J. psychiat. Rer., Vol. 22, Suppl. Printed in Great Britain.
1, pp. 33-54,
1988.
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CG22-3956/M $3.00+ .CQ 1988 Pergmm Press plc
ANXIETY, PANIC AND PHOBIC DISORDERS: AN OVERVIEW MARTIN ROTH*
and NICK ARGnEf
*University of Cambridge Clinical School, Level 5, Addenbrooke’s Hospital, His Road, Cambridge CB2 2QQ, U.K. and TPsychiatric Research Unit, Old Addenbrooke’s Hospital, Trumpington Street, Cambridge CB2 2QE, U.K. (Revised 23 February 1987) Summary-Thispaper reviews anxiety, panic, and phobic disorders as they were described in landmark works, along with more recent epidemiologic studies of the disorders. The author discusses clinical syndromes of anxiety as outlined in the DSM-III: agoraphobia, social phobia, generalized anxiety disorder, panic disorder, simple phobic states, and obsessive-compulsive disorder, relating them to Phobic Anxiety-Depersonalization Syndrome and to earlier descriptions by Westphal and Benedict. The paper addresses the problem of delineating anxiety and phobic states from depressive disorders, with regard to diagnosis and treatment outcome. Various etiological bases of agoraphobia, panic, and anxiety disorders are suggested: heredity, life events and circumstances, family background and developmental history, the premorbid personality, and some psychological aspects. Several questions are explored on the relationships of agoraphobia, anxiety and panic attacks. For example, is agoraphobia a new disease or one stage in the development of severe chronic anxiety? Are the phobias of agoraphobia acquired by conditioning or learning? Are “panics” spontaneous or physiological? Are panic attacks the first event in the primary cause of agoraphobia? For future work the authors propose a reassessment of the prevalence of agoraphobia and related disorders, a more careful definition of the agoraphobic disorders, and thorough clinical investigation of the various treatment modalities in well-defined populations. The past twenty years’ achievements in behavioural and pharmacological treatments for agoraphobia are briefly recapitulated. DO STATES OF ANXIETY EXIST?
attempts at wrestling with the task of arriving at a precise definition of anxiety are on record, and many contestants have conceded defeat. At the end of his well-known paper, LEWIS (1970) favoured “. . . substituting the term fear for it, with adjectival qualification . . ., ” while RADo (1959) was in favour of dropping the term altogether. Yet at the end of his critical review of the literature, Lewis was able to compile an inventory of features which provides a satisfactory foundation for clinical diagnosis and for operational definition in scientific inquiry. It would also command wide agreement. Lewis’ summary depicts clinical anxiety as an unpleasant emotional state experienced as fear or something close to it. It is unconnected with or disproportionate to environmental threats, and is associated with bodily discomforts such as chest constriction, difficulty in breathing, tightness in the throat, and weakness in the legs. Some of these symptoms are manifest in physiological disturbances, which are susceptible to measurement. Anxiety is an emotion directed in anticipation of the future, to ordeals which are yet to come (SLATER and ROTH, 1977). A number of these features can be found in FREUD (1953) and in the earlier accounts of DARWIN(1872). A feature that deserves to be added derives from the evidence that mild anxiety enhances performance while severe anxiety
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impairs or disorganizes it. Attention has been drawn to the fact that in a state of acute peril, anxiety may be retroactive; it backfires after the individual’s intact emergence from the ordeal. However, investigation of such apparent exceptions tends to substantiate the general rule while also shedding new light on states of anxiety (NOYESand KLETTI, 1977). An affect such as anxiety must resist unequivocal and precise definition, for the emotions merge insensibly with one another in mental life, and cannot be expected to have sharp boundaries. The boundaries are artificial, created to reduce the task of investigating affective states to manageable proportion. Clear-cut and unambiguous accounts of anxiety as an emotion are not necessary for delineating and defining the disorders that present in clinical practice. Here, the covariation of a whole cluster of features simplifies definition. In clinical practice, we can start with syndromes of distinctive, readily recognizable character such as anxiety with doubt-laden fears of disease or anxiety in the setting of agoraphobia or social phobia, and move outwards to evaluate the status of other conditions in which anxiety is a salient feature. As JAMB (1907) has pointed out, elucidation of the character of morbid states of mind will often illuminate the nature of the kindred but more intricate and elusive phenomena of normal psychological experience, and simplify the task of defining them. “Phobic anxiety state” and “anxiety neurosis” are no less or more precise than “obsessive-compulsive neurosis” or “depressive illness”. The premature imposition of strict and unambiguous definitions on difficult concepts in the early states of their development is counter-productive. Such terms are hypotheses that require the challenge of further inquiries; precise definitions come only with closer investigation of clinical phenomena that are always incompletely delineated in the first instance. As POPPER(1973) has pointed out “words are to be used in order to formulate theories” and excessive preoccupation with words and their meanings and definitions can lead only to an “empty verbalism”. With such reservations in mind, at this stage a brief definition of the two remaining terms in the title, “Phobia” and “Panic”, is appropriate. Phobic disorders refer to states of exaggerated and sustained fear experienced in contact with certain situations or objects which are rationally understood to constitute no dangers, but give rise to aversive behaviour. “Panic” refers to an abrupt attack of overwhelming fear accompanied by a massive autonomic discharge with palpitations, faintness, nausea, pallor, sweating, and feelings of imminent collapse, loss of control, or death. Detailed criteria are given in DSM-III-R. Panic may be regarded as an extreme form of anxiety or fear, but it also has the quality of being directed towards the present rather than the future. Anxiety is felt in anticipation of real or imagined future events, and it often increases as phobic situations approach. However, during a panic attack, the patient may feel that he is losing control or suffering from some disastrous physiological event. His fear of the future may be transformed into terror of the present. Even after the lapse of more than a century, the description by DARWIN (1872) of depression and anxiety in his Expression of the Emotions in Man and in the Animals remains illuminating. “After the mind has suffered from an acute paroxysm of grief, and the cause still continues, we fall into a state of low spirits; or we may be utterly cast down and dejected. Prolonged bodily pain, if not amounting to agony, generally leads to the same state of mind. If we expect to suffer, we are anxious; if we have no hope of relief, we despair”.
