production of hysterical symptoms. Boyle remarked that it is common for one hysterical woman when she observes another undergoing a fit to be “infected with the like strange discomposure”. These authors were thus approaching the possibility of a physical symptom which might be induced by example or by a thought. In the one case Descartes had clearly foreshadowed the Freudian
Some traditional concepts
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theme of association of unconscious ideas, and in the other case Boyle was explaining a physical symptom by imitation and example. Perhaps the most important 17th-century author was Carolus Piso (Charles Le Pois), who was the dean of the medical faculty at Pont-à-Mousson, and who attributed hysterical symptoms to the brain. Piso attributed hysterical symptoms to both men and women. Before long others took an essentially similar view. Briquet (1859, p. 12) gave Le Pois credit, saying of him that he was “the first to shine the light of observation on the traditionally accepted means of hysteria”, and the first to dissociate it from the uterus. The next radical change in the basis of the concept was made by Thomas Willis (1684), who located the source of all convulsive attacks in the brain. Using the terminology of his period he attributed the fits to explosions of the animal spirits inhabiting the brain. Epilepsy was supposed to be due to explosions in the middle part of the brain, hysteria to explosions at “the beginning of the nerves within the head”. A discharge at these lower points would be more likely to affect the vagi and intercostal nerves and involve visceral functions. Since “distemper of the mind” could affect the animal spirits, psychological causes could also provoke fits, of either type. The post-Renaissance view is well presented in the opening remarks of Sydenham (1697) in his discourse on hysteria when he considers the effects of mental trauma on bodily function. It will be seen, however, that in Sydenham’s day hysteria included much that would nowadays be considered to be organic disease: “When the Mind is disturb’d by some grevious [sic] Accident, the animal Spirits run into disorderly motions; the Urine appears sometimes limpid, and in great quantity; the sick persons cast off all hope of recovery; .... Whatsoever part of the body the Disease doth affect (and it affecteth many) immediately the symptoms that are proper to that Part appear; in the Head, the Apoplexy, which ends in a Palsy of one half of the Body, comes presently after Child-bearing; sometimes they are seiz’d with Convulsions, that very much resemble the Epilepsy, and are commonly called the Suffocation of the Womb, in which the Belly and Entrails rise upwards towards the Throat; At other times they are miserably tormented with the Hysterical Clavus [nail], in which there is a most vehement pain in the Head, which you may cover with your Thumb, the sick person in the mean time vomiting up green Matter like to that sort of Choler that has its name from Leeks.” (Sydenham, 1697, p. 6)
This extract tells us that following a severe stress both emotional and physical changes appear. Some are observable alterations in
10
History and concepts
bodily functions, such as changes in the urine, apoplexy or hemiplegia, but others are changes that would still be deemed hysterical today, such as non-epileptic fits. Sydenham goes on to mention subsequently other pains, diarrhoea, dropsy, tears and laughter. Overt emotional changes are also seen to be part of the illness, but the treatment remains physical, with venesection and medicines. Although Sydenham wrote of hysterical suffocation, he did not believe in a mobile uterus. He seems rather to have accepted the conventional label for the illness. Since Sydenham regarded hysteria, which he allied with hypochondriasis, as the most common chronic illness, it seems likely that he used the term to cover much of the wide range of emotional disturbances, with or without somatic complaints or disease, which physicians are wont to see. He was certainly explicit in attributing the condition to the mind, and argued (p. 157) that: “The External Causes of this Disease are either violent motion of the Body, or more frequently vehement Agitations of the Mind by the Assaults of Grief, Anger, Fear and such like Passions. And therefore when my Advice is demanded by a Woman, concerning a Disease whose nature I cannot discover by the Assistance of the vulgar Axioms, I observe always to enquire carefully, whether her Distemper is not exasperated as often as her mind is disturb’d by Passions; and if she returns an affirmative Answer, I am abundantly satisfied that her Distemper belongs to that set of Distempers, which are the subject of my present Discourse.”
Sydenham may deserve the credit for being the first to note explicitly that the syndrome of hysteria was related to emotional causes. I cannot say this firmly because there may be a section in the writings of Le Pois where this is mentioned, but, so far as I have been able to understand him, Le Pois writes principally about accumulations of fluid in the head causing hysterical symptoms. Despite the advances which Sydenham made in understanding, he still retained some of the old phraseology, for example “Sometimes they are seiz’d with convulsions that very much resemble Epilepsy, and are commonly called the Suffocation of the Womb, in which the Belly and Entrails rise upwards towards the Throat” (Sydenham, 1697, p. 6). After Sydenham, Purcell (1707) likewise saw hysteria as a bodily illness (occasionally but not usually fatal). For Purcell the immediate cause was a “Disorder of the Spirits”, especially indigestion, but this was not an adequate cause. Women were more liable to it than men for various reasons, including the effects of retention of menstrual products and because the weaker texture of their brain and nerves made them more subject to
Some traditional concepts
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violent passions, whilst psychological causes could also provoke attacks. Blackmore (1725, pp. 102–103), a rather verbose author, also recognised both physical and mental symptoms, which in the latter case he attributed to bad humours affecting the passages of the brain. Hysteria and hypochondriasis for him differed only in degree, the former being more linked to psychological causes and manifestations. He gave the good advice not to interfere with the patient during a convulsive fit. Blackmore was aware of Piso, and referred to his work. Blackmore observed (p. 99): “Terrible Ideas, formed only in the Imagination, will affect the Brain and the Body with painful Sensations. Thus we find that dreadful Objects presented to the Mind in Dreams; for instance, the empty and unsubstantial Forms of Ghosts and Spectres, will, by their violent Instigation and Impulse on the Spirits, put them into such a Hurry and Confusion, as shall cause great Inquietude and grievous Pains.”
It is worth emphasising that all these authors wrote in a tradition which automatically assumed that the mind could influence the body and the body could influence the mind. Rather (1965, pp. 1– 2) points out that: “it seemed plain to most of them that the will and the emotions did in one way or another produce far reaching and sometimes harmful or even fatal changes in the body, and they believed it their business as physicians to set forth the circumstances, extent and means of control of the interaction between mind and body. They believed also, in keeping with an unbroken tradition originating in ancient Greek medicine, that the mind could be influenced corporeally, that is, by means of drugs, diet, climate and other factors acting primarily on the body. Clinical observation had convinced them that the cause of a bodily disturbance could lie in the mind, and that where this was so treatment of the body alone was sometimes ineffectual. On the other hand, it had also convinced them that the causes of some mental disorders lay in the body, and they drew the obvious inference regarding treatment.”
The evidence that earlier generations believed that the mind could influence the body is particularly well stated by FischerHomburger (1979), who demonstrated the persistence of the view that ‘imagination’, conceived by Van Helmont as an internal force arising within organs such as the spleen and the uterus, could produce far-reaching and specific effects like birthmarks or even an immaculate conception. In 1637 the parliament of Grenoble
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History and concepts
ruled that a woman could be impregnated via imagination when dreaming of her husband who had been absent for four years, about which a critic remarked, “Here the president of the parliament or another man seems to have been instrumental” (Ammann, 1670). We can speculate that the decision might have something to do with the unwillingness of a court to label a child as a bastard, and was therefore not quite as stupid as it appears. By the middle of the 18th century, traditional views of the relationship between the mind and body were being strengthened and extended. The influence of the mind in causing physical symptoms – as distinct from physical disease – could not be worked out, given the limited anatomical and physiological knowledge of the time. Nevertheless, a relationship between somatic complaints (whether from disturbances of the autonomic nervous system or due to thoughts) and the state of the emotions was clearly becoming more detailed and more sophisticated. Whether or not the concept was sophisticated, it could still be benevolent. Risse (1988) has shown very well that the diagnosis of hysteria was not restricted to the leisured or wealthy classes. Women admitted with this diagnosis to the Edinburgh Infirmary in the 18th century were mostly poor, young, unmarried, living in squalid quarters, and suffering great deprivation. The medical care offered for social difficulties under the diagnosis of hysteria offered a way to support and assist the patients, not least with accommodation, food and warmth, while treating them with medical measures ranging from irritating salts to electric sparks and from purgatives to blisters.
A psychosomatic view Robert Whytt (1751) provided a notable development in 18thcentury views of hysteria and hypochondriasis. It is probably relevant that he was not only a perceptive doctor who was keen to treat his patients with a variety of physical remedies (including electric shocks on occasion) but also an active experimental physiologist and pharmacologist. His works include, for instance, detailed reports of the effect of opium applied to various sites of the body in laboratory preparations of the frog, and numerous experiments on the functions of individual nerves. As Hunter & MacAlpine (1963, p. 389) point out, he was the first to establish: “that movement could be initiated not only by an effort of will or by external stimuli, but by a nervous impulse independent of either. He thereby discovered what are called today autonomic and reflex activity.”
Some traditional concepts
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Whytt particularly emphasised the importance of ‘sympathy’ of the nerves in producing effects in one part of the body as a result of psychological effects or diseases elsewhere. In these respects he instances nausea on seeing others vomit, “the Flux of saliva into the mouth of a hungry person, at the sight of savoury food” (Whytt, 1767, p. 41) and tears of sadness. A good illustration of his technical approach is to be found in his comment that although Vesalius had shown that there was no communication between optic nerve fibres in their course from the brain to the eye, nevertheless “we find a most remarkable sympathy between the motions of the two pupils” (p. 43). All kinds of somatic responses are attributed to the emotions: pallor from anger; palpitations of the heart from fear; sudden flushings from heat; shiverings; a sense of cold in certain parts; flying pains in the arms and limbs; cramps or convulsive motions or sudden startings of the limbs; long faintings; giddiness; pains in the head; and still others. Although Whytt was not the first to be aware of the link between mental stress and physical disease, undoubtedly he had a deep understanding of the implications of what are now called psychosomatic disorders. Perhaps as a result of this he had recourse, in accounting for hysteria, both to the general state of the nervous system and to the traditional view that there are local causes. In his opinion: “the hypochondriac and hysteric affections often proceed from a morbid state of the alimentary canal, uterus, or other viscera of the abdomen; yet as there are several of their symptoms which seem independent of any disorder in those parts, and as there is often no trace of those diseases appeared after death in any of the abdominal organs, it was highly probable that they may frequently arise from some less visible fault in the body.” (Whytt, 1767, p. 108)
He ascribed this fault to “I. A too great delicacy and sensibility of the whole nervous system” and “II. An uncommon weakness ... in some of the organs of the body” (p. 109). These two categories provided predisposing causes. “Particular occasional causes” were found in visceral disturbances and in “violent affections of the mind”. His list of visceral disturbances is disappointingly odd and includes wind, a tough phlegm and/or worms – all in the stomach or bowels – the wrong food and scirrhous or other obstructions in the viscera (p. 183). But his overall perspective entitles him to great credit as one who looked both for the precise physical mechanisms of illness and the influence of psychological factors in its production.
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History and concepts
Finally, it is worth quoting his comments upon sex and hysteria (p. 105): “Upon the whole ... the symptoms of the hysteric disease in women, seem only to differ from those of the hypochondriac in men, in so far as the former sometimes proceed from the uterus, and are, on account of the more delicate frame of the sex, more frequent and often more violent than the symptoms of the hypochondriac affection in men.”
This is surely a perceptive conclusion. Pomme (1765) recognised “a host of symptoms” (p. 51), including suffocation (p.109), haemoptysis (p.115), toothache (p.140) and hysterical insanity (délire maniaque) (p.128). In one case anorexia, nihilistic delusions and agitation were combined. In the 18th century hypochondriasis was also identified with melancholia or depression. Boswell (1777–83), for example, wrote a column in The London Magazine entitled “The Hypochondriack”. The diagnostic confusion perhaps stems from authors like Cheyne (1733), who readily included the more usual hysterical symptoms like convulsions and spasms as members of one great class of complaints ranging from melancholy through apoplexy, paralysis and weakness to imbecility. Micale (1990a) observed that: “in the 18th century, the disorder slid imperceptibly into hypochondria, ‘the vapours’, and ‘the spleen’, and in the 19th century it often overlapped with neurasthenia, nymphomania, general nervousness and out and out insanity. Many ... have used the word in reference to any nervous malady with spastic or convulsive complication.... Many physicians have complained vociferously about the vagueness and indefinability of hysteria.”
Despite this, the terms ‘suffocation of the mother’, ‘hysterical suffocation’ and ‘fits of the mother’ persisted well into the 19th century. Dubois D’Amiens (1833) wrote of a rounded foreign body, or globus hystericus, and Landouzy (1846, p.6) described a ball mounting from the abdomen to the neck and constriction of the throat. The term ‘globus hystericus’ which they used is still used today – whatever its meaning.
A revival of older themes Sydenham’s ideas were largely maintained for over 100 years, until the early 19th century, when there was active discussion of the view that hypochondriasis and hysteria were distinct. A decisive
Some traditional concepts
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shift of opinion appears to have followed a prize competition of the Académie Royale of Bordeaux won by Dubois d’Amiens (1833), who, like the other entrants, argued the two syndromes were distinct, especially because of the following differences: “Hypochondriasis usually affects males, hysteria only women. The former is slow of onset, the latter sudden. Hypochondriasis occurs in three stages, the first one of exaggerated fantasies of illness, the second one of severe anxiety, with multiple somatic complaints which may remit, the third one of irreversible organic change. Hysteria occurs in two grades of severity, the first marked by heaviness of the limbs, widespread somatic discomforts and paroxysms of the limbs despite the presence of consciousness. The second grade goes on to wild and painful cries and generalised convulsions with incomplete loss of consciousness. The prognosis as always in a functional illness is good.”
The full details tabulated by Dubois d’Amiens are given in Appendix A. By 1846 the distinction was so well accepted that Landouzy commented that it was hard to understand how anyone could have followed Sydenham. At that time the common concept appears to have been as follows (Landouzy, 1846): “1. It is a disease usually, or even only, affecting women, almost always young ones. 2. It is characterized by pains in any part of the body, paralysis of limbs, speech, sight and hearing, anaesthesias, certain types of fits, dyspnoea, pharyngeal globus, dysphagia, hiccough, vomiting, meteorism, dysuria and urinary retention. The illness has a prodromal phase of gradual onset marked by changes of mood and appetite. The fits have a more vigorous prodromal phase which can include photophobic involuntary movements of the eye-balls and eye-lids, disturbances of vision, sadness, facial pallor, extensive jerking, clutching movements, ringing in the ears, incoherent words, laughter and tears without cause, eructations, disturbances of appetite, palpitations, sudden sweating, shivering and cold feelings (refroidissements), pains and paraesthesiae in the limbs, and sometimes spasmodic or convulsive movements. A clear and limpid urine is produced sometimes at the start and often at the end of an attack.”
Landouzy observed: “These precursory phenomena being infinitely variable like all nervous phenomena, one would seek in vain for an exact relationship between particular prodromes and particular types of attacks. However, observation indicates that shivering, clutching movements, and palpitations usually herald the non-
16
History and concepts convulsive form, especially syncope, whilst disturbances of sight, headache and mild spasms usually precede the convulsive attacks. 3. There is an organic cause for this affliction, the great majority of recorded cases with pathological evidence showing some type of lesion of the female reproductive apparatus, and particularly the uterus and ovaries. 4. Typically according to the generally accepted view of Sir Benjamin Brodie [1837], ‘it is not the muscles which refuse to obey the will, but the will itself which has ceased to work’.”
Other factors predisposing to hysteria besides youth and female sex include, according to Landouzy, warm climates, the spring, civilised societies, a nervous temperament, heredity, and menstrual irregularities and sexual disturbances. It would be easy to poke fun at the apparent naivety of some of these ideas, yet they were frequently supported by careful and close observation, studious analysis of the literature, and a shrewd appreciation of some of the psychological causes which could be relevant. Although the boundaries of the syndrome may be hard to define, there seems to be a recognisable pattern which the honest observer would often find, even if it was not infrequently depicted more convincingly with the help of the patient’s unconscious awareness of what the doctor thought was appropriate. At the same time one has to respect the intellectual penetration which argued that this condition, with a supposed organic aetiology, nevertheless produced its effects by an impairment of willpower. Many of the elements of this syndrome are still recognisable in textbooks and journals today under the heading of hysteria, and occasionally that of hypochondriasis, or the hysterical personality. The reality of the suffering of the hysterical patient seems to have been called more into question as knowledge of the anatomy and physiology of the central nervous system increased. As has been pointed out elsewhere (Merskey & Spear, 1967), pains became either ‘real’, that is, due to organic or functional afflictions of the nerves, or else ‘imaginary’. Inman (1858), who accepted the reality of hysterical pain, sought to prove that it had a physical basis and that the term should be dropped because it implied that it was fanciful. He observed that: “In medicine pain is no pain, and suffering no suffering, in an hysterical sense ... a hysterical pain is one which a patient feels but has not; which has no existence; which being thought upon may grow until it is unbearable.”
Nevertheless, the general view of hysteria at that time still seems to be one of a physically based illness, but requiring skilful
Some traditional concepts
17
management, both psychological and physical. This was to change. Shorter (1989) has made the sad point that as technical medicine became more powerful in diagnosis and treatment, so the psychological skills needed in the care of patients were neglected, which is another aspect of the same process. It appears that between the 17th and 19th centuries, the notion of hysteria commonly included the following features: a relationship to the womb or the female constitution, the occurrence of diverse somatic symptoms, and a link with emotional causes. How these symptoms were produced provoked much argument. Many of them today would be called psychophysiological and be due to anxiety or depression. Others, such as fits and multiple symptoms, still tend to be regarded as hysterical. A problem also existed in distinguishing depression and hypochondriacal complaints (in the modern sense) from hysteria, and older ideas were often revived, despite penetrating observations like those of Whytt. The more precise analysis of the physical complaint required the development of more profound psychological analysis of the idea that the willpower of a patient had a bearing on the symptom. A reserved view of the matter was taken by Sandras (1851, pp. 168–169), who wrote as follows: “The illness to which we have given the name hysteria is a chronic nervous condition in which at intervals of varying length, paroxysms appear, characterized by a particular sensation of choking, a severe discomfort of respiration, a pain in the head of varying severity, and clonic convulsions in all, or almost all, the parts of the body. It is said to be an illness of women; there is no doubt that it appears in men. I am sure that I have observed it in men several times with all its symptoms without any exception.”
Sandras also wrote: “Hysterical women feel a ball leaving the womb? ... The great majority of hysterical women have never felt this ball and this sensation, when it exists, arises most often from the epigastrium.”
He added that since he had had reports of the sensation of a ball in the throat from men, that was enough to dethrone the uterus. This concept of hysteria, like earlier notions, could accommodate a large number of variations of nervous states and was applicable to patients with anxiety and depression. Georget (1821) and Brachet (1847a,b) thought hysteria was a neurosis, meaning that the seat of the affliction resided in the brain, and the idea that the brain was the site of the dysfunction gained strength. Although it remained an ‘organic’ concept caused by
18
History and concepts
disturbance of brain function, it might still be precipitated by ill treatment by parents, worry, stress, business setback, and broken love affairs. The essential idea was that brain function was disturbed by some cause, which was hard to characterise, but possibly related to excessive stimulation. Briquet (1859) presented a solid extensive clinical and demographic study of hysteria (Mai & Merskey, 1980a,b). He described the clinical patterns in detail under seven categories, namely: (a) hyperaesthesias, including pain, (b) anaesthesia, (c) perversions of sensation, such as visual, auditory or olfactory hallucinations, (d) spasms affecting systems such as the gastrointestinal tract and central nervous systems, (e) seizures, (f) paralyses affecting various muscle groups, causing, for example, paraplegia or monoplegia, and (g) abnormalities of muscle contraction, secretion and exhalation, causing increased secretion of saliva, sweat or urine (Mai, 1982). Briquet did not describe the syndrome which was later named after him by Guze (1970), but did destroy its historic association with physical pathology of female genitalia. The influence of his systematic approach can be glimpsed in the way in which Charcot (1872) refers to his findings with respect and with attention to Briquet’s statistics, even when he proceeds to disagree with him.
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2
Early neurological analyses
The distinction from organic illness An unprecedented change in the clinical analysis of hysteria occurred with the work of Sir Benjamin Brodie (1837). This change was the increasing recognition of the precise effects of different sensory and motor nerves in the production of anaesthesias or paralyses or pain, and hence the existence of a difference in hysteria. Walters (1969) pointed out how Brodie was aware of Bell & Bell’s (1826) work in distinguishing separate motor and sensory nerve roots. Bell had actually gone so far as to establish at operation that the frontal area of the brain did not possess sensibility. He satisfied himself that different nerves had specific functions in controlling sensation or movement in different parts of the body, and he argued that there was localisation of function within the brain. In accordance with the tradition of John Hunter and with the spirit of his own times, Brodie was devoted to demonstrating which signs and symptoms were associated with morbid anatomy and which were not. Brodie was a famous surgeon with an extensive practice concerned with bone and joint disease, and in a much-quoted observation he remarked that “among the higher classes of society, at least four-fifths of the female patients, who are commonly supposed to labour under diseases of the joints, labour under hysteria, and nothing else” (Brodie, 1837, p.37). As Walters also indicates, Brodie recognised that the motor paralysis of hysteria was due to a lack of exercise of the function of volition and not an incapability of muscle, and he satisfied himself by postmortem examination that there was no morbid anatomy to account for the hysterical symptoms of his patients.
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History and concepts
Notwithstanding Brodie’s work, bodily complaints allegedly due to dysfunction of the nervous system remained very popular. Shorter (1992) traces the early 19th-century craze for the diagnosis of spinal irritation, the mid-century attachment to “reflex neurosis” based upon notions of ovarian dysfunction, and later predilections for extravagant habits or complaints. These range from hypnosis and the induction of multiple personality to fits, paralysis and the variety of symptoms which are still called hysteria today, such as conversion symptoms and other dissociative disorders. Yet these symptoms were not understood in their modern sense, which requires a specific type of finding on physical examination, that is, function present when the patient thinks it has been lost. They were still part of a concept which would last until after Freud’s first work. According to this quite persistent concept, hysteria was any general neurosis without specific localisation (Hirschmuller, 1989). The recognition that the local complaints called hysteria were not accompanied by any physical disorder becomes more apparent from the pen of another surgeon, F. C. Skey (1867). This author is notable for his robust and hearty advocacy of wine and brandy to restore physically enfeebled patients, rather than bleeding. When it comes to hysteria he observes “every part of the body may become, under provocation, the seat of an apparent disease which in reality does not exist” (p.43). This combination of acceptance and rejection which is so typical of medical attitudes to hysteria is well shown in Skey’s concluding words: “A class of diseases involving the nerves or nervous system ... carry with them so much resemblance to real disease or disorganisation of structure as to deceive the most experienced ... But that they are destitute of some of the most prominent features which characterise real disease; ... that of local or general hysteria is the product of a disturbed, not a diseased condition of the brain or spinal cord, and that ... it is difficult to deny their relationship which appears to exercise some mysterious or occult influence over them.” (p.107)
In the same period the recognition that hysterical symptoms were not due to lesions of specific nerves or pathways was firmly stated by Althaus (1866): “The commencement and progress of all the distinct forms of hysterical paralysis, leave no doubt in the mind that it is a functional disorder ... and in no way connected with structural lesions in the nervous centres, the peripheral nerves, or the
Early neurological analyses
21
muscles. Affections which come on so suddenly, which may vary in degree from day to day, and are sometimes cured by a single application of galvanism, cannot be due to organic lesions of important organs but are produced under the influence of mental emotions and chiefly determined by them in their further progress. In accordance with this view we find that in cases which have ended fatally the most careful post mortem examinations have failed to show any structural lesions to which the affection might have been fairly traced.” (p.60–61)
Althaus was not the only neurologist to make points of this nature. For example, R. B. Todd, in his lectures on diseases of the nervous system (1854), had already observed that in a hysterical hemiplegia the tongue did not deviate to the affected side as it did in an organic hemiplegia.
The psychogenesis of a defined syndrome A radical change from the views typified by Landouzy appeared in 1853 in a book entitled On the Pathology and Treatment of Hysteria by Robert Brudenell Carter. Carter was initially a general practitioner working in Leytonstone and had evidently acquired many of his ideas from a recently deceased friend – Mr Stephen McKenzie – to whom he makes full acknowledgement. Incidentally, Carter later became a correspondent of The Times and Consultant Ophthalmological Surgeon to St George’s Hospital and to the National Hospital, Queen Square. Carter’s book has many features which are either interesting or impressive, or both. He recognises that the term hysteria has been put to very wide use, then goes on to define the condition as one which commences with a convulsive paroxysm of a very variable type, ranging from a brief attack of laughter or sobbing to very energetic prolonged involuntary movements terminating in catalepsy or coma. The condition may be complicated by neuralgias, disorders of spine, knee, and so on. In Carter’s view hysteria results from a direct effect of the emotions upon the body, acting through the only possible channel – the nervous system. He argues that “it is the natural tendency of an emotion to discharge itself either through the muscular, the secretory or the sanguiferous system” (p.15). Having added to this the opinion “that emotion is a force adequate to the production of very serious disorders of the human frame” (p.25), Carter is ready to expound a psychogenesis of hysteria as a physical disorder resulting from a psychological disturbance.
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History and concepts
The emotional disturbance in question may be secret. In women the most common feeling responsible is terror; and the most violent is “the sexual passion” (p.34). “An hysteric paroxysm produced by terror is so common among servant girls and in fourth-rate boarding schools and may be set on foot by so many causes it is needless ... to cite examples.” But men, especially those who are continent, can also suffer from hysteria and, because the disorder can affect men, Carter summarily dismisses the view that it is due to uterine disease. He clearly recognises the valetudinarianism of some patients and the secondary gain from being nursed or being treated as sick. He even notes the deceitfulness of other patients. Like his contemporaries, he considers numerous other bodily symptoms, from hypochondriacal pain to leucorrhoea, to be associated. When an author proposes a new theory it is often instructive to see what has gone before. Carter quotes from Dr Theophilus Thompson’s article on hysteria in the Library of Medicine. He arranges the hypotheses quoted in four groups: (a) “doctrines altogether indefinite” (sic); (b) “doctrines requiring the female reproductive system”; (c) “doctrines requiring the existence of specific disorder in important or vital organs”; (d) “the views of Cheyne, Parry and Pitcairn recently revived in the form of a ‘toxic hypothesis’” (pp. 78ff). He has little trouble in disposing of all of these. Treatment consists essentially in outmanoeuvring the patient by such techniques as removing her completely from her family (normally to the doctor’s household) and, when a fit occurs, leaving her alone indefinitely in a locked room until she proclaims her own recovery. But physical ill treatment, for example with cold water, is firmly rejected on both moral and practical grounds. Indeed, “it must be remembered that the patient often inflicts upon herself much more pain than any medical attendant could possibly propose”. The doctor always has to be fully in command of his own mood and to desist from attempting treatment on any occasion when he cannot be sure of having sufficient patience. Carter’s work illuminates many aspects of hysteria and shows some of the admirable skills in psychological relationships displayed by at least a few other 19th-century doctors. As Veith (1965) points out, it also makes it abundantly clear that a sexual aetiology for the condition was well recognised many years before Freud. There is still no real distinction, however, between a psychophysiological pattern of causation and one due solely to the patient’s thoughts and ideas and not involving change in peripheral physiological pathways, although (pp. 12–15) Carter carefully distinguishes between the effects produced through the agency of the sympathetic
Early neurological analyses
23
nervous system and those involving the voluntary musculature. Kane & Carlson (1982) give an excellent account of his ideas and conclude that he was unique among the English physicians of his time in his perception of these relationships. Although Carter’s work was the most thorough and the most penetrating on the topic, he was not the only one to recognise the contribution of sexual difficulties to hysteria. In Vienna, Baron Ernst von Feuchtersleben (1845) made a classical analysis of hysteria which also tended to separate the use of both that term and the word hypochondriasis from their early identification with melancholia. Among its symptoms he included pains in various parts of the body and for its cause he laid great stress on sexual frustrations. Similarly Anstie (1871), dealing not with hysteria but with pelvic neuralgias in women, remarks that they may be aggravated by persistently dwelling “in a conscious manner on sexual matters, especially if by an evil chance she becomes addicted to self abuse”. In some cases with neuralgia “a restless hyperactivity of mind and perhaps of body also seems to be the expression of Nature’s unconscious resentment of the neglect of sexual function” (p. 241).
Symptoms from ideas The next logical step was to recognise that the hysterical symptom might arise from the patient’s ideas. The first author to indicate this appears to have been Sir John Russell Reynolds (1869), who described three paralysed patients in whom he was able to show positive evidence of motor function in the paralysed limbs together with a history of incidents which determined in them the belief that they were paralysed. The increasing appearance of complaints of paralysis or pain after railway accidents was one of the contemporary influences leading to the recognition of ideas as a cause of symptoms. This is very noticeable in the discussion of Reynolds’ paper when it was presented to a meeting of the British Medical Association. Another feature evident in the same discussion was the tendency only to accept as hysteria those complaints which occurred in patients who also had convulsions. Hysteria was seen as a symptom complex, and paralysis alone was not classed as hysterical. A modern form of this notion still has strong support from authors like Guze, who reserved the word hysteria for a group of symptoms which they later named Briquet’s syndrome (see Chapter 13). Reynolds separated the conditions which he described under cases “dependent upon idea” from insanity, hypochondriasis or
24
History and concepts
hysteria, noting “an entire absence of anything like hysterical spasm, or general habit of either mind or body”. He added that “at the same time it is most obvious that such patients are often as far removed as it is possible to be from anything like the wish or the habit of deception”, which was a common allegation against patients with hysteria. Charcot was impressed by Reynold’s ideas and stated (Charcot, 1872, p. 282) that the idea of paralyses from thoughts had long been known but only Reynolds had studied them in a methodical and systematic way. Thus he explicitly acknowledged the importance of Reynold’s paper. He went on to suggest very firmly that the implantation of the idea of paralysis, or loss of use of a part by means of hypnosis, confirmed that hysteria could be produced in accordance with an idea which was provided for the patient. It was from this basis that Freud, as is well known, developed his ideas of the dynamic origin of hysterical complaints. Möbius (1888) is also credited with recognising that symptoms might be caused by thoughts or ideas, and his work too was known to Breuer and Freud (see Schiller, 1982). Like Reynolds, Paget (1873a) was reluctant to diagnose hysteria for single symptoms. He wanted to discard the term hysteria in surgery, but keep it for convulsions, suffocation, flatulence, and associated signs of nervous disorder. He agreed with Brodie’s observation on joint pains in the upper classes, noting, however, that such pains were hysterical in only one-fifth of instances in the lower classes. But he held that pain alone was not enough to prove organic disease (Paget, 1873b). These discussions were advancing the task of distinguishing between physical and psychological causes. The development of neurological examination had enabled Reynolds to recognise the importance of the idea. Paget (1873a) elucidated the volitional aspect. Emulating Brodie’s comment, he observed: “They say, ‘I cannot’; it looks like ‘I will not’; but it is ‘I cannot will’”. Brodie, Reynolds and Paget in turn provided important sources for the work of Charcot, who was well versed in both the English and German literature in addition to that of his native language, French (Guillain, 1959).
The school of Charcot The second half of the 19th century is dominated by the school of Charcot at the Salpêtrière. In its work it is possible to trace most of the lines of inquiry and the opinions which have already been
Early neurological analyses
25
mentioned from other authors. The work of Charcot and his school has been so well translated into English (Charcot, 1872; Goetz, 1987) and is so well known that it needs only a brief description. The text contains beautifully written descriptions of his patients and very clear statements of his views. Among the findings (some erroneous) which his school obtained are the occurrence both of hysteria and epilepsy as episodic disorders and the hysterical fit as having a pattern described as grande hystèrie, extending to the production of opisthotonos so extreme as to cause a position of arc en cercle. Hysterical motor signs were carefully analysed, and often well depicted by Richer (1892) and Charcot himself (Figs 2.1 and 2.2). Stigmata supposed to be characteristic of hysteria were demonstrated in the interval phase between fits, including narrowed
Fig. 2.1. Generalised contractures following a major attack of hysteria (from Richer, 1885)
26
History and concepts
Fig. 2.2. Astasia-abasia (from Richer, 1892; sketch by Charcot)
or tubular vision, hemianaesthesia, and ‘ovarian tenderness’. Thus pressure over the ovarian region, whose discovery was attributed by Charcot to medieval physicians, became a means to treat hysterical fits. Like the arc en cercle, these phenomena are now thought to be artifacts of the relationship with the doctor or with other patients. However, I have seen arc en cercle once, completely unexpectedly, and the late Dr Allan Walters told me he had seen it at least twice in 45 years of practice. The similarity of hypnotically induced symptoms and hysteria was also recognised (Gilles de la Tourette, 1887, 1891), although the school of Charcot believed much more strongly than others that hypnosis was a special trance state (James,
Early neurological analyses
27
1890). The latter is a view which is now scarcely tenable (see Barber, 1969; Merskey, 1971; and Chapter 15). Other hysterical symptoms such as paralyses were shown further to be distinguishable from organic syndromes by clinical examination, and by comparison with the neuropathological findings in cases of organic disease (Charcot, 1889; Gilles de la Tourette, 1891; Richer, 1892). The importance of suggestion was also recognised, especially by Babinski (Babinski, 1901; Babinski & Froment, 1918a,b), who went so far as to call hysteria pithiatisme, that is, suggestibility. Charcot much admired Brodie’s contribution (Walters, 1969). Nevertheless, Charcot still had a profound conviction that physical changes, of which the patients knew nothing, occurred in hysteria. For example (Lectures I, 249) he described how leeches yielded very little blood from the side of a hysterical hemianaesthesia, while blood flowed freely from the other side. He supposed that there was alteration of the blood vessels which reduced bleeding. Although he recognised that hysterical symptoms ordinarily correspond to the patient’s expectations of the effects of a lesion, and emphasised Reynolds’ contribution, nevertheless, he seems still to have believed that a physical disorder was induced within, so to speak, the territory of the idea. This continued emphasis on the local physical changes is paralleled by the persistent belief in a physical or constitutional background to the development of hysteria. Although Charcot had moved away from the mid-19th-century position of Landouzy and others that there was an organic cause for hysteria in the reproductive system, he still thought of it as an illness with enduring, discernible physical characteristics. The stigmata mentioned were taken to be signs of this persisting diathesis and it was supposed, correctly enough, that they could be demonstrated by suitable examination at times when overt symptoms did not occur. The latter were the paroxysmal or episodic features of the illness. Very similar views were held in England by Gowers (1892–93). Variable resistance on examination of motor power was noted by him as well as contraction of the flexor muscles on extension. The ‘idea’ of a loss of power was recognised and ovarian tenderness found. Hereditary predisposition, affections of the sexual organs, egotistic personality characteristics, increasing civilisation and emotional precipitants were all acknowledged as causes. This is an English parallel or derivation of the traditional picture as redrawn by the school of Charcot, although there were some differences. One of those differences from Charcot’s findings, which was not reproduced to the same extent in England, was the finding
28
History and concepts
of stigmata and ovarian pressure points. Gowers considered that ovarian tenderness was unquestionably frequent, but also that it was not invariable nor confined to the subjects of hysteria. Altogether the manifestations of hysteria as observed by Gowers seem less dramatic than those found by Charcot. Two causes may have been responsible for this. The first was the total dependence of Charcot’s patients upon him and his institution. They were usually poverty-stricken, young girls from the country who were sheltered in the Salpêtrière by virtue of their illness and at the price of their cooperation with the doctor. Axel Munthe, in his autobiographical work The Story of San Michele, gives a very vivid, although rather sanctimonious, account of these matters. Gowers’ patients, by contrast, had more opportunity for independence, being most often private patients or outpatients or only temporary in-patients. Secondly, the Industrial Revolution came later in France than in England. As subsequent chapters will indicate, it is common to find that more extreme forms of hysteria occur relatively frequently in non-industrial populations (Chapters 10, 17). Geschwind (1976) suggested that the tendency for more extreme hysterical phenomena to appear in Charcot’s patients is related to their rural origin and to the influx of simple country girls to Paris during the period of Charcot’s working life. Setting aside the detail and the errors, the following are the essential points of Charcot’s substantial contribution to the analysis of hysteria. Firstly, he reaffirmed with authority the view of many others that psychological factors promoted hysterical symptoms. Secondly, he developed the neurological examination, which permitted a distinction to be made on positive grounds between symptoms due to physical illness involving nerve tracts and pathways, and those with an emotional origin. Thirdly, he emphasised how the idea of the symptom determined its pattern. Charcot’s pupils included Janet and Freud. Their work, together with that of Charcot, provides the origins for most of the modern discussion of hysteria.
29
3
The turn of the century
In the middle of the 19th century Sandras (1851, vol. 1, p. 168) summarised the view of hysteria as follows: “hysteria is a chronic nervous condition in which at intervals of varying length, paroxysms appear characterized by a particular sensation of choking, a severe discomfort of respiration, a pain in the head of varying severity and chronic convulsions in all, or almost all, parts of the body.”
This sort of perspective provided the general background against which Briquet, Charcot, Janet, Breuer and Freud were all to offer their contributions. Hirschmuller (1989) points out that when Breuer was a student, hysteria was looked upon as “a so called general neurosis”, without definite localisation in the nervous system. If there were psychological changes it was called a psychosis as well (without necessarily carrying the later strong implications of insanity). Romberg (1851) believed hysteria was “a reflex sexual neurosis”, a notion which persisted in the Continental literature up to the end of the century, but more attention was probably paid to the broad division, summarised as late as 1909 by Savill, between neurasthenia, hysteria and hypochondriasis. At that time hysteria was seen as being based on deficient willpower and a hysterical constitution, but manifesting itself in paroxysmal complaints, especially seizures, with the usual variety of other associated bodily complaints. Figure 3.1 shows Savill’s comparison with neurasthenia and hypochondria. Of all the authors discussed so far, Briquet gets the most attention and the warmest recommendation. In 1894 Janet published his book L’État Mental des Hystériques, The Mental State of Hystericals (Janet, 1901), which was based on his 29
30 History and concepts
The turn of the century 31
Fig. 3.1. A table of diagnoses in the early 20th century (from Savill, 1909)
32
History and concepts
studies in the school of Charcot. In that work he repeated Charcot’s idea of characteristic hysterical phenomena, especially anaesthesia, amnesia, abulia, motor disturbances, and modifications of the character. The character change was divided into two components, intellectual and emotional. The intellectual change was marked by deterioration and the emotional change by exaggerated reaction to a diminished number of emotions, because “these patients are in general very indifferent, at least to all that is not directly connected to a small number of fixed ideas”. This type of argument is less attractive now than originally. However, Janet made certain notable observations in regard to subconscious thoughts (1894). He spoke of hysterical patients organising their emotional patterns, their movements, and their ideas “more or less through a kind of subconscious meditation”. The fixed idea that characterised hysteria was developed “below consciousness”, remaining “outside of normal consciousness”. He said, “the subconscious character of the fixed ideas ... plays an important part in the therapeutics of these affections”. Janet also said “we formerly showed that it was necessary to look up so to say, these subconscious phenomena in order to attack them and that one could not treat the hysterical accident before having reached those deep layers of thought within which the fixed idea was concealed. We are happy to see today Mm. Breuer and Freud express the same idea. ‘It is necessary,’ they say, ‘to make this provocative event self conscious; bring it forth to the full light. The accidents disappear when the subject realises those fixed ideas’.” (Janet, 1901, p. 412)
Here Janet is citing Breuer and Freud’s original article, “The psychical mechanisms of hysterical phenomena”. Janet (1889, pp. 436–440) had already published the case of Marie, on which these observations were founded. The concepts are similar to the Freudian explanation of unconscious ideas producing the hysterical conversion symptom. There has been a dispute over who first recognised the unconscious and the place of unconscious ideas in causing hysteria. Freud was not wholly original in this respect and acknowledged the fact himself (Freud, 1917, p. 218). However, the dynamic aspect of unconscious mental activity was emphasised much more by him, and indeed Janet’s description of the discovery of Marie’s unconscious ideas and their cure relies far more on deconditioning than on cathartic release. Thus, the dynamic aspect of unconscious mental activity was not evident to anything like the same extent in Janet’s description as in Freud’s.
The turn of the century
33
As Veith (1965) and others have pointed out, the real weakness in Janet’s position was his aetiological theories. He believed that there were agents which might precipitate hysterical accidents, but these were mostly physical in type and included haemorrhage, chronic disease, localised infection, typhoid fever, autointoxication, organic disease of the nervous system, and various alcoholic and other intoxications. Psychological provocations were admitted but not emphasised. All these agents appeared to Janet to work by weakening the organism and increasing the depression of the nervous system. The people most exposed to risk of such events were those with a degenerate heredity, but insufficient explanation was given as to why and how such symptoms might come and go. While Freud acknowledged Janet’s priority in publishing the relationship between symptoms and unconscious ideas, he pointed out that Breuer had actually undertaken a cure earlier on the same basis. He also emphasised how psychoanalysis showed the phenomena in which Janet was interested to be the result of dynamic factors – mental conflict and repression (Freud, 1935, p. 54). The state of ideas about hysteria and the extent to which Breuer and Freud provided an innovation is well characterised in a long review of the Studies in Hysteria published in Brain (Clark, 1896). Clark points out: “the authors were careful to speak of ‘the psychical origin of hysteria phenomena’ rather than ‘of hysteria’, because they do not wish to claim for their view an unlimited importance. They neither believed that all hysterical phenomena arise in the above described way, nor do they agree with Möbius that they are all dependent upon idea.”
Clark adds “it seems certain that many hysterical phenomena do not arise through idea,” and later says “the fundamental morbid change is an abnormal irritability of the nervous system; and it is a further question as to how far this is of psychical origin”. Janet was associated also with a tendency of the Parisian group to identify increasing numbers of traits which characterised hysterical personality. Briquet (1859) only mentioned seven such traits, but Axenfeld (1864) identified 12, including affective features, with which he also mentioned sensitivity, vivid imagination, simulation and egocentricity or selfishness. Successive workers with Charcot identified 15 (Du Saulle, 1883) or 17 (Richer, 1885, 1892), and ultimately the numbers rise to Janet’s 23 in 1907. It appears that Janet worked partly from the ideas
34
History and concepts
of others and partly developed his own notions. His items comprised the common features of depression, fearfulness, emotionality, lability and excitement, but also included exaggeration, suggestibility, deficient judgement, poor self-control (egocentricity), vivid imagination, erotic problems (frigidity), self-destructive tendencies, regression, jealousy, shame and diminution of the field of consciousness and dual personality (Janet, 1889, 1892, 1901, 1907, 1919; Alam & Merskey, 1992). He attributed the tendency of hysterical patients towards simulation and mendacity simply to their forgetfulness or to lack of interest in their own earlier statements, promises or facts of life, rather than to character defects. He considered that an underlying weakness of personal synthesis, a ready tendency to dissociation, produced both hysterical symptoms and hysterical traits. The symptoms were peculiar to the fully developed hysterical illness but the traits were shared with other ‘degenerates’ such as criminals and imbeciles. Successive breakdowns would weaken the predisposed constitution, with a resultant mental disintegration which could be permanent and complete. Janet was able to give more of his attention and appreciation to the personality traits of the hysterical patient than Freud, whose contribution is discussed in Chapter 4. Perhaps this resulted from his attempt to relate the symptoms to the personality of the individual in whom they arose. This was in contrast to Freud’s approach, which was to explain the symptoms in terms of specific determination, probably Freud’s greatest achievement in his study of hysteria. A further picture of the view of hysterical symptoms and patients is provided by Kraepelin, whose lectures, translated into English in 1904, contain an account of what he called ‘hysterical insanity’. A lecture of the same title is a masterpiece of description and is printed here in Appendix B. So many of the notions which were common to Janet and his predecessors are to be found in Kraepelin’s writing that it would be a hindrance rather than a help to recapitulate them; and any restatement would be inferior. What can be said is that the pattern of symptoms, the emphasis on personality, the response to treatment, and the use of many treatments with some considerable suggestive power, resemble with great precision experiences which can readily be encountered with hysterical patients today. By the turn of the century hysteria and hysterical traits were understood to involve at least three major elements. The first is
The turn of the century
35
those symptoms which now are regarded as dissociative, a term defined in Chapter 4. These include fits, attacks of loss of consciousness, impairment of memory, loss of use of the limbs, anaesthesias, and so on. The second element was the occurrence of a variety of these and other symptoms together, and the third was peculiarities of personality and of the relationship with the doctor; these were also recognised before Freud. One might add that there was a recognition of some motive in at least a few patients, but this recognition was not, before Freud, given more than intermittent attention. The definition of these symptoms and their patterns probably became more exact as a result of their separation from other groups of illness. By the end of the 19th century schizophrenia, or chronic delusional insanity, and manic–depressive illness were all recognised as independent conditions, usually different from the hysterical pattern in ways which could be defined acceptably. The main problem remained to distinguish the hysterical syndrome from other types of neurotic illness. Savill (1909) gave the most common diagnoses as neurasthenia, hysteria and hypochondriasis. Hypochondriasis tended to be the male equivalent of hysteria and neurasthenia that of affective illness in both sexes. Ellenberger’s (1970) classic study, The Discovery of the Unconscious, has enormously advanced our appreciation of the work of Janet and of many of the 19th-century developments. This study and the specific biographical study of Breuer by Hirschmuller (1989) illuminate the social, medical and personal context of the development of ideas about the unconscious, and frequently about hysteria. At the same time there has been a wide range of other writing which Micale (1989a,b) describes as “the historiography of hysteria”. This comprises intellectual histories of hysteria, studies related to Freud and the history of hysteria, feminist historical criticism, studies of Charcot and the history of hysteria, and nonfeminist social and political accounts of the subject. Micale’s studies (1989a,b, 1990a,b) provide an irreplaceable perspective on the role of hysteria as a concept both in medicine and in society at large. Further developments in the notion of hysteria were to take place as discussion spread through Europe and the Englishspeaking world and was affected by the theories of Freud, and also by the impact of World War I.
36
4
History and concepts
The contribution of Freud
The contribution of Freud to hysteria, which dates from 1893 (Breuer & Freud, 1893–95) gradually attracted increasing attention in the English-speaking world. By 1914 Ormerod, an English neurologist, was dealing with psychoanalysis and hysteria – not particularly favourably – although, in 1917, Craig, in a popular textbook, refers in passing to the term ‘anxiety neurosis’ as being introduced by Freud, but does not mention him in connection with the brief discussion of hysterical insanity. Freud’s work is now so well known and so much described that an extensive presentation will be avoided here, not because it is unimportant but because its considerable advances and failings have been well evaluated elsewhere by such authors as Dalbiez (1941), Fenichel (1945), Jones (1953), Brown (1961), and many more current authors. It has also been the starting point for the subsequent exploration of the nature of the hysterical personality by many writers with a psychoanalytic orientation. The latter topic is considered in Chapters 22 and 24. In this chapter, while merely noting the fact that the history of psychoanalysis begins with a publication on hysteria, only the main features of Freud’s theory of the matter will be briefly outlined. Studies on Hysteria (Breuer & Freud, 1893–95) represents Freud’s first papers on psychoanalysis. The introductory essay to the volume, “On the psychical mechanism of hysterical phenomena”, puts forward the view that ideas which were completely absent from the patient’s memory in a normal psychical state (or only present in a “highly summary form”) could be revealed by hypnosis. These memories related to psychic traumas which had not been disposed of either by abreaction or by normal “associative wearing away” in consciousness. The abnormal state was supposed to be produced either because of the strength of the undischarged 36
The contribution of Freud
37
affect attaching to the trauma or else because of a disposition to hypnoid states. This formulation provides the basis for the hypothesis that unconscious mental conflict may result in hysterical symptoms. If the symptoms affect the body, for example paralysis, pain, anaesthesia, they are conventionally called conversion symptoms, while others are known as dissociative symptoms (e.g. amnesia); notwithstanding, all conversion symptoms are also, by definition, dissociative and the 10th revision of the International Classification of Diseases now entitles the relevant section: F44 Dissociative [conversion] Disorders (World Health Organization, 1992a). According to the above view, the symptom solves a conflict which is too unpleasant to be faced or resolved in consciousness. In the first four patients whom Freud treated by his technique, pain was a prominent symptom, and he laid gradually increasing stress on the way in which these pains resulted from psychic conflict. For Elisabeth von R. he described them explicitly as a successful conversion phenomenon which spared her from the conviction that she loved her sister’s husband. “She repressed her erotic idea from consciousness and transformed the amount of its affect into physical pain.” It should be noted that this idea of quantitative conversion of (psychic) affect into a physical disorder is not maintained in later dynamic formulations. It was part of Freud’s first steps en route to a wholly psychological formulation of the aetiology of symptoms and appears also in his distinction between actual neuroses, such as anxiety due to sexual repression or even coitus interruptus, on the one hand, and psychoneuroses on the other. In these latter cases the causal mechanism was seen as wholly psychological (Freud, 1912). Where the causal mechanism was wholly psychological and the symptom resulted from a repressed conflict, the primary gain to the individual lay in escaping the dilemma and making it unconscious, if it was not unconscious already. In more advanced psychoanalytic argument the primary gain is often held to result from resolving a conflict which is basically unconscious. For example, a woman may develop hysterical symptoms because a forbidden oedipal wish – to be closer to a man who to her represents her father – is in conflict with unconscious feelings of guilt that she is thereby displacing her mother in such a relationship. The resolution of both these unconscious wishes with a symptom like a paralysis which prevented the man courting her would constitute the primary gain of the illness. This notion of primary gain is basic to the Freudian dynamic theory.
38
History and concepts
In common discussion of hysterical symptoms, secondary gain is more often mentioned. This represents the advantages which follow from the sick role, from the loss of the use of the limb or some part, for example such advantages as extra attention, nursing, special consideration, and so forth. They are an important part, of course, of the reinforcing mechanism in the maintenance of hysterical symptoms. But primary gain is part of the causal system. The hypothesis that the function of the hysterical symptom was to solve a problem itself solved the problem of another 19thcentury observation. It was recognised by the school of Charcot that many patients seemed to be content with their symptom, did not complain, and indeed appeared to be indifferent to it, or complacent about it. Hence the use of the term ‘belle indifference’. The Freudian theory gives an excellent explanation for belle indifference. Provided that the solution to the problem over which conflicts exist is adequate, then there should be no undue feeling of sadness, anxiety, or other emotional turmoil in the patient who has successfully solved a problem with a conversion or dissociative symptom. Indeed, at that juncture the patient may be rather pleased for reasons of which he or she is not aware, or at least is not wholly aware. Accordingly, we have a plausible explanation for what was otherwise a paradoxical and inexplicable human reaction after injury to illness. Mace (1992a) has nicely taken up the observation of Hunter & MacAlpine (1963) who drew attention to the use of the term “hysterical conversion” by the English physician John Ferriar (1795) a century before Freud. Ferriar discussed a general concept of the “conversion of diseases” by which, “new symptoms arise ... which require a different destination, and which either put a period to the original disorder, or combining with it, alter the physician’s views regarding the prognostics, or the method of cure.” (p. 1)
When one recognised disease developed into another, that was conversion. It was also conversion if one recognised disease predisposed to the subsequent development of another, or if the ill-advised therapeutic suppression of a first disease led to the appearance of a second. Fevers were often held to terminate in hysterical disorders, especially in women, but also in men on recovering from typhus “for they experience a capricious disposition to laugh or cry, and a degree of the globus hystericus” (p. 37). In the case of hysteria, another disease could supervene while hysteria was still undeniably present. Also, with hysterical conversion, the body might counterfeit the most hazardous
The contribution of Freud
39
disorders without incurring danger. According to Mace, Ferriar showed little interest in the pathogenesis of hysteria, but conversion was a unique property of the relationship which hysteria enjoyed with other diseases. The propensity for imitation that Sydenham had recognised (and Cullen had evaded) became the essential quality of hysteria. Ferriar’s usage of the term was not followed by other writers, perhaps because of a shift in interest away from classification on the basis of formal resemblance towards a classification more related to pathological understanding. Freud’s use of “hysterical conversion” in the 1890s was taken for a complete innovation and, in any case, the concept is quite distinct in its implications from the earlier one. In his early work Freud quickly noted the symbolic significance of the symptom and the possibility of symptoms being learned or revived on the basis of previous experience. Mace (1992a) points out that Freud explicitly distinguished between symbolisation and conversion as psychological mechanisms, holding that the mechanism of symbolisation had its place “in some sense, midway between autosuggestion and conversion” (Breuer & Freud, 1895, p. 180). According to Freud it was uncommon for the determining cause of the hysterical symptom to be merely a symbolic relationship. More was made by Freud’s followers of the importance of symbolism (see Chapter 24). Freud’s ideas on the relationships between motives and symptoms in hysteria were part of a set of concepts concerning conflict, repression, and mental mechanisms, as already indicated. At first, some of the explanations of symptoms which solved problems were complicated by the use of the label anxiety-hysteria. This term was employed to cover phobias and free-floating anxiety (e.g. Freud, 1917) and to distinguish them from such hysterical complaints as paralyses, anaesthesias, and other symptoms with loss of function, which were called conversion-hysteria. Conversionhysteria, anxiety-hysteria and obsessional neurosis were then all linked together as subgroups of the so-called “transference neuroses” (Freud, 1917), on which the theories of psychoanalysis were founded. Indeed, Freud claimed that it was with these conditions that psychoanalysis was most successful as a treatment. Despite the above complication and despite the inaccuracy of Freud’s claim of therapeutic benefits, his concepts have dominated the notion of hysteria ever since they were first enunciated. Psychoanalysis has been no more successful and much less efficient than many rival techniques of treatment in the therapy of conversion and dissociative symptoms. However, the use of psychoanalytic hypotheses for understanding the patients has been
40
History and concepts
largely unavoidable. We cannot really talk about hysterical complaints without using the general scheme of dynamic psychiatry, even when we have reason to reject some of the specific hypotheses. Like Freud, both Charcot and Breuer had held that sexual problems were an important cause of hysterical symptoms, but they were unwilling to declare the fact publicly. As is well known, Freud found, in his first researches into hysteria, that his patients related to him episodes of seduction by close members of their family as the basis for the conflicts producing their symptoms. He soon discarded this view, after some embarrassment, but in its stead he arrived at the formulation that sexual wishes in childhood formed the basis for adult conflicts (Freud, 1905). In this view the hypothesis of infantile sexuality was linked with the idea of the Oedipus complex: every child is said to desire the parent of the opposite sex, to have repressed this wish and to have a consequent castration anxiety or penis envy. The notion of sexuality was broadened to that of libido, in which all forms of primary pleasurestriving are included. This theory does not command widespread acceptance. Most psychiatrists agree that it can be found to fit some patients precisely and in detail. Others seem to have their symptoms and conflicts for reasons which are not mainly sexual. The businessman who develops amnesia when faced with bankruptcy, or the soldier who is afraid to fight or to show cowardice and so develops a paralysis, does not have a problem in which sex plays the leading role. Freud (1917) argued that narcissistic attachments of the libido to the ego provided the basis on which traumatic neuroses occurred. In other words libido, which may originally have been fixated at a genital level, becomes fixated to the ego. The businessman might have been attached to his work as much for the gratification of his emotional needs, which it provided, as for the money which he earned from it (and might have over-reached himself as much for psychological reasons as for financial ones). The soldier’s paralysis may be engendered by a castration anxiety as well as by fears of battle. The libido theory provides a theory of how irrational emotions may underlie seemingly rational dilemmas. Abraham (1921b), who had worked with psychiatric casualties of the war, supported this view with case histories and with the argument that fully healthy individuals did not succumb to traumatic neurosis. They were able to renounce all narcissistic privileges (i.e. self-interest), to give up their narcissism and to sacrifice their ego for the community. The few cases he quotes, although well described, are not enough, however, to support the general argument. The argument itself lacks cogency if we consider
The contribution of Freud
41
the very large numbers of previously normal men who broke down in the trenches. Freud (1926) took a more sophisticated line when he dealt again with this topic. He wrote: “any ... contradiction has long since been disposed of by the introduction of the concept of narcissism which brings the libidinal cathexis of the ego into line with the cathexis of objects and emphasizes the libidinal character of the instinct of self-preservation.”
This argument permits a comfortable escape from the original, narrow formulation. For practical purposes a sexual aetiology of hysteria is often not accepted in routine work with individual patients, or else it is considered of minor importance. In other instances, sexual abuse is now taken very seriously as a possible cause not only of hysterical symptoms but also of personality disorders and chronic pain (see Chapter 12). The cases where sexual abuse seems least relevant are particularly those seen during wartime and in connection with monetary issues such as claims for compensation (Henderson & Gillespie, 1950). A tendency also to interpret symbolically such events as the phenomena of epilepsy has not found favour. For example, the views that tongue-biting in convulsions “is no more inconsistent with hysteria than with love-making” and that incontinence “merely represents the infantile form of a violent pollution” (Freud, 1909) are neither logically sound nor pragmatic. They have, in fact, encouraged some of the more extreme and less realistic speculations which disfigure the psychoanalytic literature. The very first case of Breuer & Freud has itself been subjected to a good deal of reinterpretation. The patient, described as Anna O., was actually Bertha Pappenheim. Her name was disclosed by Jones (1953) on the grounds that she deserved to be commemorated as the real discoverer of the cathartic method. This notion of the release of feeling is actually much older. It dates from Aristotle and was described by Jacob Bernays (the uncle of Freud’s wife) and employed and reported by Janet (1886) among others before the publication by Breuer & Freud (Jackson, 1994). Since the disclosure by Jones, a good deal of biographical information and a lot more discussion has been devoted to her. The interest of this discussion is that it has highlighted the possibility – I would say the strong likelihood – that the principal diagnosis in this case is not what we would now call hysteria but rather a severe depressive illness. Although there were unquestionable hysterical manifestations during the course of the illness, I have argued that the disorder is best characterised as a severe depressive illness
42
History and concepts
provoked by the illness and subsequent death of the patient’s father (Merskey, 1992b). She was 21 years old when she first fell ill in the period between July and December 1880, and does not appear to have fully recovered until more than two years later, while some relapses occurred over another five years. For a while, she became dependent upon morphine, which had been used as a sedative by injection, and also, during her illness, experienced frightening hallucinations of black snakes among others, and rapid fluctuations of mood. Some of the latter may well be attributable to the fact that Breuer was hypnotising her regularly, and producing what the hypnotists of the day called ‘somnambulism’, which currently would be regarded as a hypnotic state with, in her case, ‘absences’ and a ‘condition seconde’. After recovery Bertha Pappenheim became a very energetic and distinguished social worker and author, writing short stories, theatrical pieces on social themes, travel accounts, and studies on the conditions of Jewish women and on the occurrence of criminality among Jews. She founded the League of Jewish Women in Germany and a magazine of social work and also campaigned actively against white slavery (i.e. enforced prostitution). The evidence that she was depressed includes low spirits, even melancholy, weakness or fatigue, loss of appetite, insomnia and hypersomnia, anxiety, gloomy thoughts and suicidal ideas, which all persisted or recurred repeatedly. Superimposed on, or accompanying this pattern, were some prominent hysterical symptoms. Today it is hard to know whether these were there initially or whether – as seems more probable – most of them were provoked by the patterns of treatment, which involved hypnotism and a good deal of suggestion inherent in the manner in which she was examined (Merskey, 1992b). This diagnosis of depression was first suggested by Spitzer et al (1981) and seems the most likely, although many other diagnoses have been offered, including schizophrenia, a borderline state, a toxic psychosis based on morphine addiction, multiple personality disorder, tuberculous meningitis, sarcoid, and complex partial seizures. However, a depressive illness is the most economical diagnosis, particularly when viewed in terms of the patient’s subsequent recovery and highly energetic temperament thereafter. The above considerations do not take away the diagnosis of hysterical symptoms but do change the view we would have of the principal illness. Interestingly, this is not necessarily very different from that of Breuer in the 1880s, inasmuch as Hirschmuller (1989) points out that hysteria was seen as a condition in which there were acute episodes and also widespread nervous change,
The contribution of Freud
43
together with such particular psychological phenomena as loss of function in speaking or writing, which were quite obvious in this case. There was no requirement at the time for Breuer and Freud to reject or minimise the diagnosis of hysteria simply because the patient was also depressed, and Hirschmuller observes that in Breuer’s student days hysteria was looked upon as “a so-called general neurosis” without definite localisation in the nervous system. Thus the function and significance of hysterical symptoms was probably first worked out by Breuer and Freud with respect to a patient who was primarily depressed and in whom the hysterical phenomena were relatively secondary (Merskey, 1992b). Notwithstanding the above, the ideas which Freud contributed remain important, as already indicated. His consistent emphasis on psychological motives in the causation of symptoms; his description of repression and the mechanisms of defence; his recognition of conflict as the basis for symptoms; his description of the transference; his acknowledgement of motives, like sex, which were not previously acceptable in open discussion; and his attribution of symbolic meaning of symptoms – these have all been powerful tools in the elucidation of hysterical phenomena. Freud made a further contribution with his views on emotional relationships in the hysterical personality. The recognition of hysterical personality traits is common both to him and to others, like Kraepelin (1904) (cf. Appendix B; Janet, 1894; Jaspers, 1913; Alam & Merskey, 1992), and was inherited by them from the clinical awareness of previous generations of physicians. Freud did not actually write about the hysterical character or the hysterical personality, although he did initiate the analytic study of personality with his article on character and anal eroticism (1908). Perhaps he took certain hysterical traits for granted in his work, but later analysts, starting with Wittels (1930), saw the hysterical character as one in which there was a failure of emotional development, libido being fixated at an infantile level. This is an important concept which will be discussed in detail subsequently (see Chapter 24).
Psychophysiological symptoms Another issue requires brief mention at this point. In the light of the notion of symptoms due to conflict and affected by the will, we are able to think of hysterical symptoms as independent of any local physical disturbance; they are not attributable except in an indirect manner to a lesion of nerve pathways. Yet some of Freud’s
44
History and concepts
followers have not been able to drop completely the idea that there is a pathological, local ‘innervation’ of the affected portion of the body. Franz Alexander provides a good illustration of this trend. Alexander (1950) adopted a view which is widely accepted that symptoms due to autonomic disturbance are involuntary and can be distinguished from conversion symptoms because unconscious control over them is not possible. It is at least very unusual, even though some work with biofeedback suggested it might sometimes occur (Miller, 1974), but that work could not be replicated. In any case, the extent of voluntary control over autonomic symptoms is very limited. Those symptoms which are due to muscle tension are in a similar category to autonomic effects in that, like the majority of autonomic nervous system responses, they are generally accepted as psychophysiological. If they are related to an unconscious emotional state, they are not problem-solving, but rather epiphenomena of physiological adaptation which may be poorly controlled and maladaptive. Alexander expresses this common view when he says: “the only similarity between hysterical conversion symptoms and vegetative responses to emotions lies in the fact that both are responses to psychological stimuli. They are basically different, however, in their psychodynamics and physiology.”
For some reason Alexander (1952) and Alexander & Szasz (1952) blurred this excellent distinction and Alexander (1963) continued to confound it. Alexander (1952) wrote about conversion as follows: “The pent-up tension may ... be relieved by changes in the field of the skeletal and laryngeal muscles or in the sense organs. These changes (paralyses, muscular contractions, spasms ... blindness, deafness) have a symbolic meaning and serve both the expression and the negation of the repressed ego-alien tendencies.”
Alexander & Szasz (1952) talked of “expressive innervations” which were “specific physiological processes such as weeping, laughing, blushing, sighing, etc. which take place under the influence of specific emotional factors”, and Alexander (1963) commented: “Physiologically, conversion is no different from any normal innervation by which we express emotions, such as weeping, laughing or blushing or from voluntary behaviour ... Repression inhibits action, and since the tension caused by the unconscious tendency cannot be relieved it becomes a chronic innervation.”
The contribution of Freud
45
These last views contradict his original statement and are not compatible with the definition of a conversion or dissociative symptom as a problem-solving mechanism, originating in emotional conflicts, except when the physiological response happens inadvertently to solve a conflict. They muddle together the idea of biological adaptive responses, which is the normal function of psychophysiological symptoms, and the idea of conflict-solving thought processes, which is the fundamental Freudian notion of conversion hysteria. They also throw away the whole point of the neurological and psychiatric distinction between symptoms due to lesions or dysfunction of pathways and those due to unconscious ideas expressed through the voluntary musculature. Others besides Alexander altered the meaning of conversion. Ferenczi (1919), in Mace’s expression, readopted the term to distinguish one subset of physical symptoms from those which he attributed to a mental origin which caused “materialization”. The products of conversion were distinct from other materialisations because they were displacements of a genital impulse only and were couched in “a peculiar symbolic language” that he termed the “hysterical idiom” (Ferenczi, 1919, p. 100; Mace, 1992a). These comments seem to retain the purely psychological hypotheses without mixing them, as did Alexander, with psychophysiological effects. Fenichel (1945, p. 236) seems to have had a similar degree of caution, saying “not all somatic changes of a psychogenic nature should be called conversions because not all are translations of specific fantasies into a body language”. For the latter he introduced the category of “organ neurosis”, which may or may not be an improvement. In this whole group of confusing comments the palm probably goes to Deutsch (1959), who remarked (p. 95), “The symbolization of external objects leads to a retrojection of these lost objects via sensory pathways onto and into the body where they remain immanent and dormant”. In the subsequent pages of this book, many bodily symptoms are considered which may be either psychophysiological or due to a conversion or dissociative process. While any symptom, organic, psychophysiological or hysterical, may be used to serve a hysterical function, it remains the case that organic and psychophysiological symptoms are demonstrably different in their mechanism of production from those which are primarily hysterical in origin. Some later analysts (see Chapter 24) have unfortunately followed Alexander’s confusing example.
46
History and concepts
5
Combat hysteria
The effects of fear on men in battle must have been known and recognised since the dawn of history. Philippopoulos (1981) suggested that one of the earliest accounts, or even the first one, was given by Herodotus (c. 484–420). A Greek soldier at the battle of Marathon who had fought well was neither stabbed in any part nor shot but went permanently blind. Whether or not Herodotus’ case was one of hysteria, it exemplifies brave behaviour under stress followed by a permanent symptom without a physical explanation. These phenomena were particularly prominent in World War I. Overt hysterical symptoms seem to have occurred on an unparalleled scale during World War I. The conditions under which it was fought, the social attitudes to which it gave rise, and an initial lack of understanding by physicians, all contributed to produce large numbers of men with somatic complaints of psychological origin. These complaints included a wide variety of hysterical manifestations. Despite the horrors of World War II, the casualty rate for combatants was much less than in the war of 1914–18. The persistent bombing of civilian targets, the Nazi campaign of genocide against Jews and gypsies, the appalling barbarity of the Gulag Archipelago described by Solzhenitsyn (1973), the terrible outrages practised by Japanese on prisoners, and the destruction of two Japanese cities by atom bombs all affected people who were noncombatants or no longer engaged in a fighting role. Those who suffered were not then bearing arms, nor could they escape from their danger by a retreat into illness. In concentration camps this merely hastened death. Flight from bombed cities was, of course, open to some civilians. On the other hand, soldiers in World War 46
Combat hysteria
47
I experienced conditions of great discomfort and danger but could, if ill, escape from those miseries and hazards which oppressed them. The miseries and hazards were substantial and the death rate enormous. At the same time popular feeling fiercely condemned men who would not fight, while the gallant wounded were praised and esteemed. It is hardly surprising that large numbers developed symptoms of illness without any organic foundation, so being honourably relieved of military service and perhaps even securing a pension. The phenomenon occurred equally among the forces of the central powers and France, Britain and their allies. Reading Kretschmer’s (1948) descriptions of his wartime cases, and the various British writers on the topic, one obtains an impression of the same problems, faced in the same way with similar results. After the war, the lessons which had been learned had a direct influence on the practice of physicians in subsequent decades as well as on the theory of the illness. This chapter will deal mainly with the British literature, noting also the views of Babinski, which derived from the analysis of French experience. Kretschmer’s views are dealt with in Chapter 6. The French experience was, of course, very extensive, and is comprehensively documented by Southard (1919), together with many of the papers from other languages. Comparable problems were apparently elucidated by Russian authors during the Russo– Japanese War of 1904–6 (Baker, 1975). They recognised a condition amounting to traumatic war neurosis and marked by confusional states and brief hysterical excitement going on to irritability, fearfulness and emotional instability. The literature immediately before World War I contained a number of ideas which led to the characterisation of hysterical symptoms in the British forces as shell-shock. The groundwork for this term evolved from a concept of ‘commotion’ or ‘concussion’ of the brain and spinal cord. The story is worth telling in some detail as a classic example of hysteria on an exceptionally large scale. It also has a number of other implications in psychiatry. ‘Concussion’ comes from the Latin words ‘con’, meaning together, and ‘quatere’, meaning to shake, strike, or dash. The Oxford English Dictionary cites a work by R. Copland, Galyen’s Terapeutyke of 1541, as follows: “The solution of contynuyte called ecchymosis in greke cometh most often with concussyon and ruption”, and in 1656, Ridgley in Practical Physic says “Concussion of the Brain is made from an external cause”. Courville (1953) reviews the history of theories distinguishing between concussion, contusion and compression of the brain.
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History and concepts
Bailey (1906) wrote (p. 91) that: “Concussion occurs in varying degrees. In the mildest form, after a blow, there is a dazing or confusion which is only momentary.... In the more severe degrees concussion is a much more serious matter.” By comparison, contusions of the brain were described as “bruisings, by which nerve tissue, connective tissue, and blood vessels are injured”. Charles Bland Radcliffe (1880), physician to the Westminster Hospital and to the National Hospital for the Paralyzed and Epileptic, described concussion of the spinal cord in a standard textbook A System of Medicine, edited by Sir John Russell Reynolds, as follows (pp. 1016–1017): “Concussion of the spinal cord, like concussion of the brain, is the result of a fall or some other accident, and its symptoms vary with the intensity of the shock.... The appearances after death may be those of haemorrhage more or less extensive.”
These opinions reflect a general view that some type of disturbance to the nervous system might be physically produced, without haemorrhage, either by temporary disablement of cells, or perhaps by the disruption of their connections. Erichsen (1866, 1886) developed the idea strongly in relation to railway accidents. With the spread of railways throughout the 19th century, accidents and collisions inevitably occurred. According to Erichsen (1886, p. 1): “These injuries of the spine and of the spinal cord occur not infrequently in civil life ... but in none more frequently or with greater severity than in those sustained by persons subjected to the violent shock of a railway collision.”
Trimble (1981) points out that one of the themes of Erichsen’s book is that organic lesions can follow relatively mild trauma. Naturally, this position supported claims for compensation for injury. Page (1883) objected. He analysed Erichsen’s case histories, and often found evidence of significant physical injury, such as fractured vertebrae. He argued that “purely physical causes” could explain the symptoms of general nervous shock after frightening railway accidents. Page also reasoned that those cases of a “concussion of the brain”, in which symptoms persisted, generally had “definite structure lesions” and that transient loss of consciousness without disruption of brain tissue would normally be followed by a full recovery. He claimed that a similar “shake” of the spinal cord would have no lasting effect. There were also some American writers (e.g. Hodges, 1881; Putnam, 1883; Walton, 1883) who were sceptical of Erichsen’s theory.
Combat hysteria
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In addition to the above, Reynolds (1869) and Charcot (1889) had both shown that physical complaints might be due to psychological causes related to specific ideas. Clearly, Freud’s work in which the hysterical symptom was understood to be the result of conflict and repression was also available, but not very well regarded for the most part. In contrast to these, Oppenheim (1889, 1911) attributed the symptoms of concussion to functional disturbances “produced by molecular changes in the central nervous system”. Richards (1910) reviewed the then current information available from the Russo–Japanese War. For the most part the patients seem to have been classified in traditional categories such as depression with hypochondriasis, depression with acute mental confusion, or stuporous conditions, but the most immediate results of battle were recognised as hysterical excitements and confused states. These were held to clear up usually in a few days, but irritability, fearfulness and emotional instability remained for weeks. Russian soldiers greatly feared Japanese grenades, which on bursting released quantities of brownish-blue poisonous gas, and it was said that men in the immediate vicinity were prostrated by the gases and often remained unconscious for several hours; on awakening these men were deaf and dumb but after some weeks gradually regained their speech and hearing. Since the gas only spread over an area of ten feet or a little more and physical signs were limited, there was an impression that many of the cases had a large hysterical element. Many cases of neurasthenic and hysterical conditions were recognised, including hysterical fright with great excitement and confusion, ending finally in the semi-conscious state with great mental and bodily weakness. Traumatic psychoses were also recognised. “Traumatic neurosis (no evident wound)” is listed by Richards from one report as occurring among 25 350 soldiers who had been examined. Two well known French catastrophes also contributed substantially to knowledge of the topic. The ships Iéna and Liberté had exploded at Toulon in 1907 and 1911, respectively. Hésnard (1914) described the effects on survivors, after eliminating cases in which physical commotion of the brain or other direct organic causes might have been relevant. He recorded typical symptoms of post-traumatic psychological responses, which were previously recognised and have been repeatedly observed in wars and catastrophes in this century. These included an initial state of semi-somnambulism, automatic mental activity, absorption in some trivial occupation such as an exclusive preoccupation in the attempt to save some garment, a strange lucidity and feeling of exaltation, and a period of amnesia. The rescuers also showed symptoms of
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History and concepts
disturbance for several weeks, including recapitulation of the scene, terrifying dreams, diffuse anxiety, fatigue, and various minor phobias. This knowledge of emotional change after explosions, quickly abstracted in English, became part of the contemporary climate of ideas (Brown & Williams, 1918).
Shell-shock The exact origin of this term is unknown, but it caught on among the forces of the British Empire like wildfire. In December 1914, Elliott described four cases of “transient paraplegia” from shell explosions. In three, he recognised significant physical injury: all three were considered to be at risk of being diagnosed as hysterical. In the fourth case, however, Elliott accepted that his patient’s symptoms were indeed hysterical. He emphasised both that organic disease could be overlooked and that “functional disorders of the nervous system” were common after a “big shell explosion”. Two months later, on 13 February 1915, Myers (1915) seems to have used the term in the medical literature for the first time, although the Oxford English Dictionary (Murray et al, 1986) incorrectly states that Evans was the first to use the term in December 1915. Myers’ first patient, a private, had experienced shells exploding both in front of and behind him. “Curiously, the one in front cut his haversack clean away, and bruised his side, and apparently it burned his little finger. His eyes burned and were blurred and he developed hysterical blindness as well as loss of the sense of taste and smell. He was cured by suggestion.”
After describing this and two other patients in considerable detail, Myers writes, laconically, “Comment on these cases seems superfluous.... The close relation of these cases to those of ‘hysteria’ appears fairly certain.” Viets (1917) states that Myers’ article is the first recorded use of the term known to him, but that it came into use in the British Army in the latter part of 1914. A search of The Times from the onset of the war to 13 March 1915 found only one reference to ‘shock’, on 6 February 1915 (p. 5), but without the prefix ‘shell’. This related that the War Office was arranging to send soldiers suffering from shock to be treated in special wards at the National Hospital for the Paralysed and Epileptic, Queen Square, London.
Combat hysteria
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Table 5.1. Official British figures for psychiatric illness in soldiers in 1914: “Functional nervous diseases among imperial troops, August–December 1914” United Kingdom officers other ranks Neurasthenia Traumatic neurasthenia Hysteria Shock Shell-shock Totals
20 – – – – 20
321 10 50 15 – 396
officers 65 – – 23 2 90
France other ranks 279 8 11 114 18 430
From Macpherson et al (1923).
The official history of the war (Macpherson et al, 1923) gives a table of functional nervous diseases from the outbreak of war to the end of December 1914 (Table 5.1). Using slightly different criteria, the following numbers of British battle casualties in France, combining officers and other ranks, were recorded as cases of shell-shock: September–December 1914, 9; January–June 1915, 141; July–December 1915, 1246; January– June 1916, 3951; July–December 1916, 16 138; January–June 1917, 3010; July–December 1917, 4038. The rise in numbers was associated with the first battle of the Somme, which took place from July to November 1916, and was not a success for the Allied forces. Colonel A. B. Soltau stated to the post-war War Office Committee of Enquiry into Shell Shock (1922, p. 72): “there were one or two cases in the fighting line in May, 1915, and September, 1915, but nothing which really attracted attention.... It was not until the Somme that it became an appreciable problem in the field ambulance.... We were flooded ... with cases in the latter stages of the Somme.”
The official figures by month and year also show the gradual growth of the notion. However, the fact that in the official history some cases of shell-shock are dated 1914 does not prove that they were actually given the label in 1914. These were probably patients who, having spent time in hospital, were thus labelled on discharge. ‘Shell-shock’ was rare in earlier wars. The only direct evidence was an account of nervous injuries produced at a distance by the projectiles of war, given by Professor Octave Laurent, in his book La guerre en Bulgarie et en Turquie, published in 1914 (War Office Committee of Enquiry into Shell Shock, 1922, p. 109). In one chapter, Laurent (p. 367) describes a condition which he terms
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History and concepts
“Commotion Cérébrospinale” or “Nervous Injuries Produced by Projectiles”. They follow the explosion of a shell and may or may not be accompanied by signs of contusion. The effects of commotion may be slight, manifesting numbness, formication, and hyperaesthesia, with or without loss of consciousness, or they may be serious, provoking arrest of functions, where the injured falls into a torpor, inert as if struck by lightning, with all four limbs and the sphincters paralysed (War Office Committee of Enquiry into Shell Shock, 1922, p. 109). It was expected that the effects of shells might be worse in 1914 than ever before; all observers recognised that exposure to explosions had multiplied. Instead of round cannonballs, which only killed where they hit, shells were available which travelled to their destination with increased velocity and better aerodynamic qualities. They carried high explosive of greater force than formerly, and would burst on impact. The gases generated by the explosion produced a shockwave in the air, more destructive than a single cannonball. In battle, men near whom a shell exploded might be seen being thrown for a distance of 15 yards (Mott, 1916b), while others had been seen to be thrown 12 or 15 feet upwards into the air (War Office Committee of Enquiry into Shell Shock, 1922, J. C. Dunn, p. 105). Squadron Leader W. Tyrrell (War Office Committee of Enquiry into Shell Shock, 1922, p. 105) had observed the death of men blown up without external signs of injury. Stones, earth, walls, buildings, the ramparts or dugouts – all might crumble. Soldiers were exposed to continuous bombardment from many guns, with numerous shells exploding in the vicinity. The prolonged noise and physical disruption of their environment could be enough to make many feel that they were being subjected to ‘shockwaves’. General Lord Horne (War Office Committee of Enquiry into Shell Shock, 1922, p. 1) commented that: “shell shock became a serious factor in this war owing to the peculiar character of the war. The high explosives and the bombardments had never been known before.”
He added prophetically that, “In moving warfare we should not experience anything like it” (p. 60). The French also described nervous changes from ‘concussion’ (in French ‘commotion’) (Sollier & Chartier, 1915). Ravaut (1915) like Mott (1917) reported the death of individuals from the bursting of a shell without external signs of injury and looked for postmortem findings of haemorrhages in the nervous system which could account for death. The search for an organic explanation was
Combat hysteria
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perhaps supported also by an increasing recognition that many men who had given very good service and were thought of as basically courageous (even one winner of the Victoria Cross) manifested similar symptoms after having been subjected to prolonged and often serious stress and danger. The Royal Society of Medicine held a “Special Discussion on Shell Shock Without Visible Signs of Injury” on 25 January 1916 in the Section of Psychiatry, presided over by Major F. W. Mott, MD, FRS. Mott (1916a) pointed out that: “the forces producing shell shock are most commonly generated by the explosion of large shells, but also by mines, aerial torpedoes, whizz-bangs, trench mortars, bombs and hand grenades charged with high explosives. In a large number of cases, although exhibiting no visible injury, shell shock is accompanied by ‘burial’. Sandbags may be dislodged from the parapet of the trench and strike the individual on the head or spine, and cause concussion without visible injury, or the roof of a dugout may fall in. While lying partially buried he may be subject to the inhalation of noxious gases, so that a combination of causes may account for the severe effects of shell shock.”
The tenor of his view at that time was clearly to accept the reality of shell-shock as a frequent physical effect, even though he readily recognised alternative diagnoses. By contrast, Henry Head vigorously rejected shell-shock as a category, holding it to be “a heterogeneous collection of different nervous affections from concussion to sheer funk, which have merely this much in common that nervous control has at last given way” (Head, 1916). The forces which might cause nervous control to give way were formidable. The battle of the Somme, which lasted four months, cost the British 420 000 casualties, the French 194 000 and the Germans 440 000. It was calculated that in World War I the allied and associated powers mobilised more than 42 million men and lost more than five million lives. Russia and France contributed some 60% of the dead. Another 21 million men were wounded. In Britain, the social atmosphere which advocated persistence in the face of these awful figures was one of intense patriotism and loyal service. The misery of all and the stoicism of many emerge alike from the poetry of Wilfred Owen and the writings of men like Siegfried Sassoon (1936), Robert Graves (1929), and Edwin Vaughan (1981), or the historian John Keegan (1976). To the man in the ranks, the war meant being willing to serve, being ostracised, imprisoned, or shot for evasion of duty, or perhaps being ‘lucky’ enough to be ill. Judge Babington’s book For the Sake of Example:
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History and concepts
Capital Courts Martial 1914–1920 (1983) describes the execution of 269 men for desertion, cowardice, or quitting the post in the face of the enemy. Illness provided a respectable escape. Ritchie (1986) explored the attitudes of ‘imperial man’ to warfare. The stereotype of the good soldier or officer was of someone marked by comradeship, loyalty, the stiff upper lip, courage and endurance, who played by the rules without complaint. Doctors identified with these ideals: in fact, to function well as a medical officer, the doctor had to operate as an agent of the military purpose. His role was not simply to attend to sick men and see they were sent into battle, or to repair the injured. He also needed to promote self-control, moral stamina, and military devotion. It was his responsibility to certify either that a man had ‘shell-shock’ or ‘neurasthenia’ and should be removed from the firing line, or that he was a coward, shirking duty, who deserved to face a court martial and even perhaps capital punishment. Babington pointed out that the medical officers were frequently more indignant about the cowardice of deserters than were other army officers. However, the medical officer himself was at least one stage less involved in battle than the men whose cowardice he was rejecting. The special emphasis on shell-shock was not followed in Germany. In September 1916, German neuropsychiatrists meeting in Munich rejected the hypothesis of organic causation decisively, with respect to the majority of cases. This is described in English in the Journal of the American Medical Association (1917). Oppenheim opened the discussion and argued that a neurosis produced by psychic causes would have the same brain patterns as one due to concussion. ‘Fright neurosis’ and ‘commotion neurosis’ were both traumatic neuroses. Disturbances could be found which were not hysterical, although he admitted that he had underestimated the spread of hysteria. Nonne opposed him strongly. Traumatic neurosis was not a distinct entity. The shell-explosion neuroses were purely functional and curable by psychological techniques. Neurasthenia could occur in stable individuals through fatigue and exhaustion. (We note that this excuses illness in the brave.) Oppenheim’s views were against the economic interests of the state and the therapeutic needs of the patient. Most cases were hysteria. Gaupp and the majority of those present supported Nonne. Oppenheim retired from the argument, disappointed but without changing his view. The British meeting in January 1916 at the Royal Society of Medicine clearly achieved much less than the German one eight months later. However, understanding of the
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psychological basis for the symptoms was developing in Britain in 1917, and a new procedure was adopted, perhaps prompted initially by Myers (see Myers, 1940, p. 92). Early in 1917, all cases presenting symptoms of functional nervous disorder were sent to special hospitals as ‘NYD’ (not yet diagnosed). If there had been direct contact with the effect of explosions, even though there was no visible external wound, a diagnosis of “shell-shock (wound)” was made, while other cases of ‘nervousness’ were classed as neurasthenia, hysteria, and so on. After June 1917, when special neurological centres had been established in each army area, all cases of functional nervous disorder were marked ‘NYDN’ (not yet diagnosed, nervous) and transferred to the centres. Army Form .3346 was introduced to determine whether the man was ‘wounded’ or ‘sick’, but this procedure turned out to be unfair and unworkable. In September 1918, it was eventually decided to abolish the classification of “shell-shock (wound)” in France and to use it only if the patient’s disability was so serious as to necessitate transfer to England. There the decision to classify the patient as a battle casualty would depend upon the recommendation of a neurological board at a special centre (War Office Committee of Enquiry into Shell Shock, 1922, p. 119). This sequence of events and the time at which it began clearly reflect the efforts of the army medical authorities to resolve the difficult practical issues which were arising out of the concepts of shell-shock. In time, the literature on this topic provided a series of monographs. The authors included Harris (1915), Hurst (1916), who produced two more editions of his original volume in 1918 and 1940, modifying his views each time, Hurst (1920), Smith & Pear (1917), MacCurdy (1918), Yealland (1918), Lépine (1919) and Babinski & Froment (1918). Mott (1919) moved away from his original view that shell-shock was mostly due to organic causes. Among American authors, Southard provided a tremendous collection of reports from all the belligerent countries, with brief comments of his own and, together with Fenton, compiled an extensive bibliography (Southard, 1928). In addition to the British official war history, there was also the United States Army Report (Salmon & Fenton, 1929), and a collection by Brown & Williams (1918) which comprised a bibliography with abstracts from the different combatant countries. Fenton (1926) wrote a personal appraisal. The most notable American work was probably that by Salmon (1917), The Care and Treatment of Mental Diseases and War Neuroses (‘Shell Shock’) in the British Army. Salmon’s work brought
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History and concepts
together the most important lessons of World War I, and his recommendations were applied immediately to the American expeditionary forces. The fact that the German authors rejected the diagnosis of shellshock and the organic explanation is probably due in part to the greater success of the German armies at the onset of the First World War. Holmes (War Office Committee of Enquiry into Shell Shock, 1922, p. 38) observed that more cases of shell-shock occurred during prolonged engagements, especially when these were not successful, and much less frequently when the fighting was successful, for instance during the autumn of 1918. Noy et al (1983) showed that battle stress was an accurate predictor of psychiatric casualties in Israeli forces in Lebanon, battles with low stress having few physical and psychological casualties and battles with high stress having many. In general when winning wars easily, as in the Suez Campaign of 1956 and the Six Day War in 1967, Israeli attitudes and policies discounted the occurrence of post-traumatic stress disorder, but this attitude changed in the face of the greater numbers of casualties which occurred in 1973 in the Yom Kippur War and in 1982 in Lebanon. Copp & McAndrew (1990) described the evolution of the same problems in Canadian soldiers. In the end a large proportion of the symptoms of shell-shock was recognized as hysterical and another segment as related to anxiety. The hysterical symptoms listed by Hurst (1920, 1940) under war conditions included: cutaneous anaesthesias and hyperaesthesias, similar disorders of the mucous membranes, blindness, deafness and hyperacusis, stammering, aphonia, mutism, contractures, bent back (camptocormia), tremor and paralysis. These were differentiated from true cerebral and spinal concussion and soldier’s heart and anxiety neurosis. As well as Hurst, Mott described most of these and also mental confusion and delirium, neurasthenia, astasias, ataxia, tics and choreiform movements. In the end Mott took his definition of hysteria from Babinski (1901), as follows: “Hysteria is a pathological state manifested by symptoms which it is possible to reproduce by suggestion in certain subjects with a perfect exactitude and which are susceptible of disappearing under the influence of persuasion (contra-suggestion).”
Like others, he regarded neurasthenia as equivalent to anxiety neurosis. But it is worth remarking that Babinski’s definition – despite the assertion by Mott that it commanded widespread acceptance – was rejected in France during extensive discussion in 1908 by Raymond, Dejerine, Janet, Claude, Pitres, Crocq and
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many others (Guillain, 1959). Some of the grounds for rejection included the fact that many hysterical attacks did not depend upon previous suggestion and also that emotion, contrary to Babinski’s concept, played a very important role in the genesis of these phenomena. Hurst, Myers, Yealland and others all agreed, however, that suggestion was an important factor both in the onset and in the cure of wartime hysteria. As was mentioned above, it had been noted quite quickly that the notion of shell-shock was rapidly contagious (Myers, 1940) and that it readily affected many men once the first case appeared and was known to them. Another term which was ‘respectable’ for longer than shellshock was ‘disorderly action of the heart’ (DAH) or ‘soldier’s heart’. These were popular diagnoses. Abrahams (1917) caustically characterised the excessive enthusiasm of many witnesses who were either greatly in favour of this diagnosis or denied its existence entirely. Mott and the other writers all tended to agree in regarding those cases of shock which recovered quickly as belonging to two classes: hysteria and neurasthenia. Lewis (1918) was never really happy with the diagnosis of neurosis. In his study The Soldier’s Heart and the Effort Syndrome he argued that the term ‘effort syndrome’ applied to physiological sensations (breathlessness, palpitation, precordial pain, etc.), the abnormality lying in the circumstances in which they arose. These circumstances were, for example, poor physical or mental endowment, the effects of exposure, hard work, unrecognised infection, and so forth. Graded physical exercises were recommended as an important part of treatment. It was left to Hurst (1940) to observe that “soldier’s heart is often nothing more than a manifestation of anxiety neurosis”. This alternative diagnosis, based on cardiac symptoms, is a story in itself, told among others by Gallavardin (1917), Jarcho (1966), Skerritt (1983), Wooley (1986, 1987, 1988), and Wooley & Boudoulas (1988). No one seems to have noticed that Da Costa’s first case of “irritable heart” (Da Costa, 1871) had an aphonia for ten months. Today, Wooley (1988) indicates that despite the associations of DAH or neurocirculatory asthenia with anxiety, it also has a relationship with mitral-valve prolapse and mitral regurgitation.
Treatment It became evident that treatment included both prevention and suggestion. The War Office report (pp. 43, 132, 158) gave great
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attention to questions of morale and its management in order to inhibit shell-shock. Babinski & Froment (1918), although they gave credence to the notion of structural damage from shellshock, also laid greater emphasis on the notion of suggestion, just as did Hurst (1920). Yealland (1918) was one of the most vigorous exponents of the role of suggestion in causing battle hysteria and removing it. He regarded hysterical symptoms as being produced by suggestion and thought that they should, therefore, be removable in the same way. In his early article with Adrian (Adrian & Yealland, 1917) he reported on patients treated at Queen Square at the National Hospital for the Paralysed and the Epileptic, as it was then. As a result many more patients came his way. His subsequent book describes in detail over 40 patients, nearly all soldiers, representing only a small proportion of the numbers treated. Their symptoms included mutism, aphonia, stammering, deafness, blindness, blepharospasm, foot drop, wrist drop, monoplegia, paraplegia, hemiplegia, tremors and fits. They were all treated with personal persuasion, in which he showed much resourcefulness, varying his approach according to the individual; at times ‘faradic electrical stimulation’ was employed extremely vigorously. Yealland makes no secret of the fact that he was curing resistant cases with whom others had failed, although hypnosis, psychoanalysis and faradic stimulation had been attempted for these patients elsewhere. Yealland’s work led to the conclusion that the doctor had to treat the patient with faradism himself and not delegate treatment to an auxiliary. An example may illustrate how a determined and resourceful doctor could secure an impressive remission of symptoms, albeit in a fashion which would today cause concern at the propriety of the measures employed. The treatment of case A2, a private who was mute for nine months, is described by Yealland (1918) as follows: “He was taken to the dark room and a faradic battery employed, the pad electrode being as usual over the lumbar spine and a key electrode attached. Then I said to him ‘I shall apply shocks to your neck over the larynx which is the seat of the trouble. When you feel the shock you will have an uncontrollable desire to explode a sound, but I want you to suppress it. Remember do not utter a sound; suppress it ... I fear that you will shout out but I warn you not to ...’. Immediately the current was applied to his neck he shouted out. This, of course, was what I expected from him. I said to him ‘shout again’ and he did so without the aid of faradism. Then he began to half-laugh and
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half-cry, recognising his voice had returned, and he attempted to take my hand and made an effort to kiss it, but I instantly refused, knowing that any sympathetic measure of this kind would prolong the period of re-education. Instead I said to him ‘there is no time now for you to yield to your emotions; you must be practical and put forth every effort to speak’. I then told him to repeat the alphabet while I quickly and abruptly faradised the neck during the time he was exploding each sound. In five minutes he talked quite normally. In a very pleased but less demonstrative manner he expressed his thanks.”
Yealland’s techniques appear to have been very successful. This was not just because of the invariable threat from roller electrodes, wire brush electrodes and so forth and their quite frequent painful use. He set out to establish a dominant role with his patients and did not give up. And despite the rough treatment he often supplied he never seems to have been contemptuous towards them on their recovery. Invariably he would say ‘your condition is curable’ and thus indicate that he regarded it as an illness. He left the patient in no doubt that he intended to provide the cure. Many of the same skills were employed by Hurst, although as a rule perhaps not so drastically. One viewpoint, however, which no one seems to have discarded completely was that true ‘shellshock’ could occur if there was actual cerebral concussion, as in civil life with loss of consciousness. Stupor, headache, amnesia, irritability and exhaustion could follow with quick recovery. Spinal concussion with or without a penetrating wound was also held to occur. Symptoms were long lasting and they tended to be a hysterical sequel to the physical organic ones, such as a hysterical paraplegia following an organic hemiplegia. Hurst’s main conclusions were very well summarised as follows (Hurst, 1940): “In the first two years of the war cases of this kind were given the unfortunate name of ‘shell-shock’ in the belief that they were organic in origin and the result of actual concussion caused by the explosion of powerful shells. Consequently no attempt was made to cure them by psychotherapy, and treatment by rest and sympathy helped to perpetuate the symptoms. This was all the more likely to occur owing to the use of the word ‘shell-shock’, which gave the patient the idea that he was suffering from some new and terrible disease. When at last the true nature of the condition was recognised, it was found that psychotherapy not only resulted in the immediate disappearance of the symptoms, when they were treated in the special advanced hospitals opened for the purpose by the British and French and later by the
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From the military viewpoint, these lessons were well learnt and by 1917 the United States Forces in Europe were operating neurological hospitals which returned about 60% of their patients to duty within 14 days. Most of these were suffering from neurosis (Baker, 1975). As in Britain, this did not completely coincide with jettisoning the notion of shell-shock as an organic condition. Mills (1919) wrote of it, “the designation has meaning ... in many cases it would appear that purely psychic influences have played the major role, but in others physical injuries have not been lacking”. The impact of all this military experience on subsequent views on hysteria was substantial. The first conclusions that were drawn, which continued to be accepted, were that hysterical symptoms are psychological in origin and serve a purpose: and that in literally scores of thousands – perhaps hundreds of thousands of cases – it was unnecessary to consider a sexual aetiology for the purpose of successful management of patients. Indeed, to have done so would probably have been a hindrance in many cases.
Effects on psychiatry One of the effects of the wartime experience was to emphasise the distinction between the psychiatrist and the neurologist in the treatment of so-called nervous disorders. Myers (1940) reports a direct personal clash between himself and Turner in this respect, but setting aside such a ‘turf war’ it became clear that psychological methods of management were of considerable importance and direct use. They were best practised by individuals
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with some inclination and training, who were identified as ‘psychologists’, albeit medically qualified. This was an extension of the skills in psychotherapy which had been practised by some, but perhaps a minority of psychiatrists. Those associated with the care of the insane had been much less concerned with this than others who, before the war, were involved in the study of emotional change in response to suggestion and hypnosis. It may well be the case that the maturation of psychiatry occurred in the course of World War I; it then became a specialty with potential for the community. Rees (1945), who recalled the period well, stated that the provision for exservicemen “led to the establishment of clinics for civilians” (p. 29) but did not give any decisive evidence. Stone (1985) also suggested that the clinics of the Ministry of Pensions led to the development of reforms and innovations in psychiatry in Britain after World War I; those psychiatrists who qualified just before World War II, or practised during it, shared the impression. Dr Myre Sim commented (personal communication) that prominent figures like T. A. Ross, D. K. Henderson, and Millais Culpin all received an impetus to work outside the psychiatric hospitals from their own wartime experience. Nevertheless, the influence of the war upon ideas about psychiatry, which Stone observes, was weak in respect of the creation of services. There is little evidence of new provision for civilians before the Mental Treatment Act 1930. The late Sir Charles Symonds told me that he had had great difficulty in finding psychiatric help for patients in London before World War II. This was so much the case that he would occasionally select patients from his hospital practice and arrange to treat them himself, as well as he could, at his consulting rooms. He gave them psychotherapy several times a week, in accordance with Freudian recommendations, and made no charge for this treatment. He gave this up because he was disappointed with the results, and felt that he was not succeeding with this technique as he should have done. However, some psychiatric provision was available in teaching hospitals in London in the early 20th century. In 1918, Bernard Hart functioned as the first physician for mental diseases to the Outpatient Department at University College Hospital. Hart had pointed out to the hospital authorities the year before that departments for mental diseases already existed at St Thomas’, Guy’s, Charing Cross, and St Mary’s Hospitals. In 1918, Hart wrote to the Dean of University College Hospital Medical School to draw attention to the inadequate arrangements for treating functional nervous diseases. There was only one
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private hospital, in Brighton, which could do this, but because of the problems of functional nervous disorders in the British army, special hospitals had been set up and medical officers were being carefully trained, for example at Maghull Military Hospital near Liverpool (Merrington, 1976, p. 227). Since the Ministry of Pensions was forced to set up over 100 treatment centres in an effort to cope with the flood of ‘neurasthenic’ ex-servicemen, Stone (1985) argued that it was the war and the consequent mass epidemic of mental disorders which set the mechanism of psychiatric change in motion. He claimed that the major innovations between the two wars, “Psychotherapy, and the 1930 Mental Treatment Act”, which promoted out-patient clinics and ‘voluntary’ treatment, were mainly the result of these pressures. The evidence for his contentions is still rather limited. Mayou (1989) described the history of general hospital psychiatry in Britain and showed that widespread, but very patchy, efforts at such treatment were known from the 18th century. He remarked on the interest of some other physicians in treating their patients’ minds as well as their bodies, but showed that out-patient clinics and general-hospital provisions were very limited between the wars. Approaches to psychological management and to psychotherapy were also known before World War I, even though their bias was towards hypnosis and suggestion (e.g. Tuckey, 1891). In particular, Myers argued that in the 25 years leading up to 1916, and following the work of Janet, Prince, Freud, Adler, Hart, Rows, Jones, and many others, psychotherapy was by then an established skill. As discussed below, the experience of the war probably did contribute to the spread of knowledge about psychological techniques but caused little institutional change, although it is plausible to suppose also that another ten years from 1913 might in any case have seen some spread of Freudian ideas and psychotherapeutic skill. The idea that symptoms could be motivated also often worked against patients and psychiatry to belittle both the sick and the therapist who accepted them. Morton & Wright (1987, p. 75), examining the pensions of Canadian veterans, described attitudes which are equally representative of those found in Britain (and were usually drawn from European experience): “Worst off were the ‘functional’ or ‘shell-shock’ cases. Whether doctors took them seriously or dismissed them as cowardly malingerers the consequences were virtually identical. Such men had subconsciously willed themselves into a primitive state [explained a neurologist, and army specialist on neurasthenia]. To give them pensions only encouraged them: ‘You have thrown away the four aces’.”
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It seems likely, nevertheless, that the war did make a difference in demonstrating the usefulness of the psychotherapeutic skills which were most developed by psychiatrists. Smith & Pear (1917) campaigned vigorously for the provision of services outside the asylums. They concluded (p. 132) that: “Excuses for inertia brought forward before August 1914 can be accepted no longer. The thousands of cases of shell shock ... have proved beyond any possibility of doubt, that the early treatment of mental disorder is successful from the humanitarian, medical and financial standpoints.”
Pensions were indeed a matter for concern. Macpherson et al (1923, p. 56) provide figures from the Ministry of Pensions which suggest that in February 1921, 65 000 men were drawing pensions for neurasthenia and allied conditions, and that by January 1922 this number had fallen to 50 000. However, in February 1921, 14 771 men were attending either boards for assessment or clinics for treatment. The number of people in these categories increased to 16 393 by November 1921, including some who had not previously been ill. If anything, the numbers of men receiving pensions seemed to increase after 20 years, in spite of the downward trend of the initial figures quoted above, and in contradiction to the ordinary expectation that the numbers would decline by attrition caused by death and, occasionally, recovery, without being replenished. Ahrenfeldt (1958, p. 10) summarised the situation with regard to pensions in Britain, some 20 years after the end of the war, as follows: “In March, 1939 there were about 120,000 pensioners who were still in receipt of pensions or had received final awards for primary psychiatric disability (including ‘neurasthenia’, ‘shellshock’, effort syndrome, epilepsy and insanity). ‘Neurasthenia’ itself accounted for some 100,000 men, costing 10 million pounds a year, and representing about 2% of total serving troops. These 120,000 cases represented about 15% of all pensioned disabilities.”
I have discussed this topic at length, partly because of the wealth of material which demonstrated the production of hysterical symptoms, and also partly because it has so many implications for future attitudes to hysterical symptoms and their explanations. This will appear in Chapter 7 and in discussions of compensation and the diagnosis of hysteria. Meanwhile, in connection with World War I, it is also important to review next the original and fundamental contribution of Kretschmer.
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6
Ernst Kretschmer
As has been indicated the experiences of World War I with regard to hysteria had a similar effect upon medical opinion on either side of the firing line. Ernst Kretschmer, who is well known for his description of the relation of constitution to mental illness, was one of the numerous German doctors who acquired ample knowledge of combat hysteria. His experiences led him to put forward a theory of hysteria which offered a fresh way of looking at the topic, without rejecting existing views. His work on hysteria was badly translated, is not well known in the English-speaking world and deserves to be better appreciated. Kretschmer recognised the current opinion, observing, “the notion that hysteria is a psychogenic pattern of reaction has won universal acceptance”. He noted that the line of demarcation from other psychogenic reactions was vague. However, ‘hysteria’ subsumed a nucleus of syndromes ranging from spasmodic seizures through paralyses, anaesthesias and hyperaesthesias to certain manifestations of the reflexes and the autonomic system, and he accepted that sexual immaturity and problems of sexual adjustment were common causes of hysterical manifestations in ordinary life (Kretschmer, 1948, pp. 29, 33). At the same time he looked at hysteria in a biological fashion, saying in his introduction: “The clinical designation ‘hysteria’ subsumes a certain nucleus of syndromes – spasmodic seizures, catatonic stupors, tremors and convulsive tics, paralysis and muscular contractions, anaesthesias and hyperaesthesias and certain manifestations of the reflexes and of the autonomic system, all in so far as they are of psychic origin.”
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He regarded these forms of behaviour as “ontogenetically determined patterns of reaction”, and he then went on to argue that they represented primitive forms of reaction with a survival value. Interestingly, Freud (1926) also perceived anxiety as being determined at birth, albeit by the universal birth trauma. Kretschmer pointed out that Mörchen, in discussing combat hysteria, had made the same sort of point as himself. Thus Mörchen is quoted as distinguishing between: (a) actions related to defence mechanisms and the like (b) the instinctive use of primitive means of self-preservation through automatic release of motor, sensory and autohypnoid mechanisms (c) systematic use of primitive means of self-preservation culminating in simulation. These distinctions were partly in the tradition of Freud and of Kraepelin. An alternative but overlapping viewpoint, expressed by Bonhoeffer, held that hysteria represented “a deliberately induced or self-imposed sickness, or a weakness or constitutional defect”. In Kretschmer’s opinion either definition would fit the majority of clinical pictures of hysteria; thus he came to the conclusion that “hysterical means psychogenic patterns of reaction in which a tendency to dissimulate finds expression through an instinctive, reflexive or other built-in survival mechanism”. Interestingly enough, he did not think that typology could contribute much to an understanding of these patterns. “Not characterology but the effects of an experience and external conditions are most important for many hysterical reactions.” Conditions which were to be related to hysteria included disability neurosis and fear neurosis. Disability neurosis was seen as a condition based upon an existing or previous illness, in which simulation was present, but reflex or instinctive mechanisms were absent. Fear neurosis was a condition in which anxiety and panic predominated, resulting in forms of stupor, convulsions and hypnoid states, as well as in a general affective disturbance. These neuroses were held to border on hysteria, since it was often difficult to make a sharp distinction. The essence of Kretschmer’s view is that primitive patterns of behaviour exist which show poor organisation but have survival value, and that these are the basic stratum in the structure of a hysterical condition. Two primitive patterns which human behaviour may resemble are the ‘instinctive flurry’ and the ‘death feint’. He illustrates ‘instinctive flurry’ as follows.
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When a young lady is faced with the problem of an undesirable marriage, she has two choices. She may proceed calmly and deliberately to take advantage of her adversary’s weaknesses, now resisting him energetically and now cleverly eluding him – with the result that by selecting words and actions appropriate to every new development, she finally reaches her goal. Or she may suddenly break down, tremble and quiver convulsively, roll and toss and work herself up into a frenzied state; she will behave in this way until she frees herself from the unwanted suitor. Two men cannot adjust themselves to the horrors of war. The first takes advantage of his superior penmanship, technical ability, and political connections; after weighing all the pros and cons, he manages by deft manoeuvring finally to sit behind a comfortable desk. The second is found wandering aimlessly through the trenches one morning following a heavy bombardment; taken away, he succumbs to violent trembling; he is placed in a psychiatric ward and subsequently in an office where he sees his more talented comrade already at work behind a desk. These are two possible courses of action. The first is for the most part peculiar to man. The second is a characteristic biological reaction common to all members of the animal kingdom, from one-celled creatures to human beings. When a swimming infusorian approaches a zone of hot water, it reacts by producing a flurry of rapid movements; this flurry persists until one movement carries the infusorian away from the zone of danger, whereupon it again swims calmly on. When a bee or a bird is imprisoned in a room, the creature does not retreat to a corner and try to determine how it can escape through an opening in the windows or door. Instead, instinctively drawn toward the light, it unleashes a flurry of movements; frantically and blindly it moves back and forth until at last one movement accidentally carries it through a crack in a window. Having won its freedom, it immediately resumes its placid flight. The ‘instinctive flurry’ (Bewegungssturm) is a typical reaction of animals to situations that threaten or interfere with their existence. It is a built-in mechanism with a biological function. The whole array of movements at the disposal of an organism is called into action, one after another they are resorted to and repeated over an ever-widening area. One of these countless blind movements accidentally removes the creature from the danger zone; then it speeds serenely on its way. Thus the instinctive flurry, viewed in the most favourable light, makes it possible for the organism quickly to choose or select from all possible movements the one appropriate to a given situation, and the choice requires, not
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deliberation at a high level, but a set of movements which are almost wholly mechanical or which are at most activated by a dull, undifferentiated affection. Viewed as an inflexible pattern of instinctive behaviour and one that fails to adapt to special situations, however, it is senseless or manifestly injurious. During the course of evolution the instinctive flurry was pushed further into the background. Over the older type of biological defence reaction were superimposed more recent and, for the most part, more useful structures. In dogs and even more distinctly in apes we find the rudiments of methodical searching and calm deliberation. When a mature person is faced with new situations, deliberation is the dominant pattern of behaviour; only under certain circumstances are instinctive flurries produced (Kretschmer, 1948, pp. 3–5). Another circumstance which provokes a useful instinctive flurry is the earthquake, which leads people to rush out of their homes. Childish overactive behaviour – pushing, jerking, screaming and thrashing about as a reaction to unpleasant stimuli – is held to have similar characteristics. The ‘hysterical hyperkinesias’ stand midway between panic and childish behaviour. Strong emotional crises, fugues, hysterical outbursts, trembling and convulsive paroxysms are held to be related forms of behaviour. The flurry then is seen as an ‘instinctive defence reaction to frustrating stimuli’, and consists of an “overproduction of aimless movements”. It is generated by “a diffusely intensified affective condition” (in other words, strong anxiety) and it meets with success when it results in an escape from the zone of danger and disturbance. A higher biological pathway is, of course, one of deliberate, selective behaviour. The alternative primitive mechanism, of the ‘death feint’ or immobilisation reflex, is illustrated by fishes which change to a camouflage colour and lie still in the presence of a predator; and by insects, crabs, snakes, hens and horses, among others, which in certain circumstances will all develop conditions of immobility and unresponsiveness even to strong external stimuli in particularly frightening circumstances. Kretschmer identifies this response with human hypnosis and stupors, but there is reason to think that hypnosis in man does not correspond to it (cf. Chapter 19). Kretschmer found a further form of hysterical primitive response in man, the ‘Ainu phenomenon’, which he describes, quoting Uchimura, as follows: “Under the stimulus of fear, a ‘ripe’ Ainu woman will regress automatically to a state of agitation. If the stimulus is a certain
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When I saw for the first time the ever recurring, monotonous appearance of Ainu I remembered at once the primitive defense reaction of lower or underdeveloped organisms. As noted earlier, the defense reaction is characteristic of the symptom picture of hysteria. According to Kretschmer the instinctive flurry and immobilization reflex are the most important defense reactions of lower organisms that are disturbed by external stimuli; it would, therefore, seem logical to compare the acute Ainu state with the instinctive flurry. The counterpart of the death feint is seen in acute catalepsy, which occurs sooner or later in all Ainu women though it tends generally to escape observation on account of other more striking symptoms. In any case it is certain that the symptom picture in general lies in the frame of Kretschmer’s so- called ‘hypobulic mechanisms’. Furthermore, I find in Ainu an indication of a primitive built-in defense reaction. This would explain why widely dispersed peoples evidence the same symptoms.” (pp. 15–18)
Hypobulic mechanisms are conditions in which the will or volition of the individual is impaired. It will be seen that a unifying notion is thus provided for a wide range of phenomena which are often called hysterical. Battle hysteria and culturally sanctioned outbursts alike can be viewed as primitive responses with a biological purpose. These primitive responses can be related to the more sophisticated phenomena of emotional conflict and repression, which are equally manifest in the traditional patterns of hysteria seen under less exciting medical conditions. Kretschmer further recognised two main subdivisions of hysteria, which he called ‘social’ and ‘endogenous’. The ‘social’ forms were those due to disability, war, and accident neurosis. The ‘endogenous’ resulted “mainly from the reactions of women and young people to certain erotic and family situations and from strong inclinations towards hysterical behaviour under certain psychopathic conditions, as in the pathological swindler.” (p. 50)
While these hysterics were not readily distinguishable from the social hysterics, they evidenced a stronger predisposition. He was careful to say that they did not correspond particularly to any of his three main constitutional types (pyknic, muscular, asthenic) but they did tend to have autonomic disturbances (“severe stigmatization in the vegetative system”) and “pronounced disturbances in the sexual constitution, especially sexual and general
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infantilism”. Statistical gynaecological evidence is cited in support. He also regarded a partial emotional retardation or failure of maturation as an important aspect of hysteria, especially the ‘endogenous’ form. Clearly, while accepting many standard and well established views on the nature of hysteria, Kretschmer developed certain ideas which help to complete the full appreciation of hysterical phenomena. His ideas can be used further to help sort out a common clinical problem. In the conditions of hysteria described in wartime and also in a number of civilian cases, two kinds may be observed. One is for patients to show the characteristic paralysis in accordance with, and accompanied by, the well recognised – although not invariable – belle indifference. These patients typically show the phenomenon which is often held to be most characteristic of hysteria (Yealland, 1918) in which, when movement is attempted in a paralysed limb, both agonists and antagonists contract. On the other hand, there are patients who show, for instance, an inability to walk which is accompanied by overt anxiety; they may believe they can move their legs but they tremble and resist doing so from fear of falling. The panic elements predominate and the disability (a partial immobilisation phenomenon?) is one of conscious fear of movement. The conflict may be only partly repressed; fear is experienced and the failure to move is openly protective, rather than unconsciously imposed. Both of these types are explicable in terms of Kretschmer’s biological explanation, although for the former, more commonly noticed pattern, a dynamic type of explanation based on the notion of unconscious conflict will be necessary in addition.
The predisposition to hysteria Turning aside a little from this main theme, it is now worth considering two other aspects of hysteria on which Kretschmer commented. His typology has already been mentioned and it was natural that he should consider whether there was a hysterical type. He commented as follows: “One may well ask whether certain types are inclined toward hysterical reactions but not whether people with hysterical reactions fit a definite type. In the second sense, there is no such thing as a hysterical type. A pre-disposition towards hysterical reactions is widespread and, in the last analysis, deeply rooted in the instinctive
Ernst Kretschmer mechanism common to all men; the triggering of these reactions depends as much on external stimuli and living conditions as on the structure of the individual. Therefore, if we take as one large statistical corpus, all those who manifest hysterical reactions and try to abstract from this corpus a hysterical type, we can never establish one that is distinct and uniform. To be sure, there are very general characteristics that have been positively identified, such as heightened lability, intensified and accelerated commutation involving the psychophysical apparatus (Kraepelin; Bleuler). For the most part, however, the expression ‘hysterical type’ is used to designate much more; it is used to designate a plastic, detailed personality portrait, and such a portrait can never be statistically realised. We glimpsed ... the heterogeneous groups that often manifest many hysterical reactions: on the one extreme a host of undifferentiated deviants – including the feeble-minded, prostitutes, and criminals – and on the other the holy men given over to religious mysticism. Or take the cosmopolitan esthetes, dandies, and poseurs – the ‘professionals’ in the world of hysteria – who manifest an exaggerated refinement in their tastes or in their attire; they are matched by Kraepelin’s hardy farm girls. In one group we find the colourless, morose indifference of the stunted ‘old maid’; in another the resilient vitality and sulking charm of the ‘flapper’ or the cold eyes of the hysterical ‘canaille’. No psychological artifice could possibly bind diverse groups into a single, unified hysterical type. But in a modified statistical sense we can rightly designate the pathological swindler as a hysterical type. Not for the reason that within the sum total of the hysterical patterns of reaction the pathological swindler resorts most frequently to one type (any particular pattern is but a small part of the general pattern), but for the opposite reason that the pathological swindler frequently does incline toward hysterical reactions. In our discussion of hysterical types, we are therefore, justified in calling attention to the pregnant group, marked by elegant flexibility, engaging patterns of behaviour, theatrical lability, a peculiar blending of refinement and infantilism and narcissism. The same holds true for the feminine type characterised by early puberty – the ‘flappers’ ... and others obviously predisposed to hysterical reactions. Among these hysterical types in the strict sense, we find to a striking degree the most important characteristics of the hysterical patterns of reaction: on the one hand lability of the psychophysical apparatus and on the other blocks in the development of the sexual constitution. And these hysterical types are especially good examples of secondary features or signs of overcompensation in Adler’s sense. They are lifelong attempts, with the help of the labile commutation apparatus, in a limited sense to conceal the defects of the sexual constitution and in a broader sense to gloss over shortcomings in love and social relations. As a secondary development they spring with a certain consistency from the interactions of both basic
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History and concepts constitutional components. And these attempts bring the theatrical, spuriously iridescent behaviour into the total picture of the hysterical personality.”
Current work on the hysterical personality, which is considered in Chapter 22, is very much in accordance with these views, as is clinical experience. A wide range of groups share a loose assortment of traits. The common features occur more often than by random variation, but there is no unique pattern characteristic of all cases.
Automatic responses The remaining topic on which Kretschmer seems especially worth quoting is the way in which hysterical symptoms can become ‘automatic’. Here he deals with a normal mechanism which probably plays an important part in many patients and which is not often discussed. There seems little point in paraphrasing his remarks and a direct quotation again follows: “During a wet spell a man develops in his right knee rheumatic pains accompanied by swelling and fever. He painfully and carefully holds his leg motionless in a half-flexed position. He can bend and stretch his leg at will; he feels some pain but not much. When he gets up after a few weeks, he still favours his right foot; yet the joint functions perfectly and the rheumatic symptoms have disappeared. Only under continued coercion does he straighten out his knee, and as he does so even then, he is visibly under great strain; even after he straightens out his knee and walks correctly for a while, he suddenly and automatically falls back into the old pattern. If he is permitted to continue in the old way, after another month any attempt to stretch his leg meets with resistance; again his knee elastically assumes the flexed position, without effort on his part; this flexion is independent of his conscious will. Even at night when he is asleep, his knee retains its flexed position. The man is unable, even by exerting all his strength, to stretch his leg. A few months later a rigid contracture of the flexors makes it impossible for anyone to straighten out his knee. As a rule, we are not fully aware of the small role actually played in our daily life and activities by the conscious will. Consciousness serves for the most part merely to give the starting signal; thereafter the whole complicated process continues without recourse to the will in the performance of the customary individual steps, whether through phylogenetically established patterns not
Ernst Kretschmer previously learned – various attitudes, gestures, and expressions of affect, for example – or through secondary automatisms learned at an earlier time – such as standing, walking, sitting, and participating in different recreational and professional activities. These secondary automatisms, long since relegated to the status of set formulas, are reorganised as new patterns based on automatic controls relating to tone and equilibrium, and on such reflexes as gripping and sucking.”