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Depression is, therefore, concerned with the past, with events completed; anxiety, with expectations of the future, with ordeals requiring a special effort for which the time has not yet arrived. RANGELL’S (1978) paraphrase of Darwin “Depression is about a certainty, anxiety about a possibility” does not quite capture the element of tormenting doubt, that the highly improbable hazards that are dreaded may materialise. The anguished anticipation that the impossible may just happen, is at the kernel of morbid states of anxiety.
EPIDEMIOLOGYOF AGORAPHOBIAAND RELATEDDISORDERS The reported prevalence of 2-4.7% anxiety states (SNMTH etal.,1971;AGRASetal.,1969) and the supposed rarity of limited agoraphobia cannot be accepted at face value. The symptoms of these disorders are a source of embarrassment to the patients, who have a strong tendency to conceal them. All forms of anxiety disorder show a female predominance. They have been considered rare in old age, but this view is not consistent with the community studies of BERGMANN (1971) who found neurotic symptoms to occur at a high prevalence (30-40%), and phobic and anxiety neuroses as well as depressive states to be relatively common. Three recent American studies have shown a prevalence for panic disorder over 6-12 months of between 0.4 and 1.5% (WEISSMANand MYERS, 1978; UHLENHUTHef al.,1984; NIMH Epidemiologic Catchment Area Study, first three sites). Comorbidity rates are high between the anxiety states, being of the order of 80% for agoraphobia and either generalised anxiety disorder or panic disorder. Further studies are needed to determine whether panic attacks can be differentiated from generalised anxiety either in terms of the detailed symptomatology or severity and time course. A history of nonspecific fears and other minor neurotic features in early childhood is often elicited from agoraphobic patients. But neurotic symptoms in childhood usually prove transient, and even school phobia is rarely reported as having occurred in the early life of agoraphobics. When it does appear in the first decade, it has a favourable outcome and is rarely followed by an agoraphobic neurosis in adult life. In contrast, school refusal commencing nearer adolescence is more liable to culminate in lasting disability and a small minority of severe agoraphobic neuroses evolves in uninterrupted fashion from such a starting point (WARREN, 1965; TYLER and TYRER, 1974). The history of subsequent development usually yields further evidence of anxious neurotic traits of a circumscribed kind. But the disabilities entailed are usually limited, and until a critical age span of 20-30 years is reached, the life history is relatively free of episodes of clear-cut, neurotic breakdown. Anxiety before ordeals such as examinations, interviews, and social occasions is common, although these features do not prevent many patients from achieving conspicuous success in their educational career and work. The breakdown into a clear-cut agoraphobic neurosis occurs in a high proportion of patients after marriage or the establishment of a relationship with a consort. The term “housebound housewife” has entered common language in some countries, and it is of interest that it is married rather than single women to whom the description specifically refers.
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MARTINROTHand NICK ARGYLE THE CLINICAL SYNDROMES OF ANXIETY
Faithful and accurate description and a valid classification provide the most solid foundation for clinical practice and scientific investigation of the morbid states of anxiety. The operational definitions of the different anxiety syndromes within DSM-III (1980) have performed a valuable service to contemporary psychiatry by promoting more consistent and reliable clinical and scientific practices. There is, however, an inevitable element of arbitrariness in the framing of operational definitions on the basis of a consensus of cooperating psychiatrists. The weight and importance to be attached to individual items of a syndrome should be proportionate to their value in description and discrimination. But the relevant quantitative data are not available. It is essential, therefore, to keep the system open to prevent it from becoming an orthodoxy. The descriptions are largely crosssectional in character having been mainly derived from examination of the present mental state. This is inescapable for the present, as standardised methods of investigating the remaining part of the picture are not available. But anxiety, phobic, and panic states arise in vulnerable personalities with an important historical and developmental dimension. This context of the anxiety disorders is difficult to investigate in a stringent manner at the present time, but it cannot be ignored without over-simplification in clinical or scientific work. With these points in view, the rubrics to be found within DSM-III under the heading of “Anxiety Disorders” and certain conditions regarded by psychiatrists in some countries as having an affinity with morbid states of anxiety, though not included in DSM-III-R, will be critically considered. Agoraphobia This disorder, given pride of place in the classification, has been intensively investigated in recent years and provides an excellent paradigm for anxiety disorders. Fear-laden avoidance of a wide range of situations leads to life patterns of restricted activities, and the helpless disability that evolves is well described. But the striking relief, often with freedom from panic, provided by the presence of a relative or close friend is a consistent feature that deserves a place among diagnostic criteria. So do the terror of death, collapse, of losing control, running berserk, falling unconscious, developing a heart attack, or suddenly becoming insane. Lurking behind them are the shame and humiliation engendered by the fear of lying prostrate, exposed in a state of helplessness, and having to be beholden to observers who are strangers. This last feature conveys something important about the personality traits of these patients. The condition almost invariably evolves against a background either of a general anxiety state or more limited anxiety symptoms often well compensated and concealed for years. Developments within the marriage or in interpersonal relationships that threaten security or other onerous life events are generally found to have occurred as antecedents to the early symptoms (ROY-BYRNE et al., 1986). It is in such a stressful setting that one or more panics or the early phobias evolve as a prelude to the more disabling phase of the illness. The very first panic is often experienced in a shop, queue, or crowd (SNAITHet al., 1971). In the first 6-12 months, agoraphobia is often a pan-neurosis with a wide range of symptoms including many phobic but also depressive, hysterical, and obsessional symptoms, threatened or actual syncopal attacks, and depersonalization.
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The evidence about the basic personality traits of agoraphobic patients is ambiguous, and further investigations are indicated. The helpless and dependent manner in which the patient often leans on relatives or close friends seemed, in early studies, to be a parody of personality features manifest in the patient’s premorbid state and not merely secondary effects. However, in investigations with objective measures of dependency, only 27% of patients reported awareness of dependency, together with resentment about it (~UGLASS et al., 1977). There is no necessary contradiction between these findings. Both are consistent with clinical observation. The study of BUGLASS et al. (1977) suggests that account has to be taken of the tendency of agoraphobic patients to camouflage their dependence on others. Recent enquiries have confirmed the close association between the agoraphobic syndrome and dependant personality disorder (REICH et al., 1986). The presence of an historical and developmental dimension in agoraphobia is further suggested by the frequency with which marital and earlier psychosexual difficulties are manifest. Although sexual frigidity may follow the first appearance of phobic symptoms, it often precedes it, developing in many patients after a first or second pregnancy. The dependent state and sexual coldness of agoraphobics have been well described by EY et al. (1974). In an early investigation (ROTH, 1959), a group of agoraphobic women was found to be married more often than women of comparable age in the general population, confirming the hypothesis that they were more often in quest of a secure haven. Their mothers had often had prominent anxiety traits or neuroses, and the attitudes of the agoraphobic daughters toward them were often ambiguous. Agoraphobia rarely arises out of the blue or in response to adverse life events alone, but evolves in personalities predisposed and rendered vulnerable in certain ways. Hence, there are developmental and historical dimensions to be defined to complete the picture gained from the present mental state of patients with agoraphobia and related neuroses. Certain questions are posed by the subdivisions of agoraphobia in DSM-III. The meaning of “agoraphobia without panic attacks” is obscure since acute anxiety attacks are indistinguishable from “panic” as defined in DSM-III, which refer to the usual antecedents of avoidance behaviour in agoraphobia. At present much interest is focused on the presence of spontaneous panic attacks that do not occur in association with phobic situations. It has been proposed that the presence of spontaneous panic attacks merits the diagnosis of panic disorder to which agoraphobic avoidance would be secondary, whereas panic attacks that only occurred in a phobic situation (whether it was agoraphobic or related to a social phobia or mono phobia) would be considered as secondary to the phobic illness. Social phobia The description of this disorder in DSM-III should include agoraphobics, who have similar aversions to those described as specific for social phobia. Despite this overlap, the condition does occur independently with a higher proportion of males, earlier onset, and more frequent complication of alcoholism. Generalized anxiety disorder Although the account given in DSM-III implies that the anxiety is free floating,
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ARGYLE
investigation often reveals anxiety to be centered upon a multitude of possible fears and dangers, one improbable disaster giving way to apprehension about the next. In one form of general anxiety state, predominately in males, the individual hovers between doubt and near certainty that he suffers from illness; cardiac disease gives place to cancer, venereal infection, leukemia, or brain tumor. These ideas differ from the nihilistic beliefs of psychotic depressives; it is the doubt-laden fear that there may be, rather than the certainty that there is disease, that constitutes the torment in anxiety states. Nonetheless, such patients may present a considerable suicide risk. There is a relatively sharp distinction between agoraphobic and other anxiety states, yet the initial emotional disorder in many agoraphobic patients is a general anxiety state. Incapacitating phobic symptoms develop in stepwise fashion, usually after exposure to severe stress. This is among many reasons for grouping phobic states with anxiety rather than with obsessional neuroses, as advocated by some authorities in the past. Panic disorder Panic disorder is found only in DSM-III-R, appearing neither in ICD-9 nor in the various national classifications that depart from ICD-9. Certain problems posed by this concept remain to be resolved. The occurrence of frequent “spontaneous” panic attacks in the absence of an associated anxiety or phobic neurosis is not generally recognized, and more stringent evidence for its existence as an independent form of anxiety disorder is needed. As spontaneous panic attacks have been given a role of central importance in the genesis of subsequent avoidance and dependent behaviour (KLEINet al., 1978; KLEIN, 1981), patients so affected are presumed to be in a transitional phase in the development of agoraphobia. But information regarding the course and outcome of “panic disorder” is lacking. These questions are discussed more fully in the etiology section. The separation of panic disorder as a diagnostic category derives from therapeutic response to imipramine and monoamine oxidase inhibitors (M.A.O.I.‘s) rather than recognition of a distinct group of patients. There is great overlap between patients who suffer from panic attacks and those who have different forms of phobic avoidance and also generalised anxiety, although with the recent increased interest, more patients are being reported with panic attacks without phobic avoidance. The majority of patients with panic attacks have so far been reported as having agoraphobia. Some patients may be described as phobophobic, that is they have anticipatory fear of the panic attacks themselves rather than associated situations. There is also evidence, mentioned later, for panic attacks being biologically different from anxiety. If this is substantiated, it may be more sensible to recognise anxiety-panic as one dimension of classification ultimately explicable in physiological terms, and the presence or absence of phobic avoidance as a separate dimension, which may be explained with the aid of cognitive and behavioural concepts. Simple phobic states Simple phobias of animals, heights, or other specific circumstances (thunder, etc.) require little comment. Their characteristics and responses to treatment conform to predictions from theories of learning. In these respects, they differ sharply both from agoraphobia and social phobia.