Kretschmer quotes Bleuler with approval speaking of: “a certain psychic causal apparatus [Gelegenheitsapparat] fashioned expressly to prevent the conscious will from having to be attentive even at the outset to every detail in certain mental performances. His formulation is doubtless correct. We quote from his own description: I write a letter and put it in my pocket with the intention of dropping it into the next letterbox. I need no longer think about it. The first letter-box that comes into view causes me to dispose of the letter. Or I am engaged in an activity that I cannot or will not interrupt. Somehow the notion enters my mind that I ought to bring a book from another room, this idea stays in my mind for perhaps only a fraction of a second and is then pushed out of my consciousness. But when the moment comes for me to get the book, I go to the bookshelf and take the book. This happens a thousand times, and so obviously that I am generally unaware of it. The whole mechanism is brought to my attention only when something fails to fall into place. Since I am predominantly a motor type, dislocation serves as the best illustration. Not infrequently I find myself at the place where the book is, near the person to whom I have something to say, but must first try to recall what I want, why I have come there. Or I subsequently realise that I do not need the book, yet go for it at the critical moment. When we make a decisive choice, we fashion an apparatus in our brain; this apparatus is set to react later – for example, a movement of the right hand on a green signal and of the left on a red one. With the specific reaction the conscious ego has little or often nothing more to do; the reaction occurs automatically. If it is somewhat difficult, then the objective results are often not in accord with the subjective controls of the conscious ego. At the moment of the assigned reaction the ego may be involved in something else, yet the apparatus may still react properly and promptly; against this, the ego may, by becoming involved, interfere with the reaction. In these cases we have constructed through one specific decision a cerebral apparatus for a definite occasion; this apparatus executes the decision in the same way that habit creates automatic apparatuses or that phylogenetic forces
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History and concepts construct in our central nervous system apparatuses for reflexes and instincts. Such an apparatus is created by each decision, each undertaking, from the simplest automatic course of action resembling a reflexive response to a definite stimulus (a simple psychological response) to a whole pattern of existence whose cessation is brought about only by death and whose execution is interrupted a thousand times by compelling activities that claim all our strength. We prepare ourselves to awaken or not to awaken when the alarm rings, to find a certain plant, to see misprints, etc.”
This sort of automatic establishment of behaviour patterns also occurs with skills, and was much discussed earlier by William James (1890) and by others like him who were interested in ‘subconscious’ as distinct from ‘unconscious’ processes. The way in which it can be employed for the development of hysterical patterns of disuse is clearly described in Kretschmer’s quotation from Uchimura and needs no extra illustration. But it is probably worth pointing out that there are times when an explanation of this sort may be conveniently employed to train a patient away from an established symptom for which the original motivation has become less strong. As for Kretschmer’s views on instinctive behaviour, I think that these might need some modification in the light of advances in ethology, but the fundamental notion appears sound. To my knowledge Yap (1952) and Ludwig (1972) are the only authors writing in English who have taken due note of Kretschmer’s views. Ludwig accepts the basic considerations outlined above and also argues that a number of regressive phenomena such as urinary incontinence, babbling, rocking, head-bobbing, crying, vivid fantasy construction, and the like, all bear some resemblance to the violent motor reaction of sham death, and contribute to the posture of helplessness and defencelessness which, like the sham-death reflex, wards off attack, especially from members of the same species. He holds that hysterical psychoses, ageregression phenomena, puerilism and the Ganser syndrome of pseudo-dementia represent comparable primitive behaviours which may occur as a result of the dissolution of higher function. A parallel is thus drawn with the concepts of Hughlings Jackson (1884) and provides a biological basis for the behaviour listed. As Kretschmer saw, the success of such behaviour may serve to promote its recurrence. Ludwig conceives that such events are due to operant conditioning, and observes:
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“ the systematic rewarding of planned or ‘accidental’ behaviour will result in the increased frequency and, finally, establishment of those behaviours. It also provides an alternative way of accounting for the ‘secondary neurotic gain’ ... [which] may be translated as the continued reinforcement of the symptomatic behaviour.” I think that these views of conditioning are reasonable and justified but not necessarily an advance on the dynamic formulation, perhaps because to a considerable extent, if not entirely, they are saying the same thing in another set of terms. Kretschmer’s contribution merits considerable respect and it is probably the best revision of the theory of hysteria to have resulted from the experiences of large-scale war. It contrasts less with the views of Freud than might appear superficially. Although they took different routes and arrived at certain different conclusions, their basic approaches were similar. Both looked at a range of phenomena, from primitive instincts or feelings to sophisticated motives and their expression. Both emphasised, ultimately, the biological basis of the conditions with which they were dealing and both recognised the importance of motive in regard to hysterical symptoms. In due course we will need to discuss some of the types of motive which may be important and those conditions where the motive for possible hysterical symptoms seems nearest to consciousness.
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7
History and concepts
Post-traumatic stress disorder
The decay of the concept of shell-shock was not enough to cure the men who had suffered stress syndromes under that guise. As indicated in Chapter 5, many pensioners remained after World War I. When World War II began, the lessons of World War I, which to some extent had been put aside, were recognised and quickly applied. The removal of affected individuals from the firing line and the quick treatment of psychiatric casualties reduced the impact of stress (Grinker & Spiegel, 1945; Sargant & Shorvon, 1945). Many others besides wrote of the effectiveness of appropriate treatment of psychiatric casualties in World War II. The treatments were primarily rest, sedation, encouragement and abreaction. Torrie (1944) reported 1000 cases of anxiety and hysteria from North Africa, including 86 with fugues and 77 with paralysis or loss of function. Of these 899 returned to duty; 586 went back to full duty and only 54 were invalided. The United States adopted similar approaches. Some have held that the selection processes reduced the impact in terms of numbers of soldiers affected because the most vulnerable were kept out of the firing line, but Chalke (1954) has expressed doubts about the success of the efforts to select suitable soldiers. In any case, psychiatric illnesses were again produced by stress in World War II, and it was widely understood that the extent of exposure to danger carried a risk of anxiety and other symptoms almost pari passu. During World War II an additional theory also began to emerge from observations of men’s reactions to stress. Sargant & Shorvon (1945), in fact developed ideas based on Pavlovian concepts. They describe some of their observations as follows: “Among the patients who came direct to us from the Normandy battlefields, there were, aside from those who showed the usual
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anxious and depressive symptoms, men with states of simple but profound exhaustion; others with gross, incoordinated, irregular jerking and writhing movements of the limbs and trunk, often accompanied with aphonia or stammer or explosive speech, and yet others in various states of stupor. It was in these patients with hysterical reactions that parallels to Pavlov’s experimental observations could most frequently be seen, not only during their period of observation in the hospital but in their behaviour of the past as preserved in the field records.”
Some patients were found who had broken down into intense excitatory states. One man banged his head repeatedly against a tree, rushed around wildly calling for an ambulance and then had to be strapped down when it came. Others passed into stupor or amnesias or were “literally paralysed by fear”. These events are explained as states of either excitation or inhibition caused by excessive stimulation. These sudden states of total inhibition or collapse were thought to be possible examples of Pavlov’s ultraparadoxical phase, in which widespread inhibition is held to abolish normal conditioned reflexes. Treatment was usually by sedation or abreaction, the latter being much assisted by narcoanalysis or the administration of ether. Results were held to be good if treatment was provided promptly. Grinker & Spiegel (1943) had reached similar conclusions in regard to the clinical phenomena encountered and their treatment. Sargant & Shorvon also noted an analogy between these states of excitation or inhibition and the response of sudden converts to the preaching of evangelists in the style of early preachers like John Wesley. Sargant (1957) later linked many types of revivalist and socially induced trance to the same phenomena. In his view, excessive stimulation or arousal leads to Pavlov’s ‘ultra-boundary’ inhibition, a rupture of higher nervous activity and the extinction of recently acquired conditioned reflexes. There is then a greatly heightened readiness to accept new orientations. Religious conversion and brainwashing may thus operate similarly at least to some extent, although the former lacks the cruelty and imposed constraints of the latter. Sargant’s views present a tenable hypothesis for this group of phenomena and include reference after Pavlov to the relevance of individual differences, with ‘strong’ or ‘excitatory’ dogs and men being more resistant to breakdown than ‘weak’ or ‘inhibitory’ types. The theory lacks a basis for determining when excitation will result and when inhibition. In addition, the theory has not been extended, with evidence, to the wide diversity of hysterical phenomena which are open to consideration, and the methods of
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treatment have very limited success outside acute stress situations and, possibly, the attempted reversal of brainwashing. However, awareness of the phenomena has substantially influenced disaster planning.
The spreading awareness of stress disorders The two world wars were not, of course, the only occasions that gave rise to stress for soldiers or civilians. The Vietnam War (1964–73) probably contributed most to changing the emphasis from dissociation to anxiety. We expect anxiety to burgeon in the face of danger. The challenge is to control or subdue it. The prominent nature of conversion and dissociative symptoms, when present, means that they are promptly acknowledged. Initially, anxiety under stress is a matter of course, but may be masked by dissociative responses. Likewise depression, which is liable to follow the anxiety, is easily taken for granted in its turn. However, once anxiety and depression become recognised and acceptable, hysterical symptoms become less necessary. In DSM–II (American Psychiatric Association, 1968) the view was taken that overwhelming stress could cause transient situational disturbances, but that if “the symptoms persist after the stress is removed the diagnosis of another mental disorder is indicated”. Twelve years later DSM–III (American Psychiatric Association, 1980) described post-traumatic stress disorder (PTSD) in detail as an anxiety disorder. It took some while for awareness to emerge of the prolonged effects of psychological stress in American soldiers returning from Vietnam. Hostile attitudes within America to the Vietnam War made many veterans keep back their feelings and symptoms from others. Nevertheless, a common pattern of post-traumatic stress was increasingly recognised, marked by depression, an explosive aggressive reaction, sleep disturbance with nightmares, startle responses, discomfort at stimuli associated with previous lifethreatening experiences, constriction of ego interests and adaptive functions, and possible dissociative reaction, that is, ‘flashbacks’ (Figley, 1978; Haley, 1978). An enormous literature developed on such illnesses induced by catastrophic stress, including reports from many countries and campaigns as far apart as Afghanistan and Vietnam, as well as on the suffering of concentration camp survivors and prisoners of war in Japan and the USSR; the effects of torture in a wide range of countries; and the misfortunes of civilian survivors of catastrophes in Australia, Britain, the United States and elsewhere (Choy & De Bosset, 1992; Wilson & Raphael,
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1993). Most, if not all, of this literature makes principal reference to anxiety and depression and little formal mention of dissociative disorders; for example Miller et al (1989) describe effects in former United States prisoners of war in Germany and Japan in which anxiety and depression are prominent while such personality changes as were found on the Minnesota Multiphasic Personality Inventory and Millon Inventory were quite varied. In response to the Vietnam veterans the United States Congress mandated a National Centre for Post Traumatic Stress Disorder (PTSD) in 1984, which carries out a broad range of multidisciplinary activities in research, education and training, including the publication of a PTSD research quarterly. Acute disasters in civilian life commonly give rise to the same sort of initial responses as those found in soldiers, often with automatic behaviour and confusion, overt panic, anger and guilt (Edwards, 1976). Defensive reactions with hysterical dissociations are likewise recognised (Kinston & Rosser, 1974). As with former soldiers, there is a tendency for evidence of anxiety and depression to be much more prominent than hysterical symptoms, provided that the environment after the event is friendly. Gersons & Carlier (1992) provide a discussion of the evolution of this concept of PTSD, recognising how it is related more to problems of anxiety and adrenal function than necessarily to the psychodynamic resolution of emotional conflict. This must apply particularly in civilian cases (especially when compensation is not an issue) and where the danger of having to fight again or be exposed to the same hazards is no longer present. Nevertheless, civilian responses to acute disaster have shown a remarkable similarity to those in wartime. The Buffalo Creek dam collapse of 1972 produced PTSD in a significant portion of the sample, while major depression was the next most common diagnosis. Anxiety disorders were also common. The overlap with other diagnoses was quite similar to that found in a sample of Vietnam veterans, whom the same authors had studied earlier, except that the disaster sample had fewer dysthymic disorders, substance abusers and cases of antisocial personality disorder (Green et al, 1992). McFarlane & Papay (1992) also found a high rate of additional diagnoses (77%) in fire fighters who already had PTSD after exposure to a natural disaster (an extensive bush fire in southeast Australia). Again, the tendency was for depression to be the most common concurrent disorder. More prolonged exposure to stress also tends to produce syndromes which are mainly related to anxiety and depression. Bauer et al (1993) describe a series of complaints in former
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political prisoners in East Germany marked by sleep disturbance, sadness, general anxiety, irritability, exhaustion, lack of contact, headache, nightmares, nervousness, and so on. Watson (1993) describes PTSD in former Australian prisoners of the Japanese. Weisaeth & Eitinger (1993) observed such common themes as depression and anxiety after wars, disasters and traumatic events. Eitinger et al (1985) also point out that in the most severely abused persons who were subjected to the sustained trauma of Nazi concentration camps, a combination of somatic and anxiety symptoms predominates. They note that the constellation of somatic and psychiatric symptoms was so typical that it became known as the ‘concentration camp syndrome’ or ‘survivor syndrome’. The main symptoms of the concentration camp syndrome include weight loss, pathological fatigue, periodical constant diarrhoea, dizziness, headache, hot flushes, nightly sweating, sleep disturbances, reduced sexual potency, depression or moodiness, emotional lability, nightmares or other fear phenomena and reduction in memory and/or ability to concentrate (Turner & Gorst-Unsworth, 1993). The range of physical effects related by Eitinger (1964) in his classic study covers many more somatic symptoms than can be easily attributed to anxiety but also does not demonstrate a predominance of dissociative ones.
A scarcity of dissociative complaints While the above reports demonstrated the predominance of anxiety in patients with PTSD, this was in contradiction with previous expectations. Even though Kretschmer demonstrates a shift in his understanding of what was happening with his patients, the sort of material outlined in Chapters 5 and 6 is still rich in classic hysterical symptoms. However, not all reports showed the trend away from hysterical symptoms. Breslau & Davis (1992) presented some results on PTSD which might seem to be at variance with the tendency to find less evidence of dissociative symptoms. In a random sample of young adults selected from the membership of a large health maintenance organisation in the Detroit area, reported in detail by Breslau et al (1991), psychogenic amnesia was observed in one-quarter of the affected subjects. The subjects found to have chronic PTSD all related a variety of symptoms to a series of traumatic events. In the base study six factors were found to be associated with greater vulnerability to PTSD after such events: female sex, prolonged childhood separation from parents, family history of anxiety, family history of antisocial
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behaviour, pre-existing anxiety or depression, and neuroticism. The events included violence such as sudden injury or accident, physical assault and rape (the latter causing an exceptionally high rate of PTSD). Vicarious experiences such as seeing someone seriously hurt or killed or receiving news of a violent death or of injury to a close relative or friend were apparently as traumatic as direct injury, except for rape. In association with these findings Breslau & Davis note the usual PTSD symptoms of recurrent recollections and dreams in a very high percentage of their subjects and flashbacks in 49–50%. There was avoidance of thoughts or activities connected with the traumatic events in over 80% of cases, psychological reactivity, particularly to symbolic stimuli, diminished interest, sleep problems, irritability, difficulties in concentration, hypervigilance, startle, and so on. The least frequent of these symptoms apart from flashback was diminished interest, which still affected 62% of their subjects. Of those with chronic PTSD, 24.5% were said to have “psychogenic amnesia”, but this is the only dissociative symptom noted in their study. Carlson & Rosser-Hogan (1991) reported high scores among Cambodian refugees on measures of trauma, dissociation, depression and anxiety. The scores for dissociation were based on responses to the dissociative experiences scale of Bernstein & Putnam (1986), which is considered in Chapter 21. Eighty-six per cent of the subjects met DSM–III–R criteria for PTSD (American Psychiatric Association, 1987) and 96% had high dissociation scores on this scale. Eighty per cent could be classified as suffering from clinical depression. When we look at the item content of the dissociative experiences scale it is questionable whether it necessarily measures dissociative experiences. Their values, however, are similar to some of those found by Bernstein & Putnam in a sample of war veterans. Mollica et al (1993) gave a detailed report on 993 adults, sampled at random from refugee households in camps on the border of Thailand and Cambodia. Eighty-five per cent had suffered lack of food, water, shelter and medical care, brainwashing and forced labour; 54% reported murder of a relative or close friend; 18% reported rape or sexual abuse; 8% torture. Symptoms reflecting probable depression appeared in 55% and PTSD in 15%. No definite dissociative symptoms were mentioned in a very thorough and detailed report. The more recent literature on PTSD contains numerous systematic studies, summarised regularly on different aspects of the subject in the PTSD Research Quarterly. There are not many
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articles in that quarterly in which more than a small minority of patients who have PTSD are found to have conversion, somatoform or dissociative disorders. We must look to other sources, dealing with multiple personality disorder or supposed recovered memories in adults with alleged histories of childhood abuse, in order to discover current reports of the frequent occurrence of conversion, somatoform or dissociative complaints. In the modern reports indicated above, dealing with recorded disasters, anxiety and depression predominate in PTSD. In one study by Kuch et al (1991a) who described 60 patients with fibromyalgia, 33 had had road vehicle accidents while 27 had not had such an experience. The road vehicle accident patients had at least twice as many phobias and other anxiety symptoms as the remainder. Both groups had the same small proportion of cases with possible somatisation disorder. The sensitive and thorough book by Solomon (1993) is firmly based on repeated systematic examination of Israeli soldiers. In that volume the data consistently demonstrate the common anxiety phenomena of PTSD and scarcely ever present symptoms either as conversion symptoms or dissociative ones or somatoform disorder. It is true that in one place Solomon discusses as a conversion symptom a complaint of burning feelings in a patient who had previously been burned and who later saw colleagues burned. The provenance of that symptom is of considerable theoretical interest, but it was almost unique in Solomon’s material. With respect to those who have been through battle we find, again and again, that if the military medical culture does not expect conversion symptoms – and expects anxiety ones – the former largely vanish. The idea that dissociative symptoms are a common part of PTSD is prejudged by the assumption that besides amnesias, such experiences as flashbacks, depersonalisation, daydreaming and a number of other questionable items are to be regarded as dissociative rather than due to anxiety or normal behaviour (see Chapter 21). The situation does not seem to differ after torture. A rather low figure, comparatively speaking, for dissociative or conversion symptoms can be seen in the report by Ramsay et al (1993), “Psychiatric morbidity in survivors of organised state violence including torture”. There the commonest psychiatric diagnoses recorded were PTSD, major depression and somatoform disorders. Of the somatoform disorders, somatoform pain disorder in 29 was considered the most common (out of 300 patients). However, the diagnosis of somatoform pain disorder has been radically changed (American Psychiatric Association, 1994) and although many of
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the subjects acknowledged a relationship between their psychological state and the severity of their pain many of them also had been beaten or subjected to musculoskeletal damage. Hence, here too, although one can certainly anticipate some cases of conversion or dissociative disorder, just as with PTSD, the primary phenomena do not appear to be hysterical, and some symptoms which were regarded as essentially conversion disorder may well be organic in origin or have an alternative explanation. As a rule, PTSD is distinct from hysteria. It can also be very long-lasting. Bende et al (1994) described an 80-year-old man who had had recurrent flashbacks since World War II and frequent nightmares. They diagnosed this patient as having PTSD with enduring personality change, secondary alcohol misuse with alcoholic hallucinations and depression. He improved very substantially with a combination of alcohol withdrawal, behavioural management, desensitisation for social phobia and treatment with 20 mg paroxetine each morning. A long-term Australian study (Tennant et al, 1986) of 170 former prisoners held by the Japanese during World War II found that these veterans had more contemporary depression and anxiety disorders and more post-war psychiatric illness than a control group of veterans from the Pacific and South East Asian campaign who had not been prisoners of war. The prisoners of war also had more duodenal ulcers than controls, but otherwise the physical health of both groups was similar, as was the age-adjusted mortality in the post-war years. The authors of this report point out that the prisoners of war had suffered from malnutrition, chronic infection, lack of shelter, forced work, arbitrary brutality and execution and systematic humiliation. At the end of the war 70% of the prisoners of war who survived in Japanese hands were in abject physical health and resembled survivors of Nazi concentration camps. In the early post-war years they were all admitted to medical wards (often repeatedly) for treatment, usually of their nutrition-related disorders. It is thus not surprising that the prisoners of war had significantly more post-war medical admissions than non-prisoners of war, but what does seem remarkable, in the authors’ words, is that after 40 years their medical health was no worse than that of the comparison group. It is equally notable that their psychological changes were principally those of anxiety and depression. Kral (1951), who gave a detailed account of his experiences and observations in a concentration camp (Theresienstadt), pointed out that overt neurotic symptoms were relatively rare there. It was not an extermination camp and the great majority of prisoners were sent east to their death in other camps in Poland but, even
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for those who remained there, living conditions were appalling and life was much at risk. The initial response to removal to Theresienstadt was a state of depression and retardation and loss of initiative accompanied by anorexia, sleeplessness, constipation and in most of the women amenorrhoea. Suicidal attempts or panic reactions were not observed. Many patients who were known to have had severe chronic psychoneuroses such as phobias and obsessive–compulsive neuroses improved completely or greatly. Gastric ulcers became rare but a few hysterical reactions, seizures, pareses and demonstrative suicidal attempts were observed. Overall, if one is cautious about what constitutes dissociation, it seems that dissociative and other hysterical symptoms, such as somatoform or conversion complaints, are not the most common reaction to prolonged stress or even acute stress. An additional feature in the environment may serve to promote them at times and some conversion symptoms are to be expected as well as dissociative disorders, but not in the substantial majority of cases with PTSD. Social upheavals, more than acute, life-threatening disasters or concentration camp experiences, tend to be part of the cause of the mass hysterical phenomena discussed in Chapter 16.
Delayed post-traumatic stress disorder Two types of supposedly delayed PTSD have been discussed in the literature. The first of these is the appearance after more than six months of PTSD symptoms in individuals who had previously not presented them. To some extent this may be a matter of the reactivation of adverse combat-related memories (Long et al, 1994). In this case we are presumably dealing with the establishment of an increased predisposition to symptoms, which is well recognised (Solomon, 1993), or with the exacerbation of symptoms which have been present for some time but were less severe. It is well agreed that soldiers who have experienced PTSD in previous combat are more susceptible to reactivated PTSD on exposure to further combat (Solomon et al, 1987a,b). Alternatively, Solomon et al (1989) showed that a small proportion of cases which appeared to manifest delayed-onset PTSD (10%) had bona fide delay. Four other subcategories of apparent delay were noticed as well, including exacerbation of previously subclinical symptoms, delayed help-seeking for symptoms already present, reactivation and the occurrence of other psychiatric disorder. Even the typical case of this phenomenon which Solomon (1993) describes includes some
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element of reactivation by new threat. A man in the reserve who had served in Lebanon in active fighting without incident and who had again served in the same campaign without active involvement fell into a severe anxiety disorder resembling PTSD when he received his call-up papers for his third brief period of service. It seems possible that delayed-onset symptoms may occur when something happens which raises the sense of threat to the individual once more. Overall, there are indications that as time goes by stress symptoms decline in most individuals who have suffered some initial post-traumatic stress response (Solomon, 1993, Falk et al, 1994). Falk et al, after a review of over 50 studies, conclude that the impact of trauma can be long lasting but may wax and wane, although the question of whether extended chronicity represents delayed onset or delayed recognition has not been answered, and they note that the true course of the disorder remains unclear. Long et al (1994) report, perhaps most typically, that New Zealand soldiers who had served in Vietnam found that media coverage of warfare in the Gulf War (which occurred in 1991) revived memories of early combat and this increased their PTSD levels. In summary, although there is a most important relationship between hysterical symptoms and acute battle problems, and this relationship has taught much about the production of those symptoms per se, the symptoms do not necessarily follow from acute or even chronic stress in the absence of other contributory environmental factors.
Recovered memory and post-traumatic stress disorder This is the second type, of supposedly delayed, PTSD. In the last few years, especially since about 1988 or 1989, an increasing number of individuals have claimed that they suffered trauma in childhood and only recovered the memory of it in adult life. Psychodynamic theory has conventionally assumed that that was possible as a result of the overcoming of repression in psychotherapy. So long as these ideas were confined to the therapeutic process they did not arouse much opposition, but when they began to be used increasingly in accusations of abuse, made against parents and others, more resistance developed. There is now a vigorous dispute about the validity of recovered memories at all, and particularly about their use in criminal charges without corroborating evidence or in law suits for damages. Chapter 21 deals with this topic in detail. It deserves some attention here for
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two reasons. First, leading proponents of the recovery of buried memories argue that the syndromes with which they are dealing are those of ‘trauma’, and they align themselves and their subject matter with the treatment of PTSD in other types of trauma (e.g. Herman, 1992). Here it may be useful to note a small amount of evidence concerning long-lasting memory in survivors of natural disasters and of wartime experiences, and also to note briefly the logical status of the claim that recovered memory identifies genuine survivors with post-traumatic stress conditions. Green & Grace (1988) conducted a follow-up study of survivors of the Buffalo Creek flood in West Virginia which occurred in February 1972, whom they had examined in 1974 and whom they approached again in 1986. In order to determine the reliability of survivors’ recall of their flood experiences over a 12-year period they undertook a number of procedures. Rater generalisability coefficients (a form of inter-rater reliability) were established at 0.80 for bereavement and 0.59 for initial flood stress. (Bereavement meant the extent of loss of possessions, friends and family members). The correlation between 1974 and 1986 ratings of bereavement was r = 0.58, but the average level of bereavement did decrease significantly, from 1.84 in 1974 to 1.54 in 1986. Ratings of the scale of the threat to life of the initial flood were much less reliable (r = 0.36). While the correlations noted are significant for the 81 individuals who were examined, they also show another important finding. In the case of the recollection of bereavement, 34% of the variance was in common and in the case of the actual threat to life or its evaluation only 13% of the variance was in common. In other words two-thirds of the information was unreliable with the one measure and 87% was unreliable with the other measure. Thus, the accuracy of memories for which it was apparently assumed that continuous recall had always been available (and everybody knew about the events) was very limited after 12 years. This finding in relation to the impact of stressful events is of considerable significance in evaluating the reliability of past memory. It confirms there is something in past memories but that detailed recall is very uncertain. A second consideration which applies to the purported link between recovered memories and ‘trauma’ has to do with the nature of the cases. A substantial body of evidence holds that childhood experience is important in determining adult characteristics. The most common characteristics which are said to follow from severe childhood deprivation of affection and associated physical and sometimes sexual abuse are changes in personality in the direction of sociopathy and severe emotional
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instability. Currently the former is described in ICD–10 (World Health Organization, 1992a) as dissocial personality disorder and the latter as emotionally unstable personality disorder (with impulsive and borderline subtypes). DSM–IV describes comparable conditions as antisocial personality disorder and borderline personality disorder. It is ironic that after the rather questionable diagnostic category of borderline personality disorder had been used for many years in DSM–III and DSM–III–R, it has been adopted by the WHO classification at a time when it is becoming increasingly unpopular in North America on the grounds that it is politically incorrect, since it is applied most often to women and tends to be pejorative. Others may have reservations about that diagnosis, as I do, for various reasons, including particularly the fact that the diagnosis overlaps greatly with that of depression, as Akiskal and others have shown (Davis & Akiskal, 1986). Be that as it may, the patterns of personality disorder which are typically associated with childhood deprivation and stress are very different from those of standard post-traumatic disorder occurring in adults subjected to stress once their childhood was over. Moreover, there is also evidence that children subjected to typical stresses of the sort which produce PTSD in adults also tend to produce a PTSD syndrome of the DSM–III–R type (Shannon et al, 1994), such symptoms being particularly marked by trait anxiety (Lonigan et al, 1994). Shannon and Lonigan and colleagues studied children in three groups (pre-adolescents, 9–12 years old; early adolescents, 13–15 years old; and late adolescents, 16 years and older) in relation to hurricane experiences. Thus, what is called ‘stress’ in childhood does not seem to have the effects in adult life which recovered memory believers anticipate, even in those individuals for whom stress has been completely authenticated in childhood. It is true that the experience of childhood deprivation is said to affect personality most often when the children in question are below the age of six or seven years, while sexual abuse is more likely to occur in children above that age. However, the existing literature on recovered adult memories of childhood sexual abuse tends not to make distinctions between the types of adult symptoms to be expected from sexual abuse at different ages, and all abuse is considered likely to result in a similar amorphous mass of symptoms, as discussed in Chapter 21. If the claims about recovered memory are correct, there should be much more evidence of antisocial personality disorder in the psychotherapy patients who have recovered memories of early childhood abuse.
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8
Malingering, self-damage and anorexia nervosa
The simplest distinction between malingering and hysteria suggests that in the former the symptoms are developed as a conscious pretence, while in the latter they arise unconsciously. In theory such a view is excellent even if, as Kretschmer recognised, both states may be equally based on self-preservation. In practice it is often hard to make the distinction, since the form of malingered symptoms will be identical to that of hysterical ones. In the latter case they will be due to the thought that there is a disability – which will lead to mimicry of illness. In the case of malingering the intention to mimic an illness will have the same effect. Most allegations or reports of malingering arise in situations where either life or money may be at stake. Physical danger from military service (or at least very unpleasant conditions) or financial compensation for accidents, or the opportunity to receive disability payments, are common incentives for malingering when it occurs. Children sometimes malinger to escape unwelcome duties or tasks at school, and prisoners or accused persons are known to be potential malingerers. The attitude of the medical profession to such cases can be quite robust: “AD who covered a wound 1/16 ” in size with an ointment, lint, three bandages and a large gout-boot, seemed surprised, and I fancy not a little indignant, when most of his dressings were put in the fire, and he was told to resume work that day.” (Collie, 1922)
Sir John Collie was an examiner for numerous employers and gives pungent accounts of his visits to the homes of claimants whom he thought were malingering. Pilowsky (1985) characterises 91
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many medical attitudes ironically as “malingerophobia”, defined as an irrational and maladaptive fear of being tricked into providing health care to individuals who masquerade as sick, but either have no illness at all or have a much less severe one than they claim. He adds, “Although described as a ‘phobia’ in some instances this condition may be more like a delusion (although this is relatively rare) and, in other cases, more like an ‘overvalued idea’ or morbid preoccupation with no real or lasting insight into its irrational qualities.”
His touch is light but his brush draws a clear picture of the hostility which physicians often manifest towards ‘the hysteric’ and of their concern not to be duped. Hysteria provides the physician with some of the same problems of feelings about being tricked; these will be discussed later. At this point it is worth noting that hysterical symptoms arise more often than malingered ones in the context of interpersonal problems and difficulties in adjustment to stress. They may also arise in the same situations which produce malingering. Hurst (1940) gives two criteria for the detection of malingering. The first is detection in flagrante delicto, the second an unforced confession. However, few malingerers are so helpful as the soldier who wrote a letter on lined paper without a heading, purporting to be signed by the matron of a hospital, to the effect that private X “is unfit to return to duty because he has a broken ankel” (sic). Some patients are encountered who acknowledge that they are at least partly aware that they ‘bring on’ their symptoms (e.g. the girl with epilepsy mentioned on p. 153) or could do better if they tried, but do not wish to try. Others with hysterical symptoms appear genuinely unconscious of their mechanism. A former nurse whose symptom of hysteria was an abnormal gait who managed to read her own notes was horror-struck and indignant at the diagnosis. Some who have recovered through hypnosis or other means show no apparent awareness that their symptoms were self-induced, even though they accept that they were psychological in origin. Yet Charcot said that malingering was found in every phase of hysteria. Thus while the extremes of hysteria and malingering are recognisable, there is a group of patients with hysteria (whose size will vary with the circumstances and with the sample of patients) who show evidence both of conscious and unconscious mechanisms promoting their psychologically induced disability. Sir Charles
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Symonds (Appendix C) points out that in his experience fugue states of a hysterical type were always associated with a degree of conscious simulation. By contrast, other fugue states, especially those associated with depressive illness, appear not to have the same degree of conscious production. Flicker (1956) considered that 10% of malingerers were normal and that 5% of 100 000 inductees for military service malingered. This was nearly the same proportion that occurred in service hospitals, but very few of the latter were officially diagnosed, namely 17 out of 60 000 (0.028%). In his view malingering was encountered in five situations: psychosis, oligophrenia, constitutional psychopathic states, neurosis and fear states or morale deficiencies. The pathology can occur through a defect of the social environment. “When a man mirrors the faults of society at large, society and not the mirror is to blame.” But one might think that society will not readily hold this view, nor will it always be the most useful short-term one for society. Anderson et al (1959) observe that “it was nearly always found impossible during war in the services to charge offenders ... with malingering, although this was often strongly suspected”. From an extensive review, citing 15 authors, they also concluded that it was generally agreed that “simulation of mental illness usually occurs on a basis of some form of psychic abnormality”. Interestingly, in the same study as Anderson, Trethowan demonstrated that with few exceptions subjects attempting to simulate mental disorders failed to produce anything which closely resembled well defined psychiatric disorders or syndromes. The assessment of malingerers laying claim to psychological illness is discussed by Rogers (1988) and others and depends, like that of physical illness, on demonstrating incompatibilities, inconsistencies and the like. Perhaps in all cases, the most convincing criteria are Hurst’s original requirements of the patient being found in flagrante delicto or giving an unforced confession. Despite all this, doctors and psychologists are not particularly good at detecting liars. Ekman & O’Sullivan (1991) showed videotapes of 10 people who were either lying or describing their feelings truthfully to a variety of detectives, judges, psychiatrists, college students and working adults. Only the United States Secret Service performed better than chance, and they were significantly more accurate than all the other groups. Those who were accurate appeared to rely on different behavioural clues from those who were not accurate. Accurate observers were also significantly younger than inaccurate ones.
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Jones & Llewellyn (1917) charitably say: “there is little doubt that the consensus of expert opinion is substantially correct – viz., that feigned insanity only occurs in those more or less mentally deranged, or predisposed by heritage to mental instability.”
They add the important comment from Bernard Glueck that the detection of malingering in a given case by no means excludes the presence of actual mental disease (p. 288). This is confirmed by Pope et al (1982), who describe recovered schizophrenic patients prolonging their symptoms because they preferred in-patient residence to poor living conditions outside hospital. Pankratz & Lipkin (1978) recognised another variant of simulated psychiatric illness, in 13 patients who presented suicidal ideas of questionable truth, and one who offered paranoid symptoms in order to gain admission to more comfortable circumstances in hospital than outside. These actions are not irrational and resemble the behaviour of David, who simulated insanity when seeking refuge from Saul in the territory of the Philistines (I Samuel, 21, 11–15). Fraser (1984) briefly described the repeated production of rectal bleeding from a small tear at the anal margin by a young man under his care. He happened to be a German spy and Fraser comments “Our object of course had been to get him well so that he could be shot; his was not to get well so that he would not get shot”. This was a case of successful induced illness which was apparently maintained for very rational reasons until peace was declared. Besides those with overt malingering there are several groups in whom the production of illness may be wholly or substantially conscious, and yet severely self-damaging. These patients include those with hospital addiction, the so-called Munchausen syndrome, others to whom the term ‘deliberate disability’ (Hawkings et al, 1956) has been applied, and anorexia nervosa. Attempted suicide is a further category of this type, although it is by no means necessarily hysterical in pattern nor manipulative by intent. In addition, there are patients with pseudodementia or the Ganser syndrome whose symptoms are often both transparently false and evidently aimed at self-exculpation. A relationship between all these syndromes is easy to remark upon, yet hard to analyse. The clinical problem which they present has been illuminated by studies of the Munchausen syndrome, and although those studies do not offer a complete explanation for all the phenomena of the syndromes just listed, they provide an important part of it.
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Simulated illness and hospital addiction Simulated illness and hospital addiction can now be discussed, together. Buinewitsch (1939) provides an account of the literature on the former. Good (1942) reported six cases of malingering to escape the burden of military service. His cases gave evidence of a degree of anxiety which was unrelated to their circumstances (they were in Britain and not in combat zones) and one of them even wanted to return to deep-sea fishing which, particularly in wartime, was very much more dangerous than serving on a base at home. They also showed a lack of guilt, but they were evidently not typically sociopathic since several of them gave evidence of shyness or phobias. They displayed a marked attitude of infantile dependence. One, a man with a wife and child, was desperate to get home to look after his mother. Although in Good’s cases ‘mother’ was seen as an idealised figure, she had often beaten or rejected the patient and the dependent attitude was therefore linked with a masochistic one. This phenomenon of masochism appears in a pronounced form in the Munchausen syndrome. Asher (1951) described a group of patients who tended to be admitted to hospitals repeatedly with supposed acute physical illness, supported by an untruthful, plausible but dramatic history, which could often be characterised as pseudologia fantastica. They underwent many operations and were usually discharged after arguments with doctors or nurses, following which they would move on to another hospital, repeating the process. Buinewitsch (1939) gives an early account of the literature. Bagan (1962) indicated a close relationship of these patients towards the medical profession. Barker (1962, 1966) described six British cases whom he regarded as severely disturbed hysterical psychopaths. The term Munchausen syndrome was given to them by Asher because their extraordinary adventures and travels were reminiscent of the tales of Baron von Munchausen related by Rudolph Erich Raspe (1785). According to Chapman (1957) Hieronymus Carl Friedrich Munchausen was a real man whose adventures were elaborated by Raspe. Patterson (1988) reports that von Munchausen was an honourable man, and a raconteur who told stories which were recognisably exaggerated for comic effect. Ironically Raspe had a fugitive lifestyle, incurred large debts, was wanted by the authorities in Germany for theft, and fled from Edinburgh to Ireland because of a mining scandal. But since Munchausen was not self-damaging or hypochondriacal, but was an engaging raconteur, the term hospital addiction (Enoch et al, 1967) is
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much to be preferred and is probably better than a number of others which have been suggested. Various types of Munchausen’s syndrome have been described, depending on the type of complaint, such as renal (Nickel, 1984), cardiac (Dickenson & Evans, 1987), meningitis (Marchant & Brown, 1990), pulmonary and hypoglycaemic (Mitchell et al, 1985). Other types of somewhat similar factitious illness have included factitious plumbism (Stephenson & Lewis, 1985), hypoglycaemia (Roberts et al, 1985) and chronic pain (Rimon et al, 1980; Fishbain et al, 1988). The two cases of Rimon et al (1980) show more features of chronic pain (possibly of psychological disorder) than of the artifactual Munchausen’s syndrome. Another case of Munchausen’s syndrome or factitious hypoglycaemia has also been noted in conjunction with alleged multiple personality disorder (Freeland et al, 1993). Factitious fever and self-induced infection present very taxing problems of diagnosis. Aduan et al (1979) reported 32 cases, together with important details of methods of investigation. Sixteen of the patients had a link with the health professions. Ten were students. Psychiatric findings most often indicated underlying severe personality disorder, most often called “borderline”, but also included “psychotic depression”. Reich & Gottfried (1983) identified 41 factitious cases in a teaching hospital over 10 years. The disorders identified included one that was fatal and others that were chronic, severe, and life threatening. The disorders fell into four subgroups: self-induced infections, simulated illnesses, chronic wounds, and surreptitious self-medication. Most of the patients were regarded as immature, passive and hypochondriacal. None had a major mental disorder. A somewhat similar problem of patients who sought multiple operations was described earlier and analysed dynamically by Menninger (1938). Enoch et al (1967) appraised the literature on hospital addiction succinctly and in detail, and Berney (1973) produced a further review. Cramer et al (1971) noted the occurrence of hysterical symptoms and suicide attempts in a number of these patients, all of whom simulated illness. Bursten (1965) and Cramer et al (1971) provide valuable discussions of these patients’ motivation. At least three out of four patients had had severe infantile emotional deprivation. One of them, for instance, was abandoned by both parents and sent to an orphanage when six months old, where he claimed he was brutally treated. In all cases there had been a good relationship with a physician during the period of ill-treatment, with the
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doctor being either helpful or powerful, or both, in the eyes of the patient. In later life many of these patients worked in paramedical jobs (as assistant nurses, etc.). This point is well made by Hawkings et al (1956) in their study of deliberate disability. This category describes mainly young, single women who fake illness and also may engage in procedures which endanger life. Their work provides both a partial identification with the doctor and a knowledge of medical detail which is helpful to the subsequent career of deception. The severity of the cases need not be doubted. Besides self-inflicted injuries, chronic self-poisoning may occur. One patient, a nurse, put herself into high output heart failure by excessive ingestion of thyroid hormones. One of the observations by Cramer et al (1971) is particularly worth noting. They write: “The patient usually arranges to foul up his own plot and to have the hoax uncovered. At this point, the staff responds with an angry condemnation of the patient, and with total loss of interest in his fate. The patient signs out – accusing the physicians of incompetence or malpractice – or he is discharged. At this point, it is difficult for the physician to recognize the psychological suffering of the patient and to refer him to a psychiatrist, and the patient is off until his next hospitalization.”
Occasional cases where a Munchausen-like syndrome has been produced in other adults have also been reported. Sigal et al (1986) described a case of a man who was sent to prison for producing physical illnesses in both his wife and his girlfriend, his wife eventually dying and the girlfriend becoming paraplegic from poisonous substances injected into her lower back. This man developed a possessive relationship with his male cellmate (himself a murderer) and repeatedly put him to sleep by administering sleeping pills mixed with alcohol, and injected turpentine, stolen from within the prison, into various parts of the body of the other man. Ultimately he inserted a safety pin into the urethra of his cellmate, who became critically ill and was saved only because of immediate surgical and medical treatment. The perpetrator was sentenced this time for attempted murder. Sigal et al (1991) consider that this behaviour functioned as a way of commanding the attention and respect of his surroundings by taking care of the partner with whom he was emotionally associated. The injections of the wife, girlfriend and cellmate made them ill, with the intention of forcing them to stay with
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him as dependants and fulfil his need for respect and admiration. The Munchausen’s syndrome by adult proxy is extremely rare and I know only this single report. Janofsky (1986) has described Munchausen’s syndrome as a presentation of folie à deux. In this case a relatively passive daughter, aged 25, appears to have adopted the life pattern of a more dominant mother who had already demonstrated the behaviour of Munchausen’s syndrome. Hyler & Sussman (1981) also described a case in which wife and daughter developed Munchausen types of behaviour and the husband and son (who was a physician) tended to support the multiple referrals and illness behaviour of the wife and daughter. Meadow (1977) was the first to identify cases of infants and older children being subjected to ‘Munchausen’s syndrome by proxy’, and a number of other cases have been described (e.g. Verity et al, 1979; McKinlay, 1986; Amegavie et al, 1986). Fisher et al (1993) describe a mother who insisted that her son was psychotic. In the Verity report the name Polle was chosen as the supposed name of the daughter of Baron von Munchausen, but it has been pointed out that this name is the name of the town where Maria Wilhelmina, the daughter of the baron’s second wife, was christened, the child was not his, and Polle was not the child’s name (Meadow & Lennert, 1984). Black (1981) further describes the extension of Munchausen’s syndrome to more than one child. The risk to children in these cases is a matter for immediate concern, especially for general practitioners, paediatricians, social workers and nurses. Meadow (1989) describes five main consequences for children who are falsely labelled as ill: (a) they will receive needles and harmful investigations or treatments (b) a genuine disease may be induced by the mother’s actions (c) they may die suddenly as a result of the mother misjudging the degree of insult (d) they may develop chronic invalidism (e) they may develop Münchausen’s syndrome as an adult – the children have learned and then take over the lying behaviour of their mother. According to Meadow the mother is the deceiver in nearly all cases: the father does not know what is going on and the mother tends to be the dominant person in the marriage and to be more intelligent and capable than her husband. The husband tends to
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be in the background and not supportive of his wife’s needs. The mothers themselves often have had a difficult childhood. Many have worked as nurses. About a fifth are “personal illness addicts” and notorious for presenting with unexplained illness. The explanation of this maternal behaviour is not well developed. It is suggested that the mothers more than appreciate the attention of doctors and specialist hospitals but do not have a mental illness, although they do have a personality disorder. Meadow observes “immense selfishness” in the mothers, who are “able to do horrific things to children because of their own unhappiness and to satisfy their own needs”. Sometimes also there is envy and violence and hatred towards the abused child. Fisher & Mitchell (1992) suggest that there are many psychiatric pathways to inducing illness in a child. Depression, personality problems and functional illnesses are often noted and about one-third of mothers may demonstrate Munchausen’s syndrome themselves. The more severe cases (in the mothers) are likely to have suffered severe sexual abuse and to have developed a severe personality disorder (Sugar et al, 1991). The prognosis of Munchausen’s syndrome is largely unknown. It has appeared to be intractable. However, Higgins (1990) described the notable management of a patient who was admitted at least 91 times to at least 29 hospitals over 14 years and treated for a wide range of conditions she did not have. She appears to have remitted. Firmness, frankness, patience, sympathy, support and medication all appear to have contributed to this response. Pallis & Bamji (1979) described a relatively long-term study of one busy case showing that from 1944 to 1979 he had been a patient in at least 68 hospitals and had at least 207 admissions. Pallis & Bamji called this man Stewart McIlroy, and Cruickshank et al (1979), writing about the report of Pallis & Bamji, called him William McIlroy, saying that he had been admitted to their care in one hospital and “much to his satisfaction” transferred to an old people’s home, where he was a model patient, helpful to the nurses, cooperative with the physiotherapist, and devoted to his books and the television. They added “typical of these patients, he appears genuinely unable to explain his behaviour: ‘You tell me – I’m wonky in the head’”. They reported that he felt secure in hospital and preferred it to the usual alternative of a hostel for down-and-outs and claimed to have engineered admission in recent years in response to “nerves” and a feeling that he might do others harm. To return to the adult who inflicts disability on himself or herself, Hawkings et al (1956) indicate that the psychopathology
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of deliberate disability is not fully understood, but for the following reasons suggest that it is related to an overdetermined masochism: (a) the actual infliction of the injury is a masochistic act (b) these patients usually come into teaching hospitals for investigations and these, in view of the obscure nature of the disease, are usually exhaustive, again catering for the patient’s masochism (c) they run the constant risk of detection and as many are nursing personnel, they are fully aware of this, yet voluntarily expose themselves to this risk (d) they are essentially conscientious and reliable people, but during this stage adopt a form of behaviour, with its lies and subterfuge, which is the antithesis of their moral code (e) they nearly all have inadequate sexual outlets and therefore sexual relations cannot be offered as a substitute for their excessive masochistic needs.
Aduan et al (1979) undertook sympathetic factual confrontation, but only after a plan for social and psychiatric care had been arranged for the patient. This usually caused considerable anger and matters were so arranged that this anger or rage tended to be directed at the attending physician or psychiatrist, allowing the primary physician, nursing staff and social worker to remain supportive. Improvement was obtained by this approach. Reich & Gottfried (1983) also recommended a sympathetic approach of frank disclosure or confrontation. After their procedure only 13 patients acknowledged causing their disorders but most improved and four of the most chronic became asymptomatic. None signed out of the hospital or became suicidal. Bursten (1965) takes the analysis of these matters further. Although recognising the comparison with hysteria, he notes the deliberate imposture involved and emphasises that the patient assumes a pretended identity. According to him impostors have high, unattainable ego ideals and use their imposture as a means of defence against the anxiety associated with feelings of inferiority. The patient he described gave evidence of feelings of genital inadequacy. Unlike the conventional impostor pretending to be a hero or great man or person of standing, these patients appear to be victimised and pitiful, their imposture taking a masochistic form in which they play a role inverse to that of the physician. In regard to the relationship to physicians, Cramer et al (1971) argue that this provides a re-enactment of the
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relationship with the parents. At first what the patient seeks is the re-establishment of a state of comfort and dependency, where the hospital setting and the physician play a care-taking, maternal role. However, a man who fills the role of parent for these patients must also take on the role of the bad, abandoning parents, against whom there are strong sadistic aggressive wishes. The initial pleasure in dependency and identification with the physician oscillates to antagonistic feelings. One way of subduing the antagonistic feelings is to turn them – masochistically – against the self. The competing operation of all these mechanisms can be seen in the persistent attendance at hospitals, the seeking of self-damage and the deliberate fouling up of the relationship once admission to hospital has been secured. The importance of the foregoing analysis is twofold. First, it provides us with some understanding of the strange and exceptional behaviour of these varied types of patients. Secondly, in the light of this understanding and of the severe trauma which they undergo, it becomes possible to view severe selfdamage as a sign of true and severe emotional disturbance; it is then not a whim or conceit aimed merely at deceiving doctors and living a pretentious, exhibitionist hospital-based life, which might be warmer and better fed than life in the outside world. It is an intelligible although very abnormal response due to overwhelming problems of emotional adjustment. Lesser degrees of similar emotional disturbance may be recognised in patients with less severe disability: in patients with anorexia nervosa, which is considered shortly; in patients with hysteria; and even in normal people under certain environmental pressures. There are occasional reports of brain damage associated with Munchausen’s syndrome or with hospital addiction. Barker (1962) suggested that cerebral damage might provide a basis for some cases. Fénelon et al (1991) have described quite extensive and prominent changes in the cerebral white matter in a 35-year-old patient with behaviour typical of the Munchausen’s syndrome. Neurological signs of the case were always transitory and obviously factitious, but magnetic resonance imaging showed patterns which are unusual in a patient of that age except in the presence of other illness. In this case earlier behaviour, such as episodes of induced hypoglycaemia, might have contributed to these changes, although the patient was never in coma; a prior acute illness in childhood or adolescence might have caused the changes which then predisposed to the adult behaviour, or there may have been a brain disease – unidentified – responsible for the Munchausen syndrome. This type of explanation at
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present remains quite insufficient to account for the behavioural phenomena.
Self-injury Tantam & Whittaker (1992) distinguish between self-harm, which is the broadest term and covers attempted suicide, and self-injury, which deals with self-mutilation and self-wounding. Self-mutilation (or the agreement to be mutilated as in religious flogging or voluntary crucifixion) can have a cultural background, and they cite many instances of this. Self-wounding refers principally to slashing or cutting – without suicidal intent – and is relatively common. They estimate that one out of 600 adults wound themselves enough to require hospital treatment. Johnson et al (1975), in a prospective study, observed an annual rate of 730 episodes per 100 000 in general practices, nursing homes, jails and hospitals, committed by 559 individuals per 100 000. They estimated a ‘true’ rate of 1433 per 100 000 per anum. In their survey of 240 females who regularly wounded themselves, Favazza & Conterio (1989) found that the commonest method was cutting (72%). It is salutary to recognise that self-mutilation can be a consequence of prison conditions (Johnson & Britt, 1967), sometimes in men who were putatively normal before their incarceration (Yaroshevsky, 1975). Solzhenitsyn (1973) and Kuznetsov (1975) described striking specific instances in the USSR. Yaroshevsky, who was himself imprisoned and worked as a surgeon, treated prisoners who had cut their veins, sewed up their mouths, sewed buttons on their bodies, disembowelled themselves, slashed off fingers, toes, genitals or ears or swallowed foreign bodies. Only one patient out of the five whom he describes as having swallowed foreign bodies was extremely psychopathic. The others “committed the mutilations as a result of the insufferable conditions of their lives”. It should be added in parenthesis that severe self-mutilation may occur in psychoses, post-encephalitic Parkinsonism (Goodhart & Savitsky, 1933), after taking hallucinogenic drugs (Vallotton, 1974), and with various organic brain syndromes and mental retardation. The most severe forms of self damage other than suicide are not usually thought of as being hysterical. They include selfenucleation of an eye (Ananth et al, 1984), other self-inflicted eye injuries (Tapper et al, 1979; Griffin et al, 1982; Rogers &
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Pullen, 1987; Soulios & Firth, 1986). In these cases the association with hallucinations or religious delusions and schizophrenia is common, but occasional patients show no formal psychiatric illness, such as case 1 reported by Rogers & Pullen, and the case of Griffin et al, who was considered to have a borderline personality disorder in addition to epileptic convulsions. Selfincineration as a suicidal attempt, likewise, usually appears to be a psychotic act by young, simple people with chronic severe disorders (Jacobson et al, 1986). Four cases of amputation or partial amputation of a hand described by Stewart & Lowrey (1980) also reflect severe psychotic illness – in their cases, depression. Hunger-strikers in prison camps and prison mental hospitals, (e.g. V. Fainberg, personal communication) choose a mode of protest which in fact exerts pressure on the prison authorities; they tend to be political prisoners, and a few have been convicted terrorists. Self-mutilators tend to be criminal convicts (Yaroshevsky, 1975). In both instances, however, there is some realistic hope of obtaining an alteration in the prisoner’s circumstances. Selfmutilation in a severe Soviet prison regime can be regarded as a response by normal or relatively normal people to extreme suffering. Its dynamic mechanisms may, however, resemble those of other self-mutilations. Less severe self-mutilation is a feature of malingering in relation to military service. Flicker (1942) regarded it as an extreme form of malingering. Quoting Buinewitsch (1939) and Hulett (1941) he cites a variety of remarkable and bizarre ways of producing self-damage, and after reporting a case of his own, where loss of the right index finger resulted, he argues that the self-inflicted injury may be produced by a man who is neither amoral, nor a physical coward, but who does not accept the normal community goal. The least degree of self-wounding is discussed by Ping-Nie (1969) under the title “The syndrome of delicate self-cutting”. Delicate self-cutting is perhaps a hysterical gesture, but selfdamage of a comparable degree with self-applied constricting bands has been known quite commonly as the result of a delusional illness (Dawson-Butterworth et al, 1969). Self-cutting appears to be a rather special example of deliberate self-harm which may have links with hysteria but also involves other traits and mechanisms. Gardner & Gardner (1975), in the first published controlled study of repeated self-cutting in patients of normal intelligence, noted that the act was initially private and most often served to relieve an unpleasant feeling of tension. Compared with other psychiatric patients, the self-cutters were
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much more obsessional on the Middlesex Hospital Questionnaire and the Tavistock Inventory. Obsessionality has also been noted in criminal self-cutting psychopathic learning disabled patients (McKerracher et al, 1968) . Although hysterical traits are often thought of as being the opposite end of the spectrum from obsessional ones, the two may occur together. Imitative cutting (Offer & Barglow, 1960; McEvedy, 1963), frigidity (Gardner & Gardner, 1975) and prominent dependency needs may all have a special association with self-cutting. It can therefore be supposed that hysterical mechanisms may play a part, but certainly not the sole and perhaps not the main part, in this pattern of activity. Pattison & Kahan (1983) reviewed 56 published case reports of self-harm and noted that they revealed a typical pattern of onset in late adolescence, multiple recurrent episodes, low lethality, harm deliberately inflicted upon the body, and extension of the behaviour over many years. They felt that this differed from suicidal behaviour and other classes of self-destructive behaviour. These patterns appear to match the other reports just discussed, but not the prison cases. Even if these phenomena may be minor, they can also be quite common. Ballinger (1971) reviewed the populations of a hospital for the learning disabled and a psychiatric hospital and noted that 93 out of 626 learning disabled patients (14.9%) and 20 out of 584 psychiatric patients (3.4%) had injured themselves in the previous month. Even in many of the non-prison instances, patients engaging in self-injury have been regarded as having a hysterical psychopathic personality. Mechanisms of regression and dependence are said to characterise the personality of patients with hysteria (see Chapter 22). The symptoms or behaviour pattern in deliberate disability or hospital addiction constitute a manipulative form of behaviour which provides a primary emotional gain. In military and prison circumstances there is an environmental gain and perhaps an emotional one as well. Except for the lack of conscious deliberation in hysteria, there are thus at least three major similarities between the other syndromes and hysteria, that is, gain from solution of a conflict, dependency and regression in the personalities involved, and a strongly manipulative effect upon the environment. By comparison with malingering and the extreme forms of hospital addiction, which are rare, attempted suicide is very common. Some have chosen to call this self-poisoning (Kessel, 1965) or parasuicide (Kreitman et al, 1969), terms which represent no advance because one, self-poisoning, does not cover all the cases (there are attempted suicides by other means), and the
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other, parasuicide, may take away the generally valid implication that there is at least an attempt to die, no matter how slight, involved in the act of attempted suicide. However, the term parasuicide is now very widely used. Stengel & Cook (1958) showed that attempted suicide represented a mixture of motives – some directed towards death, some towards life. The manipulative element in many attempted suicides is well established, and an interest in the environment and its reaction is often remarkably strong even in those who most effectively set out to kill themselves. The appeal and manipulative qualities of so many attempted suicides gives them a hysterical character, as has been noted clearly by Carter (1972). Stengel (1964) commented as follows: “the so-called hysterical personality ... tends to react to frustration with physical symptoms or transient abnormal mental states such as memory loss. These people have an insatiable urge for love and attention from their fellow men and sometimes they consciously exploit the appeal effect of the suicidal act for this purpose. It would however be a mistake to regard the majority of suicidal acts as hysterical because they have an appeal effect. Their impact on other people only emphasises why hysterical personalities should so often be tempted to risk their lives in that way.”
Goldney (1981) showed that young women who attempted suicide did not score overall in a more hysterical manner than women in a comparison group when assessed on the Hysteroid Obsessoid Questionnaire. However, among those whose attempts were least lethal there was a subgroup who scored in a more hysteroid manner than the remainder. As Stengel & Cook (1958) and many others have shown, attempted suicide can occur with all forms of psychiatric diagnosis and personality, and is certainly not limited to those who have conversion symptoms or hysterical personality. It therefore represents a common expression of motives and of patterns of reaction which are selectively strongly represented in patients with hysterical manipulative traits. It is worth remarking here that there are other circumstances in which self-injury may sometimes be induced as a result of hysterical personality or traits. Patients with analgesic-induced renal nephropathy have a high incidence of abnormal personality traits (Murray, 1973). They do not pursue their addiction in order to manipulate others, but rather, in the same way as some alcoholics who also damage themselves, for the sake of the gratification which their practice offers.
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Winchel & Stanley (1991) note that the main groups of individuals who manifest self-injurious behaviour are mentally retarded patients, psychotic patients, prison populations and patients with character disorders. There is an increasing tendency to treat self-injurious behaviour with alternative pharmacotherapeutic treatments. Winchel & Stanley conclude from their review that self-injurious behaviour may be associated with serotoninergic dysfunction. Thus, serotonin reuptake inhibitors may be potentially useful. Other medications have also been tried, including neuroleptics, lithium, carbamazepine, minor tranquillisers, propranolol, baclofen, stimulants and various antidepressants, but especially serotonin reuptake inhibitors. The relevance of these observations here is that there is an increasing tendency to see certain types of behaviour, some of which were regarded as hysterical, as being linked more to obsessional illnesses (which respond notably well to serotoninergic antidepressants) or to specific biochemical dysfunctions. For example, a case of trichotillomania described by Primeau & Fontaine (1987) responded extremely well to fluoxetine.
Anorexia nervosa Anorexia nervosa is a further condition in which the production of physical illness necessarily follows from the psychological state. Between it and the hospital addiction syndrome there is a borderland occupied by patients with deliberate disability. Their characteristics are like anorexia nervosa in several particulars, as shown in Table 8.1. They differ from hospital addiction in that the threat to life in the latter, although important, is more incidental and also in the fact that hospital addiction is apparently much commoner in men. They differ from hysteria in respect of the risk to life which, except in hysterical attempted suicide, is usually minimal; and indeed hysteria may have life-preserving characteristics, for example in soldiers, as indicated in the discussions of shell-shock in Chapter 5 and of Kretschmer’s views in Chapter 6. Anorexia nervosa was described as early as 1689 by Morton under the title “nervous atrophy”, by Gull in 1868, who gave it its current name, and by Lasègue in 1873 (see Theander, 1970). Lasègue actually called it “anorexie hystérique”. A full discussion of this syndrome is beyond the scope of this work and is provided by a number of writers, including Dally (1969) and Theander (1970). Smart et al (1976) indicate that the personality profile of the typical sufferer is of a highly neurotic and introverted
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person with moderately severe obsessional features and average intelligence. The patients are nearly all single, young women with loss of weight, amenorrhoea and unwillingness to eat. This unwillingness to eat consists of a refusal to take nourishment, often despite a strong desire to do so. The syndrome is frequently associated with other psychiatric conditions; for example, Kay & Leigh (1954) found 50% of their patients to be depressed and 40% hysterical. Other estimates of ‘hysteriform’ characteristics range from one-third to one-half of patients. Dally described the main types of clinical picture in anorexia nervosa as the obsessional, comprising 57 out of 97 patients (59%), and the hysterical comprising 19 (21%). Other patients presented a mixed picture, including a further three with conversion symptoms. Conversion symptoms are thus rare but have been described by others as
Table 8.1. A comparison of hysteria, anorexia nervosa and deliberate disability (a) Hysteria
(b) Anorexia nervosa
(c) Deliberate disability
Age
Wide distribution
Majority 16–20 (Kay & Leigh, 1954); in 70% onset before 26
Majority 15–25
Sex
Mainly female, not same extent as b, c
Mainly female (Kay & Leigh; 34 women, 4 men)
Mainly female
Marital status
Both married and single
Commoner in Commoner in single single women women (Kay & Leigh; 32 single, 6 married)
Personality
Often inadequate, with tendency to dissociation
More effective in a; More effective than a obsessional traits common
Intelligence
Broad distribution, but frequently low
Usually average or above
Psychopathology
Symptoms directed to immediate gain
Not usually directed Not usually directed to immediate gain to immediate gain
Suggestibility
Common, often illsustained
Rare
Degree of morbidity
Physical suffering or threat to life sometimes present
Gross disfigurement; Gross disfigurement; threat to life threat to life common common
After Hawkings et al (1956).
Usually average or above
Rare
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well. Anxiety symptoms, manic–depressive illness and schizophrenia have also all been described in conjunction with anorexia nervosa. Bruch (1973) only rarely found the diagnosis of hysteria to be appropriate in her patients, but considered that the words ‘weak ego’, ‘diffuse ego boundaries’ or ‘narcissistic character’ were often applicable in conjunction with rather broad and nonspecific formal diagnoses. Thus anorexia nervosa may arise independently or in association with a variety of psychological states. Among other features, Dally characterises his hysterical patients as markedly frigid and as denying concern, anxiety or depression at not eating. Almost all patients employ subterfuge or deception to avoid eating, even when under pressure to do so, and the two commonest groups of personality traits described are those of emotional immaturity and obsessionality. The pathogenesis of anorexia nervosa appears to be multifactorial. Concern with dieting is always present, but genetic predisposition, family attitudes, prior gastrointestinal illness, mood changes, recent stresses, and personality disorder may all contribute. However, few if any of these factors appear to be essential to the development of the illness, including personality disorder (Garner, 1993). Garfinkel et al (1980) emphasised the heterogeneity of anorexia nervosa. Bulimic patients, who have only lately been distinguished from anorexic ones, are marked by self-induced vomiting and purging, and also display a variety of impulsive behaviours including use of alcohol and street drugs, stealing, suicide attempts and self-mutilation. Garfinkel et al (1983) looked at differences between patients with anorexia nervosa, weight loss and vomiting, and patients with conversion disorder who were admitted to hospital for the treatment of vomiting. The diagnosis of conversion disorder was based upon a chart review and a decision that the presenting symptoms were related to “a manifestation of core conflicts that were represented at a symbolic level”. Judgements of that sort present some difficulties in reliability, and unusually for a group with conversion symptoms the supposed conversion patients were older than the anorexia nervosa ones (although anorexia nervosa does tend to affect a young population). In any event, the two groups were readily distinguished, the non-anorexic patients having significantly less preoccupation with weight, body size and dieting, underestimating their actual size, and giving a larger estimate of their ideal size, in contrast with the anorexic group. They also display a stronger sense of self-control, less obsessive–compulsive behaviour, and more consistent social
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relationships. They had also had more medical illness and illness requiring surgery. These patients may not have been typical of hysterical conversion illnesses but, insofar as their patterns reflect a hysterical disorder, this is another group that does not readily resemble anorexia nervosa. Crisp (1970), like others, emphasises the way in which anorexia nervosa serves as a means to overcome sexual conflicts. The obsessional characteristics of so many patients, and the ascetic mechanisms of defence which are prominent in adolescence (A. Freud, 1937, 1946), are used to the limit in anorexia nervosa. Obviously, conflicts occur particularly in relation to oral drives, but also in relation to genital satisfactions and the acceptance of the future maternal role by girls. Such conflicts are not hard to find in patients with hysterical characteristics, in whom frigidity and immaturity are common (although not invariable). The occurrence of motor conversion symptoms has even been described in a case of anorexia nervosa (Scherrer et al, 1972). Hawkings et al (1956) (Table 8.1) related the characteristics of patients with deliberate disability to those with hysteria. Szyrynski (1973) observed that hysteria resembles anorexia through some superficial similarity of the mechanisms of denial and “blissful indifference”. In his view hostility is prevalent in both conditions, the secondary gain is more clearly manifested in hysteria, and self-destructive tendencies are less severe. Goldney & Simpson (1975) have seen a link between selfmutilation, hysterical personality and disturbances of appetite. Their article describes three female patients who showed an association between these symptoms. Their leading example is a married woman who had four children out of seven pregnancies. Three of the pregnancies terminated early, allegedly as the result of spontaneous abortion. In one pregnancy she spent seven months in hospital, and in another, five, for vaginal bleeding, and after her seventh pregnancy she underwent two subsequent curettage operations for bleeding and a hysterectomy. A history was obtained of her using a metal comb to cause bleeding. Apart from the occasions of conception, sexual relationships appear to have been relatively infrequent and she was regarded as having a severe hysterical personality disorder. In addition she gave evidence of anorexic symptoms, with associated vomiting, abdominal pains and loss of weight. Another patient, with clear evidence of anorexia nervosa and bulimia, shaved her pubic hair after she developed an aversion to body hair, particularly to that in the pubic area. A third patient gave a history of eating troubles, not quite enough to satisfy the
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authors that she had anorexia, which were also associated with the shaving of pubic hair and hysterical personality characteristics. The authors note other papers (Goldfield & Glick, 1970; French & Nelson, 1972) which discuss self-mutilation in women; Goldfield & Glick emphasised its link with many admissions to hospital, a complicated gynaecological history and the hysterical personality, while French & Nelson emphasised the link between mutilation and dysorexia as defined by Guiora (1967). Another patient, described by Simpson (1973), was also noted to have evidence of both dysorexia and genital mutilation. Goldney & Simpson argue that the combination of dysorexia, female genital self-mutilation and hysterical personality represents a triad of features which has a particular clinical pattern, and they call it the Caenis syndrome, after Caenis, described in the Metamorphoses of Ovid. Caenis was the loveliest of all the girls in Thessaly but refused to marry anyone and was raped by Neptune. In recompense Neptune granted her one wish and she said “The wrong I have suffered evokes the fervent wish that I may never be able to undergo such an injury again. Grant that I not be a woman and you will have given me all.” They argue that the circumstances preceding this wish and the feeling expressed in it appear to embody many aspects of the patients whom they describe with the triad of clinical features outlined. Such a combination of rare phenomena is surprising and its reported occurrence in a number of patients gives good grounds for the assumption that the association has a meaning. It certainly supports the idea that there is a link between phenomena of deliberate disability and anorexia nervosa and hysterical personality. Apart from these special associations, it is evident that all types of psychological illness may promote anorexia nervosa. Hysterical personality characteristics, including infantile dependent traits, contribute to or are associated with its development in a significant number of patients, and this provides some linkage with hysteria. The second major link is that all types of anorexia nervosa involve either conscious or unconscious production of symptoms and the denial of a problem. This problem may be similar dynamically to the problems of a number of patients with hysteria, that is, a difficulty in dealing with sexual relationships as a result of childhood experiences and family attitudes. Crisp (1970) sees the particular difficulty of patients with anorexia nervosa as being due to a ‘weight phobia’. It may be argued that – just as other phobias are not uncommon in patients with hysteria – we can suppose that a ‘weight phobia’ leading to anorexia nervosa could be one expression of the problems of
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patients with hysterical characteristics. It could equally of course, like other phobias, be either symptomatic of or associated with depression, anxiety, or schizophrenia. However, what is special to patients with anorexia nervosa compared with those with hysteria could be a higher degree of masochism and a lower, albeit still excessive, degree of narcissism.
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Amnesia, pseudodementia and the Ganser syndrome: denial of illness
“To think that two and two are four And neither five nor three The heart of man has long been sore And long ’tis like to be.” (A. E. Housman, Last Poems, XXXV)
The question of deception often arises in two more groups of patients who apparently have memory disturbances of psychological origin. They are those who display pseudodementia, or features of the Ganser syndrome, and those who have a claim to compensation. It is convenient to discuss the first group in this chapter, and the second group in Chapter 10. The supposed syndrome of multiple personality disorder, which is linked with fugue states and amnesia, requires a separate discussion (Chapter 20).
Hysterical amnesia Symonds observed (Appendix C) that hysterical amnesia, in his experience, was associated with awareness by the patients’ that they were counterfeiting their symptoms. Others find that it is wholly genuine in the sense that some patients appear truly lost, and on recovery give evidence of troublesome personal stresses which account for their condition. In civilian life, hysterical amnesia is rare. Lewis (1961) reports that in 1259 patients admitted within a period of 12 months to a hospital receiving psychiatric emergencies in London, 58 had 112
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organic amnesic syndrome, but only two patients were admitted during the same year because of hysterical amnesia for the details of their personal identity and experience. Lewis (1953) showed that a famous case of hysterical amnesia, which became the subject of a book on multiple personality, occurred in a man with a history of severe brain damage (cf. Chapters 11 and 20 for an account of this patient). A very famous case of carbon-monoxide poisoning with probable organic memory impairment which initiated a subsequent hysterical amnesia resembling the dysmnesic syndrome was originally described by Grünthal and Storring. This has been much argued about in the German literature and carefully reviewed by Zangwill (1967). The long persistence of the syndrome was ultimately shown to be due to deception. There is other evidence (Chapter 11) that hysterical symptoms are linked with brain damage. Occasionally fugue states with a hysterical pattern arise in depressive illness (Stengel, 1941). At the National Hospital for Nervous Diseases at Queen Square, a neurological hospital receiving patients from the whole range of a large metropolitan area and beyond, more cases of hysterical amnesia are seen than in general psychiatric practice, but these patients tend to have significant organic disease. Mr J. Stevenson (personal communication) kindly provided the following striking findings from Queen Square. “of 5000 consecutive patients seen in the psychology department between February 1969 and September 1974, 57 (1.14%) were classified as having pseudodementia either on its own or in conjunction with other psychological abnormalities. This classification also included patients with pseudoamnesia without pseudodementia. Of these 57 patients only 4 were passed by the doctors as being free from any neurological complaint; 93% of the pseudodements therefore also had some neurological disorder and only 7% were neurologically normal.”
The differentiation of a pseudodementia in the elderly from Alzheimer’s disease is important. The former is most often due to a depressive illness, whether or not the patient has a mild degree of dementia as well. Wells (1977, pp. 8,21) and Fisman (1985) have both discussed the features which help to distinguish the two groups of patients. These patients tend to have less immediate evidence of depression and the amnesia is the presenting problem. Careful inquiry almost always yields some evidence of depression in the patients with pseudodementia. The distinction is important because correct treatment of the depression may be highly beneficial, and the erroneous diagnosis of dementia may lead to
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long-term inappropriate care. However, Liberini et al (1993) have shown that a pattern of pseudodementia can occur in dependent elderly persons without depression. The topic is less relevant to hysteria than was once thought. The principal criteria of hysterical amnesia are a loss of knowledge of personal identity combined with preservation of environmental information and, often, complex learned information or skills. If patients have evidence of memory impairment combined with an impulse to wander, this constitutes a fugue state. Although we have noted that hysterical amnesia is rare in many settings, there are a few busy clinics which have come across numbers of patients, and there are at least seven reports of a series of patients with amnesia for personal identity or with a fugue state. Abeles & Schilder (1935) described 63 patients (31 men, 32 women), of whom 80% were in their second, third or fourth decades. Usually there was some preceding depression. Of these, 47 recovered spontaneously, and head injuries and carbonmonoxide poisoning were ‘not rare’. Four cases of simulation were recognised. Kanzer (1940) described 71 cases (41 men, 30 women) from Belle Vue Hospital, again, mostly between 20 and 40 years old. He noted that headache was a frequent complaint in his patients. Eight cases were atypical, having epilepsy or an organic disturbance and some resemblance to confusional states. Alcohol was a possible factor in 17 of his patients and emotional problems were established in at least 43. Experiences such as jilting, severe marital conflicts or bad financial difficulties were common. Most of his patients were depressed or agitated on admission. Wilson et al (1950) from the Philadelphia General Hospital described 59 cases of amnesia seen over eight years in private practice or in the neurological or psychiatric hospital services. Of these, 28 were held to be malingering, 15 were cases of central nervous system diseases, 7 were cases of psychosis and only 5, in their view, had hysteria. Of the 28 ‘malingered’ or ‘volitional’, three admitted deceit. This is an unusually high estimate of the numbers malingering and perhaps reflects exceptional confidence on the part of the authors in diagnosing that condition. It indicates, however, that there are some people who feel that deceit is a recognisable aspect in many patients with hysterical amnesia. Unfortunately, no indication is given of how Wilson et al were so successful in establishing the occurrence of malingering when other authors find it such a difficult problem for many cases. Kapur (1991) provided a useful description of a patient who reported memory loss of five days, during which he had wandered
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extensively. A recognition memory test was designed to assess his memory for public events which had taken place over the past six months. He had used his chequebook during the period of his wandering and he had looked after his needs and his personal hygiene, but he was unable to recall important personal information. The discrepancy between personal and public memory established the psychological basis of the memory loss rather than a neurological cause. McKinney & Lange (1983) reported a fugue state in an individual who had had previous episodes of fugues and whose father had behaved similarly. They noted that this offered a “learned” basis for the development of the fugue in their patient. Their patient did have a history of head injury, with a four-week hospital admission, but that was very remote from the time of his most recent fugue. The use of the chequebook in Kapur’s case raises the issue of malingering. Pankratz et al (1975) described a technique called symptom validity testing to detect malingering. It is based upon finding a response pattern which is clearly worse than chance and its successful use was described in further cases by Pankratz (1983) and Binder & Pankratz (1987). Stengel (1941) described 25 patients with fugues and is responsible for specifying the importance of depression in such patients. Ten of his patients had epilepsy, one schizophrenia, and the rest had typical manic–depressive, hysterical or psychopathic conditions. He described many instances of traumatic childhood experiences in his patients. Parfitt & Gall (1944) added another series on fugues. Berrington et al (1956) examined 37 cases of fugue seen at a psychiatric hospital (Runwell Hospital) and compared them with 37 psychiatric patients matched for age and sex. Sixteen of the index patients had severe head injury, and three had doubtful head injury. Three of the controls had head injury. Depression was prominent in both groups. They agreed with Stengel that lying and depression were prominent in fugue states but their patients had less evidence of a disturbed childhood. Hysterical mechanisms were common in their group of fugue patients, and from the figures quoted it is clear that cerebral trauma was very much more common than in controls (P < 0.01). They noted that this might produce indirect facilitation of the psychiatric symptom. Kennedy & Neville (1957) put together a series of 74 patients with sudden amnesia examined variously in Shropshire, London and Newcastle-upon-Tyne. It was found that 37% had gross organic
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disease of the central nervous system, 12% major epilepsy, 47% hysterical amnesia, 27% psychopathy or a very bad employment record, 16% a fear of arrest or disciplinary action, and 10% a functional psychosis. Seven per cent admitted malingering. The categories overlapped and, in addition, feeble-mindedness or illiteracy affected 3%, senility another 3%, and 4% of the patients were under 12 years of age. Dual organic and psychological aetiology were observed in 41% of the patients. Responses to suggestion were carefully considered, and the authors held that malingered amnesia is not usually difficult to detect but that hysterical amnesia frequently resembles malingering, and malingering may be admitted under pressure when in fact there is strong evidence of an organic or psychological cause. They remark that a confession cannot therefore be accepted as certain evidence of malingering. Their figures for the frequency of established malingering are much more typical of the general view than those of Wilson et al (1950). Taylor & Kopelman (1984) found that 19 out of a sample of 212 men (9%) charged with a number of offences claimed amnesia for the activity for which they were subsequently convicted. The amnesia only occurred in those who had committed violence and was most frequent following homicide. Four had a primary depressive illness and the remaining diagnoses were almost equally divided between schizophrenia and alcohol abuse, and none of the amnesias had any legal implications. The circumstances in these cases suggest that a variety of mechanisms accounted for the amnesia, including repression, dissociation and alcoholic blackouts. Even in the alcoholic cases, psychological defence mechanisms were probably of some importance. It appears that various situations, and especially severe emotional conflict and a background of brain damage, account for the bulk of cases of hysterical amnesia in civilians in the major Englishspeaking countries. Depression is also common, particularly in fugue states. Cases of amnesia with an organic basis are relatively more common in military populations than in civilian ones. Military psychiatrists have frequent experience of patients with circumscribed amnesia, usually, as Sim (1974) points out, with a powerful associated motivation related to over-riding duty, such as sailors who have jumped ship, men who have married bigamously and, in the writer’s experience, soldiers who are absent without leave. As already noted, the classic features of hysterical amnesia are a loss of memory for personal experiences and identity up to the point at which the loss of memory is discovered. Past skills (e.g. at arithmetic, chess playing) are preserved and extensive
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stores of information may be used about the government of a country, its geography and history and so forth. The patients often look somewhat puzzled, but ongoing information provided to the individual is retained. Unlike in Korsakoff’s syndrome, long conversations may be engaged in without patients repeating themselves. “I know my name is Private Thomas Atkins and I belong to X Regiment because it is on my identity card.” This is the paradigm of the military hysterical amnesic patient. In such cases differentiation from the organic dysmnesic syndrome is not difficult. Other patients, however, present a more confusing picture. A difficult minority, as in the Grünthal–Storring case, present with features perhaps partly organically based which are hard to discriminate, the differential diagnosis being made on the basis of considerations like the extent of retrograde amnesia, and inconsistency in responses and behaviour. Some medication may induce anterograde amnesia or partial amnesia. Intravenous benzodiazepines are quite well known for this effect, which may be confused with a psychologically induced loss of memory. Even oral lorazepam can have this effect (Scharf et al, 1983) and presents a problem on occasion with differential diagnosis.
Pseudodementia and Ganser syndrome A more bizarre pattern is presented by certain other patients overlapping with the above who claim to know nothing about their identity or large tracts of their past experience and also claim to lack knowledge of established skills. Objects may be correctly used but misidentified and their use wrongly described. A knife may be called a soup ladle, a spoon is said to be used for cutting bread. There is a pattern of behaviour which the patient thinks indicates madness, such as drinking urine because this is thought to be what lunatics do (Sim, 1974). In this pattern, known as pseudodementia, the patient may give answers which are commonly described as ‘Vorbeigehen’ or ‘Vorbeireden’ (Moeli, 1888), meaning to pass by or to give approximate answers, such as a cow has six legs, or 2 + 2 = 5, or the patient counts a simple series with omissions, for example 1, 2, 4, 6, 7, 8, 10, 11, 13, 18, 19, 21 (Snell, 1855; cited by Bucknill & Tuke, 1862, p. 372), the colour of the sky on a fine day is pink, and so on. Such answers are plainly silly, although the individual shows coordinated behaviour and coherent speech.
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This phenomenon, perhaps indicating feigned insanity, was noted as long ago as 1608 by Guazzo and in the 19th century by Snell, Tuke, Maudsley and Moeli (see Enoch et al, 1967). In 1898 Ganser in fact described three prisoner patients who showed the central feature of Vorbeireden and a number of additional features, namely altered consciousness with impaired grasp of attention and concentration, a memory defect, anxiety, perplexity, hallucinations and manifestly hysterical motor and sensory symptoms. The differential diagnosis has to be made from the occasional schizophrenic patient whom Bleuler (1950) and later Sim (1968) noted to show ‘a buffoonery syndrome’ which is, however, associated with positive evidence of schizophrenia. Enoch et al (1967) and Whitlock (1967a) have reviewed the literature. Whitlock notes that the full Ganser syndrome is very rare. Some authors use the terms pseudodementia and Ganser syndrome interchangeably. Others hold that they are distinct syndromes. Whitlock reasonably enough supports the suggestion of Scott (1965) that the Ganser symptoms should be distinguished from the Ganser syndrome, the latter being characterised both in Ganser’s patients and Whitlock’s by impairment of consciousness. Whitlock further points out that the condition is not confined to prisoners. He himself described six patients, of whom five had convincing evidence of brain damage and the other a schizophreniform psychosis. He draws attention to further reports of the syndrome in non-prisoners; only 4 of the 18 described with adequate detail in the English literature between 1934 and 1962 were in prison, and Sim (1974) mentions a case found in association with a large parasagittal meningioma. Anderson & Mallinson (1941) described three most convincing cases in naval personnel, one of whom had evidence of schizophrenia and the two others retarded depression. Tsoi (1973) reported 10 cases of amnesia from Singapore, where none of the patients could answer simple questions or add or count. Seven had fugue or trance-like states, six had auditory hallucinations (four of these also had visual hallucinations) and one had conversion hysteria. Head injury or brain damage (with a claim for compensation) was present in one only. The patients were Indians, Malays and Chinese, the first group particularly being over-represented in proportion to their numbers in the population. Three faced trial for murder, five wished to leave the army or retire early on medical grounds, and one was seeking to escape from domestic problems. Tsoi found the disturbances of consciousness hard to confirm, being “too subjective and ill-defined to be good criteria”. Milder forms of pseudodementia may be associated with depression in younger people, just as they are in the elderly.
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Friedman & Lipowski (1981) describe such a case of a conversion symptom associated with reactive depression. Weller (1988) described hysterical behaviour in four patients from communities with a patriarchal social pattern, including hallucinations in one patient, and a state of being found “unconscious” in her sister. There were more prominent Ganser symptoms in the third woman, a spinster, aged 28, and fainting and weakness in the voice of a patient who was in conflict with her parents about her wish for more education. The emergence of Ganser-like symptoms in one of these patients was due to substantial stress, but not associated with either organic brain disease or involvement in criminal activities. Rieger & Billings (1978) reported yet another association with Ganser syndrome: being a litigant. The patient was a 38-year-old married, retired, police officer who was involved as a plaintiff in three separate substantial actions for damages. He showed memory impairment and the syndrome of approximate answers, and the authors considered that he was showing the syndrome of approximate answers with dissociative phenomena, and conversion symptoms. This does not appear to have been a full-blown case of Ganser syndrome, but certainly demonstrated Ganser symptoms. Feinstein & Hattersley (1988) found a Ganser syndrome with approximate answers and evident dysprosody in one patient, with a number of changes in the quality of speech, including a rising inflection at the end of a sentence, halting, laboured and telegraphic speech, and a tendency to omit indefinite articles or auxiliary verbs. No organic damage was found and the illness was attributed to psychological causes. Yet another case of Ganser syndrome has been described in an Indian boy, aged 11 (Dabholkar, 1987). Two major lines of evidence have to be accepted both with hysterical amnesia and with other hysterical symptoms. One is that this type of syndrome may be promoted by organic cerebral illness; the other is that appropriate motivation is a sufficient cause, especially in unsophisticated subjects. A hysterical syndrome, which may be provoked either organically or psychologically, presents an important theoretical problem to which we will return again (Chapter 11). Meanwhile, we can recognise that the unsophisticated, the immature and the brain-damaged, when under sufficient stress, can all produce symptoms which attempt to solve a conflict. If, as Housman pointed out, the heart of man may want 2 + 2 to make 5 or 3, the unconscious mind of man often has little difficulty in satisfying itself that it has done so. The motivation may be conscious, unconscious, or both. If the patients do not show organic illness, they show evidence of psychological difficulties and even classic functional psychoses. They also indicate a
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continuum of clinical phenomena between awareness and unconscious motivation in the production of hysterical symptoms. Ganser syndrome may be regarded as a factitious mental illness, but not all factitious mental illness is the same as the Ganser pattern. Various reports exist of the simulation of psychotic symptoms somewhat resembling the Munchausen syndrome or occurring just once on their own. As discussed in the previous chapter, King David (I Samuel, 21, 11–15) provides one of the earliest examples of feigned psychosis, and Jones & Llewellyn (1917) state that the simulation of psychological illness is very rare. Jefferson & Ochitill (1982) have questioned whether the syndrome exists at all as a free-standing entity. However, Hay (1983) describes the apparent simulation of psychosis occurring as a prodromal phase of schizophrenia in extremely deviant premorbid personalities. Perhaps the commonest situation of feigned psychosis which psychiatrists encounter occurs in patients who have had a schizophrenic illness and either feign recurrence (Ritson & Forrest, 1970) or claim the continuation of symptoms which have been put into remission by treatment (Pope et al, 1982), in order to stay in hospital. Sale et al (1979) have described three cases of ‘Munchausen syndrome’ presenting in a psychiatric context, and Cheng & Hummel (1978) described another two cases, one presenting with apparent rambling talk, loose associations, and so on, and the other presenting with depressive complaints, both of whom appear to behave like Munchausen patients, becoming angry or demanding and discharging themselves. All these seem to reflect an effort to make use of some social or economic benefits which admission to hospital might provide, but are likely only to be undertaken by individuals who either have had a psychosis or have a severe personality problem as well. Anthropologists have also been known to arrange the feigning of psychotic illness for their own purposes in studying the operations of psychiatric units (Rosenhan, 1973). Feigned illness has been present following bereavement (Snowdin et al, 1978), in alcohol abuse (Caradoc-Davies, 1988) and in posttraumatic stress disorder (Sparr & Pankratz, 1983). In some circumstances the need to solve a conflict may produce not an illness but denial of one which is present. This provides an important contrast to the foregoing.
Denial phenomena Mechanisms of denial are frequently discussed in writings on hysterical and simulated illness. In such situations it is the denial
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of problems which is noted, while claim is laid to the status of illness. However, an intermediate phenomenon, denial of concern, is implicitly evident in the notion of belle indifference. From this it is a fairly easy step – perhaps too easily made – to the idea of denial of illness. Patterns of denial of illness show a curious polarity in relation to hysteria. They occur clearly in anorexia nervosa, whose links with hysteria we have explored. And they are at the same time opposed in logic to the basic hysterical symptom. Perhaps it is reasonable to regard denial, tout court, in psychological illness as a fundamental phenomenon; and to expect its application to specific situations to produce the polar contrasts just mentioned. Thus denial may be of a conflict, when it will cause a symptom; or of a symptom or fear, when it will cause detachment of some sort in mood. The disposition to use the basic mechanism of denial can thus be seen as a mechanism of defence which we regard as typically but not invariably hysterical. The psychiatric settings in which denial occurs are varied. Weisman (1972) has reviewed the matter. Besides those which we have been considering, bereavement and mourning have been widely regarded as providing occasions for denial of the loss. Hallucinations of the dead person may occur in more than 50% of bereaved individuals (Rees, 1971). Mourning phenomena, especially keeping a little museum of relics of the departed, but also the more common and culturally accepted practices of visiting cemeteries, laying flowers and uttering prayers, represent a potential for maintaining links which objectively have been ruptured, even though emotionally they may still persist. Denial of cancer or of approaching death is likewise a common phenomenon. Numerous reports indicate the readiness with which doctors believe that patients do not wish to be told of these conditions (medical denial?) and with which patients ‘forget’ the prognosis which they have been given (Saunders, 1966; Hackett & Cassem, 1974). Anyone who is faced with disaster or bad news tends to react initially with disbelief or denial, but successful denial is difficult to sustain, and a fuller realisation overtakes most people, whether or not information is given to them in words (Saunders, 1975). Thus persistent denial may be more related to individual personalities and their favourite defence mechanisms. Hackett & Weisman (1962) observe that the processes of denial are notoriously active in the dying patient and that it is not uncommon to hear a moribund patient speak of going on a vacation. They think that this type of global or massive denial seems to be more common among patients facing sudden death than among those dying slowly. For example, 16 out of 23 patients
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on a cardiac pacemaker for heart block flatly denied fear or concern with death, in spite of the fact that they had been fully informed of the danger. Interestingly, those who have studied the dying make little, if any, mention of the sort of conversion symptoms with which we are concerned in the traditional type of discussion on hysteria. Perhaps the presence of various prominent and impressive physical problems – in this setting – obviates the need for additional physical symptoms as a means of psychological or social adjustment. Tauschke et al (1990a) obtained evidence from another direction which supports this view. Patients with chronic pain had less reported evidence of poor care in childhood and employed more mature defence mechanisms than psychiatric out-patients. The methods of defence which the pain patients used, as measured by the Defense Mechanisms Inventory (Gleser & Ihilevich, 1969), were more often reversal and principalisation. Reversal includes negation, denial, reaction formation and repression, while principalisation refers to intellectualisation, isolation and rationalisation. Vaillant (1976) has provided a ranking of defence mechanisms according to which reversal and principalisation are more mature than turning against the self, turning against the object, or projection. Moreover, there are positive relationships between principalisation and reversal and parental care (Tauschke et al, 1990b). In patients who are not necessarily bound to die, the coping mechanism of denial has been regarded as the principal way in which acute coronary patients manage the psychological stress of their illness (Hackett et al, 1968). This school does not regard denial as a specific defence mechanism so much as a process by which many other defence mechanisms can be employed in the service of reducing stress, for example by rationalisation, intellectualising or displacement (Froese et al, 1974). As Hackett & Cassem (1974) point out, these phenomena of denial are very common among the physically ill. In a series of 345 male patients who had just experienced their first myocardial infarction, Croog et al (1971) found that 209 did not admit to thinking that they had had a heart attack, despite the fact that the patients had good reason to know better. Interestingly, there is some evidence that effective denial produces a better survival rate in the coronary care unit (Hackett et al, 1968), perhaps by reducing anxiety with its possible morbid effects. Successful deniers of this sort deny danger and are unruffled, cool, perhaps projecting their fear, “My wife was scared, but I wasn’t” (Hackett & Cassem, 1974). Weisman & Hackett (1961) defined denial as the conscious or unconscious repudiation of part or all of the total available
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meaning of an event, to allay fear, anxiety or other unpleasant affects. This is in contradistinction to the wider-ranging traditional view, evident in Anna Freud’s writing (Freud, 1937) that denial is a fundamental defence mechanism. It suffices for our main purpose to note that the more widespread use of denial is that which is found with physical illness and objective reasons for fear. A more special use is found with hysterical symptoms, and the two uses should not be identified with each other arbitrarily.
Neurological illness The occurrence of denial with neurological illness requires separate consideration. Some authors have argued that anosognosia, that is, denial of disease, is the result of failure of recognition of its presence, but other authors do not agree. Weinstein & Kahn (1955) observe that while denial in most physical illness is implicit, in neurological illness it is often notably explicit. These authors point out that patients will deny that they cannot lift their left arm, or give excuses for not doing so, despite being confronted with evidences of failure. Similarly, they note that the patient will deny or show unconcern not only for disabilities on the side opposite the brain lesion, but also for those on the same side. Thus, such a patient may make excuses for not lifting a right arm which is tied down, or may show unconcern about the amputation of a leg for cancer. Geschwind (personal communication) pointed out that denial or unconcern with illness is much more common with right-hemisphere lesions than with left-hemisphere lesions, a fact long familiar in the neurological literature. He noted that the most striking feature of these patients is a change in emotional behaviour, and argued that the right hemisphere is dominant for certain types of emotional expression. He cited the study of Gainotti (1972), which showed that in a large series of patients right-hemisphere lesions typically produced indifference, while left-hemisphere lesions were more likely to produce concern. Geschwind maintained that inattention to the left side is related to unconcern with illness only indirectly, and should not be regarded as its cause. The view that the right hemisphere is usually ‘dominant for emotion’ has much evidence in its favour. Lishman (1968) showed that affective disorders and somatic symptoms tend to occur disproportionately in association with right-hemispheric injuries. Flor-Henry (1978) reviews the other evidence on the topic, which includes laterality effects in affective syndromes occurring with
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temporal lobe epilepsy, neuropsychological data, and results from power spectral analysis of the electroencephalogram. Enough has been said here to indicate that the phenomena of denial require careful definition in discussion. Only some of them, namely denial of a conflict, or neglect of certain disabilities, as in belle indifference and anorexia nervosa, have an immediate relationship to hysterical phenomena. Other relationships may be disclosed in time between hysterical conversion and more wideranging phenomena of denial, but these are not part of our immediate topic.
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10 Compensation issues
The same continuum between conscious and unconscious motivation that was discussed in the last chapter appears when financial compensation is an issue. In one respect a hysterical symptom for which compensation may be a motive is no different from any other hysterical complaint. It represents a relevant and obvious reason for the individual to have a symptom. In two respects, however, it differs from most other hysterical symptoms. First, as in the Ganser group and prison psychoses referred to in Chapter 9, the motive is readily available to most people’s conscious minds and the suspicion, and indeed the possibility, of malingering occur very readily. Secondly, any help rendered to the patient or claimant by the doctor may affect the interests of other people or institutions adversely. This is a besetting problem for many psychiatric situations where the patient’s needs can conflict with those of relations or associates. More needs to be said about this in psychiatric teaching or in psychiatric monographs than is usual. These basic facts of common-sense psychology permeate numerous cases which are argued about between doctors and lawyers. In particular, a tone of hostility to alleged ‘compensationitis’ is prominent in writers like Miller (1961), who seemed to be called mainly by insurance companies. In contrast, a judge (Lawton, 1969) noted the improved and useful opinions which have been obtained in Britain since reasonable provision for care became available under the National Health Service, and it became the custom to seek opinions from those who have been engaged in treating the patients. Miller (1961) offered evidence that patients with ‘minor’ head injury almost invariably recovered on settlement of their claims. He quoted to powerful effect the aphorism of Kennedy (1946) that “a compensation neurosis is a state of mind, born out of fear, 125
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kept alive by avarice, stimulated by lawyers and cured by a verdict”. Although all the facts that he mentioned may have a role in producing symptoms after injury, it is probably true to say that every part of the statement was more wrong than right. At all events, Mendelson (1982) demonstrated that out of 10 studies of compensation following accidents, not one had confirmed Miller – although he still has his defenders, such as Sim (1992). As well, Tarsh & Royston (1985) followed up 35 claimants with so-called accident neurosis, in which there were gross perplexing somatic symptoms without demonstrable organic pathology. They found that few claimants recovered after settlement and such recovery as did take place was unrelated to the time of compensation. The legal process and the delays involved, however, caused great distress. I am not suggesting that the irritation or hostility which Miller reflected and which is sometimes felt in reaction to patients with compensation claims is entirely unjustified, but it should not colour clinical judgement or be expressed in consultations. As Gowers (1892, vol. I, p. 594) observed about patients with spinal complaints: “the sinister influence of litigation on the intellect may be traced very widely. I believe that it is rare for symptoms to be purely mental. It is often asserted by those employed for railway companies that subjective symptoms quickly subside when the sufferers’ ‘claims’ are settled. It should be remembered that mental anxiety is a potent cause of diseases of the nervous system and must be strongly opposed to recovery from genuine disorders. The occurrence of improvement when suspense is at an end, is thus no proof in itself of the nature of the case, its significance has been unquestionably over-estimated; moreover, in a great many individuals whom I have had an opportunity of observing long after they had received their ‘damages’ (as the expression curiously runs) this subsidence had not occurred and even the ‘sovereign balm’ of substantial compensation appeared to do very little for the relief of the sufferer.”
Three particular situations deserve attention. The first follows from any alarming but physically harmless accident, whose effects relate solely to psychological stresses. The second arises after injury to the body without injury to the head. The third situation occurs after head injury: this involves questions related to the emotional stress sustained, to the psychological significance of the part of the body, and to the possible occurrence of brain damage. Some accidents are moderately distracting to the average person and extremely so to the vulnerable individual. To be stuck in an
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aerial cablecar for an hour or two may cause some fear in all but the most sanguine. Such fear ceases completely for most people within an hour or two after the event, but for a small percentage it will persist for a day or two, or even several weeks. It can return unexpectedly – at least after a short interval – and in a few cases may serve as a starting point for a more protracted bout of anxiety. Any anxiety lasting more than a few days could be accompanied by hysterical manifestations – or possibly replaced by them. To witness a catastrophe, especially if it affects a close and loved relation, can be similarly – or even more – disturbing. Kinston & Rosser (1974) reviewed the consequences of mass catastrophes. They noted the widespread and sometimes persistent occurrence of anxiety in many survivors who were physically unharmed. Nightmares, irritability and complaints of exhaustion and depression are common after such experiences. In individual cases Keiser (1968), who has explored the problems of traumatic neurosis in detail, has no difficulty in showing the understandable nature of many complaints which arise in patients independently of the issue of compensation. Prolonged psychological stress – accompanied both by realistic threats to personal integrity and to the survival of loved ones, as in concentration camp inmates – has also produced prolonged psychological, and even psychotic, illness (Eitinger, 1964; Matussek et al, 1971, cited by Low-Beer, 1972; Kinston & Rosser, 1974) as discussed earlier (Chapter 7). Physical suffering involving the body may equally give rise to prolonged fear. A miner whose abdomen was crushed and who suffered a painful rupture of the pancreas from a fall of stone became understandably frightened of returning to underground work. Traffic injuries provide yet another circumstance in which posttraumatic neurosis may occur, and where the possibility of gain is frequently alleged, both in Canada and in Britain, to be the major factor in producing the patient’s symptoms. In Canada, Kuch et al (1991b) have shown that as many as 70% of a series of patients who were injured in motor vehicle accidents demonstrated phobic symptoms in relation to car travel even though this was not their principal or leading complaint. In the Netherlands, Brom et al (1993) studied victims who were involved in an accident described as “moderately serious to serious”, by five independent judges from the police records. Severe or moderately severe symptoms of intrusive thoughts or a need to avoid situations which reminded the subject of the accident were found six months afterwards in up to 25% of the patients. The exacerbation of injuries by purely hysterical symptoms can also occur and, although the problem does not often appear at
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psychiatric clinics, orthopaedic surgeons are concerned with this situation and the difficulties it presents. These are especially troublesome with back injuries, which constitute a very awkward clinical problem. The discomfort and pain which can arise from organic back disorders (e.g. facet joint disease) are often both real and hard to quantify. Whether or not there is reliable evidence of a displaced disc, it is common for patients to present in orthopaedic, neurological and physical medicine clinics with a disabling pain which is worse on activity and relieved by rest. This is frequently associated with a claim related to injury, but often occurs without such a claim. However, even in the latter case it may establish the right to continuing social security payments, invalidity benefits or pensions. In this context individual differences in personality are regularly recognised as important. Some patients with proven disc lesions struggle on despite often making their pain worse. Others with no physical evidence of illness (which does not necessarily mean there is no physical cause) ‘give in’ quite readily. The latter are liable to be referred to psychiatric attention and present a worrying problem. In one of the writer’s own cases, for instance, gross osteoarthrosis appeared in the dorsal vertebrae of a woman, aged 39, who had been very thoroughly investigated, with negative results, for complaints of pain in the relevant area in the preceding two years. Her original complaints were coupled with an untenable charge of negligence against doctors who had treated her in childbirth, as well as gross resentment and substantial problems in her relationship with her husband. Waddell and his colleagues (Waddell, 1987a,b; Waddell et al, 1980, 1984) have offered evidence that certain types of clinical signs found in orthopaedic examination are non-organic, since they are more common in patients who lack conventionally strong evidence of organic disease like disc prolapse. This will be true on occasion, but the extent to which certain less well defined presumed organic conditions (mechanical back pain, fibromyalgia and myofascial pain) contribute to these signs remains to be determined. The diagnosis of chronic hysterical pain is particularly difficult because there are no signs which will unequivocally prove that such pain itself is hysterical. This may seem surprising to those who have been brought up on the idea that a regional syndrome is evidence of a symptom in the mind of the patient and therefore of a psychological cause. However, exciting neurophysiological evidence has appeared over the last 15–20 years in studies by Wall and his colleagues (see Wall, 1984, 1989; McMahon & Wall, 1984; Cook et al, 1987). Intracellular recording in the spinal cord will
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identify second-order dorsal-horn neurones which will respond to local stimulation by pinch or some other mild noxious stimulus, but not to light touch. After injury in a neighbouring area, responses to noxious stimuli may be demonstrated in these cells by stimulating adjoining parts which previously would not induce a response from them. In other words, the area which can hurt enlarges and sensory stimulation will give new and anomalous responses; noxious stimuli from outside the usual receptive field will influence spinal neurones and a stimulus which previously would only give rise to evidence of light touch may give rise to the response normally found with nociceptive activity. These changes cross nerve boundaries and overlap from one anatomical region to another. They are based upon pathophysiological changes in receptive fields of the second-order neurones. Such changes do not respect basic anatomical distributions of the nervous system but are nevertheless physiological. Hence, altered sensation to light touch or pin prick or spreading areas of pain following an initial lesion, or in the presence of an initial illness or injury, are not necessarily evidence of hysteria but are quite likely to be evidence of physiological changes and the severity of the pain. The diagnosis of hysterical symptoms on the basis of sensory phenomena has also been shown to be unreliable. It has long been known that the responses found on sensory testing might say more about the suggestibility of the patient and the dominance of the examiner than about the actual disorder from which the patient suffered. Additional information indicates not only that changes in regional phenomena might be physiological, but also that the traditional signs of hysteria, examined in another way may be unreliable. Gould et al (1986) studied 29 patients with acute stroke and one other patient with acute neurological disease. They examined them for seven traditional signs of hysteria, namely a history suggestive of hypochondriasis, potential secondary gain, belle indifference, non-anatomical or patchy sensory loss, changing boundaries of hyperalgesia, sensory loss to pin prick or vibratory stimulation that splits at the midline, and give-way weakness. All the patients demonstrated at least one. Twenty-nine showed at least one feature of a supposedly non-physiological sensory examination. The mean number of these items per patient was 3.4. The authors infer that hysteria is easily misdiagnosed if the above signs or items of history are accepted as pathognomonic and that these tests, which are said to provide evidence of hysteria, lack validity. Findings like these reinforce hints from other directions of an organic or physiological element in chronic pain syndromes, for
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example the results of intravenous barbiturate investigations of patients with pain may now be seen to tend in that direction. Walters (1973) found many patients who retained cutaneous superficial tenderness after the first level of anaesthesia had been reached (e.g. eyelid areflexia). This tenderness only goes away at the next lower level of anaesthesia, when deep tenderness may persist. Walters considered that the syndrome of superficial tenderness was associated with psychogenic regional pain, as he called it, but he inferred that the syndrome had at least some basis in psychophysiological change and was not malingered. It was often found in association with compensation claims. But if the symptom was of psychological origin, perhaps it should have disappeared at the first level of anaesthesia. Still more notably, there is a growing body of evidence that a number of syndromes which were somewhat hard to analyse because they lacked standard physical signs, nevertheless have a substantial organic basis. It is now well recognised, particularly since the work of MacNab (1964, 1973), that individuals who have been involved in rear-end collisions causing cervical sprain injuries (‘whiplash’) are likely to have suffered from damage in the structures of the neck, including torn muscle fibres, ruptured ligaments, haematomas in the muscles, retropharyngeal haematomas, and even occasionally partial separation of cervical discs. This sort of evidence (found experimentally in monkeys subjected to appropriate deceleration) showed a strong organic basis for a condition that had often been held to persist without any physical justification. Still later work (Taylor & Kakulas, 1991) showed that injuries to the cervical motion segments in deceased trauma victims were much more common than fractures of the cervical vertebrae. In two young adult male survivors of neck injury who later died, necropsy findings showed a good correlation between the sites of disc injuries and the segmental distribution of pain. Neither of these patients had signs which were demonstrable by imaging during life, but transverse clefts were found in four discs in one of the patients and cord damage in the form of demyelination and gliosis of the left lateral column with overlying dural fibrous thickening in the other patient. With hindsight the latter patient, who was said by an orthopaedic surgeon to have “a very strong functional element in his symptoms”, seems to have had traumatic posterior prolapses of the C5–6 disc and possibly the C4–5 disc. Clefts in trauma patients which persist for a year or more in the innervated parts of the anterior anulus may develop adjacent scarring, possible calcification, and vascular and neural in-growth
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into the disc clefts. These findings may account both for the initial onset of pain and for a later exacerbation of pain which has declined after an initial cervical sprain injury. Cervical sprain injuries are also twice as common in individuals who have been wearing seat belts and have suffered rear-end collision than in those who were not. It is unlikely that this is due to the psychology of the patient; probably the seat belt fixes the body but leaves the neck free to move, saving patients from severe head injury but preserving them for a cervical hyperextension flexion injury (Allen et al, 1985). Interestingly, Sir John Erichsen (1886) observed with respect to “concussion of the spine” occurring in railway accidents that those individuals who suffered most were those who had their backs directed towards the site of the impact, rather than those who were facing it. In the days when railway passengers sat in two rows facing each other in compartments they seem to have provided a controlled comparison for studying the effects of collisions in which the impact was behind the subject. Notwithstanding the difficulties posed by an organic diagnosis, which cannot initially be made and may take months or years to be established, it remains the case that a large aura of neurotic problems surrounds patients with neck injuries or with chronic low back pain, whether or not this is related to injuries for which compensation can be claimed. Wolkind & Forrest (1972) showed a clear predominance of neurotic symptoms in those patients with low back pain who failed to improve with physiotherapy, while a larger group with low back pain from whom these non-responders were drawn had no more evidence of recovery than a control group of men in industry. They considered that the association of neurosis with non-improving low back pain was established but that it was not possible to say whether a mood state caused the pain or vice versa. In a selected population of American veterans who mostly (or all) qualified for various benefits, Sternbach et al (1973) showed an equivalent degree of change on the Minnesota Multiphasic Personality Inventory (MMPI) in patients with and patients without definite evidence of physical lesions. A similar situation was found among patients with chronic pain from neurological lesions compared with psychiatric patients with pain who had no organic lesions (Merskey & Woodforde, 1972). Sternbach et al (1973) showed further that patients with chronic low back pain had more MMPI evidence of hysterical and hypochondriacal symptoms and depression than those with acute back pain. Sternbach & Greenhoot (1974) also found that patients who had active treatment became
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less neurotic in terms of their modest but significant reduction in scores on the MMPI. Thus there is some reason to think that many patients who have neurotic symptoms related to pain, including low back pain, might have these symptoms as a secondary effect of their physical status. Even those patients who can be shown by techniques of physical examination to have, say, hysterical exacerbation of their disability may, nevertheless, have an important organic basis for their complaint. The value of the MMPI evidence is limited, however (see Chapter 13), because the recording of symptoms or responses on that test has frequently been carried out without regard for the possible presence of organic disorders. Among the author’s patients with chronic severe pain, the commonest psychiatric condition found was a depressive illness, usually of the severity of a major affective disorder (Merskey et al, 1987). The obvious explanation of this is that many patients who suffer from chronic pain, financial deprivation subsequent to unemployment, loss of status as bread winners, marital changes and other social difficulties – as well as the actual unpleasantness of persistent pain – will become depressed. In a prospective study of cervical sprain injuries, Radanov et al (1991) have nicely shown that the depression and impairment of concentration which can be found with such injuries are related to the severity of pain at onset and not to emotional changes. Other authors (Atkinson et al, 1991) found that depression occurred about twice as frequently after injury in workers receiving industrial compensation, as before. In recent years attention has also been given to more sophisticated analyses of the claim that those receiving compensation have more psychological symptoms. When the cases receiving compensation were compared with those not receiving compensation, and both groups were controlled for the presence or absence of unemployment, little difference appeared between them (Melzack et al, 1985; Dworkin et al, 1985). Pelz & Merskey (1982) also found that within a group of patients with chronic pain attending a nerve block clinic, those in receipt of compensation did not differ significantly from each other on the SCL-90 (Symptom Check List – 90), which is a measure of the psychological state. This is not to suggest that the opportunity to be off work while continuing to receive income may not be a significant factor in promoting some sickness absence. Bigos et al (1991) found that workers who had previously indicated that they did not like their job were 2.5 times more likely than others to stay off work with complaints of minor back injury. However, these were short-term studies, and even there, the occurrence of prior back complaints was also a significant indicator. In practical terms, the finding
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meant that about 20% of the variance for those who were off at any one time might be attributable to dislike of the job rather than to the patient’s physical status. These findings are important in the case of brief complaints but have not been shown to count for much with respect to long-term disability. The larger problems with chronic pain and allegations of hysteria have to do with long-term unemployment. Here there is some evidence (Sander & Meyers, 1986) that the financial rewards of compensation prolonged the recovery of those injured at work. A group of patients injured on duty took 14.2 months to return to work compared with another matched group, injured off duty, who returned within 4.9 months. Mendelson (1993) reviews additional evidence on this topic and comes to the conclusion that the availability of compensation benefits and litigation may have an adverse effect on the response to treatment, but this effect can be modified by specific rehabilitation programs (e.g. Catchlove & Cohen, 1983; Weisel et al, 1984). Mendelson further notes the relevance of psychosocial factors to repetitive strain injuries and the frequency with which they can increase in numbers in relation to social acceptance and the opportunities for benefits. Despite the perplexing difficulties the effort must be made to sort out the psychological and organic issues for each patient. For this the standard techniques of both physical and psychological examination have to be carried out thoroughly and patiently, and supplemented, where necessary and appropriate, with suitable but not excessive investigations. In the psychiatric cases motive other than compensation may be disclosed: bereavement; job problems; interpersonal difficulties; and so on. A minority of cases will remain uncertain and may require observation over some months or longer, but in the remainder, it will frequently be reasonable to assume that compensation motives are relevant.
The relationship of hysterical symptoms to bodily injury It was noted above that hysterical symptoms can complicate posttraumatic neurosis in which injury does not occur. It is therefore not surprising that bodily injury may give rise to hysterical symptoms. It has to be accepted that accidents giving rise to physical injury will be liable to provoke conversion symptoms. Despite the doubts and uncertainties about financial motivation, it remains true that accidents may cause genuine hysterical disability, usually over and above either minor or major physical problems.
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The management of these cases sadly requires platitudes for its description. Doctors must be patient, tolerant, cautious, sceptical, fair to the sick and not fooled by the malingerer. They must endeavour to minimise the factors which promote disability, to solve the patient’s problems, and to produce an evaluation in perfect wisdom and detachment. It cannot be done but it has to be attempted. For this reason many doctors take refuge in the following, not wholly ignoble, formula: ‘the patient can be expected to recover soon after the settlement of legal proceedings’. I have already referred to Gowers’ view of this attitude . Nevertheless, the formula is frequently correct with regard to psychological complaints like depression, for the following reasons. First, many illnesses have a limited time course – some patients actually recover before the conclusion of legal negotiations (Kelly & Smith, 1981). Secondly, malingerers take their gains and cease visiting the doctor. Thirdly, many genuine patients have some of their problems resolved by knowing where they stand, clearing the debts which have followed their injury, and feeling free from the fear of being the subject of legal argument. Being called upon to give testimony and face cross-examination in the setting of a court is normally worrying even to those with a good conscience. Release from these worries enables patients to make the best of their circumstances. On the other hand, pain is not usually influenced by legal settlement.
Repetitive strain injury Repetitive strain injuries (RSI) form a particular case where organic dysfunction initiates the disorder in some cases but psychological factors are liable to play a more important role when there is a large number of cases. The latter type of cases might be considered in Chapter 16, dealing with epidemic illness, but both because of the possibility of organic causes and because of their relationship to compensation they are discussed here. In one example of organic dysfunction, a female worker on an assembly line was required to complete the attachment of two metal parts by raising the heavier portion (weighing some 7 to 10 pounds) and then making a twisting motion with it. Within three weeks she was permanently disabled by chronic wrist pain. This ergonomic disaster occurred in a small factory which has since closed down under economic pressure. The patient was aware of at least two others out of a workforce of approximately 25 who developed similar complaints. More often, currently, the organic
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cause of chronic RSI is sustained typing at a keyboard. The emergence of this problem appears to be linked to the lack of rest between lines of typing. With typewriters the carriage return provided a brief but important break in repetitive fine movements which has been lost with word processor keyboards. Such effects of overuse have long been known in various circumstances and include several where negative motivation is not an issue. On the contrary, the demands of training make overuse injury endemic in modern sport (Sperryn, 1994) and the problems of musicians are well recognised (Fry, 1986; Bird, 1989; Hochberg et al, 1993), and in both these groups when emotional problems occur they are ordinarily secondary to the disorder (although a particular grip or pattern of tension in holding string instruments is relevant for some musicians). Histological evidence related to clinical severity also exists in favour of an organic diagnosis in patients with continuous pain, tenderness and weakness of the wrist (Dennett & Fry, 1988). Hocking (1987) described an epidemic of RSI in Telecom Australia between the years 1981 to 1985, telephonists and keyboard staff members being the most affected. He found little evidence of a consistent dose–response relationship between keyboard rate and RSI, age, or job duration, and he noted that others had questioned the importance of posture. He argued that social factors had promoted the epidemic and his view was supported by Cleland (1987) and Ferguson (1987). A greater tradition of trade union activism was cited as one reason for the issue being most prominent in Australia (Willis, 1986). The evidence for social factors was not conclusive either for all cases or – in some views – for the majority, but it seems to be generally agreed that claims declined after a number of court judgements against claimants. In addition to those with more conventional opinions, Willis (1986), a sociologist with evident Marxist leanings, supported a social interpretation and put down the medical model as follows: “It is necessary to understand the social process by which this paradigm of medical knowledge became dominant and the manner in which certain types of medical knowledge served dominant class interests and were sponsored by capital as a result. The biomedical paradigm became articulated in capitalist societies in corporatist terms. Disease came to be understood in individual and biological terms rather than social and political terms and the industrial analogy developed, viewing the body as a machine with replaceable parts and requiring engineering and ergonomic solutions.”
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Thus from two ends of the political spectrum the view was supported that the complaints were of psychological origin. The argument is not yet dead, however. The effects of denying the right to a claim at law furnished no proof that a disorder or illness is not present, and other reasons may be put forward to explain a decline in reported cases. They include ergonomic changes in the workplace and education on alternative techniques. Mann (1994) states that most people claiming such injury in Australia are still successful, and points out that: “There are peaks of occupational illness and accidents accompanying many innovations. These abate not because of brain washing but because workers and employers modify the work place and teach their employees how to avoid the problem.”
It seems that, as so often in medicine, both organic and psychosocial factors influence this field.
Head injuries The third category of post-traumatic symptom which deserves comment is that which occurs after head injury. Severe closed head injuries are nearly always associated with protracted unconsciousness, subsequent neurological signs, and demonstrable intellectual impairment. Retrograde amnesia of more than a few minutes’ duration and unconsciousness lasting more than an hour indicate moderately severe head injury. Moderate and severe head injuries are accepted as causing organically determined symptoms. They are also the cause of overt hysterical symptoms, usually at some point in the later phases of recovery; but the greater the dementia, the less the headache. Weinstein & Lyerly (1966) found the actual frequency of conversion hysteria in this setting to be 16 in a series of 200 military patients who had had evident neurological disturbances. ‘Minor’ head injuries of less than one hour’s unconsciousness and only a few seconds’ retrograde amnesia also give rise to symptoms. Indeed, this can happen with head injuries in which there is no loss of consciousness. The symptoms typically include headache, giddiness and memory difficulties, difficulty in concentration and some irritability, depression, anxiety and impairment of libido. The provenance of these symptoms has been much discussed. Many authors have taken the view that they result largely from neurotic mechanisms and even from a conscious wish for financial gain (Miller, 1961). The view has also been
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argued that they are primarily due to organic dysfunction (Taylor, 1967). Cerebral blood flow studies (Taylor & Bell, 1966), otoneurological evidence (Toglia et al, 1970) and psychological tests of difficulties in concentration (Gronwall & Wrightson, 1974) all support the organic view. Dr R. Kelly and Dr A. Walters (personal communications) have both observed that some patients with the minor head injury syndrome recover before settlement of their claim, and I have also encountered this outcome, which favours the view that the syndrome is a true illness and not malingering. The symptoms persist in a minority of patients even after legal compensation has been awarded or where it is not relevant (Merskey & Woodforde, 1972). The psychological problems of illness, interruption of work and legal claims, of course, complicate the situation. These factors in turn may promote a hysterical elaboration of symptoms, but much of the typical post-concussional syndrome seems likely to be due to a combination of organically based difficulties, partly unrecognised or not sufficiently appreciated, made worse by the effort to return to work too early and arousing in turn anxiety and depression (Gronwall & Wrightson, 1974). In recent years there has been a substantial accumulation of additional evidence for the organic component in the postconcussional syndrome. This is detailed extensively by Levine et al (1988) and Evans (1993). The development of a quantitative electroencephalographic method to provide a discriminant analysis of mild head trauma has also become available (Thatcher et al, 1989). Accordingly, the arguments which this syndrome has provoked seem less fierce now than formerly. Psychiatrists who recognised it as ‘genuine’ tended to find reasons for it in terms of dynamic mechanisms. These now appear to be an unlikely explanation for the basic syndrome. On the other hand, those neurologists who tended to regard the syndrome as essentially ‘compensationitis’ are fewer and perhaps less vehement. The fact that loss of consciousness or neurological signs of brain damage do not always occur can no longer be taken as grounds for thinking that the condition is unassociated with cerebral organic dysfunction. Only in films and television programmes do those who have had blows to the head fall down, stay in coma briefly, wake, shake their heads and proceed symptom-free to rout the villain. Real people suffer longer, and postmortem studies of those dying after minor head injuries, but from other causes, indicate evidence of neuronal change in the brainstem (Oppenheimer, 1968).
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In these circumstances there is less need to suppose that hysterical symptoms after head injury are due to cupidity, even though occasional blatant liars do sometimes try to reinforce their claim by making consciously false statements. One person, for instance, seen for his own solicitors, had actually had a significant head injury with a small subdural haematoma, but laid claim to having damaged his chest severely as well. He had been carefully examined at the Neurosurgical Unit where he was treated and a note made that there was no chest disease. Such cases, however, are relatively rare. Few doctors actively concerned with compensation cases see more than one or two cases of this sort in a year. My own overall experience has been that the great majority of claimants suffer genuine distress, and, in both Britain and Canada, effectively recoup less financially from their claim than they have lost.
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11 Organic brain disease
“If hysterical symptoms may thus complicate general and local diseases, it is not surprising that they still more frequently accompany various diseases of the nervous system, functional and organic.” (Gowers, 1893, vol. 2, p. 988)
It is clear from the preceding chapters that there is a wide range of symptoms regarded as hysterical and any complaint, somatic or psychological, may be the subject for hysterical mechanisms. Like most topics in psychiatry, hysteria also requires the notion of multiple aetiology. This is often necessary for individual cases, and it is invariably necessary for a complete account of all cases. In this section, a number of different causes of hysterical symptoms and a wide variety of those symptoms are considered. The topics have been selected for their clinical importance or interest and to provide a comprehensive description of hysterical phenomena. The association of hysteria with organic disease has been the subject of lively, sometimes acrimonious, discussion in recent years. Like those who attacked Freud, in apparent ignorance of the work of his distinguished predecessor in Vienna, von Feuchtersleben (1845), the controversialists about hysteria and organic disease often seem to have ignored the record. Gowers (1893) clearly recognised that hysterical symptoms were common in association with organic disease, and a variety of subsequent writers repeated the message. Kraepelin (1904), among others, noted that hysteria was not uncommon with epilepsy. Guttman (1932) cited numerous authors who had recognised the simultaneous occurrence of organic brain disease and hysterical symptoms. He noted that Credner (1930) found 73 patients with frontal lobe lesions among a series of 260 suffering from hysterical 141
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symptoms. Guttman remarked that patients with epilepsy often had hysterical attacks which required special discussion; and he pointed out that unless patients were aware of a defect they could not get a ‘hysterical overlay’. Paul Schilder (1935), in his famous work The Image and Appearance of the Human Body, developed the exceptional concept of ‘organic repression’. The book is not easy to read but we can draw many ideas from it and the following quotation with regard to patients with Korsakoff’s syndrome seems clear enough (p. 32). “When I use the term ‘organic repression’, I wish to emphasize that we are concerned with a phenomenon, which, on a structural level, repeats what is going on in other repressions in the so-called psychic level.”
It should follow from this concept that the same symptom might be the end result either of an organic illness or of a psychological disturbance. A particular symptom which Schilder specified in this connection was anosognosia, a tendency to neglect some part, usually one-half, of the body. Schilder (1939) carried forward some of these ideas and linked them with additional clinical observations. He wrote: “The conversion is based on childhood experiences, but the later organic trauma may be the nucleus and pattern for the final formation of the symptoms. For instance amnesia and memory disturbances often occur in patients who have suffered from an organic unconsciousness due to trauma or CO poisoning.... Our material accordingly contains a great number of cases of organic disease with hysterical symptoms.”
He also wrote about neuroses following head and brain injuries (Schilder, 1940) as follows: “Cerebral organic syndromes may change functions of the brain in such a way as to provoke neurotic attitudes. One cannot claim similar mechanisms for traumas which afflict other parts of the body.”
Four main conclusions can be drawn from these observations. First, organic illness might take effect through the repression of a conflict. Secondly, from this it follows that the same symptoms could have either an organic or a psychological cause. Thirdly, organic disturbances of brain function can provoke neurotic attitudes. And fourthly, organic disease and hysterical symptoms frequently coexist.
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The first of these lines of argument is conceptually difficult and has not proved popular. The second and third are well illustrated in a case report by Lewis (1953). This concerns an Englishman who first suffered from a confusional state due to neurosyphilis and then contracted malaria. Some years later, while living in America, he was written up at length as a classic case of dissociative memory disturbance in a book entitled Persons One and Three: A Study in Multiple Personality (Franz, 1933). He returned to England, showed evidence of a manic–depressive syndrome, was readmitted to the Maudsley Hospital, London, and was shown still to have positive serology for general paralysis of the insane (GPI). After treatment with induced malaria he still showed some organic memory disturbance. Unless the American diagnosis was wholly wrong, it seems likely that this patient had a memory disturbance to which both organic and psychological causes contributed and in which organic and psychological patterns appeared. It would be by no means certain that the psychological or the hysterical pattern of memory disturbance was unrelated to the presence of a defect due to organic disease. The occurrence of hysterical symptoms with multiple sclerosis was discussed by Langworthy & Legrand (1952). They were interested in the relationship of personality to the development of illness, and considered that there was a special group of patients with multiple sclerosis in whom poor emotional adjustment was a problem, even before the symptoms of organic disease developed. They thought that the diagnosis of conversion hysteria was often made at the onset of the symptoms, not merely because of the bizarre nature of the complaint, but especially because of a personality structure consistent with this diagnosis. It might perhaps be thought that if all the patients were seen subsequent to the development of the disease, some of the personality changes could be attributed to the disease. In this respect it is worth remarking that they noted that “conversion symptoms had been observed developing long after the organic signs of multiple sclerosis are apparent”. Considerable attention has been focused upon the topic of hysteria and organic brain disease by Slater (1965) and Slater & Glithero (1965) in a nine-year follow-up of 85 patients. These were drawn from an initial sample of 112 seen by Slater and colleagues and given a diagnosis of hysteria. Of these 85 patients, 4 had died from suicide and 8 from organic disease; 19 were originally considered to have organic disease with a “hysterical overlay”, and 22 were later found to have an organic basis for
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their symptoms. A further 32 had no organic pathology. Among these, 2 developed schizophrenia and 9 had affective illness. There was a nuclear group of only 7 young patients with classic conversion symptoms in response to stress, and 14 with chronic personality disorder and multiple symptoms. This latter group was of the type studied so intensively by Guze and his colleagues (cf. Chapter 13) and described so clearly by them. From this Slater drew the conclusion that the diagnosis of hysteria was “a delusion and a snare”. He remained willing to use the word hysteria as an adjective but not as a noun. Whitlock (1967b) followed Slater’s study with a report of 12 personal cases seen in Brisbane, Australia, together with a casenote study of 44 others from the University Department of Psychiatry, Newcastle-upon-Tyne, England, presenting over a four-year period. He found that 63.5% of his cases had an accompanying cerebral disorder or preceding organic brain disease. This included a history of head injury. There were 20 men and 36 women in his series. A similar history of organic disease was obtainable in only 5.5% of a control group of patients with depression or anxiety states. In a further study at the National Hospital, where Slater’s work was first conducted, Merskey & Buhrich (1975) reported a series of 89 patients seen personally and diagnosed as having motor conversion symptoms (Code 342.2 in the International Classification of Diseases). The patients were seen from September 1968 to December 1971. The criteria for inclusion in the series were that these patients should have been referred in consultation to the present writer and shown by neurological examination to have what Head (1922) called positive signs of hysteria, that is, it had been possible to demonstrate motor signs of good function in a supposedly paralysed part. A psychological cause could be presumed to be operative in producing these conversion symptoms but no presupposition was required about its nature or mechanism. Thus the diagnosis of a conversion symptom was essentially a neurological procedure although its explanation, if found, would be expected to be psychological. Matching control patients of the same age and sex and from the same clinical psychiatric setting were found for 24 patients. Three groups were defined: group L, 89 patients with conversion symptoms; group H, the smaller, matched subgroup from group L; and group C, the matching control group. It was found that 67% of group L had some organic diagnosis, 48% of the total having an organic cerebral disorder or systemic illness likely to affect brain function. Comparable figures for groups H and C
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were 67% and 79%, respectively, with an organic disorder, and 50% and 58%, respectively, with organic cerebral disease likely to affect the brain. The main relevant organic disease was epilepsy, affecting from 21% to 33.3% of the different groups. Other fairly common diagnoses were cerebrovascular disease, multiple sclerosis, head injury and dementia. Migraine was accepted as an organic disease in four patients from group L and one from group H, on the grounds that it could promote disturbed pathophysiological functions. Apart from this, the allocations of organic diagnoses were scarcely controversial. It is clear from these findings that there is an even higher incidence of organic disease in the control group than in the H group. This is not necessarily surprising, since the purpose of the Psychiatric Department at The National Hospitals for Nervous Diseases at Queen Square and Maida Vale is to provide a service primarily for neurologically ill patients. Nevertheless, even in the hysteria group the figures are at least as high as those which we found in any other published series dealing with the incidence of physical illness in psychiatric patients (Merskey & Buhrich, 1975). After making allowances for differences in the presentation of data, we found the lowest figures for cerebral and systemic illness to be 4% (Eastwood et al, 1970), the highest 28% (Davies, 1965); while other physical illness ranged from 11.2% (Eilenberg & Whatmore, 1961) to 37% (Marshall, 1949). The last of these figures came from in-patients at a psychiatric teaching hospital. The highest overall figure, 66.5% of psychiatric patients in a Yale, New Haven Hospital sample is given by Kligerman & McKegney (1971). Roy (1977a) sought further evidence to determine whether there was a relationship between hysteria and organic brain disease. He collected a consecutive series of 34 patients with convulsions seen personally in a period of two and a half years for investigation and treatment of epilepsy and whose discharge diagnosis was hysterical neurosis. Twenty-six of these patients were seen at the Maudsley and King’s Hospitals Neurology Unit or at the Maudsley Epilepsy Unit in London, England, and eight were seen in general psychiatric units. He compared them with 34 matched control patients from two general psychiatric units at the Maudsley Hospital whose discharge diagnosis was depressive neurosis. Thirteen of the 34 patients in the hysterical neurosis group had organic brain disease compared with one of the 34 patients in the depressive neurosis group, and these results were highly significant statistically (P < 0.001). In this study 26% of the total group of patients with conversion symptoms had cerebral disorder, of whom all but two had epilepsy. Roy
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considered that his findings suggested the possibility that in the group with hysteria and epilepsy the associated cerebral disorder might predispose to hysterical convulsions mainly because of psychological factors, like identification with the epileptic convulsions, rather than because of an organic factor. In another study, Roy (1977b) showed that epileptic patients at the Maudsley Epilepsy Unit who had a current chronic hysterical symptom had hysterical fits which were thought to account for over three-quarters of their current attacks. The nature of the hysterical fits closely resembled the type of epileptic fit the patient had. This resemblance was held to support the idea that the hysterical fits were related to modelling on known organic disease. Both in this paper and in another article (Roy, 1979a), Roy presented evidence indicating that significant differences between patients with hysterical seizures and those with epileptic seizures were found with respect to family and personal history of psychiatric disorder, attempted suicide, sexual maladjustment and a current affective syndrome. The practical implication of this latter group of findings was that: “a female patient referred for investigation of seizures, who is currently depressed, has a personal and family history of psychiatric disorder, and has attempted suicide may best be admitted to the hospital for further investigation and observation of her attacks before anticonvulsants are prescribed.”
In a fourth report (Roy, 1979b), a retrospective examination of case notes at a different centre (the Clarke Institute of Psychiatry, Toronto), 31 patients with hysterical neurosis were compared with 31 with depressive neurosis. Significantly more of the hysterical patients had a preceding head injury and 29% a past history of hysteria. The head injury was apparently mild in at least three of the five patients with a history of hysteria. Roy argued from his data that there was no special evidence of an association between organic disease and hysterical symptoms. In centres where patients were admitted for organic brain disease, hysteria was found with it, and in centres where patients were admitted for psychiatric illness, hysteria was found without brain disease. One of the difficulties with Roy’s argument is that although his samples are not small, they still reflect only very limited populations of patients, either with hysteria or organic brain disease. There is no dispute that the modelling of symptoms which are already known to the patient from intimate personal experience is one source of hysterical symptoms. The problem is that it is hard to explain the remarkably high occurrence of organic brain disease
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in the relatively small groups of patients who now seem to be available for study. In the past when hysteria was much more common – as is discussed in the next section of this chapter – Roy’s explanation in terms of selection would be highly appropriate. Today, when the pool of patients is so much smaller, the cases with classic conversion symptoms still stand out as having an unusually high frequency of organic cerebral disease. Roy also argues (1977a) that the patients in his group with hysterical convulsions only had no epilepsy and thus had no personal symptom to model or identify with. In this group any association with cerebral disorder could be attributed mainly to an organic factor, but no such association was found. However, his group without organic disease is distinguished from the rest of his patients with hysterical convulsions by not having epilepsy. Having excluded from his group of patients with hysteria all those who have the most common organic disease with which hysteria may be found, he then concludes that there is no association. This does not seem to be a valid argument. All the same, I am bound to agree that, in Roy’s systematic studies, evidence of a link between cerebral organic disease and the production of hysterical symptoms, as distinct from their modelling, is absent. Notwithstanding the above, there are important individual observations which keep alive the possibility that some cases of organic disease contribute to hysterical symptoms. The most striking is the relative frequency with which epileptic patients with hysterical symptoms have been noted to have toxic levels of phenytoin and to remit soon after this is corrected. (See ‘Hysteria and epilepsy’, below; some of the other findings from comparative studies in that section also support the view that physical illness is a common finding in patients with hysterical convulsions.) In addition, Gould et al (1986) (see Chapter 10) found a plethora of supposedly hysterical signs in a series of patients with acute organic brain disease, and Weinstein (1966) observed that 16 out of 200 patients with acute closed head injuries showed conversion/hysterical signs at some point during recovery. Such signs did not appear in aphasic patients with lesions on the left side of the brain.
The significance of the data Some further reasons should be noted for the view that physical illness may play a special part in producing hysterical illness. Conversion hysteria involving paralyses or anaesthesias is not a common disorder in routine psychiatric work. In times of
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peace, general psychiatrists in Canada and in Britain usually see only a few such cases in a year. Military psychiatrists regularly meet the problem – especially in times of conflict – and psychiatrists working in conjunction with neurologists often meet patients with such complaints. Otherwise, in our experience, and in that of a number of colleagues whom we have questioned, patients with conversion symptoms are not often encountered; Lewis (1974), in Wisconsin, makes this point very strongly, as follows: “Ask any experienced psychiatric clinician ... how many cases meeting the classic definition of hysteria he or she has seen, and you will receive varied answers ... neurological, industrial, military and orthopedic consultations tend to skew the answers toward greater frequency. General psychiatric practice yields a lesser number and psychoanalytic work, even less. The surprising fact is that if you press your informant to limit his or her answer to the number of cases he or she feels reasonably sure meet the textbook criteria, the frequency will be no more than a few per year of active practice – more commonly (based on informal inquiries I have made) less than a score in a practice of many year’s duration.”
A number of clinicians have noticed the same trend. Abse (1966) remarked upon this and showed that of 370 Indian soldiers with hysteria seen in Delhi, 188 had fits, 83 had pains in the abdomen, 25 had amnesia and the remaining 74 had variously aphonia (12), deafness (11), paralysis (10), blindness (7), tremors (7), vomiting (6), contractures (5), sciatica (5), headache (3), speech defect (3), enuresis (3) or anaesthesia (2). By contrast, among 161 British soldiers with a similar diagnosis, 44 had headaches, 43 pains and paraesthesiae, 17 enuresis, 11 paresis or ataxia, 10 amnesia, 13 fits or black-outs and the remainder various symptoms including insomnia, weakness and sleepwalking. Apart from fits, major motor phenomena were rare in both series, and the presumably more sophisticated British soldiers had headache as a complaint more than any other symptom. Abse also noted that although classic hysterical symptoms are generally rare in Western society, they are common in rural areas such as North Carolina. Parker (1962) cites six other studies supporting the conclusion that classic hysteria is common only in developing societies or subgroups. Watson & Buranen (1979) also observed that conversion symptoms as they encountered them were very different in frequency and pattern from the symptoms which were most commonly mentioned in textbooks. They examined 18
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textbooks of abnormal psychology and psychiatry, all except one being from the United States. They were chosen on the basis of their stature, frequency of use and recency of publication in about 1978. The textbooks most often listed paralysis, anaesthesia, blindness, deafness, mutism, tunnel vision, convulsions, paraesthesias and tics as signs of hysteria. Non-headache pain or hyperaesthesia and various types of motor loss and analgesia were also often listed, besides. Among 40 patients of their own, studied retrospectively in case records, the largest percentages of symptoms were found to be non-headache pain or hyperaesthesia, heart attack or chest pain, paresis, headache, fainting and dizziness. Data taken from Woodruff et al (1974) dealing with a series of patients and providing frequency of symptoms showed similar trends to their own. The largest numbers of patients were described as having fatigue or drowsiness, paresis, non-headache pain or hyperaesthesia (all of equal frequency), heart attack or chest pain, blurred vision, anorexia, fainting, weight loss and tremor. There was a significant correlation between their series and the data of Woodruff et al. They noted that five of the seven symptoms mentioned most commonly in textbooks appeared only rarely in the two study populations. While there may be some doubt about the hysterical provenance of a number of the symptoms which Watson & Buranen have accepted as conversion symptoms, the actual pattern of presentation supports the findings by Abse and the comments by Lewis. Quite a few additional studies support this idea and are discussed further below. From 1968 to 1970 inclusive, an annual average of 28 outpatients and 39 in-patients at the National Hospital for Nervous Diseases, Queen Square, were diagnosed as having conversion reactions (ICD code 324.2). This relatively high rate of presentation contrasts strongly with my own experience in other settings such as general hospitals, psychiatric hospitals, in-patient departments and out-patient clinics, my experience there being similar to that described by Lewis (1974). The only places where I have personally observed or obtained evidence of frequent classic manifestations have been during military service, in contact with medical services to indigenous North American populations or in work associated with a neurological hospital or department. Psychiatrists in the United Kingdom generally also find that they see few patients with motor conversion symptoms unless they practise in close association with a neurological department or in one of the other special settings to which Lewis refers. It is obvious that patients are likely to be referred to neurological departments with physical symptoms for differential diagnosis. It is surprising that so many
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patients with known neurological disease should be found to have overt conversion symptoms, unless the physical illness contributes in some way to the production of conversion symptoms.
Hysteria and epilepsy Certain links between hysteria and epilepsy have a bearing on the question of hysteria and brain dysfunction. Niedermeyer et al (1970) made the particularly important observation that anticonvulsant intoxication may be associated with hysterical symptoms. At the National Hospital for Neurology and Neurosurgery, Queen Square, and also at the National Hospital, Chalfont Special Centre for Epilepsy, it is a common experience that hysterical conversion symptoms are likely to appear in association with phenytoin intoxication and remit not long after it is corrected. In the patients in the L group in the series by Merskey & Buhrich described above, the frequency of epilepsy was 23 out of 89. This is higher than the usual frequency of epilepsy at the National Hospital, Queen Square, where approximately 7.2% of in-patients and 14.2% of out-patients have a diagnosis of epilepsy. The finding suggests a possible special link between some aspect of epilepsy and hysterical symptoms. This view is further supported by the observation of Henson and his colleagues (Currie et al, 1971) that patients with gross hysterical symptoms were actually more frequent in their series of patients with temporal lobe epilepsy (17 out of 666) than were patients with a schizophreniform illness (12 out of 666). Friemert (1970) found that 20 out of 263 epileptic patients had hysterical fits, and Standage (1975), reviewing 4 hysterical patients of his own and 21 from the recent literature, noted that physical illness was a common finding, and 32% of subjects had a history of neurological disease. Rabe (1970) described 41 case histories in which both hysterical and epileptic attacks appeared to occur in the same individual. This is a long-standing theme, from the time of Charcot onwards. According to Rabe any form of clinical epilepsy, whatever the aetiology, may be accompanied by hysterical attacks. He did not think that ‘hystero-epilepsy’ and psychomotor epilepsy were more especially associated with each other than with hysteria and other forms of epilepsy. While it was not possible to find adequate differential criteria to explain combined attacks of hysteria and epilepsy in the same individuals, Rabe thought that common causative factors might be present. These were principally disturbances of physiological and psychological maturation. A variety
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of causes and effects could be observed, ranging from cases of single hysterical attacks, reactively determined, occurring in chronic epileptics with severe personality change, to patients with marked neurotic features and symptoms in whom epileptic attacks occurred in psychologically relevant situations. Taking his argument further, Rabe observed that: “the well-grounded finding of a mutually dependent alternation of hysterical and epileptic attacks allows us to assume the existence of a pathology which forms the basis of both symptoms, the roots of which could not be found in physiological or psychological processes but were comprehensible only on the basis of the individual case history.”
Both types of attack, hysterical as well as epileptic, were thought to be the manifestations of a disturbed relationship between the ego and the environment, and anticonvulsant medication alone was not enough to cope with management and treatment. It is convenient to note here the most elegant technique for demonstrating the biological difference between hysterical and epileptic seizures. Trimble (1978) argued that since electrochemical stimulation of the medial basal hypothalamus in animals increases the release of prolactin, if the abnormal electrical activity in epilepsy passes through the midbrain it should raise the serum prolactin concentration. He then compared baseline measures of serum prolactin with those found after a fit in nine patients with generalised epilepsy, seven with presumed hysteria, and 11 having unilateral electroconvulsive therapy. All the patients with generalised epilepsy had higher scores than any of those with hysteria after the fit. All but one of the patients receiving unilateral electroconvulsive therapy also exceeded the highest value found in a patient with hysteria. In an additional study, Dana-Haeri et al (1983) confirmed the rise in serum prolactin at 20 minutes after a fit in men and women with generalised attacks. Luteinising hormone was elevated at 20 minutes and remained elevated at 60 minutes, while folliclestimulating hormone increased in women only, at 20 and 60 minutes. Following complex partial seizures, prolactin was elevated at 20 minutes. However, with simple partial seizures the estimation of prolactin was found unlikely to be of diagnostic value. Hysteria and temporal lobe foci Margherita et al (1967) have noted a relationship between hysterical behaviour and temporal lobe foci. They consider that
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this association is recognised in the literature, including that of Italy. They themselves described one man and four women with left temporal lobe foci, only some of whom had epileptic attacks but all of whom had hysterical falling to the ground and jerking, with response to stimulation during the attacks. Ljungberg (1957) also observed that 3.3% of his patients with hysteria had epilepsy – a rate much above the expected. Stefansson et al (1976) found 7 out of 64 patients seen in a consultation service with the diagnosis of conversion neurosis, hysterical type also to have a seizure disorder, and 36 of the 64 (56%) had physical illness. In a neurological consultation service Lipowski & Kiriakos (1972) found pseudoseizures or hysterical fits either alone or in combination with cerebral seizures to be the most common conversion symptoms. There is thus a great number of reports linking these two conditions, a link which has been recognised ever since the days of Charcot, when they were first clearly distinguished. We have already noted (Chapter 9) the recurrent finding by a number of authors (e.g. Abeles & Schilder, 1935; Kanzer, 1940; Berrington et al, 1956; Kennedy & Neville, 1957) that a link existed between cerebral organic disorder and hysterical amnesia. It is worth re-emphasising that the controlled study of Berrington et al showed a significant excess of head-injured patients among those with hysteria. Yet another condition with which conversion symptoms have been associated is Klinefelter’s syndrome. Christodorescu et al (1970) described four cases of this syndrome with conversion reactions. Lastly in this connection, it is worth noting the substantial evidence (Graham & Rutter, 1968) to show that organic disease, especially of the brain, is one of the most important factors in the production of childhood neurotic difficulties. Hysterical fits At this stage it is worth a brief diversion to consider some further aspects of the relationship between epilepsy and hysteria, which is a notoriously complicated one. A hysterical fit is a state of subjective loss of consciousness without ictal discharges, usually in response to psychological stimuli. Ideally these fits should be shown to serve the purpose of solving a psychic conflict, and the patient may subsequently recognise that he or she was not subject to an epileptic form of impairment of consciousness. Such fits, as has been emphasised already, most often occur in patients who have epilepsy. They have to be differentiated from hyperventilation and
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simple syncope, which are common causes of loss of consciousness, especially in children, adolescents or young adults. Occasional epileptic fits may follow from hyperventilation. Hysterical fits are often associated with other hysterical symptoms, such as paralyses, which can be adequately defined as hysterical by means of the neurological examination, and Head’s criteria discussed earlier. However, it is probably true to say that there are no absolute criteria by which the occurrence of a hysterical fit can be proved by clinical examination at the time; the presence of a hysterical paresis is very helpful, and confirmation is sometimes obtained from patients subsequently that they are aware that they generated the attack themselves and did not lose consciousness in the same way as during an epileptic attack (Betts et al, 1976). Many epileptic discharges, especially temporal lobe ones, are so modified in their expression by the use of anticonvulsant medication that they may appear as brief episodes of loss of consciousness, states resembling petit mal and even seemingly hysterical behaviour. Pond (1974) has indicated that a brief epileptic discharge may be followed by a post-ictal state in which consciousness is modified and in which an unruly, so-called hysterical, state may appear. In such a state the patient may respond with kicking or jerking or screaming if touched; or merely act on commands in a way which suggests that he or she is aware of the environment and ‘putting on an act’. Yet careful examination may demonstrate, as in one of the writer’s cases, a concurrent dysphasia or other evidence of impaired cognitive function (Betts et al, 1976). Similarly, a patient who woke at night with screaming attacks was found to have a terrifying brief aura which was subsequently elaborated with a hysterical reaction. In addition to the direct organic provoking factors, psychological problems must contribute to the production of hysterical fits. The fact that fits are the favourite symptom is readily understandable, the patient modelling the psychological complaint on the pattern of an existing physical one. A variety of emotional problems may be responsible, including difficulties with relationships, dissatisfaction with work and jilting. But it also seems that, apart from the organic factors and drug intoxication, a failure to control the epilepsy or adjust to it plays a large part in upsetting the patient and generating extra fits. It seems paradoxical that an individual wishing to be rid of an illness should enhance its effects, but it is recognised often enough in clinical practice that patients respond in a way which overemphasises their disability (Betts et al, 1976). However, the consequence is often the opposite of that intended. A pathetic girl with many problems who produced hysterical fits
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was diagnosed as attention-seeking and was rejected rather than retained in hospital for the better control of her epileptic fits. She was partly aware of what she was doing and was later contrite at ‘faking fits’. Other patients do not have even her degree of awareness of what they are doing. The type of fits which have traditionally been called hysterical are also frequently known as pseudoseizures. Slavney (1994) has suggested that this term be used whenever a non-epileptic attack occurs which, consciously or unconsciously, is intended to mimic an epileptic seizure. Snyder (1994) objects to this mainly, but not only, on the grounds that intentionality is a very difficult judgement in cases of this sort. I, also, do not like the element of rejection which the term ‘pseudo’ often entails and suggested that we should use the term ‘doxogenic seizures’ (from the Greek doxe (opinion) and genon (to produce)) for those attacks which are thought to be due to the patient’s thought processes (Merskey, 1994). For this usage we should exclude cases where anxiety triggers a physiological event such as temporal lobe epilepsy. The same label of a doxogenic disorder may be applied to multiple personality disorder and to false memories obtained in recovered memory therapy (or from any other source). The word doxogenic in the latter cases is better than ‘iatrogenic’ because doctors and other therapists do not always deserve the blame for producing these syndromes, which may also be encouraged by other agents. Since, whatever the cause that leads to the thoughts, the thoughts are the source of the symptoms, the word doxogenic covers these problems quite well. It is not that I particularly seek to replace the term hysterical, but for those who wish to avoid it or use an alternative doxogenic should serve.
The relationship to other causes The earlier discussion has concentrated on motor symptoms because they are the most easy to prove clinically and are of most practical importance (apart from hysterical deafness or blindness). But anaesthesias are commonly demonstrated concurrently with motor conversion symptoms. As hysterical anaesthesias are rarely of practical importance (if they are, the diagnosis is probably wrong) they can normally be ignored in the management of the patient. Pain may also be an important hysterical symptom (Merskey & Spear, 1967) but one which is difficult to prove; its significance is discussed later (Chapter 12). Motor hysterical symptoms still occur
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frequently in unsophisticated populations, such as in East Africa (Kagwa, 1964), in South Korea (Chang & Kim, 1973), in Sri Lanka (Wijesinghe et al, 1976), in North American Indians (Armstrong & Patterson, 1975; Lehmann, 1975) and in Inuit (Eskimos) (Lehmann, 1975). Lambo (1956) noted them to be common in Nigerian patients both from villages and from urban areas. Several additional reports from other countries support this view. Okasha (1968) found an incidence of hysterical symptoms in 10.9% of patients in Egypt, Hafeiz (1980) reported 10% from the Sudan, and El Sayed et al (1986) found 8% with the diagnosis of hysteria in 324 new cases referred to a university psychiatric department in a city in Dammam, Saudi Arabia, over six months. El Sayed notes that hysterical reactions thus still appear to be more common there than in sophisticated societies. Pu et al (1986) demonstrate this with a series of 100 consecutive cases of hysteria seen in the Benghazi Psychiatric Service for the first time between November 1983 and July 1984. Of these, 59 had fits while the other symptoms included paralyses, blindness, aphonia and involuntary movements. Such figures are unparalleled in any non-neurological Western centre. Nandi et al (1992) have also demonstrated a decline of hysteria in two Indian villages. These villages were surveyed in 1972 and 10 years later in one case and 15 years later in the other case. The second surveys show very little change in the rate of total mental morbidity, but the rate of prevalence of hysteria declined significantly in both villages, dropping from 16.9 to 4.6 per 1000 in 10 years in the one village and from 32.3 to 2.05 per 1000 in the second village over the 15 years. In a personal communication Pu makes the comment that in Malaysia and Burma hysteria per se is not diagnosed frequently, although he has many reports in Indian journals. He suggests that in Southeast Asia ‘hysterical’ patients seek treatment elsewhere, for example through religious authorities, faith healers and so on, and when hysterical symptoms do appear they tend to be of a psychological type such as trance states, multiple personality, fugue states and similar responses rather than physical symptoms. He thinks that cultural factors may play some part in the choice of symptoms, which seems a very reasonable conclusion. Some members of rural or immigrant populations moving to an urban environment may also display classic conversion hysterical symptoms without organic disease. N. Geschwind (personal communication) observed this as a transient phenomenon in successive recent immigrant populations who attended the Boston City Hospital for treatment. However, from the preceding
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evidence it seems that in more urbanised, developed countries hysteria has a definite link with physical illness and perhaps especially with organic cerebral disorder. Whitlock (1967b) observes that no theory can be sufficient which fails to take account both of the psychological and the organic factor. He says this particularly because no emotional precipitants could be detected in nearly 40% of his cases. However, Merskey & Buhrich (1975) found that a relevant emotional factor could be detected in all their group H patients (allowing physical illness as such a cause in three cases). Physical illness was actually more relevant as a psychological precipitant in Merskey & Buhrich’s non-hysteria control group, since it appeared in 10 out of 24 patients. Nevertheless, the part played by physical illness in precipitating hysterical symptoms cannot be assumed to be only an emotional one. There are conceivably five ways in which physical illness may relate to hysterical symptoms. The first is that an independent emotional stress may lead the patient to elaborate the basic effects of a lesion which has already disturbed function in a part. Perhaps in such a case the most organically affected part is liable to acquire the extra, hysterical signs, but this is not obligatory, and an organically based monoplegia could well be elaborated as a hemiplegia. Secondly, the unpleasant psychological implications of a physical illness, the discomfort and the fear attaching to it, may lead the patient either to elaborate an existing symptom or to produce a fresh one. Thirdly, the occurrence of past or intermittent physical symptoms, as in epilepsy, may lead to modelling of the hysterical symptom upon the organic pattern which the patient has experienced. Psychological stress would more easily produce a form of illness of which patients had some knowledge rather than one of which they had no knowledge. (Past illness in a relation or close acquaintance is well known to serve the same function). The last two situations and their frequent unfortunate outcome are summed up in the words of the patient with epilepsy quoted earlier who actually simulated fits in order to increase the attention paid to her organic condition. “I had fake fits so that they would pay more attention to my real ones and then they said I had hysteria and would not do more for my real ones.” Fourthly, it may happen that physical illness will lead to a regression in behaviour. The advantages of the sick role range from ‘get well’ cards, fruit and flowers, to relief from painful
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responsibilities and intrapsychic dilemmas. These advantages are much canvassed and need no special description, except for the qualifying remark that they are sometimes bought at the price of relinquishing other enjoyments and functions which may be actively desired. The most difficult problem is the fifth possible mode of effect. That is the notion that cerebral damage may operate in a more specific way to produce conversion symptoms. Schilder (1940) thought that this was particularly liable to appear and argued, as mentioned, that: “Cerebral organic syndromes may change functions of the brain in such a way as to provoke neurotic attitudes. One cannot claim similar mechanisms for traumas which afflict other parts of the body.”
Slater & Glithero (1965) extended this view to hysterical personality traits, saying, “Organic disease may bring about a general disturbance involving the personality which results in modes of behaviour (exaggeration, attention-seeking, etc.) which we naturally think of as manifestations of the hysterical personality.”
If this view is correct, cerebral disease should give rise to more hysterical symptoms than peripheral (non-systemic) physical illness. Merskey (1975) showed a trend in this direction but the figures, although quite large, were not statistically significant. In the L group with hysteria (Merskey & Buhrich, 1975) the ratio between central and peripheral lesions was 43:21 in those patients who had only organic illness in one or the other of these distributions. In a non-hysteria group with somatic illness matched to the L group for in-patient and out-patient distribution, the ratio was 137:98. The trend is in the anticipated direction but the figures from the raw data were not statistically significant. Using a psychological test, the Middlesex Hospital Questionnaire (MHQ), Gadd & Merskey (1975) found that female patients with conversion symptoms and higher-level cerebral organic lesions or disturbance also scored very significantly lower on scales for anxiety and other measures of neurosis than did other patients with conversion symptoms. This in turn supports the idea that cerebral organic disease may be comparable in some way to neurotic illness or abnormal personality in promoting conversion symptoms. The conclusion cannot be made firmly, however, because there was a significant effect in the opposite direction among the small group of male patients.
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It appears that there is now a number of studies indicating a possible connection between hysterical symptoms and organic brain disease. The special links which appear to exist with epilepsy and drug intoxication are perhaps the most notable, but paralyses occurring with tumour or with early dementia also provoke reflection, as do the pseudodementias and hysterical amnesic disturbances which may be seen with cerebral tumours or diffuse cerebral disturbance. An adequate explanation of these associations is not available, although Ludwig (1972) offers one systematic attempt. He takes up the suggestion (Whitlock, 1967b) that the lack of attention or concern paid to symptoms on the part of the hysterical patient is due to a “selective depression of awareness of a bodily function” brought on by corticofugal inhibition of afferent stimulation at the level of the brainstem reticular formation. Ludwig reviews the neurophysiological evidence which might support this view, acknowledges that some of it is controversial, but concludes that hysteria is essentially a dysfunction of attention and recent memory due to increased corticofugal inhibition of afferent stimulation, while hypochondria, as the counterpart of hysteria, is presumed to be related to decreased corticofugal inhibition of afferent stimulation. He offers a number of ways in which this theory might be tested, emphasises its speculative nature, and affirms that it could only be part of “a complete account of” the disorder, since cultural, cognitive and psychophysical correlates would also require attention. In my view this theory will probably prove to be wrong for three reasons. First, it does not have adequate initial neurophysiological data. Second, the neurophysiological evidence cited is highly controversial. Third, it seems very likely that such changes in attention as occur in hysteria are secondary to the patient’s motives and would not otherwise differ from normal. The situation is somewhat like that with hypnosis (Chapter 17), where we now have no grounds for believing that there is any physiological difference between a hypnotic ‘trance’ and responses to suggestions occurring without special trance-induced changes. Unfortunately, it seems to be too early for us to be able to offer any useful theory on how cerebral disturbances may promote conversion symptoms. It is likely even that the view that they do so at all will still encounter some strong opposition. A more fruitful approach will perhaps emerge from the careful study of the relationships between gender, hemispheric specialisation, and psychopathology. Some evidence indicates differences in the cerebral lateralisation of function for affect, as well as a
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distinct tendency for left-hemisphere functions, such as linguistic skills, to be stronger in females while right hemisphere functions, like spatial skills, are stronger in males. Flor-Henry (1978) reviewed these topics, and it is not too fanciful to suggest that the differential development of the hemispheres, combined sometimes with brain damage, contributes to the relative frequency of affective and hysterical syndromes in women, and psychopathic and schizophrenic syndromes in males. Besides the evidence on affective change and right-sided cerebral lesions discussed in Chapter 19, Lishman (1968) noted that somatic complaints such as headache, dizziness, fatigue and hypersensitivity to noise were more common after right-hemisphere damage than after left-sided injuries. Another pointer in this direction comes from the report (Stern, 1977) that conversion symptoms are localised more often on the left side of the body than would be expected by chance. This is not to deny the many other important causal factors in these illnesses, but to recognise that there are indications from systematic studies that we shall know much more in a few years’ time about the links between cerebral function and psychiatric illnesses other than just the pure brain syndromes. One sad note about hysteria and organic illness is provoked by Kraepelin’s case described in Appendix B. This patient died of tuberculosis, 12 months after her admission to Kraepelin’s care. We can guess that infection had been present for some years and had been a contributory factor in making the patient more liable to neurotic complaints. However, Kraepelin evidently did not think she was physically ill when he described her case, and it seems more likely that she acquired her infection as a result of the asylum conditions. In a sense her death was iatrogenic, as are a number of other misfortunes, especially the frequent operations (Chapter 13) which some hysterical patients undergo.
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12 Pain
In the last chapter the place of organic causes in producing hysterical symptoms and releasing hysterical behaviour was considered. We now need to look at the commonest somatic symptom in medicine, pain, and to assess its relationship to hysterical mechanisms. The historical association of pain with hysteria has already been mentioned. In analysing the dynamics of hysteria, Freud (Breuer & Freud, 1893–95) often used examples of patients with pain. He either concluded or implied that pain was a common conversion symptom, that unpleasant affect was converted to bodily pain, that the choice of symptoms was determined by precipitating events, and that pain often had a symbolic meaning. One of the difficulties in regarding pain as a conversion symptom is that there is rarely any direct evidence to prove that the specific symptom has a psychodynamic basis. Many patients have pain for psychological reasons (Merskey & Spear, 1967; Sternbach, 1968). The proportion of patients who have pain for psychological reasons may reach 38% in general medical clinics (Devine & Merskey, 1965) and 65.6% in psychiatric clinics (Spear, 1967). But it is frequently hard to demonstrate a relevant dynamic mechanism.
Changing views In general, psychiatric patients with pain show features of depression, anxiety and hysteria (Merskey, 1965a; Spear, 1967). The incidence of hysterical features either in terms of personality traits or other conversion symptoms is greater in those whose painful illness is of longer duration (Merskey, 1965b). Formerly, it was thought that this increase of conversion symptoms in the 160
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chronic cases was quite large (Merskey, 1965b). More stringent views about what can be accepted as a hysterical symptom led to a revision of that opinion. Previously the diagnosis of hysteria was accepted in the case of patients who had a history of possible hysterical symptoms such as ‘blackouts’ (which of course may have other causes) or who showed marked hysterical personality features. The thresholds for such diagnoses have risen considerably and it has been demonstrated (see Chapter 22) that the link between hysterical personality and conversion symptoms is relatively poor. The diagnosis of hysterical pain should require the following: (a) the absence of an adequate organic explanation (b) the absence of schizophrenia or a depressive illness or a psychophysiological mechanism which could account for the symptom (c) the presence of a very well marked syndrome, such as somatisation disorder, identified by detailed criteria (see Chapter 13) (d) or, ideally, the presence of an emotional conflict which has caused repression. Good proof, both of such a conflict and of its repression, is quite rare. Thus the importance of hysteria in relation to pain has diminished, although it is still of much theoretical significance and still has some practical implications. These theoretical aspects are reviewed next, followed by an appraisal of the reasons for reducing the importance of hysteria in relation to pain.
Pain from an idea The received notion of a hysterical symptom requires that it should correspond to pain from an idea and be a result of thought processes. It should be noted that alternative explanations, other than a conversion mechanism, could conceivably be appropriate for pain resulting from an idea, but they are not generally the most ready way of viewing the matter. It is not known how often hysterical symptoms occur in these ways in the total population of patients who complain of pain and, as already emphasised, it is hard to diagnose hysterical pain in practice. But some noteworthy evidence exists that pain may be produced either by an idea or by hysterical mechanisms. One of the best examples is the couvade syndrome.
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Reik (1914) provided an extensive discussion of the couvade syndrome. This word, believed to be derived from a Basque root meaning ‘to sit upon eggs’, is used to describe behaviour known since antiquity in the husbands of pregnant women or of those giving birth. The husband may go to bed and mimic the pains of childbirth or, more often, develop complaints such as headache, toothache, heartburn, gastralgia and other localised pains. This syndrome of pains of various sorts has occurred in Indian soldiers of varying ranks (Bardhan, 1965a,b), in mining communities (Dennis et al, 1956) and elsewhere in modern urban society (Curtis, 1965; Trethowan & Conlon, 1965; Trethowan, 1968). Bogren (1984) undertook a prospective study of couples expecting their first child. Twenty per cent of the men suffered from the couvade syndrome. They were older than the unaffected men and more often had older parents. More of them showed attachment to and identification with their mothers. Men with the couvade syndrome suffered from a greater number of mental symptoms during the pregnancy than did the unaffected men. The couvade syndrome was also commoner when the woman was anxious about the pregnancy. The women’s anxiety seemed to be more important for the development of the syndrome than the men’s. Bogren interpreted his findings as suggesting that the couvade syndrome was commoner in men who tended to identify more with their wives. The pains of the couvade usually have no plausible physical cause, not even such a mechanism as muscle tension. Moreover, they show very clearly how sympathy, identification, imitation or thought processes based on feelings might give rise to them. If the pain solves an emotional conflict it will be appropriate to regard it as a hysterical conversion symptom. A similar situation exists with some other pains which can be observed clinically. For instance, an educationally subnormal youth who was responsible for an extramarital pregnancy developed pains in his head, in his face, neck, arms, trunk, limbs and penis. He was unwilling to marry the girl, who was even less prepossessing than himself, but he was under pressure to do so. The pains could be seen as a retreat into illness, a temporary solution of his conflict and perhaps as an expression of guilt. He did not describe these ideas directly, but when he was asked how he thought his pains arose he said: “I imagine a nail or hammer on the back of my head or a razor catching or just laying against where you pittle. When I imagine that, it starts to pain a bit. The thought of the nail fetched the pain on.”
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In this case there was a reasonably acceptable psychological explanation as to why he had developed pains (which were not solely due to tension) and a direct account by the patient of the origin of the pains in his thoughts. This was obtained despite his low intelligence. In another case there was evidence of a hysterical amblyopia in a painful eye of a 25-year-old girl who complained of an episodic jabbing pain in her left eye and a continuous dull ache in the area, present for two years and commencing when the buckle of a car safety belt accidentally struck her. The car, in fact, belonged to her boyfriend, whom her parents disliked. The vision in her left eye was blurred and a diagnosis of hysterical amblyopia was supported by evoked potential studies. She was an immature, dependent girl and was thought to have psychosexual conflicts, but these were not helped by a series of interviews. Hypnosis, about the time that she had decided to give up her boyfriend, produced a complete recovery. It is reasonable to suppose that the pain in this case was due to a repressed conflict over her boyfriend which was solved, not by analytic exploration, although this was attempted, but by giving up her boyfriend. Perhaps not all the pains which are due to thought processes in this way are conversion symptoms. However, not only are they usually regarded in this way but also the classification of them as prima facie hysterical symptoms appears theoretically correct.
Pain and emotion Historically, pains have always had a prominent place in the diagnosis of hysteria. Instances of this were cited in Chapters 1 and 2, and the rich material of Appendix A provides another example of how many pains in different parts of the body were regarded as part of the syndrome of hysteria. Sydenham (1697), Whytt (1761), Briquet (1859), Charcot (1889), Gowers (1893) and Savill (1909) all expected pains to be hysterical, and the statement of Brodie (1837) that “in upper class women” four-fifths of joint pains were hysterical is often quoted. Sydenham regarded pain as an emotion, but in the second half of the 19th century, when pain was increasingly regarded as a sensory phenomenon, pains, if they were ‘real’, were thought to be due to organic disease or were dismissed. Inman (1858), who was quoted in Chapter 2, still favoured the older view that hysteria was in some sense an organic affliction. A more developed view is evident in Anstie (1871), who believed that neuralgic (organic) pains were an ultimate consequence of emotional disturbance, even including “unconscious resentment
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of the neglect of sexual functions”. He was not wholly original in this, since Brodie (1837) and Carter (1853), among others, had dealt with concepts of the unconscious and repression, whilst von Feuchtersleben (1845) had attributed hysteria (with pains) to sexual frustration. Perhaps many of the pains in question, such as premenstrual pains, are not so much hysterical as a consequence of anxiety and local physiological dysfunction, but the link between pain and the emotions is undoubtedly enduring and for many pains, as has already been indicated, a hysterical mechanism appears to be ineluctable. Rawnsley & Loudon (1964) provided an important example of the link between pain and hysteria. Like pains due to thought processes, those due to the couvade syndrome and those in many parts of the body without any plausible physical mechanisms, the examples given by Rawnsley & Loudon suggest a purely psychological or conversion process. Their patients belonged to the island of Tristan da Cunha. In 1937–38 a Norwegian scientific expedition visited the island and was able to record an epidemic of hysterical ‘spells’ affecting many persons. In 1961, because of a volcanic eruption, the islanders were evacuated to England. Rawnsley & Loudon investigated their health and noted a high incidence of headaches, including headaches of psychological origin. The latter were very significantly associated with the history of ‘spells’ in the 1937–38 epidemic, and there was a marked tendency to seek extra medical consultations. The spells and headaches of psychological origin were more frequent in women married to leaders of this humble group. This is striking evidence in support of the view that hysterical mechanisms are likely to be at work in the patients who consult frequently and develop pain for psychological reasons. Another worker who has documented hysterical symptoms in relation to pain is Walters (1961). Although rightly concerned to show that hysteria was by no means the only feature of patients with pain of psychological origin, Walters found 26 out of 430 psychiatric patients with pain to have pure conversion hysteria and a further 336 out of the total to have mixed neuroses and situational states. Other psychiatric abnormalities were prominent in his patients, so Walters preferred to label pain in these circumstances as ‘psychogenic regional pain’, but he clearly did not reject the occurrence of hysterical mechanisms. Still another important element in the traditional view of hysteria encompasses patients who have multiple symptoms without an adequate organic basis and whose symptoms cannot be explained satisfactorily by the presence of another psychiatric disorder, such as an anxiety state, a mood disorder or hypochondriasis. This type
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of patient was commonly called hysterical as long ago as the 18th century (e.g. Pomme, 1765; cf. Chapter 1). In the 19th century, as discussed in Chapter 2, Dubois d’Amiens, Landouzy, Briquet and most other authors recognised patients with multiple symptoms of this nature as having hysteria. Currently, many such cases are now accounted for by diagnoses of anxiety or depression, but a residual group was defined, and this is now generally known as somatisation disorder. This group of cases also provides reason to think of pain as being related to hysteria. It receives separate discussion in the next chapter. The functions which hysterical pains may currently serve are easy to document, at least in some cases. Pain conforms to the common idea of an illness with some physical basis, and does so at least as well as the dramatic fits and major hysterical symptoms which are traditionally more typical of an unsophisticated population. The latter group of symptoms has become less common at the present time, except in certain special settings, or in rural residents, either at home or newly arrived in big cities (cf. Chapter 11). As the major and traditional symptoms of hysteria other than pain decline, pain remains acceptable as a somatic complaint. But in any case, pain could still tend to be unconsciously preferred as a dissociative symptom since it is notoriously the commonest sign of suffering. It readily confers the status and role of an organically ill patient upon the affected person. The emphasis on hysterical causation in pain has a long and venerable history, some of which may well be attributable to the long-standing association of headache and psychological illness. If, as is known, headache is very common in psychological illness, including both anxiety and depressive states, and if hysteria was once – as we have shown – a general term covering much neurotic illness, the association with pain is understandable, even though the mechanism of headache in these conditions may be either psychophysiological or linked in some fashion – without conversion – to depression. The psychodynamic authors also adopted the idea that pain could be a common physical complaint, as discussed in Chapter 4 with respect to psychodynamic writers such as Alexander, and this has led to a continuing emphasis on the explanation of pain as a conversion symptom.
Psychodynamics of pain The dynamics of pain of psychological origin have generally been a matter of speculation rather than proof. Merskey & Spear
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(1967) noted 27 authors who stressed the association of guilt, hostility, resentment and pain. Almost all the evidence was anecdotal except for one or two experimental attempts to induce or abolish headache in relation to conflict over hostile impulses and some controlled studies by Spear (1967) and Merskey (1965b). The most influential psychodynamic contributor in this field, Engel, first described atypical facial pain (Engel, 1951) as a form of hysterical symptom and then gave a detailed account of what he called “psychogenic pain” in the “pain prone patient” (Engel, 1959). He regarded his subjects as suffering from a hysterical conversion symptom, but emphasised that they uniformly presented a character structure which he termed “masochistic”. He emphasised the frequency in their cases of unnecessary surgery, the occurrence of other somatic symptoms, the alleged tolerance of pain of organic origin – often with gusto – and remission of the pain at times of misfortune, or when there was other cause for suffering, whether physical or mental. Like previous psychodynamic writers, only rather more clearly, he argued that pain served as a warning of bodily damage, had a communicative function, and was linked with punishment, aggression, guilt, sexual feelings and the loss of an object. There was no statistical or quantitative proof of his claims, but the life pattern of many of his cases supported his argument. Most of them gave evidence of hysterical conversion mechanisms. If Engel is correct, certain consequences should follow with regard to repression and hostility in patients with chronic pain. Spear investigated the presence of overt or covert hostility in psychiatric patients with pain and little evidence of organic illness (Spear, 1967), and his results did not support Engel’s hypothesis. The patients with pain showed no more overt or covert hostility than other psychiatric patients. Both Spear (1967) and Merskey (1965b) found that the patients with pain had more operations, more consultations with specialists, more investigations and so on, findings which have been repeatedly confirmed. My patients with pain also had an increased frequency of past painful illness (P < 0.01) and an increased frequency of resentment but not of aggressive actions. Here, Engel’s theories were partly, but incompletely, confirmed, and it is worth noting that there is an alternative explanation of resentment (or hostility when it occurs) in patients with chronic pain. If pain is a signal of danger to the body, then preparation for action, either fight or flight, must be a normal response, and this may well explain the frequency with which cutaneous pain is associated with obvious irritability. Blumer (1975) went over the same clinical ground as Engel with respect to chronic persistent pain in a series of 388 patients
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mainly originating in neurosurgical and orthopaedic practice. He found the ‘pain-neurotic’ to be an individual with marked conflicts and prominent sadomasochistic and infantile dependent needs which result in guilt, and which are also denied. “The pain handily solves these conflicts, requiring dependency and providing atonement for guilt while at the same time allowing a good measure of revenge ... [against the long-suffering partner]”. Like that of earlier writers, his evidence was not controlled and in fact there is probably no good systematic work to confirm the boldly drawn picture of Engel, Blumer and others in the pain patient. Nevertheless, a reasonable idea lingers that, although it has perhaps never been scientifically proven, pain sometimes may have symbolic features, which could include a sadomasochistic function. Some of these patients with chronic pain fall into the group who undergo excessive surgery and are linked with the hospital addiction types (Chapter 8). Findings of this sort, discussed at length by Engel (1951, 1959), Merskey & Spear (1967) and Blumer (1975), indicate that if there is a link between pain and hysteria, that link will depend dynamically upon pregenital fixations. This is relevant to the subsequent discussion (Chapters 22–24) of the psychodynamic characteristics of patients with hysteria. Adler et al (1989) made another attempt to confirm Engel’s findings, in a controlled clinical investigation of patients’ retrospective views of their childhood experience. Patients with a diagnosis of “psychogenic pain” were compared with three other groups having “organic pain”, “psychogenic bodily symptoms”, or “organic disease”. The authors found evidence which they felt confirmed Engel’s characterisation of the parents of patients with chronic pain of psychological origin as being more verbally or physically abusive of each other and abusive of the child, while the child deflected aggression from one parent to the other onto him/herself. This work was done very carefully but has certain drawbacks in interpretation. There were significant differences between the “psychogenic pain” group and some of the others with respect to age and sex. Moreover, the diagnosis of “psychogenic pain”, which was based upon DSM–III criteria (American Psychiatric Association, 1980), is under attack, as discussed later, and no description was provided of the patients with “psychogenic bodily symptoms”. This is a pity because their patterns of response did seem to be more like those of the two organic groups than the other “psychogenic” group, although the patients with “psychogenic” bodily symptoms were younger than those in the other three groups.
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The paper by Adler et al gives only uncertain support for Engel’s main hypothesis, as does a report by Merskey & Boyd (1978) on the recollections of childhood experience by patients with emotional or organic causes for chronic pain. The first group more often had experience of punishment or rejection by their parents, but these findings had only a modest degree of statistical significance (P < 0.05). Although the effect was significant it was not large, and may be attributable to patients with psychiatric illness having a higher rate of childhood problems compared with the patients with physical illness. Thus one of the leading theories of the hysterical aetiology of painful illness still lacks adequate corroboration, while other hypotheses have come forward to vie with it for the interpretation of emotional change in association with pain, the strongest of which is that depression and other psychological changes occurring in conjunction with chronic pain of physical origin are frequently a consequence of the pain (Merskey, 1989). The other favourite explanation for the special association of pain and emotional change is that minor physical lesions, or other non-progressive painful disorder, will present more often for attention because of a selection effect, the patients having pain for physical reasons but presenting it more often for medical care because of their increased concern. In a closely related field, Kellner et al (1985) examined several groups of patients (including some with pelvic pain) and control subjects on self-rating scales with respect to anger–hostility, somatic symptoms, and hypochondriacal fears and beliefs. Somatic symptoms were positively correlated with anger–hostility, but were associated more strongly with symptoms of anxiety and depression than with those of hostility. The correlations between hostility and somatic symptoms were inconsistent, and varied between groups. The authors concluded that their findings did not support the view that anger or hostility are main or specific aetiological factors either in somatisation or in hypochondriacal fears, or both. They mention several alternative possibilities which could explain their findings. It is worth noting that the construct of “psychogenic pain” offered in DSM–III corresponded essentially to ideas of a hysterical conversion disorder, but was distinguished from other types of hysterical conversion symptoms. The criteria for this diagnosis were modified in DSM–III–R (American Psychiatric Association, 1987), when it was labelled “somatoform pain disorder”. They were still thought to be unsatisfactory, and the revised criteria for DSM–IV dropped them completely (American Psychiatric Association,
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1994). Instead “Pain Disorder” is listed among the diagnoses. Two types of pain disorder are now recognised. In pain disorder associated with psychological factors, in addition to troublesome pain, psychological factors “are judged to have the major role in the onset, severity, exacerbation or maintenance of the pain”, and the pain is not better accounted for by a mood, anxiety, or psychotic disorder and does not meet criteria for dyspareunia. In the second type, both psychological factors and a general medical condition are judged to be important. The first of these types provides a place for pain as a conversion symptom in the way in which it has been regarded in the past, while the second introduces an alternative approach which fits much better with the realities of the pain clinic, where few cases present without a significant organic basis. Despite the above, there is still reason to think that pain may occur as a result of an idea on occasion. It is one of several possible mechanisms by which pain may follow from psychological illness rather than from physical causes. The other mechanisms include the production of pain as a hallucination or delusion, as in schizophrenia or sometimes in severe depression, pain from psychophysiological causes, as in muscle contraction, and perhaps pain as a consequence of depression or related to depression, by virtue of a common biochemical mechanism (Magni, 1987). In addition, pain may be increased by a hypochondriacal focus upon minor bodily symptoms, and this will be discussed in the next chapter. It has been pointed out elsewhere (Merskey & Spear, 1967) that there is a drawback to the attractions of pain as a conversion symptom, if one adopts the point of view, which I accept, that the patient experiences pain as unpleasant. Pain is then a poor solution to the problem which one postulates that it must be intended to resolve. Why choose a symptom which hurts? One answer to this is to say that people do undoubtedly frequently hurt themselves and involve themselves in suffering either by limited self-injury or suicidal attempts or other actions when on rational grounds they could be expected to avoid such misfortunes. In view of this it has often been postulated that these acts are self-punishing or masochistic. The argument for masochism is an ad hoc explanation, and we need to look carefully at the assumptions which have promoted the idea of pain as a hysterical symptom, in addition to the historical association. The upshot of the discussion just concluded is that there are many reasons to be cautious anyhow about the diagnosis of pain as hysteria. A point of much practical importance follows from this conclusion. No matter how often a pain may be thought to be
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hysterical, it is frequently unwise to use this diagnosis overtly. In the first place, this is because it is relatively easy to be mistaken about the hysterical provenance of an individual symptom where there are few or no positive signs of hysteria. In this respect, pain is markedly distinct from motor conversion symptoms. Secondly, patients are often unable to appreciate the nature of the explanation that a symptom like pain, ‘which hurts’, is due to an unconscious conflict. It is much easier and potentially more accurate to talk of pain resulting from an emotional state affecting the body. Thirdly, for complete proof it is necessary to obtain the dynamic explanation for the genesis of a particular symptom. Strictly speaking, that explanation has to be provided by the patient from her or his own thought associations. Despite the examples quoted, this rarely happens with pain. Physicians are, therefore, best advised to recognise the importance of hysterical mechanisms in pain and to manage the patient with them in mind, but not to assume that they have proved a pain to be hysterical unless they have fulfilled the criteria outlined. The same is true in regard to multiple pains. Gout, disseminated lupus erythematosus, rheumatic conditions and hypothyroidism may occasionally present in a way which is mistaken for multiple pain of psychological origin. However, if the patient also meets the criteria of Briquet syndrome, a psychiatric diagnosis is then likely to be on safer ground. This re-emphasises the well established principle that negative organic findings are not enough to make a psychiatric diagnosis. Positive findings of emotional disturbance proportionate to the trouble, or meeting suitable criteria, must also be present before a complaint can be assumed to be psychiatric. The motivation for pain due to an injury which is subject to a compensation claim is usually obvious and not repressed – and the pain may be organically explicable – so the diagnosis of hysterical pain is exceptionally difficult. This is the more true because we lack good ‘positive signs’ by which pain may be diagnosed as hysterical. Positive signs are discussed in Chapter 14. The model for them is given by motor symptoms, such as a paralysis, where the patient can be demonstrated to have a capacity which he or she believes has been lost. Thus, a patient lying supine with a hysterical paralysis of a leg may not press the heel down hard on the examiner’s hand when asked to do so. However, when the patient lifts the other leg, the ‘paralysed’ one may press down in a synergistic counterpoise. There are no good techniques to compare with this in patients with pain, unless the patient also happens to have a classic motor conversion symptom or a symptom like hysterical blindness or deafness. In any case, the sensory signs
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which were relied on in the past as indicators of hysterical disorders are much less sure than they were previously (see Chapters 11 and 14).
Pain and psychiatry There are several other relationships of pain to psychiatry and they are more important in practice than conversion symptoms, somatoform complaints or hysteria at large. These relationships include pain associated with anxiety or depression. Anxiety and depression may cause pain, for example headaches, or may make pain worse – which is thought to happen very frequently. Also, chronic pain often causes secondary depression or other emotional changes (Merskey, 1989). Other works (e.g. Wall & Melzack, 1994) deal with this at length.
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13 Somatisation disorder and somatisation
The tacit view of pain as a hysterical symptom is particularly common among doctors when they use the word ‘polysymptomatic’ to describe patients. There is a well recognised group of patients who present in medical and surgical out-patient departments with numerous somatic complaints, including pain, very little evidence of significant physical illness, and a tendency to chronicity. Ruesch (1946) documented the relatively low social status of this group. Hollingshead & Redlich (1958) and Strole et al (1962) also gave evidence of its existence; the writer’s own findings (Merskey, 1965a,b) supported the view that hysterical pain in Western society has a social-class distribution, or at least presentation, tending to appear most often in women who are semi-skilled or unskilled workers, or married to men in comparable occupations. In addition, this view must now be qualified by the observation from epidemiological work that chronic musculoskeletal pain is much more common in groups with a low income than those with a high income and in association with depression (Magni et al, 1990, 1991, 1993, 1994). Such a distribution, of course, is never absolute, and there are plenty of examples of women from higher social classes with hysterical pain. Patients of this type are often known as ‘thick-folder’ patients, their hospital records bulging uncomfortably and weighing much more than the average. Other workers also find pain to be prominently associated with hysteria. Ziegler & Meyer (1960) found it as a primary complaint in 134 patients diagnosed as having conversion symptoms, and Purtell et al (1951) found the majority of 50 patients with hysteria to have pains in various places (28 had back pains, 14 joint pains, and 31 pains in the extremities). Pilling et al (1967), taking pain 172
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as a presenting symptom, found an association with hypochondriasis and conversion symptoms and high Hs (hypochondriasis) and Hy (hysteria) scores on the Minnesota Multiphasic Personality Inventory (MMPI). Sternbach et al (1973) obtained similar MMPI results in patients with back pain, and Kenyon (1964) observed pain to be the most frequent symptom in patients with hypochondriasis. In this context, the MMPI has some serious limitations, since it is assumed that complaints of bodily symptoms are evidence of hypochondriasis but this assumption has frequently been made without any effort to determine whether or not the symptoms were physically based. Thus all patients with bodily complaints were treated in a fashion which made them bound to appear, at least to some extent, as if they were hypochondriacal or subject to hysterical symptoms. This misreads the response patterns of patients with chronic pain on the MMPI. Pilling et al (1967) showed the conversion V triad to be common in patients with chronic facial pain. In this distribution on the MMPI the scores for hypochondriasis and hysteria tend to be elevated and those for depression are raised relatively less. Sternbach (1974) obtained similar results, and many subsequent investigators have found the identical pattern. Fordyce (1976) recognised that this pattern is common to pain patients whether or not they have physical lesions. Watson (1982) showed that chronic pain patients obtained elevated hysteria and hypochondriasis scores on the MMPI because they endorsed items that were relevant to their problem (e.g. back pain, poor sleep or fatigue) and not necessarily because they were hypochondriacal. Smythe (1984) and Merskey et al (1985) emphasised that the use of these scales in the MMPI can be misleading because they rely to a considerable extent upon symptoms like pain in different locations, fatigue, other bodily complaints and insomnia as evidence for high scores on hypochondriasis, depression and hysteria. In the presence of physical illness this will often be invalid. Love & Peck (1987) reviewed 56 studies and concluded that the MMPI should not be used in the attempt to distinguish psychological causes of pain. Pincus et al (1986) showed that elevations in the Hs, D (Depression) and Hy scores in patients with rheumatoid arthritis were explained largely by five MMPI statements related to their diseases, and their responses to other questions resembled those of normal subjects. It follows that the so-called conversion V phenomenon, which earlier led us to believe that hysterical phenomena were a common part of chronic pain, has been seriously misunderstood. The limitations of the MMPI in this context have been noted, but multiple symptoms still require discussion. Guze and his
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colleagues at Washington University, St Louis, Missouri, have conducted a valuable systematic study of patients with multiple symptoms for a number of years (Perley & Guze, 1962; Guze & Perley, 1963; Guze, 1967; Woodruff, 1968; Farley et al, 1968; Cloninger & Guze, 1970a,b; Woodruff et al, 1971; Bibb & Guze, 1972; Guze, 1973; Cloninger & Guze, 1975). Their numerous publications started from a particular definition of hysteria: First the patient must demonstrate a dramatic or complicated medical history beginning before age 35. Second, the patient must admit to 25 symptoms in 9 of 10 special review of symptoms areas. Third, no other diagnosis can be made to explain the symptoms. (Guze, 1967)
The areas of symptoms shown in Table 13.1 (Woodruff, 1968). In regard to this type of patient, Guze (1967) observes “frequent visits to the physicians, the use – often simultaneous – of an amazing number of medications, excessive hospitalization, and excessive surgery, parallel the florid symptom picture”. He proposed the term Briquet’s syndrome for this group (Guze, 1967, 1970). It has been found in full in 1 out of 50 consecutive women under investigation in a university hospital medical ward Table 13.1. Woodruff’s (1968) groups of symptoms of hysteria Group
Symptoms
1 2
Headaches; sickly most of life Blindness; paralysis; anaesthesia; aphonia; fits or convulsions; unconsciousness; amnesia; deafness; hallucinations; urinary retention; ataxia; other conversion symptoms Fatigue; lump in throat; fainting spells; visual blurring; weakness; dysuria Breathing difficulty; palpitation; anxiety attacks; chest pain; dizziness Anorexia; weight loss; marked fluctuations in weight; nausea; abdominal bloating; food intolerances; diarrhoea; constipation Abdominal pain; vomiting Dysmenorrhoea; menstrual irregularity; amenorrhoea; excessive bleeding Sexual indifference; frigidity; dyspareunia; other sexual difficulties; vomiting nine months of pregnancy, hospitalised for hyperemesis gravidarum Back pain; joint pain; extremity pain; burning of the sexual organs, mouth or rectum; other bodily pains Nervousness; fears; depressed feelings; need to quit working or inability to carry on regular duties because of feeling sick; crying easily; feeling life was hopeless; thinking a good deal about dying; wanting to die; thinking suicide; suicide attempts.
3 4 5 6 7 8 9 10
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(Woodruff, 1968) and in 1 out of a sample of 100 ‘normal’ postpartum women (Farley et al, 1968), corresponding to a distribution of 1–2% in such patients and agreeing with similar findings by Majerus et al (1960) and Murphy et al (1962). About 10% of psychiatric in-patients in university hospitals were similarly affected (Bibb & Guze, 1972) and between 5% and 11% of psychiatric out-patients (Guze et al, 1971). (The figures from the latter paper are the writer’s interpretation.) Guze (1970) has emphasised that this syndrome is in contrast with the definition of conversion symptoms. He observes: “it is precisely because conversion symptom and hysteria were used to refer to different phenomena that a gratifying degree of diagnostic validity was demonstrated. The term conversion symptom is used in these studies in a purely descriptive way to refer to unexplained symptoms suggesting neurological disease of which amnesia, unconsciousness, paralysis, ‘spells’, aphonia, urinary retention, difficulty in walking, anaesthesia and blindness are the most common and classical examples. (These are the socalled ‘pseudo-neurological’ or ‘grand hysterical’ symptoms.) Unexplained in this context, means only that the history, neurological examination and appropriate diagnostic test have failed to uncover a satisfactory explanation for the symptoms. Furthermore, this use of the term conversion symptom carries with it no etiological pathogenic implications. Conversion symptoms must refer simply to a limited group of certain individual symptoms. Even though the term arose from the psychoanalytic theory of the unconscious conversion of psychic energy, it is proposed that its use be restricted to the descriptive function just outlined.”
There is of course a substantial overlap between patients with conversion symptoms and those with Briquet syndrome. This is recognised (Guze, 1967; Guze et al, 1971), although occasionally patients appear with Briquet syndrome and without a history of conversion symptoms (cf. Guze et al, 1971; Table 13.1). Conversion symptoms as such affected or had affected 27 of the 100 postpartum women studied by Farley et al (1968), 30% of 50 medically ill women studied by Woodruff (1968), and 24 of 100 psychiatric clinic out-patients studied by Woodruff et al (1971). These are remarkably high figures. The earliest paper from this group (Perley & Guze, 1962) indicated that this syndrome remained stable in 90% of the cases and no other illness which might have explained the original symptoms developed during the period of follow-up. Arkonac & Guze (1963) further reported that 9% of the parents, siblings and children over 15 years old of the affected individuals suffered from the same syndrome (15% of the female
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relations). Anxiety neurosis affected 9% of the relatives (not more than the likely population incidence) but 33% of the male relatives were diagnosed as alcoholic or sociopathic. Woerner & Guze (1968) enlarged the study, included husbands in it, and obtained similar findings. In a further study it was shown that conversion symptoms in male criminals were associated with significantly higher prevalence rates for alcoholism or drug addiction, anxiety neurosis, attempted suicide, and psychiatric admission to hospital, than for other criminals. When examining female felons, Cloninger & Guze (1970a,b) made at least one psychiatric diagnosis on every female patient. Sociopathy, alcoholism, drug dependence, hysteria and hypochondriasis were encountered more frequently than would be expected in the general female population. The most striking finding was a 20-fold greater incidence of hysteria than normal (27 out of 66 women). With the development of DSM–III and DSM–III–R (American Psychiatric Association, 1980, 1987) a category was incorporated of somatisation disorder which was intended to identify similar patients but with somewhat fewer questions and categories. As now described in DSM–IV (American Psychiatric Association, 1994), this category requires a history of many physical complaints over several years and beginning before the age of 30. They must result in treatment being sought or significant impairment in social, occupational or other important areas of functioning. At least four pain symptoms, two gastrointestinal symptoms, one sexual symptom, and one “pseudo-neurologic” symptom are required to meet the criteria. DSM–III–R described 35 potential symptoms, divided into gastrointestinal symptoms, pain symptoms, cardiopulmonary symptoms, conversion or pseudoneurological symptoms, sexual symptoms for the major part of the person’s life after opportunities for sexual activity, and some female reproductive symptoms. Shorter forms of the original Briquet categories modelled upon them in this fashion proved successful in further research exploring the implications of somatisation disorder. In particular, epidemiological studies have used algorithms to identify a pattern related to somatisation disorder, for example Sigvardson and his collaborators (Sigvardson et al, 1984; Cloninger et al, 1984; Bohman et al, 1984; Deighton & Nicol, 1985). Studies of concordance between different ways of diagnosing somatisation disorder in the community have also been conducted (Schwartz et al, 1987) and alternative criteria such as the Feighner criteria (Feighner et al, 1972) or the Research Diagnostic Criteria (Spitzer et al, 1978)
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have been compared with DSM–III criteria. These paved the way for the somewhat shorter DSM–IV version. Guze (1983) summarised the usefulness of the Briquet category, demonstrating, a high degree of diagnostic use over the years, the strong familial increase in the risk of Briquet’s syndrome, and the increased risk of antisocial personality among first-degree female relatives. On the other hand, the study by Deighton & Nicol found that the prevalence of Briquet syndrome, as determined by a screening instrument, was 2.04 per 1000, much less than that found in previous studies. Further, many other patients showed both the high consultation rates and the other correlates of Briquet syndrome, bringing the usefulness of a discrete syndrome into doubt in their opinion. Still lower rates have been found for somatisation disorder in community surveys, for example 0.03% (Escobar et al, 1987) and 0.7% (Canino et al, 1987). However, more studies using these criteria seem to have found interesting if not important information. For example, the adoption study of somatoform disorders by Cloninger et al (1984) demonstrated an increased rate of somatic complaints among young women adoptees. They had repeated brief sick leave for multiple somatic complaints in a pattern that was consistently associated with psychiatric disability, as well as four times the frequency of sick leave from occupational disability compared with others. Most of the sick leaves were not medically certified and the authors gave reasons for thinking that these complaints were primarily psychiatric in origin. The cases were split into two discrete patterns, one with a high frequency of a limited number of complaints and the other of less frequent disability but a greater diversity of complaints. The first type combined features of somatisation disorder, hypochondriasis, agoraphobia, and agitated depression. The second type appeared to be associated more with generalised anxiety, but no previously described and validated diagnostic category fully described the symptoms and course of a typical patient in this group. Bohman et al (1984) then reported that the genetic and environmental antecedents of the two groups differed from those of the other subjects in their study. The risk of the second type, “Diversiform somatization”, was increased in the adoptedaway daughters of men treated for what they characterised as “male limited” alcoholism, while the biological fathers of cases with high-frequency somatisation (the first type) often had a history of recurrent convictions for violent crime since adolescence, but no treatment for alcoholism. These differential patterns of
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inheritance, which tended to replicate earlier findings of an association between criminality and Briquet syndrome, reinforced the view that patterns of somatic complaining have a hereditary component. Liskow et al (1986) offered evidence that Briquet syndrome presented a heterogeneous disorder. Among 78 female psychiatric out-patients with the diagnosis, 68 (87.2%) had a lifetime prevalence of major depressive disorder, 35 (44.9%) had experienced panic disorder, 21 (26.9%) had had a diagnosis of schizophrenia, and 31 (39.7%) a diagnosis of mania. Twenty-one (26.9%) also had a diagnosis of obsessive–compulsive disorder, and 30 (38.5%) a diagnosis of phobic disorder. Lesser numbers had drug dependence (18), alcohol dependence (13), antisocial personality (13), anorexia nervosa (5), and homosexuality, organic mental disorder or mental retardation. While Briquet syndrome may or may not be heterogeneous, these data show that it clearly has other concomitants and might well be the end result of several different causes. From the findings of the National Institute of Mental Health Epidemiologic Catchment Area study (ECA study), a populationbased survey of psychiatric morbidity among more than 18 000 residents of five US communities, Simon & Von Korff (1991) also noted that somatisation symptoms showed strong associations with anxiety and depression, an intermediate association with symptoms of psychotic disorders, and the weakest associations with symptoms of substance abuse and antisocial personality. This reflects consideration of all somatisation symptoms, and one might anticipate that whereas a few somatisation symptoms in any given person will be likely to show the links with anxiety and depression which have been noted, it is the sustained concentration of somatisation symptoms which have the links with personality disorder. One of the most interesting findings is a relationship between a tendency to somatisation and genetic liabilities within the family to antisocial personality. The St Louis group has shown this phenomenon repeatedly, and Lilienfeld (1992) considers a number of sex-related factors which might be responsible for differences in aggression and dependency, leading to the patterns that have been observed. Such factors might be either hormonal or social in origin. Further work on the family structure and social patterns in patients with Briquet syndrome will be mentioned later. Although Briquet syndrome probably does not represent a specific defined entity, but rather one end of a continuum, the work of the St Louis group has left little doubt that pain can function as a
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psychological symptom which is often associated with the disease syndrome of conversion symptoms and other somatic complaints. In clinical practice also there is no doubt about the durability of pain as a psychological symptom in this relatively limited group. Briquet himself did not really describe this syndrome (Mai & Merskey, 1980a,b). His own patients had a variable course, often showing hysterical personality traits and a relationship to environmental events and to the emotional state. He himself criticised the use of the word ‘hysteria’ since the etymology was both clinically and pathologically unsound, but he concluded that he would have to continue using it because it had been in use since Hippocrates and because everyone understood its meaning. He hoped – forlornly as it has turned out – that in the course of time the word would lose its pejorative connotations. Interest in the diagnosis also differs on both sides of the Atlantic. Although the work of Guze and his colleagues was published in the British Journal of Psychiatry at a time when American psychiatrists were less receptive to his efforts to produce systematic studies of clinical categories than is now the case, Briquet syndrome has not proved to be as popular in Britain as it has become in North America. Stern et al (1993a) demonstrated that the majority of a large sample of senior British psychiatrists endorsed the view that the US health system encourages patients with multiple somatic complaints to consult specialists and leads to over-investigation, and agreed that that reflected the interest shown in the disorder by particular psychiatrists in the USA. The British psychiatrists preferred alternative diagnoses, such as hypochondriasis or personality disorder, affective disorder and other neurosis for patients whom they thought fulfilled ICD–10 criteria for somatisation disorder (World Health Organization, 1992a). Stern et al conclude that the marked discrepancy in diagnostic practices did not reflect a genuine difference in prevalence. Chertok (1975) raised another issue which has provided objections to the use of the term Briquet syndrome. He pointed out that Briquet himself made no distinction between a monosymptomatic and a polysymptomatic form of hysteria, and that conversion symptoms were included in Briquet syndrome as well as separated from them. While unwilling to relinquish the term hysteria, the author finds Briquet syndrome or somatisation disorder useful as a description of one of the major forms of hysterical illness. This is so despite the fact that it seems to represent one end of a continuum of hysterical disorders rather than an isolated group of cases and contains other diagnoses. In addition to this question of terminology, the work of the St Louis
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school must be considered in relation to the distinctions and similarities between hysteria and hypochondriasis, which will be discussed in Chapter 14.
Contributions to somatic complaints Somatisation disorder can also be explored from another direction. We need to think of the different ways in which somatic complaints can be produced in addition to conversion or dissociative disorders or hypochondriasis. One of the factors which promote somatic complaints may be preoccupation with being in good health. Classically this is described in part by the term valetudinarianism, which implies anxiety over health. Such concerns are also part of the topic of hypochondriasis (Chapter 14) and are related to the forceful presentation of symptoms which is encountered in patients with the problem of somatisation disorder. Simple preoccupation with bodily functions may also be incriminated without there being a strong emphasis on anxiety (or obsessionality), and the contribution of such concerns has to be considered. Stern et al (1993b) found that more than 72% of 25 female patients with somatisation in a general hospital clinic had a personality disorder, compared with 36% of control female patients in the same clinic. Passive–dependent, histrionic and sensitive– aggressive personality disorders occurred significantly more often in the somatisation disorder patients. This parallels some of the findings in other settings with respect to conversion symptoms and hysteria (see Chapter 22). It may only mean that personality disorder promotes the referral of patients with somatic complaints more often than do other psychiatric diagnoses. This leads us to the question as to what else may be related to somatisation disorder, and also to the use or otherwise of the term somatisation.
Somatisation – a bad term? About 80% of healthy individuals experience somatic symptoms in any one week (Reidenberg & Lowenthal, 1968; Pennebaker et al, 1977). Thus bodily discomfort is a regular, normal experience. It is commonly accepted in general practice that psychological problems are frequently linked with physical complaints and
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may affect up to 30% of patients (Kessell, 1960; Shepherd et al, 1966). As little as 3% of symptoms experienced by patients may be reported to their doctors (Banks et al, 1975). An enormous margin exists, accordingly, for somatic symptoms to be presented to physicians if a need arises or to be ignored if they are not felt to be important. It is of obvious interest for us to know when physical symptoms reflect a psychological problem. The frequency with which this occurs is a matter for epidemiological investigation and the information obtainable about it should help to guide the provision of health care. Moreover, even more important in dealing with patients, it is plainly necessary to understand which aspect of the illness most requires treatment. It follows that there has been much interest in somatic symptoms which reflect psychological ones. In a sense that is the topic of the larger part of this book. The different ways in which this may happen are reviewed in many chapters. Here I wish to consider the implications of the term somatisation, which is presumed to describe the above situation. Kirmayer & Robbins (1991) point out that psychosomatic medicine has traditionally been concerned with investigating and treating the psychological components of disease, and psychodynamic theory attempted to study the role of specific psychological conflicts or personality dimensions in disease. They note that this strategy did not live up to its promise and had the unfortunate effect of encouraging clinicians to think of certain diseases as being especially ‘psychosomatic’ in nature. They point out that the recognition that there is no unique class of psychosomatic disorders – only particular clinical instances in which psychosocial factors play what they call an over-riding role in causing or aggravating a patient’s condition – led to the elimination of the category of psychophysiological disorders from DSM–III and the substitution of the label “psychological factors affecting physical condition”. Hence, somatisation was introduced as a term which would focus attention on the experience and expression of illness in which psychological factors were important. Lipowski (1968) originally defined somatisation as “the tendency to experience, conceptualize and/or communicate psychological states or contents as bodily sensations, functional changes or somatic metaphors”. He amended this to “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 them” (Lipowski, 1988).
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In a substantial review of the topic, Kellner (1990) has indicated that the term somatisation was first used by Stekel (1943, p. 580), who defined it as a bodily disorder arising as the expression of a deep-seated neurosis. He regarded this as identical with Freud’s concept of conversion. This is only of historical interest. Today, one has to take somatisation to mean having conditions that are described in DSM–III or DSM–III–R or DSM–IV under the category of somatoform disorders. This would include conversion disorders, somatisation disorder and hypochondriasis, but it is clearly not enough, since symptoms of anxiety and depression are very common with bodily complaints. Kellner points out that different authors do not agree wholly on the definition of somatisation. For example, Katon et al (1984a) described somatisation as “an idiom of distress in which patients with psycho-social and emotional problems articulate their distress primarily through symptomatology”. Kleinman & Kleinman (1985) defined it also as “the expression of personal and social distress in an idiom of bodily complaints with medical help seeking”. Ford (1983) defined it as the use of somatic symptoms for psychological purposes, and Bridges & Goldberg (1985) used operational criteria for somatisation based on consulting behaviour, the patient attributing the somatic manifestations to a physical problem but having a psychiatric illness which responds to psychiatric treatment. Kirmayer (1986), among others, has concluded that somatisation is neither a discrete clinical entity nor the result of a single pathological process, and that somatisation cuts across diagnostic categories. Kirmayer & Robbins (1991) made three operational definitions of somatisation: (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 in the absence of evidence of serious illness (c) exclusively clinical presentations among patients with current major depression or anxiety. In a sample of 685 patients attending two family medicine clinics, 26.3% met criteria for one or more forms of somatisation. The three forms of somatisation are associated with different sociodemographic and illness behaviour characteristics. However, a majority of the patients met criteria for only one type of somatisation, suggesting that distinct pathogenic processes may be involved with each of the three types.
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In primary care only a minority of presenting symptoms can be given an adequate organic explanation (Kroenke & Mangelsdorff, 1989) and, in addition, somatisation is said to be more, not less, likely in the presence of organic disease (Katon, 1993). Smith (1992) reviewed the epidemiology and treatment of depression when it coexists with somatoform disorders, somatisation or pain. He concluded that there is a high prevalence of depression in patients with somatisation disorder, while in patients with major depression there are substantial levels of hypochondriacal and somatising symptoms. Depression in the face of coexisting somatisation disorder can be successfully treated. Further, in chronic pain patients there is a high prevalence of depressive disorders and in patients with major depression pain is a frequent complaint. Pain also improves with the treatment of depression. Fabrega et al (1988) looked at somatoform disorder in a psychiatric setting and made systematic comparisons with depression and anxiety disorders. They concluded that patients with somatoform disorder resemble patients with depression, but harbour traits that reflect personality and interpersonal difficulties. Somatoform disorder itself is noted to be a rare condition, whereas, of course, somatic complaints with depression and anxiety are common. According to Fabrega et al the diagnosis of somatoform disorder appears to be much influenced by the cultural biases of patients and physicians, a point which Kirmayer (1984) made. Very large differences, however, can be cited to show that, even with formal evidence of depression, somatic complaints can rise greatly in different populations. Magni et al (1992) compared two groups of Hispanic patients in the United States, Puerto Ricans and a combined group of Mexican-Americans and CubanAmericans, with respect to abdominal pain. Chronic abdominal pain was observed in 4.6% to 5.8% of the Cuban-Americans but in 8.3% of Puerto Ricans. The data came from a formal epidemiological study undertaken at the United States National Center for Health Statistics, with careful representative sampling of the population. In either population those who complained of pain were found to be depressed more often than those who did not complain of pain. The result of the high rates for pain and high rates for depression in the Puerto Rican population was to demonstrate that 40.8% of the Puerto Rican patients with pain were depressed to an extent likely to require intervention, compared with 18.7% of the two other groups combined. Using more conservative figures based upon the Diagnostic Interview Schedule, 6.8% of Mexican- and Cuban-Americans with chronic pain and 12.6% of Puerto Ricans with chronic pain had depression.
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In clinical practice and in research reports the term somatisation is evidently used in a variety of ways, which may be summarised, perhaps not completely, as follows: (a) (b) (c) (d)
somatisation disorder conversion symptoms hypochondriasis heightened bodily awareness (alerting), resembling hypochondriasis but unlike the latter in 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 (e.g. hypochondriacal psychosis) (g) any of the above combined with organic disease. This variety of meanings almost rivals the number of meanings or subdivisions which currently have been offered for hysteria, although somatisation is a far younger term. In clinical practice the word is also used to imply that the person who has the symptom is ‘somatising’, or actively producing physical symptoms, perhaps by tension, even though the intention may be unconscious. In clinical practice it is also used somewhat indiscriminately, in my observation, without the effort to determine the correct psychiatric diagnosis. It seems to me that we would be better off without the term, while continuing to look at the topics which it has brought under one umbrella.
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14 Hypochondriasis
“I have sent for you doctor, to consult you about a distemper of which I am well assured I shall never be cured.” (B. de Mandeville, A Treatise of the Hypochondriack and Hysterick Diseases, 1730, p. 1)
The relationship between pain and hypochondriasis was touched upon in the last chapter. Many patients with pain were noted to be ‘polysymptomatic’. Many treat their symptoms in a way which may be called hypochondriacal. The case has been stated for regarding pain as a symptom which can sometimes reflect hysterical mechanisms. We need next to consider the relationship between hysteria and the notion of hypochondriasis. The word ‘hypochondriacal’ is used to refer to both symptoms and behaviour, often without a careful distinction being made and often in a fashion which is dismissive of the complaint or the individual who makes it. When careful distinctions are made there are plenty to be found, and Kenyon (1965) lists 18 different usages of the terms ‘hypochondria’ and ‘hypochondriasis’, as follows: (a) synonymous with mad or senseless (b) a mental disease due to a disorder of the digestive tract (c) a term of abuse, that is, either actually malingering or all complaints simply imaginary (d) a general sense of preoccupation with bodily or mental health or functions (e) a personality trait or attribute (f) a mechanism of defence (g) a neurotic manifestation, especially in lower social classes or in those of poor endowment (h) an anxiety substitute or affective equivalent 185
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(i) an actual neurosis (j) closely allied to or a manifestation of neurasthenia or depersonalisation (k) the same as hysteria, only in the male (l) transitional state between hysteria and psychosis (m) a nosological entity, primary or essential hypochondriasis (n) a symptom of almost any of the other commonly recognised psychiatric syndromes, especially depression (o) a prodromal stage of another illness, such as schizophrenia (p) a form of schizophrenia (q) a form of coenaesthesiopathy (r) a part of a symptomatic psychosis or exogenous reaction. Despite this, Bianchi (1971) observes that lack of definition has plagued the study of hypochondriasis in general and disease phobia in particular. This is also the case with regard to distinguishing hysteria and hypochondriasis, which is often said to be the male form of hysteria. However, some important distinctions can be made, and definitions increased in number with DSM–III and DSM–III–R (American Psychiatric Association, 1980, 1987). Barsky & Klerman (1983) conceptualised hypochondriasis in four ways: (a) as a psychiatric syndrome composed of ‘functional’ somatic symptoms, fear of disease, bodily preoccupation and the persistent pursuit of medical care (b) psychodynamically as a derivative of aggressive or oral drives or as a defence against guilt or self-esteem (c) as a perceptual amplification of bodily sensations and their cognitive misinterpretation (d) as socially learned illness behaviour, eliciting interpersonal rewards. Gillespie (1929, p. 66) foreshadowed the last of these categories when he remarked: “The common sense view of hypochondria is that, like most other abnormal mental reactions, not the direct expression of organic brain disease, it is a mode of reaction to difficulties, external or internal – an excuse or an avoidance. The peculiar intensity and fixity of the symptoms is attributed to an habitual self centredness on the one hand, and on the other to the insoluble difficulty of the external circumstances – insoluble at least by the patient in question, in view of his peculiar self-centredness.”
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Gillespie, of course, was defining as hypochondriasis one end of a spectrum of behaviour, the other end of which might be merely a modest amplification of bodily sensations and some anxiety, topics covered more comprehensively by Barsky & Klerman (1983), Barsky & Wyshak (1990), Barsky et al (1991, 1993) and Kellner (1986). In an admirably clear and thorough monograph, Kellner (1986) established the fact that functional somatic symptoms are extremely common. About 60–80% of the general population will experience at least one somatic symptom in any one week and in most, as we observed in the previous chapter, the cause is not established or is uncertain (Reidenberg & Lowenthal, 1968). Such functional somatic symptoms may be found with organic disease or associated with depression, anxiety, pain or hypochondriacal patterns of behaviour, which include worry about illness and fear of disease, panic attacks and schizophrenia. Broadly speaking, there is agreement that the salient features of hypochondriasis may be found with a number of diagnoses but that the particular phenomena which are most specific to the term are fear of disease (disease phobia), often accompanied by a conviction of its presence (disease conviction), a combination which was established with most clarity by Pilowsky (1967). In addition, an amplifying perceptual style is common or important among some, or indeed many, patients. Barsky et al (1994) have also demonstrated that hypochondriasis and panic disorder co-occur to some extent in a primary care population. They point out that the overlap is by no means complete and that these patients are phenomenologically and functionally differentiable and distinct and are viewed differently by their general practitioners. Before analysing the current understanding of the patterns of hypochondriasis in more detail, we should note some important features of the historical aspect. They are well reviewed (in French) by Henne (1955), who also discusses the main phenomena briefly. Kenyon (1965) provides a helpful survey, and Ladee (1966) contributes a useful and extensive historical and theoretical discussion as well as an analysis of 225 cases. Kellner (1986) presents the historical information very clearly and with extensive references. Sydenham (1697) wrote “of the disease called in women the hysterical, in men the hypochondriacal passion,” in which “when the mind is disturbed by some grievous accident, the animal spirits run into disorderly motions,” and physical changes or complaints ensued. Others, such as Highmore (1669) and
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Willis (1670), distinguished hysteria from hypochondriasis or hypochondria. Henne (1955) points out that the initial notion of hypochondria associated it with a physical disorder, especially of the gastrointestinal organs. It was identified with numerous other bodily complaints, while hysteria and the vapours (which originally denoted emanations from the uterus) seem to have been more identified with fits (e.g. Purcell, 1707). The gradual evolution of thought in the 17th and 18th centuries tended to change the notion both of hysteria and hypochondriasis from visceral maladies to disorders which resulted from a change in the brain. De Mandeville (1730) and Cheyne (1733) tended to put hysteria and hypochondriasis side by side, the latter author incorporating them as “the English malady”. A different association is emphasised in Burton’s Anatomy of Melancholy (1651), where hypochondriacal melancholy appears as a subcategory. Similarly, when James Boswell (1777) in The London Magazine wrote of himself under the title of “the Hypochondriack” he meant someone prone to melancholy or depression. However, many writers, especially Whytt (1761), subsequently recognised a difference between depression and concern with multiple bodily symptoms. Ladee (1966) emphasises the trouble which Whytt took to make a sharp distinction between melancholia on the one hand and hypochondriasis on the other. There is certainly a major link between depression and concern with somatic complaints. For example, Kenyon (1964) obtained substantial evidence of a relationship between depressed mood or anxiety and hypochondriacal symptoms, whilst Kreitman et al (1965) also described this combination. It has long been accepted that the two may go together, and other instances were noted in Chapter 13. If such complaints are related to affective illness, as in agitated depression, which used to be called involutional melancholia, the combination may sometimes recover with treatment of the depression. Patients with persistent somatic complaints in the absence of severe depression are more refractory. In the 19th century specific distinctions were made between hysteria and hypochondriasis by Dubois D’Amiens (1833) and Landouzy (1846), who firmly adopted the table of Dubois which is set out in Appendix A. This table gives an interesting and impressive indication of the detail with which the syndromes of hysteria and hypochondriasis were then studied. Much of the later 19th-century and the 20th-century discussion of hypochondria is concerned with delusional illness. It was increasingly recognised that hypochondriacal disorders might be
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a part of a schizophrenic illness or a sequel of dementia. However, others, especially Gillespie (1929), described hypochondriasis as a separate syndrome, to be differentiated from hysteria and from affective illness. Some comprehensive studies (Kenyon, 1964; Ladee, 1966) support the view that no distinct syndrome of hypochondriasis exists and that the cases found can be broken down into other syndromes with no clear-cut primary syndrome emerging. Kenyon (1976) argued very strongly for this conclusion, suggesting that the words hypochondria and hypochondriasis should be dropped and only the term hypochondriacal retained. Kellner (1986) held that the findings surveyed in his volume support the view that hypochondriasis can coexist with any psychiatric disorder, most commonly with an affective disorder, but can also occur in people who have no other psychiatric illness. He saw hypochondriacal neurosis as occupying the opposite end of a continuum to mild functional somatic symptoms. The latter could grow into a hypochondriacal reaction, which if severe enough would amount to a hypochondriacal neurosis satisfying the criteria of DSM–III. Among 20 patients with marked hypochondriacal features, seen in a psychiatric hospital, Baker & Merskey (1983) described one who satisfied criteria for the diagnosis of primary hypochondriasis in accordance with DSM–III, and nine more who would have been classed as having hypochondriasis or somatisation disorder as a secondary diagnosis provided DSMIII had allowed the identification of hypochondriasis in the presence of a different primary diagnosis. DSM–III–R allowed this secondary diagnosis. DSM–IV (American Psychiatric Association, 1994) permits it provided that the patient’s symptoms are not better accounted for by a diagnosis of generalised anxiety disorder, obsessive–compulsive disorder, panic disorder, a major depressive episode, separation anxiety, or another somatoform disorder. Kenyon’s argument was reasonable in the light of the available systematic evidence of the time, but in view of the findings of Kellner and of Baker & Merskey it is probably wrong. The typical case of pure hypochondriasis will lack the criteria to justify anxiety or depression as the main diagnosis. Warwick & Salkovskis (1990) argue strongly that hypochondriasis is not only a secondary disorder. Kenyon (1964) based his argument on the similarity which he demonstrated between primary cases and secondary ones, and upon the frequency of depression in the former group, suggesting that all his apparently primary cases examined retrospectively were secondary to
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depression. Warwick & Salkovskis emphasised the importance of time relationships in such an argument. Just as obsessive–compulsive disorder may be a primary diagnosis when it appears in advance of depressive change, or a secondary diagnosis when it follows from a depressive illness, some cases of hypochondriasis can be primary, appearing before any other phenomena, while in other individuals a different illness may appear jointly with hypochondriacal manifestations. Warwick & Salkovskis further point out that the patients seen in hospital usually come from a selected series and such a series will miss cases in primary care, where it is likely that examples of primary hypochondriasis can be found. Another reason for dissenting from Kenyon’s argument is that it resembles too closely the one which Slater (1965) advanced about hysteria. The latter diagnosis is still alive and its validity or the validity of its components is supported in Chapter 25. Perhaps the same arguments apply to hypochondriasis. Whatever the correct final view may be, certain patterns of behaviour occur which can be recognised and distinguished either adjectivally as hypochondriacal or substantively as hypochondriasis. From this point on the reader may, according to taste, substitute ‘hypochondriacal states’ for the words hypochondria or hypochondriasis, but the actual phenomena and their explanation should concern us more than this problem in classification.
Patterns of hypochondriasis The mildest form of hypochondriacal complaint is to be concerned over such somatic symptoms as palpitations or headache, which are due to anxiety, and to respond with satisfaction to a medical examination which establishes their cause as harmless. Some patients with anxiety develop these symptoms more readily, and more often than others, and have a recurring need for re-examination and reassurance. An element of dependency is evident in their behaviour. More often those who have such symptoms do not respond to the reassurance of negative examinations and investigations, and show both a fear that they have illness and a conviction that it is present. They may be frequent attenders in the physician’s consulting room but do not show overt dependency so much as dissatisfaction. The doctor is not fulfilling their requirements, and it is among patients of this group that the complete pattern of extreme hypochondriasis appears. Perhaps the best distinctions with respect to severe cases were drawn by Henne (1955), who first of all distinguished between
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simple hypochondria and delusional hypochondria. In his view the latter reflected an association with melancholia, or with delusional illnesses, or with states of dementia. The delusional states could very well be evidence of a schizophrenic process. He considered that primary hypochondria showed four major types. The first he called arganism after the famous character of Molière, the sufferer being sombre and taciturn, ruminating on his complaints, associating with few people except close friends and doctors, giving a meticulous and stereotyped description of his symptoms with, to him, logical explanations from his own reading in medicine, following every detail of treatment to a ridiculous extent, and tyrannising his family with his egotism. The second type, the hysteric, shows a marked need to complain and has a more ostentatious hypochondria which is more labile, requires the interest of other people, and is more susceptible to removal by suggestion. The third type, the psychasthenic, suffers from hypochondria in the form of an obsessional fear of illness. Beset with the idea that they are going to suffer from or indeed are already suffering from an incurable illness, they reject with vigour the idea that obsesses them but are in fact unable to give it up. The fourth type is a transitional intermittent delusional hypochondria which has links with arganism and with psychotic states as well. All these descriptions have the ring of clinical truth, even if we might consider arranging the categories differently. Additional important features which emerge here after separating the delusional and the depressive hypochondriasis from the others are as follows: preoccupation with multiple complaints; meticulous and pedantic characteristics; self-centredness in regard to the illness; fear of disease; and, finally, a conviction which does not respond to reassurance that disease is indeed not present. These matters have been elegantly dissected by Pilowsky (1967) using questionnaire and factor-analytic techniques. Pilowsky has established three major elements in the pattern of hypochondriasis. The first is a preoccupation with bodily symptoms, the second is a fear of such symptoms, and the third is a conviction that disease is present despite the lack of objective evidence and, usually, despite the completion of all appropriate examinations and investigations. The satisfaction of these criteria can serve as the defining process for the presence of hypochondriasis. The writer thinks it reasonable to conclude that patients who show these patterns and do not have other conditions represent a defined syndrome. Warwick & Salkovskis (1990) offer another slant on concepts of hypochondriasis. They suggest that individuals who have a
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previous experience or perception of illness in themselves or the family, or medical mismanagement, or who have been brought up with a pattern of consulting physicians readily in case they had something serious, will form dysfunctional assumptions about bodily symptoms. They will tend to feel that bodily symptoms are always an indication of something wrong and it should be possible to find an explanation for them. If such individuals experience a critical incident, such as the death of a friend or acquaintance or relative from cancer, they are at risk of interpreting some minor symptoms of their own in accordance with their long established pattern of expectation. This leads them to negative automatic thought and to health anxiety or hypochondriasis. These ideas are well known and accepted by many and appear to fit quite a few clinical cases. Nevertheless, while such arguments describe the sort of personality background and life patterns which may promote hypochondriacal complaints, they do not account for their persistence or strength in most patients. One would expect the power that drives hypochondriacal patients to have more to do with significant illnesses that may arise independently, such as the depressive phase of a bipolar affective illness or a major affective disorder arising because of burdensome environmental stress. The model which Warwick & Salkovskis offer is a cognitive model of hypochondriasis. They applied this model with apparent success to two patients (Salkovskis & Warwick, 1986). It is supported somewhat by other notions of the amplification of symptoms discussed both by Kellner (1986) and by Pennebaker (1982a). The logical extension of their argument was to treat hypochondriacal patients with cognitive behavioural methods, not using reassurance after the first full examination had been undertaken but rather encouraging activities which distracted them from health preoccupation, and denying repeated reassurance. This approach worked well, at least in the short term, in the two patients whom they reported. More evidence would be needed before this approach could be taken to have compelling evidence in its favour. Although the topic does not appear to have been formally studied, there are some items in Pilowsky’s basic criteria which might separate these patients from those whom Guze (Chapter 13) and others call hysterical. First, patients with fear of disease do not normally develop the classic motor symptoms of conversion hysteria which are included in Briquet syndrome. Second, there may be some satisfaction on the part of the hysterical patient with the presence of somatic symptoms, while the hypochondriacal patient manifests more concern. This is not to say that all hysterical patients are unconcerned nor that all
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hypochondriacal patients are without evidence of satisfaction in their symptoms, but rather that a trend exists which provides some distinction. The disease phobia which hypochondriacal patients manifest is often associated with persistent obsessional concern over the trivia of bodily function and defines their particular group. It can be seen from the views cited above that Henne reached a very similar conclusion about the difference between hypochondria and hysteria. Schmidt (1994) also considered this topic and agrees that it is at least possible that hypochondriacal patients fear a serious disease while ‘somatisation patients’ fear the consequences of the state of their health, but such a conclusion would require corroborative evidence which has not yet been sought. Third, as we shall see, hysterical symptoms are perhaps more susceptible to a current psychodynamic formulation than hypochondriacal symptoms. Fourth, not all hysterical symptoms (e.g. amnesia) are somatic.
Diagnostic groupings It may be helpful at this point to set out the main distinctions which the writer recognises and then to define hypochondriasis. The initial subject matter, as it were, is all those complaints without physical basis. Monosymptomatic cases are for the moment left out of consideration. Among patients with excessive concern over multiple symptoms, the following groups can be recognised. (a) In delusional hypochondriasis, the symptoms are part of a schizophrenic illness or of a definite affective disorder. (b) In symptomatic hypochondriasis, the patient’s complaints appear to result from the development of a dementia; this group may or may not show delusional features. (c) Hysterical hypochondriasis includes some cases of somatisation disorder, and is marked by the occurrence of detectable motor conversion symptoms and some degree of satisfaction on the part of the patient, together with a relative lack of disease phobia, and sometimes the classic labile, histrionic features of hysterical personality (cf. Chapter 22); hysterical hypochondriacal complaints may also be subjective, non-somatic ones (e.g. amnesia). (d) Hypochondriacal reaction, according to Kellner (1986), presents functional somatic symptoms about which the patient is unduly worried but which do not yet amount to a full-scale diagnosis of hypochondriacal neurosis. Mayou (1976) furnished reasons for the view, which is probably correct, that minor elements of hypochondriacal characteristics may appear both in
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Varied causes and symptoms
the normal population and in other psychiatric patients. This is the group to which the theories of Salkovskis & Warwick (1986) and Warwick & Salkovskis (1990) will most apply. Pennebaker (1982a) has demonstrated and emphasised the important influence of the perceptual context, attention to symptoms, the selective search for information, negative affectivity, and the dispositional and genetic bases of symptom reporting. Pennebaker & Watson (1991) comment that “it is easy to see how extreme variants [of the processes studied] could lead to the greatly magnified symptom reporting” that characterises somatoform disorder. (e)Patients with hypochondriacal neurosis without another primary condition and without conversion symptoms or non-somatic complaints show excessive concern with bodily function, a failure to respond to sympathetic management and reassurance by relinquishing their complaint, a marked fear of physical disease, and a continuing or markedly recurring belief that they have got a disease. They show dependence on medical personnel and often are dissatisfied with them. A pattern of cultivated meticulous valetudinarianism may be prominent, together with detailed ordering of the smallest items of daily life in terms of health and illness, cupboards overflowing with laxatives and home remedies, and punctilious compliance with dietary fads, and so on. Their mood, as in arganism, may be sombre and pessimistic. Their attitudes are primarily egotistical but may extend to concern for others, for example Mr Woodhouse, in Emma by Jane Austen, not only cosseted himself and anxiously considered every item in his own diet, but also extended the same concern to others, as the following bears witness: “Mrs. Bates, let me propose your venturing on one of these eggs. An egg boiled very soft is not unwholesome. Serle understands boiling an egg better than anybody... You need not be afraid – they are very small, you see – one of our small eggs will not hurt you... Mrs. Goddard, what say you to half a glass of wine? A small half-glass – put into a tumbler of water? I do not think it could disagree with you.” (Austen, 1816, Vol 1, p. 24)
Besides this Mr Woodhouse made a friend of his apothecary, Mr Perry, derived great comfort from his visits, believed he could not stand the noise and commotion of more than eight people at dinner, did not think his daughter should go to church on Christmas Day because the ground was covered with snow, and held that “the dews of a summer evening are not what I would expose anyone to”. Treating everyone with consideration he was loved because he was a “kind-hearted, polite, old man”.
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Of course, attitudes to hypochondriasis are not always so tolerant. Indeed, attitudes to illness can sometimes be rather hostile, as the following extract indicates. “Lady Bracknell: ... I think it is high time that Mr. Bunbury made up his mind whether he was going to live or to die. This shilly-shallying with the question is absurd. Nor do I in any way approve of the modern sympathy with invalids. I consider it morbid. Illness of any kind is hardly a thing to be encouraged in others. Health is the primary duty of life. I am always telling that to your poor uncle, but he never seems to take much notice ... as far as any improvement in his ailment goes. I should be much obliged if you would ask Mr. Bunbury, from me, to be kind enough not to have a relapse on Saturday, for I rely on you to arrange my music for me. It is my last reception ....” (Wilde, 1895, The Importance of Being Earnest, Act 1, pp. 39–40)
In those for whom the label of pure hypochondriasis is appropriate, these phenomena are dominant in daily life and in the clinical presentation. A monosymptomatic complaint of an illusory disease or deformity may be a reflection especially of early schizophrenia. It may also, rarely, reflect a depressive or dementing illness – perhaps in association with some minor or undeclared local physical disturbance which it magnifies. In the absence of psychotic or cerebral organic features, monosymptomatic hypochondriasis has to be regarded as more akin to disease phobia than to hysterical conversion patterns. There is a profound conviction that something is seriously wrong, whether it is the amount of hair on the upper lip or a terrible pain without any organic basis, and yet the patient gains no satisfaction from the symptom. Unlike most isolated conversion symptoms, it is accompanied by insistent concern and a fear of the condition. While it may not be associated with a general valetudinarianism or with special regimens of daily life it seems closer, in its significance to the patient, to the symptoms of the disease phobic than to the classic conversion symptom or to somatisation disorder. Another unusual manifestation is that the patient may believe that the shape of some part of the body is wrong, rather than that there is a disease process. However, it is important to recognise monosymptomatic delusional hypochondriasis because it is thought to have a specific treatment which can be quite
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Varied causes and symptoms
effective, namely the use of pimozide (Munro, 1978; Munro & Chmara, 1982) or alternatively a serotonin reuptake inhibitor (Phillips et al, 1993). To summarise, hypochondriasis can now be defined as behaviour marked by persistent fear of disease and an erroneous conviction that a disease or deformity is present. There are usually symptoms of multiple somatic complaints but occasionally there is only one strongly held symptom. Minor forms of hypochondriacal behaviour may be typical in some individuals. Major forms reflect other conditions, such as schizophrenia, affective illness or dementia, or perhaps exist as a rare and extreme behavioural pattern. Monosymptomatic delusional hypochondriasis represents one particular and possibly specific type of psychotic hypochondriasis associated with major psychiatric illness. Hysterical hypochondriasis or somatisation disorder is distinguished from pure hypochondriasis particularly by classic conversion symptoms and the more satisfied attitude which the patient has with his or her complaints. It has been found (Chapter 13) that this category frequently overlaps with other diagnoses. Pure hypochondriasis – hypochondriacal neurosis – occurs rarely but is recognisable. Minor forms of hypochondriacal behaviour also overlap with anxiety and probably exist on a continuum with abnormality. The minor forms can readily be conceptualised as related to anxiety about some specific event which suggests illness and which is then augmented into hypochondriacal behaviour. We lack information on the extent to which such illnesses occur sui generis or are secondary to anxiety or depression.
Aetiology of disease phobia Kellner (1986) reviews the development of hypochondriasis, and concludes with respect to twin studies that there is suggestive but insufficient evidence to prove that there are genetic factors in hypochondriasis. However, he notes the well supported view that such factors exist in functional somatic symptoms (Bohman et al, 1984; Cloninger et al, 1984; Sigvardson et al, 1984) as noted in connection with Briquet syndrome in the previous chapter, and argues that there are genetic components in some forms of hypochondriasis. Physical disease in childhood is also thought to act as a predisposing factor for functional somatic symptoms and for hypochondriacal tendencies, and some aspects of the family constellation may encourage this as well. A culture or subculture can also apparently pattern attitudes towards, beliefs about, and the display of distress.
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Barsky et al (1991) found that whereas it used to be thought that there was a strong relationship between hypochondriasis and age this was not the case when a group of consecutive patients at a general medical clinic were studied systematically. They note that hypochondriasis is found to some degree in all patients and appears to be unrelated to age. Kramer-Ginsberg et al (1989) found that it was common in the depressed elderly. Hypochondriasis was associated with anxiety but not with depressed mood, suicidal tendencies or short-term outcome. The persistence of some hypochondriasis after relief of depression suggested that the patients had manifested a combination of state and trait phenomena. Both hysteria and hypochondriasis have in common the frequent occurrence of somatic symptoms without physical basis, a manipulative attitude in the consultation, certain attitudes of dependency, and some aspects of childhood experience. There may also be some similar aetiological factors in both conditions. The aetiology of hysteria has not yet been fully discussed, but in anticipation it may be mentioned that hysterical symptoms can arise in the functional psychoses, and, as we have already stressed, as a consequence of physical illness. Similar associations plainly exist for a number of hypochondriacal illnesses and were well shown by Ladee (1966). The psychogenesis of hypochondria also has links with hysteria. From his systematic study, Bianchi (1971) commented that in comparison with control psychiatric patients, the disease phobic patients showed more self-pity and were weak and sickly in childhood: “and in adult life, pallid inhibitors of anger, low in self-esteem. Even prior to the phobia they evidenced a prophylactic attitude and preoccupation with vitamins and patent medicines ... carefulness is seen also in the trend towards less accidentproneness and fewer attempts of suicide. They are more often the youngest sibling. From overprotection and excessive babying and from the kindling evidence of much disease and death among their relatives, they are wellschooled in the lesson of a personal vulnerability. With anxiety and bodily turbulence added to the ferment, background disquiet becomes active disease-phobia.”
Ladee (1966) observed: “Almost without exception, it is noted of all of them that they are highly unsure of themselves though with great – sometimes open, but usually carefully hidden – assertiveness, and that they
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Varied causes and symptoms live in a striking dependence-relation to a certain figure, one of the parents or a representative of the parent.”
Among his male patients he particularly emphasised slavish submission to the mother or fear and admiration of the father, and a tendency to be the youngest child or the only son, or both. Many of these features may well be found in patients with conversion symptoms or with Briquet syndrome, and in people who are unaffected, and it is evident that these groups present overlapping problems in aetiology, in management, and in their relationship to the physician. Maternal overprotection appears to be the most notable background factor predisposing patients to hypochondriacal behaviour. Levy (1932) seems to have been the first to state this clearly, but others who have agreed with him include Katzenelbogen (1942), Ladee (1966) and Bianchi (1971). Baker & Merskey (1982) undertook a controlled investigation of the hypothesis. Twenty hypochondriacal patients in a psychiatric hospital were matched with a control group from the same wards or the out-patient department and were examined using the Parental Bonding Instrument (PBI) of Parker et al (1979). This measures the retrospective views of patients about their childhood. Maternal overprotection was reported much more frequently in the hypochondriacal group than in the control group (P < 0.005), giving support to the maternal overprotection hypothesis. Hypochondriasis occurs quite often in men and women who were formerly athletic. It then presents the obverse side of pride and narcissistic gratification in the body. This is less common in hysteria, although narcissistic and exhibitionist features are often characteristic of hysterical patients. Patients who fall ill or become injured and develop chronic pain or other disability, and who have been athletic during their lives, usually tolerate the restrictions from which they have come to suffer rather less well than those who were never particularly athletic or physically active previously. It may be supposed that the unconscious mechanism of symptom production in hypochondriasis is analogous to that in somatisation disorder but a difference arises, either on the basis of premorbid personality traits, or as a result of the failure of the hypochondriacal patient to separate affect from bodily symptoms when the latter are produced. In other words, hysterical patients are more successful at dissociating affect from symptom. Further detailed comparison of the childhood experience of patients with disease phobic hypochondria versus those with Briquet’s syndrome might give some indication as to why this happens.
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The psychopathology of hypochondriasis was not discussed much by Freud, who tended to regard it as one of the “actual neuroses” (Freud, 1912), that is, one like neurasthenia and anxiety neurosis, which stemmed from a change of a physical disturbance into anxiety or other symptoms. Many writers recognise the importance of narcissism and Henne (1955) also mentions bodily aggression turning against the self or the masochistic conversion of an instinctive aggression arising from repressed unconscious guilt. Perhaps psychoanalysts have less interest in hypochondriasis than in some other topics because they have regarded it (no doubt correctly) as a poor indication for psychoanalytic psychotherapy. Kellner (1986, pp. 10–11) gives a detailed summary of the sources available in both the psychoanalytic literature and the general psychiatric literature where the psychopathology is discussed.
Prognosis The prognosis of hypochondriacal illnesses often depends upon the underlying conditions. With depression, schizophrenia, organic brain syndromes and so on it is likely to be determined to a considerable extent by the prognosis of the underlying illness. Kellner’s hypochondriacal reaction is relatively mild and has a good prognosis. Hypochondriacal neurosis or fixed hypochondriacal ideas used to be thought of as having a poor prognosis. Kellner states that three syndromes can be distinguished which differ in prognosis, although they are not clearly differentiated from each other: the hypochondriacal reaction, hypochondriacal neurosis, and developmental hypochondriasis. These appear to be somewhat similar in their onset, course and prognosis to adjustment reactions, neuroses and personality disorders, respectively. Hypochondriacal neuroses in patients attending specialist clinics have a somewhat worse prognosis than other neuroses. The proportion showing improvement, or recovery, varies across studies and this is probably attributable to a number of factors, including differences between the patients studied, methods of evaluation employed, and types of treatment, although controlled studies of treatment do not appear to be available. Contrary to widely held beliefs, a substantial proportion of patients treated for hypochondriacal neurosis completely recover or improve to the extent that they no longer believe that they have a physical disease, and their social and occupational performance improves. In some of the follow-up studies reviewed by Kellner, the proportion of these patients approached or exceeded 50%.
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15 The diversity of hysterical complaints
The last three chapters, like the earlier ones, have shown that a wide range of bodily symptoms have been classed, reasonably enough, as hysterical. Certain personality traits have also been noted to have a bearing on the notion of hysteria. It is still too early in this account to discuss the notion of hysterical personality, but it is time to review certain phenomena which may or may not be hysterical and to discuss the interactions of patients and physicians. This chapter discusses a number of symptoms and signs, and their understanding. As Watson & Buranen (1979) recognised, the symptoms written about most often are not the same as those that are found most often. This is probably because the classic symptoms, such as fits, paralyses, blindness and deafness, were once the most frequent and prominent but also continue to provide the clearest examples of what is meant by a hysterical or doxogenic symptom. The discussion here deals first with symptoms which are important theoretically and which help towards the clearest understanding of the concepts of conversion or dissociation. The most common symptoms are considered both here and in earlier chapters dealing with pain or hypochondriasis, and in Chapter 17, dealing with fatigue. These very common symptoms provide the largest problems in differential diagnosis. It is also convenient to include here some notes on the prognosis of individual hysterical symptoms. Chapters 16–21 describe some of the other major hysterical phenomena, and then the notions of hysterical personality and psychoses are reviewed in Part IV, with a further look at psychodynamic hypotheses. 200
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Motor symptoms Hysterical symptoms may be motor, sensory, cognitive or affective. The existing reports offer different frequencies for the occurrence of motor and other symptoms. Table 15.1 sets out the percentages of selected symptoms from three different sources. Carter (1949) was treating English civilians at a time of stress (wartime bombardment); Hafeiz (1980) reported from the Sudan; and Ljungberg (1957) from the university centre and psychiatric hospital in Stockholm. As discussed in Chapter 11, the figures vary from country to country and according to some social factors. Today, in developed countries, motor symptoms and seizures are the most easily diagnosable hysterical symptoms, and they present more often to neurologists than to other specialists. Diagnostic habit may well be responsible for some of the differences. It is not uncommon for patients with paralyses, or weakness of the limbs, also to have astasia abasia (a disorder of gait defined below), and those with fits may have astasia abasia as well. It is possible that a number of Carter’s patients were classified initially under other headings than astasia which may also have been present. There might be dispute today about whether vomiting is more than a very rare hysterical symptom. Likewise, some doctors would classify dyspnoea under anxiety. One of the commonest motor presentations is hysterical aphonia, loss of speech. Head (1922) describes how patients may become completely mute while writing voluble accounts of their condition. The patient who cannot whisper can cough loudly because, as Head points out, “from a psychological point of view, the resonant sound of a cough has nothing to do with articulated speech”. In the larynx, the vocal cords remain apart on phonation, although with a cough they close normally. Hysterical aphonia provides a good example of what Head calls “positive signs”. Head emphasised that in order to diagnose hysteria it was necessary to demonstrate two phenomena. First, there should be an absence of relevant organic disease, or proportionate organic disease. Second, there should be proof of these positive signs. A third condition is necessary for the psychiatrist; the demonstration of a psychological aetiology, often confirmed by the patient, or psychiatric illness in sufficient proportion to the symptom. Flaccid paralysis may affect one or more limbs, or one side of the face. Spasm is theoretically an alternative form of hysteria, for example both arm and leg being contracted on the same side of the body, the hand closed tightly, the knee flexed, perhaps the
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Carter (1949) Ljungberg (1957) Hafeiz (1980)
n
Paralysis
Tremor
Astasia abasia
Fits
Aphonia
Vomiting
Dyspnoea
Blindness
Amnesia
100 381 61
23 10 10
10 10 3.3
– 47 –
6 20 10
29 1.3 20
6 – 16
– – 20
3 0.8 3.3
23 – 3.3
After Hafeiz (1980). Not all symptoms are included and therefore the rows do not add up to 100%.