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Obsessive-compulsive disorder This condition is classified in DSM-III with anxiety disorders. Neurotic disorders having been excluded from the DSM-III system of classification. It was difficult to include obsessive and related disorders under any other rubric. Yet the features are qualitatively distinct in some respects. The everchanging range of themes revolving around ideas of contamination, dirt, infestation, violence, obscenity, and the numerical and abstract philosophical speculations-the fears of committing blasphemous, indecent acts, or risking impossible dangers-and the interminable ritual acts of cleansing, ordering, checking, and expiation are far removed from the clinical picture of general or phobic anxiety states. Successive attacks of illness present a strikingly consistent pattern in the clinical picture. The disorder, therefore, deserves a category to itself separate from “anxiety disorders”. It is regarded, in most countries, as a distinct, specific form of neurosis. But the concept of “neurosis” makes only a back door entry into DSM-III. The phobic anxiety-depersonalisation syndrome (PADS) The early account of this disorder (ROTH, 1959, 1960) was an attempt to describe what has come to be known as “agoraphobia”. It incorporated the clinical picture of the early acute stages that were much more common in psychiatric clinics 25-30 yr ago, before anxiolytic and antidepressant drugs had come on the scene. The syndrome described by WESTPHAL(1871) seemed at the time different, referring to three men who feared wide empty streets and open spaces rather than crowds, shops, and queues. Most contemporary agoraphobics are female and are comforted by the presence of spouses, mothers, and intimates. The passers-by and strangers, whose help was sought by Westphal’s original agoraphobics, would have frightened and humiliated the patients studied 25-30 yr ago. The dependence and the psychosexual immaturity of the basic personality which appeared as a related and integral part of PADS had not been mentioned by WESTPHAL(1871) or by BENEDICT(1870), the latter regarding “dizziness” as primary in “Platzschwindel”. In retrospect (ROTH, 1959), it is plain the depersonalisation was given an undeserved prominence in the original description. In a recent investigation (BUGLASSet al., 1977), it has been found in 37% of cases. It is in the early and acute phases that depersonalisation and related features are most often prominent: they tend to fade, appear intermittently or not at all as the disorder enters a chronic phase. Recent inquiries have confirmed the relative specificity of the relationship of depersonalisation to states of anxiety. NOYESand KLETTI(1977) have studied 101 persons during extreme danger. More than 50% of those who thought they were about to die described feelings of unreality (81%), a changed passage of time (78%), increased speed of thinking (68%), automatic movement (63010), a sense of detachment (61@/‘0),and a blunting of emotion (57%). They also have described the phenomena of “panoramic” memory. All these features were observed in episodic form in the agoraphobic patients in the early studies (ROTH, 1959; HARPERand ROTH, 1962). The overlap of symptoms in patients with temporal lobe lesions and agoraphobia has been confirmed by recent investigations (UHDE et al., 1984). When the individual faces imminent danger of death as in near drowning or in a threatened car crash at speed, the depersonalised patient describes a part of himself as having been calm and without fear, observing the other self as a passive spectator. NOYESand
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(1977) came to a conclusion similar to our own (ROTH and HARPER, 1962), namely that depersonalisation comprised a state of heightened arousal together with dissociation of emotion and thus served as an adaptive mechanism which enhanced the chances of survival in acute danger. Some physiological evidence consistent with this view is on record (LADER, 1975; KELLY and WALTER, 1968).
~ETTI
Primary depersonalisation Feelings of unreality regarding the self or outside world appear abruptly and continue for months or years. The emotions are described as “dead”, and anxiety is usually in abeyance, but may erupt in episodes or be present as an undercurrent of apprehension. One patient described his mental state as follows: “ . . . I feel like a mind detached and nebulous without a body or physical setting . . . . Fears and anxieties of one kind and another play quite a large part in my condition. There are the fears, of course, of insanity, of sudden blackness or loss of memory. There are also fears of a sudden loss of control . . . of some violent distressing fit or an outburst of violence or of suicide. I suffer bouts of depression, but when I try to be quite honest, I cannot say that I have ever really wanted to commit suicide. Rather I feel that I might reach a state in which I would want to, or might do so unconsciously . . .; these fears involve a lack of security. When they are at their worst I feel simply unsafe, as though I could experience security only if I had some kind of constant ‘keeper’. I feel that tucked up in a hospital bed with a psychiatrist on one side, a surgeon on the other and a flock of attendant nurses, nothing really serious could happen”.
In some patients with depersonalisation, anxiety alternates with feelings of unreality, while others protect themselves from panic by avoiding bright light, the open country, crowded places, or mirrors, which tend to intensify feelings of unreality after inducing transient surges of panic. Studies of depersonalisation may shed light on some of the basic psychological and physiological mechanisms underlying this whole group of disorders. RELATIONSHIP BETWEEN ANXIETY AND PHOBIC STATES AND DEPRESSIVE DISORDERS
Anxiety and phobic disorders and depressive illnesses may constitute distinct clinical territories or may merge in insensibly with one another in the manner of continuum as the exponents of the unitary concept of affective disorders of a few decades ago, LEWIS (1934) and MAPOTHER (1926), insisted. These questions are of central importance for classification and management of the most highly prevalent groups of disorders in modern psychiatric practice. The issue is complex. On the one hand, both anxiety and phobic states may have a strong depressive colouring. There is no general concensus as to which cluster of features should receive precedence in diagnostic formulation and should constitute the main target in therapy. On the other hand, a substantial proportion of depressive disorders of every kind have concomitant anxiety symptoms. Even more subtle and difficult problems are posed by patients in whom minimal phobic disabilities, which are well-controlled over many years, are released as a crippling disability by the advent of an endogenous or major depressive disorder. Further complexities have been introduced by the recent claim that panic attacks can be effectively treated by tricyclic compounds causing associated phobic avoidance behaviour, regarded as secondary, to recede (KLEIN et al., 1981; ZITRIN et al., 1981). These claims are contested by researchers who have been concerned mainly with the study of behavioural treatment (MARKS,1981a). They believe that such results can be achieved only in patients with depressive disorders with epiphenomenal phobic symptoms (marks, 1981b).