Varied causes and symptoms
T ABLE 15.1. Percentages of selected symptoms
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legs and the foot drawn up. Paralysis with contractures appears to be one of the most extreme possible examples of the acceptance of disability as a result of hysterical illness. Spasmodic contractile patterns of hysteria are much less common in current practice than they were in the last century. I have not seen a convincing case or case report. There is reason to think that a number of these complaints are not wholly psychological in aetiology. Sometimes, as Head observed, spasm of the muscle at the knee or other joint actually resists the movement of the limb in the direction in which the contraction is supposed to be occurring. Traditionally, these phenomena are accepted as evidence of hysteria, and yet sometimes simultaneous contraction of opposing muscles can have a pathophysiological basis, such as pain or noxious irritation in a relevant part of the body, including a joint. Paralysis of the tongue is another situation where the positive signs of hysteria may be observed. It is usual to consider that finding proof of hysteria by clinical examination essentially consists in searching for discrepancies between the patient’s knowledge of the symptom and the physician’s knowledge of the physical facts. Thus when a patient walks, the manner in which he moves, takes off his clothes or dresses again, and gets on to an examining table, may indicate a global affection which is not compatible with specific nerve lesions or even a hemiplegia. Hysterical paresis is marked by simultaneous contraction of agonistic and antagonistic muscles. This provides a basis for one of the favourite signs, which is to ask a patient to press a heel down on the bed while lying supine. When the patient finds that he or she cannot do it, the hand is placed under that heel and the patient is asked to lift the opposing limb. The synergistic response of the ‘paralysed’ leg produces pressing down of the heel while the ‘good’ leg is lifted. ‘Give-way weakness’ is often used as a sign of hysterical paralysis. The term implies a sudden change in resistance during the direct testing of muscle power. Although it is often taken to be diagnostic of a hysterical condition, in fact it often occurs in individuals with pain who overtly do not wish to move their limbs as the examining physician requires, because it will hurt them too much. In the absence of pain it is perhaps more likely to be evidence of a hysterical weakness. If flaccid paralysis or spasms continue, contractures may develop. However, contractures seen in clinical practice today, both in physical medicine and psychiatry, usually follow from temporary failure of use of a part after local pain, or some other major illness, such as myocardial infarction, and true hysterical
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contractures are very rare. ‘Frozen shoulder’ is a frequent example of these occurrences, and a partially frozen shoulder, or arm which is limited in movement, is usually related to physical causes. The problem is occasionally difficult to resolve because, equally, a contracted extremity, held stiff for psychological reasons, might well develop limitation of movement. Certain abnormal movements which formerly were thought to be psychological in origin are now well removed from psychiatry across the porous boundary into the field of the neurologist. Facial tics and dyskinesias, blepharospasm, and other tardive dyskinesias are now accepted as pathophysiological or neurological in origin. Stuttering is also sometimes called hysterical, but while it may occasionally be due to psychological causes it is rarely believed to fulfil the criteria for conversion. Abnormal movements Abnormal movements illustrate the recurring dilemma of how to separate organic from psychological symptoms. As was indicated in Chapters 1 and 2, the physicians of the 19th century and earlier thought of hysteria as an organic illness. For example, Richer (1892) says that blepharospasm may follow either conjunctivitis or psychic shock, and both he and Charcot illustrate numerous examples of facial spasm (which must be very hard to produce and certainly hard to maintain, either consciously or unconsciously). In accordance with this way of thinking certain bizarre types of organic disease were classified as hysterical, including blepharospasm, facial dyskinesias, spasmodic torticollis, many tics and even hemichorea (Charcot, 1889). It has been found that certain types of torticollis appear to develop after emotional stress (Tibbetts, 1971) and might ultimately remit, and tics are often subject to emotional influences and remission (Corbett et al, 1969). But there is a lack of evidence of psychological causal factors in torticollis (Cockburn, 1971), while positive evidence exists of organic disorder supervening upon tics which have been present for some time (Tibbetts, 1971). Until very recently the example of the 19th-century masters was followed, while the frame of reference in which they viewed hysteria as somehow organic was altered by other perspectives, which saw it as a wholly psychological illness. If a symptom did not fit a recognised syndrome with a proven pathology, it was classified by tradition as hysterical. Should the patients appear depressed or beseeching, this was regarded as further evidence of the psychological nature of their affliction. Increasing experience by
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psychiatrists in the last few decades produced a jaundiced view of this hypothesis. Spasmodic torticollis, for instance, rarely responded to psychotherapy of any sort, or to any of the large range of psychotropic drugs, or even to leucotomy. The best therapists usually failed to make any progress. But peripheral nerve section could be temporarily helpful and also stereotactic neurosurgery on the basal ganglia. Other cases of blepharospasm or torticollis gradually evolved into proven cases of torsion dystonia or facial dyskinesia (Tibbetts, 1971) and careful neurological analyses of some dyskinesias would show a retrocollis or palatal movements which were not likely to be psychologically induced, or produced or sustained by voluntary action. It was also known that tics and torticollis, resembling those illnesses thought to be psychological in origin, could be produced by encephalitis lethargica (von Economo, 1929). Drugs which appeared in the 1950s, especially the phenothiazines with piperazine side-chains (e.g. prochlorperazine, fluphenazine), were liable to provoke dystonias and dyskinesias, themselves at first mistaken for hysteria (Delay & Deniker, 1958; Leeman, 1965). Then it began to be recognised that others, such as reserpine, trifluoperazine (stelazine) and haloperidol, could control both the abnormal movements of hemichorea and some of the tics. It was vigorously argued (Shapiro & Shapiro, 1971) that the syndrome of Gilles de la Tourette, including even coprolalia, was of organic origin, since it was often remarkably well controlled by haloperidol, although Morphew & Sim (1969) questioned this argument. The syndrome was removed from the canon of hysterical symptoms by the findings of poor response to psychotherapy, good response to drugs which were irrelevant to psychodynamic postulates, and the acceptance of a stronger relationship to family history than to emotional stress. Emotional disturbances were then recognised as often due to the severity of tics or torticollis rather than as the cause of nearly all of them. Some evidence was adduced that electroencephalographic (EEG) abnormality (Guggenheim & Haynal, 1964) or chromosomal aneuploidy might be associated with movement disorder. Examples occur in Klinefelter’s syndrome with tremor and Parkinsonism (Hunter, 1969), the XYY syndrome with tremor (Daly, 1969) and XYY with the syndrome of Gilles de la Tourette (Merskey, 1974). Jadresic (1992) argues that the latter syndrome particularly involves the amygdaloid complex. Levodopa, introduced for the treatment of Parkinsonism by Lloyd & Hornykiewicz (1973), was seen further to provoke many comparable dyskinetic abnormal movements in patients under treatment for Parkinsonism. Facial dyskinesias and blepharospasm,
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which also had persistently been attributed to psychological causes, changed their category after the introduction of L-dopa treatments. Neurologists became aware that a small excess of L-dopa in the treatment of their patients could lead to a switch from a Parkinsonian state to overt dyskinetic phenomena, resembling what used to be called hysterical facial abnormalities. Since that time it has generally been considered that most, or all, of the blepharospasms and dyskinesias found in clinical practice are of fundamentally neurological origin, although occasionally blepharospasm does still seem to emerge with depressive illness, or other emotional change, and remit with it. During the 1980s the change in opinion on this topic became quite dramatic. Jahanshahi & Marsden (1988) pointed out that in 1970 Engel listed spasmodic torticollis, writer’s cramp, blepharospasm and spastic dysphonia among the motor symptoms of hysteria. “All these conditions are now considered to be manifestations of torsion dystonia which is a recognized physical disorder”. Marsden (1986) had observed that 50%, or more, of patients with dystonia were still initially misdiagnosed as having hysteria. However, among 400 patients with different forms of dystonia a confident diagnosis of hysteria was made in only five cases. In one report where a psychological aetiology was favoured, impressive recent losses, marital conflict and precipitating events were observed. Symptoms of depression were found in three out of five men and less convincing pathological personality patterns in all 20 patients (Diamond et al, 1984). Even in this report the authors suggest that “neurological and psychogenic factors may interact etiologically”. A new treatment also began to have an impact with regard to spasmodic torticollis. The injection of botulinum toxin into the abnormally active muscles began to be employed with success. The toxin blocks the release of acetylcholine locally and renders the muscles weak, and its effect is thought to be analogous to that of surgical denervation, but the injections are relatively simple and well tolerated (Geller et al, 1987). The treatment has also been applied to blepharospasm. Stell et al (1988a,b) reported that their experience confirmed its beneficial effect in relieving pain in more than 90% of patients and in improving head posture in 70%. They had treated over 60 patients without serious side-effects of systemic toxicity. The notion of a psychological disorder becomes much less impressive in the light of such results – and even if there were, improbably as it now seems, a psychological aetiology, the results of the organic treatment have been superior to any of the numerous psychological approaches which have been
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attempted. Naber et al (1988) have similarly concluded from a comparative study of patients with idiopathic spasmodic torticollis and Parkinson’s disease that the groups had similar abnormal personality profiles and that the resemblance between both patient groups indicates that psychiatric symptoms in spasmodic torticollis are non-specific and represent the consequence of a chronic disabling disease. Special psychological phenomena can be observed, however, in patients with torticollis. The disease is embarrassing and distressing. For most people merely to have it is to suffer. Jahanshahi & Marsden demonstrated that 100 torticollis patients did not differ from a control group of 49 patients with cervical spondylosis in terms of personality or in self-reports of events preceding onset of their illness. The groups differed significantly, however, with regard to marital status, a higher proportion of the torticollis patients being single, but not in marital harmony. A significantly higher proportion of the torticollis patients were permanently too ill to move, and the results both of their own study and others led Jahanshahi & Marsden to suggest that depression and destabilisation of personality were both by-products of the physical and social disability experienced by some torticollis patients, as well as by sufferers from other physical disorders, such as cervical spondylosis. Of course, in torticollis, the degree of self-perceived disfigurement resulting from the postural abnormality of the head was thought likely to play a major role in the outcome, so that premorbid personality, rate of progression of the illness, symptom severity and controllability, the resulting functional disability and the extent and quality of social support were all relevant in determining which patients became depressed or developed ‘neurotic’ personality traits. Hysterical tremor is said to be a positive repeated movement of a voluntary type varying in rapidity. It ceases if the patient can be persuaded unwittingly to perform some other movement with the same limb. Care must be taken in making the diagnosis of hysterical tremor, which should not be confused with tremor due to simple anxiety or physical causes. Difficulties in walking are often considered to be hysterical and are then called astasia abasia. This is defined as a form of hysterical unsteadiness of gait (i.e. ataxia), characterised by bizarre incoordination and an inability to walk or stand still, even though all leg movements can function perfectly normally while sitting or lying down. On occasion, patients do things because of their abnormality of gait which are hard for the normal individual with full muscular control (see Fig. 2.2).
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It is clear that many abnormal movements – perhaps most – which were formerly regarded as hysterical, are now thought to be of organic origin, even though neuropathological evidence is scanty or absent. However, anxiety is still accepted as an important cause of tics or habit spasm in many children and treatment, even of the organic conditions, by behaviour therapy techniques has had some successes. Contractures The occurrence of hysterical paralysis leading to contractures appears to present one of the most extreme examples of the acceptance of disability as a result of hysterical illness. Brodie (1837) referred to “several cases of this singular affection of the hands and wrist”, and Paget (1873a) gave a detailed description of it as an example of “Nervous mimicry of organic diseases”. Charcot (1890) described the “Oedème bleu des hystériques”, which developed with contractures and is known by his name. MacAlpine & Ross (1956) point out that Brodie had in fact reported the condition earlier. According to Charcot, the extreme disorder is characterised by non-pitting oedema, coldness, purplish discoloration, altered sensation, often total anaesthesia, paresis and contracture of a hand or foot, yet with normal electrical reactions. Trophic changes and occasional pain may also occur. Charcot’s pupil, Richer (1892), thought that contractures would occur before or after convulsive attacks, with the disappearance of some other hysterical symptoms and as a result of psychological causes (impressions morales). He also thought they could follow on various physical conditions (états morbides), such as rheumatism, syphilis, chlorosis, fevers, chronic intoxications and tremor. Fluctuating weakness is common and paralyses occur relatively often among the motor conversion symptoms. Contractures are rare and are a result of disuse. MacAlpine & Ross (1956) described two patients who were referred with a view to surgery, such as sympathectomy or amputation. Both were treated by face to face psychotherapy, one with complete benefit and the other with partial benefit (while a compensation case was pending). Siomopoulos & Reissman (1969) described a patient with contractures of both hands and arms and of the legs as well, which had developed progressively over 10 years and which did not respond to treatment. The special interest of the condition, among other hysterical ones, is the degree of self-harm which is evident. Richer, in his book, linked certain facial disorders with paralysis and contractures: blepharospasm, hemifacial spasm, trismus and
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glossolabial hemispasm were all described as hysterical, like torticollis, but reasons have already been given for rejecting such a view of torticollis, facial spasms and dyskinesia. Weinberg et al (1970) reported a case of supposed hysterical trismus which required the rupture of fibrous contractures under anaesthesia, subsequent psychotherapy, and separation from his wife, all of which combined to produce a complete cure. It seems likely to me that the organic change was the most important initial one, whether or not it was produced by psychological factors, and that the other psychological changes observed later were essentially secondary responses. They emphasised that organic causes, such as tremor, infection, tumour and tetanus, may also be relevant and that the diagnosis of hysterical trismus requires positive psychological evidence. In considering contractures in general, it is worth remarking that disuse atrophy with skin and vasomotor changes is more common in the neglected hemiplegias with frozen shoulders, with nerve lesions or when use of a limb is painful after accidents than in hysteria. Complex regional pain syndromes, types one and two (International Association for the Study of Pain, 1994), formerly known as reflex sympathetic dystrophy or causalgia, frequently have such effects. Unwillingness or failure to use such a limb can be hysterical or normal. The writer has had only one patient who maintained a contracted hand. This was after a painful wrist injury and despite complete organic recovery and settlement of a compensation claim. It was worse under emotional stress and relieved variously by suggestion, relaxation and hypnosis. A deeper significant psychopathology was not found for this case, although he was undoubtedly a passive individual. Some other motor responses Hysterical fits were discussed in Chapter 11. Mutism is essentially a motor symptom. It may also be associated with other conditions (Behrman, 1973) such as schizophrenia (Kahlbaum, 1874), diencephalic disturbances (Cairns et al, 1941), ictal discharges (Jackson, 1882) and cingulate lesions (Barris & Schuman, 1953). Depression may produce stupor and mutism but the depressed mute patient rarely fails to utter some words. When hysterical mutism or stupor do occur, they are likely to be due to a conflict which is readily found. In such cases Kretschmer’s view of the hysterical symptom as a protective withdrawal may well be apposite. Hyperventilation, by contrast, is a symptom which is a good deal more likely to be due to anxiety than to hysterical mechanisms.
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The typical pattern of hyperventilation occurs in anxiety – provoking situations, such as assemblies, underground railway stations, small spaces, and so on, in people who are phobic of such places, or in relation to emotionally stressful events, such as examinations or difficult personal encounters. The patients feel uneasy and then feel they cannot get their breath. The occurrence of loss of consciousness is organically induced starting from the fall in blood pCO 2. Although hyperventilation symptoms often occur in people with hysterical personalities, they are not necessarily hysterical and they can be relieved by demonstrating to the patient how the symptom may be produced by overbreathing and removed by rebreathing into a paper bag or by holding the breath. Dizziness often accompanies anxiety and hyperventilation. It is a common complaint among psychiatric patients. A subjective feeling of unsteadiness has often been called hysterical. It is not clear that is the best label. Feelings of unsteadiness and falling are of course part of the syndrome of astasia abasia but also occur commonly with anxiety. They are distinguished from vertigo, in which the patient feels that the environment is rotating and from postural hypotension which is commonly caused by medication, or by vasomotor instability. Most current studies support the above views. Lum (1981) reported that more than 1000 patients received a course of breathing retraining and relaxation in a physiotherapy department and this usually helped to abolish symptoms. Hibbert (1984) regarded hyperventilation as a cause of panic attacks and said that it should be included in the differential diagnosis of all cases of panic disorder, whether or not there appear to be other sources of frightening somatic sensations. Bass & Gardner (1985) carefully investigated 21 patients with unexplained somatic symptoms and unequivocal chronic hypocapnia on repeated occasions. Skin tests to common allergens were found to be positive in three, and ventilation perfusion scanning was abnormal in another three patients. Ten of the 21 patients were neurotic and suffered from chronic psychiatric problems characterised by anxiety, panic and phobic symptoms, but the remainder had no detectable psychiatric disorders, although they reported proportionately more somatic than anxiety symptoms. Thus severe hyperventilation can occur in the absence of formal psychiatric or detectable respiratory abnormalities or other organic difficulties, and hence not all cases can be attributed either to a known physical cause or to anxiety. Bass (1990) observed that no single factor has been implicated in the pathophysiology of hyperventilation and that the causal
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mechanisms are likely to be multifactorial, including physical factors characterised by an increased drive to breathe, manifest as tachypnoea and exercise-induced hyperventilation, psychological factors, and environmental factors. Hyperventilation may occasionally have an organic significance, as hinted by Bass & Gardner. Freeman & Nixon (1985) described a case of coronary artery vasospasm induced by spontaneous hyperventilation, the mechanism being presumed to be vasoconstriction as a result of the hyperventilation. Unilateral symptoms with hyperventilation appear to reflect a central organic mechanism (O’Sullivan et al, 1992). However, anxiety remains much the most common cause of hyperventilation.
Visceral symptoms It has been evident so far that virtually the whole range of possible symptoms in the body may be implicated in hysterical complaints. Indeed, prima facie no symptom which may be either thought of by the human mind or experienced by the body can be immune from hysterical mimicry. Similarly, any motor complaint which can be produced voluntarily may also be produced as a hysterical symptom. The way in which psychological symptoms can be mimicked hysterically is exemplified by a girl whose depression was not thought to be profound. She developed identical symptoms to those of an older sister who had had a depressive illness. Parenthetically I might mention a 40-year-old medical student who was even more sophisticated. He saw no need to complain of symptoms but simply said “I’m sick, Doctor, treat me, I’m just sick”, producing the ultimate dependent request. On the other hand, I have always been reluctant to accept as hysterical those symptoms which are hard to produce or maintain voluntarily. For example, hysterical retention of urine to the point of bladder distention has not been a possible diagnosis in even one patient of the many seen by the writer with other hysterical symptoms; and in the case of Knowles (1963) describing chronic hysterical urinary retention there was no proof of retention but there was evidence of deceit by the patient. Among gastrointestinal symptoms, that of globus hystericus is one for which modern evidence suggests a frequent organic aetiology. A sensation of a ball or lump in the throat has, since Hippocrates, been regarded as hysterical. A precise distinction between anxiety and hysteria may be easy in theory but is often hard in practice, and was not made by traditional writers. Many
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people swallow saliva or air when tense, and feel it hard to eat or to swallow when anxious or depressed. It is reasonable to regard this symptom as possibly due to anxiety, and not a conversion symptom. Malcolmson (1968) draws attention to the fact that Purcell (1707) described the symptom and commented upon it as follows: “women in this Distemper affirm they often feel a Hard ball pressed against the outside of their throats; sometimes as it were a Stick thrust down their Throats which stretches and distends them violently, at other times, a Sensation like that of a Rope pull’d straight about their Necks almost strangling them; and lastly a Rising of something up their Throats: are not vain imaginations and groundless Fancies....”
He attributed the sensation to violent contractions of the sternohyoid and other neck muscles pressing on the thyroid cartilage, the awareness of discomfort from this being referred internally to the throat. Sydenham (1697), following Jorden (1603) as well as earlier writers, had spoken of the “Suffocation of the Womb in which the Belly and Entrails rise upwards the Throat”. Malcolmson (1966, 1968) showed in a series of 307 patients that only 21% had a completely negative physical and radiological examination. Of the remainder, 38% (92 out of 242) had a lesion in close anatomical relation to the site of the symptom, such as cervical spine osteophytes, overactive cricopharyngeus, hyperplastic tonsils, goitre, post-cricoid web or lymph nodes. Of those with lesions, 62% (150 patients) had a gut disturbance distal to the pharynx, such as hiatus hernia (104 patients), duodenal ulcer, and gastric lesions. He suggests globus pharyngis is a better term, emphasises occasional fatal causes (e.g. carcinoma) and indicates that air-swallowing may also be a consequence of the lesion. In another study (Delahunty & Ardran, 1970) an acid barium swallow given to 25 patients showed that 22 had reflux oesophagitis resulting in an acid-induced disturbance of oesophageal motility. Hunt et al (1970) showed that elevated resting pressures occurred in the cricopharyngeal sphincter in patients with gastric reflux. These pressures fell to normal after successful treatment. Watson & Sullivan (1974) further demonstrated that cricopharyngeal sphincter pressures were significantly elevated in nine patients with globus pharyngis compared with 37 controls. Lehtinen & Puhakka (1976) examined 20 such patients with globus pharyngis psychiatrically, and by oesophagoscopy and oesophageal cinematography. Two had gastro-oesophageal reflux and eight had abnormalities of the cricopharyngeal folds. No patient was free of
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psychiatric symptoms, but only eight showed any evidence of hysterical personality. A markedly obsessive personality picture predominated, all but two of the patients exhibiting obsessive features. These authors consider that there are two different types of globus pharyngis patients, one in which the aetiological factor is mainly somatic and another in which the aetiological factor is primarily psychological. Brown et al (1986) report some cases responsive to antidepressants. The studies quoted are sufficient to support the view that all cases of globus should not normally be labelled hystericus. Yet another organic cause for globus is often neglected. Dysphagia occurs in a significant minority of patients over the age of 87 (21 out of 109 in one study by Bloem et al (1990)). The collapse of the vertical dimension in the masticating (gnathic) apparatus – for example by loss of molars and wearing of obsolete dentures – may upset the balance of the supramandibular, the submandibular and the hyoid muscles. Campbell (1962) argued that changes of this type were liable to produce sensations comparable with that of a lump in the throat. Wilson et al (1988) challenged the view that globus hystericus was commonly based upon organic dysfunction or disease. In 46 patients the only organic abnormalities detected were an abnormal degree of oesophageal acid exposure in seven patients and oesophageal spasm in one patient. At the same time the 37 female patients had elevated scores for neuroticism on the Eysenck Personality Inventory (EPI), and reduced scores for extraversion. Their results were significant in these respects (P < 0.01). The male patients appeared normal (in fact the male patients had significantly lower neuroticism scores than age-matched normals). Thirteen of the females and one male patient had elevated scores, suggesting psychiatric morbidity on the General Health Questionnaire (GHQ-60; score > 12). On the one hand, it cannot be disputed that these authors found little evidence of organic disease in their patients. On the other hand, their interpretation of the psychological data is questionable, since mean trends in group scores do not demonstrate psychopathology for individual patients, and the size of the mean trends clearly did not suggest that most of the patients had psychological problems. Indeed, even using the lowest acceptable threshold for predicting psychiatric illness on the GHQ, less than one-third of all the patients ranked as potentially psychiatrically ill. This level of neuroticism is common in all general medical populations, as already discussed. Part of it may be due to secondary depression from an existing physical illness, and another part may reflect a selection pattern in which
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patients who are more concerned about a basic symptom, which may or may not be organic in origin, present themselves more frequently for hospital attention. Thus Wilson et al have not shown that globus is a psychological illness, but they have demonstrated that little organic evidence was found in their particular population. Mace et al (1988) criticised Wilson et al for relying unduly on the GHQ and the EPI in their interpretations, having regard to known problems of discrimination with both tests with respect to physical illness and hysteria. In a later study (Deary et al, 1992) evidence was obtained that scores on the Beck Depression Inventory were elevated in 25 patients with globus sensations and no organic cause compared with 25 control cases. In addition, significant independent life events had affected 52% of the patients compared with 8% of the control group (P > 0.002). This is convincing evidence that psychological factors such as depression are evident but also suggests that they apply to only about half the cases. It seems reasonable to conclude that globus is not often hystericus, although it might be sometimes. Some of the changes may be related to the various oesophageal abnormalities that have been considered, and when these occur a number of them seem to have a particular association with psychiatric diagnoses (Clouse & Lustman, 1983). Some may well be related to anxiety or depression, and, as mentioned above, a report exists of successful treatment of three patients with antidepressants (Brown et al, 1986). Clouse (1992) observes that although acute emotional events may influence oesophageal activity, no oesophageal motility disorder is recognised as resulting directly and completely from psychiatric factors. He added that the studies which have found evidence of psychological changes: “do not prove a causal role of psychiatric factors in the oesophageal process. They primarily demonstrate the prevalence of psychopathology in patient subsets seeking health care in clinical settings. A selection bias introduced by the health care setting must be expected and has been well recognized in studies with patients with irritable bowel syndrome.”
We can suppose that a few patients might have globus as a hysterical symptom. Nevertheless, an examination of the conditions in which globus has been found historically suggests that it is much more likely to be related to anxiety than either to a theoretical movement of the womb (Merskey & Merskey, 1993) or to a psychodynamically motivated conversion symptom.
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Other gastrointestinal symptoms which have been regarded as hysterical include vomiting and diarrhoea. Induced vomiting, as in anorexia nervosa, actually represents the conscious production of a symptom and is therefore, strictly speaking, malingering or deliberate disability. It is reasonable to consider that it has links with hysterical symptoms, as discussed earlier (Chapter 8). Vomiting occurs rarely, if at all, with hysterical motor symptoms, and when it appears with anxiety it is usually not persistent or frequent. Nausea and some retching are more common. Hyperemesis gravidarum is now thought to have more to do with hormonal changes than with emotion, and in general it is unwise to regard troublesome vomiting as hysterical. Gonzalez-Heydrich et al (1991) reported the results of re-examination of four children in whom a tentative diagnosis of psychogenic vomiting had been made after extensive (but sometimes incomplete) evaluation. Three had significant organic causes for vomiting as well as psychological problems. One had a vomiting disorder with no evident organic cause which responded well to psychological management. There is probably a special, small group of patients who do have vomiting for psychological reasons, but they have to be identified with the utmost care to avoid overlooking serious organic or gastrointestinal disease. Some of these patients who vomit for psychological reasons present severe problems (Hill, 1967, 1968) which even extend to hypokalaemia, which brings its own psychological symptoms (Sim, 1974). Reviewing the literature, Cleghorn & Brown (1964) noted that psychologically induced vomiting appears in dependent, immature people with impaired parental relationships whose episodes of vomiting are often related to a fear of heterosexuality. Hill (1968) points out that such common deficiencies of character formation are difficult to accept as specific determinants of the symptom, but are more likely to act as general maladaptive effects in a person otherwise predisposed to vomit. Hill’s own series comprised 20 patients (14 females and 6 males), most of whom gave evidence of being locked in an inescapable hostile relationship within their family group; they had an excessive amount of childhood parental loss, histories of recurrent vomiting at that time, and an increased family history of vomiting. Loss of weight and hypokalaemia could be serious. It has been suggested that for many people psychogenic vomiting is an occasional event associated with severe emotional stress. Apart from the severe cases just discussed, it is argued that we should work on the basis that each individual has the potential to vomit, perhaps secondary to disorders of gastrointestinal motility
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as a result of psychological stress, but that the threshold varies from one person to another. Those presenting with unexplained vomiting may be experiencing high levels of stress or have a low threshold (Lancet, 1992). The more severe phenomena are relatively uncommon in general psychiatric practice. It is possible to interpret such cases as expressing a conscious or unconscious rejection of relationships. Alternatively, as implied in the previous paragraph, they may represent a learned psychophysiological response in susceptible individuals. As with motion sickness, some people will be more liable than others because of anxiety or previous conditioning. It seems reasonable to suppose that some, but not all, of these patients might have a conversion symptom, some will induce or maintain it deliberately, and some, perhaps all, are relatively liable to vomit for physiological reasons. Some patients who have diarrhoea tend in fact to complain of constipation and to take excessive laxatives: patients with anorexia nervosa may also consume these substances. One patient in the latter group took more than 700 laxative tablets over two weeks. Her height was 152 cm and her weight on admission to hospital was 34 kg; with the development of gross oedema and inappropriate antidiuretic hormone response, her weight rose to 52 kg within seven days. Metabolic disturbances provoked in this way can be dangerous and are usually consciously induced. As with induced vomiting, they are part of the picture of deliberate disability (Chapter 8). They may also be due to bowel preoccupation of a delusional intensity or to Hirschsprung’s disease (megacolon) with chronic constipation and overflow diarrhoea. Pseudocyesis has been described under a variety of diagnostic categories (Cohen, 1982). It seems to be associated quite often with psychotic illnesses. At other times it is thought to have a link with hysterical phenomena. Among the psychotic conditions, pseudocyesis has also classically been thought of as a visceral hysterical symptom. However, it has been described in a schizophrenic man with intermittent hyponatraemia and polydipsia (Shutty & Leadbetter, 1993), and as a recurring accompaniment to episodes of hypomania in a young woman (Taylor & Kreeger, 1987). In the first of these two cases the authors took the view that the hyponatraemia and rapid weight gain observed stemmed from the ingestion of large amounts of water. In the second case the authors held that there was no evidence that the disorder related to a reduction in the availability of biogenic amines at neuronal receptor sites. Among evidence on the neurotic aspects of this disorder, Song et al (1993) studied patients with abdominal swelling
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not associated with the specific beliefs in pseudocyesis. Abdominal swelling is thought to be due to a variety of causes being found quite often with other gastrointestinal disorders but also occurring in relatively pure culture, so to speak, on its own. In a hospital sample, reflecting the work of a specialised gastrointestinal referral service, approximately two-thirds of the patients had evidence of anxiety. A potential exists for a hysterical syndrome to build upon symptoms of this type, but it apparently does not do so very often. For patients who become concerned about this syndrome it is probably more important to stress the value of relief from anxiety rather than searching for major histrionic motives. Despite some of the organic possibilities, pseudocyesis represents the triumph of an idea over reality, particularly when it occurs in men.
Sensory symptoms Among sensory symptoms, deafness, blindness (amaurosis) or visual impairment (amblyopia) are distinguished by special tests which demonstrate a function which the patient believes lost. Cerebral evoked potentials can also help to support the diagnosis. Hysterical deafness is quite rare in clinical practice, although individuals at home and at work often mention that others have not been inclined to hear what they said. Hysterical deafness was more common in soldiers exposed to blast injury and was often found in association with other hysterical symptoms such as paralysis and blindness. Those who have had their eardrums ruptured, or suffered industrial deafness, may be more liable unconsciously to prolong or magnify an original injury if some benefit will result. Absolute hysterical deafness should be detectable in sleep by the effect of noise in waking the patient. A subtle method of demonstrating this is to take a sleep EEG recording and mention the patient’s name during it. This may produce the characteristic K complex in the EEG which indicates a response to familiar material. (The response tends to extinguish on repetition.) Evoked potential studies can also be used to demonstrate intact auditory pathways. However, incomplete hysterical deafness is obviously harder to discriminate. It may be inferred from inconsistent responses on audiological testing. Tyrer (1957) gives a useful description of techniques, like those of Head (1922), which can be used diagnostically for the paralyses, anaesthesias, blindness and deafness. Hysterical blindness is common in ophthalmological practice (Kathol et al, 1983a,b; Weller & Wiedemann, 1989) and it is often
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partial rather than complete. It is perhaps found most often as blurring of vision or difficulty in reading in adolescents facing examinations. Difficulty in vision is often thought to be hysterical if the patient shows tubular or spiral fields. The measurement of visual fields by perimetry involves moving a small spot systematically from the margin to the centre, and asking the patient to detect the spot. With normal vision the fields should be wider at a distance than close to the eye. If it appears that the size of the visual field stays the same no matter what the distance from the eye, this is known as tubular vision. A spiral change in the visual fields is obtained when the examiner, starting at one point, obtains a visual field of a given magnitude which then gradually decreases as he or she moves around the field in a circle. By the time the test spot has been returned to the starting point, it may only be visualised on the axis where it started in a much lower (or higher) position than was originally found. Kathol et al (1983a), in a review of the literature, noted that as many as 60% of patients with functional visual loss had no evidence of psychiatric disease. They also found (1983b) that 20 out of 42 such patients had no psychiatric disorder on follow-up. Inconsistent spiral fields, like tubular vision, may be attributed to the persuasive skill of the examiner or to high suggestibility. They perhaps may show that some condition or stress has encouraged the patient to give inconsistent answers, but they are not proof of hysterical complaints, and are not disabling. Ophthalmologists have always had impressive skills in demonstrating that patients who claim not to be able to use their eyes could nevertheless process visual information. They are able to show discrepancies in reading different sizes of print at different distances, in what the patient reports when looking at polaroid projector charts and when using polaroid goggles, and in responses when red/green filters and perimetry are employed. None of these tests may be absolutely reliable, but they are all useful. Behrman (1969) describes the use of dark-adapted visual evoked responses as a satisfactory method of confirming the integrity of retinal and visual pathways. She used it effectively in 35 patients referred to an electrodiagnostic clinic at Moorfields Eye Hospital. Twelve patients were male, 23 female, and half were under 16 years of age. Halliday (1972) further described the diagnostic usefulness of averaged evoked responses, both to discriminate hysterical complaints and even to determine the simultaneous presence both of an organic lesion and of a hysterical element in the complaint. Theodor & Mandelcorn (1973) further report that it has proved possible to demonstrate the processing of visual
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information despite the patient’s denial. Thus a patient was shown to perform very significantly worse than chance in response to visual stimuli in a ‘blind’ area. This demonstrated the active rejection of material, as to produce this effect the material had to be processed at some level of awareness. The author’s experience of adult patients with severe hysterical amblyopia includes two in whom compensation problems and a fairly strong suspicion of malingering were present, and a third, the girl whose problems with interpersonal relationships were described on p. 163. A fourth patient, depressed at the compulsory detention of her mildly wayward son in a hospital for the criminally insane, improved suddenly with psychotherapy, strong suggestion, and brief antidepressant treatment. She gave convincing evidence of believing that her sight had failed. Problems of hysterical blindness still occur, although nowadays they are not often analysed in the psychiatric literature. Blepharospasm, which can also be tantamount to blindness, can be due to anxiety, and may be due to hysteria, but if severe is more often due to extrapyramidal dyskinesia. Hysterical visual symptoms are quite common, but blindness is much less frequent than are minor anomalies such as tunnel vision or spiral fields. Meadows (1969) considered hysterical blindness to be rare but less abnormal in children because of their immaturity. But hysterical blindness has always aroused considerable theoretical interest as well as having practical importance. The theoretical interest derives from the psychoanalytic view of hysterical blindness as a symbolic equivalent to castration, by analogy with Oedipus, who in response to his sexual guilt put out his own eyes. Vallotton (1974), who gives a long list of eye complaints and their causes, indicates that many such complaints are common. In the course of five years, he saw three cases of “the Oedipus Rex syndrome”, in which individuals plucked out their eyes under the influence of hallucinogenic drugs. Goodhart & Savitsky (1933) reported a similar case in a psychotic postencephalitic girl. Complete hysterical amaurosis is more common than self-induced blindness, although less common than the minor complaints such as tubular fields and partial visual loss (amblyopia). It is worth noting that an apparent inconsistency in symptoms sometimes results from the doctor’s failure to take a careful history. Many patients can describe their sensory symptoms only vaguely, because they are not asked specifically in what ways a symptom such as pain occurs at different times. On one occasion the patient may describe tingling in the arms or legs, on another numbness, on another a dull ache, and so forth, and unless the
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doctor is careful to establish that the patient experiences these symptoms at different times, and perhaps in different places, he or she may simply assume that the history is unreliable, when it may in fact be more precise than the doctor’s own questions. Hallucinations which are well formed, often visual, and generally of people are frequently regarded as hysterical. La Barre (1975) describes numerous reports and instances of hallucinations associated with dissociative behaviour. However, Holroyd et al (1992) found 13 patients among 100 with age-related macular degeneration who suffered from visual hallucinations. The hallucinations were associated with living alone, a lower cognitive status, a history of stroke and bilateral lower visual acuity. They note that their findings suggest a contribution both from sensory deprivation and from a possible decrease in cortical inhibition. Hallucinations may occur without any other signs of psychological illness and be unimportant; a hysterical mechanism may cause the reappearance of dead relations and may be an explanation for such experiences at seances. Profuse visual images, for example of trains of people passing before the eyes, were called phantasmagoria by Galton (1883) and they may also occur in normal people. Morsier (1936) described a clinical condition occurring in the elderly with preserved intellectual functions which was characterised by vivid, elaborate and dynamic recurrent visual pseudohallucinatory phenomena of a pleasant or neutral nature. These are often associated with ocular pathology. Morsier pointed out that Charles Bonnet (1760) had described this pattern in the case of his grandfather. Damas-Mora et al (1982) have reviewed the phenomena and described additional cases. Schultz & Melzack (1991) have emphasised the sensory deprivation framework in which these hallucinations occur. Other types of hallucinations, especially those which occur at night, may result from anxiety, sensory deprivation or partly impaired consciousness, or a mixture of these causes. Hysterical mechanisms can play a part but need not be assumed to do so. Hysterical mechanisms may also be relevant to the hallucinations which occur with depressive illness. In general, if hallucinations are associated with serious psychiatric or organic illness, this will be evident. Anaesthesia of the skin or mucous membranes is rarely troublesome. Both anaesthesia and hyperaesthesia have been shown to have a potential physiological basis, as discussed in Chapter 10. Skin burns or similar lesions suggest an organic disorder. When demonstrated, hysterical hyperaesthesia and anaesthesia carry the
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same lessons as tubular vision and spiral fields. Similarly, deep points of tenderness, particularly in the ovarian region, which were a special subject of interest to Charcot, are now scarcely ever sought, and do not reflect any significant psychological meaning except, again, that the patient is suggestible.
La belle indifférence One aspect of hysterical symptoms which has been long accepted is that patients show a lack of concern with their symptoms, or an acceptance of them which would be surprising in someone who has suddenly developed a significant disability. This does not appear in all patients, but is common and sometimes striking. The notion that the symptoms solve a conflict provides a ready explanation of the findings. If the patient is happy to be ill in order to escape a more difficult problem, then la belle indifférence is readily understood. This may not, however, be the whole story. Lader & Sartorius (1968) examined 10 patients with well defined conversion symptoms and compared them with 71 people with anxiety and phobic states and 75 controls. Patients with conversion symptoms rated themselves significantly lower than anxiety phobic patients in respect of overt anxiety, but higher for current anxiety. On measures of habituation and spontaneous fluctuation of the galvanic skin response (GSR), the patients with conversion symptoms, unlike those with anxiety states, showed no tendency to habituate. Lader & Sartorius comment that the hypothesis of lower anxiety in the conversion symptom patients was not upheld and they had significantly higher autonomic (‘arousal’) activity than the anxious phobic patients. The inferences from this study are that a superficial impression of belle indifférence will often not correspond to the patient’s physiological state, which may be typical of high anxiety, and in any case some patients with conversion symptoms will show evidence of anxiety – a common clinical finding. Rice & Greenfield (1969) studied nine patients, of whom three had pareses and four less certain hysterical symptoms (torticollis, asthenia, chest pain, head pain). When compared with patients with organic disease, they tended to show somewhat more physiological reactivity to anxiety-provoking stimuli. Significant differences in this direction were found at times in the GSR and frontalis muscle tension, leading the authors to conclude that “the defensive process represented in la belle indifférence does not prevent the arousal of covert physiological correlates of emotion”.
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Rosen (1951) reported an opposite finding: patients with conversion hysteria displayed less response to the cold pressor test compared with other psychiatric patients. The systolic blood pressure of the conversion hysteria patients actually showed a reduction. More work on this topic would be welcome. Meanwhile it is clear that, despite Rosen’s paradoxical findings, belle indifférence is not a regular or pathognomonic sign of hysteria. When it occurs it has to be seen as only superficial evidence and, in any case, in clinical practice, it is a very unreliable diagnostic sign, as already noted in the discussion in Chapter 10 of the paper by Gould et al (1986). The attraction which the idea of belle indifférence has always held for doctors can itself be understood psychologically. It is impressive to find patients who treat their symptoms with remarkable unconcern; it is satisfying to have a neat dynamic explanation that the patient is pleased because an unconscious problem has been solved and the disturbing affect removed from consciousness. But the preoccupation with it has also led to confusion. This was particularly so in multiple sclerosis, where hysterical signs are not uncommon. Cottrell & Kinnier-Wilson (1926) showed that euphoria was frequently present in patients with multiple sclerosis. They did not look for mild degrees of dementia and ignored the fact that 13% of those they had examined were obviously demented. It was only when later work (e.g. Braceland & Giffin, 1950; Canter, 1951; Pratt, 1951; Surridge, 1969) showed that organic cerebral changes were common in multiple sclerosis that the euphoria, or relative lack of depression, in such a grave illness was seen to result from dementing changes. Meanwhile multiple sclerosis with hysterical symptoms was often taken to show belle indifférence (e.g. Langworthy & LeGrand, 1952).
Depression In contrast to la belle indifférence, more attention has been paid recently to the association of hysteria and depression. In Slater’s series of 85 cases of hysteria, eight developed endogenous depression and one another form of affective illness (Slater & Glithero, 1965). Lewis (1975) traced 98 cases, of whom two developed schizophrenia, and of those who had not recovered, eight had a depressive syndrome. Merskey & Buhrich (1975) found significant depression in 16% of patients with conversion symptoms and McKegney (1967) found it in 22% of cases. These figures should be compared with findings that 6–8% of the general
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population have diagnosable depression. Fifty-eight per cent of those with hysteria in McKegney’s series had some depression and particularly high rates of depression have already been noted in fugue states (Stengel, 1941). Bibb & Guze (1972) found depressive symptoms to be prominent in 80% of patients hospitalised with Briquet syndrome. There is an increasing tendency to favour the idea that many hysterical symptoms occur in the context of depression. This is more evident in those studies discussed above, where somatisation disorder and similar conditions have been examined. There the principal overlap of hysterical symptoms has been with depression, but most of the studies which I have been able to review connected with monosymptomatic conversion symptoms – or of patients who only have one or two such complaints – do not seem to find a prominent depression.
Examination and the doctor’s response The psychological problems for doctors in dealing with hysteria are considerable. It is not only for intellectual understanding that Paget (1873a), following Brodie, worked out, “They say, ‘I cannot’; it looks like ‘I will not’; but it is ‘I cannot will’”. An explanation which allows sympathetic management becomes invaluable for doctors and others who are presented with a demand to treat the patient. Almost all hysterical patients produce such an implicit demand and are liable to lead doctors into feeling that a deception is being attempted. In the sense that the symptom is produced for the patient’s benefit it is certainly manipulative or even counterfeit, notwithstanding the fact that the simulation is unconscious. Doctors are as liable to have an unconscious resentment of this circumstance as the patient is entitled to benefit from it. Add to this the facts that many hysterical, and especially hypochondriacal, patients demand time and attention, and present their symptoms in circumstances where full and proper inquiry may be inconvenient; the doctor is then wrongly tempted to accept the surface, organic version of the matter. It is no wonder that ‘hysteric’ is a well established medical term of abuse. Few doctors object to being told that they show some obsessional traits, or even an anxious, driving temperament. By contrast, few would accept happily the least hint that they have hysterical personality traits, even though they may well have a fairly strong narcissistic need for gratification from the attitudes of their patients, above average acting ability in presenting clinical
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demonstrations, considerable sensitivity to the psychological minutiae of daily relationships, and a willingness to be obliging and helpful in serving people. All of these are in some measure traits, whether good or bad from the social and practical point of view, which have been linked with hysteria. The wide range of hysterical phenomena, both in terms of symptoms and of personality traits, has not yet been fully discussed, but it is already clear that the conditions in which they arise are very varied, the problems they present multiple, and the resources which the doctor needs in both medical skill and personal confidence are considerable. The reader is invited to study the address by Emil Kraepelin in Appendix B for an illustration of the picture of hysteria which retains the same immediacy as on the day it was spoken. Anyone who has read that extract will at least have a feeling for the major characteristics and many of the subtleties of hysterical patients with regard both to their complaints and to their handling. In that extract Kraepelin, a psychiatrist, can be seen using both psychological and neurological techniques of observation and management. In Appendix C, Sir Charles Symonds has permitted the reprinting of a lecture on hysteria where he, as a neurologist, used both neurological and psychiatric techniques. Sir Charles’ lecture tackles many issues and is equally notable for the clinical skill and psychological understanding which he employed to diagnose and treat his patients. There is no false sentiment, nor the slightest rejection of a patient, although the doctor’s own problems in finding the necessary time and the right moment in which to deal with the patient are clearly recognised. These extracts, from two masters, give us the first essentials for diagnosis and management of the patient with hysteria. The examination of hysterical patients must be as careful as of other types of patient: full and competent inquiry must be made into symptoms and into the history; physical examination must be complete and skilful; and the subsequent management of the patient neither hurried nor aggressive. If this pattern is followed and all appropriate investigations are also completed, patients with hysterical symptoms can be treated with confidence and will accept a psychological approach to their symptoms. They will still need to be managed with flexibility and resourcefulness, but there will be few who will not benefit from treatment in these circumstances. When engaged in treating hysterical patients, the doctor needs to be aware not only of organic technical traps, but also of emotional ones, which are equally technical. The doctor should not be too ready to sympathise or to give promises of special help
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in some matter because the patient is beseeching. It will not do to indicate that the husband must change his ways, without seeing him first, and perhaps not even after that. The doctor should similarly negate any hostility that may be felt. The standard psychiatric advice of neutral sympathy is more necessary for patients with conversion hysteria or hysterical personality than for any other group. There are occasions when the psychiatrist may intervene on behalf of the patient to change circumstances or advise changes in relationships (Merskey, 1980), but hysteria is not often one of them where relationships are concerned. Throughout all this, it remains necessary to base a diagnosis firmly upon two criteria: the absence of proportionate organic disease, and the presence of proven hysterical phenomena. If these cannot be shown in full, management must be the more tentative, and should always be undogmatic. A third criterion, the discovery of adequate psychological evidence for the syndrome, is helpful. The diagnosis of hysterical symptoms may be neurological; its treatment is psychiatric, no matter who undertakes it. In doing all this, care must be taken not to over-investigate or over-treat physically, even though the presence of relevant organic disease must be carefully sought. The problems of the relationship with hysterical patients are those of transference, whether positive or negative. It would be repetitious to engage in a further discussion of this important phenomenon, which is fully treated in numerous texts. Nevertheless, the positive and negative aspects of the transference have been implicit and substantial throughout this discussion.
Prognosis Carter (1949) showed that 70% of 90 patients followed for four to six years were well and only seven could not work. This is in accordance with the view that the prognosis for monosymptomatic conversion hysteria is normally good, despite the fact that a small percentage of the patients in most series has committed suicide, and there is also a slight increase in mortality compared with the general population. Slater (1965) observes that two authors who selected patients by the presence of conversion symptoms in an uncomplicated setting both found favourable recovery rates. Carter (1949) traced 90 out of 100 patients. All were alive and all but seven, as just mentioned, were able to work. In Ljungberg’s large personal follow-up series (Ljungberg, 1957) suicide was no more frequent among men than
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among the general population, but the rate for women was raised. Seven per cent of the male patients and 12% of his female patients had attempted suicide, but the differences between the sexes were not significant for either suicide or attempted suicide. However, the average expectation of life in his patients was 15% below that of the general population. In Slater’s own series, 85 out of 112 patients were traced. Four had died by suicide, eight from natural causes, but from his own data this was a physically vulnerable population, a fact confirmed by Merskey & Buhrich (1975) and discussed in Chapter 11. Using somewhat different selection criteria based on the diagnosis of hysterical neurosis (conversion type), Stefansson et al (1976) found 72 deaths, six of which were suicides, among 1374 patients in Monroe County over a 12-year period. However, 20 of the deaths occurred within one year of diagnosis – a significant excess. Thus it appears that there is probably a small but significant excess of deaths from natural causes and from suicide among patients with a diagnosis of hysteria. The explanation for the deaths from natural causes is partly misdiagnosis, but also associated and recognised physical disease. In epidemics of hysteria (Chapter 16) recovery is normally 100% in respect of the individual symptom. The same is true for endemic, culturally induced conditions, provided the patient survives any extreme activities which may occasionally arise. The incidence of psychoses as determined in follow-up studies is also modest, although above expectation for a normal population. Two of Carter’s patients became schizophrenic, as did two of Slater’s, while the latter also diagnosed seven patients with recurrent endogenous depression. Ljungberg gives the morbidity risk for schizophrenia as 3.1 ± 1.1%, for manic–depressive psychoses as 2.4 ± 1.1%, for presenile psychoses as 1.8 ± 1.3%, for psychogenic psychoses as 2.0 ± 0.9%, for alcoholism as 2.0 ± 0.9%, and for drug addiction as 1.3 ± 0.6%. The figures for schizophrenia are above those for most populations and so are the figures for psychoses in general. There is general agreement, therefore, that patients diagnosed as hysterical have a modest increase in the rate of physical illness, suicide and psychoses. Ljungberg’s valuable study also shows that the proportion classed as recovered after initial treatment declines with time. After one year, 43% of the men and 35% of the women had residual symptoms. After five years 25% of the men and 22% of the women still had symptoms. And at 15 years the combined figure was 20%. Lewis (1975), with the help of Seward, traced 73 women and 25 men who had been given the diagnosis of hysteria at the Maudsley
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Hospital over a five-year period. The follow-up ranged from 7 to 12 years. Seven of the women had died, three from independent conditions, three from a probable affection of the central nervous system, and one by suicide. Of the rest, 40 were well and working and free from disability or troublesome symptoms. A third of the remainder were consistently better than at the time of the original admission, though still troubled, a fifth were worse and the rest were little changed. Among those who had not recovered, eight had a depressive syndrome, sufficiently accounted for by their circumstances and showing a strong tincture of hypochondriasis. In none did the retrospective diagnosis of schizophrenia seem to be justified. In the male group, 14 were well and working, two were improved, four were little changed and five were worse. Two of the latter were in mental hospital with diagnoses of schizophrenia and another, who had had a severe fall, was evidently in a state of dementia. Considering the fact that the Maudsley Hospital tends to receive patients who are difficult to diagnose or therapeutically intractable, these outcomes suggest an impressively high success rate for patients diagnosed as having hysteria. Hafeiz (1980), working in a general hospital in the Sudan, treated 61 of 80 patients who had been seen by himself and the other psychiatrist in their unit over 1975–78. Treatment employed various forms of suggestion. All symptoms were removed and only 12 patients had relapsed after 12 months. Symptom substitution was minimal. The prognosis was related to the duration of illness before treatment. Chandrasekaran et al (1994) reported that in India hysterical neurosis is still one of the commonest mental disorders. In a five-year follow-up study of 38 women who also satisfied ICD–10 criteria for dissociative (conversion) disorder (World Health Organization, 1992a) they found that 63% of the patients remained totally asymptomatic. Among the 14 patients regarded as having hysterical personality only six (47%) had recovered. In all cases the setting and environment of the individual patient will play an important part in determining outcome. For individual symptoms an adequate solution to the provoking cause may be enough to provide a satisfactory long-term result. In an undetermined proportion of patients, more profound resolution of conflicts is necessary because fresh symptoms arise or the life situation is seen to be provoking unhappiness. These patients merge into those with intractable personality disorders and perhaps multiple symptoms. The prognosis of that group defined as suffering from Briquet syndrome is very poor. A universally applicable figure for prognosis is scarcely feasible. Where a condition ranges diversely from brief individual symptoms
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to multiple, long-standing complaints, it must be the case that a continuum of prognoses will exist. But it is possible to summarise the situation in adults simply by saying that acute individual symptoms will nearly all clear up relatively promptly, while chronic problems tend to remain chronic. The treatments of hysteria have long been recognised as impressive in their frequent striking successes, their great diversity, and their recurring failure in some patients. Hysteria has served as the starting point for the study of the placebo response. Yet the patient will respond only when ready to do so. This does not mean that placebo measures should not be used, only that they should be undertaken with due awareness of this point. They are appropriate because patients often need a face-saving excuse for recovery, and because anyone is entitled to feel better in response to interest, sympathy and encouragement, particularly if lonely. On close consideration we may observe that occasional or repeated reinforcement, which the intervention of a father or mother figure may give, can enable a dependent individual, whose personality is not going to be changed, to function better, nevertheless, in life and social relationships. There is also a place for more exploratory therapy. While psychoanalysis is no longer required or recommended for the vast majority of patients, it may sometimes be helpful. It will be more usual for ‘brief psychotherapy’ (Malan, 1963) and further interviews to be arranged, ad hoc, according to the needs of the case. Narco-analysis or hypnosis may have a place in acute cases where it is necessary to abolish symptoms, such as mutism or paralysis, before further psychological treatment can be pursued. Narco-analysis is not helpful in chronic cases, although hypnosis sometimes may be. Some of the best results have been obtained with behavioural techniques in which the patient is placed in a ‘double bind’ by being told that his or her symptoms may originally have been organic but were followed by a maladaptive response which actually continues to make the patient worse. If the original symptoms were organic the maladaptive response will be removable by treatment. If not, it has to be regarded as so ingrained that it will be incurable. Thus a failure to recover will be evidence of the non-organic nature of the problem (Kräupl-Taylor, 1969; Neeleman & Mann, 1993; Teasell & Shapiro, 1993). This approach requires the patient to be somewhat misled, but it has been found to be very powerful therapeutically in some intractable cases. It should be emphasised that symptom substitution is not a necessary or even frequent consequence of symptom removal. Carter (1949) showed that symptoms could be removed by
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suggestion in many patients without such problems developing. Nevertheless, symptom removal should normally be undertaken with safeguards. There will always be a few patients in whom symptom removal will disclose a conflict which gives rise to the risk of impulsive action, especially suicide. The situation can be adequately handled, so long as due care is taken to maintain contact and to ensure that hospital admission is available if required. In their concern with Briquet syndrome, members of the St Louis School of Psychiatry (Scallett et al, 1976) have reviewed some 23 reports on the management of ‘chronic hysteria’ or chronic nervous illness. They note that their own work, as well as the explicit findings or inferences from many of these reports, indicates that specialised methods of treatment such as intensive psychotherapy, electroconvulsive therapy or behaviour therapy are no better than each other. Sixty-two per cent of out-patients from all sources and 65% of in-patients improved, although in many instances it is by no means clear how long the improvement lasted. They conclude that the best policy is to use low doses of anxiolytic drugs, reassurance, suggestion and regular periods of relaxation. This is clearly good advice for Briquet syndrome, and applies to many patients with monosymptomatic hysteria, at least as far as the avoidance of extreme measures is concerned. However, where specific conflict can be recognised, as in many monosymptomatic cases, it would be foolish to neglect the possibility at least of brief psychotherapy and management of the situation with regard to personal relationships. It would also be unduly dogmatic to refuse the possibility of a behavioural approach in patients to whom the above does not apply and for whom some retraining in their attitudes to the use of a part of the body could be of specific value. While all treatment may seem to be equally effective, it is worth reflecting that the more powerful the procedure for selecting patients becomes, the better they will be allocated to relevant treatment and perhaps the more likely it is that appropriate, but different, treatments will have an increased success rate because each patient has been given what is suitable for her or his needs. We should also recognise that the solutions to problems which give rise to hysterical symptoms need not be medical and can be very varied. Conversion and strong attachment to religious models or group practices – from evangelism to football teams – provide a greater or lesser degree of libidinal attachment and catharsis for most of us. One danger which deserves a mention is that of unwise group involvement. Hysterical personalities are relatively liable to
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follow new cults, and if these involve physical or social upheavals such as the use of illicit drugs, participation in witchcraft, unorthodox groups, and so forth, there is a risk of causing the patient other troubles.
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16 Epidemic or communicable hysteria
The last major special case of hysteria which we need to examine is that of mass outbreaks of unusual behaviour, and the epidemic spread of somatic complaints without any important organic basis. These patterns are usually known as mass or epidemic hysteria, and have also been called mass psychogenic illness. The work of J. F. Hecker (Appendix D) presents an outstanding description of many instances of mass hysteria. The extracts show the widespread communication of many sorts of hysterical behaviour, including prolonged dancing, paroxysmal and other movements, and fits. Hecker showed that all classes of society and all ages could be affected, but children and younger people were more often influenced than others. He attributed the occurrence of the epidemics to disturbed social conditions, seeing them as the aftermath of plague, war, famine and civil disturbance.
Cargo cults The cargo cults of Melanesia provide a modern example of primitive, widely diffused, anomalous behaviour. In these cults islanders abandon their normal activities because of a prophecy that a ship, or sometimes an aeroplane, will arrive laden with many welcome goods, such as building materials, axes, food, tobacco, firearms and cars. The ship is expected to be manned by the benevolent spirits of ancestors. The prophecy is usually announced by a leader who acquires a following, and the people make preparations to deal with the expected changes. They construct wharves, airstrips or helipads in readiness for the 231
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ancestral spirits, who will bring in the highly valued cargo (Burton-Bradley, 1973, 1975). Traditional customs, beliefs and practices may be rejected, new clothing adopted and new systems of law and ethics come into being. Valid currency is destroyed, food gardens are neglected and livestock killed on the theory that they will no longer be needed. Burton-Bradley (1973) reviewed the general literature, which is considerable, and the psychiatric aspects, noting the occurrence of psychological contagion and mass hysteria. Dreams and hallucinations are prominent in patients in whom cargo thinking is pronounced. Cult leaders may display a variety of psychopathological disturbances; grandiose paranoid reactions may occur and even human sacrifice (Burton-Bradley, 1972). Most authors concerned with the topic have been interested in group characteristics and social organisation, but they have also briefly reported shaking fits, compulsive twitchings, trances, hysteria, bizarre behaviour, destructiveness, and hallucinations. Detailed discussion of the social and anthropological aspects is not relevant here. It is easy to see the changes as a response, which is quite often maladaptive, to social upheavals, and to the disturbing impact of Western culture, although Burton-Bradley (1975) also points out that cargo cult activities have been reported under different descriptions since the late 19th century, and considers it highly likely that they have existed in Papau New Guinea from time immemorial, since the circumstances giving rise to them are not of recent origin. Indeed, Inglis (1957) argued that if there is a single element common to all cults it is a psychological one, and that a similarity of mental states is necessary for similar external manifestations. This is particularly so in the case of the leaders who are unusual men, either more ambitious and more intelligent than the others or, sometimes, mentally unbalanced.
Widespread patterns Calmeil (1845) described numerous epidemics of hysteria in convents and elsewhere in the 16th to 18th centuries. In his descriptions overt hysterical phenomena were very common but were often found to complicate hallucinations and delusions (e.g. Vol. 1, p. 86). As Sirois (1974) notes, he also recognised a possible contribution from feeding (Vol. 1, p. 255), which might have been ergotism, sexual and self-damaging aspects (Vol. 1, p. 157; Vol. 2, pp. 9, 74).
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One of the most notable 17th-century incidents occurred at Loudun, and was of particular interest to the school of Charcot (Legué & de la Tourette, 1886), which was keen to secularise the understanding of hysteria (Goldstein, 1987). Later, Huxley (1952) also described these events in detail. Constans (1863) reported an epidemic of “hystero-demonopathy” occurring as late as 1861 in a remote and poor part of the Haute-Savoie, which he attributed to poor physical and social circumstances. Evidence of mass hysteria persists even in more settled times and places than those described by Hecker (1844), found in Melanesia, or evident in the last century. Schuler & Parenton (1943) pointed out that in the United States the index catalogue of the library of the Surgeon General’s office contained roughly 100 titles on the topic, but that descriptions were rare from 1900 to the time of their paper, which recorded an epidemic in 1939 in a girls’ high school in Louisiana. However, a number of British and American examples have been described since then (Moss & McEvedy, 1966; McEvedy et al, 1966; Lyons & Potter, 1970; Benaim et al, 1973; Adomakoh, 1973; Levine et al, 1974; Polk, 1974). Levine et al (1974) list 16 English-language reports, not including Benaim et al (1973), Adomakoh, Polk, Stahl & Lebedun (1974), Taylor & Hunter (1958), Sirois (1974, 1975), Wong et al (1982), Tam et al (1982) and Dhadphale & Shaikh (1983). Sirois (1974) gives an excellent survey of 70 reports which he was able to obtain out of 78 which appeared in the world literature from 1872 to 1972. Adomakoh reported an epidemic from Ghana, and Sirois two epidemics in schools in Quebec. In these last reports all the affected were school children, mostly girls, but attacks have also been described in a more varied age group in East Africa (Kagwa, 1964), in a psychiatric hospital ward (Taylor & Hunter, 1958), among factory workers (Kerckhoff & Back, 1968; Stahl & Lebedun, 1974) and in nurses and other health personnel (McEvedy & Beard, 1970a,b). Phoon (1982) described six outbreaks in workers in Singapore. Colligan & Murphy (1982) and Schmitt & Fitzgerald (1982) have examined eight examples of mass psychogenic illness in the United States which were investigated by the United States National Institute for Occupational Safety and Health. Even epidemics of male genital shrinkage, or koro, have been described in Thailand (Harrington, 1982) and Assam (Dutta et al, 1982). In Canada, Yassi et al (1989) also reported an epidemic of “shocks” in telephone operators which spread from initial symptoms in three operators, following power failures, to a total of 55 operators, helped by alarming headlines and leading to a costly and lengthy investigation. The authors say that this result
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underlines the danger in regarding collective stress reaction as a diagnosis of exclusion. Bartholomew (1990) offers another perspective on mass hysteria and wishes to reject the term as an invention of Western psychiatry. He takes the view that “what constitutes ‘the’ correct social order is a function of a researcher’s historical socio-cultural and/or scientific milieu,” and sees the practice of observing socially shared psychopathology in epidemic illness as characteristic of “objectivist practitioners” who categorise a variety of culture-specific behaviour relative to the values and norms of their own culture, or personal beliefs, or the standards of their scientific cultural milieu, rather that appraising it in terms of the society in which it occurs. This ignores the substantial evidence of individual psychopathology which is revealed in many of the reports, the fact that the concept was first presented in Western society about members of Western societies, and denies that events such as the Melanesian cargo cults are maladaptive. He offers in place of mass hysteria the phrase “collective exaggerated emotions”, which seems unsatisfactory for several reasons, including the fact that sometimes the emotions are not exaggerated as such (although the behaviour may be excessive), and suggests that a relativist position to medical diagnosis is necessary. Bartholomew (1994) goes further and argues that dancing manias, tarantism and demonopathy seen in Europe in the Middle Ages have been mislabelled with terms like mass psychogenic illness. The participants may often be: “normal rational people who possess unfamiliar conduct codes, world views and political agendas that differ significantly ... from those of western trained investigators who often judge these illness behaviours independent of their local context and meanings.”
Perhaps we should see them as “crazes” or cults and aberrant behaviour rather than as illness. However, a relativist position in medical diagnosis may still – and perhaps readily – accept as illness or disorder certain disturbances which are related to social causes, particularly when they take a somatic form. Conventional Western psychiatry has been very willing to recognise that people in trouble will express themselves very differently according to their individual socioeconomic and political circumstances and their culture patterns. It still seems reasonable to me to classify the responses of groups which have a dissociative element as mass hysteria, emphasising that not all members of the same society take part and that people in trouble essentially find ways of expressing their dilemmas in
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concert in ways which are shaped by the phenomena of their time and place. In the epidemics described, a number of the symptoms, which include hyperventilation, could be related to anxiety, but the pattern of complaints frequently involves grouped psychological symptoms which are not based on physiological disturbance. Schuler & Parenton (1943) described convulsive jerks. In the report by Levine et al (1974) there were headaches, sore throats, abdominal pains, sore or burning eyes, arthralgia, shortness of breath, numbness, fainting, nausea, vomiting and diarrhoea without any physical cause. Lyons & Potter (1970) found complaints of fainting, nausea and abdominal pain, headache, dizziness and weakness in their patients. Over-breathing, dizziness, fainting, headache, shivering, pins and needles, nausea, pain in the back or abdomen, hot feelings and general weakness affected the majority of the patients of Moss & McEvedy (1966). Fainting, sometimes with convulsive movements, appeared in the cases of Benaim et al (1973). A suspicion of food-poisoning was common and careful steps had to be taken to disprove it in several instances (e.g. Moss & McEvedy, Lyons & Potter, Levine et al). The factory workers believed in a ‘June bug’ (Kerckhoff & Back) or a ‘mystery gas’ (Stahl & Lebedun). It hardly needs an acute observer to point out that whereas sufferers from medieval epidemics elaborated the suspicious beliefs of their time, the schoolgirls and factory workers of an age which was familiar with the scientific notions of infectious illness evolved some of their symptoms in the light of that theme. Even so, the medieval addicts of the tarantella have a still closer parallel in adolescents at pop concerts shrieking, jerking and raving to the beat of their stars. Those who recorded school and other epidemics have regularly remarked on certain characteristic features. There is often an atmosphere of constraint or stress in the institution, or a number of dissatisfied individuals, or an occasion of some note when the epidemic arises (Schuler & Parenton, Moss & McEvedy, Benaim et al, Kagwa, Adomakoh, Kerckhoff & Back, Stahl & Lebedun). Schuler & Parenton pointed out that their epidemic began with a girl of high status in her peer group who was in a state of some unhappiness. Benaim et al described a possible epidemiogenic personality: a girl, also of high status, with a formidable background of emotional disturbance. Most authors anticipate that the epidemic will spread from persons of higher status to those of lower status and will be transmitted more readily within close-knit groups. Kerckhoff & Back considered the theoretical aspects extensively and argued that the probability of acceptance of a social belief
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or behavioural innovation is proportional to the closeness of relationships with those who believe already. Acceptances increase proportionally to the number known to accept the belief, increasing the prestige of those who have accepted it, to the extent to which it becomes consistent with existing, culturally sanctioned beliefs, and serves the needs of the person. Stahl & Lebedun found that the people most dissatisfied with their bad work conditions had the most severe symptoms and reported having friends who also experienced more severe symptoms. Accordingly, they emphasise the importance of sociological variables governing the spread of symptoms. In this respect they state one commonly accepted truism, while ignoring the equal truisms that personality factors and emotional adjustment are relevant. From a review of industrial episodes, Colligan & Murphy (1982) establish that certain conditions recur as potential precipitating factors. These include sociodemographic characteristics (e.g. sex), nature of the work (e.g. highly repetitive, routine, boring jobs), uncomfortable physical environment (e.g. noisy, temperature variations, dust/odours in the air), and psychological stressors (e.g. high work pressure, poor labour–management relations). In their survey the most powerful predictors of an effect were not individual or personality factors but negative reactions to the physical and social environment at work. In social psychological studies of individuals, Pennebaker (1982b) demonstrated that internal sensations are subject to attention, schemes which guide attention and expectation, and selective search. Social influences which favour the reporting of particular internal sensations can be expected to promote the increased presentation of such symptoms by groups. Wessely (1987) divided mass hysteria into two syndromes. One form consists of episodes of acute anxiety, occurring mainly in school children. Prior tension is absent and rapid spread is brought about by visual contact. Treatment consists of separating the participants and the attacks end quickly. The second form, “mass motor hysteria”, consists in abnormalities of motor behaviour. It occurs in any age group and prior tension is present. Initial cases can be identified and the spread is gradual. Treatment should be directed towards the underlying stressors, but the outbreak may be prolonged. In mass anxiety hysteria, the abnormality is confined to group interaction; in mass motor hysteria, abnormal personalities and environments are implicated. This distinction is original and impressive. I have some doubts about the criterion of absent prior stress, which in any case is probably the most difficult item to determine with reliability,
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but hope that future reports of episodes will evaluate this very promising differentiation between patterns of syndromes. Moss & McEvedy developed a valuable scientific approach. They recognised three meanings of the word hysterical. “To the layman it means an exaggerated emotional display; to the psychiatrist it means personality distinguished by such displays, by failure in social and sexual relationships and various more morbid traits; physicians in general and neurologists in particular apply the term to long-standing dysfunctions for which they can find no organic cause, conversion hysteria being the textbook example. It is generally accepted that laymen and psychiatrists are talking about the same class of behaviour the difference being one of degree.”
These are certainly not all the meanings of the word hysterical. It may also be defined neurologically or psychiatrically as the production of symptoms by an idea (Chapter 2), as the type of symptom which belongs to the group in Briquet syndrome (Chapter 12), and as the behaviour associated with the hysterical personality (Chapter 22). Nevertheless, Moss & McEvedy are broadly correct in stating that laymen and psychiatrists are talking about the same class of behaviour. Presuming that the tendency to hysterical behaviour is normally distributed and noting the view that “the hysterical constitution” (I would prefer ‘liability to hysterical behaviour’) is more common in females, they make the following predictions, which were tested in the population which they had studied: (a) “Hysterical reactivity, being to a considerable extent constitutionally determined, the same population should be affected on each occasion.” There were four distinct days on which larger numbers of girls were affected. There was an extremely strong tendency for girls affected on the first day to be affected on the other two days. (b) “The contagion in an hysterical epidemic being behavioral, the epidemic should disseminate more rapidly when the social group is unified than when it is sub-divided.” It turned out that the number of new cases, as predicted, was higher in break periods than in lesson time and the majority of cases occurred in places of social contact such as the hall and playground and the corridors, in contrast to the classroom. (c) “The younger being more susceptible, the incidence of new cases can be expected to move to the lower end of the school as the epidemic progresses.” As predicted, the
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epidemic showed a pattern of increase among the younger students subsequent to the older ones. (d) On Eysenck’s hypothesis that extroversion and neuroticism should predispose to hysterical symptoms, the affected girls should be rated high on these characteristics. This was found consistently in students examined. Those who had shown evidence of behavioural morbidity in the past would be more likely to be involved. It was predicted that any girl attending a child guidance clinic would have a higher than average chance of being involved and this was confirmed for the three girls to whom it was relevant. Between them they had six admissions because of the epidemic, where the average of the school was 0.12. On the basis of these predictions being so readily confirmed, Moss & McEvedy (1966) concluded that the illness which they had studied could be regarded as psychological in origin. Their claims appear well justified, although the attempt must inevitably be made to exclude organic illness as well. Such an attempt may not wholly clinch the decision and, in that event, if there is doubt about the possible cause of any epidemic, the predictions which Moss & McEvedy offer provide a sound basis on which to establish the psychological nature of an outbreak. Prompt action which discourages the spread of the alarm will in effect observe principles drawn from their predictions and from past experience. Persons of high prestige such as schoolteachers and doctors can effectively allay anxiety (Lyons & Potter, 1970). Press publicity can be harmful, but publication of the view that the disorder is psychological can be helpful (Adomakoh, 1973). Closure of the school or separation of those affected from the rest may be required, and psychological treatment of the more epidemiogenic patients may also be necessary. One preventive measure from this group may also be relevant to a much more common situation where undesirable behaviour can spread to a number of individuals. Violence among football spectators is widely thought to result from the examples which they sometimes see on the playing field. If players of high prestige behave well, so may their supporters. Good manners do follow from good examples, and this argument may be extended to violence on the television screen and in the communications media.
Induction of illness An example from the cinema shows well how susceptible individuals may indeed develop bizarre hysterical symptoms.
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Ingall (1974) reported six psychiatric casualties seen in Providence, Rhode Island, after the showing of the film The Exorcist. Bozzuto (1975) reported a further four in Cincinnati and referred to press reports of numerous cases of traumatic neurosis from the same cause. The belief of possession by demons affected all of Ingall’s patients. Two of the three patients whom Ingall describes in detail were considered psychotic and one had an acute hysterical neurosis. Culturally sanctioned bizarre behaviour may also explain the ‘jumpers’ of Maine (Kunkle, 1966). According to Kunkle, ‘jumping’ was first described by Beard in 1878, but it has, apparently, been part of the folklore of Maine for many generations. Kunkle described the basic phenomenon as an excessive startle response. Associated aggressive actions may occur, a celebrated example being the man who started violently at the whistle of the passing train each night and repeatedly struck his wife. Most ‘jumpers’ are male factory employees or other semi-skilled workers. Automatic obedience to sudden command has been noted on some occasions, but echolalia only very rarely. Various racial backgrounds are represented and neurological examinations were unremarkable. Kunkle considers that there is much to suggest that the ‘jumper’ may be acting out or otherwise releasing considerable concealed hostility, especially when his response includes threatening gestures or blows. While excessive startle responses have been well documented in various diseases, particularly chronic encephalopathies, and in some degenerative brain disorders, such as Jakob–Creutzfeld disease, these patients show no evidence of significant degenerative disease. The problem remains a mystery, although it may have some affinities with the syndrome of Gilles de la Tourette, in which case it might be supposed to be a genetic anomaly. The lack of evidence of physical disease inclines me to believe that it is more likely to be a cultural phenomenon, but no firm conclusion can be drawn. A much more intensive pattern of induced beliefs than that found in the usual phenomena of mass hysteria occurs in folie imposée or folie communiquée. These terms, introduced in connection with folie à deux, folie à trois, and so on, have been used to describe the situation in which, usually, one dominant individual imposes or communicates false beliefs to others – typically a sister or other family member living an isolated life in conjunction with the first person. This effect was recognised by Digby (1658). Baillarger (1890) claims to have described four patients in 1860, but Lasègue & Falret (1877) provide the key description. Gralnick (1942) reviewed the English literature.
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It is well recognised that in small family groups one member who is dominant may cause the others to accept a delusional system of ideas. Affected family groups of various sizes have been described. Evans & Merskey (1972) reported one family comprising two parents and two daughters, but folie à douze (Waltzer, 1963) has been attained and small religious groups have been collectively (probably wrongly) labelled as mad (Bender & Yarrell, 1938). There is little proof of psychosis in such situations and much more suggestion of group influences comparable to epidemic hysteria, but restricted in their orbit. Hartmann (1931; Hartmann & Stengel, 1932) found that a certain paranoid type tended to impose delusions on overdependent relatives, that guilt feelings towards the sick person on the part of the relatives made them liable to sacrifice reality for him and identify with him (or her); and that the group was usually isolated and formed a group within a hostile society. In Hartmann & Stengel’s cases the victims of induction were usually over-dependent on the originator of the delusion and felt that they had let him or her down, for example where a woman had the delusion, the man who accepted it might be impotent or a failure in other respects. Ilechukwu (1992) gives a good account of four families where affective illnesses in the index cases led to somatic complaints which were accepted also by the spouses (and also a child in one family). The transmission of a belief in illness, under conditions of stress, is very clear in these patients. All these phenomena and the responses of children in the affected families indicate the importance of the dependency relationship. The situation has been called folie partagée (Evans & Merskey, 1972) to emphasise the occurrence of shared illness, shared in greater or lesser degree. This of course replicates the pattern of epidemic hysteria, and Lehmann (1975) notes that the boundary between induced mental disorders and collective illnesses is not well defined. Folie partagée or folie communiquée also conforms to several of the criteria of Kerckhoff & Back, and Moss & McEvedy. It often takes place on the basis of delusions of infestation (Wilson & Miller, 1946; Bers & Conrad, 1954; Liebaldt & Klages, 1961; Evans & Merskey, 1972). This is frequently a highly credible delusion (Giacardy, 1923). Ideas of infection such as the ‘June bug’ are frequent in the modern epidemics described. In the family group the role of the dominant family member corresponds to that of the emotionally disturbed influential individuals who start off any epidemic from cargo cults to schoolroom attacks. All the groups tend to be under
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stress, the religious groups perhaps do not enlarge because the ideas are not generally acceptable, and separation of affected individuals is therapeutic for the dependent ones. Folie à deux is the microcosm of epidemic hysteria. Such group phenomena can also be found in families which have not proceeded to the level of psychosis. Muluka et al (1985) described a family of six children among whom the first four developed fits under the influence of a dominant father and were joined in this by one cousin who was close to one of them. Family treatment lead to prompt recovery. Apart from the psychological, psychiatric and sociological approaches to mass hysteria which are evident in the literature, Penrose (1952) developed an interesting arithmetical approach. He argued that certain formal consequences follow from the number of persons comprising a group. In a small group of people a fixed opinion held by a few of its members may easily alter the attitude of the whole group. If most of the members are indifferent, or randomly divided in their opinion, it is comparatively easy for a surprisingly small set of resolute members to control any decision. “Thus in a group of three, one person who knows his mind will obtain a majority vote in three times out of four provided that the other two members vote at random. About the same degree of control can be exercised by a bloc [sic] vote of 3 over an indifferent population of 20. The remarkable fact is that, although the power of an individual or a bloc vote becomes gradually less, as the group becomes larger, this power only decreases as the square root of the number of indifferent voters.... For a given degree of control, the number n R in the bloc, equals K/Ön 1, where n 1 is the number of indifferent voters and K is a constant quantity. When n R = 1/Ön 1, the resolute group carries 84.1 per cent of all decisions. A bloc three times this size (K = 3), will only be in the minority once in a thousand divisions.”
Penrose gives an elegant further discussion of the mathematical formulae which affect group decisions. For our immediate purpose the relevant point is the potential for influence exercised by a small number of individuals whose behaviour is firmly decided. The theoretical significance of mass or epidemic hysteria can now be assessed. First, it provides many repeated examples of group effects under the influence of an idea which produces either physical or behavioural responses, or both. Logically this is on a par with the individual hysterical symptom. The mechanics of both spread and resolution are partly determined by group
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characteristics, such as the effect of a small decided group in influencing a larger one, spread through close contact, abatement by isolation, the presence of appropriate culturally sanctioned beliefs, convenient notions of illness, and so on. The dynamics of the event are related to emotional disturbance in some individuals, emotionally charged events affecting many or all of them, and dependency to a greater or lesser degree in numerous individuals among those affected.
Cultural influences The assumption that cultural influences affect the presentation of hysterical symptoms has already been taken for granted in a number of places. They will be discussed again in Chapter 23, on psychosis, where a number of the more extreme presentations of epidemic psychosis, which are thought to be hysterical, are regularly related to culture patterns. Here, we may note not only that the frequency of presentation of hysterical symptoms may be culturally determined but also that some patterns which are not necessarily psychotic – inasmuch as the patient does not appear to have lost touch otherwise with reality – are strongly linked to particular group beliefs. One of the most notable examples of this is the belief in the shrinking of the penis. This syndrome, most often known by the Malay word koro, has usually been attributed to Chinese subjects (e.g. Gwee, 1968). The disorder is said to have been first described in the Yellow Emperor’s Book of Medicine in 3000 BCE. Its cardinal manifestations are a belief in the retraction of the penis and impending death from shrinkage of the genitalia into the abdomen; and a panic syndrome with fear, a feeling of collapse, palpitation, sweating, breathlessness and bodily spasms (Ngui, 1969). An epidemic of 450 cases was reported in Singapore in 1970. Ninety-five per cent were young Chinese men. It became a common sight to see men appearing at admission rooms, with chopsticks and other mechanical aids tied to their sex organs to prevent retraction (Mun, 1968; Ngui, 1969). Tseng et al (1988, 1992) describe two recent epidemics in China and present evidence relating them, and other outbreaks, to periods of social crisis. The subjects affected were shown to be characterised by low intellectual endowment, and strong adherence to folk beliefs in koro, as well as increased anxiety. Tseng and his colleagues favour the view of Mo et al (1987) that koro epidemics reflect the occurrence of panic states or anxiety
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in vulnerable subjects with appropriate cultural beliefs, and do not see koro as a dissociative disorder. Occasional cases are based on schizophrenia (e.g. Devan, 1987). Berrios & Morley (1984) described a koro-like symptom in a non-Chinese subject and reviewed its occurrence in the nonChinese. As already mentioned, epidemics have been reported in Thailand and Assam. Other individual cases have been described in an Israeli Jew of Iraqi origin (Modai et al, 1986) and an American man (Kendall & Jenkins, 1987) and also secondary to a tumour of the corpus callosum (Kumar & Moloney, 1988). The last authors point out that 27 cases had been reported in non-Chinese subjects up to that date, without taking account of the Thailand and Assamese instances. An additional case was described in a Zulu (Holden, 1987). This case was complicated by substantial physical illness (alcoholic hepatitis, avitaminosis and urinary tract infection) and Holden notes, as did Berrios & Morley, that most non-Chinese cases appear to be partial or incomplete syndromes. Isolated individual cases are also more likely to be related to psychotic illness (e.g. Devan, 1987; Westermeyer, 1989). Turnier & Chouinard (1990) described an occidental patient with depression and koro which responded to trimipramine. They suggest that in the East the syndrome is primarily sociocultural, but that in the West it arises most often on the basis of cerebral pathology or depression. Another example of a culturally adopted physical symptom is ‘brain fag’ in East Africa, where a loss of function appears to follow from specific stress and to solve a conflict. These phenomena are well seen in the case described by Harris (1981). Versions of hysterical illness which are culturally determined may be as varied in individual cases as in those related to epidemic occurrences. Seltzer (1983) described three cases of spirit possession among Inuit (Eskimo) subjects in Canada. All of them faced considerable problems of social adjustment and depression. Griffith et al (1984) conducted individual interviews with 20 members of an independent urban black church who frequently attended services at which they experienced “An ineffable and explicitly religious experience”. It might be appropriate to describe the effects as dissociative but not as disorders, seeing them as adaptive human responses within an accepted cultural context. Another variant of a culture-bound sex neurosis is reported in dhat syndrome (Chadda & Ahuja, 1990), where the patient believes that dhat, a whitish discharge which is semen, is being
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passed in the urine, even in the absence of objective evidence of such discharge. The diagnoses which can underlie this complaint are thought to include neurotic depression, anxiety, neurosis, hypochondriacal neurosis and psychogenic impotence. Seven patients out of 52 received a diagnosis of pure dhat syndrome, which presumably is a stress reaction of a conversion type. Of course, not all culturally related expressions of feeling should be regarded as hysterical. Whakama is a New Zealand Maori response associated with feelings of shame, self-abasement, feeling inferior, inadequate and with self-doubt, shyness, excessive modesty and withdrawal. Sachdev (1990) describes it as an important construct in order to understand the interaction of the Maori with each other and with the Caucasian New Zealander, the behaviour of Maori in cross-cultural settings, and the clinical presentations of some Maori patients. But it does not appear to contain any elements either of dissociation or somatic complaints. One particular type of epidemic affecting medical personnel invites consideration. In the 1950s an illness known as epidemic myalgic encephalomyelitis appeared in various parts of the world (British Medical Journal, 1957). Acheson (1959) reviewed 14 such epidemics and Daikos et al (1959) described a further episode. Henderson & Shelokov (1959), Graybill et al (1972) and Dillon et al (1974) specifically entitled their reports of three similar episodes “Epidemic neuromyasthenia”. In recent years this condition has often been assumed to be a manifestation of much the same phenomena as chronic fatigue syndrome (e.g. Wessely & Powell, 1989; Komaroff, 1993; Manu et al, 1993; Shorter, 1993). It is also commonly agreed that the patterns of illness which occur under the title of chronic fatigue syndrome are varied and heterogeneous, both in type and origin. Many are more endemic than epidemic. It is logical to consider myalgic encephalomyelitis in connection with chronic fatigue and the discussion of these two topics follows in the next chapter.
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17 Chronic fatigue syndromes
With perhaps only a tiny number of exceptions, fatigue, like pain, is a universal human experience. Hannay (1979) found that an increase in feeling tired, or run down, or both in the previous two weeks was reported by 22.7% of 1334 people of all ages seen in a community survey in Glasgow, Scotland. Kroenke et al (1988) surveyed 1159 patients in two adult primary care clinics in San Antonio, Texas, and found that a “major problem” of fatigue, present for more than 30 days, was reported by 28% of women and 19% of men (24% overall). Laboratory testing was not useful in detecting unsuspected medical conditions in these patients or in determining the cause, but depression or somatic anxiety were suggested by psychometric instruments in 80% of 82 fatigued patients and in 12% of controls. This association of fatigue with depression and anxiety is no more than anticipated, although the absolute figure should be interpreted with caution because of the possibility that somatic complaints – including the report of fatigue itself – contributed to the scores on some of the instruments used. In a survey of 686 patients attending for primary care, Cathébras et al (1982) found that only 17.2% of their patients with fatigue had a current psychiatric diagnosis on the Diagnostic Interview Schedule (DIS) compared with 8.8% of controls, while 45.2% received a lifetime diagnosis of depression or anxiety disorder compared with 28.2% of controls. They contrasted their findings with much higher rates of lifetime psychiatric illness in patients with chronic fatigue reported from tertiary care clinics. They also found that 44% of patients followed up for one year had experienced physical illness consistent with a feeling of fatigue over that time, most often infections (12 cases), chronic obstructive pulmonary disease (7 cases), cardiovascular disease (4 cases) and 245
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complications of alcohol or drug abuse (6 cases). In addition, they observed that patients with fatigue and no depression did not differ significantly from control patients. This is a noteworthy finding, since even if depression or other psychological problems are found, patients cannot always be assumed to have fatigue for psychological reasons. It goes without saying that when depression or another psychiatric diagnosis cannot be made, a psychological interpretation is still more dubious. Hagnell et al (1993) provided the only report of a complete community survey of tiredness with a 25-year follow-up. Tiredness was recorded if it was present as a complaint for more than one month, and tiredness as the main phenomenon was separated from tiredness occurring with anxiety or depression or with gastric symptoms. Of 91 men and 114 women who started out with an episode of tiredness, two-thirds of the men (63) and half of the women (58) did not relapse into any mental illness in the 25 years of follow-up. Those who did have an initial accompanying psychiatric complaint such as depression or anxiety were more likely to relapse or develop psychiatric illness. These findings match well those of Cathébras et al, that patients with no psychological signs are more like other patients in general. Hagnell et al imply that their patients were not investigated somatically, but despite this their work, like that of Cathébras, suggests that there is an important population in the community with chronic fatigue to which psychological interpretations will not apply.
Benign myalgic encephalopathy As mentioned at the end of Chapter 16, myalgic encephalomyelitis and chronic fatigue syndrome have been identified as similar, if not identical, and yet they have also been called heterogeneous. There is always uncertainty when such apparently confusing ideas are presented, but it is safe to accept that the different patterns which are placed in the one envelope will overlap with each other. There is reason to suppose that the earlier version of ‘benign myalgic encephalomyelitis’ had some features which were ‘organic’, at least in a significant number of those affected. With regard to the best-known English epidemic (British Medical Journal, 1957) symptoms and signs were noted of mild pyrexia, enlarged superficial lymph nodes, malaise and headache out of proportion to the moderate fever, sore throat, gastrointestinal disturbance, fluctuating paresis with hypotonia, muscle tenderness, severe pain on movement, and emotional instability. Convincing
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evidence of reflex disturbance or organic electromyographic changes was not obtained, the cerebrospinal fluid was normal, and the signs varied markedly from case to case in severity and in the evolution of the disease. McEvedy & Beard (1970a) suggest that this report contained little evidence of organic disease and that epidemic hysteria was a much more likely hypothesis. To support their view they cited the high attack rate among women, compared with men; the intensity of’ the malaise compared with the slight pyrexia; the presence of subjective features similar to those seen in a previous epidemic of hyperventilation (Moss & McEvedy, 1966), the rarity of cases where the pyrexia exceeded 100°F (40°C), and the rarity of changes in the erythrocyte sedimentation rate (ESR) and white cell counts, as well as the frequency of normal findings in other special investigations. They also noted the glove-and-stocking distribution of sensory changes. Their report presents a formidable critique of the organic view, especially since no conclusive evidence of a virus was found. In a second article, McEvedy & Beard (1970b) argued that a lot of similar epidemics reported up to 1959 could be explained as psychosocial phenomena, which might be of two types. Either they could be due to epidemic hysteria on the part of the patients, or they could be the result of altered medical perception of illness in the community. In other words, a tendency to think that such a diagnosis might be made could lead to a number of minor infections and non-infective anxiety complaints being described as benign myalgic encephalomyelitis. Acheson (1959) in fact noted that the question of hysteria had been raised in five outbreaks, and that Galpine & Brady (1957) and Ramsay (1957) had discussed the possibility with respect to their endemic cases. Most authors had agreed that some hysterical manifestations occurred in a few patients but none felt that hysteria contributed significantly to the pattern of the disease. Some of the patients described had undoubted organic illness (e.g. ocular, facial and palatal pareses). Although he did not accept it, Acheson held that a reasonable view would be to say that the majority of cases constituted a hysterical reaction to a small number of cases of infection of the nervous system. He argued that the lack of a constant relationship with poliomyelitis was a reason for discounting fear of that disease as a factor promoting hysteria, and he did not consider whether other causes for anxiety might have been present. He also discounted the view that the mental changes in the various outbursts were due to hysteria because such symptoms as emotional lability, disorders of
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consciousness, impaired memory and concentration, and depression all seemed to him more consistent with organic cerebral changes rather than with hysteria. He noted also the analogy of the psychoneurotic-like effects of encephalitis which von Economo (1929) recognised. On balance he concluded against the view that hysteria was a cause. Poskanzer (1970) strongly criticised McEvedy & Beard. Albrecht et al (1964) had found a considerable increase in creatinuria in an outbreak in New York State and Poskanzer found the epidemic was consistent with person-to-person spread. In addition, he argued that most authors rejected the notion of mass hysteria because cases varied within the same household, separate illnesses occurred at random intervals, not simultaneously, and the illness had a consistent cause and affected a variety of people and communities. None of these arguments appears to me to be very strong. Personto-person endemic spread could well occur with hysteria in disturbed communities, and individual variation in illness is the stock-in-trade of psychiatric work. Moreover, in their study of an outbreak in Punta Gorda, Poskanzer et al (1957) observed “the paucity of physical findings ... was striking”, and that there were “problems inherent in an attempt to define a non-fatal illness with a broad array of symptoms that blend into the host of psychoneurotic and minor medical complaints endemic in a community”. Among others with direct knowledge of epidemic malaise Scott (1970), a general practitioner, objected firmly to the views of McEvedy & Beard because she felt that in a local epidemic between 1964 and 1966 she saw many patients (about 370) in whom there was a regular and consistent pattern of illness; 20 cases were seriously ill and ‘hard’ evidence in some cases included hypoglycaemia, ankle clonus, extensor plantar responses and nystagmus. The ages ranged from four years to late middle age, and patients from a wide variety of occupations were affected. Wookey (1976), a physician, indicated her belief that she had suffered from myalgic encephalomyelitis and that it was not hysterical. Compston et al (1970) defended their original report from the Royal Free Hospital, observing that widespread sporadic cases had occurred independently and that the signs among their patients included fever (79%), ocular palsy (43%), facial palsy (19%) and lymphadenopathy (79%) which disappeared as the illness passed. They held that the epidemiological characteristics were at least as compatible with an infectious disease as with a psychological disorder, and this is certainly a reasonable argument. Although they recognised psychological factors in the symptoms,
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they concluded that “the large majority of cases were affected by an organic illness”. In an epidemic occurring after the publication of the paper by McEvedy & Beard, Graybill et al (1972) considered their arguments and observed that there was an excess of females among their cases, as McEvedy & Beard would have predicted. However, Graybill et al found a number of factors which contradicted the idea of a hysterical aetiology. These included the fact that the epidemic was well advanced before it was appreciated, and detection was more fortuitous than deliberate. Second, some of the affected contacts included unlikely psychiatric cases, such as very young children. Third, organic manifestations, such as encephalopathy and transverse myelopathy, were very definite in several patients. Fever, adenopathy, stomatitis and scattered laboratory abnormalities such as leucocytosis and altered liver function were found. No causal agent was isolated and they concluded that epidemic neuromyasthenia was a poorly defined syndrome rather than a specific disease, but also held that it was principally organic in aetiology. Ramsay (1986) summarised the evidence on epidemics of myalgic encephalomyelitis (ME) and had no difficulty in establishing the frequent occurrence of organic disease of this type. He further presented evidence that the Royal Free Hospital outbreak arose explosively from a nidus of infection which had been present in the population of northwest London, and that the presentation of the illness was typical. He did not disagree that there might have been “an hysterical or functional overlay ... in many cases of M.E.”. He notes the further work of Kendell (1967), who described psychiatric sequelae in two young women whose overall clinical picture was very typical of myalgic encephalomyelitis, with accompanying pathognomonic electromyographic changes. Kendell had concluded that “damage to the cerebral mechanisms underlying the control of mood and behaviour must be postulated to underlie such severe and prolonged disturbances”. Accordingly Ramsay concludes, on the basis of this and other evidence, that McEvedy & Beard were radically wrong in their principal hypothesis that the epidemic was mainly psychological. On balance, I think that, while a significant minority of patients in the Royal Free Epidemic correctly received the description ‘hysterical’, the majority did have an unusual infectious disease. Nevertheless, McEvedy & Beard have done a considerable service by promoting recognition of the part played by psychological factors in increasing both the number of persons affected and their symptoms in such epidemics.
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Chronic fatigue syndrome The original discussion of benign myalgic encephalomyelitis has been enlarged and developed with the concept of chronic fatigue syndrome formulated by Holmes et al (1988). Patients who present to special centres for treatment of chronic fatigue and those who are found in the community, perhaps a few in each family practice, with protracted disabling problems of fatigue clearly represent a very different sample from the above. It is to this latter sample that the term chronic fatigue syndrome has been given by Holmes et al as a descriptive label. The extent to which the community cases can cast light on the more severe and disabling ones is uncertain, but at least they establish that there is a group of patients with chronic fatigue in whom psychological illness is not clearly apparent and at least some of these may be more severe and may appear in the samples at special centres. Holmes et al (1988) describe how, in the 1980s, interest developed in a very similar pattern of illness to chronic fatigue which was attributed to the Epstein–Barr virus. A pattern of nonspecific symptoms was recognised, characterised by chronic or recurrent debilitating fatigue and various combinations of various other symptoms including sore throat, lymph node pain and tenderness, headache, myalgia and arthralgia. Laboratory investigations of mononucleosis failed to confirm any correlation between serum Epstein–Barr virus titre and the presence of chronic fatigue symptoms. Considering that it was premature to focus research and diagnostic efforts on Epstein–Barr virus alone, Holmes and the group at the Center for Disease Control in Atlanta, Georgia, recommended the following criteria to define a chronic fatigue syndrome: (a) the new onset of persistent or relapsing debilitating fatigue or easy fatigability in a person who has no history of similar symptoms, that does not resolve with bed rest, and that is severe enough to reduce or impair average daily activity below 50% of the patient’s premorbid activity level for at least six months (b) other clinical conditions that might produce similar symptoms must be excluded by thorough evaluation (c) six out of the 11 following symptoms or features should be identified – mild fever, sore throat, painful or swollen lymph nodes, unexplained general muscle weakness, muscle
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discomfort or myalgia, prolonged (24 hours or greater) generalised fatigue after levels of exercise that would have been easily tolerated in the patient’s premorbid state, generalised headaches (differing from headaches the patient might have had in the premorbid state), migratory arthralgia, one or more neuropsychologic complaints (such as photophobia, forgetfulness, excessive irritability, confusion, difficulty in thinking, inability to concentrate or depression), sleep disturbance, and onset over a few hours to a few days (d) two physical criteria must be documented by a physician on at least two occasions at least one month apart out of a list including low-grade fever, non-exudative pharyngitis, and palpable or tender anterior or posterior cervical or axillary lymph nodes. Australian criteria were described by Lloyd et al (1990) for epidemiological use, and a British consensus meeting (Sharpe et al, 1991) also offered similar criteria. Sharpe et al noted that patients presenting with the principal complaint of disabling fatigue of uncertain cause have received much attention in recent years. There is much disagreement, and a number of clinical syndromes have been described, all apparently referring to similar groups of patients, but different enough to preclude ready comparison of published studies. Various names have been used, including epidemic neuromyasthenia, idiopathic chronic fatigue and myalgia syndrome, benign myalgic encephalomyelitis, chronic infectious mononucleosis, Royal Free disease, post-viral fatigue syndrome, fibrositis–fibromyalgia, and chronic fatigue syndrome. Sharpe et al (1991) recognised two broad syndromes. Chronic fatigue syndrome (CFS) has fatigue as the principal symptom, is of definite onset, but is not lifelong, and is marked by severe disabling fatigue which affects physical and mental functioning and should have been present and occurring for more than 50% of the time for a minimum six months. Myalgia, mood disturbance and sleep disturbance may also be present and patients with established medical conditions known to produce fatigue should be excluded, as should patients with a current diagnosis of schizophrenia, manic–depressive illness, substance abuse, eating disorder or proven organic brain disease. Depression, anxiety and hyperventilation were not necessarily reasons for exclusion. The second syndrome, which these authors recognised as a subtype of CFS, either follows an infection or is associated with a current infection, is present for a minimum of six months after the onset of infection, and has been corroborated by laboratory
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evidence. These distinctions were endorsed by 27 prominent investigators from a variety of disciplines. The second of these two groups is the easier to confirm – if present. Where an organic diagnosis is being offered it fits with the requirement that there should be not only a set of symptoms but also some reliable physical or laboratory findings. It can be accepted that at least a minority of patients who have complaints of chronic fatigue may have such a condition. Sharpe et al (1992) reported on 200 patients who believed that they had such a syndrome and had attended an infectious-disease clinic. They observed that the short-term prognosis for recovery of function was poor but the condition improved with time. Of 177 who fulfilled inclusion criteria, 144 (81%) returned completed questionnaires; most had made a functional recovery after their initial clinic attendance. The clinical picture of chronic fatigue syndrome was described by Komaroff (1993) as always comprising very troublesome fatigue and including symptoms in the following order of importance: impaired cognition and depression (50–85%), pharyngitis (50–75%), anxiety (50–70%), post-exertional malaise, pre-menstrual worsening, stiffness/‘gelling’, visual blurring and nausea (50–60%), muscle weakness (40–70%), tachycardia and headaches (40–50%), dizziness and paraesthesias (30–50%), and substantial minorities with dry eyes, dry mouth, diarrhoea, anorexia, cough, finger swelling, night sweats, painful lymph nodes, rash, low-grade fever, myalgia and sleep disorder, in descending order of minimum frequency. In some series low-grade fevers, myalgia and sleep disorder occurred at a very high rate. In his view both physical and psychological evidence was common. Whatever the cause of CFS, patients suffering from it have reduced aerobic work capacity compared with normal subjects (Riley et al, 1990). Most cases are managed in general practice, and laboratory tests generally have a low yield and clinch the diagnosis in only 8% of patients (Sugarman & Burge, 1984). Landay et al (1991) support the view that significant immunological changes occur in some individuals with CFS. They compared a total of 147 consecutive patients (30 males, 117 females) with a normal control group and also with some patients with virallike illness and depression and a number of family members and other individuals in contact with CFS cases. They undertook extensive studies of immunological reactions and concluded that while there was no serological evidence of any aetiological association between various human viruses and CFS, evidence of immune activation was found in many cases. Lloyd et al
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(1993) felt that there was circumstantial support for the hypothesis that CFS results from a disordered immune response to infection. A number of studies have demonstrated strong psychiatric evidence in patients subject to CFS. The interpretation of that evidence has been subject to a good deal of disagreement. Hickie et al (1990) determined the psychiatric status of 48 patients, and observed that 22 had a major depressive (non-endogenous) episode during the course of their illness, while seven had a current episode of major (non-endogenous) depression. This incidence resembles the findings in patients with some other medical disorders. Only 12.5% had a premorbid history of major depression. Only one patient matched the criteria for somatisation disorder. These patients were all individuals who had been extensively evaluated within a tertiary referral service, and the authors concluded that there was no evidence in their well defined sample to support the hypothesis that CFS is a somatic presentation of an underlying psychological disorder. In particular, there was no evidence that it was a variant or expression of a depressive disorder. They thought, rather, that their patients’ current psychological symptoms were a consequence of the disorder. Manu et al (1993) conducted a prospective study of 405 patients (65% women) and found that psychiatric diagnoses explaining the chronic fatigue were identified in 74% of patients and physical disorders were diagnosed in 7%. The most common psychiatric conditions in their series were major depression (58%), panic disorder (14%), and somatisation disorder (10%). Primary sleep disorders were diagnosed in 2% and chronic infections were confirmed in 1.6%. Thirty per cent of all these patients met criteria for CFS and had a similarly high prevalence of current psychiatric disorders (78% versus 82% in the rest) but were significantly more likely to have somatisation disorder (28% versus 5%) and to attribute their illness to a viral infection (70% versus 33%). White (1989) thought that the present evidence suggested that a chronic fatigue syndrome does exist, certainly after particular infections, but that the reliability of the concept over time was uncertain. If symptoms persisted, treatable psychiatric disorders would be found in two-thirds of patients. On the basis of the available physical evidence, Coakley (1989) firmly rejected muscle fatigue as a cause. Meanwhile, a case of chronic fatigue syndrome (with negative investigations) recovered when the patient developed mania (Sharpe et al, 1991). This case suggests that in at least one instance depression was the principal reason for the complaint of fatigue.
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Moldofsky (1993) points out that various research studies have shown that the amalgam of disordered sleep physiology, chronic fatigue, diffuse myalgia and cognitive and behavioural symptoms constitutes a non-restorative sleep syndrome that may follow a febrile illness, as in CFS. Where rheumatic complaints are prominent such a constellation of disturbed sleep physiology and symptoms also characterises fibromyalgia. In other words, the fundamental finding in common in both conditions is that there is a sleep disorder of a similar type. Moldofsky suggested that the evidence supported a reciprocal relationship of the immune and sleep–wake systems. Interference either with the immune system (e.g. by a viral agent or by cytokines such as alpha-interferon or interleukin-2), or with the sleep–wake brain system (e.g. by sleep deprivation) has effects on the other system and will be accompanied by the symptoms of CFS. The syndrome of fibromyalgia shares some of the features of CFS but can be effectively distinguished from it by the criteria established by the American College of Rheumatology (Wolfe et al, 1991). These criteria include pain above and below the waist and on the right side of the body and on the left side of the body together with tenderness at not less than 11 out of 18 specified tender points. This diagnosis has high reliability and consistency (Wolfe, 1993). At one extreme, the view of Shorter (1992) that CFS is the 20thcentury equivalent of hysterical paralysis in the 19th century has aroused predictable objections from people and organisations identified with the sufferers. The evidence cited so far shows that at least some patients will have depression rather than an infectious viral condition as the basis for their complaints, and could be helpfully treated by the usual psychiatric measures for depression. Others may have a time-limited fatigue related to a viral illness. Abbey & Garfinkel (1991, 1992) propose that the largest number will have psychopathological or psychophysiological problems. This fatigue will not clear up in the usual week or two but ultimately can be expected to remit in the great majority of cases. White (1990) summarised the evidence as follows. Chronic fatigue is common and leads to considerable disability. The fatigue syndrome is characterised by both physical and psychological symptoms and may be caused by many physical illnesses and several psychiatric illnesses, but often there is no obvious single cause. Physical and psychosocial factors are often active at the same time, but will have different relative importance in different patients. This conclusion inevitably means that some patients are likely to have the syndrome as a solution to emotional problems.
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Accordingly a number may be regarded as having hysterical complaints and probably do, but they are probably a minority of all those affected. Wessely & Newham (1993) observe that the frequency of cases with CFS who fulfil Research Diagnostic Criteria or other criteria for psychiatric disorder is such that the consequences of physical disease cannot alone account for the clinical features of the syndrome. Abbey & Garfinkel (1991) as well as Ray (1991) and David (1991) all discuss the fact that affective disorder is a frequent finding in hospital samples of CFS and this association also extends to community samples. At the same time Wessely & Newham note that two authoritative reviews (Straus, 1988; Buchwald & Komaroff, 1991) have concluded that although there is evidence of some abnormalities in immunological function, acceptance of their importance has been hampered by their inconsistency, nonspecificity, and lack of relationship to clinical findings. However, they are unwilling to ignore such possible findings entirely, and observe that current studies with improved methods are in progress. In summary, this too seems to corroborate the view that the greater part of chronic fatigue syndrome which becomes persistent will not be related to physical illness and may be due to depression or other psychiatric disorders. However, it is not clear that more than a small minority have chronic fatigue syndrome on the basis of a dissociative or conversion disorder. This conclusion may well be less applicable to the cases of benign myalgic encephalomyelitis who also showed hysterical behaviour, a number of whom had symptoms on a hysterical basis. White & Lewis (1987) described two patients who developed delusional depression after infectious mononucleosis, one of whom had encephalopathy. This reminds us of the established view that occasional severe depressive illnesses may follow a variety of cerebral insults and that less severe ones are also commonly believed to occur in the immediate wake of other infectious diseases. The problems of chronic fatigue and chronic fatigue syndrome are clearly among the most complex in psychiatry and internal medicine. Even if we accept the view that we are dealing with a symptom of chronic fatigue which occurs in a variety of circumstances, both physical and psychological, we are still left with vexing problems to sort out as to the relative contribution of each factor to the causation of the disease and to its final picture. On the one hand there are patients (and some doctors) who insist that physical causes must be found, and there are others who wish to treat the situation as one in which anthropological inquiry and
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psychological evaluation demonstrate the role of symptom attribution, which depends upon the culture and circumstances of individuals. Most but not all cases among the chronic group show evidence of psychiatric illness, but even there the argument has been offered that many of the psychological changes may be secondary to the distressing physical state. It is a mistake to insist too much upon certainty. It is also a mistake to blur notions of aetiology with the erroneous notion that attempting to find both physical and psychological causes is ‘dualistic’. The end result of any disease process may be a physical change or a psychological state, but both occur in a social context which influences the severity of the condition so far as the patient is concerned, and the social context in turn is influenced by the condition of the individual. Yet it is of vital practical importance to treat some aetiologies as organic and others as psychological, and it is equally practical to determine treatments according to all relevant causes, no matter what the theory. At the moment among the treatments which will work best, those for depression stand out (Manu et al, 1993), while general measures such as adaptation, graded rest and activity all apply. The spread of the condition to some cases may reflect mimetic behaviour and may thus be seen as hysterical, albeit this does not appear to be a frequent element of the problem. It is certain that the interaction of some patients and doctors – and especially patient groups and physicians – is liable to become tense when one view or another is adopted uncompromisingly. Both myalgic encephalitis and CFS may overlap or be the same, and also may be varied within themselves, and no single approach is sufficient. For my part I find the best unifying hypothesis in Moldofsky’s ideas which, incidentally, offer something to the psychiatrist, the immunologist and the rheumatologist.
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18 Children
Hysterical symptoms are generally thought to arise readily in children. A pain in the tummy is quickly copied from another child if it promotes absence from school, and cured if it calls for unwanted rest in bed, deprivation of icecream, or failure to attend a party. Hysterical visual failure tends to arise more easily in the young teenager at the time when he or she is under school and examination pressures. For example, the report by Behrman (1969) on hysterical visual difficulty included 18 out of 35 patients under the age of 16 years, and she cites three other papers on hysterical amblyopia (Yasuna, 1951; Schlaegel & Quilala, 1955; Krill, 1967) in which there was similarly a high proportion of children, especially girls. Reported epidemics of hysteria (Chapter 16) include several affecting school children. Proctor (1958) has given a good review of the earlier literature on a variety of hysterical symptoms in childhood and Rock (1971) discusses further literature clearly. Garralda (1992) provides an excellent up-to-date survey, and the Lancet (1991) gives a concise and well informed discussion. Taylor (1989) offers some graphic examples. Severe conversion or troublesome individual conversion reactions are less common in children (Creak, 1969) but typical conversion symptoms are, nevertheless, found in children, and abdominal pains and headaches, which are quite common, are also thought to be hysterical in some cases. Malmquist (1971) considers that tics are the most common motor symptoms of hysteria in children, but have to be distinguished from Tourette’s syndrome, hyperkinesis, torticollis and choreo-athetosis. Tics are also more often anxiety symptoms than hysterical ones. However, Proctor (1958) described 25 out of 191 unselected consecutively diagnosed child patients under 16 years as having frank conversion and/or 257
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dissociative reactions: an incidence of 13%. In discussing this paper, Schneer (1958) noted a much lower incidence at King’s County Hospital, Brooklyn: one out of 940 male in-patients, 14 out of 481 female in-patients, 5 out of 798 male out-patients, and 3 out of 798 female out-patients. Both authors attributed the difference to a more primitive and relatively static pattern of child-rearing practice in a population of low educational attainment, low socio-economic status and rural background, in the case of Proctor’s patients. In Arkansas, Forbis & Janes (1965) had a high incidence in their patients: 16% of their referrals had conversion symptoms. In Eastern Kentucky, Looff (1970) found that eight of 100 children admitted to hospital had pure conversion reactions and a further eight had mixed conversion and psychophysiological reactions. Feehan (1993) reported on a pilot study among children admitted to all departments of a district general hospital in Britain between December 1989 and May 1991. From the case notes it appeared that 191 of 8517 children admitted to hospital might have had functional illness. Of these, 160 were suffering from abdominal pain which did not result in surgery. The remaining 31 had a variety of complaints of pain or loss of function. Four fulfilled diagnostic criteria for hysterical neurosis, conversion type. Over a similar time period, two local child psychiatry in-patient units each admitted one patient with hysterical neurosis, conversion type. The admission rate for hysterical conversion was thus 0.4% for paediatric units and 1.4% for in-patient child psychiatry units, which is a relatively small rate in either case. Taken together, these findings suggest that troublesome conversion symptoms, necessitating referral to child psychiatry services, are rare except in rural and relatively poorly educated populations. This view corresponds to general experience and is supported by Looff’s specific observation that children with conversion reactions compared with other patients had a marked difficulty in the verbal expression of affect. Children are not immune from conflict in the attribution of symptoms to physical or psychological causes. Psychogenic cough is a good example of a condition which, when not related to physical causes, has been characterised as a habit tic rather than necesssarily a psychological syndrome (Milner, 1985). Overall, it appears that the frequency of conversion disorders may vary from as little as 0.5% to as much as 10% of clinical series (Lehmkuhl et al, 1989; Leslie, 1988). The systematic compilation of data on hysterical syndromes of childhood is incomplete and controlled evidence is lacking. Much of the more systematic information now available has appeared in
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the last decade. Leslie (1988) and Grattan-Smith et al (1988) found that when conversion disorder is diagnosed by ICD–9 and DSM–III–R criteria, disturbances of motor function are the commonest complaints, thus supporting the earlier work of Rock. Many of the patients of Grattan-Smith et al also had “psychogenic pain”. Multiple symptoms are common but visual disturbances were not reported in younger children. Others (Lancet, 1991) emphasise the frequency of episodic loss of awareness such as pseudoseizures and syncope, motor dysfunction and sensory abnormalities. It is said that headaches, dizziness, sleep difficulties, eating disorders, vomiting, hiccups, psychogenic cough and tremors are common accompanying complaints (Spierings et al, 1990) and that multiple organ systems are often involved, especially in older children (Lehmkuhl et al, 1989). Garralda (1992) and Taylor (1986) both emphasise that children with conversion disorders and their parents make reluctant psychiatric patients. They are usually seen by many other medical specialists before the referral to psychiatry, which is almost universally made by paediatricians, often in the face of initial parental opposition and even hostility. Taylor (1986) argues that the symptom arises out of an intolerable predicament for which all apparent solutions are blocked and that, secondly, an ally who is helping to promote the sickness is required. A model of the sickness has to be available and hysteria can only be promoted by persons with the necessary skill in social affairs or by those who derive that skill from their allies. Taylor (1986) adds that there is little evidence to support the idea of psychopathology in patients with hysterical symptoms. The organic differential diagnosis is not easy. Woodbury et al (1992) describe a patient who was very reasonably thought to have psychological problems causing him to complain of right leg pain and an inability to walk, who was admitted to hospital and then treated for a further two months, until medical examinations showed a progressive atrophy in the right calf and a positive right Babinski reflex, which led to a further readmission and discovery of a spinal cord tumour in the lower sacrum. In an adolescent, one form of acute dystonia, the Pisa syndrome, involving transient tilting of the trunk, was mistaken for a conversion disorder (Fichtner et al, 1992). Others have noted spinal cord tumours, epileptic seizures and neurodegenerative diseases being confused with conversion disorders (Bangash et al, 1988; Spierings et al, 1990; Rivinus et al, 1975). When conversion symptoms do occur in children, the psychopathology is sometimes quite slight, making it all the more difficult to determine whether or not the apparent absence of physical
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evidence should lead to more far-reaching physical investigations or psychological exploration. Families with serious domestic troubles may have children whose physical illness mimics conversion disorder, and cases with little evident reason for psychopathology may still have hysterical complaints. Also, although one of the largest studies (Grattan-Smith et al, 1988) sought information on sexual abuse they found only one confirmed history and three with possible abuse out of 52 children with a median age of 10 years and range from 6 to 15. Turgay (1980, 1990) reported studies of children in different countries, spanning a range of social conditions. He described a series of 80 children from Ankara, Turkey, and later reported on a total of 135 children and adolescents with conversion disorders, including many seen in North America. In his Ankara population, he noted that the female:male ratio of patients was 2:1, this pattern being somewhat higher in those aged nine or over, and either it was reversed in younger children or else younger boys and girls were almost equally represented. The commonest symptoms were seizures, muscle contractions in the extremities, or other motor disturbances. Blindness affected only one of his 80 patients, and other sensory changes, apart from parathaesias in the extremities in four cases, are not mentioned. This group of symptoms was the most frequent clinical picture in the Ankara University Department of Child Psychiatry. He emphasised that conversion reaction occurred more often in Turkey than in Western culture. Reporting on Canadian and American cases, he observed that conversion disorder in children and in adolescents is uncommon in North America. Compared with a control group of patients with obsessive–compulsive neurosis, far more of Turgay’s patients lived outside cities. In general, it appears that the same problems of diagnosis and explanation that exist for adults occur also with children. The theories and understanding of the cases appear to be the same in both groups. Sexual abuse is likely to be a difficult, unspeakable predicament in a small number of children with conversion syndromes (Volkmar et al, 1984; Leslie, 1988). Garralda (1992) points out that for others major family disruption would represent the impossible situation, and a number of alternative explanations for conversion symptoms, besides abuse, are offered. These include the disgrace of feeling unable to perform academically according to the child’s own expectations or the family’s high expectations, emotionally close but psychologically inarticulate family relationships and communications, and the existence of sensitising health problems.
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The last considerations are frequently applied to children with aches and pains in different locations. Apley (1975) particularly emphasised the relevance of psychological causes to abdominal pain in children. Psychiatric control studies have recently been undertaken (e.g. Crossley, 1982; Hughes, 1984; Hodges et al, 1985; Wasserman et al, 1988). An increased incidence of depression in the children with abdominal pain is found in these studies but, as discussed earlier in connection with pain (Chapter 12), the interpretation of painful symptoms as hysterical in children, just like in adults, must be qualified with respect to its implications. We have to be much more cautious than was formerly the case in assuming that pains may be hysterical. The same applies to headaches. While headaches in children might well come under the same psychological influences and selection processes as headaches in adults, the interpretation of these as hysterical is subject to the same qualifications as those mentioned in Chapter 12. In a rather different country (Poland), Sulestrowska (1973) found 36 child patients with hysterical symptoms occurring between 1947 and 1972 in the children’s psychiatric ward at Gdansk. Ninety per cent had been admitted between the ages of 11 and 14 years and “encephalopathy of a light degree” was found or, more frequently, suspected in nearly 60% of cases. “Thus so-called minimal brain damage is conducive to hysterical reactions.” Twentyfour were traced at long-term follow-up. Ten of the 24 showed full remission of their initial symptoms, so that as adolescents they did not need psychiatric care, although some of them suffered from transient neurotic symptoms such as headaches, phobias or neurasthenic hypochondriacal symptoms. Ten subsequently attended psychiatrists and five required readmission to a psychiatric hospital. In the American literature the most important follow-up study is that of Robins & O’Neal (1953), who used a broader notion of hysteria and included cases of hypochondriasis and mixed psychoneuroses. They found 41 patients, an incidence of 8.3% of psychiatric admissions to a children’s hospital excluding cases of mental deficiency, and 0.09% of all the admissions. Thirty-seven of these patients were located and 23 examined. Of the latter 23, four, all girls, had hysteria in terms of the Perley & Guze (1962) criteria at follow-up. All 23 had originally had classic hysterical symptoms and multiple additional symptoms. Five patients had anxiety neurosis and six patients each had one of the following conditions: psychopathic personality; alcohol addiction; bilateral macular degeneration; cardiospasm; idiopathic epilepsy; and a
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congenital orthopaedic disease. Six patients had symptoms for which a diagnosis could not be made, and two were completely well. Many useful hints emerged from this study, in particular the occurrence of anxiety in adult life as a sequel to possible hysteria in childhood, the fairly frequent occurrence of misdiagnosis of organic illness because the original symptoms were found in a ‘nervous’ child and held to be disproportionate to the physical situation, the absence of cases of hysteria among the boys on follow-up and the persistence of hysteria in those with classic symptoms combined with multiple symptoms. A small and significant nucleus thus emerges of patients for whom the diagnosis is appropriate, even if hedged about with problems. This finding is relevant to the controversy about the existence of hysteria as a substantive diagnosis (Chapter 25), since it supports the view of Lewis (1975) and Reed (1975) that the persistence of the diagnosis in a defined pattern in certain individuals validates the conclusion that a syndrome of ‘hysteria’ is a recognisable and distinguishable entity. In general, one can expect that normal children and those with hysterical symptoms will show many of the personality features which have often been attributed to adults with conversion symptoms or with the hysterical personality. By definition they are immature and by circumstance dependent. Their imitative drive to learn by modelling themselves on adults leaves them open to the effects of suggestion and the accusation of acting, both individually and en masse. They are inevitably more primitive and open in their responses, more labile and more vulnerable to the reactions and mood changes of the adults around them. It is hardly surprising that these characteristics are evident in hysteria in childhood. It will be of theoretical and some practical importance to consider if they are evident in adults with conversion symptoms.
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19 Suggestion and hypnotic phenomena
“When we speak of suggestion our first difficulty is to come to an agreement as to the meaning of the term. Furthermore, questions of words are at the same time questions of things; a definition is a theory.” (Baudouin, 1920, p. 19) “to be able to attribute a given occurrence to suggestion is with many a complete solution of the problem” (Jones, 1910, p. 242)
Over and above the different symptoms so far considered, certain special phenomena or situations have extended our notion of what constitutes hysteria. They include the reactions of children and the phenomena of mass outbreaks of hysteria, discussed in the two previous chapters. They also include suggestibility and hypnosis, which rank high in this respect, and these topics are discussed in this chapter. Some of these special phenomena have been of considerable historical importance, especially hypnosis, which figured prominently in the work of Charcot (Chapter 2), Freud and others in the late 19th and early 20th centuries. I hope to show how suggestion, suggestibility and hypnotic phenomena are the outcome of individual motivation in a stylised setting. In consequence what is called ‘hypnosis’ functions to produce hysterical manifestations. Both sentences in the quotation from Baudouin, opening the chapter, apply to hypnosis as well as to suggestion, but suggestion will be considered first. It is, of course, widely agreed that patients with hysterical symptoms or personality may show an unusual degree of ‘suggestibility’. It is also true that this ‘suggestibility’ is by no means consistent either between or even within individuals. Different people at different times vary in degrees of suggestibility. 263
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If the patient is ready to be cured, anything will work. If the patient is either not ready or fundamentally unwilling, nothing will persuade him or her. Baudouin ultimately defined suggestion as the subconscious realisation of an idea; and for this only the idea was necessary. Another person was not required to convey the suggestion. The placebo response is often held to be an indication of suggestion, but in clinical practice it may represent several different events. An apparent placebo response may result from spontaneous improvement, or because a disease has run its allotted course; an environmental change, unnoticed, but promoting recovery may also be responsible (e.g. an irritating boss being diverted in another direction). In the light of Shapiro’s (1964a,b) discussion, we can note that a true placebo response would depend on the false belief that a particular substance or procedure was specifically efficacious. It may be promoted by the emotional support which a physician gives through attention to the patient. If these qualifications are observed it still appears, however, that some people are more responsive to overt or implied suggestions. Shapiro et al (1968) consider that tests of suggestibility do not correlate with each other, with placebo effects, or with clinical course. However, there are reports (e.g. Joyce, 1959) that some behavioural measures such as autonomic awareness and certain scores, for example on the Bernreuter Personality Inventory, may predict placebo responses in normal individuals. Black (1966) found that patients with extrovert characteristics were significantly more liable to respond to placebos, as were those with shorter duration of the illness. Shapiro et al (1968) also showed that anxiety correlated positively with placebo responses and depression correlated negatively. Fisher & Fisher (1963) found that acquiescence, measured on the Bass Social Acquiescence Scale, correlated positively with the placebo effect. But the extent to which observations of this sort can be related to hysterical symptoms is very much open to further study. The main conclusion is that suggestibility, for which various tests exist, is distinct from the placebo response, and that while suggestibility may well be related to hypnotic susceptibility (see Hilgard & Hilgard, 1975, for examples) we cannot yet with certainty correlate the phenomena of suggestibility with those of hysterical symptoms and personality characteristics. Nevertheless, the suspicion remains that an appropriate definition for hysterical characteristics would lead to the demonstration of a relationship with suggestibility. Perhaps the most relevant
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consideration is that while patients with hysteria may be suggestible, the suggestions which most influence them are their own and not those of the investigator, notwithstanding the far-reaching suggestions which are now common in the treatment of dissociative disorders (Chapters 20 and 21). As Baudouin emphasises, suggestion does not need a proponent other than the subject himself or herself. When we consider hypnosis it seems likely that the effective suggestions are shared by both parties to the procedure. At the same time the literature on hypnosis is replete with the induction of phenomena which, if they occurred spontaneously or were generated by the patient without the encouragement of a hypnotist, would immediately be classed as hysterical. Amnesias, anaesthesias, paralyses and hallucinations induced under hypnosis have been recognised, at least since the work of Charcot, as resembling hysterical phenomena. Indeed, Charcot thought that hypnosis occurred only in sufferers from hysteria. The nature of hypnosis therefore calls for consideration, as well as its relationship to suggestion.
A dissociation of consciousness A commission appointed by Louis XVI and headed by Bailly (1784) disentangled hypnosis from the notion of animal magnetism. The Bailly report attributed the production of various hysterical phenomena to ‘imagination’. Braid (1843) coined the term hypnosis to indicate that the phenomena had, as he thought, a neurophysiological basis. But others (e.g. Bernheim and Liébeault) regarded suggestion as the principal factor in hypnosis. Chertok (1966) produced a good review of the fascinating history of these matters. Ellenberger (1970) provides an authoritative scholarly discussion. Charcot had a different view from Bernheim, and their argument is well described by William James (1890), as follows: “The Theory of Suggestion denies that there is any special hypnotic state worthy of the name of trance or neurosis. All the symptoms above described as well as those to be described hereafter, are results of that mental susceptibility which we all to some degree possess, of yielding assent to outward suggestion, of affirming what we strongly conceive, and of acting in accordance with what we are made to expect. The bodily symptoms of the Salpêtrière patients are all of them results of expectation and training. The first patients accidentally did certain things which their doctors thought typical and caused to be repeated. The
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As has been pointed out elsewhere (Merskey, 1971) James could not rid himself of the idea that a special nervous trance state, or some form of dissociation of consciousness might be occurring. Others, including Charcot (1872), Janet (1894), Prince (1905)
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and Tuckey (1891), similarly regarded it as a dissociation of consciousness. Janet (1925) believed, after Bernheim, that it was a true derivative natural sleep. Hilgard (1973) favours a neodissociation theory in which different segments of experience may be either accessible to consciousness or inaccessible, depending on the route used to tap sources of information. Schilder (1956) emphasised the resemblance to sleep. It is easy to sympathise with this view as one watches the loss of facial tone and general relaxation of some hypnotised subjects, but it is not sustained when their electroencephalograms, which show no sleep changes, are examined. Many workers (e.g. Gill & Brenman, 1959; Shor, 1959; Delay & Pichot, 1962; Abse, 1966; Tart, 1969) have seen it in terms of altered consciousness. Electroencephalographic findings are against this view, and it is important to note that there appears to be no firm evidence that there is any physiological difference between hypnosis and other states of relaxation or altered mood which might be produced by determined suggestions.
Physiological changes In the past it has been supposed that abolition of pain, and autonomic changes affecting the bronchioles, circulation, and the skin, might occur with hypnosis; and differences have been shown in immunological responses (Black 1963a,b; Black et al, 1963; Black & Friedman, 1965). But these studies did not show that subjects given suggestions might not have produced the same response. If one doubts the physiological efficacy of hypnosis, over and above a state of relaxation, then a very typical result may be seen in the report of Malmo et al (1954). Muscle potentials and eye blink were recorded in a study of hysterical deafness and hypnotically induced deafness. Describing their first hypnotic subject, the authors report: “in interview following the hypnotic session [she] denied hearing any sounds during the period of hypnotic deafness. Motor data ... showed clear reaction to the first stimulus.”
In a detailed examination of the evidence, Barber (1963) finds that hypnotic analgesia may be accompanied by signs of pain and produces an unwillingness to state directly to the hypnotist that pain was experienced. Among the most famous cases of ‘painless’ surgery under hypnosis, those of Esdaile (1850), Barber finds such reports as “she moved and moaned”, “About the middle of the
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operation she gave a cry”; “The man moved and cried out, before I had finished ... on being questioned he said that he had felt no pain”. Of six patients on whom Esdaile operated for scrotal tumours, three showed no gross signs of pain, but two of these showed marked elevations of pulse rate, of the order of 40 beats per minute. The sympathetic review of the literature by Hilgard & Hilgard (1975) indicates that most operations conducted under hypnosis give rise to some indications of pain in the subject. The percentage of recorded cases in which successful analgesia is achieved, in the sense of absence of all signs of pain and a satisfactory subsequent report by the patient, is very low (10%). Examining physiological changes associated with pain, Shor (1962) found experimentally that galvanic skin response, respiration, limb movement and heart rate were favourably influenced by hypnosis but equally influenced by the reduction of anxiety without hypnosis. The present author (Merskey, 1971) reviewed further evidence on this topic. He owes much to the classic work of Barber (1969), who argued that task-motivating instructions are usually as effective as hypnosis and it is not necessary to assume a special trance state for the explanation of hypnotic effects. Halliday & Mason (1964) carried out some decisive experiments with regard to the physiological aspect. They recorded somatosensory and auditory evoked potentials and found no difference in the potentials between the normal state and that following hypnotically induced sensory loss. This negative finding is important, particularly because it was not the result which the investigators anticipated (Halliday, personal communication). But it fits extremely well with the view that hypnosis (and hysteria) do not prevent registration of sensory impulses or even their cerebral processing. A subsequent report (Levy & Mushin, 1973) indicates that stimulation of the skin of patients with hysterical hemi-anaesthesia at near threshold levels induces an increase in the amplitude of averaged evoked responses, while stimulation at higher levels is equivalent to that in normal subjects.
A definition of hypnosis From this rather brief discussion it may be concluded that hypnosis is not physiologically different from a normal waking state of attention, concentration, or relaxation, or some
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combination of these. If we accept Barber’s view that the phenomena of hypnosis depend upon the subject’s expectations and also on those of the hypnotist, then the following definition of hypnosis appears appropriate (Merskey, 1971): “Hypnosis is a manoeuvre in which the subject and hypnotist have an implicit agreement that certain events (e.g. paralyses, hallucinations, amnesias) will occur, either during a special procedure or later, in accordance with the hypnotist’s instructions. Both try hard to put this agreement into effect and adopt appropriate behavioural rules and the subject uses mechanisms of denial to report on the events in accordance with the implicit agreement. This situation is used to implement various motives whether therapeutic or otherwise, on the part of both participants. There is no trance state, no detectable cerebral physiological change, and only such peripheral physiological responses as may be produced equally by non-hypnotic suggestion or other emotional changes.”
Transference phenomena As the quotation from Jones at the beginning of the chapter indicates, psychoanalysts tended to feel that the word ‘suggestion’ masked further phenomena. Freud (1917) emphasised that ‘suggestibility’ depended on sexuality, or on the functioning of the libido. He had abandoned hypnosis because he discovered that it led the hysterical patients he treated to become unduly dependent upon him. In his view the power which motivated patients to accept the hypnotic procedure was evidently not just a wish to recover: it was sexual love, which would attach itself inevitably to the therapist. Hypnosis even resembled love, with its humble subjection and absence of criticism towards the hypnotist, as towards the loved object (Freud, 1921), together with the development of other feelings as the nature of the transference changed. For our purposes it is not necessary to discuss transference phenomena in detail. It is sufficient to indicate that the idea of motives leading individuals to accept hypnosis, or to practise it, cannot be ignored, and that these may be extra-therapeutic.
The use of hypnosis The foregoing does not mean that the practice of hypnosis need not be or is not ethical, proper, or useful. It can provide a
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convenient and helpful way of treating patients, sometimes offering them a face-saving opportunity to relinquish a hysterical symptom. Only, in such cases, it is important to make sure that subsequent attention is given to the patient and to his or her needs once the symptom has been abolished. Further, the motives for accepting hypnosis need not always be profound, dynamic ones. The roles of hypnotiser and hypnotised can be accepted for specific purposes, such as the relief of asthma or pain, the removal of a hysterical symptom, or a variety of other uses for which hypnosis may or may not prove useful. However, the more one is unwilling to accept that it provides a special physiological state, the harder it is to practise. In this situation, suggestion is a function with which the subject and hypnotist mutually endow each other to produce the desired result. There is two-way suggestion, perhaps even double unconscious bluff. One of the results for the patient is that the phenomena of hypnosis are identical with those of hysteria: they involve self-deception and the production of alternative symptoms or behaviour to solve a problem, even if not a conflict. If phenomena of this sort can be established by the mutual influence of one person upon another, it is not surprising that mass hysterical phenomena may occur, where increasing numbers of individuals in certain conditions influence each other, with the production of a common symptom pattern, as reviewed in Chapter 16. The reasons for scepticism concerning the nature of hypnosis were expressed in the first edition of this book in 1979, and founded on earlier arguments as long ago as 1971. That is a short time span in the history of hypnosis, and it still continues to be practised and approved as a treatment in many, if not all, parts of the world with sophisticated medical systems. Its use in a legal context has come under question, and evidence obtained under hypnosis has no special status in a number of American states and Canadian provinces although more accept it. Police forces sometimes favour its use with victims in order to encourage the recall of memories, although there is no reason to think that these will be any better under hypnosis than in a normal state of awareness. Sheehan (1988) noted the controversy concerning the accuracy of memories obtained under hypnosis and undertook a programmatic series of studies to investigate possible memory distortions in hypnosis. There was no increment in accurate memory due to hypnosis, and the accuracy of memory reports in hypnosis was, at times, significantly reduced.
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The Council on Scientific Affairs of the American Medical Association found that “recollections obtained during hypnosis can involve confabulations and pseudo-memories and not only fail to be more accurate, but actually appear to be less reliable than non-hypnotic recall” (Council on Scientific Affairs, 1985). It discouraged the use of hypnosis with witnesses and victims for the purpose of testimony. It was doubtful whether the use of hypnosis with witnesses and victims for the purpose of investigation was beneficial, but allowed that it might be attempted. Piper (1994b) has reviewed the use of Amytal as a ‘truth serum’. The evidence from studies with good research methodology indicates that people interviewed under Amytal are more suggestible than they are in their normal waking states, lies can be told during Amytal interviews, and patients demonstrate numerous phenomena characteristic of hypnotic states. The reservations which apply to the use of hypnosis in obtaining recovered memories thus apply equally strongly to the use of Amytal. Hypnosis remains actively used by experimental psychologists and also in conjunction with the treatment or diagnosis of the supposed condition of multiple personality disorder, which is the subject of the next chapter.
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20 ‘Multiple personality disorder’
‘Multiple personality disorder’ has recently been renamed by the American Psychiatric Association (1994) in DSM–IV as “300.14 Dissociative Identity Disorder (formerly Multiple Personality Disorder)”. Dissociative identity disorder (DID) is then defined as follows: A. The presence of two or more distinct identities or personality states (each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self). B. At least two of these identities or personality states recurrently take control of the person’s behavior. C. Inability to recall important personal information that is too extensive to be explained by ordinary forgetfulness. D. The disturbance is not due to the direct physiological effects of a substance (eg. blackouts or chaotic behaviour during alcohol intoxication) or a general medical condition (e.g. complex partial seizures). There is a note that in children the symptoms are not attributable to imaginary playmates or other fantasy play. (American Psychiatric Association, 1994)
This reflects a change in name from the much criticised concept of multiple personality disorder but not a lot of change in the criteria. The emphasis on personalities has been softened a little with the introduction of the term identities and the statement that they recurrently take control of the person’s behaviour has been altered by the deletion of the word ‘full’. Thus it is possible for a personality to take partial control, or for two or more personalities to share this control, according to this definition. How this can happen while memory is lost may puzzle the thoughtful. Since the concept and the data which are being discussed in this chapter are essentially what was developed as multiple personality disorder I have retained that title, but I have used DID when the revised criteria are under discussion. 272
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Multiple personality disorder (MPD) is a controversial diagnosis. There is little reason to think that the new version (DID) will be significantly less controversial. Although it is widely employed in North America it is very little used elsewhere, and it is questioned by the World Health Organization in ICD–10, its most recent classification of psychiatric disorders (World Health Organization, 1992a). It is said of MPD that if it exists at all it should be categorised under “F44.8 Other Dissociative [conversion] Disorders”. No further description is given of it there, unlike other categories, such as dissociative amnesia, dissociative fugue, or dissociative stupor. Putnam (1989), one of the authors of the American Psychiatric Association’s (1987) (DSM–III–R) definition, says that there is a patient profile which should suggest MPD. The core features are a profusion of psychiatric, neurological and medical symptoms, a host of diagnoses, and a failure to respond to treatment for those diagnoses. The symptoms include depressed mood, suicidal attempts and ideas, impaired concentration, fatigue, sexual difficulties, crying spells, and insomnia. Often there is enough superficially to suggest the diagnosis of major affective disorder. Nightmares are prominent, along with terrifying hypnagogic and hypnopompic hallucinations. Closer inquiry discloses that the depression is more labile than is usual with major affective illnesses and that there may be several mood swings each day. Amnesia or ‘time loss’ may affect as many as 90% of patients, and fugue episodes and feelings of depersonalisation occur in more than 50%. There is sleepwalking in many subjects, anxiety, phobic symptoms, substance abuse, and hallucinations during the day as well. Self-mutilation occurs in about a third of patients. The life history is almost always marked by sexual abuse. The great majority of patients are women. Some patients declare their diagnosis. Otherwise, says Putnam (1989, p. 90), the therapist who wishes to “elicit alter personalities” should ask gentle questions about whether the patient has ever felt like more than one person, searching for another part, and ultimately asking, “Do you ever feel as if you are not alone, as if there is someone else or some other part watching you?” In the event of a response, the therapist looks for “any ... attribute, function or description to use as a label to elicit this other part directly”. This is a very clear and honest statement, but with such an approach there is a likelihood that the therapist will produce the phenomenon. The more dramatic examples of this syndrome attract much attention, ranging from The Three Faces of Eve (Thigpen & Cleckley,
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1957) to an unfortunate 27-year-old waitress in Oshkosh, Wisconsin, who claimed to have 46 different personalities, of whom six were sworn in and gave testimony in a trial (Daniels, 1990). Publicity must also be suspected of producing such events. Many of these patients have had terrible experiences and awful problems in their lives. The question at issue is not whether or not the patients need treatment – they do – but rather under what label and with which ideas.
The increasing numbers of cases Scepticism about the diagnosis has been increased by a great growth in numbers of cases. The pattern of this growth is noteworthy. The first supposed case of MPD recorded in detail is that of Mary Reynolds of Pennsylvania (Mitchill, 1816; Plumer, 1860; Mitchell, 1888). The initial report by Mitchill (1816) is thirdhand and brief. Plumer (1860) described the history six years after the patient’s death, from interviews with her relatives. Weir Mitchell described the case again in 1888 from Plumer’s report and from the papers of his father, J. K. Mitchell. He also reinterviewed some of the same relatives Plumer had consulted. About that time there was lengthy discussion of several cases, especially by Azam (1876, 1887, 1892), Janet (1887, 1888, 1889), James (1890), Prince (1908), and Sidis & Goodhart (1904). Prince (1908) cited some 24 reported cases. He held that in the more fully developed forms the secondary or ‘disintegrated’ personality would approximate to that of normal life and might pass before the world as mentally healthy. Hacking (1991, 1992) has argued that MPD was created, as it were, in 1875. Azam was aware of the active discussion in France of “bizarreries of amnesia” and recalled a case he had described in 1860 when he had “introduced scientific hypnotism to France” (see Hacking, 1992, for this account). He then recalled his case, first treated in 1858, and re-described it in January 1876, inspiring imitators. Hacking traces some additional cases which might be added to the classic small group, or ‘canon’, which characterises the 19th century, and he observes a cascade effect, following initial reports. Hacking (1992) estimated that the reports of numbers of cases occurred in waves. Thus, Dwight (1818) followed the initial brief report about Mary Reynolds by Mitchill (1816) and described three cases seen in 1802. This first wave, with very few cases, essentially lasted until 1875. A small increase occurred after 1875 with the publication of the case of Azam followed by
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those of Janet. Mitchell (1888) re-described the original case of Mary Reynolds after the French publications had become well known. The interest in France at the time of Azam and Janet was strong, partly because the concepts supported the views of positivist philosophers and psychologists, such as Ribot, who gained ascendancy in French academia. As the numbers grew, the name changed. In France both Azam and Janet used the words “doublement de la vie” and occasionally “le doublement de la personnalité”. After 1876 the latter form became standard for French writers, and then Myers (1886) used the phrase “case of double or multiple personality”, which by 1885 had become the received form for Ribot and Janet. Even so, in the whole of the 19th century there were only some 20 cases, apart from the small additional group which Hacking (1991) has since identified. After Prince’s report (1900) at the International Congress of Psychology, and after the first and second editions of his book (Prince, 1905, 1908), the numbers increased again until Taylor & Martin could identify 76 cases by 1944, and suggested that there might be as many more unreported. In 1954 Thigpen & Cleckley reported a case. Their book The Three Faces of Eve appeared in 1957, and a film was made of it. From that point, cases multiplied. Boor (1982) recognised 79 reports after 1970. DSM–III established a category for MPD in 1980. Kluft (1982) mentioned 130 such patients, of whom he had treated 70. Bliss had seen 100 cases, and Jeppsen another 50 (Bliss & Jeppsen, 1985). Putnam et al (1986) reviewed 100 cases. Ross (1987) found an incidence of 4.4% among his patients and claimed that MPD can be readily discovered with a reliable and valid screening instrument (Ross, 1989). Scepticism has also grown with the increase in the numbers of personalities that have been described. Greaves (1980) notes that Christine Beauchamp (Prince’s case) had four personalities; others have had 16 (Schreiber, 1973), 22 (Sizemore & Pittillo, 1977), and even 35 (Allison & Schwarz, 1980). Kluft (1982) described 60 cases in some detail, of whom only 11 had 2 personalities, 8 had 3–5 personalities, 20 had 6–10 personalities, 19 had 11–20 personalities, and 2 more than 20 personalities. Hilgard (1988) observed that such numbers “as well as those reported by several others, are bound to raise doubts about diagnoses”. Kluft (1988) lays claim to patients with more than 4000 personalities or personality fragments. DSM–III–R allowed that as many as 100 personalities, or fragments of personality, may exist within the same individual. This reductio ad absurdum of the concept wrecks most, or all, of its face validity.
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Sutcliffe & Jones (1962) give one of the most explicit discussions. They considered various conceptions of multiple personality; as a diagnostic fashion; as a product of shaping in therapy; as a product of hypnotic suggestion; as simulation; and as an extension of characteristics found in ‘normal’ personalities. We now have a strong diagnostic fashion for the topic in some countries. Hypnotic suggestion accompanies innumerable reports. Simulation is always possible but, if therapists can create the condition by suggestion, the need for simulation is slight. Explanation by an ‘extension’ of normal personalities is disputable since the patterns presented are distinct. In the light of the growth in numbers and some of the increasingly improbable stories associated with MPD, it seemed worthwhile to seek a further method by which to probe the origin of the phenomenon. I noticed some examples in which shaping by therapy was the most plausible explanation (Prince, 1908; Janet, 1913) and decided to examine a sample of the literature for information on other diagnoses and on the moments of emergence of secondary personalities. It appeared to me that the widespread modern publicity made it impossible to determine reliably whether any new case was emerging without the benefit of prior suggestion. It seemed worthwhile to look at the 19th-century literature, on the assumption that the patients would not have been ‘primed’ by prior publicity. Thus we could hope that the events at the time when their second and third personalities emerged might indicate how these conditions arose naturally (Merskey, 1992a).
The first cases Benjamin Rush mentioned the earliest known possible cases of MPD (Carlson, 1981). Ellenberger (1970) states that case histories of MPD began to appear in mesmerist writings and later in the medical literature, only after the disappearance of the phenomena of possession, although possession and exorcism sometimes still occur (Peters & Schwarz, 1978; McKellar, 1979). Ellenberger cites Gmelin’s (1791) report of a German woman aged 20, in Stuttgart, who was impressed by refugees from the French Revolution and their aristocratic manners. She “suddenly ‘exchanged’ her own personality for the manners of a French-born lady ... speaking French permanently, and German as would a French-born woman”. Sufficient context is not available to evaluate this case for its onset. French and German states alternated with loss of memory for each other. “With a motion of his hand Gmelin was easily able
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to make her shift from one personality to another” (Ellenberger, 1970). Despine (1840) reported a case of alternating states in an 11year-old Swiss girl, Estelle, who had been diagnosed as having a spinal paralysis and severe pains, which ultimately responded to ‘magnetism’. A comforting angel, Angeline, talked to Estelle in her ‘magnetised’ condition, advising support for her whims. The angel prohibited all foods that Estelle disliked and ordained that she should have anything she desired, including snow. The angel said, “Let her act according to her whims; she will not take advantage of the situation”. The book provides no evidence for a second ‘personality’. The case of Mary Reynolds was first described in 1816 by Mitchill on a report from a relative described as “Major Ellicot”, the professor of mathematics at the United States Military Academy at Westpoint. The Reverend Plumer (1860) wrote up the patient’s history in Harper’s Magazine, and Weir Mitchell (1888) described it at length also. William James (1890) gives a relatively brief, but quite informative, account of the case, and Kenny (1986) provides a valuable account of the background and situation of Mary Reynolds. The first report on Mary Reynolds describes two independent states of consciousness, the first appearing after sleep. Some of her changes followed the anticipated pattern of the mesmerisers of the day, when they produced ‘somnambulism’ (i.e. hypnotism). Nevertheless, one also finds embedded in the descriptions some striking material which suggests manic–depressive illness. For example, Plumer (1860) wrote as follows: “In her first state she was quiet and sedate, sober and pensive, almost to melancholy, with an intellect sound though rather slow in its operations, and apparently singularly destitute of the imaginative faculty. In her second state she was gay and cheerful, extravagantly fond of society, of fun, practical jokes, with a lively fancy, and a strong propensity for versification and rhyming... In her natural state the strange double life which she led was the cause of great unhappiness. She looked upon it as a severe affliction from the hand of Providence, and dreaded a relapse into the opposite state, fearing that she might never recover from it and so might never again in this life know the friends of her youth, nor her parents, the guardians of her childhood... In the abnormal state, though the prospect of changing into her natural state was far from being pleasant to her, yet it was for different reasons. She looked upon it as passing from a bright and joyous into a dull and stupid phase of life.”
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Mitchell (1888) confirmed Plumer’s account with Mary’s relatives, the Reverend John V. Reynolds and his brother, Mr William Reynolds. Using material which also appears in the earlier reports, he portrayed Mary Reynolds as having a profound sleep, after which she awakened in a state of unnatural consciousness. Her memory had fled. “All ... that remained to her was ... a few words”. She had to be taught their significance, who were her relatives and friends, and her duties. She quickly re-learned reading and writing. “Formerly she had been melancholy, taciturn and reserved, but now she was jocose and unrestrained. She had no fear of rattlesnakes, copperheads or bears ... in this peculiar state Mary’s parents had no control whatever over her. She was very fond of exercising her ingenuity, inventing tricks at the expense of theirs, ... for the purpose of enjoying a laugh and causing others to join in it, at the ludicrous figure in which she never failed to make them appear.”
After five weeks she reverted to her former state, which alternated with the new condition at intervals of varying length for 15 or 16 years. Once her natural disposition returned, “Her melancholy was deepened by the information of what occurred”. When she was cheerful, her buoyancy of spirits was so great that no depression was produced; in her other state she was quiet and shy, and there were times when she manifested an unusual degree of nervousness and restlessness. When she was 35 or 36 the alternations ceased, leaving her “permanently in her second state” until she died, aged 61. Apart from the amnesia, this case resembles bipolar affective illness. However, Mary apparently awoke with an amnesia and communication was employed to build up her knowledge of the world. During re-education the original pattern may be reintroduced or new patterns encouraged. So much must depend upon the response by others that it is unlikely that anyone waking with a hysterical amnesia would develop a ‘new personality’ without assistance. In fact, Reynolds kept her identity but changed her mood. Mitchell described her later phase as a gradual change “from a gay hysterical mischievous woman, fond of jests and subject to absurd beliefs or delusive convictions, to one ... sobered down to levels of practical usefulness”. At the reading of Mitchell’s paper, Dr H. C. Wood said that ‘double consciousness’ was about as bad a term as could be selected. He compared the case with that of a lady who suffered from melancholia and who alternated between being rather coarse
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and rude and thoroughly disregarding the rights of others on the one hand, and suffering from the deepest religious melancholia on the other. In the same discussion, C. K. Mills said that the case resembled “insanity of double form”, which we would now call manic–depressive illness. The case of Skae (1845) is a further striking example of such bipolar illness. The patient was a man of regular and retiring habits, and extremely temperate, who “commenced with the usual symptoms of dyspepsia”, which gradually passed into “hypochondriacism” and then into a state “bordering between hypochondriasis and mental alienation”. At its height, “Feelings of gloom and despondency were at the same time developed:– the most trifling errors of the past were magnified into crimes of unpardonable magnitude, and the future was contemplated with the utmost dread”. He spent much time reading and incessantly turning through the Bible, sat up the greater part of every night, lay in bed during the day, and “under the influence of the bodily distress and mental despondency ... he not infrequently spoke of drowning himself, or of throwing himself out of a window, and on several occasions begged earnestly that he might have his razors”. After nine or ten years the symptoms, which had been aggravated somewhat on alternate days, became distinctly periodic: “On each alternate day, the patient is affected in the manner just described and will neither eat, sleep nor walk, but continues incessantly turning the leaves of a Bible, and complaining piteously of his misery. On the intermediate days he is comparatively speaking, quite well, enters into the domestic duties of his family, eats heartily, walks out, transacts business, assures everyone he is quite well, and appears to entertain no apprehension of a return of his complaints.”
This is evidently a patient who began with depression and dependency and moved into a regular fluctuation from cheerful indifference to depression on alternate days. The case of Mayo (1845) is described only briefly, but also resembles a bipolar disorder, a dull, quiet phase contrasting with one of extreme excitement.
Janet and Azam Most early cases showed only “dual consciousness”. Authors such as James (1890) and Janet (1889, 1904) were very interested in dissociative phenomena as a means to understanding the operations
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of the conscious mind. Independent personalities were of secondary importance initially. When they were proposed it was often done overtly. Jules Janet (1888), the brother of Pierre, hypnotised Blanche W., a patient with hysterical symptoms at the Salpetrière, and restored normal function. This lady appears in the famous picture reproduced by Owen (1971) and by Goetz (1987) of Charcot demonstrating hysterical dystonia. Janet says, “She willingly accepted the name Louise, which I suggested to her,” but she still regarded herself as Blanche. More personalities with stronger delineation only emerged later. Greaves (1980) states that the description of multiple selves appeared in the 20th century. There are hints, however, in several famous French cases. Azam (1876, 1887, 1892), a professor of surgery interested in hypnotism, described Félida X. at the age of 47 after 32 years of observation. She was hysterical with convulsions and “was industrious, intelligent, and of a serious, almost sad, character” (Azam, 1876). In what was taken to be her basic condition, “she thinks unceasingly about her morbid state which causes solemn preoccupations, and suffers from sharp pains in several parts of the body especially the head. The symptom called hysterical nail [i.e. sharp localised pain in the head] is prominent. One is particularly impressed by her sombre manner and the lack of desire which she has to speak; she responds to questions but that is all ...” (Azam, 1876)
Azam describes how then almost every day, without any apparent cause or any excitement, she enters on her second condition. Suddenly, after a pain in the temples, she falls into a profound sleep, which lasts from two to three minutes. Then she awakes, merry and laughing. She hums a tune as she goes on with the work she is engaged upon, makes jokes with those about her, and does not suffer from the neuralgic pains of her supposedly ordinary state. “In this state, which we call the second condition, Félida has a complete knowledge of the whole of her life” (Azam, 1892): “For the last nine or ten years the periods of the second condition have diminished in time of duration to lasting a few hours only and appearing only every 25 to 30 days. So that Félida is almost cured, and will be perfectly so at ... the menopause.”
Azam (1892) denied the diagnosis of dual personality and explained doubling of consciousness in terms of somnambulism. The correct diagnosis today might be a rapid-cycling bipolar state modified by cultural expectations.
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Pierre Janet described a number of cases, particularly Léonie, Lucie, Rose, Marie, and Marcéline. Léonie was much treated previously by ‘magnetisers’. Janet (1889, p. 260) writes, “the magnetizers called her Léontine during somnambulism and recognizing that they had reason to give a new name I kept it”. In 1889 he was to say, “formerly we gave the subject different forenames ... condition of Léonie, condition of Léontine, etc. The confusion caused by this practice was recognized. Now following Azam, we will say condition 1, condition 2, condition 3, for each subject....”
He then identified patients in different states according to the pattern Lucie 1, Lucie 2, Lucie 3, and so on. Typically for these cases, Léonie distinguished between herself as Léontine and Léonie, of whom she said “That good woman is not myself. She is too stupid.” Léonie 1 knew only of herself; Léonie 2 (Léontine) of herself and of Léonie 1. A third Léonie emerged who knew of herself and of both the others. The early history of how Léonie 2 emerged is lost, but obviously there is suspicion of production by her ‘magnetisers’. Janet seems to have rediscovered her through automatic writing produced in response to a post-hypnotic suggestion made over two months previously. There was a letter in her normal style of Mme B. (the original name of Léonie) and another one on the back of the page signed by Léontine, saying how much trouble Léonie was giving to Léontine (Janet, 1889, pp. 252–253). Léonie was hypnotised repeatedly from 1860 onwards and by Janet himself many times, at least from 1885 onwards. Myers (1886) describes her as Janet’s classic case of factitious secondary personalities. Janet (1887) describes at length his practice with Lucie, a much younger girl with a history of many hysterical symptoms. In this principal description, repeated and varied somewhat two years later (Janet, 1889), he distinguishes between three phases, namely the original individual, a hypnotised state, and another character who emerged under automatic writing. In his 1889 volume and later editions, which appear simply to be impressions, he describes hypnotising Lucie and establishing this state of altered awareness which he called Lucie 2 (Janet, 1913, p. 87) . One day she failed to obey the hypnotic suggestion and, to augment her response, he made hypnotic passes on Lucie 2 as if she were not already hypnotised. After various changes, a new personage, Lucie 3, emerged.
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The following exchange occurred with Lucie under hypnosis and through automatic writing. “How are you?” “I don’t know.” “There must be someone there who hears me.” “Yes.” “Who is it?” “Someone other than Lucie.” “Ah indeed. Another person. Would you like us to give her a name?” “No.” “Yes. It would be more convenient?” “Alright, Adrienne.” “Very well Adrienne. Do you hear me?” “Yes.”
Janet adds: “Without a doubt I suggested the name of the personage and gave it a lot of individuality but we saw how much it develops spontaneously ... this naming of the unconscious personage greatly facilitates the experiences.” (1913, p. 318)
Janet was nevertheless convinced that although these hypnotic states were often imperfect and rudimentary, they could also constitute a new existence, more complete than the normal existence of the individual. The life or vitality of a psychological system, in favourable circumstances, would constitute different personalities with various hypnotic somnambulistic states. However, the act of asking a hypnotised subject, especially under hypnosis, if someone, or someone else, is there, clearly encourages the production of an artificial entity. Janet actually also declares about these subjects (p. 178), “We consider that we have been able to establish, even to produce at will, somnambulisms which are completely the same as those of Félida”. Binet (1891, p. 146) made the telling comment about the above exchange with Lucie, “it is plain that M. Janet by christening this unconscious person, and, more still, by declaring that someone must exist in order to answer him, aided materially in the formation of a person; he himself created her by suggestion”. Rose and Marie, like Léonie and Lucie, had numerous variations under hypnosis. The exact origin of these cases and their second forms of personality is either dubious or is not described in detail in any of the original sources listed here. However, all had hysterical symptoms and multiple changes under hypnosis. Janet describes two
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of the subjects, Lucie and Marie (1913, p. 131), asserting their identity. One says, “It is I Lucie but you have changed me,” and Marie says, “It is still always me ... but not at all the same thing”. Janet goes on to remark that Deleuze had observed that some ‘somnambulists’ talk of themselves in the third person. Janet (1907) had another case, which he called an “artificial Félida”, referring to the moods of depression in both cases. Janet (1907) wrote of: “a double personality ... produced artificially ... in 1887 a young woman of 20, whose name was Marcéline, entered the hospital ... For several months past she had not taken any food [and] ... had reached the last stage of emaciation.”
She was fed under hypnosis. After hypnosis she forgot what had happened. Before hypnosis she could not get out of bed and had retention of urine, which hypnosis relieved without catheters. Repeated hypnosis kept her lively, cheerful, intelligent, and active by day. At night she was allowed to relapse, inert and immobile. The treatment begun by Jules Janet in 1887 was continued by his brother Pierre, for over 10 years. Janet (1907, 1913) never gave Marcéline another name. He studied differences between two phases in which memory, mood and behaviour alternated, but the individual was still the same person. At times Marcéline fell into profound depression. Janet (1913) finally concluded “dual personality is the hysterical form of periodic depression”. The strongest reason for calling Marcéline an “artificial Félida” was the induction of alternating retarded or withdrawn states, and cheerful, alert ones. We may wonder how many other cases of recurrent depression have been cast in a pattern of dissociative disorder, from Mary Reynolds onwards. Certainly, a relationship between hysterical symptoms and depression has been suggested on other grounds as well (Slater, 1965; Gadd & Merskey, 1975). Félida (Azam, 1876, 1887, 1892) and Janet’s cases (Janet, 1889, 1913) offer 19th-century instances where more than two such conditions emerged. In Félida, a frequent state of an elevated mood alternating with the primary personality was observed, and briefly a third state in which the patient had some terror. In Léonie all three personalities had similar names, and the secondary personalities had knowledge of those revealed earlier. Lucie, Marie and Rose resemble Léonie. There is so much evidence of active shaping of Janet’s cases that it would be unjustified to accept any of them as spontaneous examples of MPD without
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strong positive evidence for the syndrome, which is lacking. We also see that Léonie came to Janet fully formed by ‘magnetisers’, the naming of individual personalities was a practice which he took from them, and there is open acknowledgement of pressure on his other subjects to develop secondary personalities. On occasion he appears to indicate this for all his cases, not only Marcéline, who is frankly described as an “artificial Félida”.
Other late-19th-century cases Another leading French case, Louis V. described by Camuset (1882), Bourru & Burot (1885) and Myers (1886), is complicated and varied with hysterical paralysis, mood changes and a motive to avoid punishment. The emergence of the personality changes is also not described in detail. Hacking (1995) describes the history in full and sees Louis V as the first real case of MPD. Richet (1883) describes women with partial striking amnesias. He says of his cases, however, that they have lost the memory of their personality. They gave to their moi, forms which were different from their real forms. He sees this as a transformation of personality for which it was enough to pronounce one word with sufficient authority. He describes the activities of M. in different roles of peasant, actress, general, priest and nun. Another case is a general, sailor, old woman, little girl and pastry cook. These cases appeared to be frank examples of play acting under the command of the hypnotist, rather than any form of spontaneous individual variation into alternate personalities. Similar dramatic changes were obtained by Rochas (1887), who presents a case where a change of name and role was produced by post-hypnotic suggestion. On the other hand, the case of Proust (1890) was a lawyer with hysterical fugues, easily hypnotised, convicted of dishonesty, and pardoned on the grounds of automatism. None of these cases shows a valid pattern of independent personalities, and Proust presents his case as one of automatism. Dailey (1894) described a melodramatic case with initial head injuries and clairvoyance. According to Dailey, both George M. Beard and W. A. Hammond denied the validity of his case. Janet (1907) wrote about it: “The history is strangely related; you feel in it ... an exaggerated seeking after surprising and supranormal phenomena. Mollie Fancher ... at least five persons, who have very poetical pet
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names: Sunbeam, Idle, Rosebud, Pearl, Ruby.... The complication of this case is very amusing.”
Many early cases had evidence of organic disease. Among 14 cases before 1905 at least two, and possibly three, had significant evidence of brain damage, while another three had evidence of epilepsy (Sutcliffe & Jones, 1962). Other patients had fugues or somnambulistic states, or were hypnotised, although some of the remaining cases were said to demonstrate true MPD. An embarrassing failure to recognise an organic element appears later in a case described by Franz (1933) and discussed below. It appears that the leading 19th-century cases were examples of bipolar illness (Reynolds, Skae’s patient, Félida), organic cerebral disorder (see Myers, 1903; Sutcliffe & Jones, 1962) or hypnotic induction. The last was sometimes overt and frequently persistent, if less obvious. It is possible that Félida also represents the effects of hypnotism. Azam investigated hypnosis with her but says it failed to cure her, and he also described a number of hysterical features in her, including nervous episodes, multiple vague pains, the ‘hysterical nail’, unexplained haemoptyses, globus hystericus, impaired taste and olfaction, anaesthetic points on the body, and convulsions for the least emotional matter, without loss of consciousness. On balance, a depressive fluctuation seems more likely, bearing in mind that, like others of the period, Azam might well call general nervousness or mood change ‘hysteria’. Like others, too, he would have been oblivious in 1858 of the enormous impact of suggestion on a distressed patient. In any event, the non-organic causes are clearly made up of these two groups, namely affective disorder or suggestion under hypnosis (or both), and Myers (1903, p. 322) describes Janet’s cases as “factitious”, saying that he thought they arose from selfsuggestion under hypnosis. We have seen that patients were not the only source of suggestion.
The turn of the century At the turn of the century three notable American cases were added to that of Mary Reynolds: the Reverend Ansel Bourne, the Reverend Thomas Hanna, and Miss Beauchamp. The Reverend Ansel Bourne of Rhode Island (James, 1890; Hodgson, 1891) was an itinerant preacher who disappeared from home. Two weeks later a man calling himself A. J. Brown rented a small shop at Norristown, Pennsylvania. Some seven weeks
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subsequently he woke in a fright and asked where he was. He said that his name was Ansel Bourne; he was entirely ignorant of Norristown. Under hypnosis he recalled the lost initial two weeks, which included visits to Boston, New York, and Philadelphia, resting, reading and looking around. Coons (1984) denies that this was a case of MPD and emphasises the misdiagnosis of many early cases. This case seems to represent a fugue in which the patient established a new identity. Unlike most MPD cases, the persistence of the role was very brief and the alternate state was less happy or lively than the usual secondary and tertiary personalities which are described. Stengel (1941) noted the importance of depression in many fugue states. The Reverend Thomas Carson Hanna was born in 1872 (Sidis & Goodhart, 1904). On 15 April 1897, he fell from his carriage and was picked up unconscious. Large doses of strychnine were administered hypodermically, and on waking the Reverend Hanna appeared to be offering to push one of his physicians. He was strong but was overcome and bound with straps. He lay quiet and the straps were removed, after which it was recognised that he had lost his speech and appeared to be in a state of “complete mental blindness”. He was re-educated, like an infant. In May 1897 the observers remarked: “No memory of his previous life spontaneously occurs to him. The time of the accident may therefore be considered as the boundary line between two distinct and separate lives of the same individual.... We may say two personalities dwell within the same individual.”
The Reverend Hanna was investigated through dream analysis, interview, and hypnosis. He was encouraged to establish recollections. Incidents from his past life were recalled, or reconstructed (or created). After two months the personalities were reconstituted, apparently spontaneously, in a state resembling mental stupor. No second personality is described, only the recall of primary experiences alternating with the impaired awareness of the external world associated with an amnesia, possibly organic initially, with hysterical elaboration. The most famous case is Christine (Sally) Beauchamp. Prince described her first in 1900, reported her at length in 1905 in The Dissociation of a Personality, and extended the description subsequently in 1908 and 1920. Before Prince’s case, most examples were patients with episodes of altered consciousness in which
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information about the world and themselves was merely reduced, or individuals who entered into a second mood state, or condition of activity. The birth of Sally Prince ultimately described four different personalities in his patient. It is instructive to examine his description of “the birth of Sally” from Miss Beauchamp. He first presents the contents of a hypnotic session in which he was taxing her with not remembering material which she had clearly referred to on previous occasions. He then says that he was startled to hear her, when hypnotised, speak of herself in her waking state as “She”. He writes: “but now the hypnotic self, for the first time, used the pronoun ‘She,’ in speaking of her waking self, as if of a third person; but used ‘I,’ of herself in hypnosis. The tone, address, and manner were also very different from what they had been ... my experience of this case entirely contradicted the view that I had held up to this time. My conviction had been growing that so-called personalities, when developed through hypnotism, as distinct from the spontaneous variety, were purely artificial creations, ... in opposition to this view the personality known as B III, or Chris, which first made its appearance during hypnosis, ... originated and persisted against my protests and in spite of my scepticism asked who ‘She’ was. The hypnotic self was unable to give a satisfactory reply. ‘You are “She,”’ I said. ‘No, I am not.’ ‘I say you are.’ Again a denial. ... I made up my mind that such an artifact should not be allowed to develop. I pursued her relentlessly in my numerous examinations, treated the idea as nonsense, and refused to accept it ... Finally: ‘Why are you not “She”?’ ‘Because “She” does not know the same things that I do.’ ‘But you both have the same arms and legs, haven’t you?’ ‘Yes, but arms and legs do not make us the same.’ ‘Well, if you are different persons, what are your names?’ Here she was puzzled, for she evidently saw that, according to her notion, if the hypnotic self that was talking with me was Miss Beauchamp, the waking self was not Miss Beauchamp, and vice versa. She appeared to be between the horns of a dilemma, was evasive, unable to answer, and made every effort not to commit
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Varied causes and symptoms herself. On another occasion, in answer to the question why ‘She’ (the apparently hypnotic state) insisted that Miss Beauchamp in her waking state was a different person from herself at that moment, the contemptuous reply was: ‘Because she is stupid; she goes round mooning, half asleep, with her head buried in a book; she does not know half the time what she is about. She does not know how to take care of herself.’ The contemptuous tone in which she spoke of Miss Beauchamp (awake) was striking, and her whole manner was very different from what it formerly had been when hypnotized. The wary, resigned, attitude was gone; she was bold, self-assertive, unwilling to accept suggestions, and anything but passive. A few days after this, when hypnotized, all became changed again; the former hypnotic manner returned. ‘Who are you?’ I asked. ‘I am Miss Beauchamp.’ Then, after a number of questions on another point: ‘Listen: now you say you are Miss Beauchamp.’ ‘Yes ...’ ‘The last time we talked you said you were not Miss Beauchamp.’ ‘You are mistaken. I did not. I said nothing of the sort.’ ‘Yes, you did.’ ‘No.’”
McDougall (1948, p. 497) observes, “It has been suggested that in the course of Prince’s long and intimate dealings with the case, involving as it did the frequent use of hypnosis ... he may have moulded the course of its development to a degree that cannot be determined. This possibility cannot be denied.”
Perhaps Prince did not discourage multiple personality as much as he suggests. Despite his statement to the latter effect, he asked for names, and he strongly reminded the patient of another ‘she’. We cannot know what would have happened had he ignored minor discussion of the patient’s self in the third person.
After Morton Prince Bernard Hart (1912) had a patient who had an angry outburst followed by a partial amnesia. He was told in psychotherapy that he was like a person who was not whole, sometimes like four-fifths of the whole individual, sometimes like one-fifth chipped off. Hart says “The ‘1/5th man’ underwent a rapid development, and was subsequently a much more complicated person than on the occasion of his first appearance”. The more prominent cases in this period were mostly described in America. Doris Fischer (Prince, 1916) is reported in a rambling fashion. The emergence of the first personality is associated with
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strong hints of possession and hysterical delirium or “sleep”. Two secondary personalities are said to have emerged at the age of three, when the patient was physically ill treated. The information given is essentially retrospective as well as jumbled. Goddard (1926, 1927) met his case, Norma-Polly, when she was 19, on admission and an established patient with at least two different phases of personality. Good reasons are given for emotional disturbance in this patient’s life, but the process of appearance of the second personality is not specified. A strong hint is offered on page 115, where it is suggested that at the age of 18 the patient had the opportunity to visit a sister, aged four, who was being very well cared for, when she was not. She would have been expected to imagine herself in her sister’s place. Such legitimate wishes could have developed into the evolution of a personality with another name. However, the proof of this is lacking. Hacking (personal communication) has obtained evidence that Norma was admitted to a psychiatric hospital in 1923 with a diagnosis of mania, although Goddard claimed she had been cured. One of the most interesting cases is briefly described by Cory (1919). A young woman sitting alone in the house at the piano felt as if something said to her “take a deep breath”, and the sound of singing which she had never heard before came from the same direction and frightened her. Just before the song she had shuddered, and felt as if something had possession of her; she went to the kitchen to get a drink then and asked, mentally, who was it that sang, and she acquired another name. It was several weeks, however, before this other person learnt to emerge or to submerge the original personality of the patient. This appears to have been a daydream or wish for fulfilment of another role partly granted by the unconscious. The new person began to speak garbled Spanish, which fitted the needs of that personality. On close inspection this case looks rather like one which might have to be treated as an example of conscious fantasy. It is also not outlined in very much detail.
Misdiagnosis and overt production The case of Franz (1933) reflects partial misdiagnosis. The patient suffered from a confusional state due to neurosyphilis and then contracted malaria, which probably halted the syphilis, or slowed it down, but left brain damage. The original physicians did not recognise the diagnosis of neurosyphilis. The patient moved to America and was examined and reported by Franz
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(1933) simply as a case of multiple personality. Before the book appeared the patient returned to England, gave evidence of a manic–depressive syndrome, was admitted to the Maudsley Hospital in London in 1931, and was shown to have positive serology for general paresis of the insane. After treatment with induced malaria, he still showed some (organic) memory disturbance (Lewis, 1953). Lewis provides a compelling argument that this patient had some organic brain change and hysterical symptoms at the time that he was diagnosed as a case of multiple personality. The conclusion of Sutcliffe & Jones (1962) and the organic evidence in the case of Thomas Hanna were noted above. Sara, the case of Lipton (1943), had repeated attacks of amnesia. Lipton wrote: “In discussing ... violent behaviour with the ... staff, as well as with Sara, one was constantly saying, ‘Sara changed again,’ or ‘Sara had one of her violent spells,’ or some similar expression... it was decided to call the patient by another name, Maud, when she appeared different ... this was merely for convenience...”
A determined effort was made to be kind and considerate to Maud. Soon two different personalities emerged. Sara was mature and intelligent, with an IQ of 128. Maud had an IQ of 43. Numerous other differences developed. Later, a third personality emerged: “She identified herself as Sara and denied the existence of any other personality as did the other two. She was dubbed Ann.... The failure to discover Ann in 7 months of observation in the hospital, for a time even after diagnosis of dissociated personality was made, is evidence of the skill with which the various personalities ‘covered up’.”
The question arises to what extent a similar manufacture occurs with other cases, albeit less obviously. We remarked upon frank suggestion previously, with hypnosis by Pierre Janet (1889, 1913), and Jules Janet (1888), as well as the highly questionable evolution of Hart’s patient.
Recent cases: from Eve to Billy Milligan Relevant detailed accounts are available on a number of recent cases. Among them the most notable, Christine Costner Sizemore, called “Eve” by Thigpen & Cleckley (1957), has also provided her own version (Sizemore & Pittillo, 1977). She was seen for headaches
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as an out-patient. She seemed to be “neat, colourless, gentle, humble, not under-nourished”. During one interview she spoke of a voice she heard, apparently wishing to say more and finding herself at a loss for adequate expression. The medical authors write: “Eve seemed momentarily dazed. Suddenly, her posture began to change. Her body slowly stiffened until she sat rigidly erect. An alien, inexplicable expression then came over her face... suddenly erased into utter blankness... Closing her eyes she winced... A slight shudder passed over her entire body. Then the hands lightly dropped. She relaxed easily... There was a quick reckless smile. In a bright, unfamiliar voice that sparkled, the woman said ‘Hi there Doc!’. With a soft and surprisingly intimate syllable of laughter, she crossed her legs, carelessly swirling her skirt ... in a manner which was playful and somehow just a little provocative.”
Sizemore says that after a discussion of ‘hearing voices’ she changed. “As she sat ... eyes downcast, unable to hide her pain, she moaned softly. Then ‘slowly the head raised, straight and proud; the sparkling eyes gazed back at him sardonically. ‘Hi Doc,’ she chirped, changing the tired droop of her body to a sensuous slouch with one almost imperceptible wiggle. She asked the doctor for a cigarette which he gave to her hesitantly. He lit it for her and said ‘Who are you?’ ‘I’m me’, she flipped. ‘And what is your name?’ he pursued. ‘I’m Chris Costner’. ‘Why are you using that name instead of Chris White?’”
Thigpen & Cleckley described their case as Eve White, who altered to become Eve Black. The patient described herself as Chris White who altered to become Chris Costner. Costner was the maiden name and there were substantial marital difficulties. As with Prince’s Sally, the second personality disparaged the first. Dr Thigpen witnessed a dissociative episode. The important difference between the two accounts is that Eve used her maiden name, a point mentioned two pages further on in The Three Faces of Eve, where the authors note that the pseudonym ‘Black’ stood for the patient’s maiden name. We can see denial of the marriage, for reasons well described by both doctor and patient. A different pose and set of attitudes were adopted, but this might not have been another ‘personality’; it was an affirmation of a previous (real) single state which the patient regretted leaving. However, the patient’s account does partly support the earlier psychiatric account. Sizemore indicates that, as Miss
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Costner, she denied having a child and defended herself by saying that her body might have had the baby but not when she was in it. In any case, once the decision was made to accept a denial of marriage as a second personality, a different pattern followed. From then on, Sizemore had repeated dissociative episodes and ultimately she described up to 22 different personalities. Sizemore was emaciated and depressed on admission. Her childhood as described included some frightening experiences, but not childhood abuse, unlike nearly all recent cases. In searching the literature of individual descriptions of the emergence of a new personality, I only found one other example which might favour the view that it occurred spontaneously in an adult. Congdon et al (1961) described the following instance during a series of therapeutic interviews. The patient was known originally as Betty. “The patient stated that as a child she had created an imaginary playmate she called Elizabeth... During one interview ... she was describing her imaginary playmate to the therapist when she suddenly seemed to become that personality. She sat bolt upright in her chair, at the same time assuming a more relaxed and friendly demeanour, and said to the therapist, ‘I think it’s about time I started telling you about me’. The astonished therapist said, ‘What do you mean?’, and the patient replied, ‘About me, not about her’. She then proceeded to describe herself (Elizabeth) and her career more fully.”
This second personality, Elizabeth, lasted for four months. This case might have been influenced by the publicity from The Three Faces of Eve or similar discussions. No report is given about inquiry into the possible sources of knowledge that the lady might have had concerning multiple personality. Since the widespread publicity about The Three Faces of Eve and Sybil, all subsequent cases are suspect of having been prepared by prior information. Sybil herself (see below) had read a good many psychiatric case histories, and even the change which occurred in Eve, as she describes it, is less impressive in a significant particular than the way in which it was described by Thigpen & Cleckley. If she did indeed principally deny her marriage status, choosing her maiden name once more, and secondarily defended her decision by denying associated items, the creation of the secondary personality was not a pure transformation. Horton & Miller (1972) reported ‘Gloria’, a very disturbed 16-yearold with varied moods, fainting turns and somnambulism, who said one day, “Four years ago I ... went by the name Sue,” and ultimately described four different personalities. Preferring a different name probably served here as a springboard for new personalities.
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Sybil (Schreiber, 1973) was five foot five inches tall, and weighed 79 pounds, when, after repeated amnesias, she entered treatment with Dr Wilbur. Early on during treatment she read many psychiatric case histories. During one session she abreacted violently, regressed in her age, changed her accent, and spoke atypically and ungrammatically. She described an incident in which a child was killed. Dr Wilbur said to her, “Who are you?” She answered, “I’m Peggy”. Peggy then admitted to living with Sybil and her mother, but denied that she was the daughter of Sybil’s mother. The doctor concluded that Sybil was a case of multiple personality. Sybil’s mother was probably psychotic, treated her appallingly, and called her by different names which she preferred, including Peggy. Victor (1975) held that Wilbur persuaded Sybil to believe in extra personalities, but the patient’s reading in the existing literature may also have contributed. Dr Herbert Spiegel has stated in a television interview (Spiegel, 1993) that Sybil came to him from Dr Wilbur for further assessment. When talking about a particular phase of her life, she asked him if she had to become one of the personalities, Flora, or whether she could talk to him in an ordinary way, and when he explored what she meant, she replied, “Well when I’m with Dr. Wilbur she wants me to be that person”. Spiegel concludes that extra personalities were created by the therapist. Sybil was also said to be subject to sexual abuse, and Hacking (1991) points out that the expectation of sexual abuse in the history of patients with MPD (and its widespread discovery) dates from the case of Sybil. Both the last two cases had conscious awareness of the adoption of different imaginary roles. Henry Hawksworth (Hawksworth & Schwarz, 1977) had five personalities, also adopted consciously. The second one appeared when he was three years old and persisted for 40 years. He was abused and later suffered from marked depression and elation and abuse of alcohol. He pretended (p. 23) that another version of himself, an imaginary playmate ‘Johnny’, lived inside a ventriloquist’s doll. Even if he blamed ‘Johnny’ for his misdeeds, he recognised that he himself still got punished at home and at school. Hawksworth recalls being in the playground, thinking of himself as Dana. His teacher said: “Henry Hawksworth, you are to report to the principal’s office immediately.” “‘Yes Ma’am’, said Dana, uncertain why the principal would want to see him.” He was punished for bad language, spoken by Johnny.
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In this case serious adult misbehaviour occurred, alternating with phases of sober, calm, settled and successful work as a law-abiding citizen. The adoption of multiple personalities was conscious and grew out of childhood fantasies with an obvious motive, which are also presented as overtly conscious. There is another difficulty, as well. Like others in this group, the story is not always told consecutively like a psychiatric history, but often in the screen-play, flash-back pattern, which makes it hard to establish an adequate picture of the full sequence of events and the life history. Christina (Peters & Schwarz, 1978) was terribly abused. A brutal father killed one of her baby siblings, terrorised her mother, and raped her when she was five. She lost consciousness or recollection, and woke in an orphanage as Marie. She became an alcoholic and a drug addict, fantasised about spirits, and believed she was possessed. Her doctor claimed to exorcise her. Afterwards he introduced her to the idea of multiple personalities, and she developed them. As a child she had retreated into an alternative identity. Her adult condition was taught to her. W. S. Milligan (Keyes, 1981) committed repeated rapes. He was found not guilty by reason of insanity, that is, multiple personality, and has been kept in a psychiatric forensic institution. In his first year of life he was in and out of hospital. His alcoholic father committed suicide. A brutal stepfather abused him physically and forced anal intercourse when he was eight or nine years old. From the age of three years and eight months he had an imaginary playmate. When he wanted to play with his baby sister, his mother said he could not do so. When he woke he had the identity of ‘Christene’, who could play with the baby. It is not clear if this was an unconscious switch. By the age of nine, he had six other imaginary identities, seemingly often conscious. Every situation called out a new role, such as Adalana, a girl who would enjoy washing dishes when it was required. Eve and Sybil had depression, severe anorexia, and hysterical amnesias or fugues. The first appearance of a ‘secondary personality’ in Eve was an episode of denial of her marital relationship. We are not informed if she knew of multiple personality before the change. Once she became a case of ‘multiple personality’, the stage was set for 22 individual forms to emerge. Thigpen & Cleckley (1984) have been reluctant to diagnose subsequent cases, but ‘Eve’ has been the model for hundreds more, perhaps for all the cases that followed. Before the full adult syndrome emerged, Christina had direct instruction from her doctor about multiple personality. Elizabeth followed Eve. Sybil probably read descriptions of multiple
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personality and was persuaded by her therapist, at least in part. The two male cases and Sybil, Christina and Gloria consciously used their alternate roles for emotional relief, or social advantage. Eve’s case has the most convincing descriptions and yet a doubt remains. In her case it is uncertain whether there was prior knowledge of the concept of multiple personality. On the other hand, it does not appear to have been ruled out, there is a strong lead to another explanation, the childhood experience is not apparently typical, and the more sceptical we become about personality number 22, the more we may question the first alternate. Milligan also raises doubts and his reliability has been strongly questioned already (Thigpen & Checkley, 1984). In these cases the role of a secondary personality, at any age, developed out of depression, or severe emotional conflict, and as a protection from experiences which could not otherwise be tolerated. In most or all of them spontaneous origin of anything that we should call MPD, without some awareness, is either doubtful or disproven. This need not imply malingering. I take malingering to mean the conscious adoption of a symptom in order to achieve a deliberate or unfair benefit, ordinarily at the expense of others or society. Here the patient, with some awareness, adopts a role which at least part of the environment favours. Cases like the Reverend Ansel Bourne suggest that brief spontaneous second identities might emerge in vulnerable individuals with the help of depression and environmental stress. Secondary identities might appear in others, like Gloria, Sybil or Henry Hawksworth, as a result of fantasies of imaginary companions, social encouragement, or some combination of these items. However, the persistence of such individual discrete identities, if any, is not evident without the artifactual medical, psychological or social processes which we have been noting here. Lastly, among case reports, Allison & Schwarz (1980) describe several patients. Their first presented fully formed. Analysis of her process suggests spontaneous developments as a child, but the origins of the adult patterns are not clear. Another patient was treated by exorcism. No example in the book, which is written for the general reader, is convincing.
The weaknesses of MPD A different perspective The examination of the above cases suggests we need a new perspective on the 19th century and its contribution to MPD, as
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well as those who, in the 20th century, emulated the original pioneers. It appears from my review of the literature that the early cases show limited development of dual consciousness. Their changes are related to fluctuations of mood, anorexia, hypnotism, overt suggestion, or organic disease. Dual personality as distinct from dual consciousness is sometimes explicitly denied (Azam, 1887). James, Azam and Janet were concerned with somnambulism, awareness, automatic behaviour, attention, memory, dissociation, and ultimately, recognition of the self and awareness of the self. These topics were prominent for Herbert Spencer in his book, The Principles of Psychology, in 1870, and are described by Coupland (1892), among others. They continued into the 20th century (e.g. Myers, 1903; Stout, 1919). The discussion centred on ways to understand the operations of the mind, in quite another direction from the issue of multiple selves. A number of the early cases raise questions of diagnosis. Three of the most famous have a strong spontaneous streak of bipolar fluctuation or depression persisting for many years, namely Mary Reynolds, the case of Skae, and Félida. Others have a prominent organic contribution which, as mentioned, seems to be quite well accepted already, for example by Myers (1903) and by Sutcliffe & Jones (1962). In the 20th century, the cases of the Reverend Thomas Hanna and Franz/Lewis’ patient also had undisputed organic problems. All the cases of Pierre Janet, as well as most of the other French ones, emerged with hypnosis. Marcéline was severely anorexic, like Eve and Sybil later. Interestingly, Hacking (1995) noticed that towards the end of his long professional career Janet (1925, Vol. 2, p. 842–846) remarked that his patients were like those with folie circulaire, that is, having bipolar affective illness: “The changes ... in hysterical patients are only peculiar forms of the oscillations that can be observed in periodic depressions. The excitations we have just been speaking of are no longer so extra-ordinary if we assimilate them to the excitations which occur spontaneously in these other patients. The earlier French alienists had carefully studied the cases of what they called folie circulaire...”
Janet went on to describe a patient whom he considered differed from his earlier ones because she had these phases of mania and depression, as well as one of normality every month. Alcoholism was overt in later cases (Hawksworth, Christina). Louise (Janet, 1888) and Sara (Lipton, 1943) were openly created, probably like Léonie and several others.
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No case has been found here in which multiple personality, as now conceived, is proven to have emerged through unconscious processes without any shaping or preparation by external factors such as physicians or the media. In respect of this argument, we may have reached a situation comparable to Heisenberg’s principle of uncertainty: observation of the phenomenon changes it. If this is true, it means that no later case, probably since Prince, but at least since the film The Three Faces of Eve, can be taken to be veridical, since none is likely to emerge without prior knowledge of the idea. It is likely that MPD never occurs as a spontaneous persistent natural event in adults. The cases examined here have not shown any original dissociative conditions which are more autonomous than a fugue or a second identity promoted by overt fantasies or conscious awareness. The most that might be expected without iatrogenesis is that an overt inclination for another role could cause the adoption of different conscious patterns of life, as in Cory’s (1919) case, or perhaps the case of Horton & Miller (1972). Without reinforcement such secondary changes would ordinarily be expected to vanish. Suggestion, social encouragement, preparation by expectation, and the reward of attention can produce and sustain a second personality. Admittedly, if only those physicians who expect the disorder can see it, those who do not believe in it cannot see it. However, like others, I was willing to entertain its existence and never found it myself before the dramatic rise in reported cases occurred, or since. Meanwhile, it is not necessary to treat patients who have had terrible childhoods and who have conversion symptoms by developing in them additional beliefs in fresh personalities. Enthusiasm for the phenomenon is a means of increasing it. Lack of enthusiasm discourages it. We should consider how patients, and doctors, come to believe in multiple personality, or to present the popular pattern. Four suggestions are appropriate to explain the way in which MPD is created. The first is the misinterpretation of organic or bipolar illness, as already argued. The second is the conscious development of fantasies as a solution to considerable emotional problems, which has also been discussed above. The third is the development of hysterical amnesia, followed by retraining. The fourth is creation by implicit demand under hypnosis or repeated interviews. Retraining may arise in a purely dissociative amnesia, or one which is triggered by a head injury or depression but followed by hysterical patterns of memory loss. This learning effect is evident in Mary Reynolds. Mitchell reported (1888):
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Varied causes and symptoms “The first lesson in her education was to teach by what ties she was bound to those by whom she was surrounded, and the duties devolving upon her accordingly. After a while some striking mood fluctuations were observed between depressed and elated, sad and retiring, or outgoing and over-confident.”
Two personalities were not evident here; only two mood states. The natural effort to retrain the individual is described. The same natural effort comes out very clearly in the case of the Reverend Hanna (Sidis & Goodhart, 1904). One can imagine the consequences if this patient had been in touch with someone who wanted to suggest that he might have thought that he had another mood characterised, say, by the name William. The potential for creating a new story would have been strong. Miss Beauchamp is but another example of the fourth scenario. Prince first describes verbatim a gentle argument with his patient, under hypnosis, about what she could recall and what not. As he attributed the power of recollection to her, she presumably began to distance herself, under hypnosis, from that power and role. Ultimately, in one of her sessions under hypnosis, she used the word ‘she’ for herself at another time, and Prince pounced upon it. Despite his conviction that other selves appearing under hypnosis were not produced by suggestion, he explored the question as to ‘who’ she was and then said, “You are ‘She’”. Despite her denial, he persisted with his assertion and went on, in due course, to ask her for the name of the other personality and later to remind her of ‘she’. Today, patients are better trained. Spanos et al (1986) obtained telling experimental evidence that procedures employed routinely to diagnose MPD encourage and legitimate enactments of the syndrome. The change which occurred in Eve, as she describes it, is less impressive in a significant particular than the way in which it was described by Thigpen & Cleckley. If she did indeed principally deny her married status, choosing her maiden name once more, and secondarily defended her decision by denying associated items, the creation of the secondary personality was not a complete transformation. The development of the condition in some of the other cases in childhood is a kind of conscious make-believe, by necessity, and may be carried through with insight into adult life. Again, this does not amount to spontaneous functioning alternates who should be granted a life of their own for pragmatic, legal or therapeutic purposes. A relevant human mechanism appears in patients with paralysed limbs, or dysfunction of a part. A patient with hemiballismus,
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unable to control the erratic and violent movements of her left arm, described it separately as ‘George’. The tendency to distance oneself from an unpleasant phenomenon is common and easy to adopt. Multiple personality offers a mode of separating, splitting, and isolating particular subjective problems. However, the evidence so far implies that it requires assistance and that the majority of cases are produced by an artificial mechanism. All the cases are probably elaborated by medical interaction or other support. Proponents of the diagnosis of MPD point to the high frequency of sexual abuse in the histories of patients diagnosed as having the condition. Ross et al (1990) found that 90% of 102 patients were so affected. In Canada, where this work was done, a national survey (Report, 1984) has indicated findings of some sexual abuse by touching or attempted assault in 45.6% of females. This is apart from incidents of exposure or threatened abuse. More cases of sexual abuse are also found among patients with chronic pelvic pain. Walker et al (1988a,b) reported that 64% of patients with chronic pelvic pain had a history of sexual abuse, whereas 23% of a control group had comparable experiences. Many of these patients with pelvic pain also had symptoms of a type associated with depressive and somatic complaints. Sexual abuse from childhood is probably much more common than we have been prepared to recognise to date, but is not specific to a particular diagnosis. The frequency of childhood deprivation and other abuse in current patients with symptoms related to hysteria has been recognised for some time in discussions of hospital addiction and simulated illness (Merskey, 1979, p. 66). As investigators have tended to emphasise sexual abuse as a criterion for the diagnosis of MPD, it is hardly surprising that the phenomenon has increased in their sample. While it is highly likely that the troubled patients who are now called cases of MPD have had many problems of abuse and difficulty in their lives, the definition of the diagnosis in terms of that event cannot serve as a proof of the independent existence of the condition. Other criticisms We have already noted that the diagnosis is not common in many countries. Those who rejected it or said that it occurred very infrequently include Mayer Gross et al (1954) and AldridgeMorris (1989, p. 15) in Britain, Takahashi (1990) in Japan, Modestin (1992) in Switzerland, and Götestam (1993) in Norway. There are no scientific reports from most of Scandinavia but in one Norwegian town, of medium size (about 100 000 people in
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the city and local county area), a small group advocates the diagnosis of MPD, to the disapproval of their colleagues in psychiatry and psychology. Altrocchi (1992), on a visit to New Zealand, found it was rare but argued that it should be diagnosed more often. Several critical voices have offered a substantial review of the topic. Kenny (1986) examined the biographies of five prominent reported cases from an anthropological perspective and found MPD to be a play on social roles that could be properly understood only in reference to the current cultural set of “ideal types” or “root paradigms”. He regarded the diagnosis as lacking in explanatory adequacy and he suspected “cultural bias and a covert process of selection, that direct certain kinds of patients to therapists inclined to diagnose their problems in terms of multiple personality”. It was an artifact to which both doctors and the rest of the environment could contribute. Fahy (1988) maintained that the literature lacked information on the reliability of diagnosis, prevalence, or the role of selection bias, that iatrogenic factors may contribute to MPD, and that there is little evidence from genetic or physiological studies to suggest that it represents a distinct psychiatric disorder. Aldridge-Morris (1989) called it an exercise in deception and saw it as a cultural phenomenon. McHugh (1992) criticised both MPD and recovered memory treatments. The proponents of MPD currently argue that not only does the diagnosis have high reliability, but that evidence of validity has been found in a number of different ways. The issue of reliability is not proof of validity. An actor can reliably produce the same performance night after night, in which he convincingly offers a portrayal of a character to hundreds of people who will all agree that, whether well or ill done, he has represented the specific character. The argument of validity is open to further serious question. I suggested earlier that face validity for this disorder is nonexistent. Bernstein & Putnam (1986) described the Dissociative Experiences Scale, which was said to have high construct validity because of a high inter-item correlation, but such a claim is erroneous since inter-item correlation does not measure any type of validity, but rather internal consistency. Sandberg & Lynn (1992) used the same scale to identify a sample of 15% of the general population who scored high with this measure. Among this sample 6% (2 subjects) met criteria for a dissociative disorder. Among a control group of the same size from the other end of the scale, none had a dissociative disorder. However, eight other
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subjects who scored in the top 2% of the population on the Dissociative Experiences Scale had no diagnosis of a dissociative disorder. Using a screening test, to find individuals with dissociative disorder among 15% of the population allows one to ignore 85% of those who would otherwise have to be interviewed. But interviews could only be expected to yield at most one case for every 17 examined from the remainder. Hacking (1995, Ch. 7) criticises this scale radically. Ross (1989) has described an interview schedule for dissociative disorders, which is claimed to have good clinical validity on the basis of a sensitivity of 90% and a specificity of 100% for the diagnosis of MPD. This scale takes responses which indicate dissociation to include trances, sleepwalking, having had imaginary playmates, childhood sexual abuse, answers to 11 questions about amnesic episodes, blank spells, failure to recognise possessions, and a person inside who emerges or takes control, as well as other questions which might identify psychogenic amnesia, psychogenic fugue and depersonalisation disorder. The remaining half of the schedule is devoted to recognising other psychiatric conditions, such as depression. The high sensitivity and specificity cited do not prove face validity or construct validity. Face validity is conspicuously lacking in MPD, and construct validity likewise. Some of the items which are held to indicate dissociation in the schedule are open to question, including, particularly, childhood sexual abuse (which has many other diagnostic associations), and depersonalisation. It is also important that the Dissociative Disorders Interview Schedule includes sections which are bound to be answered positively by anyone who has been told that they have MPD, whatever the other issues in a case. The questions used in order to diagnose MPD disorder include the following: “Have you ever felt like there are two or more very different personalities within yourself, each of which is dominant at a particular time?”
If the answer to this is ‘yes’, the subject is asked, “Do any of the following apply to you?: The personality or part of you that is dominant at any particular time controls your behaviour. Each individual personality is complex and has behaviours and social relationships that are not shared by the other personalities. Two or more different personalities have been in control of your body on at least three separate occasions.
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Varied causes and symptoms Some type of amnesia or combination of types of amnesia exists among the different personalities.”
Questions like these, whether or not they are justified, amount to asking the patient whether or not he or she thinks that MPD is present. They lack any face validity. If a series of patients who have been given the diagnosis and accept it are asked this question by different investigators no doubt there will be a remarkable degree of agreement between the patient and the investigator on different occasions in responding to encouragement. Such reliability is of no particular scientific use, and the answers to the questions have no independent usefulness in providing validation. There is a further discussion of what constitutes dissociation in the next chapter. The journal Dissociation (vol. 2, no. 2, June 1989) has dealt specifically with the question of iatrogenesis. Ross et al (1989) claim that iatrogenic production of MPD by specialists in dissociation has not been reported in the literature. The present analysis of the most prominent cases and authors leads me to an opposite opinion. The same authors also suggest that because they have found no important demographic differences between the MPD patients diagnosed by psychiatrists with many cases and those diagnosed by psychiatrists with few cases, this means that those with many cases are not producing them differentially. This argument is not a proof of validity, only consistency of selection. One of the active authors in the field (Fraser, 1991) has described what he calls the dissociative table technique. Patients are invited to imagine being at a table with empty chairs and to fill the chairs with their other personalities. Putnam (1989, p. 86) recommends, with approval, the extreme technique of Richard Kluft, who stresses suspected MPD patients by extended interviews of several hours. Kluft (1991) himself recommends “unapologetic direct inquiry”. D. Spiegel (1993), in responding to criticisms, said: “We intend to include a tightened version of the diagnosis of MPD in the fourth edition of the Diagnostic and Statistical Manual of the American Psychiatric Association. In addition to some changes in language, we are re-introducing the requirement that the dissociative amnesia be a part of the syndrome in order to make the diagnosis.”
The DSM–IV criteria, discussed at the opening of this chapter, do not encourage the belief that this new criterion is at all restrictive, and it is hard to guess how a restriction on memory in the diagnostic criteria will function with the occurrence of partial personalities or identities of DSM–IV.
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For many years the usual concept of MPD in the literature was indicated by the following statement by Taylor & Martin (1944): the cases show “two or more personalities, each of which is so well developed and integrated as to have a relatively coordinated rich unified and stable life of its own”.Piper (1994c) points out that this conflicts with other current statements in the literature. Ross (1989, p. 109) writes: “Alter personalities are not people... Alter personalities are highly stylized enactments of inner conflicts, drives, memories and feelings... They are fragmented parts of one person: there is only one person”
On the other hand Bliss (1984) says that personalities are obviously imaginary constructs. As Piper notes, this statement is contradicted by DSM–III–R and by several other writers. Kluft (1984) claims “the major identifying characteristic [of MPD is] the presence of separate personalities in a single individual”. Kluft (1985a) also argues “What is essential to MPD across its many presentations is no more than the presence within an individual, of more than one structured entity with a sense of its own existence” (emphasis added). Kluft (1985b) also says “Overt behavioural phenomena are not basic ingredients of MPD”, and he later observed “The irreducible core of MPD is a persistent form of intrapsychic structure rather than overt behavioural manifestations” (emphasis added) (Kluft, 1991). It is hard to reconcile these different statements about MPD with a consistent concept of what it is supposed to represent or of what it is composed. Piper suggested that it is impossible to either prove or disprove comments made about this psychic organisation. A tendency to over-diagnose MPD also seems likely from the guidelines or recommendations offered by its proponents. For example, Putnam et al (1984) state that MPD is a “superordinate” diagnosis: “Once the diagnosis of MPD is confirmed it is important to consider it as the superordinate diagnosis even when other symptom clusters seem to predominate ... amnesia, anxiety, mood changes, hallucinations, somatization and anorexic, bulimic symptoms among others generally can be conceptualized as manifestations of different alternate personalities or of interactions between alternate personality states.”
There appear to be no data in the literature to support Putnam’s statement nor the remark by Ross (1987) that:
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Varied causes and symptoms “Any female between 20 and 40 years of age with a history of childhood sexual abuse, amnesic spells and auditory hallucinations who meets or nearly meets the DSM–III criteria for borderline personality disorder should be considered to have MPD until proven otherwise.”
The expansion of MPD into other diagnoses can only be fostered by the recommendation to treat it as “superordinate”, which is not defined but which presumably means it should always be made as the first diagnosis if believed to be present. It would thus have priority over schizophrenia, manic–depressive illness, and probably any other condition except perhaps for organic disorders, which are omitted from the discussion. Piper (1994b) lists authors and articles which have endorsed the following features as resembling MPD or overlapping with it: obsessive–compulsive disorder, schizophrenia, somatisation disorder, borderline or other personality disorders, rapid-cycling affective disorders, episodic dyscontrol syndrome or intermittent explosive disorder, depression, mania, bulimia, anorexia, various anxiety disorders, self-destructive behaviours, post-traumatic stress disorder, trans-sexualism or other psychosexual disorders, substance abuse of various kinds, and complex partial seizure disorder. It is also suggested that it may present with hallucinations, delusions, catatonia, or symptoms of a thought disorder (Putnam, 1989, p. 141). It is likely that the increasing profusion of symptoms or diagnoses that are linked with MPD, like the expansion of the number of personalities, occurs because once the initial step is taken of saying that somebody can change in this fashion – without critical examination of the proposition – there are no restraining features or criteria to prevent an unlimited growth of fanciful notions in any direction. This is well illustrated by the remark of Ross (1993) that the goverment agencies implanted MPD into children so that some of the alters “could carry more information”, and that present criticisms of MPD are inspired by the same agencies in order to discredit the diagnosis of MPD, so that reports of the discovery of these implanted “alters” will not be believed.
The nature of diagnosis Putnam (1992) notes that a number of dramatic psychiatric disorders such as anorexia nervosa, bulimia nervosa, obsessive– compulsive disorder, and bipolar illness, are daily topics in books, magazines, newspapers, films, radio and television, and asks why MPD is
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singled out as being uniquely susceptible to media contamination compared with other psychiatric disorders. Putnam also asserts that it is specious not to explain why two or more alter personalities should be so tractable to suggestion or to contamination effects. Hysterical symptoms are so notoriously prone to suggestion that Babinski even wanted to change the name to ‘pithiatism’, meaning an illness due to a suggested idea (Babinski & Froment, 1918). Hypnotism is institutionalised suggestion, as we have observed, and even when they do not use hypnotism, the leading practitioners in the field of MPD, including three of those just cited, overtly support procedures which are an open invitation to subjects to dissociate into secondary personalities. Not surprisingly, once the breach is made, patients and practitioners feel free to enlarge the numbers. Such an unbridled development of complaints generated collaboratively by the patient and the physician lacks even the modest homogeneity and restraint which most other psychiatric diagnoses have attained. Diagnosis in medicine is heuristic and variable (Merskey, 1986). Some diagnoses are preferable to others, either because the conditions seem to originate independently of doctors or social demands, or because they are more successful in prognosis or in explaining aetiology, or – most important – because they are the most helpful guides to treatment. They may be influenced by psychological factors or by social expectations, whether we are talking about cancer pain, endogenous depression or post-traumatic stress disorder. However, it is reasonable to reject those diagnoses which most reflect individual choice, conscious role playing and personal convenience in problem solving, provided we have alternatives which are less troublesome intellectually, and at least as practical socially and therapeutically, and not morally objectionable. Hence we can evaluate MPD as a diagnosis with the implicit view that certain other diagnoses are alternatives or better: mania, certain depressive illnesses, schizophrenia, obsessional neurosis, and even some conversion or dissociative symptoms arise in very many cases of supposed MPD, without medical induction or social facilitation.
Negative findings One of the special peculiarities of MPD is that experienced psychiatrists in many places are unwilling to make the diagnosis or
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do not see any case that can be legitimately called MPD, while others (with varying experience) diagnose endless numbers of patients. Ljungberg (1957) found no cases of MPD among 381 patients with overt hysterical symptoms. In 89 cases of classic dissociative or conversion disorder (Merskey & Buhrich, 1975) I encountered no MPD. In 41 years in psychiatry I found none among many more patients having conversion disorders. One patient dissociated and talked of herself in a detached fashion. In that instance the genesis of MPD was carefully avoided. Another, under the care of a colleague, declared she had reported her multiple personalities to please the doctors who first told her that that was her condition. A few patients referred to me as purported MPD have been given the diagnosis needlessly by others. Mayer-Gross et al (1954, 1977) said that multiple personalities were always artificial productions, due to medical attention and also literary interest. Sim (1981) likewise gives a sceptical report. Chodoff (1987) noted the rarity of cases in his own practice and that of colleagues. Fahy et al (1989) reported a patient who fulfilled the diagnostic criteria for MPD. She had seen the film The Three Faces of Eve and read the book Sybil (Schreiber, 1973). Directing her attention away from the “alternate personalities” led to their decline. Lately we reported four cases in which an unjustified diagnosis of multiple personality was made (Freeland et al, 1993). These cases were used to illustrate the concern that MPD may be the result of misdiagnosis by both patients and clinicians. Many of the patients with MPD have had awful experiences and extensive histories of child abuse. The diagnosis of MPD need not exclude other diagnoses, but it is likely to distract attention from them. Alcoholism or depression might be better treated by directing attention to problems with drink, or using non-addictive medication. The diagnosis of MPD (or production of it) may hinder the most appropriate action and damage treatment. Chodoff (1987) writes that in two cases demonstrated on video-tape, he was struck by the bolstering of defences – with a stultifying effect on psychotherapeutic progress – exerted by concentration on the characteristics of the individual personalities rather than the patient’s underlying conflicts. Whether the patient needs management of social relationships, the resolution of conflicts in psychotherapy, the recognition of physical illness, or the prescription of medication, the process of treatment will not be helped by extraneous exciting diagnoses. Concern has been raised both in Canada and the United States about the cost of treatment of MPD. In a dissociative disorders
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unit the cost exceeded $300 000 per annum (Pendergrast, 1995, p. 172). There is also no worthwhile evidence of efficacy in treatment, despite lavish expenditure of money and time (Piper 1994a), and there are prominent examples of patients getting worse in the course of their therapy for MPD (e.g. Ofshe & Watters, 1994; Seltzer, 1994; Pendergrast, 1995). While no adequate representative sample of professional opinion has been taken, the trend of comments among professionals indicates polarisation between those who believe firmly in the diagnosis and those who believe equally firmly that it is wrong. Orne & Bauer-Manley (1991) suggest that the group who believe very strongly in the diagnosis represent a small minority. Mai (1995) circularised 294 Canadian psychiatrists with respect to their experience of MPD and received 180 responses. Fifty-seven per cent reported seeing a case and 42% had not seen one. The mean number of cases seen was 3.78 (s.d. 10.26). As these values imply there was a wide range of frequency with which individuals made the diagnosis. The average number of newly diagnosed cases seen by those responding was 1.21 (s.d. 5.02). One hundred and nineteen individuals or 68% of those responding had never made the diagnosis (Mai, 1992). The figures for the frequency with which individuals make the diagnosis are clearly best explained by a small number of psychiatrists making a very large number of diagnoses – as appears to be the case also from the reports in the literature by those who have produced large series of cases. Following the publication of the article on MPD which has provided the basis for this chapter, I took the opportunity to enclose a questionnaire with reprints which were supplied in response to requests, or were sent to colleagues. Of 90 questionnaires sent out, 44 were returned promptly, of which 38 were analysable. After reviewing the material in the article, four still held that MPD was a valid entity or condition and quite common, 15 supported the view that it occurred occasionally, and 19 rejected the diagnosis. This sample cannot be considered to be representative, but it is the best we have so far. It is potentially biased by the inclusion of some colleagues whom I knew to be sympathetic to my views, although not all supported them fully. This applies, at most, to 10 of those responding. On the other hand, proponents of the diagnosis, or others considering it to be a realistic category, were perhaps more likely to write for copies of the article than those who were not interested, or who disbelieved in it, and were not bothering with the literature on the topic. So far as we know, the majority of psychiatrists and
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other interested health professionals believed that MPD is much over-diagnosed, or should not be diagnosed at all. It seems to me that both on empirical and logical grounds, psychiatry would be better off without the diagnosis. In the fullness of time it is likely that it will be seen as an outstanding example of a doxogenic syndrome. As mentioned on page 154 this term comes from the Greek doxe, meaning opinion, and genon, to produce, and implies that the disorder is a result of the individual’s own thoughts on a matter. Such a condition detracts from the treatments which patients need and another ill-effect also results from belief in it. The value and good sense of psychiatry become suspect as wonders multiply.
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21 Dissociation, repression and false memories
The concept of dissociation has always been of theoretical interest and some practical importance. Currently it has become a burning issue upon which several controversial topics hinge, particularly multiple personality disorder (MPD), the false memory syndrome (FMS), and the plausibility – or otherwise – of the whole notion of the repression of memories. For many years psychiatry took the idea of repression as a comfortable explanation of the loss of memories which might later be recalled in the course of psychotherapy, particularly psychoanalysis. Now there is reason to think that repressed memories of long duration may well not be recoverable in any reliable shape. If that is so, the widespread use of the notion of repression will require reconsideration. To consider these problems it is necessary to look at the development of the idea of dissociation. As mentioned already, hysterical symptoms which do not affect the body have been called dissociative (Chapter 4) and now ICD– 10 also calls hysterical somatic symptoms dissociative (World Health Organization, 1992a). The psychodynamic theory holds that a split occurs between the symptom, which remains conscious, and the emotional conflict, which becomes unconscious, and thus two connected phenomena become separated and amnesia occurs for an important problem. In all cases the essential phenomena are a separation of ideas and loss of memory for the relevant material. Janet and Freud are the two people most responsible for our current ideas on dissociation. Janet drew part of his concept of consciousness from John Stuart Mill and from Herbert Spencer’s book The Principles of Psychology (Janet, 1899). Consciousness was a field of variable size in which sensory phenomena – and other 309
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experiences including ideas – received attention. It is a universal experience that the direction of attention shifts and the items which remain in consciousness vary. Janet assumed, or argued, that consciousness could be narrowed or enlarged. The most extreme case of “retraction” (narrowing) was attributed to catatonia (Janet, 1899). Nowadays we might say that he believed that the contents of consciousness fluctuated in accordance with that selective attention with which we monitor first one source of sense data and then another. Visual items give way to tactile sensations or vice versa; and our own thoughts, or comments addressed to us, enter into consideration and depart from it. The extent of the field of consciousness is bound to vary a great deal with individuals and with their states of mind (Janet, 1907, p. 307). However, complete consciousness is not solely expressed by the kaleidoscope of impressions or notions. It also involves the idea “I see, I feel a movement” (Janet, 1907, p. 304). According to Janet, the ensemble includes an idea of personality or of the whole person of the individual as well as those cognitive constituents which do not necessarily involve self-reference. The ideas which come into consciousness change readily, and in hysteria Janet held that the field of consciousness tended to diminish, or become narrowed, or “retracted”, while neglected sensations might become lost altogether. Thus anaesthesia might appear in a neglected arm. The difference from normal lies in the patient’s susceptibility to such retraction, or narrowing, or losses, a consequence of “feebleness ... of thinking” (Janet, 1907, p. 311). This depends also upon abulia, or a loss of will, by the patient. Dissociation then became an important element in Janet’s definition of hysteria: “Hysteria is a form of mental depression characterized by the retraction of the field of personal consciousness and a tendency to the dissociation and emancipation of the systems of ideas and functions that constitute personality.” (Janet, 1907, p. 332)
Janet (1907, p. 332) was also happy to cite Breuer & Freud (1893–95) as having a very similar opinion with respect to hysteria when they wrote, according to his translation, “The disposition to this dissociation, and at the same time, the formation of [hypnoid] states of consciousness ... constitutes the fundamental phenomenon of this neurosis”. Although this quotation from Freud shows that he also relied upon the concept of dissociation, he took it far more for granted, would use it at first, and then would get on with other business which was more interesting to him. He attended much more to
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dynamics, drives and motives. Breuer (Breuer & Freud, 1893– 95, p. 312) emphasised that dissociation is related to “an excess of efficiency, the habitual co-existence of two heterogeneous trains of ideas”. Dalbiez (1941) expresses the generally accepted view that, in Janet’s opinion, anomalies of psychic activity have to be explained by “The purely negative idea of ‘deficiency’” (vol. 1, p. 190). Breuer & Freud’s views of hysteria differ from Janet’s in a number of respects: a refusal to trace hysteria directly to a congenital hereditary degeneration (Breuer, p. 312); offering in place of a mere description a dynamic explanation by a play of mental forces; and referring psychical dissociation not to a congenital disability but to a special process called “repression” (Freud p. 61). Freud’s system of explanation relies on the positive idea of conflict and efficient causality. Throughout the Studies on Hysteria, Breuer & Freud write about the splitting of the personality and how ideas or conflicts may become conscious or unconscious, but apart from the quotation which Janet so much appreciated, they go no further into the nature of dissociation. Janet himself later referred to the relevance of conflict (Janet, 1925) but only briefly, mentioning that Morton Prince had identified conflict as a factor in preventing the recovery of memories. Typically, Freud viewed dissociation as the removal of ideas from one compartment to another. This can be seen very readily in the Introductory Lectures (Freud, 1917, p. 248), where he used the metaphors of rooms and doorkeepers for the unconscious and conscious minds. Breuer (Breuer & Freud, 1893–95, p. 307) also wrote of splitting of the mind rather than of consciousness. William James (1890) was, like Janet, interested in studying both conscious experience and the phenomena of illness which might demonstrate changes in memory. In the first direction he remarked that experience is trained by both association and dissociation, and that psychology must be written “both in synthetic and in analytic terms” (James, 1890, Vol. 1, p. 487). His use of the idea of dissociation emphasised that “what is associated now with one thing and now with another tends to become dissociated from either”. This in turn allows the mind to create an independent abstraction on some topic. He referred this idea back to Herbert Spencer (James, 1890, Vol. 1, p. 506). The idea is isolated as the “law of dissociation by varying concomitants”. Dissociation is a means for correcting ideas of false association. This, however, is clearly distinguished from the dissociation of one part of the mind from another. In this respect James followed Janet, accepting his idea that hysterical patients have a narrow field of attention, and
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therefore may be distracted from one topic to another, losing the first. Such an approach relies on hypnosis, automatic writing, posthypnotic suggestion and similar adventures. Like Janet, he accepted the idea of splitting in consciousness associated with secondary personalities, or of material in hypnosis which is split off and “dissociated from the rest of the subject’s mind” (James, 1890, Vol. 2, p. 614; Vol. 1, p. 384ff.). The more straightforward ideas of dissociation or disintegration have been retained in our idea of the fragmentation of thought processes and consciousness in schizophrenia. Mayer-Gross et al (1954) observed that dissociation of ideas may occur in schizophrenia, and they agree with Janet that the most plausible single feature, constant in all cases of hysteria, is the tendency to dissociation, a breakdown in central nervous integration (p. 123). The idea of compartments in the mind has been used both in psychoanalysis and in the formulation of MPD. It has also been thought that dissociation of consciousness occurs more readily in patients who have had some head trauma with a mild or moderate amnesia, and that even a very partial and temporary disturbance of consciousness serves to start a hysterical dissociation, which thereafter might become self-maintaining. Mayer-Gross et al (1954) emphasise that the dissociative events in schizophrenia, where emotion may be separated from ideas, are very different from those in hysteria, where the dissociation is often transparent in its motivation and thematic in its content, and makes use of dysmnesic mechanisms. Hysterical dissociation is also said to be more massive, while the schizophrenic form is shown in minutiae. Erdelyi (1985, 1990) has demonstrated that Freud repeatedly allowed different meanings for the term repression, and that the concept included conscious processes. Repression was often used synonymously with dissociation, and on occasion repression is identified with dissociation, for example “Moreover, I ... doubt whether splitting of consciousness ... is really different from one due to conscious rejection” (Breuer & Freud, 1893–95). Erdelyi argues that the terms repression and dissociation have no formal distinction, and that the essence of repression is simply “notthinking” about a topic. Erdelyi (1990) develops his views from experimental evidence and from a refreshing reconsideration of the way in which Ebbinghaus, in his study of his own processes of forgetting, avoided thinking about the nonsense syllables which he had memorised except when recall had to be tested. As he puts it, there is a “processing bias”. This very reasonable approach seems
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to me to imply that repression/dissociation is a graded phenomenon without hard and fast boundaries. Such a viewpoint would accommodate quite well the observation of Symonds (Appendix C) that patients with hysterical fugues are aware of the problem which leads to their behaviour. For others, dissociation implies a fluidity of ‘state’ boundaries in hypnosis; for example Evans (1972) refers to “a fluidity or interchangeability of state boundaries rather than any specific features of ... dissociated states”. In this condition hypnosis is conceived of as a trance state. For those who accept hypnosis as a ‘state’, this would imply differences in levels of consciousness between different hypnotic states. Its basis as a trance condition still has supporters, the alternative view of hypnosis being that it is in effect a formula for a social role (Barber, 1969). The occurrence of dissociation in hypnosis requires the occurrence of a hypnotic or hysterical amnesia. In response to objections to the validity of hypnotic amnesia, Cooper (1972) wrote: “I am not convinced that the phenomenon of hypnotic amnesia can be entirely explained on the basis of demand characteristics, instructions, expectations, desires to please the experimenter, or role-playing. Over and above all of these variables, there is a responsiveness to hypnotic suggestions that is part of a unique subjective state and which supports the authenticity and genuineness of hypnotic amnesia.”
He gives a fair statement of the pros and cons in this discussion, and the present writer favours the cons (Merskey, 1971). Hilgard (1973, 1977, 1979) has put forward another paradigm for dissociation, offering what he has called “a neodissociative theory of hypnosis”. He argued that different segments of experience might be accessible or inaccessible to consciousness, depending on the route used to tap sources of information. If an executive ego is in overall control, individual subordinate control systems can sometimes exist in touch with each other, and sometimes not. His leading examples came from automatic writing. Hilgard’s theory is also based upon the concept that not everything people do or achieve is consciously intended, initiated or controlled, and that there may be a hierarchical order for mental contents which can be segregated. He argues that hypnotic responsiveness involves a somewhat reduced influence of executive initiative and control over hypnotically enacted behaviour. Thus the planning function is inhibited and the hypnotized person does not independently undertake new lines of thought or action.
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Suggestions under hypnosis are held to activate subsystems of control directly. Suggestion to the subject will accordingly bypass normal voluntary initiative and effort. Like other theories based upon hypnosis, this one also is at risk of foundering on the rocks of the argument that hypnotic events can be explained as actions taken for the purpose of particular social roles. In addition, there is an obvious lack of evidence regarding the qualitative and quantitative factors involved in shifts between dissociative phases, a problem which may well apply to all theories of dissociation. We noted in Chapter 19, on hypnosis, that dissociation has been said to refer to other patterns of behaviour, for example the ability of hypnotised patients to attempt to detach themselves from their immediate environment (Kroger & Fezler, 1976). Other phenomena which have been placed within the group of dissociative syndromes include depersonalisation and a number of the changes which are associated with post-traumatic stress disorder, such as a subjective state of being dazed and being unable to concentrate, feelings of detachment, blanks in memory or impairment of memory, somnambulism and feelings of detachment or of estrangement from others. Some have held that daydreaming is a dissociative state. Ross (1989, p. 324ff.) lists the following among symptoms which may be associated with MPD and are assumed to have a dissociative connotation: having forgotten large parts of one’s childhood after the age of five; having memories come back all of a sudden in a flood or like flashbacks; long periods of feeling unreal as if in a dream; and hearing internal voices. Depersonalisation disorder is also treated as a dissociative disorder in DSM–III and DSM–IV (American Psychiatric Association, 1980, 1994), and includes feelings that the feet or hands, and other parts of the body, have changed in size; out-of-body experiences; and a strong feeling of unreality. DSM–III–R and DSM–IV (American Psychiatric Association, 1994) placed depersonalisation disorder within the group of dissociative syndromes. The justification for this deserves investigation. It has to contend with the occurrence of depersonalisation in other contexts, which include schizophrenic and depressive illnesses, anxiety states and temporal lobe epilepsy, as well as other possible organic cerebral disorders. A small residual group of patients with marked depersonalisation in whom none of the other diagnoses appear feasible has been studied by different authors over the years (e.g. Davison, 1964) without being conclusively allocated either to a group with ‘hysteria’ or to any other category. Slater
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& Roth (1980) argue for a strong link between anxiety and depersonalisation. ICD–10 (World Health Organization, 1992a) describes depersonalisation – derealization syndrome (F48.1) as a rare disorder which may be part of a schizophrenic, depressive, phobic or obsessive–compulsive disorder. ICD–10 does not mention depersonalisation in connection with dissociative or somatoform disorders. Depersonalisation has also been held to be a type of dissociation in which the patient is told under hypnosis to forget who he or she is and assume the identity of the person he or she would like to be (Kroger & Fezler, 1976). It should be noted that this is quite different from the standard meaning of depersonalisation in psychiatry, in which there is a feeling of loss of reality of the self, often accompanied by feelings of being detached or cut-off from oneself. Kirmayer (1993) notes that dissociation involves a gap or disturbance in normal patterns of integration of memory, self and perception. We recognise this disruption against the standards which we have for the continuity, univocality and rationality of the self. This is expressed in a temporal narrative. In other cultures less continuity, consistency, univocality and rationality may be expected. Thus cultural concepts of remembering and forgetting time and memory shape accounts of action and experience, and may make dissociation more common and less pathological. The nature of dissociation has a cultural component, and some of the circumstances in which we are inclined to think of other cultures as expressing dissociation may not reflect dissociation in terms of their standards. Ever since detailed descriptions of psychological responses to catastrophic events began to be offered, a group of quite typical common symptoms has been recognised, whether these occurred in individuals who experienced misfortune on their own, or in groups who were involved in sudden dangerous and frightening events (see Hésnard, 1914). These symptoms included a number of very prominent anxiety symptoms closely related to high arousal, such as terror or fright, accompanied by the usual autonomic responses of dry mouth, pilo-erection, sweating, palpitation, gastrointestinal changes, and trembling. They also included some phenomena of loss of function, such as inability to move or speak. Sometimes panic is accompanied by overactive behaviour such as pushing, jerking, screaming and thrashing about, and similar outbursts. These variations, beyond panic and in the direction of either stupor or agitation, were regarded as hysterical.
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Kretschmer (1926) provided some plausible reasons why both types of response might be seen to have some value for self-preservation. In today’s usage of the terms hysterical and dissociative, to call symptoms hysterical is also to invite their classification with the rubric ‘dissociative’. Whether that is justified might be an empirical question, such as to what extent do such symptoms occur more often in individuals who show classic hysterical symptoms when not in immediate danger, or are they more notably associated with anxiety and relieved by the treatments for anxiety? Another range of phenomena has also been mentioned commonly in connection with extreme stress. These include symptoms which could be classified with those of paralysis or withdrawal, for example the numbing of sensations which is very common in the face of stress. This numbing is seen as a reduction in the powers of both observation and feeling, with a subjective state of being dazed and being unable to concentrate, feelings of detachment, blanks in memory or impairment of memory, somnambulism, that is, walking about aimlessly without evincing appropriate responses to stimuli, a restricted range of affect, and feelings of detachment, estrangement from others, and an inability to recall an important aspect of the stressful event (‘psychogenic amnesia’). Following the immediate event, psychological phenomena which are usually categorised as post-traumatic anxiety symptoms are often observed, including nightmares, recurrent intrusive thoughts of the original event, namely flashbacks, exaggerated startle response, and increased physiological reactivity, and some symptoms which may be associated with depression, such as withdrawal, difficulty in concentration, irritability and guilt. Insomnia is noted in many cases, and continuing physical complaints concerning headaches, the gastrointestinal system, musculoskeletal pains and cardiac activity may be prolonged. Carlson & Putnam (1988) used data from normal control subjects and subjects with both dissociative and non-dissociative disorders examined with the Dissociative Experiences Scale (DES). They found three factors (which differed slightly between the two groups) and identified them as “absorption/imaginative involvement” (e.g. not sure whether something really happened or was just a dream), amnesic dissociation, and depersonalisation/derealisation. The discussion here suggests that only their list of amnesic dissociation phenomena may be reasonably related to dissociative disorders, and even some of those may not definitely be linked. Typical symptoms shown by Dutch resistance workers who had been incarcerated in concentration camps include specific phobias
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and anxiety related to their incarceration and ill-treatment, flashbacks and difficulties on encountering reminders of their illtreatment, intrusive recollections and recurrent dreams, sudden acting or feeling as if the traumatic events recurred (flashbacks), diminished interest, feelings of detachment, constricted affect, hyperalertness, sleep disturbance, guilt feelings, memory impairment, avoidance of signals that resemble the trauma, and intensification of emotions at exposure to events resembling trauma (Op den Velde et al, 1993). In this context, it is more than questionable whether any of those symptoms should be regarded as dissociative. It is more appropriate to regard them as the persistent residue of conditioning to intolerable stress. ICD–10 places post-traumatic stress disorder (PTSD) (F43.1) in the anxiety group of syndromes, describes flashbacks as intrusive memories and, as with depersonalisation, makes no reference to dissociation with this condition. It also treats numb feelings, detachment, emotional blunting and unresponsiveness to the environment as part of PTSD. To what extent are any of the symptoms which have been regarded as evidence of dissociation in response to stress valid indicators of dissociation, and, if they are valid indicators, what is meant by dissociation? It appears that the only symptoms which could be regarded as dissociative are the classic hysterical ones which have long been recognised, like blindness, paralysis, circumscribed or motivated amnesia, hypochondriacal treatment of symptoms, and somatisation disorder, if it appears. Numbing, which was often combined with fear and anxiety, can be a biological response which provides emotional detachment and a reduction of the harsh impact of enormously threatening stimuli. The consequent difficulties in concentration and memory would be both physiologically and psychologically inevitable. We are forced to think again about what other symptoms can be called dissociative. In other words, although stress is a well authenticated cause of dissociative disorders (witness shell-shock), the symptoms which are found in the typical post-traumatic pattern are most often anxiety and should not be characterised as dissociative without specific justification. Reviewing the detailed contents of the latest large volume on post-traumatic stress disorder (Wilson & Raphael, 1993), and the material cited also in Chapter 7, it becomes evident that the classic hysterical symptoms are remarkably rare in the 84 chapters and 988 pages of text. Some cases of multiple personality disorder are attributed to past trauma, but the strongest statement on possible avoidance or denial of symptoms is to be found in a
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discussion of torture victims (Agger & Jensen, 1993) which quotes Horowitz’s views emphasising the place of denial and avoidance in those who have been subjected to repeated ill-treatment. Formal classic hysterical symptoms are scarce, particularly in comparison with any of the literature on World War I, where such material abounds (Merskey, 1991). Similarly, Warshaw et al (1993), in an extensive study of patients with anxiety, including a group with PTSD, only found a modest, non-significant increase in amnesic dissociation in their PTSD subjects. Examination of their results does suggest that depersonalisation and derealisation may be associated with PTSD, and so may “absorption/imaginative involvement”, as both these phenomena had a highly significant link with the presence or absence of PTSD in their patients with anxiety. The paper does not provide a measure which would indicate whether the severity of the anxiety may have differed between the two groups and whether that was responsible for the increase in depersonalisation and so on in those with PTSD. However, the subjects with PTSD had histories of a longer mean duration of episodes with major depressive disorder, which somewhat suggests that the PTSD patients were the most ill. From the evolution of ideas on dissociation so far, it appears that the main, well accepted phenomena to which the word might be applied are the break-up of mental content, the separation of ideas which were associated, some type of detachment from events, and the gross splitting of ideas or feelings into conscious and unconscious (or accessible and inaccessible) compartments. It is questionable to what extent the symptoms found with post-traumatic stress disorders, or in abstraction from daily life in other respects (where the subject is perfectly well aware of what he or she may be doing), should be regarded as dissociative. Certainly, in order for them to be treated as dissociative, such responses require evidence that they do serve to produce gross splitting and that they are preferentially associated with other unquestionably dissociative states. Care is needed in this respect, since any symptom may be utilised as a hysterical one, but to prove that a symptom is dissociative we would need to show that it functions with an unconscious motive, in other words that there is amnesia in relation to the motive in question, and that it is not simply an ordinary part of human life. Tillman et al (1994) question the routine assumption that ‘trauma’ causes dissociation. They examine this claim with particular reference to childhood sexual abuse. Among other considerations, they note the problems in defining and operationalising dissociation. They note reports which demonstrate that the DES confounds dissociative
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pathology in particular with gross psychopathology in general, and point out that when – as often happens – scores from non-traumatised patients exceed those from traumatised ones, “it is possible that the difference has less to do with dissociation per se, and more to do with gross pathology”. They point out that weaknesses of research design are prominent in this literature; at least some sexual abuse is not necessarily experienced as overwhelmingly traumatic, and broader childhood stress (deprivation, physical illness and ill-treatment, bereavement etc.) producing a pathogenic family environment has been shown to be more harmful than early sexual trauma (Nash et al, 1993). Also, the validity of many claims of sexual abuse is in doubt, as we shall shortly see. We find that not only is the wide concept of dissociation doubtful, but also its link with conventional trauma is uncertain. As with the nature of the connection between trauma and dissociation, so too Putnam’s claim (1989, p. 6) that dissociation occurs in both minor non-pathological and major or pathological forms, which is supported by a number of other authors in the literature, requires proof. The occurrence of supposedly dissociative symptoms among combat veterans does not constitute such proof, unless they occur in those veterans who more often have amnesias and traditional dissociative symptoms, compared with the remainder of the veterans with PTSD. The inclusion of such symptoms in the past under the rubric of dissociation is understandable, but current standards require more justification. The same applies to the DES, developed by Bernstein & Putnam (1986), which relies upon answers to 28 questions recorded on a visual analogue scale 150 mm in length. The items include missing part of a conversation, remembering the past so vividly that one seems to be reliving it, being able to ignore pain, talking out loud to oneself when alone, looking at the world through a fog, finding evidence of having done things one cannot remember, driving a car and realising that one does not remember what happened during the trip (is not this normal?). As indicated above in the discussion of the DES, not only is that scale unsatisfactory so far in defining MPD but it is not valid to call many of its items dissociative phenomena. This conclusion is one which could be modified in the light of empirical evidence. To summarise, the notion of dissociation has been popular for more than a century. There are differences in the way in which dissociation has been conceived, and it has been held to be synonymous with repression, while ‘not-thinking’ about a topic appears to be its principal characteristic. The phenomena which it should now include deserve keen scrutiny.
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Memories of sexual abuse and repression In the last decade, a strong movement has developed attributing MPD and other dissociative phenomena to sexual abuse in childhood. As already indicated, the proponents of the diagnosis of MPD regard sexual abuse in childhood as a virtually unfailing prerequisite for the adult condition. Sexual abuse is also discussed in the context of other possible hysterical disorders, for example chronic pain (see Chapter 12). As is well known, sexual abuse figured initially in Freud’s theories, and its theoretical importance in hysteria attracts attention to the topic. The sexual abuse of children is undeniably common. A government commission in Canada undertook a broad survey of the population and established that serious sexual abuse before the age of 16, amounting either to intercourse or genital fondling, or touching a “sex part” of their bodies, occurred in 12% of girls and 6% of boys (Report, 1984). Most adult women have encountered lesser degrees of sexual abuse, for example witnessing exhibitionists. The relationship of such experiences to other diagnoses has been canvassed. In a community sample, Winfield et al (1990) observed that sexual assault appeared to be a non-specific risk factor for psychiatric illness. They used a careful definition of sexual assault as a situation in which the subject was pressured into doing more than she wanted to do sexually to the extent of forced contact with the sexual parts of her body or the other person’s. Other historical items were also obtained. Sexual assault appeared then to have a significant relationship with major depression, substance abuse, panic disorder, PTSD, and obsessive– compulsive disorder. All of these were significantly more prevalent among sexual assault victims than among non-victims. Interestingly, somatisation disorder, schizophrenia, dysthymia and generalised anxiety disorder were not more common in the assaulted population. But the authors warn that since somatisation disorder and schizophrenia were very rare in the sample as a whole, their estimates for those diagnoses may be unstable. Brown & Anderson (1991) found that 18% of 947 psychiatric patients in a tertiary care military medical centre reported experiencing childhood abuse. Nine per cent experienced sexual abuse, with or without physical abuse, and 10% physical abuse with or without sexual abuse. Three per cent suffered from combined abuse. Alcohol abuse was more common in victims of physical or combined abuse than in the sexually abused or nonabused patients. The diagnosis of personality disorder (particularly
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borderline personality disorder) was more frequent in the abuse victims also. The patients with childhood abuse were more often suicidal. Again, the lack of association between childhood abuse and hysterical disorders in this population is noteworthy and even surprising. Some relationships have been found in studies of psychologically disturbed adolescents (Sanders & Giolas, 1991) and in case histories of female psychiatric patients (Chu & Dill, 1990) between scores on the DES and reports (but not records) of childhood abuse. In view of the weaknesses of the DES discussed above, these findings appear of lesser significance. The overall impact of childhood sexual abuse has been reviewed by Browne & Finkelhor (1986). Studies which tried to confirm empirically the effects of child sexual abuse, as cited in the clinical literature, indicate that in at least some portion of the victim population, the initial responses are fear, anxiety, depression, anger and hostility, aggression and sexually inappropriate behaviour. Long-term effects frequently reported include depression and self-destructive behaviour, anxiety, feelings of isolation and stigma, poor self-esteem, difficulty in trusting others, a tendency towards re-victimisation, substance abuse, and sexual maladjustment. Adult survivors had identifiable degrees of impairment compared with non-victims. There is no reference in this source to dissociative or conversion symptoms as a result of childhood sexual abuse. The findings are discussed more in terms of impaired sleep, eating disturbance, pregnancy, later poor sexual adjustment, or inappropriate sexual behaviour, depression, low self-esteem, nightmares, and symptoms of anxiety and tension. With respect to any evidence that childhood sexual abuse was a risk factor for bulimia nervosa, Pope & Hudson (1992) found that there were no differences in the prevalence of childhood sexual abuse between bulimic patients and the general population, and concluded that current evidence does not support the hypothesis that childhood sexual abuse is a risk factor for bulimia nervosa. The literature on childhood sexual abuse and adult conditions is now expanding rapidly. Some of the examples cited here suggest that a high percentage of individuals both in general medical clinics and in psychiatric clinics are likely to report experiences of abuse. Unfortunately, few studies appear to be comparable with each other, and many are vitiated by failure to determine if the sexual abuse reported was always known or was only ‘recalled’ in adult life, after a long period when it was not even known to the subject. Problems arise from different definitions of abuse, different techniques for eliciting reports – sometimes
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sketchy and sometimes persistent and pressing – as well as from the study of different populations in clinical samples (Pope & Hudson, 1992, 1995). Urban control groups are by no means always representative of the general population, and altogether there is a wide spread of results, usually without much, if any, effort being made to evaluate the implications of the experience for the individual. It is not acceptable to minimise the impact of the different forms of sexual abuse, but it would also be a bad mistake, scientifically and ethically, to treat all cases from a wide spectrum as equally serious. Sommers (1994) and Fekete (1994) have provided devastating criticisms of the management of some of the statistics now being put forward connected with sexual abuse of women. They have shown serious exaggeration in frequency of severe abuse in supposedly objective surveys, so that it is harder currently to get a sound estimate of the true scope of serious abuse, both physical and sexual. This is true even in the scientific literature. The best hope is that the growing demand for accuracy and care in studies of sexual abuse will provide more reliable and useful data before long. The existing climate of opinion has not only produced some innocent victims, it has also made it harder for the true victims to be recognised.
False memories The study of sexual abuse has generated the question whether memories of it are repressed and then only recovered in adult life. In order to appreciate this problem of the appearance of false memories of childhood abuse, it is helpful to observe some of the contemporary issues connected with the recognition of childhood abuse in the United States. Some of these issues, together with the widespread prevalence of child abuse, have been referred to already. In the United States the Child Abuse Prevention and Treatment Act, passed in 1973 and sometimes known as the Mondale Act, after one of its sponsors, was implemented to fight a genuine problem, namely that child abuse was rarely reported and frequently covered up. The law provided federal funding to match state spending and served as an incentive to create programmes which would detect and treat child abuse. Gardner (1992a,b), a clinical professor of child psychiatry at Columbia University, observes that today accusations of child sex abuse are burgeoning in the United States, but that when the charges arise “from vicious child custody disputes ... or
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in venues such as day-care centers where the potential pedophile has little opportunity for contact with the child alone, the prevalence of child abuse is in reality quite low”. Nevertheless, the numbers of cases of alleged child abuse has grown, and several examples give rise to profound concern about the validity of the legal process and accusations which have ensued. Gardner points out that current American laws require specific people, such as health-care professionals, law-enforcement officials, teachers and school administrators, to report suspected child abuse to the appropriate child protection agency, or incur the risk of penalties. As a result, these professionals are put on the defensive, and there has been over-reporting of even the most absurd and impossible accusations. Gardner sees the basic problem as bias in the system. State and federal money is available for treatment of children who are found to have been abused, but no funds have been specifically allocated for the protection and treatment of those who have been falsely accused. Nor has money been made available for another special and growing group – children who have suffered psychiatric disturbance because they have been used as vehicles for the promulgation of a false accusation. Evaluators who conclude that there has been abuse set in motion events which bring their offices both state and federal funds. If they conclude that there was no abuse, their facilities receive no funding for further evaluation and treatment. In consequence a ‘child abuse establishment’, comprising a network of social workers, psychiatrists, psychologists and law-enforcement officials, has come into existence, and through its very existence, frequently validates an individual’s charges. In a notorious case, Kelly Michaels, a young New Jersey nursery school teacher, was sentenced to 47 years’ imprisonment for allegedly sexually abusing 20 children under her care. Again, Gardner claims that after examining the alleged victims, the accusing parents and Ms Michaels, he was convinced that she did not engage in the variety of abominable acts attributed to her. Yet the parents’ clamour was fuelled by “over-zealous validators and law enforcement officials, leading to Ms. Michael’s conviction”. Rabinowitz (1990) has described the case in detail. Michaels, who was convicted on 115 of an alleged 131 counts of sexual abuse against 20 children, was a 26-year-old worker in a day-care nursery, first as a teacher’s aide and then as a teacher. According to the prosecutors she raped and assaulted the children with knives, forks, a wooden spoon, and Lego blocks. The prosecution maintained that she had been able to do all this unnoticed by
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other teachers, administrators, parents, and visitors to the school, or anyone working for the church on whose premises the school was conducted. “Unnoticed and on a daily basis, Michaels had also, according to the prosecutors, licked peanut butter off the children’s genitals, played the piano in the nude, and made them drink her urine and eat a ‘cake’ of her faeces. For 150 school days, not a single child ever said so much as a single word about any of these crimes because – again according to the prosecution – Kelly Michaels had forced them to keep at least 115 terrible secrets.”