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DSM-III deals with classification by the simple device of a sharp cleavage. Panic disorder, anxiety, and phobic states are assigned to a distinct category of “Anxiety Disorders” apart from depressive states which are classified under “Affective Disorders”. There is some evidence from studies of classification to justify creating a clean line of demarcation. But the creation of entirely separate categories fails to do justice to the complexity of some issues in this area. A number of investigations have adduced evidence for the existence of a qualitative distinction between depressive and anxiety neuroses (PRUSOFFand KLERMAN, 1974; DOWNING and RICKELS, 1974; RICKELSet al., 1979). The first inquiry to validate the distinction by means of follow-up studies was undertaken in Newcastle (ROTH et al., 1972; KERR et al., 1972; GURNEYet al., 1972; SCHAPIRAet al., 1972; KERR et al., 1974). The relatively clear separation of depressive states from anxiety states established with the aid of principle components and discriminant function analyses was validated by independent lines of evidence. Follow-up studies over 2l%-4 yr showed that the depressive group of patients had a more favourable course and outcome than those with anxiety. There was very little crossover between the groups in respect to the type of syndrome by patients in relapse. Finally, the index derived from stepwise discriminant function analysis for predicting outcome was made up of different groups of items in the depressive and in the anxious groups of patients, respectively. Two subsequent investigations have served to fill certain gaps in the evidence in this area. The second study (MOUNTJOY and ROTH, 1982a, b) excluded endogenous depressions, but was confined to depressive, anxious, and phobic neuroses, a territory within the affective disorders where lines of demarcation are unclear. Although personality and biographical data were excluded from the statistical analyses in this study, a demarcation line between anxiety and depressive syndromes was again demonstrated. The Hamilton Depression, the Hamilton Anxiety, and the Wakefield Depression Scales, which purport to measure severity alone, had unexpected characteristics. When stepwise discriminant function analyses were undertaken to estimate the coefficients for the items in each scale, some items emerged with positive weights while others showed negative weights. Utilizing the rating scales with their recalculated weights, 90% or more of the patients were reallocated to the two diagnostic groups made up of “anxious” and “depressed” patients in whom a confident diagnosis could be made at the commencement of the inquiry. In other words, the rating scales could be adapted to function as discriminating scales, suggesting that they had not been unidimensional scales for rating “depression” or “anxiety” in the first place. In the most recent investigation of a consecutive series of 150 patients in whom anxiety or depression were the salient features (CAETANO, 1980), the Present State Examination was used as the initial rating instrument. This entails rating each item serially on the basis of strict definitions, thereby minimizing clinical preconceptions and halo effects. Using principle components and stepwise discriminant function analyses, the distributions of scores obtained were consistent with the presence of two distinct populations corresponding to the anxiety and depressive subgroups. The Maudsley Personality Inventory and the 16 Personality Factors were administered to 89 of the patients after they had recovered from the presenting episode of illness. With the aid of an index derived from analysis of the scores on these two tests, the separation into the anxiety and the depressive groups on the basis of clinical symptoms alone was replicated correctly in 83.4% of the patients.
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Despite some methodological differences, the clusters of features depicted by these investigations as characteristics of the anxiety and phobic disorders, and the depressive disorders respectively, were very similar. Anxiety avoidance, panic attacks, autonomic manifestations of anxiety, situational anxiety, obsessive symptoms, irritability, depersonalisation, and derealisation emerged as the features with the highest loadings within the anxiety-phobic cluster; observed depression, depressed mood, persistent (in contrast to intermittent) depression, retardation, morning depression, early waking, and morbid guilt were characteristic of the depressive syndrome. Therefore, there is a large body of evidence indicating that despite substantial overlap regarding symptoms, the depressive and anxiety disorders are distinct. The inquiries in this field have yielded a number of discriminating scales, (GURNEYet al., 1972; GURNEY,1971; MOUNTJOY and ROTH, 1982a, b). These should prove valuable as algorithms. When applied alongside diagnoses made with the aid of operational criteria, they should facilitate clinical decision making and improve the replicability of scientific observations.
NONSPECIFICAND INDETERMINANCY OF TREATMENTRESPONSEIN ANXIETY-PHOBICAND DEPRESSIVEDISORDERS It is, perhaps, the failure to deal consistently with the problem of diagnosis and to heed the complexities created by overlap between affective and related disorders that has prevented emergence of any satisfactory consensus regarding the optimal treatments of anxiety, panic, and phobic states. To some extent, this reflects the lack of agreement regarding differential diagnosis and treatment in the wider area of the depressive and anxiety disorders. JOHNSTONEet al. (1980) studied 240 neurotic outpatients who were not diagnosed, but scored both depressive and anxiety symptoms by observation and self-rating scales. During a four-week trial of amitriptyline, diazepam, a combination of the two, or placebo, both anxiety and depressive features were favourably influenced by each form of medication. The interpretation of these findings is difficult; in the absence of clinical diagnosis (rating scales alone being inadequate), the character of the patient population remains uncertain. Investigating outpatient depressives and patients with a mixture of anxiety and depression, ROWANet al. (1982) studied the effect of phenelzine, amitriptyline, and placebo in a doubleblind, controlled trial. Both active substances were superior to placebo, particularly regarding depressive symptoms. Statistical analysis failed to demonstrate any differential responses to active drugs within this group. Before it is concluded that any group of antidepressant drugs discriminates in its therapeutic effects between anxiety and depressive disorders, attempts should be made in clinical trials to record information along several parameters. This should apply to all patients in whom prominent anxiety, depression, or both are central clinical features. There are complex relationships in this area between a range of psychiatric phenomena. In patients presenting with conspicuous depressive symptoms, clinical exploration is all too liable to be confined to these features alone, and chronic, severely disabling, phobic symptoms may go undetected in the absence of direct inquiries. The reverse situation is presented by some phobic states appearing “de novo” in middle or late life, when a major endogenous illness may acutely