After a total of five years in prison, including pre-trial detention, Michaels was released in 1993 aged 31, following a successful appeal, and the charges against her have now been dropped. Satanic ritualistic abuse is another field in which accusations are now being made. It involves allegations in the context of an alleged vast covert network of highly organised transgenerational Satanic cults (Ganaway, unpublished, cited by Loftus, 1993). Stated simply, the idea of Satanic ritual abuse implies that groups of adults meet secretly for the worship of Satan, and conduct a variety of organised bizarre and cruel activities. At the time of writing there have been more than 35 such allegations in North America, and one or two elsewhere, such as Australia. The numbers quoted for these cases vary. Marron (1989) states that there have been more than 100. One of the earliest reports (Smith & Pazder, 1980) took the sole alleged victim who had been identified to a meeting with the Pope at the Vatican, but no corroborative evidence of stories of bizarre events was provided. This appears to be the book that initiated the craze. In another Canadian case (Marron, 1989), allegations of child abuse were sustained against a mother and two men with whom she associated, but no ruling was made on the question of Satanic activities, including allegations of murder, cannibalism, graveyard rituals and acts of bestiality. The police could find no evidence of these activities. Despite an inability to demonstrate empirically even one example, the most extreme advocates claim that there is such an epidemic, and that there have been murders of up to 50 000 babies each year in the United States (Berg, 1988). A Department of Health inquiry (LaFontaine, 1984) investigated 84 cases of alleged ritual abuse in Britain up to 1992. Three cases of ritual abuse were substantiated in which adults laid claim to mystical or magical powers in order to entrap children and impress them (and also other adults) with a reason for the sexual abuse, keeping victims compliant and encouraging their silence. In each case there was one male perpetrator, aided in two
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instances by adult collaborators. The other 81 cases of allegations were found to have no supporting evidence of Satanic ritual abuse. However, there was clear corroborating evidence in 41% of cases that at least some children had been abused. As in other countries, there are cases in which children are abused and Satanic ritual abuse is alleged, but there were no cases where the evidence included proceedings of Satanic ritual abuse. It appears that although some of the investigations have found adults who abused children, there are also strong indications of a flood of reports of implausible activities which have never been confirmed. Because of the heavy involvement of the ‘child abuse establishment’ in some of these cases, and because of their extent, Gardner has described the present situation in the United States as “Its third great wave of hysteria”, the first being the Salem witch trials in 1692, and the second the McCarthy hearings in the 1950s over the supposed communist threat. The existence of an ‘establishment’ which is predisposed to find evidence of childhood abuse is also blamed for the emergence of what has been labelled the ‘false memory syndrome’. This descriptive label has been put forward by the False Memory Syndrome Foundation, a body established in the USA in March 1992 to combat allegations of sexual abuse which were founded solely on the recall of supposedly repressed memories. Typically, the adult daughter of elderly parents discovers during some form of reported psychotherapy that she was abused by her father during childhood. The accusations against the previously blameless father are usually not supported by the mother, and normally the other siblings reject the accusation. There is no other indication of childhood events which might have indicated an enormous single trauma, or recurring traumas. The family is not dysfunctional and has no resemblance to the many dysfunctional families with serious problems. The probable origin of the symptoms is of considerable interest. Usually, a woman faced with emotional problems has entered psychotherapy. Her complaints are non-specific, for example depression, anxiety, difficulties after a divorce, job problems, and so on. In the hands of therapists who believe in immediately searching for repressed memories of childhood abuse, the patient is quickly encouraged to recall evidence of such events from childhood. If memories do not come quickly, more pressure is exerted. Once a memory is produced, the patient is told to stay away from members of the family until they acknowledge their wickedness and guilt, and law suits may be commenced to pay for the damage done and for further therapy. Families are torn
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apart on uncorroborated evidence, based upon the solicited recall by individuals who have had no knowledge in the 20-, 30or even 40-year interval, of the events which are said to have taken place. A substantial number of stories of this type have now been reported from individuals who have subsequently recanted their recovered memories. In a study of psychotherapy, Campbell (1992) showed that therapists interpreted their clients’ circumstances in a biased fashion. All the articles published in Psychotherapy for the year 1990 were examined. Any article which contained at least one case illustration was reviewed for a therapist’s inferential comments about significant others in a client’s life. Forty-two inferential comments were encountered in ten articles. Thirty-eight qualified as negative, and four as positive. Thus those therapists in this study making inferences about significant others in their clients’ lives predominantly couched them in critical terms. “Blame and change manoeuvres” were well illustrated in the paper. Of course, positive interpretations may not have been made or recorded because they were not needed for the issue at hand, but the negative effects are still evident. Unfortunately, as Dawes (1994) has demonstrated, the clinical practice of psychotherapy is frequently based on unsustainable theories, not to say myths. The FMS Foundation (1993) reports that among 281 accusers who claimed to have recovered memories, the accusations were vague or unsettled in 44.8% of cases. The specific allegations have included fondling (13.8%), molesting (7.1%), intercourse (10.6%), rape (21.6%), sodomy (9.2%), murder (4.6%), Satanic ritual abuse (18%) and oral sex (23.7%). Among 222 accusers, the child claimed first memories ranging from before the age of one (in 12.6% of cases), before the age of two (in 32.9% of cases), and before the age of four (in a cumulative total of cases of 63.5%). Another 20.3% claimed first recollections before the age of six. Of the accusers, 80.8% were aged 20–39 at the time of accusation. Of the accusations, 9.6% were said to have been repressed for more than 10 years and less than 20; 63.7% were repressed for 20–39 years, and 7.1% repressed for 40–49 years. In 61.6% of cases the father only was accused, in 2.1% the mother only, and in 28.5% both. Siblings, grandparents and others were also accused in 45.2% of cases. Apart from the lack of corroborative events, the therapists’ urgency in soliciting the recall of memories has also made both therapists and memories seriously suspect. In this respect, a book which has been helpful to survivors of incestuous abuse has been criticised for its approach to those who do not initially recall such
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a memory. The Courage to Heal (Bass & Davis, 1988) is used by many therapists (Wakefield & Underwager, 1992), and contains statements such as “If you are unable to remember any specific instances ... but still have a feeling that something abusive happened to you, it probably did” (p. 21); “If you think you were abused and your life shows the symptoms, then you were” (p. 22); and “If you don’t remember your abuse you are not alone, many women don’t have memories, and some never get memories. This doesn’t mean they weren’t abused” (p. 81). Even stronger remarks are sometimes reported, such as that within one or two sessions of treating a patient the individual is told “You seem like someone who has been abused. Tell me what the bastard did to you” (Davis, 1991, p. 82). More than 750 000 copies of The Courage to Heal have been sold. Thus its influence is widespread. The process of memory making and the factors which contribute to it have been examined in a series of recent books which individually and together provide an exceptional demonstration of the artifactual nature of recovered memories (Loftus & Ketcham, 1994; Ofshe & Watters, 1994; Wakefield & Underwager, 1994; Yapko, 1994; Pendergrast, 1995). The result of the uproar has been to highlight the issue of how much abuse may be actually repressed or forgotten. Existing indications suggest that repeated trauma is always, or almost always, remembered and, similarly, that overwhelming single episodes of trauma produce long-lasting conscious recollections (Terr, 1991). While Terr describes children who are reluctant to talk about events of which they are aware and states that repression occurs, she does not document the actual repression, and her position has been subjected to a withering critique by Ofshe & Watters (1994), partly on the basis of profound conflicts between her testimony in a court case and her written accounts, as well as contradictory factual information which was not made available in court. Another approach has been to follow up individuals who suffered known oppression and abuse, and approach them much later to determine how often they might display overt recollection of the episodes. Williams (1994) reported a follow-up of 100 women who had reported sexual abuse in childhood in 1973, 1974 or 1975. These women were asked to participate in a follow-up study, looking at the lives and health of women who received medical care at a particular hospital. In the course of an extensive interview they were asked about childhood experiences with sex, in order to elicit their responses about sexual victimisation. Thirty-eight per cent were said to be amnesic for, or failed to report, their known childhood sexual victimisation.
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The author infers that retrospective studies which rely on selfreports of childhood experiences of sexual victimisation are likely to result in an underestimation of the true prevalence of such abuse. However, 53% of these non-reporters actually mentioned another and different sexual abuse experience which occurred at some other time during their childhood, so that only 17% of the abused women in this retrospective study would have been wrongly classified as not abused; and the study describes reports, but not all memories may be reported. In the Williams study some events occurred at ages when the subjects were too young to establish memories and this too was not analysed. Femina et al (1990) examined 69 subjects who, while in jail nine years previously, had reported sexual abuse. In this examination 18 failed to mention the past abuse, virtually the identical number to that found in the Williams study. On further questioning of eight of the 18, they all acknowledged knowing about the past abuse but indicated that they had not wished to discuss it, most often because of a sense of embarrassment, a wish to protect parents, or a desire to forget. The Williams study supports the idea that some memories are lost and may not be recoverable. The strength of that effect is uncertain. Presumably in adults it will be low, but in young children many past experiences will not be available at later dates. On the other hand, the Williams study may be used to argue that some memories do exist which could be unearthed if sufficient attention was paid to restoring them. The problems attendant on proving the validity of such recovered memories have been sufficiently canvassed here. The concept of repression has been at the core of psychiatric theory since the formulation of psychodynamic hypotheses 100 years ago (Breuer & Freud, 1893–95). Thus psychotherapy has been widely conducted on the assumption that repressed material might emerge and be resolved through abreaction. Curiously, there appears to be no independent scientific evidence apart from clinical treatment to validate the notion of repressed memories (Holmes, 1990). Holmes observes that in general repression has three elements: (a) repression is the selective forgetting of materials that cause the individual pain (b) repression is not under voluntary control (c) repressed material is not lost, but instead is stored in the unconscious and can be returned to consciousness if the anxiety that is associated with the memory is removed.
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He focuses on the view that painful material is expelled from consciousness and kept out of awareness thereafter because it gives rise to anxiety. Holmes finds from a thorough study of the relevant literature that there is no scientific evidence that repression occurs. Although Holmes’ work was published in prominent places in the psychological literature, it was neglected by clinicians who are still unwilling to give up the view that they encounter evidence from their patients which proves repression, even though we have known, at least since the days of Charcot and of shell-shock, that no phenomenon is so unreliable as the convincing individual case which supports the clinician’s theory. There is also another problem over recovered memories. They become implausible in the light of the information on memory provided by cognitive psychology. Even if the reports which show that significant items of memory can be lost are correct, this does not demonstrate that what is regained under treatment is reliable, or accurate. We know that memory may be lost for salient events which are not necessarily subjects of conflict. For example, onethird of the memories of attendances for the treatment of pain are forgotten within a year (Means et al, 1989) and accidents, too, are often forgotten. The study of memory has indicated quite convincingly that false memories can be created experimentally. Individuals shown pictures of events have been persuaded by experimental instructions to recall non-existent broken glass and tape-recorders, a moustache on a clean-shaven man, straight hair as curly, and even to report something as large and conspicuous as a barn in a rural scene which originally contained no buildings at all (Loftus & Ketcham, 1991). Loftus & Ketcham point out that new information invades us like a Trojan horse, precisely because we do not detect its influence. Any recollection of events is modified under the influence of new information which becomes incorporated into our memory, supplanting and altering the recollection. The knowledge that an event has happened, for instance that one was born on a certain date, or that a world war broke out on 3 September 1939, may be established as semantic memory, but not as a pictorial record engraved in mnemic traces among neurones and synapses. Investigations of recollections of public events have similarly shown marked unreliability, even for quite prominent, specific items connected with them (see Loftus, 1993; Loftus & Ketcham, 1994). It has been shown that a wide range of false memories can also be implanted both by incidental natural events and by experimental procedures (Loftus, 1993).
[
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Current investigations of children’s ability to recall early memories further suggest that before the age of 18 months nothing can be strongly enough registered in verbal or pictorial processing to permit subsequent recall (Howe & Courage, 1993; Usher & Neisser, 1993; Wakefield & Underwager, 1994). Dispositions and tendencies may well be created in that period, but not precise factual material which can be pulled out of ‘a memory bank’ as we would draw the ace of spades or any other card from an unchanging pack. The belief in the notion that false memories are engendered, rather than based upon original facts, is strongly supported by the number of individuals who report that they had false memories which they have subsequently recognised as erroneous. The FMS Foundation, to which in 1995 more than 12 000 families belong, knows of 700 adults who had formerly accused their parents and have now withdrawn the accusations as mistaken. The FMS Foundation knows altogether of more than 20 000 families which maintain that they have suffered a false accusation. This may be only the tip of the iceberg. Pendergrast (1995) notes information on the number of different ‘therapists’ practising in the United States, including doctoral-level psychologists and social workers, and suggests, conservatively, that there are at least 250 000. Other information (Poole & Lindsay, unpublished) suggests that at least 25% of these therapists believe in recovered memory therapy and see about 50 female cases per annum, among whom 34% recover memories of sexual abuse. Pendergrast points out that simple arithmetic with these figures suggests that more than 1 000 000 Americans per annum have been provided with recovered memories and that even if a lesser proportion of cases is found in other years (because of overlap and repeat attendances) it is likely that several million females are affected. If 2.5 million currently identify themselves as survivors, that will represent almost 1% of the American population or approximately one in 25 families. If this is the case then nearly everybody must know someone or some family in which this event has occurred (although it may not have been disclosed). Even if this estimate is three or four times higher than the truth (which I do not think to be the case), then psychiatry is exposed to the influence of an enormous social upheaval – whatever the justification for it or lack thereof. The problem is as common in its impact upon the population as were shell-shock and other causes of casualties in World War I. These events concerning memory have both a theoretical and a social impact on psychiatry. We now have to reconsider the supposed aetiology of all hysterical symptoms that are said to be
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related to the existence of long-lasting repressed memories. In a very important precedent for the United States, a New Hampshire Superior Court has held – after hearing opposing expert witnesses – that the concept of repressed memories lacked evidence of scientific support sufficient to justify its use in a criminal trial (N. H. v. Hungerford; N. H. v. Morahan, 1995) The existence of the material on false memory forces psychiatry to reappraise the role of repression in its scheme of dynamic explanations. If repression occurs at all, we have to see it as not being absolute as before and not likely, or much less likely, to be of long-lasting power in the lives of individuals. As Holmes (1990) indicates, the factors that influence selective recall are important, and the more exciting and more productive lines for future research involve information processing. Interestingly, an occasional organic cause has been reported for false memories. Hays (1992) describes the occurrence of false but sincere accusations of sexual assault made by narcoleptic patients. Four patients, all described as obviously honest, consistently reported experiences of sexual assault, which it was possible to relate to phases of narcoleptic hallucinations. As Hays states, “Many undiagnosed narcoleptics have illnesses in which dreams take place in the daytime, when the subject is apparently awake. The intrusion of REM in this fashion may lead the patient to mis-remember.... Narcoleptics who are finally diagnosed will often describe events in their past, which, by ordinary assessment of what is possible, cannot have taken place; astral travel is an example of this kind of event.”
Narcolepsy is much less common than false memory, and the organic explanation is of comparatively little importance. The overwhelming phenomenon, now, is that – as at many other times – a hysterical phenomenon has become a major social issue. In the present case, unlike some others, this must lead to important theoretical and practical changes. We may not wish to give up some aspects of the concept of repression and probably should not do so, but repression as a long-lasting event is no longer a plausible explanation for forgetting. On the other hand, some of the phenomena of dynamic psychiatry remain and should not be ignored. Selective attention, motivated forgetting and partial recall are still very liable to occur on a day-to-day basis and to have implications in human relationships, but we need a much better theory and practical application of the theory than we have had to date.
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Part IV. Individual dynamics and clinical subgroups
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22 Personality traits
The concept of personality and personality disorders has emerged gradually over the last 150 years. Terms such as personality, personality disorder, character, temperament, constitution, self, type, trait and psychopathic inferiority were all changing and exchanging meanings (Berrios, 1993). The review of this topic by Berrios provides a masterly description of the relationships between efforts at psychiatric diagnosis, the intellectual background of the concepts, and the way in which psychiatrists, who had at first thought of character types and disorders as forms of attenuated insanity, later made them into a separate group with varied causes. In 1923 Kurt Schneider, in the first version of his book Psychopathic Personalities, chose the term personality (Schneider, 1928), and thus contributed to making the words temperament and character obsolete. His description of personality disorders became the model for the great majority of subsequent attempts at the classification of personality, relying especially upon the description of behavioural traits to separate groups of individuals. Current efforts to delineate personality types or disorders attempt, like Schneider, to provide operational criteria. However, as Livesley & Jackson (1991) point out, they suffer from the absence of an accompanying rationale for the inclusion of specific clinical features, a lack of distinctiveness among features relevant to different disorders, and criteria sets that mix specific behaviours such as truancy (antisocial personality disorder in DSM–III–R) and more global stylistic behaviours and traits such as rapidly shifting and shallow expression of emotions (histrionic personality disorder) or interpersonally exploitative behaviour (narcissistic personality disorder). Ekselius et al (1993) have investigated the question whether personality disorders are to be regarded as extreme variants of normal 335
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personality or whether they should be regarded as categories, that is, psychopathological entities that can be qualitatively set apart from normal personality. Their evidence, together with that of Dowson & Berrios (1991) and Schroeder & Livesley (1991), demonstrates that DSM–III–R criteria for personality disorders (American Psychiatric Association, 1987) do not distinguish independent categories. The lack of such categories reduces the support for DSM–III–R and DSM–IV diagnostic concepts. Their findings are consonant with the observation by Widiger (1991), from a review of a series of investigations, that there is a substantial overlap between a number of the DSM–III–R personality categories which are frequently found together in patients, particularly those who are more ill. As Pfohl (1991) points out, if the personality disorder diagnoses are viewed as selections from a descriptive catalogue of behaviour, the fact that many patients meet criteria for multiple overlapping diagnoses is of no great consequence. On the other hand, if the diagnoses are intended to operationalise the diagnosis of a set of personality syndromes which are at least theoretically distinguishable on the basis of aetiology, course and treatment response, a high rate of overlap greatly complicates the problem of validating the distinctions between disorders. At least one observation appears to merit special emphasis in this connection. Dowson & Berrios (1991) suggest that for the routine assessment of patients, the most important derivative of the DSM–III–R classification of personality disorder is the total score on positive criteria for personality disorder. This is supported from an entirely different direction by the report of Mulder (1991), who demonstrated that the diagnoses of personality disorder (made according to ICD–9 categories) in New Zealand were constant as a proportion of hospital admissions from 1980 to 1986 and that the commonest diagnosis, 45% of the total sample, was personality disorder without any further specification. This also underlines the utility of the general diagnosis of personality disorder and the difficulty of the more specific subordinate categories. It is beyond the scope of this discussion to deal with the substantial literature on personality disorders in general. However, we can note that DSM–IV retains a set of personality disorders which include histrionic personality disorder and that this has developed according to a certain traditional pattern. Stone (1993) has produced a cornucopia of information and reasoning which supports the idea that there are five factors, or dimensions, against which such traditional patterns can be mapped. For the purpose of this discussion, the present chapter reviews the features
Year: 1.
Emotional lability, mood changes
2.
Exaggeration (disproportionate anxiety)
3.
Depression
4.
Mental dullness
5.
Lack of volition, deficient will, disturbed intellect
6.
Theatrical
7.
Suggestible
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Dependent
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Childlike, immature, lack of discipline or poor self-control
1600 I
1700 I
1800 I
1900 I
2000 I
11. Deceitful, malingering 12. Disturbed understanding and imagination 13. Sexual disorders
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10. Egoncentricity, self-centredness and attention seeking
14. Expansion of overall concept
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F IG . 22.1. Relative prominence of reports of different hysterical traits (from Alam & Merskey, 1992, with permission of Alpha Academic)
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which have been thought to be typical of histrionic or hysterical personality. Alam & Merskey (1992) traced the origins of this pattern through the English and French literature from the 17th to the 20th century, in order to examine the evolution of the idea of hysterical personality. Until the middle of the 19th century it was common to find that patients with a diagnosis of hysteria were described as having signs of depression with violent and labile emotions and nervousness accompanying physical complaints. Thereafter, depression was overshadowed by attention to suggestibility, egocentricity, deficient will, exaggeration, simulation, and the like. The change of emphasis appears most with the Parisian group, especially Du Saulle (1883), Richet (1885) and Janet (1907). Janet applied the largest numbers of labels of traits, reaching 23 by 1907. The most common features included depression, fearfulness, emotionality, lability, and excitement. Other traits comprised exaggeration, suggestibility, deficient judgement, poor self-control, vivid imagination, erotic problems, self-destructive tendencies, regression, jealousy, shame, and diminution of the field of consciousness and dual personality. Concomitantly with the development of the theories of conversion and dissociation, the emphasis on depression and also on deficient will or lack of volition declined. Figure 22.1 shows the relative prominence of reports of different hysterical traits in different centuries. Some tentative notions of hysterical personality were bound to arise from the numerous traits which have been linked with hysterical symptoms. It is easy to recognise that a person with many complaints but no physical cause might be thought to be demanding and hence manipulative; over-complaining and hence over-demonstrative; readily accepting minor illness as significant and hence superficial and hypochondriacal; unduly keen to attract the physician’s support and hence dependent. In this century the idea crystallised that a number of such traits, believed to be found in association with hysterical symptoms, comprised a particular pattern to which the name of hysterical personality could be given. They include frigidity and exhibitionism in women, attention-seeking behaviour, suggestibility, labile and histrionic attitudes, mendacity with self-centredness, vanity and frigidity (Chodoff & Lyons, 1958). Chodoff & Lyons challenged the association of these traits with conversion symptoms, finding that only three out of 17 patients with conversion symptoms had hysterical personality as defined above. They thought that conversion symptoms were more often associated with immaturity and dependence.
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Many of the usually accepted traits of the hysterical personality are evident in the extract from Kraepelin given in Appendix B. Dependency and suggestibility (when it is acceptable to the patient to receive the suggestion), emotional lability or shallowness of emotional responses, manipulative skill, and minor drama in the presentation of symptoms are all to be found there. The kaleidoscopic reflections of this sort of experience were built up into a traditional picture which was portrayed graphically by Aubrey Lewis (1950) in a standard textbook: “Hysterical Personality This is not found in all patients who show hysterical symptoms but nearly all people of hysterical personality show hysterical symptoms. Many of the features of this personality are socially obnoxious, but other features are not, and it is wrong to use ‘hysterical’ as a depreciatory epithet for a set of qualities that one dislikes. These people are unduly responsive to the situation they are in, especially if by their excessive response they can fulfil the wishes of which they are hardly aware, or evade what is painful in the situation, instead of meeting it and disposing of it adequately. Unsatisfied with their own capacities, they seek to cut a better figure than their endowment warrants, and are constantly posing and pretending. This, like all their behaviour and aims here described, is not done with full consciousness, but with more or less sincere ignorance or ambiguity of purpose; it is not a question of deliberate deceit, of studied histrionics or malingering. In thus responding to situations and turning the response to some inadequate end, the hysterical person is characterised by a lack of inner stability and of constant standards of behaviour, and also by a lability of affect and an exuberant fancy. The fantasies normal in childhood are here seen in physically mature adults, who, like children, can temporarily live their fantasies, absorbed in this unreal compound of past experiences and longings, yet not so wholly divorced from their real surroundings as might appear. In an attenuated form, this is evident when they almost unwittingly manufacture some situation, according to their needs – literally ‘making a scene’ – and enter into it emotionally with a rapidity and fervour impossible for more stable people. Egotism and untruthfulness (pseudologia phantastica) may be pushed to the point of delinquency. There may be a longing for prestige, sympathy, love or some other emotional relationship, which leads the hysteric to behave in a way strikingly out of keeping with his demeanour on other occasions; the inappropriateness of his behaviour even at the time may be obvious to a detached onlooker, but is not always so. Many of these people can use illness or well-acted fantasies of illness to satisfy their hardly
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Individual dynamics and clinical subgroups conscious needs; they may also gain their ends by forgetting what it would be painful to remember. Here again the onlooker may find it hard to tell how genuine or complete is this forgetfulness, but the question is of little moment compared with discovery of the motive for the hypoamnesia. Hysterics are often regarded as unduly suggestible because they respond so readily or violently to situations and to people with whom they develop an emotional relationship, often unrecognized by themselves as such. The emotional attitude of a hysteric towards others is often influenced by sexual factors. Hysterical personality is believed to be commoner in women than in men, and may be associated with psychosexual immaturity. Coquetry and frigidity are not uncommonly allied in hysterics; there may be much flirting and sexual excitation, stopping short of coitus. It is, however, juster to say that the sexual lives of hysterics show instability and inadequacy than to specify any particular aberration.”
Many aspects of this pattern exist in people who have not fallen ill. It is as easy to recognise as the driving obsessional or the anxious worrying personality, and it is a phenomenon which derives from many basic human motives. The wish to please, the need to be approved, concern over human contact, a desire to gain some particular acceptance in social or human relationships are found, in varying degree, in almost all adults of both sexes. These characteristics and attempts at manipulating people may be most evident and most open in children, but are virtually universal in some degree. Despite the pejorative associations which attach to it in medicine, the hysterical personality has many features which are useful and positive in society and appreciated in personal relationships. This is inherent, of course, in any set of traits which promotes the adjustment of drive and emotion in dealing with other people. In regard to this common pattern, there are certain questions which are most relevant to psychiatry. Is there, indeed, a particular personality which is found in association with some or all of the main hysterical groups of symptoms? If so, what are the defining features of this personality? Is it found in association with other psychiatric illness? How common is it in the general population? Are it and other personality types mutually exclusive? How is such a personality formed, and what significance does it have for the dynamic understanding of personality, temperament and emotion? Before tackling these questions it is worth setting out the general view of what constitutes the hysterical personality. The view involves two approaches. The first is essentially phenomenological, that is, it involves defining the traits of behaviour and attitudes to which the terms refers. The second is dynamic and
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interpretative, and concerns the attempt to provide a theory of the origins and varieties of the hysterical personality summarised by Chodoff & Lyons (1958), whose list of traits was largely incorporated in the group of rather unattractive attributes mentioned above.
Groupings of traits In accordance with this approach we can find a number of studies which attempt to define hysterical personality or hysterical characteristics. Lindberg (1950), for instance, follows Janet’s (1907) conception that the habitual hysteroid attitude is characterised primarily by strong suggestibility and distractibility. Characteristic traits are: “social restlessness, swift changes in the kind and tendency of activity, impulsiveness, impressionability and changeableness ... fleeting enthusiasm, vivid imagination and uncertainty with regard to the ego-experience with secondary egocentricity, often with verbalistic eloquence and dramatic talent.”
Interestingly, Lindberg & Lindegard (1963) were able to show in a large series of psychiatric patients that there was a significant excess of surgical operations among those women regarded as hysterical. This gives extra validity to the view that there is a link between poly-surgery and the hysterical personality, at least as defined in their terms. Cohen et al (1953) provided even stronger evidence of excess surgery in patients with the Perley & Guze (1962) characteristics, in whom gynaecological operations in particular were conducted extremely frequently as compared with controls. Another way of looking at the hysterical personality characteristics has been to relate them, as Eysenck (1947) suggested, to the notion of ‘extraversion’. Foulds (1965) examined this relationship. Medical and other staff rated patients for the traits of attention seeking, emotional display, speed of decision, lability of affect, conscientiousness, and shallowness of affect. On this basis, patients were classified as hysterical or obsessional. This Hysteroid– Obsessoid Questionnaire (HOQ) produced highly significant differences between these groups. The Maudsley Personality Inventory (MPI) correlated highly for extraversion with the HOQ. Hysteroid or hysterical personality traits thus appear to be related to extraversion.
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In reviewing the literature on this topic, Ingham & Robinson (1964) pointed out that if extraversion is defined in terms of the E scale on the MPI, there is a clear tendency for patients reported as hysterical to score more like normals. This tendency had earlier led to criticism of the notion of extraversion (Sigal et al, 1958). Examining a normal group, and groups with conversion hysteria (26 patients), hysterical personality (30 patients), and dysthymic cases (105 patients), Ingham & Robinson found that the conversion hysteria groups scored like normals for E but the hysterical personality group was more extraverted. Hysterical personalities scored more on the Neuroticism (N) scale than conversion patients. Conversion patients, nevertheless, scored more than normals, while dysthymic patients were much less extraverted than either the hysterical group or normals and scored high on N. From this it would seem that the specific grouping known as hysterical personality can be demonstrated by personality testing and that the conversion hysteria group stands some way between the hysterical personality group and normals. Forbes (1969) showed that Cattell’s 16PF questionnaire (Cattell & Eber, 1957) discriminated between hysteroid and obsessoid personalities among psychiatric in-patients on factors A, E, F, H and Q2, but not on factors G, I and O. Factor G is described in the test handbook as persevering, responsible, consistently ordered and conscientious, and O involves similar obsessional characteristics. Factor I represents demanding, affected, attention seeking and frivolous traits. Its failure to be discriminate the two groups may reflect the particular difficulty of showing these traits with the instruments usually employed for psychological testing. People do not normally declare themselves as having these characteristics, and it is hard to phrase questions which bring them out. Gadd & Merskey (1975) similarly failed to obtain scores with the hysteria subset of the Middlesex Hospital Questionnaire which discriminated conversion hysterical patients from other populations. It is also worth noting in this context that answers to questions thought to implicate particular traits are no proof of their validity one way or the other. (This is well illustrated by the question on the Pd scale of the Minnesota Multiphasic Personality Inventory in which sociopathic individuals answer ‘yes’ to the statement “My parents and family find more fault with me than they should”, whereas the real situation is probably the other way round (Meehl, 1956); most normal people answer ‘no’.) Lazare and his co-workers, who studied patients with depression, made a major effort to describe hysterical personality patterns (Lazare et al, 1966; Lazare & Klerman, 1968; Lazare et al, 1970). In
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these factor-analytic studies, the authors took seven traits as defining hysterical personality in the literature. They were egocentricity, emotionality, suggestibility, dependence, sexual provocativeness and fear of sexuality. At the Massachusetts Mental Health Center, 90 female in-patients and out-patients were given questionnaires and three factors were obtained which accounted for nearly 90% of the variance (Lazare et al, 1966). Each of the factors resembled one of three commonly accepted personality types: oral, obsessive and hysterical. Predicted traits of emotionality, exhibitionism, egocentricity, and sexual provocativeness had loadings on factor 1 from 0.7 to 0.57, in descending order. Dependence and related traits derived from the factor loaded at 0.4 or less, fear of sexuality had no significant loading, suggestibility had a small negative loading (–0.08) and emotional constriction had a high negative loading (–0.61). As the authors say, the agreement between factor 1 and the hysterical personality is relatively good and is consistent with the clarity and agreement in the literature on the description of the hysterical personality. In passing, one may note that the oral personality (factor 2) had the least correspondence with predicted traits and the obsessional personality (factor 3) had a good degree of loading on predicted traits. Lazare & Klerman (1968) next showed that observer rating of the hysterical personality could separate depressed in-patients into two groups, one with prominent hysterical personality characteristics (15 patients) and one without such characteristics (20 patients). Depression was measured on the Hamilton Rating Scale for Depression. Examination of the clinical records further demonstrated that the hysterical personality group had a lower mean age on admission, lower levels of educational and work attainment, and more employment in the cosmetics and women’s fashion fields. These findings were all statistically significant at P < 0.02. The hysterical patients had their first child sooner (P < 0.05), more children (P < 0.2), more extramarital affairs (P < 0.1) and more admissions to hospital (P<0.2) and gynaecological surgery (P<0.2). The trends in these last respects are noteworthy although they were unlikely to attain a high degree of statistical significance because only small numbers were examined. Hysterical symptoms, mostly of the classic type, were much more frequent in the hysterical personality group (P < 0.01). This report provides a satisfying degree of confirmation of the normal clinical view. In a third paper (Lazare et al, 1970), the first study was replicated on 100 consecutive female in-patient admissions with essentially similar results to those in the original study. It is clear that the
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concept of the hysterical personality and the majority of its accepted traits are well supported by this work. Paykel & Prusoff (1973) have since shown that a relationship exists between the set of personality dimensions used by Eysenck and that employed by Lazare and his co-workers. There is an unpublished dissertation by O’Neill (1965) which, according to Jordan & Kempler (1970), shows that it is possible to discriminate hysterical personality, diagnosed accurately by psychiatrists, with the use of objective personality testing. Clinical unanimity persists in other articles on the hysterical personality. De Alarcon (1973) provides the most recent review of the papers listing the characteristics of the hysterical personality. In 14 papers, including those by Chodoff & Lyons, Lazare and others, Ljungberg (1957) and Lindberg & Lindegard (1963), and others which have already been cited, and in DSM–II (American Psychiatric Association, 1968), he finds the following characteristics of hysterical personality to be repeatedly mentioned: histrionic behaviour (12 authors) egocentrism (11), emotional lability (10), dependency (10), excitability (10), seductiveness (8), suggestibility (8) and childishness (4). Clearly, there is a consensus that a personality pattern exists which can be labelled hysterical, or, nowadays, histrionic. Lazare & Klerman (1968) have shown that this personality pattern provides one subgroup of the patients diagnosed as having depression; and that the depression was of sufficient depth to achieve scores comparable to those of other depressed patients on the Hamilton Rating Scale for Depression. Ziegler et al (1960) also found a considerable association between the diagnosis of hysteria or hysterical personality and depression, as did Blinder (1966), who mentioned that the depression in his patients was most often not typically endogenous. On the other hand, Spitzer & Williams (1982) were not able to validate a syndrome of hysteroid dysphoria. Suicide attempts associated with this type of depression tend to be a common cause of admission of hysterical personality patients to hospital. In a report by Slavney & McHugh (1974), suicide attempts were responsible for the admission of 50% of hysterical personality patients compared with 16% of control patients, who were also mostly depressed. We find, therefore, a central core notion that hysterical or histrionic personality traits are present in a wide range of patients from the group with depression and hysterical personality, as in Lazare & Klerman’s study, and are found, also, at such extremes as malingering, deliberate disability, Munchausen’s syndrome, anorexia, or suicidal attempts, many of them gestures. There are
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also links with criminality. Alcoholism tends to occur in the fathers (Lazare & Klerman, 1968; Slavney & McHugh, 1974; Cloninger & Guze, 1973) and there is a tendency for a bad home atmosphere in childhood to be reported frequently (Slavney & McHugh). Criminality is noticeable in the male members of the family and in some of the females (Cloninger & Guze, 1970a,b, 1973).
Personality and conversion symptoms Forrest (1967) examined the link with psychopathy and conversion symptoms. He reviewed 62 patients with a diagnosis of hysteria (ICD–8 311) and anxiety state (ICD–8 310). On the basis of symptoms, number of hospital admissions, drug addiction or attempted suicide, 23 patients were categorised as hysterical psychopaths. A group of 21 patients presenting with phobic or depressive symptoms and not showing psychopathic traits, in the usual British sense of the term, was categorised as having hysterical personality problems. The residual 18 patients were a miscellaneous group, including patients with conversion reactions. Forrest concludes that conversion reactions have no diagnostic significance for ‘hysteria’, by which he seems to mean Briquet syndrome. His observations of the diagnostic patterns of hysterical personality and hysterical psychopathy are in agreement with the evidence just discussed. But the view that conversion symptoms are of no diagnostic significance in the diagnosis of ‘hysteria’ needs restating. They are part of the criteria used for Briquet syndrome, and we shall shortly state the evidence for supposing that they have a link with hysterical personality within its accepted limits. Ljungberg (1957) attempted to answer the question whether there was a special type of personality associated with conversion symptoms. He observed divergent views in the European literature on whether there was such a connection. He took a large sample of patients who had only had: “functional (not organic) bodily symptoms in the form of paralyses, difficulties in walking, tremor, fits, anaesthesia and patients with pronounced psychical symptoms in the form of derangement of consciousness and of memory.”
In assessing personality types he looked for hysterical types, after Janet (1894), psycho-infantile types (Lindberg, 1950) and psychoasthenic types (Janet, 1908). The first of these groups is defined as being characterised by suggestibility and distractibility, quickness in learning and forgetting, a tendency to impose upon people and to dupe them, ready but unsustained enthusiasm, and a pressing need
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for variety. The patient is considered to be subjective and egocentric and to enjoy being the centre of attention. The psycho-infantile type is regarded as having a strong affective fixation and dependence upon relatives, spouse and friends, and a strong need for guidance and help. This type is held to show pronounced childishness, insufficiency in the face of pressure, credulity, a tendency to be easily led, and a tendency to produce protective attitudes on the part of others. The psychoasthenic type, according to Janet, suffers from a pronounced feeling of insufficiency, easily becomes tired, lacks psychic energy, is anxious and hesitant, and avoids situations which require choice. Among 381 patients (246 female and 135 male) half had astasia abasia, 20% had fits, and 10% tremors. After one year 43% of the men and 35% of the women still had symptoms; and after five years, 25% of the men and 22% of the women still had symptoms, while those who had an abnormal personality had a significantly worse prognosis than those who did not. Among symptoms, astasia abasia had the best prognosis. Criminality (males, 17.6%; females, 4.6%) was significantly higher than in the general Swedish population. This is in accordance with the observations of the St Louis School (Cloninger & Guze) and of Forrest, mentioned earlier. There was also a significant increase in the number of women with an IQ less than 90 compared with other neurotic patients. With regard to personality, about 43% of the men and 47% of the women exhibited abnormal personalities, mainly hysterical, psycho-infantile and asthenic, as defined above. About 15% of the men and 17% of the women were classified as abnormal personalities in a restricted sense of the term. About 3% of the men and 12% of the women were classified as hysterical psychopaths. Ljungberg felt that this investigation confirmed the opinion that no uniform personality type exists which is prone to hysterical reactions. In one respect this result is inevitable. If hysterical symptoms are a mechanism to which anyone is prone then any personality type will have them. However, if hysterical personality does exist and is linked with hysterical symptoms, those in whom certain personality features predominate can be expected to have hysterical symptoms more often. In Ljungberg’s material, the frequency of the supposed types associated with hysteria is clearly substantial. It is reasonable to guess that these personality types will be more common or more pronounced in this material than in the general population, and perhaps more so than in other psychiatric populations. For instance, it is unlikely that a general population
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or an ordinary female psychiatric population would be classified as containing 12% of hysterical psychopaths, and it seems even more improbable that 43% of men even in a psychiatric clinic would be classified as having hysterical, psycho-infantile and asthenic personalities according to the definitions used. In effect, Ljungberg’s findings leave open the question of whether there is a special link between classic conversion symptoms and personality but, if anything, support the view that it exists. Certainly, they do not show that there is no relationship, but they do show that if there is a relationship it is not an automatic one. Interestingly, if one starts with a diagnosis of hysterical personality in patients admitted to hospital and looks at the frequency of hysteria, the association may be strong. Thus Liss et al (1973) found that among nine patients with hysterical personality diagnosed at Renard Hospital, St Louis, six had ‘hysteria’ (or the equivalent of Briquet syndrome). A large proportion of abnormal or unusual types, as found by Ljungberg, is unlikely to be due to a chance association. Moreover, if deviant personalities are considered, it is striking how often one finds evidence of hysterical symptoms. Dysorexia, deliberate disability, Munchausen’s syndrome, and even malingering, repeatedly give evidence of associated hysterical symptoms. Some of the personality characteristics which are recurrently described in these patients have been discussed in Chapters 8 to 10 and represent extreme versions of supposed hysterical characteristics, such as manipulative behaviour, sexual difficulties, dependent relationships and immaturity. It is argued later (Chapter 24), in accordance with a common view in the literature, that certain dynamic characteristics pertain both to these types of patients and to those with hysterical symptoms. The remarkable confluence of these groups of symptoms and characteristics, whether in terms of clinical traits or motives discerned, is scarcely attributable to chance. After these views had been formulated, Trimble (Merskey & Trimble, 1978) reviewed some data which this author had collected in 1968–70 during the study with Buhrich (Merskey & Buhrich, 1975). The selection of these patients and their general medical and psychiatric characteristics have been described in Chapter 11. In the course of examination, each patient had been classified with respect to his or her apparent personality. The categories used were hysterical personality and passive immature–dependent, anxious, obsessional and psychopathic personalities, mild character deviation, and no definite personality disorder. An H group of patients with conversion symptoms had 5 out of 24 (21%) with
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hysterical personality and the same number with passive immaturedependent personalities. It contained one patient with obsessional personality. A control group of 24 psychiatric patients had no such personality types but seven obsessionals (29%). Comparing the incidence of hysterical personality with obsessional personality and the number of passive immature-dependent personalities with obsessional personality, the difference in each case between the control group and the conversion symptom group was significant (P < 0.01). Overall, the full group of 89 patients with conversion hysterical symptoms (L group) had 17 hysterical personalities, 17 passive immature-dependent personalities, 7 obsessional personalities, 16 ‘normal’ and 32 others (anxious, psychopathic or mild character deviations). Thus this study produced very similar figures for hysterical personality in patients with conversion symptoms to those described by Ljungberg, and also by Chodoff & Lyons (1958), who found three hysterical personalities in 17 patients with conversion symptoms. Moreover, both hysterical personality and passiveimmature dependent types were significantly less common in the control psychiatric patients than were obsessional personalities. Earlier in this chapter, certain questions were asked and some answers to them have now been given. It is clear that there is, indeed, a particular personality which is regarded by psychiatrists as hysterical, and this may be found in association with some or all of the main hysterical patterns of symptoms. Salient features of that personality have been described in the studies by Lazare and his colleagues and by others and are reviewed by De Alarcon (1973). The personality pattern is clearly associated at times with depressive illness, especially non-endogenous, and I have argued that it has some links with dependent attitudes and hysterical conversion symptoms as well. Other important questions, including the genesis of the hysterical personality, remain to be considered and will be dealt with in Chapter 24. At this point, some of the evidence on the sexual identity of these patients and on their sexual adjustment requires discussion.
Gender and hysterical traits Two papers (Luisada et al, 1974; Lerner, 1974) discussed respectively hysterical personality in men and in women. Luisada et al report on 27 men meeting the DSM–II criteria for hysterical personality, found from roughly 27 000 case records. These men usually had a family history of alcoholic, unassertive fathers, and strikingly poor attainment relative to their own educational potential. They showed occupational
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instability; most were heterosexual but all had disturbed sexual relationships. Most had abused alcohol or drugs and been charged with drunkenness or robbery. Effeminacy was not prominent. In comparing their male with reports of female hysterical patients, the authors note many similar features. Two major differences are the criminality of the men and the seductive appearance and an excessive number of operations among the women. They argue straightforwardly that male hysteria is probably more common than is usually recognised. Both males and females tend to initiate psychiatric treatment in their second or third decade, to have a history of suicide attempts, to have a dominant mother, to be the last-born or only child, to under-achieve, to find other partners, and to over-use alcohol and drugs. None of their men had clinical conversion hysteria, although some had hypochondriasis. Some experienced hysterical psychoses and several had depressive symptoms. Although Lindberg & Lindegard (1963) showed hysteria to be as frequent in younger men as in women, but to decline markedly in older groups, the authors comment that hysterical personality is much less often diagnosed in men and that this could be a function of the fact that most of the examiners tend to be men. Chodoff (1987) has effectively demonstrated that it is purblind to deny the association of femininity with traditional hysterical traits but, balancing that conclusion, he shows that the ‘macho’ male provides a masculine equivalent. Blacker & Tupin (1991), adapting the earlier formulation of hysterical personality as a “caricature of femininity” (Chodoff & Lyons, 1958) cover the behavioural manifestations in both males and females by describing them as a “caricature of sex role”. Lerner (1974), in her fair and balanced paper, suggests that social and cultural factors play a major role in producing the sex difference in hysteria. Dealing with the influence of role models, she remarks that she: “cannot, for example recall seeing a television programme in which a group of women struggled effectively to solve a technical or scientific problem, while the men concerned themselves with social trivialities.”
She adds that the problem is not merely one of role models, for if we examine society’s notions of work and femininity we find that the pressures on women to adapt a hysterical style are intense and lifelong. As she says: “From the earliest years the young girl is taught to spend her major efforts in preparation [for wifehood and motherhood]
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Because of these social pressures, it may be anxiety-arousing for certain women to relinquish a flirtatious, childlike, sexualised type of interacting. It is not surprising, then, that there are many clinical reports of women who initially ‘look hysterical’ and later prove to be characterised by a far more serious emotional disturbance. Lerner adds: “I also have some doubt regarding the widely held notion that women rely more heavily on the defensive use of repression than do men. Rather an additional theory suggests that socialisation of women leads to a style of personality and cognition that in its observable outcome is not dissimilar to the effect of repression.”
In the light of such considerations, she expresses doubts about accepting a categorisation of hysterical personality based on a particular type of feminine behaviour that has a certain effect on the male observer. She suggests that the diagnostician must ask: “Is the patient’s dependent and childlike behaviour the regressive defence against genital fears of the hysteric or is it a learned aspect of feminine behaviour? Is emotional lability a defensive operation reinforcing repression or is it rather the patient’s attempt to be a vivid and exciting companion? Are sexual provocativeness and flirtatiousness reflective of Oedipal conflicts or are they the behaviour of a woman who feels she has little else to offer the male psychiatrist? These distinctions which are not mutually exclusive may be difficult ones to make in a brief diagnostic work-up and the stereotype of the hysterical female is so deeply ingrained that women are often carelessly and prematurely diagnosed.”
Despite these problems, she considers that certain psychoanalytic views of the hysterical personality, such as Kernberg’s (1967, 1970), are valuable and neither inherently feminine nor inherently masculine. These views, which are discussed in Chapter 24, depend upon an analysis of the dynamic conflicts present. Such conflicts might be found with a repressive style of defence in men and in women.
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Wells (1976) provides a very good illustration of Lerner’s theme in his discussion of Scarlett O’Hara, the heroine of Gone With the Wind, a novel by Margaret Mitchell which became very widely known as a film. Wells had little difficulty in showing that Scarlett precisely fits the criteria of Chodoff & Lyons (1958). By apt quotation he demonstrates that she was egoistic, vain, self-centred, attention seeking, histrionic, emotionally labile, and capricious. She sexualised all relationships, and coquetry and sexually provocative displays were never far beneath the surface. Demanding behaviour was constant. On the other hand, Scarlett was the very opposite of dependent. She showed a firm grip on reality and she would plan with resolution for the future. One of her most striking characteristics was a shrewd practicality. Her childhood also was a very happy one. Wells elegantly demonstrates that in appearance and behaviour, Scarlett fulfils almost perfectly our requirements for being labelled a hysterical personality, but that she does not fit our ideas of the hysterical personality in terms of favoured defence mechanisms, psychodynamic forces, and cognitive style. The rating of traits alone does not describe the hysterical personality, since surface traits may be determined by social forces or connections and belie the underlying patterns of emotional relationships, attitudes and expectations according to which the individual actually operates. Nevertheless, it is reasonable to suppose that where those traits are notably evident, the expected dynamic problems will be much more likely to be found. The occurrence of hysterical personality traits, together with conversion symptoms or frigidity, or the polysurgery and medical maladjustment of Briquet syndrome, suggest their frequent relationship with dynamic psychopathology.
Sexual adjustment Before discussing the dynamics of hysterical personality in Chapter 24, some of the evidence on the sexual adjustment of these patients should be noted, particularly since it tends to challenge Lerner’s idea that social models are responsible for the apparent hysterical traits of women. It was traditionally taught that hysterical patients are frigid, but exceptions are so often found clinically that this statement requires revision. Winokur & Leonard (1963) noted the general evidence of sexual maladjustment which is repeatedly found in papers on hysteria and hysterical personality, for instance the findings by Purtell et al (1951) that 73% of their patients obtained no sexual pleasure, and by Perley & Guze (1962) that 24% of their patients
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were frigid. Winokur & Leonard investigated the sexual life of 14 patients with hysteria defined in accordance with the criteria of Purtell et al and Perley & Guze (in other words, Briquet syndrome). They observed that eight (57%) had had gynaecological operations and that three (21%) were surgically sterilised before the age of 30. Pre-adolescent sexual experience and premarital petting were not unusual, but a striking deterioration in sexuality within marriage was found, with an unusual decrease in frequency of sexual intercourse and of orgasm. The change was much greater than would have been predicted from the data provided by Kinsey et al (1953) for the normal population. Approaching the topic with the techniques of clinical and experimental psychology, Jordan & Butler (1967) showed that students with a high score on the Hysteria Scale of the Minnesota Multiphasic Personality Inventory showed much greater galvanic skin response (GSR) deflections than normals when reading or recalling passages dealing with sexual themes. O’Neill & Kempler (1969) further showed that the hysterical subject’s behaviour in response to sexual cues fitted an approachavoidance model. Relatively neutral situations were treated as of more sexual significance, while sexual cues were avoided. Jordan & Kempler (1970) next demonstrated with female students who showed ‘hysterical’ patterns on O’Neill’s scale that the GSR response thresholds fell more than those of other students in situations where the sexual role was threatened. They concluded that their ‘hysterical’ student subjects had demonstrated anxiety over inadequacy and over incompetence in the sex role to a significant extent. This suggests that Lerner’s argument that hysterical patterns of behaviour are imposed on women may be less relevant for disturbed patients. Relatively normal women may indeed accept a number of hysterical patterns of behaviour, as Lerner suggests, but it is the more disturbed ones, who have more actual sexual or psychosexual problems, who manifest the traits of seductiveness and insecurity most notably. In the review of patients mentioned above, Merskey & Trimble (1978) found evidence in support of this view. Thirty-two per cent of the whole group with conversion symptoms, 38% in the matched (H) group, and 13% in the control (C) group were judged to have abnormal sexual adjustment – mainly long-term frigidity. The difference is significant (P < 0.05). When personality type was considered in relation to sexual adjustment, those with hysterical personality were significantly more liable to be frigid (P < 0.025) than those whose personalities had not been found to be abnormal.
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It is clear that there is a consensus based on experience, and some evidence, that patients with hysterical symptoms or personality show maladjustment in their attitudes to the sexual role. This most often manifests itself as frigidity, with a decline in sexual activity early in the course of marriage, but, occasionally, there may be heightened sexuality associated with episodes of increased emotional conflict (Prosen, 1967). Experimental work further demonstrates the insecurity and anxiety of subjects in situations which test their competence and confidence in their roles as women. Hollender (1971) presents a widely accepted view of the way in which this insecurity works in the hysterical personality, and his summing up gives the standard current opinion, as follows: “The crucial point developmentally is that young girls, who become hysterical personalities, turn to their fathers not as fathers but as substitute mothers. Since they barter sexual attractiveness, they grow up to be women who use sex as a means – often the prime means – of obtaining maternal gratifications from men. The only change is the person from whom closeness and love are sought: a suitor or husband is substituted for father.”
It follows that seeking masculine support, offering sexual partnership, and being unable to tolerate a full sexual and emotional relationship, a woman with a hysterical personality is headed for disaster in marriage, unless she has chosen a suitably unusual and compliant partner. The vicissitudes of the severe hysterical personality of either sex may not end simply with a bad marriage. There is reason to believe that not only do conversion symptoms occasionally herald a standard psychotic illness (schizophrenia, endogenous depression) but that some psychoses may be characterised as hysterical on the basis of either their phenomenology or the type of personality in which they arise, or the defence mechanisms which can be discerned in them. These topics are considered in the next chapter.
Neurotic styles It remains here to note one other aspect of the notion of hysterical personality. Shapiro (1965) identified patterns which he called “neurotic styles”. By “style” he meant “a form or mode of functioning – the way or manner of a given area of behavior that is identifiable, in an individual, through a range of his specific acts”. “Neurotic styles” were those which seemed characteristic of
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the various neurotic functions. He held that in “hysterical style” the repression of ideational contents from consciousness, the failure of one’s perceived contents to achieve the status of conscious memories or of memories available to consciousness, are characteristic, and that repression must be especially closely related to the process and mode of cognition. As he saw it, an obsessive– compulsive individual who relied upon sharply defined technical data and organisation of original cognitions would be less likely to lose memories than one who, in the hysterical style, relied upon mechanisms of repression very readily. In recalling (as distinct from forgetting), he presumed that the same features of attention (detailed and sharp in the obsessive–compulsive, and loose and poorly connected in the case of the hysterical subject) would operate as in the loss of the original cognition. Thus he suggested: “that hysterical cognition in general is global, relatively diffuse, and lacking in sharpness, particularly in sharp detail. In a word, it is impressionistic. In contrast to the active, intense and sharply focused attention of the obsessive–compulsive, hysterical cognition seems relatively lacking in a sharp focus of attention; and in contrast to the compulsive’s active and prolonged searching for detail, the hysterical person tends cognitively to respond quickly and is highly susceptible to what is immediately impressive, striking, or merely obvious.” Hysterical attention, according to Shapiro, is easily captured, and is not compatible with curiosity. It produces a relatively non-factual subjective world for ‘the hysteric’. This then extends to the experience of the subject’s own self. He or she does not feel like a very substantial being with a real and factual history. Shapiro adds: “One would think that vivid emotional life, strong feelings, would above all guarantee an equally vivid, sharp sense of oneself, but, in this case, it certainly does not have that result. It is well to keep this paradox in mind as we take a closer look at hysterical emotionality.”
For him, hysterical emotionality is also relatively shallow. These features which Shapiro identified so well can be recognised in the descriptions of patients by Carter (1853) and Kraepelin (1904). We may think that they underpin the traits described in DSM–IV for histrionic personality disorder without being expressed there quite so explicitly. Horowitz (1977), building on Shapiro’s theme, emphasised how the structure of the personality might be related to the processes of change in treatment. He noted a series of cognitive options available when the person with the hysterical personality wished to repress and
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avoid meanings, and we can note that these options are taken to be related to the personality traits of the individual. They include the following list, which Horowitz provides: (a) inhibit representation of the ideas and feelings (b) if option (a) fails, then inhibit translation of those ideas into other systems of representation (for example, do not let image meanings translate into word meanings) (c) avoid associational connections (that is, use steps (a) and (b) to avoid ideas and feelings that would be automatically elicited by information that has already gained representation) (d) conclude a train of thought by early closure or by declaration of the impossibility of any solution (e) change self-attitude from active to passive, or vice versa, depending on the direction of greater threat (f) if the above measures are inadequate, then alter state of consciousness so as to reduce reflective self-awareness. In brief, the recognition of hysterical personality traits leads to a particular process in psychotherapeutic interviews. These types of approach might be useful with the “repressive coping style”, which Weinberger (1990) sees as being marked by low anxiety and high defensiveness. An alternative process is delineated very well by Slavney (1990) with respect to more florid examples of patients with hysterical or histrionic personality disorder. This is evidently more supportive and less analytic, but at least as sensitive.
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23 Psychoses
It is well established that there is a modest increase in the incidence of subsequent psychoses among those who present with conversion symptoms. The statistical evidence for this was reviewed in Chapter 15. Certain authors have also labelled some psychoses as hysterical; such illnesses arise most often in patients who have characteristics which are considered to be part of the hysterical personality. These two matters, conversion symptoms as a precursor of psychoses and hysterical phenomena in psychoses, require further attention. The following case offers a simple illustration of a severe depressive illness associated with a motor conversion symptom. In 1966 a middle-aged man was seen with a hysterical paresis of his left hand. He worked as an engineering craftsman and it transpired that he was a very keen and conscientious workman who did about twice as much work as was the norm for his occupation. His workmates objected to his level of production because it implied that the norm should be reset and more work would be required from them for the same pay. They threatened to ostracise him unless he came down to their level. His basic temperament would not let him do this consciously. He developed the paresis of his non-dominant hand, which resulted in his work output falling to the level requested. Interpretation, support and recovery of his paresis were followed by a depressive illness of endogenous pattern which required electroconvulsive therapy to cure it. The association of hysterical symptoms with an overt pattern of affective illness is well recognised. Slater (1965) noted it in 7 of 85 patients traced at follow-up, and Merskey & Buhrich (1975) found it in 15 out of 89 patients with conversion hysteria. A different association with depression occurs as a well recognised complication of the abrupt removal of hysterical symptoms. Reactive 356
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depression with a suicide risk or attempt may then appear. This is especially liable to happen after hypnosis or similar dramatic measures for removing the symptom if these are practised without adequate psychiatric support and if a difficult problem emerges as a result. Occasional deaths are known, usually mentioned by word of mouth rather than reported in the literature. Many hysterical symptoms can be removed with impunity and without symptom substitution. Carter (1949) relieved numerous patients without such problems arising in the short term and with good results at follow-up of four to six years. Nevertheless, it is essential to provide a suitable framework of support and medical care to safeguard against the occasional risk when hysterical symptoms are removed.
Hysterical psychosis It is also recognised that hysterical symptoms may occur, although very rarely, as precursors of schizophrenic illness. This is understandable as one of a number of regressive phenomena released by the illness. Hysterical psychosis per se is a more debatable concept. Kraepelin used the term hysterical insanity for severe prolonged hysterical symptoms without the presence of delusions or hallucinations, as in the case quoted in Appendix B. Breuer & Freud (1893–95) used the term hysterical psychosis in a more usual way, but Bleuler (1950), Fenichel (1945) and Reichard (1956) criticised it. However, Hollender & Hirsch (1964) revived its use to denote psychotic symptoms of sudden onset and brief duration, arising in patients with hysterical personalities after a period of increasing stress. The symptoms included delusions, hallucinations, depersonalisation and grossly unusual behaviour, and usually lasted one to three weeks. Mallet & Gold (1964) described 13 patients, all women, with an illness which at some points had been diagnosed as schizophrenia because of unsuccessful treatment as well as the presence of emotional emptiness and bizarre depersonalisation phenomena, paranoid thinking and dramatic hallucinations, mainly visual but sometimes auditory. All the patients displayed what the authors considered to be characteristically hysterical personality traits, that is, egocentricity, psychosexual immaturity, lability of mood, and shallowness of emotional contact. In every case admission to hospital followed an acute episode of violent or negativistic and symbolic behaviour or a suicide attempt. Five of these patients ultimately committed suicide. These authors reported the illness as a pseudoschizophrenic hysterical psychosis.
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Hirsch & Hollender (1969) suggested that the illness might present in three ways: (a) as socioculturally sanctioned behaviour, that is, behaviour determined by the prevailing belief system of the given culture, for example as it is encountered among the natives of New Guinea (Langness, 1965) (b) as simulation of psychotic behaviour; psychotic symptoms are appropriated by a mechanism analogous to the use of somatic symptoms in conversion hysteria; in such a case the symptoms constitute a reinforcement of repression (c) as a true psychosis with temporary ego disruption and impairment of repression. Siomopoulos (1971) points out that the frequent confusion between hysterical psychosis and schizophrenia originates from the presence of delusions and hallucinations in both illnesses. He considers that the delusional ideas expressed by patients with a clinical picture of true hysterical psychosis do not have the characteristic of incorrigibility which is an essential feature of the delusion proper. Hysterical psychosis does not appear in ICD–10 (World Health Organization, 1992a), but several labels and descriptions are offered under categories F23, F24 and F28 which might apply to transient psychotic disorders and in which it could be included. Perhaps the most prominent of these is F23.0, “Acute polymorphic psychotic disorder without symptoms of schizophrenia”. This corresponds to the description of bouffée délirante without symptoms of schizophrenia or unspecified. Bouffées délirantes or acute paranoid reactions are generally regarded as acute psychotic disorders in which hallucinations, delusions or perceptual disturbances are obvious but markedly variable, changing from day to day, or even from hour to hour. ICD–10 indicates that emotional turmoil is frequently present within transient feelings of happiness, ecstasy, anxiety, or irritability. The polymorphism and the instability are characteristic of the overall clinical picture and the psychotic features do not justify the diagnosis of schizophrenia. Such disorders often have an abrupt onset and show rapid resolution of symptoms. The literature has typically recognised these symptoms as occurring in response to severe stress. Allodi (1982) reviewed data on such syndromes in Canada for 1969 and 1973 and observed that, in 1969, 1241 first admissions to all psychiatric institutions in Canada were diagnosed as suffering from reactive psychosis. This amounted to 8.3% of all first-admission
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psychoses and 2.7% of all first admissions. The rates increased in the province of Quebec in the four-year period. Allodi emphasised that these syndromes occurred in relatively unsophisticated patients suffering from home sickness or stress and perhaps lacking language skills as well. Phenothiazines are not helpful for these patients and they generally recover with relief of the stress following hospital admission. By way of illustration, Krieger & Zussman (1981) specifically described the importance of cultural factors in a brief reactive psychosis with respect to conflicts between Roman Catholic and Buddhist beliefs in a Thai male. The patient felt stress as a result of being confronted with a Buddhist family mortuary ritual to which he had previously adhered. He felt obliged to subscribe for his deceased mother and was tempted to an extramarital relationship, in conflict with his Roman Catholic beliefs. Another factor which may promote hysterical types of illness may be sexual disappointment. Cavenar et al (1979) described four patients who had all experienced some type of strong sexual stress or disappointment and developed brief dramatic abnormal behaviour which gave rise to a diagnosis of psychosis. Either a sexual advance had been made to the patient or the patient had been angry because one had not been made. Spiegel & Fink (1979) describe two cases in whom rather similar phenomena may be noted. One was a 15-yearold boy, jilted by his first girlfriend, who believed himself to be possessed by demons (a belief corresponding to his family’s religion). The other was a 31-year-old woman who, in response to a sexual advance, had made a suicidal gesture and admitted to both auditory and visual hallucinations. Kapur & Pandurangi (1979) made a detailed study of cases of reactive and of acute psychosis. Reactive psychosis, a syndrome recognised by Jaspers (1913), is marked by: (a) a close association with stress (b) understandability of symptoms in terms of the stress (c) a purpose served by the psychosis, such as an escape from stress or alternatively wish fulfilment (d) termination of psychosis with termination of stress. In ICD-10 it is categorised under F23.9, “Acute and transient psychotic disorder, unspecified”. There may be a case for arguing there is little difference between the latter and bouffée délirante except for the emphasis on the persecutory aspects in bouffée délirante which some favour. However, even those aspects are not found in the ICD–10 description of bouffée délirante.
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At all events, Kapur & Pandurangi compared 30 patients with reactive psychosis and 30 with acute psychosis without antecedent stress seen first as out-patients and then admitted to the Indian National Institute of Mental Health and Neurosciences. The groups were matched for age and sex and followed up for seven months, and it was noted that the reactive psychotic group had more hysterical and affective features, more vulnerable personality characteristics, more experience with stress in their life before illness, and a relatively better prognosis than the second group. In fact, on the follow-up only 10% of the reactive cases had schizophrenia, but 43% were so diagnosed in the second group. These data likewise tend to support the view that acute psychotic phenomena do appear in reaction to overwhelming stress or possibly in susceptible individuals in response to sexual difficulties. They have a better prognosis and require discrimination from manic–depressive illness, severe depressive illness and schizophrenia in particular.
Culture-bound syndromes There are several situations to distinguish with regard to the term hysterical psychosis. The first is that which Hirsch & Hollender noted, where a cultural practice sanctions extreme behaviour. Examples include latah (Yap, 1951, 1952), some Ainu behaviour (Chapter 6), amok (Westermeyer, 1972), piblokto (Brill, 1913, Ackerknecht, 1948), wihtigo (Yap, 1951), voodoo (Sargant, 1957) and phii pob (Suwanlert, 1976). Yap describes how a female Malayan subject to latah behaves in a simple, compliant way, perhaps with echopraxia, echolalia and even coprolalia. The condition usually follows a sudden fright, such as seeing or stepping on a snake. Chiu et al (1972) found that 7 out of 50 females with latah had a mental illness and another 13 had mild psychiatric disorders. They considered it to be “socially accepted as a female attention-seeking response”. The behaviour of some Ainu women (Chapter 6) is closely comparable. Johnson & Proskauer (1974) describe a more individual psychosis in a young Navaho girl. Amok is a more masculine type of behaviour, also found in Malayans, who after a period of brooding may seize a weapon suddenly and slay anyone within reach until eventually he himself is killed. Those who have survived are said to claim amnesia for the whole episode. Comparison can be made with the ‘berserk’ behaviour of the Vikings (Sim, 1974). Westermeyer emphasises that amok seems to be determined far more by social considerations than by
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individual dynamics. Fenton-Russell (1956) found that some supposed cases were misdiagnosed instances of catatonic excitement or postepileptic states. Others were addicted to hashish, but there was a group whom, he held, went through an initial phase of anxious preoccupation, succeeded by homicidal excitement, which in turn gave way to deep sleep. Amnesia after the event occurred in one patient and the acute phase was normally followed by “an unstable nervous condition lasting several months”. Most authors consider that amok is usually a response by a man to a desperate situation which he cannot remedy. Piblokto or Arctic hysteria is found among the Inuit (Eskimos). The sufferer, usually a woman, begins to scream and tear off and perhaps destroy her clothing, imitating the cry of an animal or bird, and then throws herself on the snow or ice, despite very low temperatures. The attack usually lasts one to two hours and the Inuit are reluctant to touch any afflicted person during the attack because they think it has something to do with evil spirits. On one occasion as many as 8 out of 20 women under observation suffered piblokto (Ackerknecht, 1948). Lehmann (1975) reports that among many Inuit patients who were psychiatrically disturbed, he has seen only one case in which the history resembled piblokto, and he thinks it is now rare. Piblokto has also been observed to be related to a low serum calcium level (Foulks, 1972). Wihtigo, a psychiatric illness of the Cree, Ojibway and Salteaux Indians, is yet another cultural variant. Sufferers believe that they have been transformed into a man-eating, giant monster; alternatively there may be a fear of such a possibility. Yap (1951) thinks that, like other possession states, wihtigo is essentially hysterical in nature. Lehmann (1975) again reports the condition as extremely rare. The most notable possession state is probably voodoo, which both Sargant (1957) and Lehmann (1975) regarded as exhibiting major hysterical phenomena. A classification problem nevertheless exists with culturally sanctioned behaviour and is well illustrated by phii pob, which Suwanlert (1976) described in Thailand. This is perhaps the most interesting of all the possession states. Believers consider that a spirit with power over human beings originates in a living person and then conceals itself within the body of that person, who is called the originating host. They also believe that the spirit may leave the originating host to possess another, who is then called the possessed host. The dynamics of projection and guilt which may arise from such a situation are obvious. Suwanlert (1976) considers that there are three categories of possession. The first is where there has been only one instance of
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possession, an antecedent psychological problem is evident, the possession state is socially accepted and provides a solution to conflict, and the patients cannot be said to be ill. The second occurs in people who are repeatedly possessed and show clear evidence of neurotic symptoms. A difficult or insoluble problem together with hysterical personality allows a diagnosis of hysterical neurosis or, he suggests, spirit possession neurosis. The third category comprises possessed hosts in which the phii pob refuses to depart and the native healer advises hospital treatment. These cases usually develop into psychotic states but not schizophrenia or a brain syndrome. The patients are typically females of low socio-economic status. Their chief complaints are of convulsions, trembling, shaking or spasm, and every case exhibits anxiety and depression. Delusions, persecutory ideation, and auditory hallucinations are common. The personality tends to be hysterical, “characteristically seductive, sensitive to cues, impulsive, egocentric, suggestible, with dramatizations in which they imitated folk actors”. Family conflicts are common and precipitating events with some sort of psychological stress beforehand are invariable. Hospital
T ABLE 23.1. Some characteristics of hysterical and related psychoses
Latah Amok Ainu Piblokto Wihtigo Phii pob Voodoo Negi negi Induced psychoses 1 ‘Borderline' or psychopaths Psychogenic Ganser Hysterical
Culturally sanctioned
Delusions or hallucinations
Repression (reinforced, impaired ego disruption)
Predisposing hysterical, dependent or psychopathic traits
Yes Yes Yes Yes Yes Yes Yes Yes
No No No No Yes Yes (Yes) Yes
+ (-) + + + (-) (-)
Yes No Yes Yes No Yes ? ?
(Yes) brief psychoses No No No No
Yes of Yes Yes Yes
(-)
Yes
+ -
Yes Yes Yes Yes
(-) possibly. 1. For example by terrifying experiences; or folie communiquée/partagée.
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treatment promotes prompt and satisfactory recovery, usually starting within three to seven days. Suwanlert considers that this is a culture-bound syndrome which corresponds to the hysterical psychosis of Hirsch & Hollender. From the description it would seem that repression of feelings related to conflict is reinforced. The patients with this more severe form of phii pob may be regarded as having a defined illness with false beliefs and disturbances in their grasp of reality; in other words, they are truly psychotic. Nevertheless, because repression is reinforced, they would not meet Hirsch & Hollender’s criteria for hysterical psychosis. On the other hand, it appears that some culturally sanctioned psychoses involve impairment of repression and ego disruption. This is true of amok and wihtigo and perhaps negi negi and voodoo. It may also apply to induced psychoses in the West such as folie communiquée/partagée, discussed in Chapter 16, in which case folie communiquée/partagée could be classed with hysterical psychoses except that it is not usually brief. Some of the conflicts in these criteria are set out in Table 23.1, which is presented very tentatively. Despite the conflicts, these criteria help us make the best of a difficult job.
Other brief psychoses We can now consider further, various Western diagnostic categories in relation to hysterical psychosis. If we take culturally sanctioned behaviour as the first situation to distinguish with regard to hysterical psychosis, the second major situation will correspond to appropriation of psychotic behaviour and will include the Ganser syndrome (Chapter 9), which agrees with Hirsch & Hollender’s criteria in that repression is reinforced. However, if the Ganser syndrome is part of another psychosis, as in Anderson & Mallinson’s (1941) patients, then the other psychosis usually claims the primary diagnosis. Otherwise, the Ganser syndrome is the main diagnosis. The third situation is that of the type of patient described by Hirsch & Hollender (1969) with hysterical personality traits in a stressful situation. This has many points in common with the Scandinavian notion of psychogenic psychosis (Faergeman, 1945). A fourth situation overlaps with or is an extension of the third. It corresponds to the patients described by Mallett & Gold (1964) and requires gross predisposing personality traits with perhaps less stress. These conditions require a little more discussion. The concept of psychogenic psychosis has not been widely adopted outside Scandinavia, perhaps because it tends to be used
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both for what is called elsewhere severe reactive or situational depression and for those different syndromes in which delusions and hallucinations are more prominent. On the Continent, some of the latter are called schizophreniform psychoses, in accordance with Langfeldt’s (1937) criteria. In the United Kingdom they may be called paranoid states, schizophrenia, schizophreniform psychoses, or simply psychoses occurring in hysterical psychopathic personalities, and, if appropriate, postoperative psychoses. If there is an association with epilepsy but formal schizophrenic phenomena are not prominent, they may be called psychoses of epilepsy. The least hint of confusion leads to a diagnosis of acute confusional state and a feeling of relief for the diagnosing doctor. The fourth group attracts similar labels to the third, as well as the rather unfortunate term ‘the borderline state’ (Zetzel, 1956; Schmideberg, 1959). Zetzel (1971) observes that patients in North America who attract the diagnosis of borderline personality or condition and who may develop ‘schizophrenia’ in the course of analytic treatment correspond to the types who are regarded in England as having psychopathic personalities or character disorders. Richman & White (1970) support the concept of Hollender & Hirsch (1964) and emphasise the importance of family and situational factors; they note differences from schizophrenia, particularly in the lack of classic schizophrenic symptoms and in the hysterical psychopathic characteristics of their patients and their oral and dependent traits. Abraham (1908) had pointed out already that dementia praecox differed from hysteria in that in the one case the libido is withdrawn from objects, while in the other it becomes cathected to an excessive degree. In other words, schizophrenic patients take too little notice of the world around them and of other people, while patients with hysteria are unduly attached both to external objects and to other people. The manifestation of the latter phenomena in a psychosis could perhaps serve as one means of recognising a hysterical illness, although a stronger criterion would be the observation of Hollender & Hirsch that a hysterical psychosis supports mechanisms of repression, while a schizophrenic psychosis loosens or dissolves them. However, there are difficulties with this as well if we accept amok and wihtigo as hysterical. Siomopoulos (1971) likewise argues for the differentiation of hysterical psychosis and schizophrenia. There is a fairly wide measure of agreement about the type of Western patient and the type of Western illness under discussion. Labelling the illness is another matter in which agreement has yet to be reached. The papers cited certainly show a tendency to reconstitute
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a possible use of the word ‘hysterical’. For our purpose we can recognise that immaturity, cultural patterns, a fairly characteristic type of failure of personality development in our society, and acute social or personal stress can singly or jointly give rise to a form of psychotic illness which has numerous hysterical mechanisms and, often, hysterical symptoms. Whether this is given any of the names noted, other than schizophrenia, is less important than the recognition of the phenomenon and of those mechanisms. It appears from the foregoing that the effort to classify these varied, usually brief, psychoses has not been entirely successful. What emerges is that culturally sanctioned behaviour, simulation of psychosis, reinforcement or impairment of repression, and gross regressive behaviour occur in a variable mixture in different syndromes. It is easier to ‘understand’ these illnesses than to group them systematically.
Dynamics of psychosis The differences between some of these Western phenomena and other psychoses may, however, have a bearing both on classification and on the psychodynamic theory of hysteria, which is discussed in Chapter 24. The loosening of restraints evident in amok or wihtigo has to be set against the reinforcement of repression in the Ganser syndrome or in piblokto. This raises the question of why some cultures may produce one type of psychosis and others another type of psychosis, or many neurotic hysterical phenomena. The answer to that question may help to support one view of the psychodynamics of hysteria. Parker (1960, 1962) suggests that the differences in personality style between Ojibwa Indians and Inuit (Eskimos) are culturally induced; that the personality dynamics of members of the cultures differ; and that these differences may be used to explain why the Ojibwa have been liable to the wihtigo (or wittiko) psychosis, and the Inuit to more hysterical symptoms. His excellent papers deserve to be read in detail. Summarising them briefly, it appears that the Ojibwa culture, although initially permissive in the treatment of children, soon places great emphasis on punitive techniques imposed by the mother, such as fasting and suffering. Power, acceptance and affection are secured by techniques of self-denial and suffering, while security and self-esteem are very vulnerable and must constantly be reaffirmed by tangible success. Aggressive intent associated with biting is prominent in Ojibwa practices, and cannibalism in their myths. Ojibwa adults are described as often
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sullen, hostile, introverted, hypersensitive to insults, reticent and full of exaggerated pride. Parker sees in this a striking confirmation of Abraham Kardiner’s (1939) ideas on the closeness between unsatisfied dependency cravings and fantasies of being persecuted, killed and devoured by the object of dependency. In the myths, small and dependent boys are starved and uncared for by the mother, who is killed by the father and turns into a cannibalistic monster who wishes to devour the children. The loved object turns into its opposite. When faced with severe failure, for example in hunting, the individual feels abandoned and worthless. The normal personality defences (masochism, hostility) fail to relieve anxiety and depression. With their failure regression into psychosis takes place and at the same time the psychotic symptoms serve to allay dependency cravings, by becoming one with the object of dependency, and to release aggression against the frustrating object by killing and eating it. If we regard this psychosis as related to frustrated dependency needs, then we can regard it as hysterical (although now very rare) and we can suppose that it supports the view that certain hysterical phenomena are related not to genital frustration but to much earlier unfortunate experiences. There are doubts, however, both about the occurrence of this psychosis and the validity of the personality stereotype which has been outlined. Psychiatrists with extensive practice among the Ojibwa have never seen it or heard of a live case and an Ojibwa view of the personality stereotype could well be very different from the one which Parker presents. By contrast, the hysterical phenomena found among the Inuit are generally much more benign. This culture pattern is much more indulgent and favourable to the individual throughout childhood and heavily emphasises the responsibility of members of the group to each other. The child’s individual dependent needs are fully satisfied, the adult is generally cheerful and spontaneous, emotionally demonstrative and extrovert. Except in extreme circumstances mutual help is the rule in Inuit society and friendly group activity is readily seen. Inuit men are not trained for neurotic ‘dependency’ but for individual competence, often in dangerous hunting activities. The women suffer restrictions in adult life and are generally placed in a subordinate role. Hysterical neurotic responses without psychosis are relatively common in Inuit populations while piblokto, which was normally brief, is now also rare. It can be argued that in Inuit society the position of the woman combined with the expectation of help from others will be relatively likely to foster episodes of
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hysteria in women. But even when these are severe enough to induce piblokto, they represent the persistence of repression and a much lesser degree of regression than is the case in wihtigo psychosis. We can conclude that hysterical symptoms in an individual or a culture may satisfy dependency needs of a very different type, sometimes at a relatively late level of development, at other times at a very primitive level. Depending on the degree of personality disorder and the strength of the pressures in the individual, the result of unsatisfied dependency needs may be anything from minor hysterical symptoms or traits to a major personality disorder; it may also be a psychosis which supports repression (Ganser syndrome, phii pob, piblokto) or one which loosens it (wihtigo, amok). It follows that the criteria of Hirsch & Hollender (1969), that a hysterical psychosis involves reinforcement of repression, would serve to support the presence of a hysterical psychosis, but not to rule it out. It also follows that pregenital fixation (usually oral) would have to be accepted as producing some extreme forms of hysterical psychosis. The notion that pregenital fixation characterises the hysterical personality is part of current psychoanalytic thought (Chapter 24). Another line of argument which supports the relevance of pregenital fixation was anticipated in the discussion of hysterical psychoses in this chapter. If we accept some of the more extreme instances like amok and wihtigo as hysterical, it follows that the disturbance in emotional development which contributes to them is an early and primitive one with important aggressive and masochistic elements. The extent to which psychodynamic views of this sort are applicable to the psychoses is now greatly circumscribed, if they are accepted at all.
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24 Psychoanalytic concepts
“Even as a saint the hysteric cannot be relied upon and occasionally lapses into the diabolic.” (Wittels, 1930)
Chapters 8, 9 and 23 have considered the dynamics of certain extreme hysterical manifestations or related behaviour. It is now time to examine further the ideas about hysteria and its psychodynamics which psychoanalysts have developed. These ideas are relevant to the views we may wish to take of histrionic personality and of dissociative symptoms. Before doing so, however, it is necessary to review the meanings of the word hysteria.
Semantics of hysteria Multiple meanings of the term hysteria have led to semantic confusion (Cleghorn, 1969a). Many authors remark upon this point but the issue need not present any real problem. Slater (1965) argued that the term hysteria should be dropped since certain organic causes and psychoses might not be recognised as a result of its use. However, provided that the term is used as a starting point, or with a specific defined intention, there is no reason to drop it, and I agree with Lewis (1975) that hysteria is likely to outlive its obituarists. Five types of meaning have so far been given for the word hysteria, and another can be noted here as well. The conversion symptom has been treated as one specific type, corresponding to the patient’s idea of physical disturbance and defined by neurological examination. Traditional dissociative symptoms are defined similarly, but on the basis of psychological examination and not by neurological examination. Pain is also included here, but in practice the diagnosis of hysterical pain requires great caution. These types essentially form 368
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one group which ICD–10 now subsumes under two adjectives: dissociative for the first two, and somatoform for pain (World Health Organization, 1992a). A syndrome which includes these and other symptoms without organic basis – somatisation disorder – represents another application of the noun hysteria, or the adjective, hysterical, and is also called a somatoform disorder. For those who want another term to replace hysterical symptoms, conversion symptoms or dissociative symptoms or disorders, I suggest doxogenic (see p. 308). The third main technical use of the word hysterical or hysteria is to describe a particular group of personality traits (Chapter 22). Fourthly, we have touched on the meaning of the term as a psychodynamic mechanism, and in Chapter 23 that interpretation was extended to certain psychoses. Fifthly, we have to consider the notion of a particular type of character which appears in the psychoanalytic discussions, and that is part of the further theme of the present chapter. In addition, we may note in passing that there is a sixth, vernacular, use, indicating noisy, excited, and uncontrolled behaviour. Semantic confusion has perhaps been more evident in the psychoanalytic discussion of hysteria because it has considered both mechanisms – such as oral and genital fixation – and personality features, which either follow from the mechanisms or are apparent clinically. There is nothing wrong with this in principle and it is justifiable in the attempt to understand both what patients are like and how they got to be so. But in practice, as double burdens normally do, it makes life harder. In particular, we have to distinguish between personality patterns and personality dynamics in any discussion of the hysterical character.
The hysterical character Lazare (1971) provides a review of the history of the psychoanalytic notion of the hysterical character. Cleghorn (1969b) also gives a review, while Aufreiter (1969) gives an appraisal of psychoanalytic attempts to classify hysteria nosologically on dynamic lines. Horowitz (1977, 1991) discusses the way in which the structure of the hysterical personality is founded upon cognitive processes. Lazare points out that Abraham (1921a, 1924b) had a greater influence on the current use of the idea of the ‘hysterical character’ than Freud, when he argued that the hysterical symptom was related to a failure at the early genital (phallic) level of organisation. This was not an exclusive relationship. For instance, he considered a tic to be a conversion symptom at the anal–sadistic stage (Abraham, 1921a). Like Freud, he
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did not write about the hysterical character, but his work on the dynamic understanding of the anal and oral characters (Abraham 1921c, 1924a) provided the groundwork for the study of the relationship between character and libidinal development and fixation. The first psychoanalytic description of the hysterical character dates from Wittels (1930), who accepted the existence of a hysterical type, with infantile, feminine, sometimes creative, but unreliable characteristics. “Even as a saint the hysteric cannot be relied upon and occasionally lapses into the diabolic. As a loving woman she represents a veritable martyrdom for the serious, compulsive male who ... sees himself betrayed the following day.”
According to Wittels the hysterical character never frees itself from infantile fixation, confuses fantasy and reality, and allows the law of the id to enter the ego. Some fantasy, mixed with reality, perhaps strayed into his own remarks, when in dealing with the subject of phantom pregnancy he observed: “in the search for the phallus the hysteric’s nose, her arms and legs which incline to paralysis or to excessive activity, become symbols of these conversional symptoms. Her mouth becomes a symbolic transference from below to above. Her blush is an erection. The fit of hysteria has long ago been seen through, and revealed itself as a coitus.”
Wittels also argued more reasonably that the hysterical fixation was pregenital, and that hysterical symptoms resulted from a combination of constitutional and environmental causes. Reich (1933) next put together such traits of the hysterical personality or character as sexual ambivalence, coquetry, excitability, suggestibility and pathological lying, and linked them to Abraham’s notion of genital fixation. Lazare points out that Fenichel (1945) restated Reich’s formulation, thereby acknowledging that Reich’s position was becoming generally accepted. This standpoint was not challenged until 1953, when Marmor observed that the hysterical character was not easy to change and that oral fixations are of basic importance to the hysterical character, giving it a strong pregenital cast. In consequence he held that there was a close psychodynamic relationship between hysteria, addiction, and certain types of depression and schizophrenia. In the reference to addiction he was following Wittels, and his next conclusion could be supported in terms of the links which some authors described between hysterical
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traits, addiction and depression. The same view is not adequately supported in the literature with regard to schizophrenia, as strictly defined, although it would apply to the psychoses discussed in Chapter 23. Lazare points out that if the hysterical character is related solely to genital fixation, it should be easy to treat by psychoanalysis. Genital fixation alone is not compatible with Marmor’s (1953) observations or those of Wittels, if the hysterical character is to be explained in terms of libido theory. Nor was it compatible with Freud’s comment (1931) that the ‘erotic type’ which was linked to excessive strength of the id was more liable to fall ill with hysteria; this follows because the preponderant ‘erotic type’ would have an oral and therefore pregenital fixation. No one seems to have noticed that Abraham (1921a) had already linked the supposed conversion symptom of a tic with the anal stage. The view that hysterical mechanisms are not solely determined by pregenital fixation is reinforced by the extensive personality disturbances found in anorexia nervosa, Ganser syndrome, deliberate disability, hospital addiction and the like. It is true that it could be argued that the masochistic and hostile aspects of such behaviour were pregenital and only the conflict-solving, dependency and manipulative aspects were genital. However, to do so would neglect the fact that the association between these patterns of behaviour is frequent and the link between them is too strong for it to be presumed to be accidental. The same applies to a proportion of patients with persistent pain. These difficulties are resolved by Marmor’s proposals that ego development should be taken into account as well as more than one point of libidinal fixation. We can restate this in more ordinary language by saying that the strength of an emotional drive or conflict and its manifestations will be modified by the degree to which the individual is attuned realistically to the rest of the world. Sensible people have better control over infantile emotions. At this point we might ask, why bother to state the position in dynamic terms if all that is being said is mere tautology, to the effect that people who are mature and realistic have better emotional control than those who are immature and unrealistic. It is reasonable to reply that the psychoanalytic formulation leads us to ask questions about the childhood of the hysterical patient and the quality of mothering in that childhood. Such questions can be answered clinically and by the techniques of social science and what emerges, at least from clinical observation, is that the mothering was often inconsistent or rejecting, and the oral and genital phases were perhaps equally impaired while no great demands were made for
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either superego control or self-discipline. Thus anal–obsessional characteristics were less often required or developed. Easser & Lesser (1965) took the psychoanalytic definition of the hysterical character further by recognising the importance of distinguishing between symptoms and character structure. They described six female patients whom they regarded as having hysterical personalities, although they were in no way provocative, seductive or exhibitionist. Their presenting problems revolved mainly around sexual behaviour and they showed varying degrees of sexual inhibition and malfunction. Emotional lability, an overt and covert need for love, which resulted in hypersensitivity, some irresponsible flighty qualities and a presentation of a ‘child–woman’ facade were emphasised. They argued that these modes of behaviour represented a major psychic defence based upon the hysterical mechanism, which involved: “the substitution of emotions, one for the other, or a shift in the quality of an emotional response so that it becomes, paradoxically, a substitute for itself”. By contrast, they delineated a hysteroid personality, which corresponds to the more extreme types of hysterical personality discussed in Chapter 20 and is less mature, less well integrated, more beset with pregenital fixation, and more liable to psychosis. The clinical distinction between more and less mature patients is valuable, although the terms ‘hysterical personality’ and ‘hysteroid’ are liable to cause confusion. The explanation of one group in terms of genital fixation and the other in terms of more extensive pregenital, as well as genital, fixation, provides a reasonable distinction in psychodynamic terms between possible causes of the two types. Lazare points out that Kernberg (1967) and Zetzel (1968) made the same distinction between two types of hysteria and advanced the argument that the ‘healthy’ hysteric has a predominance of oedipal over oral conflicts, and more obsessional defences, while the ‘sick’ hysteric suffers from more oral problems and more infantile fixation. The ‘healthy’ hysteric, of course, has more potential in analysis. Lazare adds that this distinction between two types, in which one has more maturity and potential for psychotherapy than the other, looks back to the Abraham/Reich libidinal hierarchy which has in effect defined ‘hysterical’ as relatively healthy and treatable. He very reasonably observes, however, that the use of ‘hysterical personality’ and ‘healthy’ to denote one group and ‘hysteroid’ or ‘sick’ for the other causes some confusion because hysteria and hysterical character, in general psychiatric terms, refer to patients with gross symptoms, gross disturbances in character traits and major ego disturbances. The current psychoanalytic concept of the hysterical character is, therefore, confusing to general psychiatrists and it
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would be better, as Lazare says, if all the patients under discussion were referred to as hysterical with an appropriate modifying adjective to indicate the degree of ego impairment. Aufreiter (1969) summarised the stages of development of psychoanalytic theory up to this point. He notes three historical attempts to provide organising systems for symptoms and classification. The first was that of psychosexual development, from which derive the libidinal fixation points, considered to be characteristic for developing symptoms. We have already discussed this. The second attempt to organise symptoms and to classify psychological entities considered ego development and ego defence, and was made by Anna Freud, Hartmann and their followers. Much current discussion of the hysterical personality and of the borderline syndrome relates to failure of ego development. The third attempt was made in connection with the ‘object relation theory’ of Melanie Klein, Fairbairn and others. The latter group of theorists consider that: “the decisive experiences for every human being are interpersonal fulfilment or frustration during early infancy, leading either to successful progression or to fixation at the oral dependent stage ...” (Aufreiter, 1969)
Hysteria would be marked by a constant unrealistic expectation of a supportive object and denial of the bad, frustrating ones. It follows from this that hysterical patients direct themselves towards a living, giving object, that is, look for emotional returns from other people and do not withdraw like the schizophrenic patient. The way in which the patient may do this will be inherently limited by the cognitive features which Shapiro and Horowitz have recognised (see Chapter 22). Conversion: later views Rangell (1959), Engel (1968) and Schmale (1969) proposed an extension of the notion of conversion with regard to somatic symptoms. This extension refers not to personality but to the mechanism of symptom formation and is, therefore, best considered here as a postscript to the major psychodynamic hypotheses. It appears to follow from the somewhat confusing views of Alexander, which were criticised in Chapter 4. Rangell wishes to use the term conversion for any repressed wish with somatic expression. Engel suggests that “the conversion process may sometimes be one step or one component in the development of a localized organic lesion (Schur, 1955; Rangell, 1959; Engel & Schmale, 1967)”. In such a case the lesion and its symptoms “neither have primary psychologic meaning ... nor serve a defensive function”. The
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timing and location of the manifestation are due to “the drive and defence aspects of the conversion contribution”, but the latter are not responsible for the nature of the lesion. Engel emphasises that psychophysiological processes such as gastrointestinal secretions which are not perceived and cannot leave memory traces are not part of the conversion. In a careful discussion of a number of examples he shows how a new symptom which is produced physiologically, such as paraesthesias after hyperventilation, may subsequently provide a perceptual basis for new conversion symptoms. This is, of course, in accordance with the accepted tendency of hysterical symptoms to mimic any organic or psychological symptoms which may have occurred previously. His view that a case of urticaria and another one of nickel sensitivity may be attributed to a conversion process which revives an effect on previous physical lesions is less acceptable. It is more plausible to suppose that excitement and generalised autonomic overactivity would have most effect in areas whose state had previously been altered, or which were currently in contact with metal. Walters (1969) also expresses doubts about the theoretical value of extending the meaning of conversion in this way. This difference of view from Engel and Schmale depends somewhat upon a different assessment of the significance which can be attached to some of the evidence offered. Schmale (1969) describes a case which we may briefly consider. In this 40-year-old woman, the very first evidence of rheumatoid arthritis developed in the ring finger of her left hand within days after the sudden onset of pain in the area covered by her wedding ring. The pain first occurred when she was getting ready for bed, while handling the medicine cabinet in which she kept a bottle of sleeping pills. In another context, she reported that, earlier the same day, her husband, in his progressive downhill struggle against cancer, had spoken of suicide by sleeping pills. She forgot to hide the pills from him. The relationship with her husband was ambivalent. Schmale considers this is not an unusual story of a progression from a conversion symptom to a somatic disease state, with the pain in the ring finger, which appeared as the first symptom, symbolising the patient’s acute conflict over her ambivalence towards her husband. Although I am entirely willing to accept that pain may occur as a conversion symptom, the evidence in this case is not good enough to prove that it had developed in that way or that it develops often in other patients as a precursor to somatic symptoms which have, as it were, an independent, organic mechanism. There is a tendency to believe in views like those under discussion
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because of the still current impression that hypnosis can produce local physical change. Following Barber (1969) the writer has argued (Merskey, 1971) that this view of hypnotic phenomena is erroneous, and the reasons are given in Chapter 19. Conversion phenomena are already sufficiently wide, interesting and controversial for it to be unnecessary to extend them in this way. If they are to be extended, the burden of proof, which must be substantial and not anecdotal, rests on the proponents. One of the factors influencing the development of Engel’s and Schmale’s ideas, and to which they refer, was Miller’s work on autonomic conditioning (Miller & Banuazizi, 1968). Miller later expressed his regret that he had not found it possible to replicate in full some of his first and most interesting experiments (Miller, 1974). With time, the effects have become steadily less pronounced. It is credible that autonomic conditioning to perceptions might occur at a somatic locus – and that these perceptions might be determined by a previous experience of some change in the part. But the proven quantitative basis for such local changes, even in the skin, which is so generally reactive to psychological stimulation, is still very slight. I conclude this chapter with the observation that the basic psychodynamic theory of the conversion symptom has not, effectively, altered since the 1920s. By that time Freud’s original notion that psychic energy was converted was being ignored in favour of the symbolic character of the symptom. Ziegler & Imboden (1962) state the view of several psychoanalytic authors who also favour rejecting the transmutation idea. The relationships between hysterical personality, conversion symptoms, sexual adjustment and psychodynamic theory have all gained attention, and some conclusions concerning these matters are drawn in Chapters 9, 10 and 25. More recently, the concept of dissociation has come under fresh scrutiny (Chapter 21) with respect to its capacity to produce enduring loss of memory, a matter which was evident earlier to the sensitive eye of Symonds (Appendix B), who remarked upon the awareness of their problems possessed by many of his patients. Chapter 25 offers a perspective on the nature of hysteria, the clinical approach to it, and the theory of its origins.
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25 The survival of hysteria
“One good reason that may be assigned to the persistent employment of the term Hysteria – a term we all know to be objectionable – is the difficulty of finding a substitute for it.” (F. C. Skey, 1867) “hysteria ... tends to outlive its obituarists.” (Lewis, 1975)
For the last few centuries, hysteria has been seen as a group, or groups, of symptoms with one unifying cause. The ebb and flow of historical argument sometimes placed that cause in the uterus (e.g. Jorden, 1603; Landouzy, 1846). At other times the view taken was essentially a psychosomatic one (Sydenham, 1697; Whytt, 1761; Carter, 1853) with the belief that mental changes provoked organic ones. This psychosomatic view went much further than we would go today since, as described, conditions like gout and dropsy were taken to be a consequence of emotional stress (Chapter 1). Concurrently with these views, the phenomena which today we class as anxiety and depression were combined under the heading of hypochondria and generally described as the male equivalent of hysteria. Both Charcot, and Freud usually considered hysteria to be a psychological disorder with physical symptoms but no organic basis. As Hirschmüller (1989) has pointed out, however, Breuer and Freud still considered it to be primarily a “general neurosis without specific localization”, which accorded with the standard view in the second half of the 19th century. Throughout the 19th century, the nature of loss of function due to an idea was being defined increasingly, with the benefit of more precise neurological analysis. However, the concept of hysterical symptoms being related to an idea, established by Russell Reynolds (1869) and Charcot (1872), had not abolished the more general notion. In consequence 379
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hysteria included a variety of emotional changes, and patients with severe depression, such as Anna O., the first case in the Breuer & Freud’s (1893–95) Studies on Hysteria, who had a severe depressive illness which even required several admissions for sanitorium treatment, were still classified as hysterical (Merskey, 1992b). Only in the 20th century have firm and widespread distinctions between anxiety, depression and dissociative disorders become established. Just at a time when the hysterical mechanism had become so well agreed, and apparently so well explained, the use of the term itself as a diagnosis began to be questioned most strongly, and became less popular. Like the psychiatric hospitals, which have changed from being lunatic asylums to mental hospitals or psychiatric hospitals, so the term hysteria has become unpopular in practice and in diagnostic classifications. In 1980 the American Psychiatric Association formally abandoned the diagnosis of hysterical neurosis, which had been used since 1968 in DSM–II. DSM–III included categories of conversion symptoms, somatoform disorders and dissociative disorders, and also abolished the category of hysterical personality disorder, substituting histrionic personality disorder in its place. The terms conversion and dissociation have thus served to minimise or replace the use of the word hysteria. DSM–II had a category “Hysterical Neurosis, conversion type”. DSM– III simply had conversion disorder and also dissociative disorders. DSM–IV (American Psychiatric Association, 1993, 1994) provides separate classifications of somatoform disorders, which include conversion disorder and dissociative disorders. Kihlstrom (1994) gives an excellent description of this evolution. Both DSM–III and DSM–IV have avoided the term hysterical personality and use histrionic personality disorder. ICD–9 (World Health Organization, 1977) allowed conversion hysteria as well as dissociative disorders and hysterical personality. In ICD–10 the World Health Organization (1992a) chose to avoid the word hysteria in any title and brought together disorders previously termed hysteria under the overall heading “Dissociative [Conversion] Disorders”. Thus in ICD–10, a hysterical paralysis is a dissociative motor disorder. Under personality disorder, ICD–10 recognises histrionic personality disorder and dependent personality disorder among others, as in DSM–III and DSM–IV. The unwillingness to continue to use the label hysteria is reinforced by an appreciation of its negative connotations: an erroneous idea of its mechanism; an apparent – or actual – sex bias, not only in the occurrence of the disorder but also in the readiness to diagnose it; patients’ discontent with the implications of the diagnosis; and the frequency with which it is wrongly made
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(Slater, 1965; Merskey 1986; Gould et al, 1986). In addition, occasional authors, especially Schilder (1940), Whitlock (1967b), Ludwig (1972), and myself seem to share the feeling that, notwithstanding the substantial importance of psychological factors in promoting the disorder, there is a link in some patients with cerebral organic dysfunction, although none of the four has given the latter mechanism pre-eminence over psychological causes. Slater (1965) was probably the most radical in seeming to relegate hysteria to the position of an epiphenomenon of another illness. Some supposed hysterical symptoms have also received other explanations, especially globus, spasmodic torticollis and multiple tics (Chapter 15). Nevertheless, the diagnosis continues to be made under one label or another, psychiatrists and physicians continue to use the concept of hysteria, and its causes and management remain a matter of concern. In the most comprehensive discussion of the history of hysteria and its literature Micale (1995) justly points out that “the very period that has witnessed the decline of hysteria as a medical diagnosis has brought a burst of professional interest in the history of the disorder”, which originates from many places in Europe and North America and includes several medical disciplines as well as a variety of the humanities. Sometimes these studies are invaluable, for example Micale’s own work, the luminous writing of Janet Oppenheim (1991) and the penetrating analyses of Jan Goldstein (1987). At other times I think the reader has grounds for complaint that neither evidence nor logical premise informs many of the productions (which are best left unreferenced), but the existence of this body of work is a testimony both to the interest of the subject and to its social importance. In any event, such a phenomenon requires a name. ‘General nervous problems’ would be a fair description for much of the extra-medical discussion, but covers even more territory, and again we see at least some need for a single term, in which case hysteria has really no competitors.
Diagnosis and subdiagnosis Whatever the full causes may be, it must be evident from the foregoing chapters that the range of phenomena encompassed in the concept of hysteria is enormous. If we accept that hysterical mechanisms are of basic importance in human psychology, that is not surprising. If we also accept that hysteria can model itself on any voluntary response, the same conclusion is inevitable. It does
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not necessarily follow from this that hysteria is an adequate diagnostic category. Recognising repression and projection as dynamic phenomena has not led to the creation of disease syndromes under those names. The situation with hysteria is, however, somewhat different. Individual symptoms or groups of symptoms occur with definable patterns, and more often than not no other diagnosis can reasonably be entertained. Many patients with hysteria do not have and do not develop schizophrenia, and are free from brain lesions. If these several conditions contribute to the production of the illness, that does not mean that they are a sufficient explanation for the phenomena, and they do not define in any way what is normally called hysteria. The latter is still a vigorous entity or set of entities, even if somewhat pleomorphic. It occurs sufficiently often on its own account, without other contaminating diagnoses, to justify its continued use. Many wartime patients could only be diagnosed as subjects of hysteria. Those with Briquet syndrome (Chapter 13), those in primitive communities (Chapter 16), those with epidemic hysteria (Chapter 16) and many children with such symptoms (Chapter 18) lack any characteristics which would require even a secondary, subsidiary diagnosis. In more conventional practice, even with neurological subjects, more often than not there is no good alternative diagnostic category. Merskey & Buhrich (1975) found 68 of 89 patients with conversion symptoms were only classifiable psychiatrically as cases of hysteria. Reed (1975), in a case-note study of a different hospital population, found a subgroup of 13 patients who originally had typical conversion or dissociative symptoms and who at follow-up varying from 3 to 19 years had had either similar psychiatric illnesses or none. He concludes that these patients showed a uniform clinical pattern and outcome, justifying the diagnosis of hysteria, and that to withhold the use of the term as a diagnosis “involves unjustifiable feats of semantic juggling”. For all these reasons hysteria is and should remain a valid substantive diagnosis. Whether one then prefers to talk of hysterical neurosis, conversion reaction or dissociative disorder is a matter of choice. With the changes in ICD–10 mentioned above, dissociative disorder is likely to be the most popular term, and with good reason, since it employs a unifying concept for all supposed cases and, so far, does not suffer from unpleasant judgemental implications which are readily recognised. If the word dissociative, which is now also undergoing some re-evaluation (Lynn & Rhue, 1994), is felt to be unsatisfactory, then the term doxogenic disorder may serve (see Chapter 20).
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The principal symptoms have been conveniently classified by Cleghorn (1969a) in the following three categories of hysterical reaction, modified from Rees (1967). (a) Dysmnesic (disorder of memory or conditions marked by gross dissociation) (i) amnesia (ii) fugues (iii) twilight, trance and possession states, Ganser’s syndrome (iv) somnambulism (b) Conversion reactions (conditions characterised by limited dissociation) (i) motor – paralysis, paresis, tremors, rigidity, abnormal gait, ataxia, fits (ii) sensory, general – anaesthesia, paraesthesia, pains sensory special – visual difficulties, including blindness, deafness, loss of taste, loss of smell, hallucinations (iii) visceral – vomiting, retention of urine, diarrhoea, constipation (iv) symptomatic super-additions or prolongation of illness (v) fictitious syndrome of conversion, surgical addiction and histrionicity (c) Hysterical or histrionic personality. This list takes into account both the occurrence of symptoms and hysterical personality disorder. Apart from some doubts expressed in Chapter 15 about the position of the visceral symptoms, I think this is a satisfactory statement of the relevant phenomena covered by the term hysteria. In fact, this grouping of symptoms is not controversial and is the basis for most discussions on the topic. In current practice in the developed world, the existence of the classic motor symptoms is best defined by physical, usually neurological examination. This will normally show that they correspond to an idea of the function of the part which is appropriate to the patient’s knowledge of anatomy and physiology. The explanation and treatment of the condition will be a matter for the psychiatrist using both Freudian notions of conflict and other notions, such as the effects of war, Kretschmer’s ideas on survival value, the impact of social and physical factors, and so forth. The hazards and the doubts with regard to making the diagnosis of hysteria have been covered by many authors and by innumerable doctors in word-of-mouth discussion. It should also be noted that failure to make the diagnosis can have substantial ill-effects. These
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include perpetuation of invalidism, the prescribing of unsuitable – and sometimes toxic – medication, over-investigation with potentially unpleasant or dangerous techniques such as lumbar puncture and arteriography, and surgical operation. Using the diagnosis of hysteria in the sense now indicated by Briquet syndrome, Cohen et al (1953) showed that women so affected underwent surgery in gross excess of what was likely to be required for their physical health, with probably no benefit and some harm to their mental health. Gynaecological operations were particularly frequent, occurring seven times more frequently in these patients than in control medical patients. One out of three such hysteria patients was rendered sterile before the age of 40. Besides all sorts of operations, patients with hysteria also use sedative drugs and opiates excessively. The authors conclude that far better diagnosis and management are required, and eschew the suggestion that the operations may be due either to masochism on the part of the patient or sadism on the part of the surgeon.
The medical role in hysteria It is clearly important to recognise hysteria when it occurs, whether as a symptom or group of symptoms, a mechanism or a pattern of behaviour or personal attributes. Szasz (1961), however, has taken the view that none of the phenomena which have been called hysteria should be accepted as illness. Illness is a category reserved for physical disease or disabilities. Doctors accept a false role in agreeing to treat hysteria medically once they have discriminated the true situation. The diagnosis of ‘no physical illness’ should be followed by the offer of a new relationship based on a contract to deal with personal problems in terms of communications and human relationships. Szasz advanced logical grounds for this position. There is a sense in which we may all agree with this formulation. When hysteria arises as a consequence of discoverable emotional problems, it is best managed by the dynamic and psychotherapeutic approach which Szasz ultimately relies upon, despite his many criticisms of other therapists. We can note this, and also note that a hysterical symptom or condition will invariably require management on lines which differ from the treatment of a simple pneumonia or a broken leg. However, it must be recognised in turn that many physical illnesses call for psychological and social management as part of the physician’s function. Some cases (e.g. Taylor, 1989) require management which only an astute doctor can provide.
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The care of the dying is another (non-hysterical) example, and changing the occupation of a silicotic or paraplegic miner is a third. A more subtle illustration of the need for psychological intervention in physical illness is the definition and treatment of emotional factors which may provoke attacks of grand mal epilepsy. At the same time, one has to note that numerous psychological disturbances are not susceptible to explicit formal psychotherapeutic techniques. There is also no way to distinguish logically with respect to the symbolic status of hysteria between those occasions when a conversion symptom results from a simple conflict and those when it is perhaps promoted by personality regression as a result of brain disease. For that we rely on somatic evidence. If all mental illness were hysteria, there might be a case for Szasz’s argument. But not all mental illness is hysteria, and even with hysteria the variety of its manifestations gives rise to situations, as already indicated, where the logic of his argument is inapplicable. Much of his argument in fact hinges on the notion that the only way to define illness is as a physical (pathological) event which provides certain consequences of social acceptance and release from particular responsibilities. Fabrega (1974) establishes that this is not so, very clearly showing that the role of being ill or having the status of a sick person is one which may be defined in terms of biological, psychological or social criteria. It is not necessary for it to be solely based on biological changes. One of Szasz’s criticisms against Charcot and Freud is that in defining hysteria as illness they were ‘changing the rules of the game’. The patient and the illness were reclassified and treated with the rules which applied to those who were physically ill. The argument just advanced regarding the criteria of illness is open to the same criticism, except that it is doubtful whether the rules were ever wholly written in the way Szasz suggests. Kendell (1975) required more stringent criteria for mental illness, arguing that the best guide to the presence of illness is the impairment of life expectancy or the impairment of fertility (provided that these are not a consequence of society’s reaction to the individual and his or her behaviour). By these standards, the purposive life-saving quality of some hysterical symptoms would exclude them from the definition of illness. But other hysterical behaviour, such as contractures, drug dependence and suicide attempts, may cause an increase in mortality, whether immediately or after some delay. Moreover, a few hysterical patients are liable to develop those psychoses such as schizophrenia which Kendell convincingly shows to be ‘illness’ in terms of the most severe
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criteria, while another group has hysterical symptoms secondary to physical illness or injury. Thus there is an important collection of patients with hysterical conditions who meet these very demanding standards for classification under the rubric of a medically approved ‘illness’. It can be argued also that the function of the physician qua physician is not only to cure or diagnose physical disorders but also to undertake the management of at least some situations which are related in time or place to physical illness and to mental disturbance. The role of healer has never been totally separate from that of personal adviser, and never will. The urge to make a break between the two functions has arisen from the triumphs of somatic medicine, so that the precise limits within which it is useful for the physician to practise in these conjoint roles has undergone re-examination. However, the abolition of the role as psychologist cannot follow either from the success of organic skills or from the substantial contribution of non-medical psychologists. Medicine and psychological symptoms are too intimately linked for this to happen, as may be evident from the preceding pages. The limits of what is a medical condition and what will be taken to be a medical role are bound to undergo continuing definition and redefinition, both with advances in medicine and with social changes (Merskey, 1986). None of this is likely to lead to hysteria being removed from the province of medicine, despite the inevitable wish of some doctors. Like Szasz, Mechanic (1962) considered the social significance of behaviour in relation to illness. Basing his work on the theories of Talcott Parsons, Mechanic described the notion of illness behaviour as “the ways in which given symptoms may be differentially perceived, evaluated and acted (or not acted) upon by different kinds of persons”. In his view, the sick role provides a “partially and conditionally legitimated state” which is granted if the individual agrees that it is “undesirable” and recognises an obligation to cooperate in recovery. These views have always been inherent in medical practice and are a common-sense assumption which normally underlies a patient’s request for medical help. Pilowsky (1969) introduced the concept of ‘abnormal illness behaviour’, which is evident when a person deviates from normal vis-à-vis the expected role “to a point at which the individual behaviour may be considered neurotic or even psychotic”. Belle indifférence, conversion symptoms, malingering, and particularly hypochondriasis and deliberate disability can be classified under this rubric. The reasons for most of these deviations have been explored already. It is relevant to point out that these patterns of
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abnormal illness behaviour are so frequently associated with abnormalities of personality, and of personal experience, that it is impossible to dismiss them as of no concern to the physician who makes the diagnosis of hysteria. To do Szasz justice, he does not suggest that such people should be dismissed from all forms of attention. His plea in essence is that it should not be called medical. Few, if any, practising clinicians would accept that such an aim is either attainable or desirable. One example only will be given. An illegitimate youth of mixed ethnic origin with a history of marked childhood deprivation, frequent changes of employment, abuse of alcohol and criminal offences injured himself with a gun and threatened suicide if returned from hospital to face further legal charges. Within the surgical unit he was also difficult to manage, often creating minor disturbances. The doctors responsible for his surgical care sought psychiatric help, and without attempting to prevent the law from taking its course, the psychiatrists construed it to be their medical role to treat his emotional disturbance, if possible, and to try to safeguard against suicidal attempts. The alternative of seeking to deal with his emotional disturbance purely through other social agencies would have been neither effective nor humane. This is not to say that the medical management was necessarily effective nor that it excluded psychological and social variables in dealing with the patient. It was simply the best approach available. Another approach to the understanding and management of hysteria which many authors from Freud onwards have advocated (see Szasz, 1961; Abse, 1966) is to consider the symptom as a communication, or evidence of an attempt at communication. This is certainly an important aspect of any dealings with patients with hysteria, and was considered in Chapter 4. But it has its limitations. All attempts to talk overtly to patients about communication run two risks. The first is that the patient will not comprehend the approach, and this is extremely likely with Briquet syndrome. The second is that the resistances of the patient will render them nugatory. This is particularly true in monosymptomatic conversion reactions, which lead patients to ignore or deflect any approaches for which they are not ready. A subclass of this second category is the possibility that the patient will talk enthusiastically about communication and not about the basic problem, and the doctor and patient then collude in an arrangement which perpetuates their meetings but does not resolve the disorder. Without wishing to dismiss the subject of communication as unimportant – it is not – I think it worth emphasising that communications are often too explicit for comfort or safety. Aggressive
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behaviour, terrorist activity and the like all provide a clear enough message for those who survive it, and one which does not need to be expanded or repeated. In patients with hysteria the need is for definition of the content of communication rather than its theory. The aspect of content, indeed, is the one which emerges most regularly from Freud’s original observations. When Slater (1965) challenged the idea of hysteria as a diagnosis he recognised, without elaborating on the matter, that there was still an important phenomenon which required attention. This was the adjectival function of the term. Symptoms or patients might be hysterical even in the absence of a diagnosis of hysteria. Interestingly, as described in Chapter 1, King (1994) has demonstrated that this is exactly how the Hippocratic collection handled the topic. McHugh & Slavney (1983) proposed that we should think about disorders in terms of four constructs: diseases, dimensions of personality, goal-directed behaviour, and life stories. With respect to hysteria, Slavney (1990) argues that it is not something which a patient has but rather reflects something a patient is and something a patient does. Why patients are what they are, and do what they do, is a question which he thinks should be answered through meaningful interpretations of the life story, which may be conflicting and inconsistent. Again, it is clear that whatever the status of hysteria as a diagnosis, these are phenomena which require understanding and medical professional help, even if the solution is likely to rest with the relationships of the individual.
Over-extension of hysteria Exaggeration is not only an objection to hysterical descriptions. It can also be a feature of the interaction between the patient and the therapist producing far-fetched phenomena, unrestrained by critical evaluation. Without it, the enormous growth of artificial conditions like multiple personality disorder (MPD), and particularly the proliferation of numerous personalities with bizarre patterns offered as a version of human adjustment, would not have taken place. The remarkable statement in DSM–III–R (American Psychiatric Association, 1987) that as many as 100 personalities or fragments of a personality might exist in any one case, raises the obvious question of whether those who agreed to that particular criterion were using the notion of personality in any sense which reflects the usual use of the word inside or outside medicine. Similarly, today, fashionable descriptions of cases with MPD are scarcely
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sufficient unless they include a personality of the opposite sex, one of another race, a child and perhaps an animal. Developments of this sort inevitably mean that anyone with a minimum amount of scepticism is bound to question the basis in medicine for such creative changes. There is much similarity between these excesses and the ovarian tender points in which Charcot believed and which were abandoned by his successors. Both appear to have been created by obliging patients responding to the expectations of physicians or other therapists. Of the two fashions, ovarian tender points are the more plausible. The only reservations I would have in defining MPD as the ovarian tenderness of the 20th century are that the phrase has been used for other conditions, such as chronic fatigue syndrome, and that, in any case, MPD also dates from the time of Charcot and his colleague Janet, although it was never developed to the same extent in their hands as it has been today. Valuable concepts may be damaged by over-extension as well as weak ones. The notion of repression has served for 100 years as a helpful means of exploring patient’s feelings, and perhaps of resolving internal conflicts. It is a fundamental part of a system of dynamic psychiatry which, for good reason, has had an immense influence both within and beyond medicine. In my view it is still plausible to suppose that the repression of serious emotional problems can occur, but we now need to review the way in which we conceptualise repression. Selective attention, shaped by motivation, may be a better approach to understanding repression than any theory advanced to date, and in any case we must modify our beliefs about the extent to which repression can affect longpast memory. The need to do so resulted essentially from the proliferation of cases of the recovery of implausible past memories, now described as part of the ‘false memory syndrome’ (FMS). In the past, psychologists have expressed occasional concern that the scientific basis of the concept of repression was uncertain and that it had never been systematically demonstrated. Nevertheless, an enormous amount of individual anecdotal information repeatedly supported the possibility of repression occurring with respect to current problems. There have indeed been experimental psychological investigations which demonstrated the production of headache in response to an emotional conflict and as an apparent solution to that conflict (Eisenbud, 1937), and the recovery of recent traumatic memories in the treatment of battle neurosis is well known. Thus as a working hypothesis to explain the treatment of current or recent events by the mind, the concept of repression has justification. On the other hand, the
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emergence of FMS has provided very strong reasons for questioning the validity of recalling supposed memories of long-past events as a result of the unblocking of repression. The grounds for believing that there is a FMS which adversely affects the lives of the relatives of those who developed the syndrome – as well as being no help to the patients – were considered in Chapter 21. It suffices here to remark again that the emergence of that syndrome has forced a reconsideration of the role of repression in psychiatry. It is not reasonable to suppose that the concept of repression, as described by advocates of the recovery of long-lost memories, can be maintained. Knowledge of the ordinary workings of the brain without repression makes it clear that memories are not stored in a crystalline fashion, only requiring a cover to be taken off them. If any memories have really been kept in a secure compartment in the brain, only waiting for the association of ideas to release a combination lock which will then slide open and release them, the material within the locked compartment cannot be what was put in there one, five or 20 years previously. This point has substantial importance in North America today, since the over-extension of the idea of repression has been used to generate criminal prosecutions as well as law suits against relatives, who are expected to pay for the fees of the therapists who have engendered the idea in the patient, and for the suffering of the patient. It was helpful to use the notion of repression as conceived to date as a means of assisting individuals to get better, and it remains justified in relation to the way in which we treat current problems, pushing them aside or even refusing consciously or unconsciously to acknowledge them. As a basis for evidence which is inherently harmful to other people, yet founded upon recollections that at best can only be distant and at worst are impossible, however, repression must now have had its day in psychiatry, as well as in court. If it is to survive it will need redefinition. The twin phenomena of MPD and FMS mean that we must look closely again at what constitutes the notion of dissociation. This has been considered in Chapter 21, where I also conclude that the criteria for what constitutes repression must be drawn much more stringently than in the past. As a tailpiece to this discussion, it is worth noting that suits against psychotherapists for using the wrong diagnostic technique and for failing to use appropriate treatment have begun to appear. One of the most notable concerned the attempt to treat by psychotherapy a physician who had a severe depressive illness and who was not given adequate opportunity to explore the benefits of
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psychopharmacology and electroconvulsive therapy, which ultimately cured him (Klerman, 1990). In California in 1994 Gary Ramona successfully sued his daughter’s two therapists. At the present time, suits are also being brought in a small town, of some 6000 people, in Ontario against a social worker and his employers, where the social worker – after attending a course on MPD – returned and told a number of women that they had this condition. Subsequently at least three attempted suicide and they are suing him and his employers for malpractice. The American Medical Association has made a strong statement about recovered memory therapy (Council on Scientific Affairs, 1994).
Clinical analysis Reasons have been given for regarding hysteria, conversion symptoms or dissociative disorders as problems requiring medical expertise, albeit very often in the context of social systems. In fact, the main difference between hysteria and meningitis in this respect is that the social systems and interpersonal relationships probably play a larger role in the production of hysteria, but in principle the same relationships obtain. Meningitis also has to be treated in terms of its social contacts and implications, where the patient should be managed, and what relationships other individuals should have with the sufferer. It therefore remains valid to study hysteria as a medical issue, to treat the patients who have it as subject to illness, and to accept that it is a valid diagnosis embracing the symptoms reviewed in this book. A few comments defining hysteria in clinical practice are indicated accordingly. The clinical groupings in which hysteria will occur are more or less outlined by the topics of this work and its chapter headings, from simple motor paralyses to hospital addiction and Briquet syndrome. For convenience and in order to draw the threads together, the following presentation pattern can be isolated: (a) hysteria with one or two symptoms, usually motor or dissociative (as in amnesia), sometimes pain (b) polysymptomatic hysteria, especially hypochondriasis and Briquet syndrome (c) hysterical elaboration of organic complaints (d) symptoms of self-induced illness or self-damage in abnormal personalities, from anorexia nervosa to hospital addiction
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(e) psychotic or pseudopsychotic disorders (Ganser’s syndrome, hysterical psychosis) (f) hysterical personality (g) culturally sanctioned endemic or epidemic hysteria. These categories cover the bulk of hysterical manifestations. The aetiology of some of these cases will ordinarily be evident from the circumstances in which they are seen, such as battle neuroses, culturally based outbreaks, compensation settings. Other cases will arise in patients with well established personality disorders or long histories of psychological illness, the evidence of which will assist in reaching a diagnosis. Apart from these, certain other considerations may be helpful for the differential diagnosis of monosymptomatic cases in practice in Westernised settings. Hysteria may be recognised and explained in cases where there is a definite conflict, which can be demonstrated. This will usually be in young people. Depression will provide a modest number of patients with classic motor conversion symptoms as a precursor or accompaniment. Schizophrenia will do this very occasionally. Lastly, organic neurological disease, especially epilepsy but sometimes an early brain tumour or a dementia, will lead to hysterical manifestations. A patient approach to the subject and recognition of these possible underlying causes will enable satisfying diagnostic work and therapy, always provided that hysteria is not diagnosed by exclusion or merely because the symptom appears bizarre or inexplicable; and provided that positive psychiatric evidence is always sought to confirm the diagnosis. Anyone who practises in this fashion need not fear that they will be using an extinct diagnosis. As Lewis (1975) points out, “hysteria is a tough subject, unlikely to be killed so long as clinicians find it useful, if not indispensable”. What clinicians ultimately make of it will always depend on their particular orientations or, more frankly, their biases. This was well understood by Wilson (1910), who observed that the originators of various theories of hysteria showed “a curious similarity in their appeal to their own clinical experience subsequent to the adoption or enunciation of their particular theory”. He went on to remark that “the exponents of the sexual theory, the suggestion theory, the sleep theory, and the ‘hysteria-only-a-symptom’ theory alike appeal to experience for confirmation of their opinion, and find it”. Following such a warning, barely noticed in the lifetime since it was penned, we can concur in not dismissing the diagnosis, but it becomes harder to advance any single theory of the origins of hysteria. We must accept that we are dealing with a disorder of
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infinite variety, determined always by human motives and circumstances. These motives derive from the fundamental experiences of childhood, from acute stress situations, especially conflict, and from the circumstances of physical illness. The numerous symptoms which may result give expression to the individual’s need for survival and for the resolution of emotional dilemmas, and the mechanism employed to attain these ends is primarily one of regression. The personality traits with which the disorder is associated probably result from the same mechanisms as the symptoms, leaving the individual more prone to these symptoms in later life. The simplest, ultimate paradigm is of the small child within the adult frame crying for his or her mother and protesting weakness and debility to secure love and affection.
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Appendix A. Comparative table of the symptoms of hypochondriasis and hysteria
E. F. Dubois d’Amiens. From Landouzy (1846) Hypochondriasis
Hysteria
Exclusive to Man, affecting both sexes, but especially males, usually between 30th and 50th years of life. Onset: slow, gradual, according to the ideas the patient has of them. Prodromal symptoms: Introspective, concern with one’s health, scrutiny of organs available to the senses, and of excreta. Scrupulous attention to certain rules of hygiene; need to consult medical books or to talk to doctors; depression is usual; loss of interest resulting from minor changes in general health. The symptoms constitute three stages.
Exclusive to woman, hysteria is the sole prerogative of women, occurs during reproductive life, between puberty and the menopause. Attacks of sudden onset. Onset provoked especially by strong feelings; sudden onset or heralded over a period of several hours by prodromal features; inappropriate elation or sadness; crying without cause; almost convulsive laughter, deep sighings, cramps in the limbs; mild rumblings in the belly; sense of constriction in the throat, etc. The symptoms are of two degrees.
First Stage Continuous and marked worry engendered by normal body sensations. Hypochondriacal self-scrutiny. Express continuous exaggerated
First Degree Heaviness in the limbs: numbness; cramps more severe; strong feeling of an ascending abdominal constriction, which is swollen or drawn in, the 397
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Appendices phantasies about their disease. False belief of having a severe and unusual disease; they assert, and in fact believe themselves, to be suffering from all the affections of which they have heard or read. Sometimes patients are preoccupied with digestive symptoms, and then abdominal disorders feature (hypochondriacal monomania); sometimes attention is focused upon the organs of the circulation or respiration (‘cardio-respiratory monomania’); sometimes the patient is concerned about the brain function (‘cephalic monomania’), etc., etc. From then on the patient’s attention is divided between the sensations and the search for a cure; hence avid reading of medical books, charlatans consulted, gossips trusted; all-stimulating diet or all-weakening diet, misuse of drugs, and henceforth increased symptoms in digestive, circulatory, respiratory, sensory systems, etc. Increase in normal anxiety (moral fear) – return to normality possible. Second Stage Development of diverse neuroses from usual causes and the added causes of the first stage; moral anxiety raised to the highest level, no relief; momentary distractions. From then on symptoms either remit or lessen. Continual fear of death. If the digestive tract is neurotic:
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umbilicus is retracted, feeling of a rounded foreign body (globus hystericus), intermittent excessive movement is noticed in the abdominal viscera. Constriction in the chest; continual sighings, insatiable need to breathe; palpitations, dyspnoea; increase of chest constriction; strangulation; feeling of a foreign body lodged in the throat, swelling of the neck; swelling of the jugular veins; fremitus of carotids; suffocation; hemicranial headache; stabbing, localized head pain (‘hysterical nail’); expressive facies; clenched teeth; generalised and voluntary tensing of muscles of locomotion; soon followed by relaxation and renewed tensing more or less sustained; limb contortion. Remain conscious during paroxysms. It is usual for convulsions to be milder and to occur more often during the bending and extending of limbs. Second Degree To the preceding symptoms are added, or appear de novo, the following features: wild and painful cries, incomplete loss of consciousness – sometimes complete, suffused facies; enormously swollen neck; violent and tumultuous heart-beats; involuntary locomotor muscle contraction; frightening generalized convulsions, violent movement requiring several others to restrain; extensive flexion and
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Appendices symptoms of dysphasia, of gastralgia, enteralgia, etc. Constipations. If circulatory organs: palpitations, dyspnoea, marked arterial pulsation, buzzing, whirring, explosions, etc. If general sensory: anergia, collapse, weakness, sweats, vague pains etc.; mental functions are disturbed, sensation and imagination pass far beyond the bounds of reason. Return to health possible. Third Stage Chronic inflammation of various organs, widespread organic change, especially with disturbances of abdominal viscera; then of respiratory organs and parenchymal organs; serious and numerous symptoms, not surprising given the organ tissue-change. Reversal to normality almost impossible. The prognosis then, as is almost always the case in an illness with organic components, is most often poor. (Jahn, 196, Hasse, 293)
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extension movements; frequent spitting; sometimes saliva a little frothy, but no frothing at the mouth. There is no foaming of the mouth and the thumbs are not bent inwards. Often imminent suffocation, breathing and circulation are almost suspended. Sometimes the patients jump about on their beds, sometimes they adopt almost tetanic postures; sometimes long-lasting syncope or loss of feeling and movement without facial pallor or cold extremities; the attacks may last several hours. Prompt return of consciousness, immediately after the convulsions. The prognosis then, as always in a functional illness, is good. (Loewenthal, 84)
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Appendix B. Hysterical insanity
Emil Kraepelin (1904) G ENTLEMEN , – The young lady, aged 30, carefully dressed in black, who comes into the hall with short, shuffling steps, leaning on the nurse, and sinks into a chair as if exhausted, gives you the impression that she is ill. She is of slender build, her features are pale and rather painfully drawn, and her eyes are cast down. Her small, manicured fingers play nervously with a handkerchief. The patient answers the questions addressed to her in a low, tired voice, without looking up, and we find that she is quite clear about time, place, and her surroundings. After a few minutes, her eyes suddenly become convulsively shut, her head sinks forward, and she seems to have fallen into a deep sleep. Her arms have grown quite limp, and fall down as if palsied when you try to lift them. She has ceased to answer, and if you try to raise her eyelids, her eyes suddenly rotate upwards. Needle-pricks only produce a slight shudder. But sprinkling with cold water is followed by a deep sigh; the patient starts up, opens her eyes, looks round her with surprise, and gradually comes to herself. She says that she has just had one of her sleeping attacks, from which she has suffered for seven years. They come on quite irregularly, often many in one day, and last from a few minutes to half an hour. Concerning the history of her life, the patient tells us that her parents died 16 years ago, one soon after the other. Her father’s step-brother attempted suicide, and her brother is most fantastically eccentric. I must add that two other members of her family give the impression of being very nervous. She did her work easily at school. She was educated in convent schools, and passed the examination for teachers. As a young girl, she inhaled a great deal of chloroform, which she was able to get secretly, for toothache. 402
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She also suffered from headaches, until they were relieved by the removal of growths from the nose. She very readily became delirious in feverish illnesses. Thirteen years ago she took a place as governess in Holland, but soon began to be ill, and has passed the last seven years in different hospitals, except for a short interval when she was in a situation in Moravia. It would appear from the statements of her relations and doctors that the patient has suffered from the most varied ailments, and been through the most remarkable courses of treatment. For violent abdominal pains and disturbances of menstruation, ascribed to stenosis of the cervical canal and retroflection of the uterus, recourse was had five years ago to the excision of the wedge supposed to cause the obstruction, and the introduction of a pessary. At a later period loss of voice and a contraction of the right forearm and the left thigh set in, and were treated with massage, electricity, bandaging, and stretching under an anaesthetic. Heart oppression and spasmodic breathing also appeared, with quickly passing disablements of various sets of muscles, disturbances of urination, diarrhoea, and unpleasant sensations, now in one, and now in another part of the body, but particularly headaches. Extraordinarily strong and sudden changes of mood were observed at the same time, with introspection and complaints of want of consideration in those about her and in her relations, although the latter had made the greatest sacrifices. Brine baths, Russian baths, pine-needle baths, electricity, country air, summer resorts, and, finally, residence on the Riviera – everything was tried, generally with only a brief improvement or with none at all. The immediate cause of the patient being brought to the hospital was the increase in the ‘sleeping attacks’ two years ago. They came on at last even when the patient was standing, and might continue for an hour. The patient did not fall down, but simply leaned against something. The attacks continued in the hospital, and spasmodic breathing was also observed, which could be influenced by suggestion. Hypnotic experiments only produced hypotaxis, suggestions of cure proving not to be lasting. But sprinkling with cold water and the faradic current were fairly effective, even against the disablement which appeared now and then. After spending eight months here, the patient went away at first to her sister’s. But after a few months she had to be taken to another asylum, where she stayed about a year, and then, after a short time spent with her family, came back to us. During her present residence here, so-called ‘great attacks’ have appeared, in addition to her previous troubles. We will try to produce such an attack by pressure on the very sensitive left
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ovarian region. After one or two minutes of moderately strong pressure, during which the patient shows sharp pain, her expression alters. She throws herself to and fro with her eyes shut, and screams to us loudly, generally in French, not to touch her. ‘You must not do anything to me, you hound, cochon, cochon!’ She cries for help, pushes with her hands, and twists herself as if she were trying to escape from a sexual assault. Whenever she is touched, the excitement increases. Her whole body is strongly bent backwards. Suddenly the picture changes, and the patient begs piteously not to be cursed, and laments and sobs aloud. This condition, too, is very soon put an end to by sprinkling with cold water. The patient shudders, wakes with a deep sigh, and looks fixedly round, only making a tired, senseless impression. She cannot explain what has happened. The physical examination of the patient shows no particular disturbances at present, except the abnormalities already mentioned. There is only a well-marked weakness, in consequence of which she often keeps her bed or lies about. All her movements are limp and feeble, but there is no actual disablement anywhere. She often sleeps very badly. At times she wanders about in the night, wakes the nurses, and sends for the doctor. Her appetite is very poor, but she has a habit of nibbling between her meals at all kinds of cakes, fruit, and jam, which are sent to her, at her urgent request, by her relations. What particularly strikes us in this picture is, first, the coming and going, in the form of attacks, of a number of disturbances of different kinds, and, secondly, the fact that they are influenced by external agencies. These two peculiarities show at once and with absolute certainty that we have to deal here with the disease known as hysteria. Its nature is, I think, to be found in this: that all disturbances on the mental side arise, with very strongly exaggerated sensations, through the agency of ideas. There is not one of the very varied appearances which might not be called up by violent emotional shock. All that is morbid is the circumstance that these disturbances appear even when there has been no cause, or only a very trivial one, for emotional excitement. In the ‘great attacks’ occurrences are repeated in dream-like recollection which the patient says have taken place before. These are, first, a gynaecological examination, to which she was very roughly subjected by a Dutch doctor, and, secondly, a curse pronounced on her by her aunt. That all the disturbances are produced by ideas having the force of sensations is very clearly shown by the fact that they can at once be put an end to by psychical influences. A contraction of the
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patient’s right hand, provoked by her former doctor by an incidental question about the disturbance, which had often been observed before, was very instructive. Next day the hand was so spasmodically clenched that the nails ran into the skin. After a little instruction in metallo-therapeutics, first a gold coin and then a key was laid on the wrist and relieved the spasm. The faradic brush worked even better, and had a more lasting effect. While real hypnotics had hardly any influence, her sleep was very much improved by distilled water, with harmless additions, and by powdered sugar. All the other various troubles gave way to measures of the same kind, working on the imagination alone. It is true that these results were only temporary, as was to be expected, considering how changeable were the patient’s feelings. After a few hours or days, with or without an external cause, one or other of the old symptoms returned. The capricious nature of hysterical phenomena leads only too easily to the accusation of intentional and artful trickery. But many of the disturbances observed can hardly be imitated voluntarily, or cannot be imitated at all, while others are only accidentally discovered, and have never come to the patient’s own knowledge – as, for instance, the limitation of particular departments of perception. These circumstances seem to me to confirm the hypothesis that in this disease we have always to deal with the involuntary effects of excited sensations, referable to the patient’s own body. Again, the morbidity of the general condition, even when disturbances are really feigned or greatly exaggerated, is shown by the patient’s whole course of life. Our patient, in spite of her very good mental endowment, has never been able to fill any place in life permanently, but has been wandering for many years out of the hands of one doctor into those of another. In this we recognize the deep disturbance of the will, which we never fail to see in hysterical patients. In spite of the usual extravagant complaints about her illness which our patient is always pouring out to the doctors in conversation or in letters, she is quite without the power of striving energetically to overcome the morbid phenomena. Indeed, her illness gives her a certain satisfaction, and she resists involuntarily when steps are taken to cure it. Hence the constant appearance of new and ever more remarkable disorders; hence the exaggerations, the calls for the doctor, and the burning desire to see proper attention given to her own condition, because invalidism has essentially become a necessity of life to her. With her growing expertness in illness, the emotional sympathies of the patient are more and more confined to the selfish furthering
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of her own wishes. She tries ruthlessly to extort the most careful attention from those around her, obliges the doctor to occupy himself with her by day or by night on the slightest occasion, is extremely sensitive to any supposed neglect, is jealous if preference is shown to other patients, and tries to make the attendants give in to her by complaints, accusations, and outbursts of temper. The sacrifices made by others, more especially by her family, are regarded quite as a matter of course, and her occasional prodigality of thanks only serves to pave the way for new demands. To secure the sympathy of those around her, she has recourse to more and more forcible descriptions of her physical and mental torments, histrionic exaggeration of her attacks, and the effective elucidation of her personal character. She calls herself the abandoned, the outcast, and in mysterious hints makes confession of horrible, delightful experiences and failings, which she will only confide to the discreet bosom of her very best friend, the doctor. Hysterical insanity is the expression of a peculiar, morbid tendency, and can be brought to further development, but not originated, by external causes. In our patient, the beginning of the illness goes back to an early age. We cannot therefore expect that treatment will be successful in altering her personality. Such patients, in whom the selfish development of feeling and will has appeared, in addition to the other symptoms of hysteria, are generally permanent thorns in the flesh of their relations and doctors. The individual manifestations of the disease may change, but the original soil in which they are always reappearing remains unaltered.* * The patient died of pulmonary consumption after having been one year in the asylum psychically unchanged.
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Appendix C. Hysteria
An address given by Sir Charles Symonds at the National Hospitals for Nervous Diseases, Queen Square, London, 27 February 1970 The last time I heard hysteria discussed in this theatre was the occasion of Dr. Eliot Slater’s Shorvon Lecture which he ended with the words ‘The diagnosis of hysteria is a disguise for ignorance, and a fertile source of clinical error. It is in fact not only a delusion but a snare.’ Sir Francis Walshe later subjected Dr. Slater’s arguments to detailed criticism, arriving at a very different conclusion. ‘The essential difference of hysteria from somatic disease,’ he said, ‘is that it constitutes a behaviour disorder, a human act on the psychological level,’ and he went on to say that diversity of symptoms from case to case, and in any single case from time to time is no argument against the unitary quality of the malady. I agree entirely with Sir Francis in this, and all else that he wrote in his masterly summary. Hysteria is not a myth but a reality. In 1941 the Brain Injuries Committee of the M.R.C. produced War Memorandum No. 4, A Glossary of Psychological Terms Commonly Used in Cases of Head Injury. At the price of one penny from His Majesty’s Stationery Office, it was not bad value for money. The Committee discussed the definition of hysteria at length, Bartlett and Aubrey Lewis, as I recall, taking the lead. This was our definition: Hysteria: A condition in which mental and physical symptoms, not of organic origin, are produced and maintained by motives never fully conscious directed at some real or fancied gain to be derived from such symptoms. . 407
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Note: The adjective hysterical may be applied either to this condition, or to the type of psychopathic personality common among those who develop this condition. James Birley, one-time physician to this hospital, wrote an interesting paper on the hysterical personality, I think in the St. Thomas’s Hospital Gazette. He concluded, as I recollect, that the capacity for self-deception in the hysteric might be regarded as a specific kind of mental deficiency, a suggestion worth reconsideration. The susceptibility to hysteria may undoubtedly be associated with uncommon ability in other directions. The pattern of hysterical symptoms is determined by variable factors. Among these medical fashion must be included. Charcot set a fashion in his day, which has long been obsolete, for grotesque convulsive spasms. Babinski who followed him was more interested in hysterical paralysis, which thus became prevalent. It was not, however, until World War I that hysterical symptoms became common in men exposed to psychological stress of a kind and degree exceeding any that had been previously endured in the mass. These symptoms were in the main exaggerations or perpetuations of the effects of physical injury or shock. Thus the man who had been buried or blasted by the explosion of a shell would exhibit paralysis, tremor or aphonia: the man who had been blinded by the intense blepharitis and conjunctivitis caused by mustard gas would fail to recover his vision when these lesions were healed. Such cases were common, and the sufferer was by no means always of a hysterical personality. Under the conditions of the Somme, and of Passchendaele, the gain to be derived from disability could be overwhelming for any normal person. As a battalion medical officer I had first-hand experience of this, and successfully treated cases of hysteria without sending them into hospital. The earlier the diagnosis was made the more easily it was treated. The idea, prevalent in the early days of that war, that shell-shock could cause paralysis, tremor and so on, as the effect of some obscure physical disorder of the nervous system resulted in a plethora of hysterical disability. Even the great ones were deceived. Froment and Babinski described a condition they named ‘reflex paralysis’, the organic nature of which was considered proven not only by the vascular changes in the paralysed limb, but the X-ray evidence of decalcification of bone in chronic cases. The reader of their manual was warned against the diagnosis of hysteria. This manual, translated into English and appearing as a paperback under the aegis of a physician to this hospital, must have been
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responsible for much chronic disability, until Arthur Hurst proved that in all such cases the paralysis could be removed by psychological treatment, and that the vascular and bony changes then disappeared. They were in fact the effects of prolonged disuse. Motivation for hysteria was still prevalent in the immediate postwar years. There was wide scale unemployment and much hardship, and the war pensions clinics yielded a considerable harvest of hysterics to the neurologist who was prepared to take the necessary time and trouble for their diagnosis and treatment. A single example will serve to illustrate the type of case encountered, that of a young man who had suffered temporary blindness from mustard gas. He had subsequently remained blind for two years. For reasons that now seem as incredible as they were obscure, the disability had been accepted as organic and he was receiving a 100 per cent pension. I saw him at a Pensions Clinic and admitted him to Guy’s. I had been trained in the treatment of hysteria by Hurst who had himself been trained by Babinski. Persuasion and suggestion, sometimes assisted by hypnosis were the methods used. Hurst laid great stress upon the importance of cure at a single session. I set aside an afternoon for the treatment of this patient, and at the end of three or four hours his vision was normal. At this moment his wife came into the ward to visit him with her two small children. Proud and exhausted I said to her ‘Your husband is cured of his blindness’ . Her immediate response was ‘Whatever shall we do without the pension!’ Between the wars gross hysterical disability in men was uncommon except in compensation cases, in which the pattern of disability varied with the nature of the injury. I gave up trying to treat these cases until the compensation issue was settled, giving the opinion that when this had been concluded the symptoms would rapidly disappear. This opinion did not always prove correct. There appeared to be two reasons for this. The first was simple. The patient’s self-respect demanded some credible reason for recovery. Electrical treatment or hypnosis were effective. I wonder if any neurologist practises hypnosis now? Hurst taught me to make good use of it. The second, and much smaller group of cases, in which there was imperfect recovery after compensation, comprised patients whose sense of injury was of almost paranoid degree and who would not be deprived of the right to nurse a grievance. Apart from compensation cases hysteria between the wars was uncommon and therefore perhaps more easily misdiagnosed. One of my appointments in my early days was that of consulting
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neurologist to the Streatham Home for Incurables, a very fine institution. I made it my business on each of my routine visits to examine a few patients thoroughly and make my own diagnosis. Many were suffering from disseminated sclerosis or Parkinsonism, in the advanced stages. But in the course of my investigations I discovered two women with hysterical paraplegia. One had been bed-ridden for nine years the other for seven years. They were both admitted to Guy’s under my care and discharged walking normally. The story of one of these cases I shall tell you as a typical example of the psychopathology of the illness. Until the age of 25 this young woman had led a life of leisure as the daughter of wealthy parents. There was then a financial disaster, and she found herself obliged to earn her own living. This she eventually did by taking work as a nursery governess – work for which she had the greatest possible distaste. At the age of 29 she went with an officer’s family to live at Gibraltar. While there she became attracted by a man some years younger than herself who made her an offer of marriage. This man was a private soldier and an officer’s servant. Now she was in two minds about this. She was very fond of the man and welcomed any opportunity of escaping from the work she disliked so much. On the other hand his age and social rank were strong arguments against the marriage. Eventually she consented to become engaged. She came home to England, the arrangement being that he would shortly follow and they should then be married. Before he arrived she had an illness, which appears to have been a polyarthritis. Some concern was expressed about her cardiac condition. She was still in bed when her fiancé arrived. The wedding was therefore postponed, and it was decided that she should name the day when she got better. Now consider her position at this time. So long as she was ill her relatives were prepared to provide for her for the time being. She was well looked after and had not to work for her living, and this without paying the price of a marriage which, at the back of her mind, she felt would be disastrous. So long as she could honestly believe that she was ill she could feel that she was doing her fiancé no injustice, because it was through no fault of her own that the wedding was delayed. Her fiancé and relatives became anxious about her and the opinion of various physicians was taken. Meanwhile she remained in bed with a progressive paraplegia which was eventually diagnosed as disseminated sclerosis. Finally her family raised the necessary funds for her admission as a permanent inmate to the home for incurables, where, as I have said, she had lain in bed for seven
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years before I saw her. I had her admitted to Guy’s, obtained her story and brought her gradually, and not without a good deal of distress and humiliation, to realize that she had been unconsciously exploiting illness to her own advantage. After this with persuasion and suggestion we soon got her walking again. We then began to help her make plans for her future. We assumed that her relatives would give her shelter while she set about finding a job. Their attitude in the matter, however, was quite definite. They were in difficult circumstances themselves. They had secured the patient’s admission to the home, where she had been for all these years, and they were not prepared to do anything more for her. She had no money apart from her small savings so that the position was indeed difficult. We made tentative arrangements with a hostel to take her while we found her a post; and discussed these plans with her. Next day she complained of a pain in her back, and her legs had become rigid and paralysed. She was convinced that there was organic disease of her spine. After all she had been told this by the two doctors who had supported the application for her admission to the Home for Incurables, and also that in her disease there might be temporary remission. No amount of argument could shake her belief. Now it was not difficult in the light of what we knew, to understand what had happened. The news we had brought her had placed the patient again in a situation that was too much for her. Unable to cope with it she had fallen back into invalidism as the only possible refuge. It is just this way of reacting to a difficult emotional situation that is characteristic of the hysteric. I then discussed the case with the excellent matron of the Streatham Home, and through her obtained the consent of the Governors to the patient returning there and staying there indefinitely as a voluntary worker, being given sewing to do, and employed on errands of shopping. We told the patient this and again began our task of explanation and persuasion, now with success. At the end of three weeks we had her walking normally, and the case seems to have come to a satisfactory conclusion. It was arranged that on a certain date she should return to the home. The day after the receipt of this news she again relapsed. She woke with a pain in the back, found her legs still and weak, and reverted to her old belief that we had still overlooked some lesion in her spine. Now it was a little difficult to understand the cause of this relapse, but on consideration there did appear to be a possible motive for it. One of the difficulties encountered by the hysteric is that of a graceful recovery. She is apt to fear, and not without
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reason, that others seeing her disability cured without any drastic treatment, will imagine she has been malingering. The atmosphere of a home for incurables is perhaps especially likely to foster such uncharitable gossip. It was at this juncture that the matron of the home proposed a plan which enabled us to put a satisfactory end to our treatment. She arranged that on the day of the patient’s return to the home a special thanksgiving service should be held in the chapel for her recovery. This she judged would be effective in stifling unkind criticism. The arrangement was made that this plan should be carried out when the patient was well enough to return, and the matron told her of this when next she visited her at Guy’s. We then began again our treatment by means of suggestion and persuasion, this time with permanent success. This woman led an active, useful and happy existence at the Streatham Home for the rest of her life and died not long ago at the age of 80. To return for a moment to the M.R.C. definition of hysteria you will note that it states that the motivation is ‘never fully conscious’. The implication is that it is sometimes partly conscious. I believe, without proof, that this is generally so, and I suspect that in the compensation cases we are often faced with pure malingering. I suspect also that all so-called hysterical fugues are examples of malingering. Forty years ago a young man was brought to this hospital as an out-patient to B room, where I was working, with loss of memory for a period of a week. I had a heavy load of patients and it was a hot afternoon. I did not want to admit him and could not face the prospect of a prolonged psychotherapeutic session. I said to him ‘I am quite sure you can remember if you try: here are paper and pencil. Write me out your story, and I will do what I can to help you.’ With that I put him into the side room, closed the door and went on with my work. At the end of my session I had forgotten about him, but just as I was about to leave there was a tap on the door of the side room and he emerged with two sheets of close written foolscap. His story was this. He worked in a shop in Birmingham, had recently married, and took £10 from the till to cover the expenses of his honeymoon. He had, as he said, ‘borrowed’ it. On his return home he found that a previous misdemeanour had been discovered, and that he had been sacked. So there he was with no prospect of repaying the £10 before his theft would be discovered. He concluded that the only way out was suicide and that the right way would be to jump off the cliffs at Lands End. So he made his way down to Lands End but there was no suitable cliff. It was dark and cold. He went to the nearest police station and declared that he had lost his
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memory and knew neither his name nor address. He was then transferred to hospital at Penzance and subsequently referred to Queen Square. Since then I must have seen half a dozen cases of so-called hysterical fugue in private practice and have adopted the following plan. I have said to the patient ‘I know from experience that your pretended loss of memory is the result of some intolerable emotional situation. If you will tell me the whole story I promise absolutely to respect your confidence, will give you all the help I can and will say to your doctor and relatives that I have cured you by hypnotism.’ This approach has never failed, and I have been told some dramatic stories. I had little experience of hysteria in World War II, a notable exception being an hysterical paralysis of an upper limb in a naval officer who subsequently became an Admiral. You never know where hysteria may be lurking. The long case history of the female patient in this lecture was also published by Sir Charles as part of an article entitled “Two cases of hysterical paraplegia”. Guy’s Hospital Gazette (1928), 42, 323–328.
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Appendix D. Epidemics of the Middle Ages
J. F. C. Hecker The spread of attacks of psychological illness to groups of people is classed as a hysterical phenomenon. This is reasonable since the affected persons develop a disability or disturbance which is not based on physical illness, follows the pattern of the ideas which they possess as to the nature of the ailment, is induced by implicit or explicit suggestion, and is relieved by psychological management. The classic author in this field is Hecker (1844), who provides a most learned and detailed account of medieval and subsequent epidemics of this type (as well as equally scholarly and fundamental studies of the black death and the sweating sickness). Rather than summarise Hecker’s writings at length, it seems preferable to present some of his own work in moderate extent in this Appendix. The whole topic of outbreaks of hysterical illness is, however, considered in Chapter 16. In Hecker’s view the hysterical epidemics “afford a deep insight into the workings of the human mind in a state of society”. Occasional outbreaks are known at least as early as 1237, when more than 100 children at Erfurt were said to have been suddenly seized with a disease in which they proceeded dancing and jumping along the road to Amstadt, where on arrival they fell down exhausted. The first widespread epidemic, which Hecker describes as St John’s dance, was perhaps called this because of the enormous leaps by which it was characterised. Another reason given is that John the Baptist was possibly seen as the protector of those affected because he himself suffered death after Salome’s dance. 414
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But Hecker also thinks that the more probable reason is that St John’s Day replaced an ancient German festival on which the Nodfyr was kindled. The belief persisted, even into Hecker’s time, that people and animals who leap through flames or their smoke on that day were protected for a whole year from fevers and other diseases, as if by a kind of baptism of fire. Another saint after whom dancing attacks were named was Vitus, a martyr under Diocletian who was much revered as a powerful intercessor for all kinds of distress, and a 14th- or early 15th-century legend attributed to him a prayer to God that he might protect from the dancing mania all those who would solemnise the day of his commemoration and fast upon its eve. St John’s dance appeared in Germany soon after the black death, and Hecker describes it as follows: “So early as the year 1374, assemblages of men and women were seen at Aix-la-Chapelle who had come out of Germany, and who, united by one common delusion, exhibited to the public both in the streets and in the churches the following strange spectacle. They formed circles hand in hand, and appearing to have lost all control over their senses, continued dancing, regardless of the bystanders, for hours together, in wild delirium, until at length they fell to the ground in a state of exhaustion. They then complained of extreme oppression, and groaned as if in the agonies of death, until they were swathed in cloths bound tightly round their waists, upon which they again recovered, and remained free from complaint until the next attack. This practice of swathing was resorted to on account of the tympany which followed these spasmodic ravings, but the by-standers frequently relieved patients in a less artificial manner, by thumping and trampling upon the parts affected. While dancing they neither saw nor heard, being insensible to external impressions through the senses, but were haunted by visions, their fancies conjuring up spirits whose names they shrieked out; and some of them afterwards asserted that they felt as if they had been immersed in a stream of blood, which obliged them to leap so high. Others, during the paroxysm, saw the heavens open and the Saviour enthroned with the Virgin Mary, according as the religious notions of the age were strangely and variously reflected in their imaginations. Where the disease was completely developed, the attack commenced with epileptic convulsions. Those affected fell to the ground senseless, panting and labouring for breath. They foamed at the mouth, and suddenly springing up began their dance amidst strange contortions. Yet the malady doubtless made its appearance very variously, and was modified by temporary or local circumstances, whereof non-medical contemporaries but imperfectly noted the essential particulars, accustomed as
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Appendices they were to confound their observation of natural events with their notions of the world of spirits. It was but a few months ere this demoniacal disease had spread from Aix-la-Chapelle, where it appeared in July, over the neighbouring Netherlands. In Liege, Utrecht, Tongres, and many other towns of Belgium, the dancers appeared with garlands in their hair, and their waists girt with cloths, that they might, as soon as the paroxysm was over, receive immediate relief on the attack of the tympany. This bandage was, by the insertion of a stick, easily twisted tight: many, however, obtained more relief from kicks and blows, which they found numbers of persons ready to administer; for, wherever the dancers appeared, the people assembled in crowds to gratify their curiosity with the frightful spectacle. At length the increasing number of the affected excited no less than the attention that was paid to them. In towns and villages they took possession of the religious houses, processions were everywhere instituted on their account, and masses were said and hymns were sung, while the disease itself, of the demoniacal origin of which no one entertained the least doubt, excited everywhere astonishment and horror. In Liege the priests had recourse to exorcisms, and endeavoured, by every means in their power, to allay an evil which threatened so much danger to themselves; for the possessed assembling in multitudes, frequently poured forth imprecations against them, and menaced their destruction. They intimidated the people also to such a degree that there was an express ordinance issued that no one should make any but square-toed shoes, because these fanatics had manifested a morbid dislike to the pointed shoes which had come into fashion immediately after the Great Mortality in 1350. They were still more irritated at the sight of red colours, the influence of which on the disordered nerves might lead us to imagine an extraordinary accordance between this spasmodic malady and the condition of infuriated animals; but in the St. John’s dancers this excitement was probably connected with apparitions consequent upon their convulsions. There were likewise some of them who were unable to endure the sight of persons weeping. The clergy seemed to become daily more and more confirmed in their belief that those who were affected were a kind of sectarians, and on this account they hastened their exorcisms as much as possible, in order that the evil might not spread amongst the higher classes, for hitherto scarcely any but the poor had been attacked, and the few people of respectability among the laity and clergy who were to be found among them, were persons whose natural frivolity was unable to withstand the excitement of novelty, even though it proceeded from a demoniacal influence. Some of the affected had indeed themselves declared, when under the influence of priestly forms of exorcism, that if the demons had been allowed only a few weeks more time, they would have entered the bodies of the nobility and princes, and through these have destroyed
Appendices the clergy. Assertions of this sort, which those possessed uttered whilst in a state which may be compared with that of magnetic sleep, obtained general belief, and passed from mouth to mouth with wonderful additions. The priesthood were, on this account, so much the more zealous in their endeavours to anticipate every dangerous excitement of the people, as if the existing order of things could have been seriously threatened by such incoherent ravings. Their exertions were effectual, for exorcism was a powerful remedy in the fourteenth century; or it might perhaps be that this wild infatuation terminated in consequence of the exhaustion which naturally ensued from it; at all events, in the course of ten or eleven months the St. John’s dancers were no longer to be found in any of the cities of Belgium. The evil, however, was too deeply rooted to give way altogether to such feeble attacks. A few months after this dancing malady had made its appearance at Aix-la-Chapelle, it broke out at Cologne, where the number of those possessed amounted to more than five hundred, and about the same time at Metz, the streets of which place are said to have been filled with eleven hundred dancers. Peasants left their ploughs, mechanics their workshops, house wives their domestic duties, to join the wild revels, and this rich commercial city became the scene of the most ruinous disorder. Secret desires were excited, and but too often found opportunities for wild enjoyment; and numerous beggars, stimulated by vice and misery, availed themselves of this new complaint to gain a temporary livelihood. Girls and boys quitted their parents, and servants their masters, to amuse themselves at the dances of those possessed, and greedily imbibed the poison of mental infection. Above a hundred unmarried women were seen raving about in consecrated and unconsecrated places, and the consequences were soon perceived. Gangs of idle vagabonds, who understood how to imitate to the life the gestures and convulsions of those really affected, roved from place to place seeking maintenance and adventures, and thus, wherever they went, spreading this disgusting spasmodic disease like a plague; for in maladies of this kind the susceptible are infected as easily by the appearance as by the reality. At last it was found necessary to drive away these mischievous guests, who were equally inaccessible to the exorcisms of the priests and the remedies of the physicians. It was not, however, until after four months that the Rhenish cities were able to suppress these impostures, which had so alarmingly increased the original evil. In the meantime, when once called into existence, the plague crept on, and found abundant food in the tone of thought which prevailed in the fourteenth and fifteenth centuries, and even, though in a minor degree, throughout the sixteenth and seventeenth, causing a permanent disorder of the mind, and exhibiting, in those cities to whose inhabitants it was a novelty, scenes as strange as they were detestable.”
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He describes St Vitus’ dance in the following way: “Strasburg was visited by the ‘Dancing Plague’ in the year 1418, and the same infatuation existed among the people there, as in the towns of Belgium and the Lower Rhine. Many who were seized at the sight of those affected, excited attention at first by their confused and absurd behaviour, and then by their constantly following the swarms of dancers. These were seen day and night passing through the streets, accompanied by musicians playing on bagpipes, and by innumerable spectators attracted by curiosity, to which were added anxious parents and relations, who came to look after those among the misguided multitude who belonged to their respective families. Imposture and profligacy played their part in this city also, but the morbid delusion itself seems to have predominated. On this account religion could only bring provisional aid, and therefore the town-council benevolently took an interest in the afflicted. They divided them into separate parties, to each of which they appointed responsible superintendents to protect them from harm, and perhaps also to restrain their turbulence. They were thus conducted on foot and in carriages to the chapels of St. Vitus, near Zabern and Rotestein, where priests were in attendance to work upon their misguided minds by masses and other religious ceremonies. After divine worship was completed, they were led in solemn procession to the altar, where they made some small offering of alms, and where it is probable that many were, through the influence of devotion and the sanctity of the place, cured of this lamentable aberration. It is worthy of observation, at all events, that the Dancing Mania did not recommence at the altars of the saint, and that from him alone assistance was implored, and through his miraculous interposition a cure was expected, which was beyond the reach of human skill. The personal history of St. Vitus is by no means unimportant in this matter. He was a Sicilian youth, who, together with Modestus and Crescentia, suffered martyrdom at the time of the persecution of the Christians, under Diocletian, in the year 303. The legends respecting him are obscure, and he would certainly have been passed over without notice among the innumerable apocryphal martyrs of the first centuries, had not the transfer of his body to St. Denys, and thence, in the year 836, to Corvey, raised him to a higher rank. From this time forth, it may be supposed that many miracles were manifested at his new sepulchre, which were of essential service in confirming the Roman faith among the Germans, and St. Vitus was soon ranked among the fourteen saintly helpers (Nothhelfer or Apotheker). His altars were multiplied, and the people had recourse to them in all kinds of distresses, and revered him as a powerful intercessor. As the worship of these saints was however at that time stripped of all historical connexions, which were purposely obliterated by the priesthood, a legend was invented at the beginning of the
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fifteenth century, or perhaps even so early as the fourteenth, that St. Vitus had, just before he bent his neck to the sword, prayed to God that he might protect from the Dancing Mania all those who should solemnize the day of his commemoration, and fast upon its eve, and that thereupon a voice from heaven was heard, saying, `Vitus, thy prayer is accepted.’ Thus St. Vitus became the patron saint of those afflicted with the dancing plague, as St. Martin of Tours, was at one time the succourer of persons in small-pox; St. Antonius of those suffering under the `hellish fire’, and as St. Margaret was the Juno Lucina of puerperal women.”
St John’s dance appeared at a time of widespread disaster. The effects of the black death had not yet subsided. The Rhine and the Maine had both overflowed, security of property did not exist, and the population in the affected areas were wretched and oppressed. Hecker writes accordingly: “If we take into consideration, that among their numerous bands many wandered about, whose consciences were tormented with the recollection of the crimes which they had committed during the prevalence of the black plague, we shall comprehend how their despair sought relief in the intoxication of an artificial delirium. There is hence good ground for supposing that the frantic celebration of the festival of St. John, A.D. 1374, only served to bring to a crisis, a malady which had been long impending; and if we would further inquire how a hitherto harmless usage, which, like many others, had but served to keep up superstition, could degenerate into so serious a disease, we must take into account the unusual excitement of men’s minds, and the consequences of wretchedness and want. The bowels, which in many were debilitated by hunger and bad food, were precisely the parts which in most cases were attacked with excruciating pain, and the tympanitic state of the intestines, points out to the intelligent physician, an origin of the disorder which is well worth consideration.”
Comparable outbreaks in Italy were described as tarantism, being attributed to the bite of the tarantula spider, which was alleged to continue its effects indefinitely: “The patients in their sudden attacks behaved like maniacs, sprang up, throwing their arms about with wild movements, and, if perchance a sword was at hand, they wounded themselves and others, so that it became necessary carefully to secure them. They imagined that they heard voices, and various kinds of sounds, and if, during this state of illusion, the tones of a favourite instrument happened to catch their ear, they com-
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Appendices menced a spasmodic dance, or ran with the utmost energy which they could muster until they were totally exhausted. These dangerous maniacs, who, it would seem, appeared in considerable numbers, were looked upon as a legion of devils....”
At the close of the 15th century, tarantism spread beyond the boundaries of Apulia, where it had originated. At this time: “nothing short of death itself was expected from the wound which these insects inflicted, and if those who were bitten escaped with their lives, they were said to be seen pining away in a desponding state of lassitude. Many became weak-sighted or hard of hearing, some lost the power of speech, and all were insensible to ordinary causes of excitement. Nothing but the flute or the cithern afforded them relief. At the sound of these instruments they awoke as it were by enchantment, opened their eyes, and moving slowly at first, according to the measure of the music, were, as the time quickened, gradually hurried on to the most passionate dance. It was generally observable that country people, who were rude, and ignorant of music, evinced on these occasions an unusual degree of grace, as if they had been well practised in elegant movements of the body; for it is a peculiarity in nervous disorders of this kind, that the organs of motion are in an altered condition, and are completely under the control of the overstrained spirits. Cities and villages alike resounded throughout the summer season with the notes of fifes, clarinets, and Turkish drums; and patients were everywhere to be met with who looked to dancing as their only remedy. Alexander ab Alexandro, who gives this account, saw a young man in a remote village who was seized with a violent attack of Tarantism. He listened with eagerness and a fixed stare to the sound of a drum, and his graceful movements gradually became more and more violent, until his dancing was converted into a succession of frantic leaps, which required the utmost exertion of his whole strength. In the midst of this overstrained exertion of mind and body the music suddenly ceased, and he immediately fell powerless to the ground, where he lay senseless and motionless until its magical effect again aroused him to a renewal of his impassioned performances. At the period of which we are treating there was a general conviction, that by music and dancing the poison of the Tarantula was distributed over the whole body, and expelled through the skin, but that if there remained the slightest vestige of it in the vessels, this became a permanent germ of the disorder, so that the dancing fits might again and again be excited ad infinitum by music.”
Tarantella music owes at least its name to these events and beliefs.
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Among the sufferers many abhorred specific colours or preferred others. Red colours, which were detested by the St Vitus dancers, were preferred by the Italians: “so that a patient was seldom seen who did not carry a red handkerchief for his gratification, or greedily feast his eyes on any articles of red clothing worn by the by-standers. Some preferred yellow, others black colours, of which an explanation was sought, according to the prevailing notions of the times, in the difference of temperaments. At the sight of colours which they disliked, patients flew into the most violent rage, and, like the St. Vitus’s dancers when they saw red objects, could scarcely be restrained from tearing the clothes of those spectators who raised in them such disagreeable sensations.”
This remarkable phenomenon lasted until the 18th century. A comparable dancing mania is described in Ethiopia as affecting individuals. Attacks of convulsions or spasms in smaller groups of people were noted in Lancashire in the 18th century, Cornwall in the 18th and 19th centuries, and the Shetlands, the United States in Tennessee and Kentucky, and Berlin in the 19th century. Paris and other parts of France experienced them in the 18th century. The 18th-century Cornishmen were Methodists known as jumpers, the French groups were known as convulsionnaires, and some of these were barkers as well. The common social features which are evident in the later groups include belonging to fanatical or extreme sectarian groups and usually in poor economic circumstances. Pentecostalists today in the United States and the West Indies perhaps show some of these features. Sargant (1957) has reviewed the common phenomena of many of these groups. Throughout these epidemics men were affected as much as or even more than women. Sexual excesses were not absent. Hecker was concerned to explain these disorders. He noted, interestingly, that physicians were rarely called upon to treat those affected, but priests often were. He saw them as a consequence of extreme social disturbance, but also liked to think that they were related to organic disease. He believed genuine cases spread by imitation and sympathetic mimicry and that imposture also played a part. Later writers (e.g. McEvedy) have sought a psychological explanation and have also attempted to differentiate the epidemic pattern of hysteria from that of infectious illness. This is discussed in Chapter 16.
422
References
References
ABBEY, S. E. & GARFINKEL, P. E. (1991) Neurasthenia and chronic fatigue syndrome: the role of culture in the making of a diagnosis. American Journal of Psychiatry, 148, 1638–1646. —— & —— (1992) Taking chronic fatigue seriously. Dr. Abbey and Dr. Garfinkel reply. American Journal of Psychiatry, 149, 756–757. A BELES , M. & S CHILDER , P. (1935) Psychogenic loss of personal identity. Archives of Neurological Psychiatry, 34, 587–604. A BRAHAM , K. (1908) The psycho-sexual differences between hysteria and dementia praecox. In Selected Papers of Karl Abraham, 1927. London: Hogarth Press. —— (1921a) Contribution to a discussion on tic. In Selected Papers of Karl Abraham, 1927. London: Hogarth Press. —— (1921b) Psycho-analysis and the war neuroses. In Clinical Papers and Essays on PsychoAnalysis. London: Hogarth Press (1955). —— (1921c) Contributions to the theory of the anal character. In Selected Papers of Karl Abraham, 1927. pp. 370–392. London: Hogarth Press. —— (1924a) The influence of oral eroticism on character formation. In Selected Papers of Karl Abraham, 1927. pp. 393–406. London: Hogarth Press. —— (1924b) A short study of the development of the libido, viewed in the light of mental disorders. In Selected Papers of Karl Abraham, 1927. pp. 418–501. London: Hogarth Press. A BRAHAMS , H. S. (1917) Soldier’s heart. Lancet, i, 442–445. A BSE , D. W. (1966) Hysteria and Related Mental Disorders. Bristol: John Wright. A CHESON , E. D. (1959) The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease and epidemic neuromyasthenia. American Journal of Medicine, 26, 569–595. ACKERKNECHT, E. H. (1948) Medicine and disease among Eskimos. Ciba Symposia, 10, 916–921. A DAMS , F. (1844) The Seven Books of Paulus Aegineta. London: The Sydenham Society. ––– (1856) On hysterical suffocation. In On the Causes and Symptoms of Acute Diseases, Book 2 of The Extant Works of Aretaeus the Cappadocian, pp. 285–287. London: New Sydenham Society. A DLER , R. H., Z LOT , S., Hü RNY , C. & M INDER , C. (1989) Engel’s “psychogenic pain and the pain-prone patient”: a retrospective, controlled clinical study. Psychosomatic Medicine, 51, 87–101. A DOMAKOH , C. C. (1973) The pattern of epidemic hysteria in a girls’ school in Ghana. Ghana Medical Journal, 13, 407–411. A DRIAN , E. D. & Y EALLAND , L. R. (1917) The treatment of some common war neuroses. Lancet, i, 867–72.
422
References
423
A DUAN , R. P., F AUCI , A. S., D ALE , D. C., et al (1979) Factitious fever and self-induced infection; a report of 32 cases and review of the literature. Annals of Internal Medicine, 90, 230–242. A GGER , I. & J ENSEN , S. B. (1993) The psychosexual trauma of torture. In International Handbook of Traumatic Stress Syndromes (eds J. P. Wilson & B. Raphael), pp. 685–702. New York: Plenum Press. A HRENFELDT , R. H. (1958) Psychiatry in the British Army in the Second World War. London: Routledge & Kegan Paul. A LAM , C. N. & M ERSKEY , H. (1992) The development of the hysterical personality. History of Psychiatry, 3, 135–165. A LBRECHT , R. M., O LIVER , V. L. & P OSKANZER , D. C. (1964) Epidemic neuromyasthenia: outbreak in a convent in New York State. Journal of the American Medical Association, 187, 904–967. A LDRIDGE-M ORRIS , R. (1989) Multiple Personality: An Exercise in Deception. London: Lawrence Erlbaum Assoc. A LEXANDER , F. (1950) Psychosomatic Medicine. New York: Norton and Co. —— (1952) Development of the fundamental concepts of psychoanalysis. In Dynamic Psychiatry (eds F. Alexander & H. Ross). Chicago: University of Chicago Press. —— (1963) Fundamentals of Psychoanalysis (3rd edn). New York: Norton and Co. —— & S ZASZ , T. (1952) Psychosomatic approach in medicine. In Dynamic Psychiatry (eds F. Alexander & H. Ross). Chicago: University of Chicago Press. A LLEN , M. J., B ARNS , M. R. & B ODIWALA , G. G. (1985) The effect of seat belt legislation on injuries sustained by car occupants. Injury, 16, 471–476. A LLISON , R. & S CHWARZ , T. (1980) Minds in Many Pieces. New York: Rawson Wade. A LLODI , F. (1982) Acute paranoid reaction (bouffée délirante) in Canada. Canadian Journal of Psychiatry, 27, 366–373. A LTHAUS , J. (1866) On Epilepsy, Hysteria and Ataxy. London: John Churchill & Sons. A LTROCCHI , J., (1992) “We don’t have that problem here”: MPD in New Zealand. Dissociation, 5, 101–110. A MEGAVIE , L., M ARZOUK , O., M ULLEN , J., et al (1986) Münchausen’s syndrome by proxy: a warning for health professionals. British Medical Journal, 293, 855–856. A MERICAN P SYCHIATRIC A SSOCIATION (1968) Diagnostic and Statistical Manual of Mental Disorders (2nd edn) (DSM–II). Washington, DC: APA. —— (1980) Diagnostic and Statistical Manual of Mental Disorders (3rd edn) (DSM–III). Washington, DC: APA. —— (1987) Diagnostic and Statistical Manual of Mental Disorders (3rd edn, revised) (DSM– III–R). Washington, DC: APA. ——, T ASK F ORCE ON DSM–IV (1993) DSM–IV Draft Criteria. Washington, DC: APA. —— (1994) Diagnostic and Statistical Manual of Mental Disorders (4th edn) (DSM–IV). Washington, DC: American Psychiatric Association. A MMANN , P. (1670) Medicina Critica. Erfurt: Hertz Ohler. A NANTH , J., KAPLAN , H. S. & L IN , K-M. (1984) Self inflicted enucleation of an eye: two case reports. Canadian Journal of Psychiatry, 29, 145–146. A NDERSON , E. W. & M ALLINSON , W. P. (1941) Psychogenic episodes in the course of major psychoses. Journal of Mental Science, 87, 383–391. ——, T RETHOWAN , W. H. & KENNA , J. C. (1959) An experimental investigation of simulation and pseudodementia. Acta Psychiatrica et Neurologica Scandinavica, 134 (suppl. 132). A NSTIE , F. E. (1871) Neuralgia and the Diseases that Resemble It. London: Macmillan. A PLEY , J. (1975) The Child with Abdominal Pains. Oxford: Blackwell Scientific. A RKONAC , O. & G UZE , S. (1963) A family study of hysteria. New England Journal of Medicine, 268, 239–242. A RMSTRONG , H. & P ATTERSON , P. (1975) Seizures in Canadian Indian children. Canadian Psychiatric Association Journal, 20, 247–255.
424
References
A SHER , R. (1951) Munchausen’s syndrome. Lancet, i, 339–341. A TKINSON , J. H., S LATER , M. A. & P ATTERSON , T. L. (1991) Prevalence, onset, and risk of psychiatric disorders in men with chronic low back pain: a controlled study. Pain, 45, 111–121. A UFREITER , J. (1969) Psychoanalytic nosology and hysteria. Canadian Psychiatric Association Journal, 14, 569–571. A XENFELD (1864) Des Névroses. Paris: Germer Baillière Libraire. A ZAM , E. (1860) Note sur le sommeil nerveux ou hypnotisme. Archives Générales de Médicine, 15, 1–24. —— (1876) Amnésie périodique, ou doublement de la vie. Révue Scientifique, 2me Serie, 26 May, 10, 481–489. —— (1887) Hypnotisme, Double Conscience, et Altérations de la Personnalité. Paris: Baillière. —— (1892) Double consciousness. In A Dictionary of Psychological Medicine (ed. D. Hack Tuke), Vol. I, pp. 401–406. London: Churchill. B ABINGTON , A. (1983) For the Sake of Example: Capital Courts Martial 1914–1920. New York: St. Martin’s Press. B ABINSKI , J. (1901) Definition de l’hystérie. Société Neurologique Paris, 7 Novembre. —— & F ROMENT , J. (1918a) Hysteria or Pithiatism (ed. E. Farquhar Buzzard). London: University of London Press. —— & —— (1918b) Hysteria or Pithiatisme and Reflex Nervous Disorders in the Neurology of War. London: University of London Press. B AGAN , M. (1962) Munchausen syndrome: report of a case and a review of the literature. Boston Medical Quarterly, 13, 113–119. B AILEY , P. (1906) Diseases of the Nervous System Resulting from Accident and Injury. New York: D. Appleton & Co. B AILLARGER , M. (1890) Recherches sur les maladies mentales. Paris: Masson. B AILLY , J. S. (1784) Rapport des commissaires chargés par le Roi de l’examen du magnétisme animale. Paris: Imprimerie Royale. B AKER , B. & M ERSKEY , H. (1982) Parental representations of hypochondriacal patients. British Journal of Psychiatry, 141, 233–238. —— & —— (1983) Classification and associations of hypochondriasis in patients from a psychiatric hospital. Canadian Journal of Psychiatry, 28, 629–634. B AKER , S. L. (1975) Military psychiatry. In Comprehensive Textbook of Psychiatry, vol. II (eds A. M. Freedman, H. I. Kaplan & B. J. Sadock). Baltimore: Williams & Wilkins. B ALLINGER , B. R. (1971) Minor self injury. British Journal of Psychiatry, 118, 535–538. B ANGASH , I. H., W ORLEY , G. & K AND t, R. (1988) Hysterical conversion reactions mimicking neurological disease. American Journal of Disease in Children, 142, 1203–1206. B ANKS , M. H., B ERESFORD , S. H. Z., M ORRELL , D. C., et al (1975) Factors influencing demand for primary medical care in women aged 20–40 years; a preliminary report. International Journal of Epidemiology, 4, 189–255. BARBER, T. X. (1963) The effects of ‘hypnosis’ on pain. Psychosomatic Medicine, 25, 303–333. —— (1969) Hypnosis: A Scientific Approach. New York: Van Nostrand. B ARDHAN , P. N. (1965a) The fathering syndrome. Indian Armed Forces Medical Journal, 20, 200–208. —— (1965b) The couvade syndrome. British Journal of Psychiatry, 111, 908–909. B ARKER , J. C. (1962) The syndrome of hospital addiction (Münchausen’s syndrome). A report on the investigation of seven cases. Journal of Mental Science, 108, 167–182. —— (1966) Hospital and operation addiction ( Munchausen’s syndrome). British Journal of Clinical Practice, 20, 63–68. B ARRIS , R. W. & S CHUMAN , H. R. (1953) Bilateral anterior cingulate gyrus lesions. Syndrome of the anterior cingulate gyri. Neurology, 3, 44–52. B ARSKY , A. J. & K LERMAN , G. L. (1983) Overview: hypochondriasis, bodily complaints, and somatic styles. American Journal of Psychiatry, 140, 273–283.
References
425
—— & WYSHAK , G. (1990) Hypochondriasis and somatosensory amplification. British Journal of Psychiatry, 157, 404–409. ——, ——, K LERMAN , G. L. (1991) The relationship between hypochondriasis and medical illness. Archives of Internal Medicine, 151, 84–88. ——, C OEYTAUX , R. R., S ARNIE , M. K., et al (1993) Hypochondriacal patients’ beliefs about good health. American Journal of Psychiatry, 150,1085–1089. ——, B ARNETT , M. C. & C LEARY (1994) Hypochondriasis and panic disorder boundary and overlap. Archives of General Psychiatry, 51, 918–925. B ARTHOLOMEW , R. E. (1990) Ethnocentricity and the social construction of ‘mass hysteria’. Culture, Medicine and Psychiatry, 14, 455–494. —— (1994) Tarantism, dancing mania and demonopathy: the anthro-political aspects of ‘mass psychogenic illness’. Psychological Medicine, 24, 281–306. B ASS , C. M. (1990) Functional cardiorespiratory syndromes. In Somatization: Physical Symptoms and Psychological Illness (ed. C. M. Bass), pp. 171–206. London: Blackwell Scientific Publications. —— & G ARDNER , W. (1985) Respiratory and psychiatric abnormalities in chronic symptomtaic hyperventilation. British Medical Journal, 290, 1387–1390. B ASS , E. & D AVIS , L. (1988) The Courage to Heal. New York: Harper & Row. B AUDOUIN , C. (1920) Suggestion and Auto-Suggestion. London: George Allen & Unwin. B AUER , M., P RIEBE , S., H ÄRING , B., et al (1993) Longterm mental sequelae of political imprisonment in East Germany. Journal of Nervous and Mental Disease, 181, 257–262. B EHRMAN , J. (1969) The visual evoked response in hysterical amblyopia. British Journal of Ophthalmology, 53, 839–845. B EHRMAN , S. (1973) Mute of malady. British Medical Journal, i, 755–756. B ELENKY , C. G. L., N OY , S., S OLOMON , Z., et al, (1985) Battle Stress: The Israeli Experience. Military Review, 65, 28–37. B ELL , J. & B ELL , C. (1826) The Anatomy and Physiology of the Human Body (6th edn). London: Longman Rees & Co. B ENAIM , S., H ORDER , J. & ANDERSON , J. (1973) Hysterical epidemic in a classroom. Psychological Medicine, 30, 366–373. B ENDE , B. C., P HILPOTT , R. M., S ALTISSI, S., et al (1994) Persistent post-traumatic stress disorder. British Medical Journal, 309, 526–528. B ENDER , L. & Y ARRELL , Z. (1938) Psychoses among followers of Father Divine. Journal of Nervous and Mental Disorders, 87, 418–449. B ERG , M. (1988) Satanic crime increasing, police, therapists alarmed. Kansas City Times, 26 March. B ERNEY , T. P. (1973) A review of simulated illness. South African Medical Journal, 47, 1429– 1434. B ERNFELD , W. (1929) Eine Beschwörung der Gebarmutter aus dem Frühen mittelalter. Kyklos, 2, 272–274. B ERNSTEIN , E. M. & P UTNAM , F. W. (1986) Development, reliability and validity of a dissociation scale. Journal of Nervous and Mental Disease, 174, 727–735. B ERRINGTON , W. P., L IDDELL , D. W. & F OULDS , G. A. (1956) A re-evaluation of the fugue. Journal of Mental Science, 102, 280–286. B ERRIOS , G. E. (1993) European views on personality disorders: A conceptual history. Comprehensive Psychiatry, 34, 14–30. —— & M ORLEY , S. J. (1984) Koro-like symptom in non-Chinese subject. British Journal of Psychiatry, 145, 331–334. B ERS, N. & C ONRAD , K. (1954) Die chronische taktile Halluzinose. Fortschritte Der NeurologiePsychiatrie, 22, 254–270. B ETTS , T. A., MERSKEY , H. & P OND , D. A. (1976) Psychiatry. In A Textbook of Epilepsy (eds J. L. Laidlaw & A. Richens). London: Churchill Livingstone.
426
References
B IANCHI , G. (1971) Origins of disease phobia. Australian and New Zealand Journal of Psychiatry, 5, 241–257. B IBB , R. C. & G UZE , S. (1972) Hysteria (Briquet’s syndrome) in a psychiatric hospital: the significance of secondary depression. American Journal of Psychiatry, 129, 224–228. BIGOS, S. J., BATTIE, M. C., SPENGLER, D. M., et al (1991) A prospective study of work perceptions and psychosocial factors affecting the report of back injury. Spine, 166, 1–6. B INDER , L. M. & P ANKRATZ , L. (1987) Neuropsychological evidence of a factitious memory complaint. Journal of Clinical and Experimental Neuropsychology, 9, 167–171. B INET , A. (1891) Alterations of Personality (ed. D. N. Robinson, 1977). Georgetown: Georgetown University Publications of America. B IRD , H. (1989) Overuse injuries in musicians. British Medical Journal, 298, 1129–1130. B LACK , A. A. (1966) Factors predisposing to a placebo response in new out-patients with anxiety state. British Journal of Psychiatry, 112, 557–567. B LACK , D. (1981) The extended Münchausen’s syndrome: a family case. British Journal of Psychiatry, 138, 466–469. B LACK , S. (1963a) Inhibition of immediate-type hypersensitivity response by direct suggestion under hypnosis. British Medical Journal, i, 925–929. —— (1963b) Shift in dose–response curve of Prausnitz–Kustner reaction by direct suggestion under hypnosis. British Medical Journal, i, 990–992. ——, H UMPHREY , J. H. & N IVEN , J. S. F. (1963) Inhibition of Mantoux reaction by direct suggestion under hypnosis. British Medical Journal, i, 1649–1652. —— & F RIEDMAN , M. (1965) Adrenal function and the inhibition of allergic responses under hypnosis. British Medical Journal, i, 562–567. B LACKER , K. H. & T UPIN , J. P. (1991) Hysteria and hysterical structures. In Hysterical Personality and the Histrionic Personality Disorder (ed. M. J. Horowitz), pp. 15–66. Northvale, NJ: Jason Aronson. B LACKMORE , R. (1725) A Treatise of the Spleen and Vapours: or, Hypochondriacal and Hysterical Affections. London: J. Pemberton. BLEULER, E. P. (1950) The Group of Schizophrenias. New York: International Universities Press. B LINDER , M. G. (1966) The hysterical personality. Journal of Neurology, Neurosurgery and Psychiatry, 29, 227–235. B LISS , E. L. (1984) A symptom profile of patients with multiple personalities, including MMPI results. Journal of Nervous Mental Disease, 172, 197–202. —— & J EPPSEN , E. A. (1985) Prevalence of multiple personality disorder among inpatients and out-patients. American Journal of Psychiatry, 142, 250–251. B LOEM , B. R., L AGAAY , A. M., V AN B EEK , W., et al (1990) Prevalence of subjective dysphagia in community residents aged over 87. British Medical Journal, 300, 721–722. B LUMER , D. (1975) Psychiatric considerations in pain. In The Spine (2nd edn) (eds R. H. Rothman & F. A. Simeone). Eastbourne: W. B. Saunders Co. B OGREN , L. Y. (1984) The Couvade syndrome: background variables. Acta Psychiatrica Scandinavica, 70, 316–320. B OHMAN , M., C LONINGER , C. R., V ON K NORRING , L., et al (1984) An adoption study of somatoform disorders. III. Cross-fostering analysis and relationship to alcoholism and criminality. Archives of General Psychiatry, 41, 871–878. B ONNET , C. (1760) Essai analytique sur les facultés de l’ame. Copenhagen and Geneva: Philibert. B OOR , M. (1982) The multiple personality epidemic. Additional cases and references regarding diagnosis, etiology, dynamics, and treatment. Journal of Nervous and Mental Disease, 170, 302–304. B OSWELL , J. (1777–83) On hypochondria. In Boswell’s Column (ed. M. Bailey, 1951). London: William Kimber & Co. B OURRU , H. & B OUROT , P. (1885) De la multiplicité des états de conscience. Révue Philosophique, 20, 411–416.
References
427
B OYD , W. (1947) A Textbook of Pathology (5th edn) London: Henry Kimpton. B OYLE , R. (1664) Some Considerations Touching the Usefulness of Experimental Natural Philosophy (2nd edn). Cit. Wright (1980). B OZZUTO , J. C. (1975) Cinematic neurosis following The Exorcist: report of four cases. Journal of Nervous and Mental Disease, 161, 43–48. B RACELAND , E. J. & G IFFIN , M. E. (1950) The mental changes associated with multiple sclerosis (an interim report). Proceedings of the Association for Research of Nervous and Mental Disorders, 28, 450–456. B RACHET , J. L. (1847a) Traité de l’Hystérie. Paris: J. B. Baillière. —— (1847b) Traité Complet de L’Hypochondrie. Paris: J. B. Baillière. B RADWELL , S. (1603) Mary Glover’s Late Woeful Case. MS Sloane, 831. London: British Library. Transcribed in MacDonald, M. (1991), pp. 4, 5. B RAID , J. (1843) Neurypnology. London: Churchill. B RESLAU , N., D AVIS , G. C., A NDRESKI , P., et al (1991) Traumatic events and postraumatic stress disorder in an urban population of young adults. Archives of General Psychiatry, 48, 216–222. —— & —— (1992) Posttraumatic stress disorder in an urban population of young adults: risk factors for chronicity. American Journal of Psychiatry, 671–675. B REUER , J. & F REUD , S. (1893–95) Studies on Hysteria. Harmondsworth: Penguin Books (1974). B RIDGES , K. & G OLDBERG , D. P. (1985) Somatic presentation of DSM–III psychiatric disorders in primary care. Journal of Psychosomatic Research, 29, 563–569. B RILL , A. A. (1913) Piblokto or hysteria among Peary’s Eskimos. Journal of Nervous and Mental Disease, 40, 514. B RIQUET , P. (1859) Traité clinique et thérapeutique de l’hystérie. Paris: J. B. Baillière et Fils. B RITISH M EDICAL J OURNAL (1957) Editorial. Benign myalgic encephalomyelitis. British Medical Journal, ii, 927–928. B RODIE , B. C. (1837) Lectures lllustrative of Certain Nervous Affections. London: Longman. B ROM , D., K LEBER , R. J. & H OFMAN , M. C. (1993) Victims of traffic accidents: incidents of prevention of post traumatic stress disorder. Journal of Clinical Psychology, 49, 131–139. BROWN, G. R. & ANDERSON, B. (1991) Psychiatric morbidity in adult inpatients with childhood histories of sexual and physical abuse. American Journal of Psychiatry, 148, 55–61. B ROWN , J. A. C. (1961) Freud and the Post-Freudians. Harmondsworth: Penguin Books. B ROWN , M. W. & W ILLIAMS , F. E. (1918) Neuropsychiatry and the War. New York: National Committee for Mental Hygiene. B ROWN , S. R., S CHWARTZ , J. M., S UMMERGRAD , P., et al (1986) Globus hystericus syndrome responsive to anti-depressants. American Journal of Psychiatry, 143, 917–918. B ROWNE , A. & F INKELHOR , D. (1986) Impact of child sexual abuse: A review of the research. Psychology Bulletin, 99, 66–77. B RUCH , H. (1973) Eating Disorders: Obesity, Anorexia Nervosa and the Person Within. New York: Basic Books. B UCHWALD, D. & K OMAROFF , A. (1991) Review of laboratory findings of patients with chronic fatigue syndrome. Review of Infectious Diseases, 13 (suppl. 1), 12–18. B UCKNILL , J. C. & T UKE , D. H. (1862) A Manual of Psychological Medicine (2nd edn). London: Churchill. B UINEWITSCH , K. (1939) Über das Simulieren von Krankheiten. Wiener Medizinische Wochenschrift, 89, 472–473. Cit. Flicker (1956). B URSTEN , B. (1965) On Munchausen’s syndrome. Archives of General Psychiatry, 13, 1–8. B URTON , R. (1651) The Anatomy of Melancholy (ed. H. Jackson, 1932). London: J. H. Dent Everyman’s Library. B URTON-B RADLEY , B. G. (1972) Human sacrifice for cargo. Medical Journal of Australia, ii, 668–670. —— (1973) The psychiatry of cargo cult. Medical Journal of Australia, 20, 388–392.
428
References
—— (1975) Stone Age Crisis. A Psychiatric Appraisal. Nashville: Vanderbilt University Press. C AIRNS , H., O LDFIELD , R. C., P ENNYBACKER , J. D., et al (1941) Akinetic mutism with an epidermoid cyst of the third ventricle. Brain, 64, 273–280. C ALMEIL , L. F. (1845) De la folie considérée sous le point de vue pathologique, philosophique, historique et juridique. Paris: Baillière. C AMPBELL , J. (1962) Facial paraesthesia accompanying facial pain. British Dental Journal, 112, 108–113. C AMPBELL , T. W. (1992) Therapeutic relationships and iatrogenic outcomes: The blame and change maneuver in psychotherapy. Psychotherapy, 29, 474–480. C AMUSET , L. (1882) Un cas de dédoublement de la personnalité. Annales MédicoPsychologiques, 7, 75–86. C ANINO , G. J., B IRD , H. R., S HROUT , P. E., et al (1987) The prevalence of specific psychiatric disorders in Puerto Rico. Archives of General Psychiatry, 44, 727–736. C ANTER , A. H. (1951) Journal of General Psychology, 44, 27. Cit. Pratt (1951). C ARADOC -D AVIES , G. (1988) Feigned alcohol abuse: a unique case report. British Journal of Psychiatry, 152, 418–420. C ARLSON , E. B. & P UTNAM , F. W. (1988) Factor analysis of the Dissociative Experiences Scale. In Abstracts of the Annual Meeting of the American Psychological Association. Washington, DC: American Psychological Association. —— & R OSSER -H OGAN , R. (1991) Trauma experiences, posttraumatic stress, dissociation, and depression in Cambodian refugees. American Journal of Psychiatry, 148, 1548–1551. C ARLSON , E. T. (1981) The history of multiple personality in the United States: I. The beginnings. American Journal of Psychiatry, 138, 666–668. —— (1984) The history of multiple personality in United States: Mary Reynolds and her subsequent reputation. Bulletin of the History of Medicine, 58, 72–82. C ARTER , A. B. (1949) The prognosis of certain hysterical symptoms. British Medical Journal, i, 1076–1079. —— (1972) A physician’s view of hysteria. Lancet, ii, 1241–1243. C ARTER , R. B. (1853) On the Pathology and Treatment of Hysteria. London: Churchill. C ATCHLOVE , R. & C OHEN , K. (1983) Directive approach with workmans’ compensation patients. Advances in Pain Research and Therapy, 5, 913–918. C ATHÉBRAS , P. J., R OBBINS , J. M., K IRMAYER , L. J., et al (1992) Fatigue in primary care: prevalence psychiatric comorbidity, illness behavior, and outcome. Journal of General Internal Medicine, 7, 276–286. C ATTELL , R. B. & E BER , H. W. (1957) Handbook for the Sixteen Personality Factor Questionnaire. Champaign: Institute for Personality Testing. C AVENAR , J. E., J R , S ULLIVAN , J. L. & M ALTBIE , A. A. (1979) A clinical note on hysterical psychosis. American Journal of Psychiatry, 136, 830–832. C HADDA , R. K. & A HULA , N. (1990) Dhat syndrome; a sex neurosis of the Indian subcontinent. British Journal of Psychiatry, 156, 577–579. C HALKE , F. C. R. (1954) Psychiatric screening of recruits: A review. Department of Veterans’ Affairs Treatment Services Bulletin, 9, 273–292. C HANDRASEKARAN , R., G OSWAMI , U., S IVAKUMAR , V., et al (1994) Hysterical neurosis – a follow-up study. Acta Psychiatrica Scandinavica, 89, 78–80. C HANG , S. K. & K IM , K. I. (1973) Psychiatry in South Korea. American Journal of Psychiatry, 130, 667–669. C HAPMAN , J. (1957) Peregrinating problem patients – Munchausen’s syndrome. Journal of the American Medical Association, 165, 927–933. C HARCOT , J. M. (1872) Clinical Lectures on Diseases of the Nervous System, Delivered at La Salpêtrière, Vol. 3 (trans. T. Savill, 1889). London: The New Sydenham Society. —— (1890) Cliniques Des Maladies du Système Nerveux. L’Oedème Bleu Des Hystériques. Paris: Veuve Babé et Cie.
References
429
C HENG , L. & H UMMEL , L. (1978) The Münchausen’s syndrome as a psychiatric condition. British Journal of Psychiatry, 133, 20–21. C HERTOK , L. (1966) Hypnosis. London: Pergamon Press. —— (1975) ‘Hysteria’ versus ‘Briquet’s syndrome’. American Journal of Psychiatry, 132, 1087. C HEYNE , G. (1733) The English Malady: Or, a Treatise of Nervous Diseases of all Kinds; as Spleen, Vapours, Lawness of Spirits, Hypochondriacal and Hysterical Distempers (4th edn). London: G. Strahan; Bath: J. Cornhill. C HIU , T. L., T ONG , J. E. & S CHMIDT , K. E. (1972) A clinical and survey study of Latah in Sarawak, Malaysia. Psychological Medicine, 2, 155–165. C HODOFF , P. (1982) Hysteria and women. American Journal of Psychiatry, 139, 545–551. —— (1987) Multiple personality disorder. American Journal of Psychiatry, 144, 124. —— & L YONS , H. (1958) Hysteria, the hysterical personality and ‘hysterical’ conversion. American Journal of Psychiatry, 114,734–740. C HOY , T. & D E B OSSET , F. (1992) Current perspectives: post-traumatic stress disorder: an overview. Canadian Journal of Psychiatry, 37, 578–583. C HRISTODORESCU , D., N EGULICI , E., Z ELINGHER , R., et al (1970) Conversion reactions in Klinefelter’s syndrome. Psychiatric Clinics, 3, 230–240. C HU , J. A. & D ILL , D. L. (1990) Dissociative symptoms in relation to childhood physical and sexual abuse. American Journal of Psychiatry, 147, 887–892. CIOMPI, L. (1969) Follow-up studies on the evolution of former neurotic and depressive states in old age. Clinical and psychodynamic aspects. Journal of Geriatric Psychiatry, 3, 90–106. C LARK , J. M. (1896) Review of Studien über Hysterie. Brain, 19, 401–414. C LAYTON, P. J. & G UZE, S. B. (1971) Hysteria, studies of diagnosis, outcome and prevalence. Journal of the American Medical Association, 215, 425–428. C LEGHORN , R. A. (1969a) Hysteria – multiple manifestations of semantic confusion. Canadian Psychiatric Association Journal, 14, 539–551. —— (1969b) Hysterical personality and conversion: theoretical aspects. Canadian Psychiatric Association Journal, 14, 553–567. —— & B ROWN , W. T. (1964) Psychogenesis of emesis. Canadian Psychiatric Association Journal, 9, 299–312. C LELAND , L. G. (1987) “RSI”: a model of social iatrogenesis. Medical Journal of Australia, 147, 236–239. C LONINGER , C. R. & G UZE , S. B. (1970a) Psychiatric illness and female criminality: The role of sociopathy and hysteria in the antisocial woman. American Journal of Psychiatry, 127, 303–311. —— & —— (1970b) Female criminals: their personal, familial and social backgrounds. The relation of these to the diagnoses of sociopathy and hysteria. Archives of General Psychiatry, 23, 554–558. —— & —— (1973) Psychiatric illnesses in the families of female criminals: a study of 288 first-degree relatives. British Journal of Psychiatry, 122, 697–703. —— & —— (1975) Hysteria and parental psychiatric illness. Psychological Medicine, 5, 27–31. ——, SIGVARDSON , S., V ON K NORRING , A. L., et al (1984) An adoption study of somatoform disorders: II. Identification of two discrete somatoform disorders. Archives of General Psychiatry, 41, 863–871. C LOUSE , R. E. (1992) Psychiatric interactions with the esophagus. Psychiatric Annals, 22, 598–605. —— & L USTMAN , P. J. (1983) Psychiatric illness and contraction abnormalities of the esophagus. New England Journal of Medicine, 309, 1337–1342. C OAKLEY , J. H. (1989) Myalgic encephalomyelitis and muscle fatigue. British Medical Journal, 298, 1711–1712. C OCKBURN , J. J. (1971) Spasmodic torticollis: a psychogenic condition? Journal of Psychosomatic Research, 15, 471–477.
430
References
C OHEN , M. E., R OBINS , E., P URTELL , J. J., et al (1953) Excessive surgery in hysteria: study of surgical procedures in 50 women with hysteria and 190 controls. Journal of the American Medical Association, 151, 977–986. C OHEN , L. (1982) A current perspective of pseudocyesis. American Journal of Psychiatry, 139, 1140–1144. C OLLIE , J. (1922) Medico-Legal Examinations and the Workmans’ Compensation Act, 1906; as Amended by Subsequent Acts. London: Balliere, Tindall & Cox. C OLLIGAN , M. J. & M URPHY , L. R. (1982) A review of mass psychogenic illness in work settings. In Mass Psychogenic Illness: A Social Psychological Analysis (eds M. J. Colligan, J. W. Pennebaker & L. R. Murphy), pp. 33–55. Hillsdale, New Jersey: Lawrence Erlbaum Associates. C OMMITTEE ON S EXUAL O FFENCES A GAINST C HILDREN AND Y OUTH (1984) Report. Ottawa: Minister of Supply & Services, Canada. C OMPSTON , N. D., D IMSDALE , H. E., R AMSAY , A. M., et al (1970) Epidemic malaise. British Medical Journal, i, 362–363. C ONGDON , M. H., H AIN , J. & STEVENSON , I. (1961) A case of multiple personality illustrating the transition from role-playing. Journal of Nervous and Mental Disease, 132, 497–504. C ONSTANS , A. (1863) Relation sur une epidémie d’hystéro-démonopathie en 1861. Paris: Adrien Delahaye. C OONS , P. (1984) The differential diagnosis of multiple personality. Psychiatric Clinics of North America, 7, 51–67. C OOPER , L. M. (1972) Hypnotic amnesia. In Hypnosis: Research Developments and Perspectives (eds E. Fromm & R. F. Shor), pp. 217–252. London: Paul Elek. C OPP , T. & M CA NDREW , B. (1990) Battle Exhaustion, Soldiers and Psychiatrists in the Canadian Army, 1939–1945. Montreal: McGill Queens University Press. C ORBETT , J. A., M ATHEWS , A. M., C ONNELL , P. H., et al (1969) Tics and Gilles de la Tourette’s syndrome: a follow-up study and critical review. British Journal of Psychiatry, 115, 1229–1241. C ORY , C. E. (1919) A divided self. Journal of Abnormal Psychology, 14, 281–291. C OTTRELL , S. & KINNIER-W ILSON , S. A. (1926) The affective symptomatology of disseminated sclerosis. A study of 100 cases. Journal of Neurology and Psychopathology, 7, 1–30. C OUNCIL ON S CIENTIFIC A FFAIRS (1985) Scientific status of refreshing recollection by the use of hypnosis: Report of the Council on Scientific Affairs of the American Medical Association. Journal of the American Medical Association, 253, 1918–1923. C OUPLAND , W. C. (1892) Philosophy of mind. In A Dictionary of Psychological Medicine (ed. D. Hack Tuke), vol. I, pp. 27–49. London: Churchill. C OURVILLE , C. B. (1953) Commotio Cerebri. Los Angeles: San Lucan Press. C RAIG , M. (1917) Psychological Medicine (3rd edn). London: J. & A. Churchill. C RAMER , B., G ERSHBERG , M. & S TERN , M. (1971) Munchausen syndrome. Archives of General Psychiatry, 24, 573–578. C REAK , M. (1969) Hysteria in childhood. Acta Paediatrica Psychiatrica, 36, 269–274. C REDNER , L. (1930) Klinische und soziale Auswirkungen von Hirnschädigungen. Neurological Psychiatry, 126, 721–757. C RISP , A. H. (1970) Anorexia nervosa, ‘feeding disorder’, ‘nervous malnutrition’ or ‘weight phobia’? World Review of Nutrition and Dietetics, 12, 452–504. C ROOG , S. H., S HAPIRO , D. S. & L EVINE , S. (1971) Denial among male heart patients. An empirical study. Psychosomatic Medicine, 33, 385–397. C ROSSLEY , R. B. (1982) Hospital admissions for abdominal pain in childhood. Journal of the Royal Society of Medicine, 75, 772–776. C RUICKSHANK , K., G IBLIN , M. J. & OLIVE , J. E. (1979) McIlroy lives. British Medical Journal, i, 1278. C URRIE , S., H EATHFIELD , K. W. G., H ENSON , R. A., et al (1971) The clinical course and prognosis of temporal lobe epilepsy. Brain, 94, 173.
References
431
C URTIS , J. L. (1965) A psychiatric study of 55 expectant fathers. Unites States Armed Forces Medical Journal, 6, 937–950. C UTLER , B. & R EED , J. (1975) Multiple personality – a single case study with a 15-year follow-up. Psychological Medicine, 5, 18–26. D ABHOLKAR , P. D. (1987) Ganser syndrome: a case report and discussion. British Journal of Psychiatry, 151, 256–258. D ACOSTA , J. M. (1871) On irritable heart; a clinical study of a form of functional cardiac disorder and its consequences. American Journal of Medical Science, 61, 17–52. D AIKOS , G., G ARZONIS , S., P ALEOLOGUE , A., et al (1959) Benign myalgic encephalomyelitis. An outbreak in a nurses’ school in Athens. Lancet, i, 693–696. D AILEY , A. H. (1894) Mollie Fancher. The Brooklyn Enigma. New York: Mary J. Fancher. D ALBIEZ , R. (1941) Psychoanalytic Method and the Doctrine of Freud (trans. T. F. Lindsay). London: Longmans, Green & Co. D ALLY , P. (1969) Anorexia Nervosa. London: William Heinemann. DALY, R. E. (1969) Neurological abnormalities in XYY males. Nature, London, 221, 472–473. D AMAS -M ORA , J., S KELTON -R OBINSON , M. & JENNER , F. A. (1982) The Charles Bonnet syndrome in perspective. Psychological Medicine, 12, 251–261. D ANA -H AERI , J., T RIMBLE , M. R. & O XLEY , J. (1983) Prolactin and gonadotrophin changes following generalized and partial seizures. Journal of Neurology, Neurosurgery and Psychiatry, 46, 331–335. D ANIELS , A. (1990) Daily Telegraph, 13 November, p. 17. D AVID , A. (1991) Post-viral fatigue syndrome and psychiatry. British Medical Bulletin, 47, 966–968. D AVIES , D. W. (1965) Physical illness in psychiatric out-patients. British Journal of Psychiatry, 111, 27–33. D AVIS , G. C. & A KISKAL , H. S. (1986) Descriptive, biological and theoretical aspects of borderline personality disorder. Hospital and Community Psychiatry, 37, 685–692. D AVIS , L. (1991) Murdered memory. Health, 5, 79–84. D AVISON , K. (1964) Episodic depersonalization. British Journal of Psychiatry, 110, 505–124. D AWES , R. M. (1994) House of Cards: Psychology and Psychotherapy Built on Myth. New York: The Free Press. D AWSON -B UTTERWORTH , K., W ALLEN , G. D. P. & G ITTLESON , N. L. (1969) Self-applied constricting bands. British Journal of Psychiatry, 115, 1255–1259. D E A LARCON , R. (1973) Hysteria and hysterical personality: how come one without the other? Psychiatric Quarterly, 47, 258–275. DE LA T OURETTE , G. (1887) L’Hypnotisme et les États analogues au point de vue médico-légale. Paris: Plon, Nourrit. —— (1891) Traité clinique de l’hystérie d’apres l’enseignement de la Salpêtrière. Hystérie normale ou interparoxystique. Paris: Plon, Nourrit. D E M ANDEVILLE , B. (1730) A Treatise on the Hypochondriack and Hysterick Diseases. London. D EARY , I. J., S MART , A. & WILSON , J. A. (1992) Depression and “hassles” in globus pharyngis. British Journal of Psychiatry, 161, 115–117. D EIGHTON , C. & N ICOL , A. (1985) Abnormal illness behaviour in young women in a primary care setting: is Briquet’s syndrome a useful category? Psychological Medicine, 15, 515–520. D ELAHUNTY , J. E. & A RDRAN , G. M. (1970) Globus hystericus: a manifestation of reflux oesophagitis? Journal of Laryngology and Otology, 84, 1049–1054. D ELAY , J. & D ENIKER , P. (1958) Hysteria and drug-induced hysteria-like states. In Symposium on Chemical Concepts of Psychosis (eds M. Rinkel & H. Denber). New York: McDowell. —— & P ICHOT , P. (1962) Abrégé de psychologie. Paris: Masson. D ENNETT , X. & F RY , H. J. H. (1988) Overuse syndrome: a muscle biopsy study. Lancet, i, 905– 908.
432
References
D ENNIS , N., H ENRIQUES , F. & S LAUGHTER , C. (1956) Coal ls Our Life. London: Eyre & Spottiswoode. DE R OCHAS , A. (1887) Hypnotisme et changement de personnalité. Révue Philosophique, 5, 330–333. D ESCARTES , R. (1649) The Passions of the Soul. D ESPINE , C. (1840) De l’emploi du magnétisme animal et des eaux minérales dans le traitement des maladies nerveuses, suivi d’une observation tres curieuse de guérison de névropathie. Paris: Germer, Bailliere. D EUTSCH , F. (1959) Symbolization as a formative state of the conversion process. In On the Mysterious Leap from the Mind to the Body (ed. F. Deutsch), pp. 75–97. New York: International Universities Press. D EVAN , G. S. (1987) Koro and schizophrenia in Singapore. British Journal of Psychiatry, 150, 106–107. D EVINE , R. & M ERSKEY , H. (1965) The description of pain in psychiatric and general medical patients. Journal of Psychosomatic Research, 9, 311–316. D HADPHALE , M. & S HAIKH , S. P. (1983) Epidemic hysteria in a Zambian school: “The mysterious madness of mwinilunga”. British Journal of Psychiatry, 142, 85–88. D IAMOND , E. L., T ROBE , J. D. & B ELAR , C. D. (1984) Psychological aspects of essential blepharospasm. Journal of Nervous and Mental Disease, 172, 749–756. D ICKENSON , E. J. & EVANS , T. R. (1987) Cardiac Münchausen’s syndrome. Journal of the Royal Society of Medicine, 80, 630–633. D IGBY , K. (1658) A Late Discourse Made in a Solemn Assembly of Nobles and Learned Men at Montpellier in France – Touching the Cure of Wounds by the Powder of Sympathy (trans. R. White). London: Lownes & Davies. D ILLON , M. J., M ARSHALL, W. C., D UDGEON , J. A., et al (1974) Epidemic neuromyasthenia: outbreak among nurses at a children’s hospital. British Medical Journal, i, 301–305. D OWSON , J. H. & BERRIOS , G. E. (1991) Factor structure of DSM–III–R personality disorders shown by self-report questionnaire: implications for classifying and assessing personality disorders. Acta Psychiatrica Scandinavica, 84, 555–560. D U S AULLE , L. (1883) Les hystériques: État physique et État mental, actes insolites, délictueux et criminels. Paris: J. B. Baillière et Fils. D UBOIS D’ AMIENS , E. F. (1833) Histoire philosophique de l’hysterie. Paris: Deville Cavellin. D UTTA , D., PHOOKAN , H. R. & D AS , P. D. (1982) The Koro epidemic in lower Assam. Indian Journal of Psychiatry, 24, 370–374. D WIGHT , B. W. (1818) Facts illustrative of the powers and operations of the human mind in a diseased state. American Journal of Science, 1, 431–433. D WORKIN , R. H., H ANDLIN , D. S., R ICHLIN , D. M., et al (1985) Unravelling the effects of compensation, litigation, and employment on treatment response in chronic pain. Pain, 23, 49–59. E ASSER , B. R. & L ESSER , S. (1965) Hysterical personality: a re-evaluation. Psychoanalytic Quarterly, 34, 390–412. E ASTWOOD , M. R., M INDHAM , R. H. S. & T ENNENT , T. G. (1970) The physical status of psychiatric emergencies. British Journal of Psychiatry, 116, 545–550. E DWARDS , J. G. (1976) Psychiatric aspects of civilian disaster. British Medical Journal, i, 944–947. E ILENBERG , M. D. & W HATMORE , P. B. (1961) Physical disease and psychiatric emergencies. Comprehensive Psychiatry, 2, 358–363. EISENBUD , J. (1937) The psychology of headache. Psychiatric Quarterly, 2, 592–619. E ITINGER , L. (1964) Concentration Camp Survivors in Norway and Israel. London: George Allen & Unwin. E ITINGER , L., K RELL , R. & R IECK , M. (1985) The Psychological and Medical Effects of Concentration Camps and Related Persecutions on Survivors of the Holocaust: a Research Bibliography. Vancouver: University of British Columbia Press.
References
433
EKMAN, P. & O’SULLIVAN, M. (1991) Who can detect a liar? American Psychologist, 46, 913–920. E KSELIUS , L., L INDSTROM , E., V ON K NORRING , L., et al (1993) Personality disorders in DSM– III–R as categorical or dimensional. Acta Psychiatrica Scandinavica, 88, 183–187. E L S AYED , S. M., M AGHRABY , M. M., H AFEIZ , H. B., et al (1986) Psychiatric diagnostic categories in Saudi Arabia. Acta Psychiatrica Scandinavica, 74, 553–554. E LLENBERGER , H. F. (1970) The Discovery of the Unconscious. New York: Basic Books. E NGEL , G. L. (1951) Primary atypical facial neuralgia. An hysterical conversion symptom. Psychosomatic Medicine, 13, 375–396. —— & S CHMALE , A. H. (1967) Psychoanalytic theory of somatic disorders. Journal of the American Psychoanalytical Association, 15, 344–365. E NGEL , G. L. (1959) Psychogenic pain. Medical Clinics of North America, 42, 1481–1496. —— (1968) A reconsideration of the role of conversion in somatic disease. Comprehensive Psychiatry, 9, 316–326. E NOCH , M. D., T RETHOWAN , W. H. & B ARKER , J. C. (1967) Some Uncommon Psychiatric Syndromes. Bristol: John Wright. E RDELYI , M. H. (1985) Psychoanalysis: Freud’s Cognitive Psychology. New York: Freeman. —— (1990) Repression, reconstruction and defense: history and integration of the psychoanalytic and experimental frameworks. In Repression and Dissociation. Implications for Personality Theory, Psychopathology, and Health (ed. J. L. Singer), pp. 1–31. Chicago: University of Chicago Press. E RICHSEN , J. E. (1866) On Railway and Other Injuries of the Nervous System. Philadelphia: Henry C. Lea. —— (1886) On Concussion of the Spine, Nervous Shock and Other Obscure Injuries to the Nervous System in Their Clinical and Medico-Legal Aspects (a new and revised edition). New York: William Wood & Co. E SCOBAR , J. I., B URNAM , A., K ARNO , M., et al (1987) Somatization in the community. Archives of General Psychiatry, 44, 713–718. E SDAILE , J. (1850) Mesmerism in India. In Hypnosis in Medicine and Surgery. New York: Julian Press. E VANS , F. J. (1972) Hypnosis and sleep techniques for exploring cognitive activity during sleep. In Hypnosis: Research Developments and Perspectives (eds E. Fromm & R. F. Shor), pp. 43–83. London: Paul Elek (1973). E VANS , P. R. & M ERSKEY , H. (1972) Shared beliefs of dermal parasitosis: folie partagée. British Journal of Medical Psychology, 45, 19–26. E VANS , R. W. (1993) The post concussion syndrome and the sequelae of mild head injury. In The Neurology of Trauma (ed. R. W. Evans). Neurological Clinics, 10, 815–847. E YSENCK , H. J. (1947) Dimensions of Personality. London: Routledge & Kegan Paul. F ABREGA , H. (1974) Disease and Social Behaviour. An lnter-Disciplinary Perspective. Cambridge, Mass.: MIT Press. ——, M EZZICH , J., J ACOB , R., et al (1988) Somatoform disorder in a psychiatric setting: systematic comparisons with depression and anxiety disorders. Journal of Nervous and Mental Disease, 176, 431–439. F AERGEMAN , P. M. (1945) Psychogenic Psychoses. London: Butterworths (1963). F AHY , T. A. (1988) The diagnosis of multiple personality disorder. A critical review. British Journal of Psychiatry, 153, 597–606. ——, A BAS , M. & B ROWN , J. C. (1989) Multiple personality. A symptom of psychiatric disorder. British Journal of Psychiatry, 154, 99–101. F AINBERG , V. (1975) Personal Communication. F AIRBAIRN , W. R. D. (1954) Object-Relations Theory of the Personality. New York: Basic Books. F ALK , B., H ERSEN , M. & V AN H ASSELT , V. B. (1994) Assessment of post-traumatic stress disorder in older adults: A critical review. Clinical Psychology Review, 14, 383–415. F ALSE M EMORY S YNDROME F OUNDATION (1993) The accusations. FMS Foundation Newsletter, May, p. 9.
434
References
F ARLEY , J., W OODRUFF , R. A. J R & G UZE , S. B. (1968) The prevalence of hysteria and conversion symptoms. British Journal of Psychiatry, 114, 1121–1125. F AVAZZA , A. R. & OMAN , M. (1978) Overview: foundations of cultural psychiatry. American Journal of Psychiatry, 135, 293–303. —— & C ONTERIO , K. (1989) Female habitual self-mutilators. Acta Psychiatrica Scandinavica, 79, 283–289. F EEHAN , C. J. (1993) Hysteria in childhood. British Journal of Psychiatry, 162, 571–572. F EIGHNER , J. P., R OBINS , E. G UZE , S. B., et al (1972) Diagnostic criteria for use in psychiatric research. Archives of General Psychiatry, 26, 57–63. F EINSTEIN , A. & H ATTERSLEY , A. (1988) Ganser symptoms, dissociation and dysprosody. Journal of Nervous and Mental Disease, 176, 692–693. F EKETE , J. (1994) Moral Panic: Bio-politics Rising. Montreal: Robert Davies Publishing. F EMINA , D. D., Y EAGER , C. A. & L EWIS , D. O. (1990) Child abuse: adolescent records versus adult recall. Child Abuse and Neglect, 14, 227–231. F ÉNELON , G., M AHIEUX , F., R OULLET, E., et al (1991) Münchausen’s syndrome and abnormalities on magnetic resonance imaging of the brain. British Medical Journal, 302, 996–997. F ENICHEL , O. (1945) The Psychoanalytic Theory of Neurosis. London: Routledge. F ENTON -R USSELL , D. (1956) Suicide. British Medical Journal, ii, 998—999. F ERENCZI , S. (1919) The phenomena of hysterical materialization. In Further Contributions to the Theory and Technique of Psycho-analysis, pp. 89–104. New York: Brunner/Mazel (1950). F ERGUSON , D. A. (1987) “RSI”: putting the epidemic to rest. Medical Journal of Australia, 147, 213–214. F ERRIAR , J. (1795) Medical Histories and Reflections, Vol. II. London: Cadell & Davies. Cit. Mace (1992a,b) F ICHTNER, C. G., P ECHTER , B. M. & J OBE , T. H. (1992) Pisa syndrome mistaken for conversion in an adolescent. British Journal of Psychiatry, 161, 849–852. F IGLEY , C. R. (1978) Stress Disorders Among Vietnam Veterans. Theory, Research and Treatment. New York: Brunner/Mazel. F ISCHER -H OMBURGER , E. (1979) On the medical history of the doctrine of imagination. Psychological Medicine, 9, 619–628. FISHBAIN, D. A., G OLDBERG, M., R OSOMOFF , H. L. (1988) Münchausen’s syndrome presenting with chronic pain: case report. Pain, 35, 91–94. F ISHER , G. C. & M ITCHELL , I. (1992) Münchausen’s syndrome by proxy (factitious illness by proxy). Current Opinion in Psychiatry, 5, 224–227. ——, —— & M URDOCH , D. (1993) Münchausen’s syndrome by proxy: the question of psychiatric illness in a child. British Journal of Psychiatry, 162, 701–703. F ISHER , S. & F ISHER , R. L. (1963) Placebo response and acquiescence. Psychopharmacologia, 4, 298–301. F ISMAN , M. (1985) Pseudo-dementia. Progress in Neuropsychopharmacology and Biological Psychiatry, 9, 481–484. F LICKER , D. J. (1942) The self-inflicted injury. A case report. American Journal of Psychiatry, 99, 168–173. —— (1956) Malingering: a symptom. Journal of Nervous and Mental Disease, 123, 23–31. F LOR -H ENRY , P. (1978) Gender, hemispheric specialization and psychopathology. Social Science and Medicine, 128, 155–162. F ORBES , A. R. (1969) The validity of the 16 PF in the discrimination of the hysteroid and obsessoid personality. British Journal of Social and Clinical Psychology, 8, 152–159. F ORBIS , O. L. & J ANES , R. H. (1965) Hysteria in childhood. Southern Medical Journal, 58, 1221–1225. F ORD , C. V. (1983) The Somatizing Disorders: Illness as a Way of Life. New York: Elsevier Biomedical.
References
435
F ORDYCE , W. E. (1976) Behavioral Methods in Chronic Pain and Illness. St Louis, MO: The C. V. Mosby Co. FORREST, A. D. (1967) Manifestations of ‘hysteria’: phobic patients and ‘hospital recidivists’. British Journal of Medical Psychology, 42, 263–270. F OULDS , G. (1965) Personality and Personal lllness. London: Tavistock Publications. F OULKS , E. (1972) The arctic hysterias of the north Alaskan Eskimos. Bulletin of the American Anthropological Association. F RANZ , S. I. (1933) Persons One and Three. A Study in Multiple Personalities. New York: McGraw-Hill. F RASER , G. A. (1991) The dissociative table technique: a strategy for working with ego states in dissociative disorders and ego state therapy. Dissociation, 4, 205–213. F RASER , I. (1984) A matter of life and death. British Medical Journal, 289, 1442. F REELAND , A., M ANCHANDA , R., C HIU , S., et al (1993) Four cases of supposed multiple personality disorder: evidence of unjustified diagnoses. Canadian Journal of Psychiatry, 23, 245–247. F REEMAN , L. J. & N IXON , P. G. F. (1985) Are coronary artery spasm and progressive damage to the heart associated with the hyperventilation syndrome? British Medical Journal, 291, 851–852. F RENCH , A. P. & N ELSON , H. L. (1972) Genital self-mutilation in women. Archives of General Psychiatry, 27, 618–620. F REUD , A. (1937) The Ego and the Mechanisms of Defence (trans. C. Baines, 1937). London: Hogarth Press. —— (1946) The Psycho-Analytical Treatment of Children. London: Imago. F REUD , S. (1905) Three Essays on Infantile Sexuality. Complete Psychological Works. Standard edn, vol. 7 (1960). London: Hogarth Press. —— (1908) Character and Anal Erotism. Standard edition, vol. 5 (1959) London: Hogarth Press. —— (1909) General Remarks on Hysterical Attacks. Standard edition, vol. 9 (1959). London: Hogarth Press. —— (1912) Contributions to a Discussion on Masturbation. Standard edition, vol. 12 (1962). London: Hogarth Press. —— (1917) Introductory Lectures on Psychoanalysis (trans J. Rivière, 1922). London: George Allen & Unwin. —— (1921) Group Psychology and the Analysis of the Ego. London: Hogarth Press. —— (1926) Inhibitions, Symptoms and Anxiety. Standard edn, vol. 20 (1959). London: Hogarth Press. —— (1931) Libidinal Types, Standard edn, vol. 21 (1961). London: Hogarth Press. —— (1935) An Autobiographical Study (trans. J. Strachey). London: Leonard & Virginia Woolf, Hogarth Press. F RIEDMAN , M. J. & L IPOWSKI , Z. J. (1981) Pseudodementia in a young Ph.D. American Journal of Psychiatry, 138, 381–382. F RIEMERT , K. (1970) Simultaneous occurrence of epileptic and hysterical fits. Psychiatrie Neurologia Medizinesche Psychologie, 22, 253–255. F ROESE , A., V ASQUEZ , E., C ASSEM , N. H., et al (1974) Validation of anxiety depression and denial scales in a coronary care unit. Journal of Psychosomatic Research, 18, 137–141. F RY , H. J. H. (1986) Overuse syndrome of the upper limb in musicians. Medical Journal of Australia, 144, 182–185. G ADD , R. A. & M ERSKEY , H. (1975) Middlesex Hospital Questionnaire. Scores in patients with hysterical conversion symptoms. British Journal of Medical Psychology, 48, 367–370. G AINOTTI , S. (1972) Emotional behaviour and hemispheric side of the lesion. Cortex, 8, 41–55. G ALLAVARDIN , L. (1917) Soldiers with disordered action of the heart. Archives des Maladies du Coeur, Paris, 10, 408–433.
436
References
G ALPINE , J. F. & B RADY , C. (1957) Benign myalgic encephalomyelitis. Lancet, i, 757. G ALTON , F. (1883) Inquiries into Human Faculty (2nd edn, 1907). London: J. M. Dent. G ANSER , S. (1898) A peculiar hysterical state. Archiv für Psychiatrie und Nervenkrankheit, 30, 633. (Trans. C. E. Schorer, 1898, British Journal of Criminology, 5, 120–126.) G ARDNER , A. R. & GARDNER , A. J. (1975) Self-mutilation, obsessionality and narcissism. British Journal of Psychiatry, 127, 127–132. GARDNER, R. A. (1992a) Modern witch hunt – child abuse charges. Wall Street Journal, 22 Feb. —— (1992b) True and False Accusations of Child Sexual Abuse. Cresskill, New Jersey: Creative Therapeutics. G ARFINKEL , P. E., K APLAN , A. S., G ARNER D. M., et al (1983) The differentiation of vomiting/weight loss as a conversion disorder from anorexia nervosa. American Journal of Psychiatry, 140, 1019–1022. G ARNER , D. M. (1993) Pathogenesis of anorexia nervosa. Lancet, 341, 1631–1634. G ARRALDA , M. E. (1992) A selective review of child psychiatric syndromes with a somatic presentation. British Journal of Psychiatry, 161, 759–773. G ELLER , B., H ALLET , M., R AVITS , J.,, et al (1987) Botulinum toxin therapy in hemifacial spasm; clinical and physiologic studies. Neurology, 37, 120. G EORGET , M. (1821) De la physiologie de la système nerveux, Vol. 2, pp. 261–262 and 265– 286. Paris: J. B. Bailliere. G ERSONS , B. P. R. & C ARLIER , I. V. E. (1992) Post traumatic stress disorder, the history of a recent concept. British Journal of Psychiatry, 161, 742–748. G IACARDY , P. (1923) Un cas d’acarophobie familiale. Journal de Médécine de Bordeaux, 53, 479– 480. G ILL , M. & B RENMAN , M. (1959) Hypnosis and Related States. New York: International Universities Press. G ILLESPIE , R. D. (1929) Hypochondria. London: Kegan Paul. G LESER G. C. & I HILEVICH , D. (1969) An objective instrument for measuring defense mechanisms. Journal of Consulting and Clinical Psychology, 33, 51–60. G MELIN , E. (1791) Materialen fur die Anthropologie I. Tübingen: Cotta. Cit. Ellenberger (1970). G ODDARD , H. H. (1926) A case of dual personality. Journal of Abnormal and Social Psychology, 21, 170–191. —— (1927) Two Souls in One Body. A Case of Dual Personality. New York: Dodd, Mead & Co. G OETZ , C. G. (1987) Charcot the Clinician. The Tuesday Lessons. New York: Raven Press. G OLDFIELD , M. D. & G LICK , L. D. (1970) Self mutilation of the female genitalia: a case report. Diseases of the Nervous System, 31, 843–845. G OLDNEY , R. D. (1981) Are young women who attempt suicide hysterical? British Journal of Psychiatry, 138, 141–146. —— & S IMPSON , I. S. (1975) Female genital self-mutilation, dysorexia and the hysterical personality: the Caenis syndrome. Canadian Psychiatric Association, 20, 435–441. G OLDSTEIN , J. (1987) Console and Classify. The French Psychiatric Profession in the 19th Century. New York: Cambridge University Press. G ONZALEZ -H EYDRICH, J., K ERNER , J. A. & S TEINER , H. (1991) Testing the psychogenic vomiting diagnosis: four paediatric patients. American Journal of Diseases of Childhood, 145, 913–916. G OOD , R. (1942) Malingering. British Medical Journal, ii, 359–362. G OODHART , S. P. & S AVITSKY , N. (1933) Self-mutilation in chronic encephalitis. American Journal of Medical Science, 185, 674–683. G ÖTESTAM , K. G. (1993) Er multippel personlighet en psykiatrisk lidelse? Tidsskrift For Den Norske Lægeforening, 26, 113. G OULD , R., M ILLER , B. L., G OLDBERG , M. A., et al (1986) The validity of hysterical signs and symptoms. Journal of Nervous and Mental Diseases, 174, 593–598.
References
437
G OWERS , W. R. (1892–93) A Manual of Diseases of the Nervous System. I & II. London: J. & A. Churchill. G RAHAM , P. & R UTTER , M. (1968) Organic brain dysfunction and child psychiatric disorders. British Medical Journal, iii, 695–700. G RALNICK , A. (1942) Folie à deux: the psychosis of association. Psychiatric Quarterly, 16, 230–263, 491–520. G RATTAN -S MITH , P., F AIRLEY , M. & P ROCOPIS , P. (1988) Clinical features of conversion disorder. Archives of Disease in Children, 63, 498–414. G RAVES , R. (1929) Goodbye to All That. Harmondsworth: Penguin (1960). G RAYBILL , J. R., S ILVA , J., O B RIEN , M. S., et al (1972) Epidemic neuromyasthenia. A syndrome or disease? Journal of the American Medical Association, 219, 1440–1443. G REAVES , G. B. (1980) Multiple personality 165 years after Mary Reynolds. Journal of Nervous and Mental Disease, 168, 577–596. G REEN , B. L. & G RACE , M. C. (1988) Conceptual issues in research with survivors and illustrations from a follow-up study. In Human Adaptation to Extreme Stress: from the Holocaust of Vietnam (eds J. P. Wilson, Z. Harel & B. Kahana), pp. 105–124. New York: Plenum. ——, L INDY , J. D., G RACE , A. C., et al (1992) Chronic post traumatic stress disorder and the diagnostic co-morbidity in a disaster sample. Journal of Nervous and Mental Disorders, 180, 760–766. G REEN M. H. (1985) The Transmission of Ancient Theories of Female Physiology and Disease through the Early Middle Ages, pp. 170–171. Princeton NJ: Princeton University; available from Microfilms International, Ann Arbor. G RIFFIN , F. N., W EBB , M. G. T. & P ARKER , R. R. (1982) A case of self inflicted eye injuries. Journal of Nervous and Mental Disease, 70, 53–56. G RIFFITH , D. E. (1975) Juvenile hysteria and primary shock: report of a case. Journal of Dentistry for the Child, 42, 299–300. G RIFFITH , E. E. H., Y OUNG , J. L. & S MITH , D. L. (1984) An analysis of the therapeutic elements in a Black church service. Hospital and Community Psychiatry, 35, 464–469. G RINKER , R. F. & S PIEGEL , J. P. (1943) War neurosis. In North Africa: The Tunisian Campaign. New York: Josiah Macy Jr Foundation. —— & —— (1945) Men Under Stress. Philadelphia: Blakiston, McGraw Hill. G RONWALL , D. & W RIGHTSON , P. (1974) Delayed recovery of intellectual function after minor head injury. Lancet, ii, 605–609. GROSZ, H. J. & ZIMMERMAN, J. (1965) Experimental analysis of hysterical blindness: a followup report and new experimental data. Archives of General Psychiatry, 13, 255–260. G UGGENHEIM , P. & H AYNAL , A. (1964) Über elektroenkephalographische Untersuchungen bei der Maladie Gilles de la Tourette. Schweizerische Archiv für of Neurologie und Psychiatrie, 94, 265–278. G UILLAIN , G. (1959) J. M. Charcot. His Life – His Work (trans. P. Bailey). London: Pitman Medical. G UIORA , A. Z. (1967) Dysorexia: a psychopathological study of anorexia nervosa and bulimia. American Journal of Psychiatry, 124, 391–393. G UTTMAN , E. (1932) Organische Krankheitsbilder hysterischen Geprages. Fortschritte Der Neurologie und Psychiatrie, 4, 82–99. G UZE , S. B. (1967) The diagnosis of hysteria: what are we trying to do? American Journal of Psychiatry, 124, 77–84. —— (1970) The role of follow-up studies: their contribution to diagnostic classification as applied to hysteria. Seminars in Psychiatry, 2, 392–402. —— (1973) Suicide, hysteria, and conversion symptoms. Journal of the American Medical Association, 225, 65. —— (1983) Studies in hysteria. Canadian Journal of Psychiatry, 28, 434–437.
438
References
—— & P ERLEY M. J. (1963) Observations on the natural history of hysteria. American Journal of Psychiatry, 119, 960–965. ——, W OODRUFF , R. A. & CLAYTON , P. J. (1971) A study of conversion symptoms in psychiatric out-patients. American Journal of Psychiatry, 128, 643–646. G WEE , A. L. (1968) Koro – its origin and nature as a disease entity. Singapore Medical Journal, 9, 3. H ACKETT , T. P.& W EISMAN , A. D. (1962) The treatment of the ageing. Current Psychiatric Therapy, 2, 121–126. ——, C ASSEM , N. H. & W ISHNIE , H. A. (1968) The coronary care unit: an appraisal of its psychological hazards. New England Journal of Medicine, 279, 1365–1370. —— & —— (1974) Development of a quantitative rating scale to assess denial. Journal of Psychosomatic Research, 18, 93–100. —— & H ACKING , I. (1986) The invention of split personalities. In Human Nature and Natural Knowledge (eds A. Donagan, A. N. Perovich Jr & M. V. Wedin), pp. 63–85. Dordrecht: Reidel. H ACKING , I. (1991) Two souls in one body. Critical Enquiry, 17, 838–867. —— (1992) Multiple personality disorder and its hosts. History of the Human Sciences, 5, 3–31. H ACKING , I. (1995) Rewriting the Soul: Multiple Personality and the Sciences of Memory Princeton: Princeton University Press. H AFEIZ , H. B. (1980) Hysterical conversion: a prognosis study. British Journal of Psychiatry, 136, 548–551. H AGNELL , O., G RÄSBECK , A., Ö JESJÖ , J., et al (1993) Mental tiredness in the Lundby study: Incidence and course over 25 years. Acta Psychiatrica Scandinavica, 88, 316–321. H ALEY , S. A. (1978) Treatment implications of post combat stress response syndromes for mental health professionals. In Stress Disorders Among Vietnam Veterans. Theory, Research and Treatment (ed. C. R. Figley). New York: Brunner/Mazel. H ALLIDAY , A. M. (1972) Evoked responses in organic and functional sensory loss. In Colloque Inserm, Tours. —— & M ASON , A. A. (1964) The effect of hypnotic anaesthesia on cortical responses. Journal of Neurology, Neurosurgery and Psychiatry, 27, 300–312. H ANNAY , D. R. (1979) The Symptom Iceberg. A Study of Community Health. London: Routledge & Kegan Paul. H ARRIMAN , P. L. (1943) A new approach to multiple personality. American Journal of Orthopsychiatry, 13, 638–643. H ARRINGTON , J. A. (1982) Epidemic psychosis. British Journal of Psychiatry, 141, 98–99. HARRIS, B. (1981) A case of brain fag in East Africa. British Journal of Psychiatry, 138, 162–163. H ARRIS , W. (1915) Nerve Injuries and Shock. London: Henry Frowde and Hodder & Stoughton. H ART , B. (1912) A case of double personality. Journal of Mental Science, 58, 236–243. H ARTMANN , H. (1932) Studien zur Psychologie des induzierten Irreseins. Jb. Psychiat. Neurol, 48, 164–183. —— & S TENGEL E. (1931) Studien zur Psychologie des induzierten Irreseins. Archives of Psychiatry, 95, 584–600. H ARVEY , W. (1651) On parturition. In The Works of William Harvey M. D. (trans. R. Willis, 1847), pp. 542–543. London: Sydenham Society. H AWKINGS , J. F., J ONES , K. S., S IM , M., et al (1956) Deliberate disability. British Medical Journal, i, 361–367. H AWKSWORTH , H. & S CHWARZ , T. (1977) The Five of Me. Chicago: Henry Regnery Co. H AY , G. G. (1983) Feigned psychosis – a review of the simulation of mental illness. British Journal of Psychiatry, 143, 8–10. H AYS , P. (1992) False but sincere accusations of sexual assault made by narcoleptic patients. Medical-Legal Journal, 60, 265–271.
References
439
H EAD , H. (1916) Quoted by Mott in special discussion on shell-shock without visible signs of injury. Proceedings of the Royal Society of Medicine, 9, Part III (suppl.), 42. Also quoted by Anonymous, Lancet, i, 306–307 (a discussion on shell-shock). —— (1922) An address on the diagnosis of hysteria. British Medical Journal, i, 827–829. H ECKER , J. F. C. (1844) Epidemics of the Middle Ages (trans. B. G. Babington). London: New Sydenham Society. H ENDERSON , D. A., K UNKLE , E. C., K ALTER , S. S.,, et al (1957) Epidemic neuromyasthenia. An outbreak in Punta Gorda, Florida. New England Journal of Medicine, 257, 356–364. —— & S HELOKOV , A. (1959) Epidemic neuromyasthenia. Clinical syndrome? New England Journal of Medicine, 260, 757–764; 814–818. H ENDERSON , D. K. & G ILLESPIE , R. D. (1950) A Textbook of Psychiatry (7th edn). London: Oxford Medical Publications. H ENNE , M. (1955) L’hypochondrie à travers les ages. Histoire de Médecine, 5, 5–27. H ERMAN , J. L. (1992) Trauma and Recovery. New York: Basic Books. H ERODOTUS (c. 484–420) (1963) Histories, Book IV, Loeb Classical Library. London: Heinemann. H ÉSNARD , A. (1914) Les troubles nerveux et psychiques consécutifs aux catastrophes navales. Révue de Psychiatrie, 18, 139–151. H IBBERT , G. A. (1984) Hyperventilation as a cause of panic attacks. British Medical Journal, 288, 263–264. H ICKIE , I., L LOYD , A., W AKEFIELD , D., et al. (1990) The psychiatric status of patients with the chronic fatigue syndrome. British Journal of Psychiatry, 156, 534–540. H IGGINS , P. M. (1990) Temporary Münchausen’s syndrome. British Journal of Psychiatry, 157, 613–616. H IGHMORE , N. (1669) Cure of hysteria and hypochondriac passion. Philosophical Transactions, B, 1089. H ILGARD , E. R. (1973) A neodissociation interpretation of pain reduction in hypnosis. Psychological Review, 80, 396–411. —— (1977) Divided Consciousness: Multiple Controls in Human Thought and Action. New York: Wiley. —— (1979) Divided consciousness in hypnosis: The implications of the hidden observer. In Hypnosis: Developments in Research in New Perspectives (2nd edn) (eds E. Fromm & R. F. Shor). New York: Aldine. —— (1988) Professional skepticism about multiple personality. Journal of Nervous and Mental Disease, 176, 532. —— & H ILGARD , J. R. (1975) Hypnosis in the Relief of Pain. Los Altos: William Kaufmann. H ILL , O. W. (1967 ) Psychogenic vomiting and hypokalaemia. Gut, 8, 98–101. —— (1968) Psychogenic vomiting. Gut, 9, 348–352. H IRSCH , J. J. & H OLLENDER , M. H. (1969) Hysterical psychosis. Clarification of the concept. American Journal of Psychiatry, 125, 909–915. H IRSCHMULLER , A. (1989) The Life and Work of Josef Breuer: Physiology and Psychoanalysis. New York: New York University Press. H OCHBERG , F. H., L EFFERT , R. D., H ELLER , M. D., et al (1983) Hand difficulties among musicians. Medical Journal of Australia, 249, 1869–1872. H OCKING , B. (1987) Epidemiological aspects of “repetition” strain injury in Telecom Australia. Medical Journal of Australia, 147, 218–222. H ODGES , K., K LINE , J. J., B ARBER o, G., et al (1985) Depressive symptoms in children with recurrent abdominal pain and in their families. Journal of Pediatrics, 107, 622–626. H ODGES , R. M. (1881) So-called concussion of the spinal cord. Boston Medical and Surgical Journal, 104, 361–365, 386–389. H ODGSON , R. (1891) A case of double consciousness. Proceedings of the Society of Psychical Research, 7, 221–257.