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exacerbate what had been for many years a mild nondisabling phobic state. The specific depressive features are manifest in such elderly patients in a “silent” form. In therapeutic trials in anxious, agoraphobic, other phobic, and anxious-depressive individuals, valuable new knowledge might be gathered if reliable information were to be recorded along a number of parameters. They should include: (1) diagnosis based on defined operational criteria; and (2) scores recorded on rating scales for (a) depression, (b) phobias, (c) anxiety, (d) panic frequency, and (e) on a measure of premorbid personality. Information on items (a)-(e) should be recorded at regular intervals throughout the trial. The sequence of changes along these parameters should provide information regarding the association between mood changes, phobias, panic attacks, and “pathoplastic” factors, that is, the colouring of clinical features lent to the picture by the premorbid personality. The much disputed causal links between a number of these variables should also receive some clarification. THE ETIOLOGICALBASISOF AGORAPHOBIA,PANICAND ANXIETYDISORDERS The etiological basis of agoraphobia and related disorders is unknown. But attempts at a synthesis of developments during the past 25 yr may provide guidelines for fresh enquiries into causation and treatment, and for understanding those affected by these disorders. Only a selected sample of studies from a large and growing literature can be reviewed here. Heredity The view that agoraphobia and related disorders are due to a specific physiological or biochemical abnormality in the central nervous system determined by genetic factors has gained some currency in recent years. CROWEet al. (1983) studied 41 patients with panic disorder and 41 controls and found morbidity figures of 17.3 and 1.8% respectively in first degree relatives, with female relatives having twice the risk of male relatives in the panic disorder group. However, the evidence regarding heredity is inconsistent. SOLYOM et al. (1974) found 31% of the mothers and 6% of the fathers of agoraphobic patients suffered from phobias. On the other hand, BUGLA~Set al. (1977) reported phobias in only 7% of 60 parents of agoraphobics as compared with 2% of control patients. NOYRSet al. (1986) found an increased morbidity risk for agoraphobia (11.6%) and panic disorder (8.2%) in first-degree relatives of agoraphobics, but only for panic disorder (17.2%) in the relatives of panic disorder probands. There is some evidence from twin studies in favour of a hereditary basis for panic disorder (TORGERSEN,1979). SLATERand SHIELDS(1969) reported a marked discrepancy in concordance between anxious monozygotic and dyzygotic pairs of twins, 41% as against 4%. Slater’s 4% figure of dyzygotic cases with all types of anxiety state contrasts with Noyes and coworkers’ (NOYESet al., 1986) overall figures of 31% for first-degree relatives and 41% for interviewed cases. It is clear that there are differences in definition to be resolved. It may be concluded that hereditary factors contribute to the etiology of states of anxiety and panic disorder. But data from adoption studies are not available in agoraphobia or panic states. It would be premature to infer that a hereditary factor of a classical Mendelian kind that would be associated with a specific biochemical deficit in the brain has already been identified
MARTIN ROTH andNICK ARGYLE
44
in agoraphobic or related disorders. This does not exclude the possibility that some biochemical correlates of agoraphobic and related disorders may exist and that they may be favourably influenced by pharmacological treatment. The familial relationships of depression and panic disorder are currently being examined. WEISSMAN(1985) has reported that the presence of panic disorder in depressed probands increased the risk of depression, alcoholism, panic, and phobic disorders in the relatives. LIFE EVENTS
AND CIRCUMSTANCES
ASSOCIATED
WITH ONSET
The first attack of panic or of phobic anxiety with aversion behaviour often appears abruptly. Many of those affected had previously lived seemingly full and normal lives. Yet, within a matter of weeks or months, they find themselves severely incapacitated by anxiety, unable to move more than yards from the safe haven of home. They may be perplexed by the rapidity with which they have been rendered helpless, and the perplexity exacerbates their anxiety. In the majority of patients, a certain amount of careful exploration and unraveling of the events in the previous weeks and months is necessary to understand the changes in life related to the onset of a neurosis in which the patient’s sense of security and independence are seriously undermined. We have to say “related to” because scientific understanding of the processes whereby the patient is rapidly reduced to crippling disability through panic attacks and avoidance behaviour is limited. But when exploration is adequate, total mysteries are few. A 34-yr old woman and her husband had undergone five years of joint investigations for infertility. A year ago, she had a hysterectomy for menorrhagia. Four months ago, the couple adopted a baby girl, and two months later, the patient discovered that her husband was having a sexual affair with his secretary. The first severe panic attacks began while she was in a large crowded supermarket four days after her husband announced his intention to leave her. Such experiences are not “sufficient” causes, but they impinge with a selective severity on the Achilles’ heels of anxiously predisposed persons. In agoraphobics, we are not studying a sample of individuals randomly drawn in respect of personality from the general population. The term “endogenous anxiety state”, which has been used as a synonym for agoraphobia (SHEEHANet al., 1982b) does not, therefore, appear appropriate. When detailed examination proves entirely negative for agoraphobia as regards psychological and social factors, organic causes such as hyperthyroidism, phaeochromcytoma, hyperinsulinism, and occult physical diseases have to be excluded with care. Family background and developmental history Evidence or presence of disturbed family background comes from a number of studies. Using a standard rating scale, SNAITH et al. (1971) found the family background of agoraphobics to be more unstable than that of other phobics. In a comparative study of depressed (“endogenous” and “neurotic”) and anxious patients (comprising agoraphobic and generalised anxiety groups) (ROTH et al., 1972), the anxious subjects differed significantly in respect to a poorer relationship with parents, a higher prevalence of neurotic traits, a poorer social adjustment, and more premorbid personality traits of anxiety,
ANXIETY,
PANICAND PHOBICDISORDERS
45
immaturity, dependence, and instability. In all these respects, the agoraphobic subgroup of patients was the most severely affected and the endogenous depressives least affected. However, the anxious patients did not differ significantly from the depressives regarding phobic symptoms in childhood, and neither in the agoraphobic nor in the generalised anxiety states was there evidence of separation anxiety. This is consistent with the findings of BUGLASSetal. (1977), who recorded no differences between agoraphobic and control subjects as far as a record of separation anxiety or maladjustment in school were concerned. It is at variance with the view of KLEIN (1981) that separation anxiety and school phobia are frequent in childhood among patients with panic disorder and agoraphobia. A study by DELTITO et al. (1986) found school phobia in childhood in 60% of those patients with panic disorder who also had agoraphobic disorder. The premorbid personality There is no sound evidence for regarding the agoraphobic illness as a recrudescence of a similar disorder in early life. As has already been pointed out, school refusal, often regarded as a form of separation anxiety, nearly always subsides without a trace when it commences under the age of 11 yrs. Cases that make their appearance after 12 yr often culminate in adult neurosis including a very small proportion of agoraphobics. Yet there is evidence from a number of sources to