440
References
H OLDEN , T. J. (1987) Koro syndrome associated with alcohol-induced systemic disease in a Zulu. British Journal of Psychiatry, 151, 695–697. H OLLENDER , M. H. (1971) Hysterical personality. Comments on Contemporary Psychiatry, 1, 17–23. —— & H IRSCH , S. J. (1964) Hysterical psychosis. American Journal of Psychiatry, 120, 1066– 1074. H OLLINGSHEAD , A. B. & R EDLICH , F. C. (1958) Social Class and Mental Illness: A Community Study. New York: Wiley. H OLMES , D. S. (1990) The evidence for repression: An examination of sixty years of research. In Repression and Dissociation. Implications for Personality Theory, Psychopathology, and Health (ed. J. L. Singer), pp. 85–102. Chicago: University of Chicago Press. H OLMES , G. (1950) Some clinical aspects of pain. In Pain and Its Problems (eds H. Ogilvie & W. A. R. Thomson). London: Eyre & Spottiswoode. ——, K APLAN , J. E., G ANTZ , N. M., et al (1988) Chronic fatigue syndrome: a working case definition. Annals of Internal Medicine, 108, 387–389. H OLROYD , S., R ABINS , P. V., F INKELSTEIN , D., et al (1992) Visual hallucinations in patients with macular degeneration. American Journal of Psychiatry, 149, 1701–1706. H OROWITZ , M. J. (1977) Structure and the processes of change. In Hysterical Personality (ed. M. J. Horowitz), pp. 329–399. New York: Jason Aronson Inc. —— (1991) Psychic structure and the processes of change. In Hysterical Personality Style and the Histrionic Personality Disorder (revised edition) (ed. M. J. Horowitz), pp. 193– 261. Northdale, NJ: Jason Aronson Inc. H ORTON , P. & M ILLER , D. (1972) The etiology of multiple personality. Comprehensive Psychiatry, 13, 151–159. H OWE , M. L. & C OURAGE , M. L. (1993) On resolving the enigma of infantile amnesia. Psychological Bulletin, 113, 305–326. H UGHES , M. C. (1984) Recurrent abdominal pain and childhood depression: clinical observations of 23 children and their families. American Journal of Orthopsychiatry, 54, 146–155. H ULETT , A. G. (1941) Malingering – a study. Military Surgery, 89, 123–139. H UNT P. S., C ONNELL , A. M. & S MILEY , T. B. (1970) The crico-pharyngeal sphincter in gastric reflux. Gut, 11, 303–306. H UNTER , H. (1969) A controlled study of the psychopathology and physical measurements of Klinefelter’s syndrome. British Journal of Psychiatry, 115, 443–448. H UNTER , R. & M AC A LPINE , I. (1963) Three Hundred Years of Psychiatry 1535–1860. Oxford: Oxford University Press. H URST , A. F. (1916) Medical Diseases of the War (1st edn). London: Edward Arnold. —— (1918) Medical Diseases of the War (2nd edn). London: Edward Arnold. —— (1920) The Psychology of the Special Senses and Their Functional Disorders. London: Oxford Medical Publications. —— (1940) Medical Diseases of War. London: Edward Arnold. (Hurst modified his views with each edition.) H UXLEY , A. (1952) The Devils of Loudun. London: Chatto & Windus. H YLER , S. E. & S USSMAN , N. (1981) Chronic factitious disorder with physical symptoms (the Münchausen syndrome). Psychiatric Clinics of North America, 4, 365–377. IASP (1994) International Association for the Study of Pain. Classification of Chronic Pain, Descriptions of Chronic Pain Syndromes and Definitions of Pain Term (eds H. Merskey & N. Bogduk). Seattle: IASP Press. I LECHUKWU , S. T. C. (1992) Is there a shared somatic disorder? Communication of nondelusional symptoms in Nigeria. Canadian Journal of Psychiatry, 37, 699–702. I NGALL , M. A. (1974) Psychiatric casualties of the Exorcist. Rhode Island Medical Journal, 57, 472–473; 479–480.
References
441
I NGHAM , J. G. & R OBINSON , J. O. (1964) Personality in the diagnosis of hysteria. British Journal of Psychology, 55, 276–284. I NGLIS , J. (1957) Cargo cults: the problem of explanation. Oceania, 27, 149. I NMAN , T. (1858) On so-called hysterical pain. British Medical Journal, ii, 24–25. J ACKSON , J. H. (1873) On the anatomical and physiological localization of movements in the brain. In Selected Writings of John Hughlings Jackson (ed. J. Taylor, 1958). London: Staples Press. —— (1882) Localised convulsions from tumour of the brain. Brain, 5, 364. —— (1884) Evolution and dissolution of the nervous system (Croonian Lectures). British Medical Journal, i, 591, 660, 703. J ACKSON , S. W. (1994) Catharsis and abreaction in the history of psychological healing. History of Psychiatry, 17, 471–491. J ACOBSON , R. J ACKSON , M. & B ERELOWITZ , M. (1986) Self incineration: a comparison of inpatient suicide attempts. Clinical features and history of self harm. Psychological Medicine, 16, 107–116. J ADRESIC , D. (1992) The role of the amygdaloid complex in Gilles de la Tourette’s Syndrome. British Journal of Psychiatry, 161, 532–534. J AHANSHAHI , M. & M ARSDEN , C. D. (1988) Personality in torticollis: a controlled study. Psychological Medicine, 18, 375–387. J AMES , W. (1890) Principles of Psychology. New York: Henry Holt. J ANET , P. (1886) Les actes inconscients et les dédoublements de la personnalité pendant le somnambulisme provoqué. Review Philosophique, 22, 577–592. —— (1887) L’Anesthésie systematisée. Revue Philosophique, 23, 449–472. —— (1888) Les actes inconscients et la mémoire. Révue Philosophique, 25, 238–279. —— (1889) L’Automatisme psychologique. Paris: Alcan. —— (1892) L’Anesthésie hystérique. Archives de Neurologie, 69–70. —— (1894) L’État mental des hystériques. Paris: Rueff. —— (1901) The Mental State of Hystericals (trans. C. R. Corson). New York: G. P. Putnam’s Sons. —— (1907) The Major Symptoms of Hysteria. New York: Macmillan. —— (1908) Les obsessions et la psychasthénie. Paris: Felix Alcan. —— (1919) Les névroses. Paris: Ernest Flammarion. —— (1913) L’Automatisme Psychologique (7th edn). Paris: Alcan. —— (1925) Psychological Healing. A Historical and Clinical Study (trans. E. & C. Paul). London: Allen & Unwin. J ANET , J. (1888) L’hystérie et l’hypnotisme d’après la théorie de la double personnalité. Révue Scientifique, 41, 616–623. J ANOFSKY , J. S. (1986) Münchausen’s syndrome in a mother and daughter: an unusual presentation of folie à deux. Journal of Nervous and Mental Disease, 174, 368–370. J ARCHO , S. (1966) Harlow Brooks on neurocirculatory asthenia in World War I. American Journal of Cardiology, 18, 892–897. J ASPERS , K. (1913) General Psychopathology (7th edn) (trans. J. Hoenig & M. W. Hamilton, 1963). Manchester: Manchester University Press. J EFFERSON , J. W. & O CHITILL , H. (1982) Factitious disorders. In Treatment of Mental Disorders (eds J. H. Greist, J. W. Jefferson, R. L. Spitzer). New York: Oxford University Press. J OHNSON , L. B. & P ROSKAUER , S. (1974) Hysterical psychosis in a prepubescent Navajo girl. Journal of American Academy of Child Psychiatry, 13, 1–19. J OHNSON , E. H. & B RITT , B. (1967) Self-Mutilation in Prisons: Interactions of Stress and Social Structures. Carbondale. Cit. Yaroshevsky (1975). J ONES , A. B. & L LEWELLYN , L. J. (1917) Malingering: On the Simulation of Disease. London: Heinemann.
442
References
JONES, E. (1910) The action of suggestion in psychotherapy. Journal of Abnormal and Social Psychology. Reprinted in Papers on Psychoanalysis (1913). New York: William Wood & Co. —— (1953) Sigmund Freud: His Life and Work, vols. I–III. London: Hogarth Press. J ORDAN , B. T. & B UTLER , J. R. (1967) G. S. R. as a measure of the sexual component in hysteria. Journal of Psychology, 67, 211–219. —— & K EMPLER , B. (1970) Hysterical personality: an experimental investigation of sexrole conflict. Journal of Abnormal Psychology, 75, 172–176. J ORDEN , E. (1603) A Breife Discourse of a Disease Called the Suffocation of the Mother. London. (Reprinted in MacDonald M. (1991) Witchcraft and Hysteria in Elizabethan London. London: Tavistock.) J OURNAL OF THE A MERICAN M EDICAL A SSOCIATION (1917) Berlin letter. Journal of the American Medical Association, 647–648. J OWETT, B. (1953) The Dialogues of Plato Translated into English with Analyses and Introductions (4th edn). Oxford: Clarendon Press. J OYCE , C. R. B. (1959) Consistent differences in individual reactions to drugs and dummies. British Journal of Pharmacology, 14, 512–521. K AGWA , B. H. (1964) The problem of mass hysteria in East Africa. East African Medical Journal, 41, 560–566. K AHLBAUM , K. (1874) Die Katatonie. Berlin: Hirschwald. K ANE , A. & C ARLSON , E. T. (1982) A different drummer: Robert B. Carter and nineteenth century hysteria. Bulletin of the New York Academy of Medicine, 58, 519–534. K ANZER , M. (1940) Amnesia: a statistical study. American Journal of Psychiatry, 96, 711–716. K APUR , N. (1991) Amnesia in relation to fugue states – distinguishing a neurological from the psychogenic state basis, British Journal of Psychiatry, 159, 872–877. K APUR , R. L. & P ANDURANGI , A. K. (1979) A comparative study of reactive psychosis and acute psychosis without precipitating stress. British Journal of Psychiatry, 135, 544–550. K ARDINER , A. (1939) The Individual and His Society. New York: Columbia University Press. K ATHOL , R. G., C OX , T. A., C ORBETT , J. J., et al (1983a) Functional visual loss: I. A true psychiatric disorder? Psychological Medicine, 13, 307–314. ——, ——, ——, et al (1983b) Functional visual loss: II. Psychiatric aspects in 42 patients followed for 4 years. Psychological Medicine, 13, 315–324. K ATON , W. (1993) Somatization: The path between distress and somatic symptoms. American Pain Society Journal, 2, 141–149. ——, R IES , R. D. & K LEINMAN , A. (1984a) The prevalence of somatization in primary care. Comprehensive Psychiatry, 25, 208–215. ——, —— & —— (1984b) Part II: a prospective DSM–III study of 100 consecutive somatization patients. Comprehensive Psychiatry, 25, 305–134. K ATZENELBOGEN , S. (1942) Hypochondriacal complaints with special reference to personality and environment. American Journal of Psychiatry, 98, 815–822. KAY, D. W. K. & LEIGH, A. D. (1954) The natural history, treatment and progress of anorexia nervosa based on a study of 38 patients. Journal of Mental Science, 100, 411–431. K EEGAN , J. (1976) The Face of Battle. London: Jonathan Cape. K EISER , L. (1968) The Traumatic Neurosis. Philadelphia: Lippincott. K ELLY , R. E. & S MITH , B. N. (1981) Post-traumatic syndrome: another myth discredited. Journal of the Royal Society of Medicine, 74, 275–277. K ELLNER , R. (1986) Somatization and Hypochondriasis. New York: Praeger Publishers. —— (1990) Somatization theories and research. Journal of Nervous and Mental Disease, 178, 150–160. ——, S LOCUMB , J., W IGGINS , R. G., et al (1985) Hostility, somatic symptoms, and hypochondriacal fears and beliefs. Journal of Nervous and Mental Disease, 173, 554–560. K ENDALL , E. M. & JENKINS , P. L. (1987) Koro in an American man. American Journal of Psychiatry, 144, 12.
References
443
K ENDELL , R. E. (1967) The psychiatric sequelae of benign myalgic encephalomyelitis. British Journal of Psychiatry, 113, 833–840. —— (1975) The concept of disease and its implications for psychiatry. British Journal of Psychiatry, 127, 305–315. KENNEDY, A. & NEVILLE , J. (1957) Sudden loss of memory. British Medical Journal, ii, 428–433. K ENNEDY , F. (1946) The mind of the injured worker. Its effect on disability periods. Compensation Medicine, 119–124. K ENNY , M. G. (1986) The Passion of Ansel Bourne. Washington: Smithsonian Institute. K ENYON , F. E. (1964) Hypochondriasis. A clinical study. British Journal of Psychiatry, 110, 478–488. —— (1965) Hypochondriasis: a survey of some historical, clinical and social aspects. British Journal of Medical Psychology, 38, 117–133. —— (1976) Hypochondriacal states. British Journal of Psychiatry, 129, 1–14. K ERCKHOFF , A. & B ACK , K. W. (1968) The June Bug: A Study of Hysterical Contagion. New York: Appleton Century Crofts. K ERNBERG , O. (1967) Borderline personality organization. Journal of the American Psychoanalytical Association, 15, 641–685. —— (1970) A psychoanalytic classification of character pathology. Journal of the American Psychoanalytical Association, 18, 800–822. K ESSEL , N. (1965) Self-poisoning. British Medical Journal, ii, 1265–1270, 1336–1340. K ESSELL , W. I. N. (1960) Psychiatric morbidity in a London general practice. British Journal of Preventive and Social Medicine, 14, 16–22. K EYES , D. (1981) The Minds of Billy Milligan. New York: Random House. KIHLSTROM, J. F. (1994) One hundred years of hysteria. In Dissociation: Clinical and Theoretical Perspectives (eds S. J. Lynn & J. W. Rhue), pp. 365–394. New York: Guilford Press. K ING , H. (1994) Once upon a text: the Hippocratic origins of hysteria. In Hysteria in Western Civilization (eds S. Gilman, H. King, R. Porter, et al), pp. 3–90. Berkeley: University of California Press. K INSEY , A. C., P OMEROY , W. B., M ARTIN , C. E., et al (1953) Sexual Behaviour in the Human Female. Philadelphia: Saunders. K INSTON , W. & R OSSER , R. (1974) Disaster: effects on mental and physical state. Journal of Psychosomatic Research, 18, 437–456. K IRMAYER , L. J. (1984) Overview: culture, affect and somatization. Part II. Transcultural Psychiatry Research Reviews, 21, 237–262. —— (1986) Somatization and the social construction of illness experience. In Illness Behaviour: A Multidisciplinary Perspective (eds S. McHugh & T. M. Vallis), pp. 111–123. New York: Plenum Press. —— (1994) Pacing the void: social and cultural dimensions of dissociation. In Dissociation: Culture, Mind and Body (ed. D. Spiegel), pp. 91–122. Washington, DC: American Psychiatric Press. —— & R OBBINS , J. M. (1991) Introduction: concepts of somatization. In Current Concepts of Somatization: Research and Clinical Perspective (eds L. J. Kirmayer & J. M. Robbins), pp. 1–19. Washington, DC: American Psychiatric Press. —— & —— (1991) Three forms of somatization in primary care: prevalence, cooccurrence, and sociodemographic characteristics. Journal of Nervous and Mental Disease, 179, 647–655. K LEIN , M. (1950) Contributions to Psycho-Analysis 1921–1945. London: Hogarth Press. K LEINMAN , A. & K LEINMAN , J. (1985) Somatization: the interconnections in Chinese society among culture, depressive experiences and the meaning of pain. In Culture and Depression (eds A. Kleinman & B. Good). Berkeley: University of California Press. K LERMAN , G. L. (1990) The psychiatric patient’s right to effective treatment: Implications of Osheroff, the Chestnut Lodge. American Journal of Psychiatry, 147, 409–418.
444
References
K LIGERMAN , M. J. & M CK EGNEY , F. P. (1971) Patterns of psychiatric consultation in two general hospitals. Psychiatric Medicine, 2, 126–132. K LUFT , R. P. (1982) Varieties of hypnotic intervention in the treatment of multiple personality. American Journal of Clinical Hypnosis, 24, 230–240. —— (1984) Treatment of multiple personality disorder. A study of 33 cases. Psychiatric Clinics of North America, 7, 9–29. —— (1985a) The natural history of multiple personality disorder. In Childhood Antecedents of Multiple Personality (ed. R. P. Kluft), pp. 198–238. Washington DC: American Psychiatric Press. —— (1985b) Making the diagnosis of multiple personality disorder, Lesson 23. Directions in Psychiatry, 5, 1–11. –––– (1988) The phenomenology and treatment of extremely complex multiple personality disorder. Dissociation, 1, 47–58. —— (1991) Clinical presentations of multiple personality disorder. Psychiatric Clinics of North America, 14, 605–629. K NOWLES , F. W. (1963) Hypnotherapy in chronic hysterical urinary retention. New Zealand Medical Journal, 63, 38–40. K OMAROFF , A. L. (1993) Clinical presentation of chronic fatigue. In Chronic Fatigue Syndrome (eds G. R. Bock & J. Whelan), pp. 43–53 (Ciba Foundation Symposium, 173). Chichester: John Wiley & Sons. K RAEPELIN , E. (1904) Hysterical insanity. In Lectures on Clinical Psychiatry (trans. T. Johnstone). New York: William Wood & Co. K RAL , V. A. (1951) Psychiatric observations under severe chronic stress. American Journal of Psychiatry, 108, 185–192. K RAMER -G INSBERG , E., G REENWALD, B. S., A ISEN , P. S., et al (1989) Hypochondriasis in the elderly depressed. Journal of the American Geriatric Society, 37, 507–510. K RÄUPL -T AYLOR , R. (1969) Prokaletic measures derived from psycho-analytic technique. British Journal of Psychiatry, 115, 407–419. K REITMAN , N., P HILIP , A. E., G REER , S., et al (1969) Parasuicide. British Journal of Psychiatry, 115, 746–747. ––––, S AINSBURY , P., P EARCE , K., et al (1965) Hypochondriasis and depression in outpatients at a general hospital. British Journal of Psychiatry, 111, 607–615. K RETSCHMER , E. (1926) Hysteria: Reflex and Instinct. London: Peter Owen. —— (1948) Hysteria, Reflex and Instinct (trans. V. & W. Baskin, 1961). London: Peter Owen. K RIEGER , M. J. & Z USSMAN , M. (1981) The importance of cultural factors in a brief reactive psychosis. Journal of Clinical Psychiatry, 42, 248–249. KRILL , A. E. (1967) Retinal function studies in hysterical amblyopia. A unique abnormality of dark adaption. American Journal of Ophthalmology, 63, 230–237. K ROENKE , K. & M ANGELSDORFF , A. D. (1989) Common symptoms in ambulatory care. American Journal of Medicine, 86, 262–266. ––––, W OOD , D. R., M ANGELSDORFF , A. D., et al (1988) Chronic fatigue in primary care; prevalence, patient characteristics and outcome. Journal of the American Medical Association, 260, 929–934. K ROGER , W. S. & F EZLER , W. D. (1976) Hypnosis and Behaviour Modification: Imagery Conditioning. Philadelphia: J. B. Lippincott Co. K UCH , K., E VANS , R. J., W ATSON , C. P., et al (1991a) Road vehicle accidents and phobias in 60 patients with fibromyalgia. Journal of Anxiety Disorders, 5, 273–280. ——, ——, ——, et al (1991b) Accidents and chronic myofascial pain. Pain Clinic, 4, 79–86. K UMAR H. V. & M OLONEY , E. (1988) Koro secondary to a tumour of the corpus callosum. British Journal of Psychiatry, 153, 251–254. K UNKLE , E. C. (1966) The ‘Jumpers’ of Maine – a reappraisal. Transcripts of the American Neurological Association, 91, 275–277.
References
445
K UZNETSOV , E. (1975) Prison Diaries. London: Vallentine Mitchell. L A B ARRE (1975) Anthropological perspectives on hallucinations and hallucinogens. In Hallucinations: Experience and Theory (eds. R. K. Siegel & L. J. West). New York: Wiley. L ADEE , G. A. (1966) Hypochondriacal Syndromes. Amsterdam: Elsevier. L ADER, M. & S ARTORIUS , N. (1968) Anxiety in patients with hysterical conversion symptoms. Journal of Neurology, Neurosurgery and Psychiatry, 31, 490–495. L AF ONTAINE , J. S. (1994) The Extent and Nature of Organized and Ritual Abuse: Research Findings. London: Department of Health. Her Majesty’s Stationery Office. L AMBO , T. A. (1956) Neuropsychiatric problems in Nigeria. British Medical Journal, ii, 1388–1394. L ANCET (1916) A discussion of shell shock. Lancet, i, 306–307. —— (1991) Neurological conversion disorders in childhood. Lancet, 337, 889. —— (1992) Psychogenic vomiting – a disorder of gastrointestinal motility? Lancet, 339, 279. L ANDAY , A. L. JESSOP , C. & L ENNETTE , E. T., et al (1991) Chronic fatigue syndrome: clinical condition associated with immune activation. Lancet, 338, 707–712. L ANDOUZY , H. (1846) Traité complet de l hystérie. Paris: Baillière. L ANGFELDT , G. (1937) The prognosis in schizophrenia and the factors influencing the course of the disease. Acta Psychiatrica et Neurologica Scandinavica (suppl. 13). —— (1956) The prognosis in schizophrenia. Acta Psychiatrica Neurologica Scandinavica (suppl. 31), 110. L ANGNESS , L. L. (1965) Hysterical psychosis in the New Guinea highlands. A Bena Bena example. Psychiatry, 28, 258–277. L ANGWORTHY , O. R. & L EGRAND , D. (1952) Personality structure and psychotherapy in multiple sclerosis. American Journal of Medicine, 12, 586–592. L ASÈGUE , C. & F ALRET , J. (1887) La folie à deux (ou folie communiquée). Annales MedicoPsychologiques, 18, 321–55. (Trans. Michaud, R. (1964) American Journal of Psychiatry, 121 (suppl.).) L AWTON , F. (1969) An English judge’s view of some medical problems to be met in the courts. In The Late Effects of Head Injury (eds A. E. Walker, W. F. Caveness & M. Critchley), pp. 431–438. Springfield: C. C. Thomas. L AZARE , A. (1971) The hysterical character in psychoanalytic theory. Archives of General Psychiatry, 25, 131–137. ——, K LERMAN , G. L. & A RMOR , D. J. (1966) Oral, obsessive and hysterical personality patterns. Archives of General Psychiatry, 14, 624–630. —— & —— (1968) Hysteria and depression: the frequency and significance of hysterical personality features in hospitalized depressed women. American Journal of Psychiatry, 124, 48–56. ——, —— & A RMOR , D. J. (1970) Oral-obsessive and hysterical personality patterns. Replication of factor analysis in an independent sample. Journal of Psychiatric Research, 7, 275–290. L EEMAN , C. P. ( 1965) Acute dystonic reactions to small doses of prochlorperazine. Three cases misdiagnosed as hysteria. Journal of the American Medical Association, 193, 839– 840. L EGUÉ , G. & DE LA T OURETTE , G. (1886) Soeur Jeanne des Anges. Supérieure des Ursulines du Loudun (XVIIe siecle). Autobiographie d’une Hystérique Possédée. Paris: Delahaye & Lecrosnier. L EHMANN , H. E. (1975) Unusual psychiatric disorders and atypical psychoses. In Comprehensive Textbook of Psychiatry (2nd edn) (eds A. Freedman, H. I. Kaplan & B. J. Sadock). Baltimore: Williams & Wilkins. L EHMKUHL , G., B LANZ , B., L EHMKUHL , U., et al (1989) Conversion disorder (DSM–III 300. 11): symptomatology and course in childhood and adolescence. European Archives of Psychiatry and Neurological Science, 238, 155–160.
446
References
L EHTINEN , V. & P UHAKKA , H. (1976) A psychosomatic approach to the globus hystericus syndrome. Acta Psychiatrica Neurologica Scandinavica, 53, 21–28. L ÉPINE , J. (1919) Mental Disorders of War (ed. C. A. Mercier). London: University of London Press. L ERNER , H. E. (1974) The hysterical personality: a ‘woman’s disease’. Comprehensive Psychiatry, 15, 157–164. L ESLIE , S. A. (1988) Diagnosis and treatment of hysterical conversion reactions. Archives of Disease in Children, 63, 506–511. L EVINE , H. S., E ISENBERG , H. M. & B ENTON , A. L. (1989) Mild Head Injury. New York: Oxford University Press. L EVINE , R. J., S EXTON , D. J., R OMM , F. J., et al (1974) Outbreak of psychosomatic illness at a rural elementary school. Lancet, ii, 1500–1503. LEVY , D. M. (1932) Body interest in children and hypochondriasis. American Journal of Psychiatry, 89, 295–315. L EVY , R. & M USHIN , J. (1973) The somatosensory evoked response in patients with hysterical anaesthesia. Journal of Psychosomatic Research, 17, 81–84. L EWIS , A. J. (1950) Psychological medicine. In A Textbook of the Practice of Medicine (8th edn) (ed. F. W. Price). London: Oxford Medical Publications. —— (1953) Hysterical dissociation in dementia paralytica. Monatschrift Psychiatrie Neurologie, 125, 589–604. —— (1961) Amnesic syndromes: the psychopathological aspect. Proceedings of the Royal Society of Medicine, 54, 955–961. —— (1975) The survival of hysteria. Psychological Medicine, 5, 9–12. L EWIS , T. (1918) The Soldier’s Heart and the Effort Syndrome (2nd edn, 1940). London: Shaw & Sons. L EWIS , W. C. (1974) Hysteria: the consultant’s dilemma. Twentieth-century demonology, pejorative epithet, or useful diagnosis? Archives of General Psychiatry, 30, 145–151. —— & B ERMAN , M. (1965) Studies of conversion hysteria: I. operational study of diagnosis. Archives of General Psychiatry, 13, 275–282. L IBERINI , P., F AGLIA , L. & S ALVI , F. (1993) Cognitive impairment related to conversion disorder: a two year follow-up study. Journal of Nervous and Mental Disease, 181, 325– 327. L IEBALDT, S. & KLAGES , W. (1961) Morphologische Befunde bei einer ‘Isolierten chronische taktilen Dermatozoenhalluzinose’. Nervenarzt, 32, 157–171. L ILIENFELD , S. O. (1992) The association between antisocial personality and somatization disorders: a review and integration of theoretical models. Clinical Psychology Review, 12, 641–662. LINDBERG, B. (1950) Psycho-infantilism. Acta Psychiatrica Neurologiva Scandinavica (suppl. 61). –––– & L INDEGARD , B. (1963) Studies of the hysteroid personality attitude. Acta Psychiatrica Scandinavica, 39, 170–179. L IPOWSKI , Z. J. (1968) Review of consultation liaison psychiatry and psychosomatic medicine. (3) Theoretical issues. Psychosomatic Medicine, 30, 395–422. —— (1988) Somatization: the concept and its clinical application. American Journal of Psychiatry, 145, 1358–1368. —— & LINDEGARD , B. (1963) Studies of the hysteroid personality attitude. Acta Psychiatrica Scandinavica, 39, 170–179. —— & K IRIAKOS , R. Z. (1972) Borderlands between neurology and psychiatry: observations in a neurological hospital. Psychiatric Medicine, 3, 131–147. L IPTON , S. (1943) Dissociated personality: a case report. Psychiatric Quarterly, 17, 35–56. L ISHMAN , W. A. (1968) Brain damage in relation to psychiatric disability after head injury. British Journal of Psychiatry, 114, 373–410. L ISKOW , B., O THMER , E., P ENICK , E. C., et al (1986) Is Briquet’s syndrome a heterogenous disorder? American Journal of Medicine, 143, 626–629.
References
447
L ISS , J. L., W ELNER , A. & R OBINS , E. (1973) Personality disorder, Part 1. Record study. British Journal of Psychiatry, 123, 685–692. L ITTLEJOHN, G. O. (1986) Repetitive strain syndrome: An Australian experience (Editorial). Journal of Rheumatology, 136, 1004–1006. L ITTRÉ , E. (1839–61) Oeuvres complètes d’Hippocrate. Paris: J. B. Baillière. L IVESLEY , W. J. & J ACKSON , D. N. (1991) Construct validity and classification of personality disorders. In Personality Disorder: New Perspectives on Diagnostic Validity (ed. J. M. Oldham). Washington, DC: American Psychiatric Press. L JUNGBERG , L. (1957) Hysteria. Acta Psychiatrica Scandinavica (suppl. 112). L LOYD , A. R., H ICKIE , I., B OUGHTON , C. R., et al (1990) Prevalence of chronic fatigue syndrome in an Australian population. Medical Journal of Australia, 153, 522–528. ——, W AKEFIELD , D. & H ICKIE , I. (1993) Immunity and the pathophysiology of chronic fatigue syndrome. In Chronic Fatigue Syndrome (eds G. R. Bock & J. Whelan), pp. 176– 187 (Ciba Foundation Symposium, 173). Chichester: John Wiley & Sons. L LOYD , K. G. & H ORNYKIEWICZ , O. (1973) L-glutamic acid decarboxylase in Parkinson’s disease: Effect of L-dopa therapy. Nature, 243, 521–523. L OFTUS , E. F. (1993) The reality of repressed memories. American Psychology, 48, 518–537. —— & K ETCHAM , K. (1991) Witness for the Defense. New York: St Martin’s Press. —— & —— (1994) The Myth of Repressed Memory: False Memories and Allegations of Sexual Abuse. New York: St Martin’s Press. L ONG , N., C HAMBERLAIN , K. & V INCENT , C. (1994) Effect of the Gulf War on reactivation of adverse combat-related memories in Vietnam veterans. Journal of Clinical Psychology, 50, 138–144. L ONIGAN , C. J., S HANNON , M. P., T AYLOR , C. M., et al (1994) Children exposed to disaster: II. Risk factors for the development of post-traumatic symptomatology. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 94–105. L OOFF , D. H. (1970) Psychophysiologic and conversion reactions in children. Journal of American Academy of Childhood Psychiatry, 9, 318–331. L OVE , A. W. & PECK , C. L. (1987) The MMPI and psychological factors in chronic low back pain: a review. Pain, 28, 1–12. L OW -B EER , G. A. (1972) Book review of Matussek et al (1971). Psychological Medicine, 2, 89–92. L UDWIG , A. M. (1972) Hysteria – a neurobiological theory. Archives of General Psychiatry, 27, 771–777. L UISADA , P. V., P EELE , R. & P ITTARD , E. A. (1974) The hysterical personality in men. American Journal of Psychiatry, 131, 518–522. L UM , L. C. (1981) Hyperventilation and anxiety states. Journal of the Royal Society of Medicine, 74, 1–4. L YNN , S. J. & R HUE , J. W. (1994) Dissociation: Clinical and Therapeutic Perspectives. New York: Guilford. L YONS , H. A. & P OTTER , P. E. (1970) Communicated hysteria – an episode in a secondary school. Journal of the Irish Medical Association, 63, 377–379. M AC A LPINE , I. & R OSS , J. (1956) Oedème bleu. Lancet, i, 78–81. M AC C URDY , J. T. (1918) War Neuroses. Cambridge: Cambridge University Press. M AC D ONALD , M. (1991) Witchcraft Hysteria in Elizabethan London: Edward Jorden and the Mary Glover Case. London: Tavistock. M ACE , C. A., R ON , M. & D EAHL , M. (1988) Is globus hystericus? British Journal of Psychiatry 153, 727. (Response by I. J. Dreary & J. A. Wilson, pp. 727–728.) M ACE , C. J. (1992a) Hysterical conversion I: A history. British Journal of Psychiatry, 161, 369–377. —— (1992b) Hysterical conversion II: A critique. British Journal of Psychiatry, 161, 378– 389.
448
References
M AC N AB I. (1964) Acceleration injuries of the cervical spine. Journal of Bone and Joint Surgery, 46A, 1797–1799. M ACPHERSON , W. G., H ERRINGHAM , W. P., E LLIOTT , T. R., et al (1923) History of the Great War medical services. Diseases of War, Vol. II. London: HMSO. —— (1973) The whiplash syndrome. Clinical Neurosurgery, 20, 232–241. M ADISON , D. C. (1953) A case of double personality. Medical Journal of Australia, 1, 814– 816. M AGNI , G. (1987) On the relationship between chronic pain and depression when there is no organic lesion. Pain, 31, 1–21. ––––, ROSSI , M. R., RIGATTI -L UCHINI, S., et al (1992) Chronic abdominal pain and depression. Epidemiologic findings in the United States Hispanic Health and Nutrition Examination Survey. Pain, 49, 77–85. M AI , F. (1982) The forgotten avant-garde. Trends in the Neurosciences, 5, 67–68. —— (1992) Multiple Personality Disorder: A Debate. Presented at Canadian Psychiatric Association 42nd Annual Meeting, Montreal, 15–18 September. –––– (1995) Psychiatrists’ attitudes to multiple personality disorder: a questionnaire study. Canadian Journal of Psychiatry, 40, 154–157. —— & M ERSKEY , H. (1980a) Briquet’s concept of hysteria: an historical perspective. Canadian Journal of Psychiatry, 26, 57–63. —— & —— (1980b) Briquet’s “Treatise on Hysteria”: A synopsis and commentary. Archives of General Psychiatry, 37, 1401–1405. M AJERUS , P. W., G UZE , S. B., D ELONG , W. B., et al (1960) Psychologic factors and psychiatric disease in hyperemesis gravidarum: a follow-up study of 69 vomiters and 66 controls. American Journal of Psychiatry, 117, 421–426. M ALAN , D. H. (1963) A Study of Brief Psychotherapy. London: Tavistock Publications. M ALCOLMSON , K. G. (1966) Radiological findings in globus hystericus. British Journal of Radiology, 39, 583–586. —— (1968) Globus hystericus vel pharyngis: a reconnaissance of proximal vagal modalities. Journal of Laryngology and Otology, 82, 219–230. M ALLET , B. L. & G OLD , S. (1964) A pseudoschizophrenic hysterical syndrome. British Journal of Medical Psychology, 37, 59–70. M ALMO , R. D., B OAG , T. J. & R AGINSKY , B. R. (1954) Electro-myographic study of human deafness. Journal of Clinical and Experimental Hypnosis in Psychopathology (eds C. F. Reed, I. E. Alexander & S. S. Tomkins, 1964) Harvard: Harvard University Press. M ALMQULST , C. P. (1971) Hysteria in childhood. Postgraduate Medicine, 50, 112–117. M ANDEVILLE , B. A (1730) Treatise of the Hypochondriack and Hysterick Diseases in Three Dialogues, 2nd Edition. London: J. Tonson. M ANN , A. (1994) A real occupational illness.... British Medical Journal, 308, 269. M ARCHANT , B. & B ROWN , J. (1990) Münchausen’s meningitis. Journal of the Royal Society of Medicine, 83, 532–533. M ARGHERITA , G., M ASTROSIMONE , F. & P OZZL , O. (1967) The association of hysterical behaviour with irritative electroencephalographic foci in the temporal region. Rassegna Di Neuropsichiatria E Scienze Affini, 21, 185–190. M ANU , P., L ANE , T. J. & M ATTHEWS , D. A. (1993) Chronic fatigue and chronic fatigue syndrome. Clinical epidemiology and aetiological classification. In Chronic Fatigue Syndrome (eds G. R. Bock & J. Whelan), pp. 23–42. Ciba Symposium No. 173. Chichester: Wiley. M ARMOR , J. (1953) Orality in the hysterical personality. Journal of the American Psychoanalytical Association, 1, 656–671. M ARRON , K. (1989) Ritual Abuse. Toronto: McClelland-Bantam Inc. M ARSDEN, C. D. (1986) Hysteria – a neurologist’s view. Psychological Medicine, 16, 277–288. M ARSHALL , H. E. S. (1949) The incidence of physical disorders among psychiatric inpatients. British Journal of Psychiatry, 468–469.
References
449
M ATUSSEK , P., G RIGAT , R., H AIBOCK , H., et al (1971) Die Konzentrationslagerhaft Und Ihre Folgen. Berlin: Springer. M AYER -G ROSS , W., S LATER , E. T. O. & R OTH , M. (1954) Clinical Psychiatry. London: Cassell. ——, —— & —— (1977) Clinical Psychiatry (3rd edn). London: Bailliere, Tindall. M AYO , T. (1845) Case of double consciousness. London Medical Gazette, New Series 1, 1202– 1203. M AYOU , R. (1989) The history of general hospital psychiatry. British Journal of Psychiatry, 155, 746–776. —— (1976) The nature of bodily symptoms. British Journal of Psychiatry, 129, 55–60. M CD OUGALL , W. (1948) An Outline of Abnormal Psychology (6th edn). London: Methuen. M CE VEDY , C. P. (1963) Self-lnflicted Injuries. University of London: Dissertation For Academic DPM. —— & B EARD , A. W. (1970a) Royal Free epidemic of 1955: a reconsideration. British Medical Journal, i, 7–11. —— & —— (1970b) Concept of benign myalgic encephalomyelitis. British Medical Journal, i, 11–15. ——, G RIFFITH , A. & H ALL , T. (1966) Two school epidemics. British Medical Journal, ii, 1300–1302. M CF ARLANE , A. C. & P APAY , P. (1992) Multiple diagnoses in post traumatic stress disorder in the victims of a natural disaster. Journal of Mental Disorders, 180, 498–504. M C H UGH , P. R. (1992) Psychiatric misadventures. American Scholar, 497–510. —— & S LAVNEY , P. R. (1983) The Perspectives of Psychiatry. Baltimore: Johns Hopkins University Press. M C K EGNEY , F. P. (1967) The incidence and characteristics of patients with conversion reactions: I: A general hospital consultation service sample. American Journal of Psychiatry, 124, 542–545. M C K ELLAR , P. (1979) Mindsplit. London: Dent. M CK ERRACHER , D. W., L OUGHNANE, T. & W ATSON , R. A. (1968) Self-mutilation in female psychopaths. British Journal of Psychiatry, 114, 829–832. M C K INLAY , I. (1986) Münchausen’s syndrome by proxy. British Medical Journal, 293, 1308. M CK INNEY , K. A. & L ANGE, M. M. (1983) Familial fugue – a case report. Canadian Journal of Psychiatry, 28, 654–656. M EADOW , R. (1977) Münchausen’s syndrome by proxy. The hinterland of child abuse. Lancet, ii, 343–345. —— (1989) Münchausen’s syndrome by proxy. British Medical Journal, 299, 248–250. —— & L ENNERT , T. (1984) Münchausen by proxy or Polle syndrome: Which term is correct? Pediatrics, 72, 554–556. M EADOWS , S. P. (1969) Retrobulbar and optic neuritis in childhood and adolescence. Transactions of the Ophthalmological Society, 139, 603–608. M EANS , R., M IGAM , A., Z ARROW , M., et al (1989) Autobiographical memory for healthrelated events. National Center for Health Statistics, Publication No. 89-1077, pp. 1–2. Hyattsville, MD: US Department of Health Services. M ECHANIC , D. (1962) The concept of illness behaviour. Journal of Chronic Disorder, 15, 189–194. M EEHL , P. E. (1956) The dynamics of ‘Structured Personality Tests’. Article 1. In Psychology and Medicine (eds G. G. Welsh & W. G. Dahlstrom). Minneapolis: University of Minnesota Press. MELZACK, R., KATZ, J. & JEANS, M. E. (1985) The role of compensation in chronic pain: analysis using a new method of scoring the McGill Pain Questionnaire. Pain, 23, 101–112. MENDELSON , G. (1982) Not “cured by a verdict”. Effect of legal settlement on compensation claimants. Medical Journal of Australia, ii, 219–230. —— (1993) Compensation and motivation in relation to musculoskeletal pain. In Progress in Fibromyalgia and Myofascial Pain (eds H. Vaeroy & H. Merskey). Amsterdam: Elsevier.
450
References
M ENNINGER , K. A. (1938) Man Against Himself. New York: Harcourt & Brace. M ERRINGTON , W. R. (1976) University College Hospital and its Medical School: A History. London: Heinemann. M ERSKEY , H. (1965a) The characteristics of persistent pain in psychological illness. Journal of Psychosomatic Research, 9, 291–298. —— (1965b) Psychiatric patients with persistent pain. Journal of Psychosomatic Research, 9, 299–309. —— (1968) Psychological aspects of pain. Postgraduate Medical Journal, 44, 297–306. —— (1971) An appraisal of hypnosis. Postgraduate Medical Journal, 47, 572–580. —— (1974) A case of multiple tics with vocalisation (partial syndrome of Gilles de la Tourette) and XYY karyotype. British Journal of Psychiatry, 125, 593–594. —— (1975) The mode of action of organic lesions in promoting hysteria. British Journal of Medical Psychology, 48, 373. —— (1980) Psychiatric Illness (3rd edn). London: Baillière. —— (1983) Hysteria: The history of an idea. Canadian Journal of Psychiatry, 28, 428–433. —— (1986) Variable meanings for the definition of disease. Journal of Medicine and Philosophy, 11, 215–232. —— (1989) Current perspectives: psychiatry and chronic pain. Canadian Journal of Psychiatry, 34, 329–336. –––– (1991) “Shell Shock”. In 150 Years of British Psychiatry. 1841–1991. (eds G. E. Berrios & H. L. Freeman), pp. 245–267. London: Gaskell. —— (1992a) The manufacture of personalities. The production of multiple personality disorder. British Journal of Psychiatry, 160, 327–340. —— (1992b) Anna O. had a severe depressive illness. British Journal of Psychiatry, 161, 185–194. —— (1992c) Correspondence, author’s reply to letters by Fahy and Chande concerning multiple personality disorder. British Journal of Psychiatry, 161, 269–270. —— (1993) Professional and lay opinions on multiple personality disorder. British Journal of Psychiatry, 162, 271. —— (1994) Conversion fits, pseudo-attacks or doxogenic seizures. General Hospital Psychiatry, 16, 246–247. —— & S PEAR , F. G. (1967) Pain: Psychological and Psychiatric Aspects. London: Baillière Tindall. —— & W OODFORDE , J. M. (1972) Psychiatric sequelae of minor head injury. Brain, 95, 521–528. —— & T ONGE , W. L. (1974) Psychiatric lllness (2nd edn). London: Baillière Tindall. —— & B UHRICH , N. A. (1975) Hysteria and organic brain disease. British Journal of Medical Psychology, 48, 359–366. —— & T RIMBLE , M. (1978) Personality, sexual adjustment and brain lesions in patients with conversion symptoms. American Journal of Psychiatry, 136, 179–192. —— & B OYD , D. B. (1978) Emotional adjustment and chronic pain. Pain, 5, 173–178. ——, B ROWN , A., B ROWN , J., et al (1985) Psychological normality and abnormality in persistent headache patients. Pain, 35–47. ——, L AU , C. L., R USSELL , E. S., et al (1987) Screening for psychiatric morbidity. The pattern of psychological illness and premorbid characteristics in four chronic pain populations. Pain, 30, 141–157. —— & P OTTER , P. (1989) The womb lay still in Ancient Egypt. British Journal of Psychiatry, 154, 751–753. —— & M ERSKEY , S. J. (1993) Hysteria or the suffocation of the mother. Canadian Medical Association Journal, 148, 399–405. M ICALE , M. (1989a) Hysteria and its historiography: A review of past and present writings. I. History of Science, 27, 223–261.
References
451
—— (1989b) Hysteria and its historiography: A review of past and present writings. II. History of Science, 27, 319–351. —— (1990a) Hysteria and its historiography. The future perspective. History of Psychiatry, 1, 33–124. —— (1990b) Charcot and the idea of hysteria in the male: gender, mental science and medical diagnosis in late 19th century France. History of Medicine, 34, 363–411. —— (1995) Approaching Hysteria: Disease and its Interpretations. Princeton: Princeton University Press. M ILLER , H. G. (1961) Accident neurosis. British Medical Journal, i, 919–925, 992–998. M ILLER , N. E. (1974) Applications of learning and biofeedback to psychiatry. In Comprehensive Textbook of Psychiatry (2nd edn) (eds A. M. Freedman, H. I. Kaplan & B. J. Sadocks). Baltimore: Williams & Wilkins. —— & B ANUAZIZI , A. (1968) Instrumental learning by curarized rats of a specific visceral response, intestinal or cardiac. Journal of Comparative Physiological Psychology, 65, 1–7. M ILLER , T. W., M ARTIN , W. & S PIRO , D. (1989) Traumatic stress disorder: diagnosis and clinical issues in former prisoners of war. Comprehensive Psychiatry, 3, 139–148. M ILLS , C. K. (1919) Introduction to Shell-shock and Other Neuropsychiatric Problems (E. E. Southard). Boston: W. H. Leonard. M ILNER , A. D. (1985) Psychogenic cough in childhood. British Medical Journal, 290, 1847– 1848. M ITCHELL, D. M., D OYLE , P. M. & S PIRO , S. G. (1985) Münchausen’s syndrome with multiple pulmonary manifestations. Journal of the Royal Society of Medicine, 78, 681–682. M ITCHELL , S. W. (1888) On Mary Reynolds. Transactions of the College of Physicians, Philadelphia, 4 April. M ITCHILL , S. I. (1816) A double consciousness, or a duality of person in the same individual. Medical Repository (New Series), 3, 185–186. M O, K. M., L I , L. S. & O U , L. W. (1987) Report of Koro epidemic in Leizhou Peninsula, Hainan Island, China. Chinese Journal of Neuropsychiatry, 20, 232–234. M ÖBIUS , P. J. (1888) Über den Begriff der Hysterie. Zeitblatt für Nervenkrankheit, 9, 3. Cit. Schiller, F. (1992). M ODAI , I., M UNITZ , H. & A IZENBERG , D. (1986) Koro in an Israeli male. British Journal of Psychiatry, 149, 503–505. M ODESTIN , J. (1992) Multiple personality disorder in Switzerland. American Journal of Psychiatry, 149, 88–92. M OELI , C. (1888) Ueber Irre Verbrecher. Berlin. M OLDOFSKY , H. (1993) Fibromyalgia, sleep disorder and chronic fatigue syndrome. In Chronic Fatigue Syndrome (eds G. R. Bock & J. Whelan), pp. 262–279 (Ciba Foundation Symposium, 173). Chichester: John Wiley & Sons. M OLLICA , R. F., D ONELAN , K., S VANG , T., et al (1993) The effect of trauma and confinement on functional health and mental health status of Cambodians living in Thailand– Cambodia border camps. Journal of the American Medical Association, 270, 581–586. M ORPHEW , J. A. & SIM , M. (1969) Gilles de la Tourette’s syndrome: a clinical and psychopathological study. British Medical Journal of Psychology, 42, 293–301. M ORSIER , G. DE (1936) Les Automatismes visuels. Hallucinations rétrochiasmatiques. Schweizerische Medizinische Wochenschrift, 66, 700–708. M ORTON , D. & W RIGHT , G. (1987) Winning the Second Battle: Canadian Veterans and the Return to Civilian Life. Toronto: University of Toronto Press. M OSS , P. D. & M C E VEDY , C. P. (1966) An epidemic of overbreathing among schoolgirls. British Medical Journal, ii, 1295–1300. M OTT , F. W. (1916a) Special discussion on shellshock without visible signs of injury. Proceedings of the Royal Society of Medicine, Part III (suppl. 9), 1–44. —— (1916b) The effects of high explosives upon the central nervous system. Lancet, ii, 331–338, 441–449, 545–553.
452
References
—— (1917) The microscopic examination of the brains of two men dead of commotio cerebri (shell-shock) without visible external injury. British Medical Journal, ii, 612– 615. —— (1919) War Neuroses and Shell Shock. London: Oxford Medical Publications. M ULDER , R. T. (1991) Personality disorders in New Zealand hospitals. Acta Psychiatrica Scandinavica, 84, 197–202. M ULUKA , E. A. P., D HADPHALE , M. & M WITA , J. M. (1985) Family hysteria in a Kenyan setting. Journal of Nervous and Mental Disease, 173, 249–252. M UN , C. T. (1968) Epidemic koro in Singapore. British Medical Journal, 1, 640–641. M UNRO , A. (1978) Monosymptomatic hypochondriacal psychosis manifesting as delusions of parasitosis. A description of four cases successfully treated with pimozide. Archives of Dermatology, 114, 940–943. —— & C HMARA , J. (1982) Monosymptomatic hypochondriacal psychosis: A diagnostic checklist based on 50 cases of the disorder. Canadian Journal of Psychiatry, 77, 374–376. M URPHY , G. E., R OBINS , E., K UHN , N. O., et al (1962) Stress, sickness and psychiatric disorder in a ‘normal’ population. A study of 101 young women. Journal of Nervous and Mental Disease, 134, 228–236. M URRAY , J. A. H., B RADLEY , H., C RAIGIE , W. A., et al (1986) A New English Dictionary on Historical Principles, Suppl. 4, p. 10. Oxford: Oxford University Press. M URRAY , R. M. (1973) The origins of analgesic nephropathy. British Journal of Psychiatry, 123, 99–106. M YERS , A. T. (1886) The life-history of a case of double or multiple personality. Journal of Mental Science, 31, 596–605. M YERS , C. S. (1915) A contribution to the study of shell shock. Lancet, 1, 316–320. –––– (1940) Shell Shock in France 1914–1918. Cambridge: Cambridge University Press. M YERS , W. H. F. (1903) Human Personality and Its Survival of Bodily Death, vol. 1. London: Longmans Green. M YRHAUG , H. (1983) (Letter) Globus hystericus – occlusal parafunction. Journal of the Royal Society of Medicine, 76, 162. NABER, D., WEINBERGER, D. R., BULLINGER, M., et al (1988) Personality variables, neurological and psychopathological symptoms in patients suffering from spasmodic torticollis. Comprehensive Psychiatry, 29, 182–187. N ANDI , D. N., B ANERJEE , G., N ANDI , S., et al (1992) Is hysteria on the wane? A community survey in West Bengal, India. British Journal of Psychiatry, 160, 87–91. N ASH , M. R., H ULSEY , T. L., S EXTON , M. C., et al (1993) Long term sequelae of childhood sexual abuse: perceived family environment, psychopathology and dissociation. Journal of Clinical and Consulting Psychology, 61, 276–283. N EELEMAN , J. & M ANN , H. (1993) Treatment of hysterical aphonia with hypnosis and prokaletic therapy. British Journal of Psychiatry, 163, 816–819. New Hampshire v. Hungerford, ; New Hampshire v. Morahan (1995), Unreported. (New Hampshire Superior Court). N GUI , P. W. (1969) The koro epidemic in Singapore. Australia & New Zealand Journal of Psychiatry, 3, 263–266. N ICKEL , J. C. (1984) Blunt renal trauma: another ploy in Münchausen’s syndrome. Canadian Medical Association Journal, 130, 349–350. N IEDERMEYER , E., B LUMER , D., HOLSCHER , E., et al (1970) Classical hysterical seizures facilitated by anticonvulsant toxicity. Psychiatric Clinic, Basel, 3, 71–84. NOY, S., NARDI, C. & SOLOMON, Z. (1983) Battle Characteristics and the Prevalence of Combat Psychiatry Casualties: Third International Conference on Psychological Stress and Adjustment in Time of War and Peace, Tel Aviv, Israel, 2–6 January. (Cited in Belenky, C. G. L., Noy, S., Solomon, Z., et al, 1985. Battle stress: the Israeli experience. Military Review, 65, 28–37.) O’N EILL , M. (1965) Validity of Hysterical Personality as a Clinical Category. Emory University: Master’s thesis.
References
453
—— & KEMPLER , B. (1969) Approach and avoidance responses of the hysterical personality to sexual stimuli. Journal of Abnormal Psychology, 74, 300–305. O’S ULLIVAN , G., H ARVEY , I., B ASS , C., et al (1992) Psychophysiological investigation of patients with unilateral symptoms in the hyperventilation syndrome. British Journal of Psychiatry, 160, 664–667. O FFER , D. & B ARGLOW , P. (1960) Adolescent and young adult self-mutilation. Incidents in a general hospital. Archives of General Psychiatry, 3, 194–204. O FSHE , R. & W ATTERS , E. (1994) Making Monsters. False Memories, Psychotherapy, and Sexual Hysteria. New York: Charles Scribner’s Sons. OKASHA , A. (1968) Preliminary psychiatric observations in Egypt. British Journal of Psychiatry, 114, 949– 955. O P DEN V ELDE , W., F ALGER , P. R. J., H OVENS , J. E., et al (1993) Post-traumatic stress disorder in Dutch resistance veterans from World War II. In International Handbook of Stress Syndromes (eds J. P. Wilson & B. Raphael), pp. 219–230. New York: Plenum Press. O PPENHEIM , H. (1889) Die Traumatischen Neurosen. Berlin: Hirschwald. (See Oppenheim, H. (1911) Textbook of Nervous Diseases for Physicains and Students (trans. A. T. N. Bruce). London: Foulis.) O PPENHEIM , J. (1991) “Shattered Nerves”: Doctors, Patients and Depression inVictorian England. New York: Oxford University Press. O PPENHEIMER , D. R. (1968) Microscopic lesions in the brain following head injury. Journal of Neurology, Neurosurgery and Psychiatry, 31, 299–306. O RMEROD , J. A. (1914) Some modern theories concerning hysteria. Lancet, i, 1163–1169, 1233–1239, 1299–1305. O RNE , M. T. & B AUER -M ANLEY , N. K. (1991) Disorder of self: myths, metaphors, and the demand characteristics of treatment. In The Self: Interdisciplinary Approaches (eds J. Strauss & G. R. Goethals), pp. 93–106. New York: Springer-Verlag. O WEN , A. R. G. (1971) Hysteria, Hypnosis and Healing: The Work of J. M. Charcot. London: Dennis Dobson. P AGE , H. W. (1883) Injuries of the Spine and Spinal Cord Without Apparent Mechanical Lesion and Nervous Shock in Their Surgical and Medico-Legal Aspects. London: J. & A. Churchill. P AGET , J. (1873a) Nervous mimicry of organic diseases, Lecture l. Lancet, ii, 511–513. —— (1873b) Lecture III. Lancet, ii, 619–621. P ALLIS , C. A. & B AMJI , A. N. (1979) McIlroy was here. Or was he? British Medical Journal, i, 973–975. P ANKRATZ , L. (1983) A new technique for the assessment and modification of feigned memory deficit. Perceptual and Motor Skills, 57, 367–372. —— , F AUSTI , S. A. & P EED , S. (1975) A forced-choice technique to evaluate deafness in the hysterical and malingering patient. Journal of Consulting and Clinical Psychology, 43, 421–422. P ANKRATZ , L. & L IPKIN , J. (1978) The transient patient in a psychotic ward: Summering in Oregon. Journal of Operational Psychiatry, 9, 42–47. P ARFITT , D. N. & G ALL , C. M. C. (1944) Psychogenic amnesia: the refusal to remember. Journal of Mental Science, 511–527. P ARKER . G., T UPLING , H. & B ROWN , L. B. (1979) A Parental Bonding Instrument. British Journal of Medical Psychology, 52, 1–10. P ARKER , S. (1960) The Wittiko psychosis in the context of Ojibwa personality and culture. American Anthropology, 62, 603–623. —— (1962) Eskimo psychopathology in the context of Eskimo personality and culture. American Anthropology, 64, 76–96. P ATTERSON , R. (1988) The Münchausen’s syndrome: Baron Von Münchausen has taken a bum rap. Canadian Medical Association Journal, 139, 566–569. P ATTISON , E. M. & K AHAN , J. (1983) The deliberate self-harm syndrome. American Journal of Psychiatry, 140, 867–872.
454
References
P AYKEL , E. S. & P RUSOFF , B. A. (1973) Relationships between personality dimensions: neuroticism and extraversion against obsessive, hysterical and oral personality. British Journal of Social and Clinical Psychology, 12, 309–318. P ELZ , M. & M ERSKEY , H. (1982) A description of the psychological effects of chronic painful lesions. Pain, 14, 293–301. P ENDERGRAST , M. (1995) Victims of Memory. Incest Accusations and Shattered Lives. Hinesburg, Vermont: Upper Access Books. P ENNEBAKER , J. W. (1982a) The Psychology of Physical Symptoms. New York: Springer-Verlag. —— (1982b) Social and perceptual factors affecting symptom reporting and mass psychogenic illness. In Mass Psychogenic Illness: A Social Psychological Analysis (eds M. J. Colligan, J. W. Pennebaker & L. R. Murphy), pp. 139–153. Hillsdale, New Jersey: Lawrence Erlbaum Associates. ——, B URMAN , M. A., S CHAEFFER, M. A., et al (1977) Lack of control as a determinant of perceived physical symptoms. Journal of Personality and Social Psychology, 35, 167–174. —— & W ATSON , D. (1991) The psychology of somatic symptoms. In Current Concepts of Somatization: Research and Clinical Perspectives (eds L. J. Kirmayer & J. M. Robbins), pp. 21–35. Washington, DC: American Psychiatric Press. P ENROSE , L. S. (1952) On the Objective Study of Crowd Behaviour. London: H. K. Lewis. P ERLEY , J. M. & G UZE , S. B. (1962) Hysteria – the stability and usefulness of clinical criteria. New England Journal of Medicine, 266, 421–426. P ETERS , C. & S CHWARZ , T. (1978) Tell Me Who I Am Before I Die. New York: Rawson Associates. P FOHL , B. (1991) Histrionic personality disorder: A review of available data and recommendations for DSM–IV. Journal of Personality Disorders, 5, 150–166. P HILIPPOPOULOS , G. S. (1981) An early case of battle hysteria. British Journal of Psychiatry, 139, 82–83. P HILLIPS, K. A., M CELROY, S. L., K ECK , P. E., et al (1993) Body dysmorphic disorder: 30 cases of imagined ugliness. American Journal of Psychiatry, 150, 302–308. P HOON , W. H. (1982) Outbreaks of mass hysteria at work places in Singapore: Some patterns and modes of presentation. In Mass Psychogenic Illness: A Social Psychological Analysis (eds M. J. Colligan, J. W. Pennebaker & L. R. Murphy), pp. 21–31. Hillsdale, New Jersey: Lawrence Erlbaum Associates. P ILLING L. F., B RANNICK , T. L. & S WENSON , W. M. (1967) Psychological characteristics of patients having pain as a presenting symptom. Canadian Medical Association Journal, 97, 387–394. P ILOWSKY , I. (1967) Dimensions of hypochondriasis. British Journal of Psychiatry, 113, 89. —— (1969) Abnormal illness behaviour. British Journal of Medical Psychology, 42, 347–351. —— (1985) Malingerophobia. Medical Journal of Australia, 143, 571–572. P INCUS , R., C ALLAHAN , L. F., B RADLEY , L. A., et al (1986) Elevated MMPI scores for hypochondriasis, depression and hysteria in patients with rheumatoid arthritis reflect disease rather than psychological status. Arthritis and Rheumatism, 29, 1456–1465. P ING - NIE , P. (1969) The syndrome of delicate self-cutting. British Journal of Medical Psychology, 42, 195–206. P IPER , A., Jr (1994a) Treatment for multiple personality disorder: at what cost? American Journal of Psychotherapy, 48, 392–400. —— (1994b) Amytal interviews and “recovered memories” of sexual abuse: a note. Issues on Child Abuse Accusations, 6, 39–40. P IPER , A., Jr (1994c) Multiple personality disorder: A critical review. British Journal of Psychiatry, 164, 600–612. P ISO , C. (1618) Selectiorum observationum et conciliorum de praetervisis morbis affectibusque praeter naturam, ab aqua seu serosa colluvie et diluvie ortis. Leyden, Boutestein and Langerak, 1714.
References
455
P LUMER , W. S. (1860) Mary Reynolds: A case of double consciousness. Harper’s Magazine, 20, 807–812. P OLK, L. D. (1974) Mass hysteria in an elementary school. Clinical Paediatrics (Philadelphia), 13, 1013–1014. P OMME , P. (1765) Traité des affections vaporeuses des deux sexes (2nd edn.) Lyon: Benoit Duplain. POND, D. A. (1974) Epilepsy and personality disorders. In Handbook of Clinical Neurology (15th edn) (eds P. L. Vinken & G. W. Bruyn). Amsterdam: North Holland Publishing Co. P OPE , H. G., J R , H UDSON , J. I. & J ONAS , B. (1982) Factitious psychosis: phenomenology, family history, and long term outcome of nine patients. American Journal of Psychiatry, 139, 1480–1483. —— & —— (1992) Is childhood sexual abuse a risk factor for bulimia nervosa? American Journal of Psychiatry, 149, 455–463. —— & —— (1995) Can memories of childhood sexual abuse be repressed? Psychological Medicine, 25 (in press). P OSKANZER , D. C. (1970) Epidemic malaise. British Medical Journal, ii, 420–421. P OTTER, P. (1988) Hippocrates: Regimen in Acute Diseases, Loeb Classical Library. Cambridge, Mass.: Harvard University Press. P RATT , R. T. C. (1951) An investigation of the psychiatric aspects of disseminated sclerosis. Journal of Neurology, Neurosurgery and Psychiatry, 14, 326–335. P RIMEAU , F. & F ONTAINE , R. (1987) Obsessive disorder with self-mutilation: a subgroup responsive to pharmacotherapy. Canadian Journal of Psychiatry, 32, 699–670. P RINCE , M. (1900) The Problem of Multiple Personality. Paris: International Congress of Psychology. —— (1905) Dissociation of a Personality (1st edn). London: Longmans, Green. —— (1908) The Dissociation of a Personality (2nd edn). London: Longmans, Green. –––– (1920) The Dissociation of a Personality (3rd edn). London: Longmans, Green. P RINCE , W. F. (1916) The Doris case of quintuple personality. Journal of Abnormal Psychology, 73–122. P ROCTOR , J. T. (1958) Hysteria in childhood. American Journal of Orthopsychiatry, 28, 394– 407. P ROSEN , H. (1967) Sexuality in females with hysteria. American Journal of Psychiatry, 124, 687–692. P ROUST . A. (1890) Automatisme ambulatoire chez un hystérique. Révue de l’Hypnotisme, Psychologie et Physiologie, 4, 267–269. P U , T., M OHAMED , E., I MAM , K., et al (1986) One hundred cases of hysteria in Eastern Libya; a socio-demographic study. British Journal of Psychiatry, 148, 606–609. P URCELL , J. (1707) A Treatise of Vapours or Hysterick Fits (2nd edn). London: Edward Place. P URTELL , J., ROBINS , E. & C OHEN , M. E. (1951) Observations on clinical aspects of hysteria: a quantitative study of 50 hysteria patients and 156 control subjects. Journal of the American Medical Association, 146, 902–909. P UTNAM , F. W. (1989) Diagnosis and Treatment of Multiple Personality Disorder. New York: Guilford Press. —— (1992) Multiple personality disorder. British Journal of Psychiatry, 161, 415–516. ——, L OWENSTEIN , R. N., S ILBERMAN , E. J., et al (1984) Multiple personality disorder in a hospital setting. Journal of Clinical Psychiatry, 45, 172–175. ——, G UROFF , J. J., S ILBERMAN , E. K., et al (1986) The clinical phenomenology of multiple personality disorder: Review of 100 recent cases. Journal of Clinical Psychiatry, 47, 285– 293. P UTNAM , J. J. (1883) Recent investigations in the pathology of so-called concussion of the spine. Boston Medical and Surgical Journal, 109, 217–220. R ABE , F. (1970) Die Kombination Hysterischer und Epileptische Anfalle. Berlin: Springer.
456
References
R ABINOWITZ , D. (1990) From the mouths of babes to a jail cell. Harper’s Magazine, May, 52–63. R ADANOV , B. P., S TEFANO , G. D., S CHNIDRIG , A., et al (1991) Role of psychosocial stress in recovery from common whiplash. Lancet, 338, 712–715. R ADCLIFFE , C. B. (1880) Diseases of the spinal cord. In A System of Medicine (American edn) (ed. J. R. Reynolds). Philadelphia: H. Hartshorne. R AMSAY , A. M. (1957) Encephalomyelitis in north-west London. An endemic infection simulating poliomyelitis and hysteria. Lancet, ii, 1196–1200. —— (1986) Post-viral Fatigue Syndrome. The Saga of Royal Free Disease. London: Gower Medical Publishing for Myalgic Encephalomyelitis Association. R AMSAY , R., G ORST -U NSWORTH , C. & T URNER , S. (1991) Psychiatric morbidity in survivors of organised state violence including torture. British Journal of Psychiatry, 162, 55–59. R ANGELL , L. (1959) The nature of conversion. Journal of the American Psychoanalytic Association, 7, 632–662. R ASPE , R. E. (1785) The Singular Adventures of Baron Munchausen by R. E. Raspe and Others. London: Max Parrish (1950). R ATHER , L. J. (1965) Mind and Body in 18th Century Medicine: A Study Based on Jerome Gaub’s De Regimine Mentis. London: Wellcome Historical Medical Library. R AVAUT , P. (1915) Les hémorrhagies internes. Presse Medicale, 23, 114. R AWNSLEY , K. & L OUDON , J. B. (1964) Epidemiology of mental disorder in a closed community. British Journal of Psychiatry, 110, 830–839. R AY , I. C. (1991) Chronic fatigue syndrome and depression: conceptual and methodological ambiguities. Psychological Medicine, 21, 1–9. R EED , J. L. (1975) The diagnosis of ‘hysteria’. Psychological Medicine, 5, 13–17. R EES , J. R. (1945) The Shaping of Psychiatry by War. New York: W. W. Norton & Co. R EES , W. L. (1967) A Short Textbook of Psychiatry. London: English Universities Press. —— (1971) The hallucinations of widowhood. British Medical Journal, iv, 37–41. R EICH , P. & G OTTFRIED , L. A. (1983) Factitious disorders in a teaching hospital. Annals of Internal Medicine, 99, 240–247. R EICH , W. (1933) Some circumscribed character forms. In Character Analysis. (1949) New York: Ferrar, Straus & Giroux. R EICHARD , S. (1956) A re-examination of ‘studies in hysteria’. Psychoanalytic Quarterly, 25, 155–177. R EIDENBERG , M. M. & L OWENTHAL , D. T. (1968) Adverse non-drug reactions. New England Journal of Medicine, 279, 678–679. R EIK , T. (1914) Ritual: Psychoanalytical Studies. London: Hogarth Press. R EPORT OF THE C OMMITTEE O N S EXUAL O FFENCES A GAINST C HILDREN AND Y OUTHS (1984) Sexual Offences against Children. Ottawa: Government of Canada. R EYNOLDS , J. R. (1869) Remarks on paralysis and other disorders of motion and sensation, dependent on idea. British Medical Journal, ii, 483–485. Discussion, 378–379. RICE , D. G. & GREENFIELD , N. S. (1969) Psychophysiological correlates of la belle indifférence. Archives of General Psychiatry, 20, 239–245. R ICHARDS , R. L. (1910) Mental and nervous diseases in the Russo-Japanese War. Military Surgeon, 26, 177–193. R ICHER , P. (1885) Études cliniques sur la grande hystérie, ou hystéro-épilepsie. Paris: Adrien Delahaye et Émile Lecrosnier. —— (1892) Paralysies et contractures hystériques. Paris: Octave Doin. R ICHET , C. (1883) La personnalité et la mémoire dans le somnambulisme. Révue Philosophique, 15, 225–242. R ICHMAN , J. & W HITE , H. (1970) A family view of hysterical psychosis. American Journal of Psychiatry, 127, 280–285. R IEGER , W. & B ILLINGS , C. K. (1978) Ganser syndrome associated with litigation. Comprehensive Psychiatry, 19, 371–375.
References
457
R ILEY , M. S., O’B RIEN , C. J., M C C LUSKEY , D. R., et al (1990) Aerobic work capacity in patients with chronic fatigue syndrome. British Medical Journal, 301, 953–955. R IMON , R., K AMPMAN , R., I KONEN , E., et al (1980) Münchausen’s syndrome: a review and two case reports. Psychotherapy and Psychosomatics, 33, 185–192. R ISSE , G. B. (1988) Hysteria at the Edinburgh Infirmary: the construction and treatment of disease, 1770–1800. Medical History, 32, 1–22. R ITCHIE , R. D. (1986) One History of Shell-Shock, PhD thesis. San Diego: University of California. RITSON , B. & FORREST, A. (1970) The simulation of psychosis: a contemporary presentation. British Journal of Medical Psychology, 43, 31–37. R IVINUS , T. M., J AMISON , D. L. & G RAHAM , P. J. (1975) Childhood organic neurological disease presenting as a psychiatric disorder. Archives of Disease in Children, 50, 115–119. R OBERTS , I., C OHEN , H. & R EEVES , W. G. (1985) Characterization of anti-bodies to insulin to help diagnose factitious hypoglycaemia. British Medical Journal, 290, 1391–1392. R OBINS , E. & O’N EAL , P. (1953) Clinical features of hysteria in children with a note on prognosis. A two to seventeen year follow-up study of 45 patients. Nervous Child, 10, 246–271. R OCK , N. L. (1971) Conversion reactions in childhood: a clinical study on childhood neuroses. Journal of the America Adademy of Child Psychiatry, 10, 65–93. R OGERS , R. (1988) Clinical Assessment of Malingering and Deception. New York: Guilford Press. R OGERS , T. & P ULLEN , I. (1987) Self-inflicted eye injuries. British Journal of Psychiatry, 151, 691–693. R OMBERG , M. H. (1851) A Manual of the Nervous Diseases of Man (2nd edn) (trans. E. H. Sieveking, 1853). London: The New Sydenham Society. R OSEN , S. R. (1951) Vasomotor response in hysteria. Journal of Mt Sinai Hospital, 18, 179– 190. R OSENHAN , D. L. (1973) On being sane in insane places. Science, 179, 250–258. R OSS , C. A. (1987) Inpatient treatment of multiple personality disorder. Canadian Journal of Psychiatry, 32, 779–781. —— (1989) Multiple Personality. New York: Wiley. —— (1990) Twelve cognitive errors about multiple personality disorder. American Journal of Psychotherapy, 44, 348–356. —— (1993) Mistaken Identities: Toronto. Canadian Broadcasting Corporation. The Fifth Estate. 9 November 1993. ——, M ILLER , S. D., R EAGER , P., et al (1990) Structured interview data on 102 cases of multiple personality disorder from four centers. American Journal of Psychiatry, 147, 596–601. ––––, N ORTON , G. R. & F RASER , G. A. (1989) Evidence against the iatrogenesis of multiple personality disorder. Dissociation, 2, 61–65. R OY , A. (1977a) Cerebral disease and hysteria. Comprehensive Psychiatry, 18, 607–609. —— (1977b) Identification and hysterical symptoms. British Journal of Medical Psychology, 50, 317–318. —— (1979a) Hysterical seizures. Archives of Neurology, 36, 447. —— (1979b) Hysteria: a case note study. Canadian Journal of Psychiatry, 24, 157–160. R UESCH , J. (1946) Chronic disease and psychological invalidism: a psychosomatic study. Psychological Medicine Monograph (suppl. 9). S ACHDEV , P. S. (1990) Whakama: culturally determined behaviour in the New Zealand Maori. Psychological Medicine, 20, 433–444. S AINSBURY , P., P EARCE , K. & C OSTAIN , W. P. (1965) Hypochondriasis and depression in outpatients at a general hospital. British Journal of Psychiatry, 111, 607–615. S ALE , I., B URVILL , J. & K ALUCY , R. (1979) Münchausen’s syndrome in a psychiatric setting: three case reports. Australian and New Zealand Journal of Psychiatry, 13, 133–138.
458
References
S ALKOVSKIS , L. P. M. & W ARWICK , H. M. C. (1986) Morbid preoccupations, health anxiety and reassurance: a cognitive behavioural approach to hypochondriasis. Behaviour Research and Therapy, 24, 597–602. S ALMON , T. W. & F ENTON , N. (1929) Medical Department of the United States Army in the World War. Vol. 1: Neuropsychiatry in the American Expeditionary Forces, pp. 273–543. Washington, DC: US Government Printing Office. S ANDBERG , D. A. & L YNN , S. J. (1992) Dissociative experiences, psychopathology and adjustment, and child and adolescent maltreatment in female college students. Abnormalities in Social Psychology, 101, 717–723. S ANDER , R. A. & M YERS , J. E. (1986) The relationship of disability to compensation status in railway workers. Spine, 11, 141–143. S ANDERS , B. & G IOLAS , M. H. (1991) Dissociation and childhood tramua in psychologically disturbed adolescents. American Journal of Psychiatry, 148, 50–54. S ANDRAS , C. M. S. (1851) Traité pratique des maladies nerveuse. Paris: Germer Baillière. S ARGANT , W. (1957) Battle for the Mind. A Physiology of Conversion and Brain Washing. London: Heinemann. —— & S HORVON , H. J. (1945) Acute war neurosis. Archives of Neurology and Psychiatry, 54, 231–240. S ASSOON , S. (1936) Sherston’s Progress. London: Faber. S AUNDERS , C. ( 1966) The management of terminal illness. British Journal of Hospital Medicine, 1, 225. —— (1975) Terminal care. In Medical Oncology (ed. K. D. Bagshaw). Oxford: Blackwell Scientific Publications. S AVILL , T. D. (1909) Lectures on Hysteria and Allied Vasomotor Conditions. London: H. J. Glaisher. S CALLETT , A., C LONINGER , R. & O THMER , E. (1976) The management of chronic hysteria: a review and double-blind trial of electrosleep and other relaxation methods. Diseases of the Nervous System, 37, 347–353. S CHARF , M. B., K HOSLA , N., L YSAGHT , R., et al (1983) Anterograde amnesia with oral lorazepam. Journal of Clinical Psychiatry, 44, 362–364. S CHERRER, P., Q UINIOU -V IDALENC , E., M AILLARD , M., et al (1972) Anorexia nervosa and hysteria. Annals of Medical Psychology, 2, 672–684. S CHILDER , P. (1935) The Image and Appearance of the Human Body. New York: International Universities Press. —— (1939) The concept of hysteria. American Journal of Psychiatry, 98, 1389–1413. —— (1940) Neurosis following head and brain injuries. In Injuries of the Skull, Brain and Spinal Cord (ed. S. Brock). Philadelphia: Williams & Wilkins. —— (1956) The Nature of Hypnosis. Madison, CT: International Universities Press. S CHILLER , F. (1982) A Möbius Strip: Fin-de-Siècle Neuropsychiatry and Paul Möbius. Berkeley, CA: University of California Press. S CHLAEGEL , T. F. & Q UILALA , F. V. (1955) Hysterical amblyopia. Archives of Ophthalmology, 54, 875–884. S CHMALE , A. H. (1969) Somatic expressions and consequences of conversion reactions. New York State Journal of Medicine, 69, 1878–1883. S CHMIDEBERG , M. (1959) The borderline patient. In American Handbook of Psychiatry (ed. S. Arieti). New York: Basic Books. S CHMIDT , A. J. M. (1994) Bottlenecks in the diagnosis of hypochondriasis. Comprehensive Psychiatry, 35, 306–315. S CHMITT , N. & F ITZGERALD , M. (1982) Mass psychogenic illness: individual and aggregate data. In Mass Psychogenic Illness: A Social Psychological Analysis (eds M. J. Colligan, J. W. Pennebaker & L. R. Murphy), pp. 87–100. Hillsdale, NJ: Lawrence Erlbaum Associates. S CHNEER , H. I. (1958) Hysteria in childhood. Discussion of paper by Proctor. American Journal of Orthopsychiatry, 28, 406–407.
References
459
S CHNEIDER , K. (1928) Die Psychopathischen Persönlichkeiten. Translated by M. W. Hamilton as Psychopathic Personalities (1958). London: Cassell. S CHREIBER , F. R. (1973) Sybil. Chicago: Henry Regnery. S CHROEDER , M. L. & L IVESLEY , W. J. (1991) An evaluation of DSM–III–R personality disorders. Acta Psychiatrica Scandinavica, 84, 512–519. S CHULER , E. A. & P ARENTON , V. J. (1943) A recent epidemic of hysteria in a Louisiana high school. Journal of Social Psychology, 17, 221–235. S CHULTZ , G. & M ELZACK , R. (1991) The Charles Bonnet syndrome: ‘phantom visual images’. Perception, 20, 809–825. S CHUR , M. (1955) Comments on the metapsychology of somatization. Psychoanalytic Study of the Child, 10, 119–164. S CHWARTZ, M., H UGHES, D., B LAZER, D., et al (1987) Somatization disorder in the community: a study of diagnostic concordance among three diagnostic systems. Journal of Nervous and Mental Disease, 175, 26–33. S COTT , B. D. (1970) Epidemic malaise. British Medical Journal, i, 170. S COTT , P. D. (1965) Commentary on a peculiar hysterical state by S. J. M. Ganser. British Journal of Criminology, 5, 120–126. S ELTZER , A. (1983) Psychodynamics of spirit possession among the Inuit. Canadian Journal of Psychiatry, 28, 52–56. —— (1994) Multiple personality: a psychiatric misadventure. Canadian Journal of Psychiatry, 39, 442–445. S HANNON , M. P., LONIGAN , C. J., F INCH , A. J., et al (1994) Children exposed to disaster: I. Epidemiology of post-traumatic symptoms and symptom profiles. Journal of the American Academy of Child and Adolescent Psychiatry, 33, 80–93. S HAPIRO , A. K. (1964a) A historic and heuristic definition of the placebo. Psychiatric Medicine, 27, 52–58. —— (1964b) Factors contributing to the placebo effect: their implications for psychotherapy. American Journal of Psychotherapy, 73–88. —— & S HAPIRO , E. (1971) Clinical dangers of psychological theorizing. Psychiatric Quarterly, 45, 159–171. ——, W ILENSKY , H. & S TRUENING , E. L. (1968) Study of the placebo effect with a placebo test. Comprehensive Psychiatry, 9, 118–137. S HAPIRO , D. (1965) Neurotic Styles. New York: Basic Books. S HARPE , M. C. & JOHNSON , B. A. (1991) Mania and recovery from chronic fatigue syndrome. Journal of the Royal Society of Medicine, 84, 51–52. ——, H AWTON , K., S EAGROATT , V., et al (1992) Follow up of patients presenting with fatigue to an infectious diseases clinic. British Medical Journal, 305, 147–152. ——, A RCHARD , L. C., B ANATVALA , J. E., et al (1991) A report – chronic fatigue syndrome: guidelines for research. Journal of the Royal Society of Medicine, 84, 118–121. S HEEHAN , P. W. (1988) Memory distortion in hypnosis. International Journal of Clinical and Experimental Hypnosis, 36, 296–311. S HEPHERD , M., C OOPER , B., B ROWN M. C., et al (1966) Psychiatric Illness in General Practice. London: Oxford University Press. S HOR , R. E. (1959) Hypnosis and the concept of the generalized reality orientation. American Journal of Psychotherapy, 13, 582–602. —— (1962) Physiological effects of painful stimulation during hypnotic analgesia under conditions designed to minimize anxiety. International Journal of Clinical and Experimental Hypnosis, 10, 183–202. S HORTER , E. (1989) Bedside Manners. New York: Simon & Schuster. —— (1992) From Paralysis to Fatigue: A History of Psychosomatic Illness in the Modern Era. New York: The Free Press. SHORTER, E. (1993) Chronic fatigue in historical perspective. In Chronic Fatigue Syndrome (eds. G. R. Bock & J. Whelan), pp. 6–22. Ciba Foundation Symposium, No. 177. Chichester: Wiley.
460
References
S HUTTY , M. S. & L EADBETTER , R. A. (1993) Case report: recurrent pseudocyesis in a male patient with psychosis, intermittent hyponatremia, and polydipsia. Psychosomatic Medicine, 55, 146–148. S IDIS , B. & G OODHART , S. P. (1904) Multiple Personality. Appleton. Reprinted New York: Greenwood Press. S IEGEL , R. E. (1976) Galen on the Affected Parts, Book 5, pp. 187–188. Basel: Karger. SIGAL, J. J., STAR, K. & FRANKS, C. M. (1958) Hysterics and dysthymics as criterion groups in the study of introversion-extraversion. Journal of Abnormal Social Psychology, 57, 143–148. S IGAL , M., A LTMARK , D. & C ARMEL , I. (1986) Münchausen’s syndrome by adult proxy: a perpetrator abusing two adults. Journal of Nervous and Mental Disease, 174, 696–698. ——, —— & G ELKOPF , M. (1991) Münchausen’s syndrome by adult proxy revisited. Israel Journal of Psychiatry and Related Sciences, 28, 33–36. S IGERIST , H. E. (1951) A History of Medicine. Primitive and Archaic Medicine, Vol. 1. New York: Oxford University Press. S IGVARDSON , S., V ON K NORRING , A. L., B OHMAN , M., et al (1984) An adoption study of somatoform disorder: I. The relationship to psychiatric disability. Archives of General Psychiatry, 41, 853–859. S IM , M. (1974) Guide to Psychiatry (3rd edn). Edinburgh: Churchill Livingstone. —— (1981) Guide to Psychiatry (4th edn). Edinburgh: Churchill Livingstone. —— (1992) Compensation Claims: Insurance, Legal and Medical Aspects. Victoria, BC: Emmess Publications. S IMON , G. E. & V ON K ORFF , M. (1991) Somatization and psychiatric disorder in the NIMH epidemiologic catchment area study. American Journal of Psychiatry, 148, 1494–1500. S IMPSON , M. A. (1973) Female genital self-mutilation. Archives of General Psychiatry, 29, 808–810. S IOMOPOULOS , A. M. & R EISSMAN , H. H. (1969) Progressive hysterical tetraplegia with contractures. A case study. Johns Hopkins Medical Journal, 125, 14–18. S IOMOPOULOS , V. (1971) Hysterical psychosis: psychopathological aspects. British Journal of Psychology, 44, 95–100. S IROIS , F. (1974) Epidemic hysteria. Acta Scandinavica (suppl. 252). —— (1975) A propos the incidence of mass hysteria. Union médicale du Canada, 104, 121– 123. S IZEMORE, C. S. & P ITTILLO , E. S. (1977) I’m Eve. New York: Doubleday. S KAE , D. (1845) Case of intermittent mental disorder of the tertian type with double consciousness. Northern Journal of Medicine, 4, 10–19. S KERRITT , P. W. (1983) Anxiety and the heart – a historical review. Psychological Medicine, 13, 17–25. S KEY , F. C. (1867) Hysteria. London: Longmans & Co. S LATER , E. (1965) Diagnosis of ‘hysteria’. British Medical Journal, i, 1395–1399. —— & G LITHERO , E. (1965) A follow-up of patients diagnosed as suffering from ‘hysteria’. Journal of Psychosomatic Research, 9, 9–11. —— & R OTH , M. (1980) Clinical Psychiatry (2nd edn, revised) London: Bailliere Tindall. SLAVNEY, P. R. (1994) In defense of pseudoseizure. General Hospital Psychiatry, 16, 243–245. —— (1990) Perspectives on “Hysteria”. Baltimore: The Johns Hopkins Press. —— & M C H UGH , P. R. (1974) The hysterical personality. A controlled study. Archives of General Psychiatry, 30, 325–329. S MART , D. E., B EUMONT P. J. V. & G EORGE , G. C. W. (1976) Some personality characteristics of patients with anorexia nervosa. British Journal of Psychiatry, 128, 57–60. S MITH , E. & P EAR , R. (1917) Shell-shock and its Lessons. Manchester: Manchester University Press. S MITH , G. R. (1992) The epidemiology and treatment of depression when it coexists with somatoform disorders, somatization, or pain. General Hospital Psychiatry, 14, 265–272. S MITH , M. & P AZDER , L. (1980) Michelle Remembers. New York: Pocket Books.
References
461
S MYTHE , H. A. (1984) Problems with the MMPI. Journal of Rheumatology, 11, 417–418. S NOWDIN , J., S OLOMONS , R. & D RUCE , H. (1978) Feigned bereavement: twelve cases. British Journal of Psychiatry, 133, 15–19. S NYDER , S. L. (1994) Commentary: contra pseudoseizure. The problem of intention in nonepileptic events. General Hospital Psychiatry, 16, 248–250. S OLLIER , P. & C HARTIER , M. (1915) Shell-shock and its effects upon the nervous system. Paris Medical, 5, 406–414. S OLOMON , Z. (1993) Combat Stress Reaction: The Enduring Toll of War. New York: Plenum Press. ——, G ARB , R., B LEICH , A., G RUPPER , D. (1987a) Reactivation of combat-related post traumatic stress disorder. American Journal of Psychiatry, 144, 51–55. ——, M IKULINCER , M. & J ACOB , B. R. (1987b) Exposure to recurrent combat stress: Combat stress reactions among Israeli soldiers in the Lebanon war. Psychological Medicine, 17, 433– 440. ——, K OTLER , M., S HALEV , A., et al (1989) Delayed onset Post Traumatic Stress Disorder among Israeli veterans of the 1982 Lebanon War. Psychiatry, 52, 428–436. S OLZHENITSYN , A. (1973) Gulag Archipelago. New York: Harper & Row. S OMMERS , C. H. (1994) Who Stole Feminism: How Women have Betrayed Women. New York: Simon & Schuster. S ONG , J. Y., M ERSKEY , H., S ULLIVAN , S., et al (1993) Anxiety and depression in patients with abdominal bloating. Canadian Journal of Psychiatry, 38, 475–479. S OULIOS , C. & F IRTH , S. T. (1986) Self inflicted eye injury: clinical and psychodynamic aspects. Psychiatric Journal of University of Ottawa, 2, 238–242. S OUTHARD , E. E. (1919) Shell-Shock and Other Neuropsychiatric Problems. Boston: W. M. Leonard. S PANOS , N. P., W EEKES , J. R., M ENARY , E., et al (1986) Hypnotic interview and age regression procedures in the elicitation of multiple personality symptoms: A simulation study. Psychiatry, 49, 298–311. S PARR , L. & P ANKRATZ , L. (1983) Factitious post-traumatic disorder. American Journal of Psychiatry, 140, 1016–1019. S PEAR , F. G. (1967) Pain in psychiatric patients. Journal of Psychosomatic Research, 11, 187– 193. S PERRYN , P. N. (1993) Multiple personality. British Journal of Psychiatry, 162, 126. —— (1994) Overuse injury in sport. British Medical Journal, 308, 1430–1432. S PIEGEL , D. (1993) Multiple personality (letter). British Journal of Psychiatry, 162, 126. —— & F INK , R. (1979) Hysterical psychosis and hypnotizability. American Journal of Psychiatry, 136, 777–781. S PIEGEL , H. (1993) Mistaken Identities: Toronto. Canadian Broadcasting Corporation. The Fifth Estate. 9 November 1993. S PIERINGS , C., P OELS , P. J. E., S IJBEN , N., et al (1990) Conversion disorders in childhood: a retrospective follow-up study of 84 patients. Developmental Medicine and Child Neurology, 32, 865– 871. S PITZER , R. L., E NDICOTT , J. & R OBINS , E. (1978) Research diagnostic criteria: Rationale and reliability. Archives of General Psychiatry, 35, 773–785. S PITZER , R. L., S HEEHY , M. & E NDICOTT , J. (1977) DSM–III: guiding principles. In Psychiatric Diagnosis (eds. V. M. Rakoff, H. C. Stancer & K. B. Kedward). New York: Brunner/ Mazel. ——, S KODOL , A. E., G IBBON , M., et al (1981) DSM–III Casebook. Washington, DC: American Psychiatric Association. –––– & W ILLIAMS , J. B. (1982) Hysteroid dysphoria: an unsuccessful attempt to demonstrate its syndromal validity. American Journal of Psychiatry, 139, 1286–1291. S ROLE , L., L ANGNER , T. S., M ICHAEL , S. T., et al (1962) Mental Health in the Metropolis: the Midtown Manhattan Study, Vol. 1. New York: McGraw Hill.
462
References
S TAHL , S. M. & L EBEDUN, M. (1974) Mystery gas: an analysis of mass hysteria. Journal of Health and Social Behaviour, 15, 44–50. S TANDAGE , K. E. (1975) The etiology of hysterical seizures. Canadian Psychiatric Association Journal, 20, 67–73. S TEFANSSON , J. G., M ESSINA , J. A. & M EYEROWITZ , S. (1976) Hysterical neurosis, conversion type: clinical and epidemiological considerations. Acta Psychiatrica Scandinavica, 53, 119–138. S TEKEL , W. (1943) The Interpretation of Dreams. New York: Liveright. S TELL , R., C OLEMAN , R., T HOMPSON , P. D., et al (1988a) Botulinum toxin in spasmodic torticollis. Journal of Neurology, Neurosurgery and Psychiatry, 51, 920–923. ——, T HOMPSON , P. D. & M ARSDEN , C. D. (1988b) Botulinum toxin treatment of spasmodic torticollis. British Medical Journal, 297, 616. S TENGEL , E. (1941) On the aetiology of fugue states. Journal of Mental Science, 87, 572–599. —— (1964) Suicide and Attempted Suicide. Harmondsworth: Penguin Books. —— & C OOK , N. G. (1958) Attempted Suicide. London: Oxford University Press. S TEPHENSON , T. J. & L EWIS , S. W. (1985) Factitious plumbism. Lancet, ii, 335. S TERN , D. B. (1977) Handedness and the lateral distribution of conversion reactions. Journal of Nervous and Mental Disease, 164, 122–128. STERN, J., MURPHY, M. & BASS, C. (1993a) Attitudes of British psychiatrists to the diagnosis of somatisation disorder. A questionnaire survey. British Journal of Psychiatry, 162, 463–466. ——, —— & —— (1993b) Personality disorders in patients with somatization disorder: a controlled study. British Journal of Psychiatry, 163, 785–789. S TERNBACH , R. A. (1968) Pain. A Psychophysiological Analysis. New York: Academic Press. —— (1974) Pain Patients: Traits and Treatment. New York: Academic Press. ——, W OLF , S. R., M URPHY , R. W., et al (1973) Traits of pain patients: the low-back ‘loser’. Psychosomatics, 14, 226–229. —— & G REENHOOT J. H. (1974) Conjoint treatment of chronic pain. Advances in Neurology, 4, 595–601. S TEWART , D. E. & L OWREY , M. R. (1980) Replantation surgery following self-inflicted amputation. Canadian Journal of Psychiatry, 25, 143–150. S TONE , M. (1985) Shell shock and the psychologists. In The Anatomy of Madness, Vol. 2 (eds W. T. Bynum, R. Porter & M. Shepherd), pp. 242–271. London: Tavistock Press. —— (1993) Abnormalities of Personality: Within and Beyond the Realm of Treatment. New York: W. W. Norton & Co. S TOUT , G. F. (1919) Manual of Psychology (3rd edn) London: University Tutorial Press. S TRAUS , S. (1988) The chronic mononucleosis syndrome. Journal of Infectious Diseases, 157, 405–412. S UGAR , J. A., B ELFER , M., I SRAEL , E., et al (1991) A 3-year old boy’s chronic diarrhea and unexplained death. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 1015–1021. S UGARMAN , J. R. & B ERG , A. O. (1984) Evaluation of fatigue in a family practice. Journal of Family Practice, 19, 643–647. S ULESTROWSKA , H. (1973) Clinical and follow-up studies of hysteria in children. Psychiatria Polska, 7, 133–134. S URRIDGE , D. (1969) An investigation into some psychiatric aspects of multiple sclerosis. British Journal of Psychiatry, 115, 749–764. S UTCLIFFE , J. P. & J ONES , J. (1962) Personal identity, multiple personality and hypnosis. International Journal of Clinical and Experimental Hypnosis, 10, 231–269. S UWANLERT , S. (1976) Neurotic and psychotic states attributed to Thai ‘Phii Pob’ spirit possession. Australian and New Zealand Journal of Psychiatry, 10, 119–123. S YDENHAM , T. (1697) Discourse concerning hysterical and hypochondriacal distempers. In Dr. Sydenham’s Compleat Method of Curing Almost All Diseases, and Description of Their
References
463
Symptoms, to Which Are Now Added Five Discourses of the Same Author Concerning Pleurisy, Gout, Hysterical Passion, Dropsy and Rheumatism (3rd edn). London: Newman and Parker. S ZASZ , T. S. (1961) The Myth of Mental lllness: Foundations of a Theory of Personal Conduct. New York: Harper & Row. S ZYRYNSKI, V. (1973) Anorexia nervosa and psychotherapy. American Journal of Psychotherapy, 27, 492–505. T AKAHASHI , Y. (1990) Is multiple personality disorder really rare in Japan? Dissociation, 3, 57–59. T AM , Y. K., TSOI , M. M., K WONG , B., et al (1982) Psychological epidemic in Hong Kong. II. Psychological and physiological characteristics of children who were affected. Acta Psychiatrica Scandinavica, 65, 437–449. T ANTAM , D. & W HITTAKER , J. (1992) Personality disorder and self-wounding. British Journal of Psychiatry, 161, 451–464. T APPER , C. M., B LAND , R. C. & D ANYLUK , L. (1979) Self-inflicted eye injuries and selfinflicted blindness. Journal of Nervous and Mental Disease, 167, 311–314. T ARSH , M. J. & R OYSTON , C. (1985) A follow-up study of accident neurosis. British Journal of Psychiatry, 146, 18–25. T ART , C. T. (1969) Altered States of Consciousness. New York: John Wiley. T AUSCHKE , E., M ERSKEY , H. & H ELMES , E. (1990a) Psychological defence mechanisms in patients with pain. Pain, 40, 161–170. ——, —— & —— (1990b) A systematic inquiry into recollections of childhood experience and their relationship to adult defence mechanisms. British Journal of Psychiatry, 157, 392–398. T AYLOR , F. K. & H UNTER , R. C. A. (1958) Observation of a hysterical epidemic in a hospital ward. Psychiatric Quarterly, 32, 821–839. T AYLOR , A. R. (1967) Post-concussional sequelae. British Medical Journal, iii, 67–71. —— & B ELL , T. K. ( 1966) Slowing of cerebral circulation after concussional head injury. Lancet, ii, 178–180. T AYLOR , D. C. (1986) Hysteria, play-acting and courage. British Journal of Psychiatry, 149, 37–41. —— (1989) Hysteria, belief, and magic. British Journal of Psychiatry, 155, 391–398. T AYLOR , J. & K REEGER , A. (1987) Recurrent pseudocyesis and hypomania. British Journal of Psychiatry, 151, 120–122. Taylor, J. R. & K AKULAS , B. A. (1991) Neck injuries. Lancet, 338, 1343. T AYLOR , P. J. & KOPELMAN , M. D. (1984) Amnesia for criminal offences. Psychological Medicine, 14, 581–588. T AYLOR , W. S. & M ARTIN , M. F. (1944) Multiple personality. Journal of Abnormal and Social Psychology, 39, 281–330. T EASELL , R. A. & S HAPIRO , A. P. (1993) Rehabilitation of chronic motor conversion disorders. Critical Reviews in Physical and Rehabilitation Medicine, 5, 1–13. T EMKIN O. (1956) Soranus’ Gynecology. Baltimore: Johns Hopkins. T ENNANT , C., G OULSTON , K. & D ENT , O. (1986) Australian prisoners of war of the Japanese: post-war psychiatric hospitalization and psychological morbidity. Australian and New Zealand Journal of Psychiatry, 20, 334–340. T ERR , L. C. (1991) Childhood traumas: an outline and overview. American Journal of Psychiatry, 148, 10–20. T HATCHER , R. W., W ALKER R. S., G ERSON , I., et al (1989) EEG discriminant analyses of mild head trauma. Electroencephalography and Clinical Neurophysiology, 73, 94–106. T HEANDER , S. (1970) Anorexia nervosa. A psychiatric investigation of 94 female patients. Acta Psychiatrica Scandinavica (suppl. 214), 1–194. THEODOR, L. H. & MANDELCORN, M. S. (1973) Hysterical blindness: a case report and study using a modern psychophysical technique. Canadian Journal of Ophthalmology, 8, 353–355.
464
References
T HIGPEN , C. H. & C LECKLEY , H. M. (1954) A case of multiple personality. Journal of Abnormal and Social Psychology, 49, 135–151. —— & —— (1957) The Three Faces of Eve. New York: McGraw-Hill. —— & —— (1984) On the incidence of multiple personality: A brief communication. International Journal of Clinical and Experimental Hypnosis, 32, 63–66. TIBBETTS, R. W. (1971) Spasmodic torticollis. Journal of Psychosomatic Research, 15, 461–469. T ILLMAN , J. G., N ASH , M. R. & L ERNER , P. M. (1994) Does trauma cause dissociative pathology: In Dissociation: Clinical and Theoretical Perspectives (eds S. J. Lynn & J. W. Rhue), pp. 395–414. New York: Guilford Press. T ODD , R. B. (1854) Clinical Lectures on Paralysis, Disease of the Brain and Other Afflictions of the Nervous System. London: Churchill. T OGLIA , J. U., R OSENBERG , P. E. & R ONIS , M. L. (1970) Post-traumatic dizziness. Archives of Otolaryngology, 92, 485–492. T ORRIE , A. (1944) Psychosomatic casualties in the Middle East. Lancet, i, 139–143. T RETHOWAN , W. H. ( 1968) The Couvade syndrome – some further observations. Journal of Psychosomatic Research, 12, 107–115. —— & C ONLON , M. F. (1965) The Couvade syndrome. British Journal of Psychiatry, 111, 57–76. T RIMBLE , M. R. (1978) Serum prolactin in epilepsy and hysteria. British Medical Journal, ii, 1682. —— (1981) Post-traumatic Neurosis from Railway Spine to the Whiplash. London: Wiley. T SENG , W. S., M O , K. M. & HSU , J. (1988) A socio-cultural study of Koro epidemics in Guangdong, China. American Journal of Psychiatry, 143, 1538–1543. ——, ——, L I , L. S., et al (1992) Koro epidemics in Guangdong, China: a questionnaire survey. Journal of Nervous and Mental Disease, 180, 117–123. T SOI , W. F. (1973) The Ganser syndrome in Singapore: a report on ten cases. British Journal of Psychiatry, 123, 567–572. T UCKEY , C. L. (1891) Psychotherapeutics. London: Baillière. T URGAY , A. (1980) Conversion reaction in children. Psychiatric Journal of the University of Ottawa, 5, 287–294 —— (1990) Conversion Disorder in Children and Adolescents. Proceedings of the 143rd Annual Meeting of the American Psychiatric Association (APA). Paper session 52, paper 156. Washington, DC: APA. TURNER, S. & G ORST-U NSWORTH , C. (1993) Psychological sequelae of torture. In International Handbook of Traumatic Stress Syndromes (eds J. P. Wilson & B. Raphael), pp. 703–713. New York: Plenum. T URNIER , L. & C HOUINARD , G. (1990) Effet anti-Koro d’un antidépresseur tricyclique. Canadian Journal of Psychiatry, 35, 331–333. T YRER , J. H. (1957) The differentiation of hysteria from organic neurological disease. Medical Journal of Australia, i, 566–571. U SHER , J. A. & N EISSER , U. (1993) Childhood amnesia and the beginnings of memory for four early life events. Journal of Experimental Psychology, 122, 155–165. V AILLANT , G. (1976) Natural history of male psychological health. V: The relation of choice of ego mechanisms of defense to adult adjustment. Archives of General Psychiatry, 33, 535–545. V ALLOTTON , W. W. (1974) Ocular hysteria, malingering and other bizarre complaints. Acta Societatis Ophthalmologica (Japan), 78, 437–440. V AUGHAN , E. C. (1981) Some Desperate Glory. The World War I Diary of a British Officer. London: F. Warne. V EITH , I. (1965) Hysteria: The History of a Disease. Chicago, IL: University of Chicago Press. V ERITY , C. M., W INCKWORTH , C., B URMAN , D., et al (1979) Polle syndrome: children of Münchausen. British Medical Journal, ii, 422–423.
References
465
V ICTOR , G. (1975) Sybil: Grande hystérie or Folie à deux. American Journal of Psychiatry, 132, 202. V IETS , H. (1917) Shell-shock: A digest of the English literature. Journal of the American Medical Association, 69, 1779–1786. V OLKMAR , F. R., P OLL , J. & L EWIS , M. (1984) Conversion reactions in childhood and adolescence. Journal of the American Academy of Child Psychiatry, 23, 424–430. V ON E CONOMO , C. (1929) Encephalitis Lethargica (trans. K. O. Newman, 1931). London: Oxford University Press. V ON F EUCHTERSLEBEN , E. (1845) Lehrbuch der artzlichen Seelenkunde. Vienna: Gerold. (Trans. H. Lloyd Evans 1847, The Principles of Medical Psychology. London: Sydenham Society.) W ADDELL , G. (1987a) A new clinical model for the treatment of low back pain. Spine, 12, 632–644. —— (1987b) Understanding the patient with back ache. In The Lumbar Spine and Back Pain (3rd edn) (ed. M. I. V. Jayson), pp. 419–434. Churchill Livingstone: Edinburgh. —— , B IRCHER , M., F INLAYSON, D., et al (1984) Symptoms and signs: physical disease or illness behaviour? British Medical Journal, 289, 739–741. —— , M CC ULLOCH , J. A., K UMMELL , E., et al (1980) Non-organic physical signs in low back pain. Spine, 5, 117–125. W AKEFIELD , H. & U NDERWAGER, R. (1992) Recovered memories of alleged sexual abuse: lawsuits against parents. Behavioural Science and the Law, 10, 483–507. —— & —— (1994) Return of the Furies: An Investigation into Recovered Memory Therapy. Chicago: Open Court. W ALKER , E. A., K ATON , W. J., H ARROP -G RIFFITH , J., et al (1988a) Relationship of chronic pelvic pain to psychiatric diagnoses and childhood sexual abuse. American Journal of Psychiatry, 145, 75– 80. ——, —— & J EMELKA . R. P. (1988b) The prevalence of chronic pelvic pain and irritable bowel syndrome in two university clinics. American Journal of Psychiatry, 149, 534–537. W ALL , P. D. & MELZACK , R. A. (1994) Textbook of Pain. Edinburgh: Churchill & Livingstone. W ALTERS , A. (1961) Psychogenic regional pain alias hysterical pain. Brain, 84, 1–18. —— (1969) Psychogenic regional sensory and motor disorders alias hysteria. Canadian Psychiatric Association Journal, 14, 573–590. —— (1973) Psychiatric considerations of pain. In Neurological Surgery (ed. J. Youmans), pp. 1615–1645. New York: Saunders. W ALTON , G. L. (1883) Possible cerebral origin of the symptoms usually classed under “railway spine”. Boston Medical and Surgical Journal, 109, 337–340. W ALTZER , H. (1963) A psychotic family: folie à douze. Journal of Nervous and Mental Disease, 137, 67–75. W AR O FFICE C OMMITTEE OF E NQUIRY INTO S HELL S HOCK (1922) Report of the Committee, Cmd 1734, pp. 43, 132, 158. London: HMSO. W ARSHAW , M.G., F IREMAN , E., & P RATT , L. (1993) Quality of life and dissociation in anxiety disorder patients with histories of trauma or PTSD. American Journal of Psychiatry, 150, 1512–1516. W ARWICK , H. M. C. & S ALKOVSKIS , P. M. (1990) Hypochondriasis. Behaviour Research and Therapy, 28, 105–117. W ASSERMAN , A. L., W HITTINGTON , P. F. & R IVARA , F. (1988) Psychogenic basis for abdominal pain in children and adolescents. Journal of American Academy of Child and Adolescent Psychiatry, 27, 179–184. W ATSON , C. G. & BURANEN , C. (1979) Short reports. Frequencies of conversion reaction symptoms. Journal of Abnormal Psychology, 88, 209–211. W ATSON , D. (1982) Neurosis tendencies among chronic pain patients: an MMPI item analysis. Pain, 14, 365–385. W ATSON , I. P. B. (1993) Post traumatic stress disorder in Australian prisoners of the Japanese: a clinical study. Australian and New Zealand Journal of Psychiatry, 27, 20–29.
466
References
W ATSON , W. C. & S ULLIVAN , S. N. (1974) Hypertonicity of the cricopharyngeal sphincter: a cause of globus sensation. Lancet, ii, 1417–1419. W EINBERG, S., V AN D E M ARK , T. B., N ATKIN , B. B., et al (1970) Hysterical trismus. Report of a case. Oral Surgery, 30, 460–463. W EINBERGER , D. A. (1990) The construct validity of the repressive coping style. In Repression and Dissociation. Implications for Personality Theory, Psychopathology, and Health (ed. J. L. Singer), pp. 337–386. Chicago: University of Chicago Press. W EINSTEIN , E. A. (1966) Conversion hysteria after brain injury. Transcripts of the American Neurological Association, 91, 361–362. —— & K AHN , R. I. (1955) Denial of lllness. Springfield: C. C. Thomas. —— & H ACKETT , T. P. (1961) Predilection to death. Death and dying as a psychiatric problem. Psychosomatic Medicine, 23, 232–256. —— & L YERLY , O. G. (1966) Conversion hysteria following brain injury. Archives of Neurology, 15, 545–548. W EISAETH , L. & E ITINGER , L. (1993) Post traumatic stress phenomena, common themes across wars, disasters and traumatic events. In International Handbook of Traumatic Stress Syndromes (eds J. P. Wilson & B. P. Raphael), pp. 69–77. New York: Plenum. W EISEL , S. W., F EFFER , H. L. & R OTHMAN , R. H. (1984) Industrial low back pain: A prospective evaluation of a standardized diagnostic and treatment protocol. Spine, 9, 199–203. W EISMAN , A. D. (1972) On Dying and Denying. New York: Behavioral Publications. W ELLER , M. P. I. (1988) Hysterical behaviour in patriarchal communities: four cases, one with Ganser-like symptoms. British Journal of Psychiatry, 152, 687–695. —— & W IEDEMANN , P. (1989) Hysterical symptoms in ophthalmology. Documenta Ophthalmologica, 73, 1–33. W ELLS , C. E. (1976) The hysterical personality and the feminine character: a study of Scarlett O’Hara. Comprehensive Psychiatry, 27, 353–359. —— (1977) Dementia. Philadelphia: E. A. Davis Co. —— (1979) Pseudodementia. American Journal of Psychiatry, 136, 895–900. W ESSELY , S. (1987) Mass hysteria: two syndromes? Psychological Medicine, 17, 109–120. —— & N EWHAM, D. (1993) Virus syndromes and chronic fatigue. In Progress in Fibromyalgia and Myofascial Pain (eds H. Vaeroy & H. Merskey), pp. 349–360. Amsterdam, Elsevier Science Publishers. –––– & P OWELL , R. (1989) Fatigue syndromes: a comparison of chronic “post-viral” fatigue with neuromuscular and affective disorders. Journal of Neurology, Neurosurgery and Psychiatry, 42, 940–948. W ESTERMEYER, J. A. (1972) A comparison of amok and other homicide in Laos. American Journal of Psychiatry, 129, 703–708. —— (1989) A case of koro in a refugee family. Journal of Clinical Psychiatry, 50, 181–183. W HITE, P. D. (1989) Fatigue syndrome: neurasthenia revived. British Medical Journal, 298, 1199–1200. —— (1990) Fatigue and chronic fatigue syndromes. In Somatization, Physical Symptoms and Psychological Illness (eds C. M. Bass & R. H. Cawley), pp. 104–140. Oxford: Blackwell Scientific Publications. —— & L EWIS , S. W. (1987) Delusional depression after infectious mononucleosis. British Medical Journal, 295, 97–98. W HITLOCK , F. A. (1967a) The Ganser syndrome. British Journal of Psychiatry, 113, 19–30. —— (1967b) The aetiology of hysteria. Acta Psychiatrica Scandinavica, 43, 144–162. W HYTT , R. (1751) Observations on the nature, causes and cure of those disorders which are commonly called nervous, hypochondriac, or hysteric: to which are prefixed some remarks on the sympathy of the nerves. In The Works of Robert Whytt (3rd edn, 1767). London: Becket & du Hondt; Edinburgh: Balfour.
References
467
W IDIGER , T. A. (1991) DSM–IV reviews of the personality disorders. Introduction to special series. Journal of Personality Disorders, 5, 122–134. W IJESINGHE , C. P., D ISSANAYAKE , S. A. W. & M ENDIS , N. (1976) Possession trance in a semiurban community in Sri Lanka. Australian and New Zealand Journal of Psychiatry, 10, 135–140. W ILDE , O. (1895) The Importance of Being Earnest. New York: Avon Books, 1965. WILLIAMS, L. M. (1994) Recall of childhood trauma. A prospective study of women’s memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167– 1176. W ILLIS , E. (1986) Commentary: RSI as a social process. Community Health Studies, 10, 210– 219. W ILLIS , T. (1670) Affectionum Quae Dicuntur Hystericae et Hypochondriacae, Pathologia Spasmodica Vindicata Contra Responsionem Epistolarum. Lugdunum Bataviorum. —— (1684) An Essay of the Pathology of the Brain and Nervous Stock in which Convulsive Diseases are Treated of (trans. S. P. Cordage). London: Dring, Leigh & Harper. W ILSON , G., R UPP , C. & W ILSON , W. W. (1950) Amnesia. American Journal of Psychiatry, 106, 481–485. W ILSON , J. A., D EARY , I. J. & M ARAN , A. G. D. (1988) Is globus hystericus? British Journal of Psychiatry, 153, 335–339. W ILSON , J. P. & R APHAEL , B. (1993) International Handbook of Traumatic Stress Syndromes. New York: Plenum. W ILSON , J. W. & M ILLER , H. E. (1946) Delusions of parasitosis. Archives of Dermatology and Syphilology, 103, 355–363. WILSON, S. A. K. (1910) Some modern French conceptions of hysteria. Brain, 33, 293–338. W INCHELL , R. M. & STANLEY , M. (1991) Self-injurious behaviour: a review of the behaviour and biology of self-mutilation. American Journal of Psychiatry, 148, 306–317. W INFIELD , I., G EORGE , L. K., S WARTZ , M., et al (1990) Sexual assault and psychiatric disorders among a community sample of women. American Journal of Psychiatry, 147, 335–341. W INOKUR , G. & L EONARD , C. (1963) Sexual life in patients with hysteria. Diseases of the Nervous System, 24, 337–343. WITTELS, F. (1930) The hysterical character. Medical Research Reviews (New York), 36, 186–190. W OERNER , P. I. & G UZE , S. B. (1968) A family and marital study of hysteria. British Journal of Psychiatry, 114, 161–168. WOLFE , F. (1993) Fibromyalgia and problems in classification of musculoskeletal disorders. In Progress in Fibromyalgia and Myofascial Pain (eds H. Vaeroy & H. Merskey), pp. 217– 236. Amsterdam: Elsevier Science Publishers. ——, S MYTHE , H. A., Y UNUS , M. B., et al (1990) The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis and Rheumatism, 33, 160–172. W OLKIND , S. N. & FORREST , A. J. (1972) Low back pain: a psychiatric investigation. Postgraduate Medical Journal, 48, 76–79. W ONG , S. W., K WONG , B., T AM , Y. K., et al (1982) Psychological epidemic in Hong Kong. I. Epidemiological study. Acta Psychiatrica Scandinavica, 65, 421–436. W OODBURY , M. M., D EMASO , D. R. & G OLDMAN , S. J. (1992) Case study: an integrated medical and psychiatric approach to conversion symptoms in a four-year-old. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 1095–1097. W OODFORDE , J. M. & M ERSKEY , H. (1972) Personality traits of psychiatric patients with chronic pain. Journal of Psychosomatic Research, 16, 167–172. W OODRUFF , R. A. (1968) Hysteria: an evaluation of objective diagnostic criteria by the study of women with chronic medical illnesses. British Journal of Psychiatry, 114, 1115– 1119.
468
References
––––, C LAYTON , P. J. & G UZE , S. B. (1971) Hysteria, studies of diagnosis, outcome and prevalence. Journal of the American Medical Association, 215, 425–428. ––––, G OODWIN , D. W. & G UZE , S. B. (1974) Psychiatric Diagnosis. New York: Oxford University Press. W OOKEY , C. (1976) Myalgic encephalomyelitis. Lancet, i, 154. W OOLEY , C. F. (1986) From irritable heart to mitral valve prolapse – World War I, the British experience and Thomas Lewis. American Journal of Cardiology, 58, 844–849. —— (1987) From irritable heart to mitral valve prolapse: World War I – the U.S. experience and the origin of neurocirculatory asthenia. American Journal of Cardiology, 59, 1183–1186. —— (1988) Lewis A. Conner, M.D. and lessons learned from examining four million wounded men in World War I. American Journal of Cardiology, 61, 900–903. —— & B OUDOULAS , H. (1988) From irritable heart to mitral valve prolapse: World War I – the U.S. experience and the prevalence of apical systolic murmurs and mitral regurgitation in drafted men compared with present day mitral valve prolapse studies. American Journal of Cardiology, 61, 895–899. WORLD H EALTH O RGANIZATION (1977) International Classification of Diseases (ICD–9). Geneva: WHO. —— (1992) The ICD-10 Classification of Mental and Behavioural Disorders. Geneva: WHO. WRIGHT, J. P. (1980) Hysteria and mechanical man. Journal of the History of Ideas, 41, 233–247. Y AP , P. M. (1951) Mental disease peculiar to certain cultures: a survey of comparative psychiatry. Journal of Mental Science, 97, 313–327. —— (1952) The Latah reaction: its pathodynamics and nosological position. Journal of Mental Science, 98, 515–564. Y APKO , M. D. (1994) Suggestions of Abuse: True and False Memories of Childhood Sexual Trauma. New York: Simon & Schuster. Y AROSHEVSKY , F. (1975) Self-mutilation in Soviet prisons. Canadian Psychiatric Association Journal, 20, 443–446. Y ASSI , A., W EEKS , J. L., S AMSON , K., et al (1989) Epidemic of “shocks” in telephone operators: lessons for the medical community. Canadian Medical Association Journal, 140, 816–820. Y ASUNA , E. R. (1951) Hysterical amblyopia in children. American Journal of Diseases of Children, l06, 558–563. Y EALLAND , L. R. (1918) Hysterical Disorders of Warfare. London: Macmillan. Z ANGWILL , O. L. (1967) The Grunthal–Storring case of amnesic syndrome. British Journal of Psychiatry, 113, 113–128. Z ETZEL , E. R. (1956) Panel report on the borderline case by Rangell, L. Journal of the American Psychoanalytic Association, 3, 285–298. —— (1968) The so-called good hysteric. International Journal of Psycho-analysis, 49, 256–260. —— (1971) A developmental approach to the borderline patient. American Journal of Psychiatry, 127, 867–871. Z IEGLER , F. J., I MBODEN , J. B. & M EYER , E. (1960) Contemporary conversion reactions: a clinical study. American Journal of Psychiatry, 116, 901–909. —— & I MBODEN , J. B. (1962) Contemporary conversion reactions II: a conceptual model. Archives of General Psychiatry, 6, 279–287. Z ILBOORG , G. & H ENRY , G. W. (1941) A History of Medical Psychology. New York: W. W. Norton & Co.