suggest that agoraphobic patients are vulnerable to breakdown before the appearance of their specific symptom. It is difficult to obtain firm and objective evidence about this question. The evidence in relation to the over-protection of agoraphobic patients is conflicting (SNAITH et al., 1971; SOLYOM et al., 1976). Dependence on others is often mentioned as a prominent personality trait, and some reports derived from systematic clinical investigation have described agoraphobic patients as being more emotionally dependent than other neurotic or control subjects (SHAFER, 1976; ROTH et al., 1972). But such findings could have been influenced by halo effects arising from the parodied form of dependence manifest during the presenting clinical disorder. BUGLASS et al. (1977), using an inclusive set of indices, found no differences between agoraphobic and control subjects and reported that 27% of the agoraphobics had a combination of dependency and resentment. This describes the ambiguity that can be defined in many agoraphobic patients with the aid of systematic and thorough investigation. Patients consciously employ strategies for concealing dependency and feelings of obligation to others. These have to be circumvented with objective measures in future studies in order to secure accurate results. Recent enquiries provide support for a close association between agoraphobic syndrome and dependant personality disorder (REICH et al., 1986). An inquiry with the aid of a standardised clinical interview (ROTH et al., 1972; GURNEYet al., 1972) has shown that agoraphobic patients score higher in measures of anxiety proneness and neuroticism than patients with nonphobic anxiety and depressive illness. In an investigation with the Maudsley Personality Inventory (KERR et al., 1970), neuroticism scores of the anxious patients were significantly higher than those of the depressive group both during presenting illness (P-0.02) and at follow up (P-0.001). The agoraphobic patients had the highest neuroticism scores. At follow-up examination, the neuroticism scores of the male patients had declined markedly, but there was no comparable fall in the scores of the female agoraphobic or other neurotic patients. The
46
MARTIN ROTH and NICK ARGYLE
anxious groups also had the lowest extraversion (E) scores, and among the women who had recovered from agoraphobic or generalised anxiety, E scores remained significantly below normal; the scores of endogenous depressives remained significantly higher. Although the increased neuroticism and introversion of patients with phobic anxiety may have been exaggerated by the illness, the deviations from the norm of these scores were largely independent of illness, having persisted after remission from it. Some physiological aspects Agoraphobia is a chronic disorder that fluctuates, or, in some cases, continues unabated for years. Its etiology is complex, but the possibility remains that some final physiological pathway can be defined and will prove susceptible to control. When exposed to phobic stimuli, agoraphobic patients exhibit an increase in skin conductance (MARKSet al., 1971; GELDER et al., 1973) and in fluctuations of conductance (GELDER et al., 1973). There is also an increase in heart rate and in blood pressure. But it has long been known that such indices of autonomic arousal are not specific for any one form of emotional disorder. Panic attacks have been induced experimentally with sodium lactate infusions by PITTS and MCCLURE(1967), FINKet al. (1969), KELLY et al. (1971), and mork recently under doubleblind conditions by LIEBOWITZ et al. (1983). These studies show that the majority of patients with panic disorder (or anxiety neurosis in earlier studies) develop panic attacks when given lactate infusion, whereas few or none of the control group do so. Prior treatment with imipramine prevents panic attacks on lactate infusion. Panic attacks have also been induced.experimentally by 5% carbon dioxide (GERMANet al., 1984) caffeine and yohimbine. Gorman suggests that increased CO, in the region of the locus coereleus is a common effect of lactate infusion and COz inhalation. A central feature of all anxiety states is constituted by the tendency of patients to project some improbable disastrous outcome from minimal and benign cues, a process into which there is usually considerable insight. The agoraphobic expects that palpitations or minor somatic discomforts will lead to losing control, running berserk, lapsing into insanity, or collapsing, and so being humiliated. In generalised anxiety states, the affect is regarded as “free floating” but, in f&t, it fastens upon the minutiae of everyday life and enlarges them to sources of threat and imminent peril in a manner that may lead to states of protracted anguish. Awareness that the predictions entail a morbid exaggeration does not help. GRAY(1982) postulates that there is a neural system specifically concerned with matching past experience and current sensory cues for the estimation of probabilities. He considered the neural substrate of anxiety is to be found in the abnormal functioning of a “behavioural inhibitory system” comprising anatomically the septohippocampal system, the Papex circuit, the prefrontal cortex, and the ascending monoaminergic and cholinergic pathways that innervate these forebrain structures. It operates by comparing predictive with actual sensory events. Behavioural inhibition is generated when the predicted event is estimated to have aversive implications. There is a partitioning of activities among the different pharmacological constituents of the system. The theory is that the noradrenergic part construes the importance of sensory input and then promotes the appropriate arousal. The serotonergic input generates appropriate motor inhibition. The cholinergic system, interacting with the other pathways, then mediates the selection of the relevant stimuli to
41
ANXIETY, PANIC AND PHOBICDISORDERS
which responses may be made or inhibited. The theory is backed by a large body of experimental data, but it is difficult at present to see any means of applying it to research with agoraphobic and other anxious subjects. QUESTIONS
ON THE RELATIONSHIPS
OF AGORAPHOBIA,
ANXIETY
AND
PANIC
ATTACKS
The sudden emergence of severely disabling agoraphobic symptoms in individuals who had achieved tolerable and effective adjustment in many facets of their earlier lives make it tempting to seek a specific physiological or psychophysiological explanation. Hypotheses that lend themselves to experimental evaluation elude us; however, a detailed study of the clinical features and historical development of the condition may define problems that lend themselves to scientific exploration. IS AGORAPHOBIA
A NEW DISEASE OF MANY
PROCESS
SEVERE
OR MERELY
ONE STAGE
CASES OF CHRONIC
IN THE DEVELOPMENT
ANXIETY?
Neither of these suggested answers is in accord with the facts. As we have seen, general anxiety has usually been present for months or years in most cases. Yet some qualitative change appears to enter with the onset of phobic symptoms. Although many patients improve considerably, agoraphobia remains a chronic disorder even with modern treatments (CLONINGER et al., 1981). It is unproductive to ignore this fact, and learning theory, psychoanalysis, or neuropharmacology cannot provide explanations of the change that has occurred. However, anxiety neurosis seems to be the common starting point. It is a much less disabling and much more treatable condition. The positive implications of this analysis are, therefore, that an attempt should be made to treat general anxiety states, particularly those in whom fleeting, well-controlled phobias are present. It is possible that this could pre-empt the emergence of agoraphobic neurosis. ARE THE PHOBIAS
OF AGORAPHOBIA
ACQUIRED
BY CONDITIONING
OR LEARNING?
Until about 20 yr ago, the predominant theory was that phobias such as those in agoraphobia had developed by classical conditioning and were maintained and reinforced by the decrease in anxiety consequent upon avoidance behaviour (EYSENCK and RACHMAN, 1965). Even in their present modified form, such theories cannot be reconciled with the facts. The setting in which the first phobic experience occurs bears no resemblance to situations that subsequently evoke avoidance behaviour. Moreover, one would have expected the situations that evoked fear-laden behaviour to have been shaped by the circumstances in the patient’s life; but this is not the case. There is a remarkable consistency among agoraphobic patients in respect to the types of situations that evoke phobic avoidance. And the persistence of severe autonomic arousal in patients during in vivo exposure treatment is inconsistent with theories of learning. ARE
“PANICS”
SPONTANEOUS
AND
PURELY
PHYSIOLOGICAL?
If panics are purely physiological events, why are they liable to occur under certain circumstances and not merely discharged at random? Why do crowded shops, queues, and
48
MARTIN ROTH and NICK ARGYLE
streets where help is readily at hand cause panic, whereas being alone at home (where one might pass out and perish unaided) is less liable to evoke panic. How are mothers or others able to provide immunity from panic by their presence, and what is the historical or symbolic significance for the patient. In a recent study, NORTON et al. (1985) questioned 186 normal young adults and found 34.4% reporting one or more panic attacks in the past year. The occurrence of isolated panic attacks does not usually lead to the development of agoraphobia, but patients who have developed agoraphobia often report dramatic increases in phobic avoidance which are punctuated by panic attacks. Patients with mono phobias and social phobias also experience the symptoms of panic attacks when actually in a phobic situation. It may be that there is a spectrum of susceptibility to panic attacks which varies genetically but can also be altered by psychological and environmental circumstances and also by-drug therapy. ARE PANIC ATTACKS
THE FIRST EVENT IN THE PRIMARY
CAUSE OF THE GENESIS OF
AGORAPHOBIA? KLEIN (1964, 198 1) and ZITRIN et al. (198 1) answer this question affirmatively. His view is important because he claims that pharmacological treatment of the panics cause the avoidance behaviour to recede and disappear. The therapeutic question is addressed later. The problem regarding etiology is the absence of a valid and reliable definition of panic. The description of panic disorder in DSM-III is difficult to differentiate from the bouts of acute tension in generalised anxiety disorder. The question-which then arises is whether panic attacks are primary causes or consequences of mounting background anxiety. Many patients report nothing like “panic” until phobic avoidance has been established, and others do not report panics at all. It should be possible to evaluate these alternative hypotheses and to choose between them by taking a detailed, systematic, standardised history. SOME TASKS FOR THE FUTURE
Prevalence Agoraphobia and related disorders are severely incapacitating illnesses which cause personal, familial, and social distress. These conditions have been identified to an increasing extent in recent years, and old figures for prevalence that are quoted probably fail to do justice to the size of the problem. There is a strong case for re-estimating the prevalence of agoraphobia in psychiatric practice and, with the aid of epidemiological studies, in community samples. There are indications that many cases may remain concealed under the heading of “affective disorder” which is often present as a mere coloring. Up-to-date findings should render practitioners more alert to the diagnosis of agoraphobia and related states. Definition The definition of agoraphobic disorder needs to be tightened to facilitate the greatest possible measures of replicability of scientific findings. In the course of several investigations of patients with affective disorder in Newcastle and Cambridge, minor distinctive phobic features were frequently discovered after specific inquiries were made. The phobic symptoms
ANXIETY, PANIC ANDPHOBIC DISORDERS
49
were variable, involved only transient anxiety, were readily overcome with effort, and never entailed flight. The patients were never housebound. The situations that aroused passing unease were similar to those in agoraphobia and, if focused upon, investigation could lead to misdiagnosis. These symptoms are nonspecific, widely distributed, and subordinate in diagnosis to affective disorder, which was the most common condition present. DSM-III carries the qualification “not due to . . . major depressive disorder . . .” But the conditions under which phobic features should be regarded as secondary and epiphenomenal need to be more explicitly spelled out. Selection of cases There have been significant advances in treatment in this area. Yet psychiatric outpatient clinics abound everywhere with patients who have been treated with methods of proven value and yet suffer from severe, incapacitating, phobic disorders. One is aware from clinical experience that therapists of every kind tend to be highly selective in the patients they treat. If a behavioural therapist confines himself to patients with a relatively limited span of phobias and other symptoms and to those with a relatively stable premorbid personality, his results will not prove comparable to those of therapists less selective. It is desirable that agoraphobic patients admitted to treatment trials should be representative of the total population of patients who come under care. The manner in which the sample was selected should be specified and its characteristics stated along relevant parameters. The results of treatment During the last 20 yr behavioural and pharmacological treatments have improved the outlook for those suffering from agoraphobia. However, the conflicting claims of those whose findings led them to suggest that behavioural therapies represent the optimal treatment in this field, and those who advocate pharmacological treatments as being the most simple, economical, and rapidly effective, can only be resolved with the aid of further controlled investigations. Although a number of well-designed trials are on record, the total number of patients studied remains relatively small. It is imperative that well-designed therapeutic investigations be mounted to settle the issues in dispute. As far as behavioural treatment is concerned, the past twenty years’ experience has served to establish that optimal results are achieved with those forms of behavioural treatment that make use of direct in vivo exposure to feared situations (CROWEet al., 1972; MATTHEWS et al., 1976; JOHNSTONet al., 1976). There is good evidence that the reduction in fear and avoidance behaviour in agoraphobic patients is significantly greater than that achieved by formal psychotherapy. The signs of autonomic arousal during exposure are relatively unaffected. There is also evidence from a number of comprehensive follow-up studies to testify to the lasting effects of behavioural treatment. A study by MUNEZY and JOHNSTON (1980) of patients treated by GELDERand coworkers (1973) and MATTHEWSand coworkers (1976, 1977) showed the therapeutic benefits in 65 out of 66 agoraphobic patients to have been sustained for the intervening 5-8.6 yr. These are impressive achievements. But full evaluation requires that residual phobic restrictions be specified and that control subjects be investigated over equally long periods. Cognitive therapies whose value has been established through the pioneering efforts of BECK (1976) is often used in conjunction with other treatments.
50
MARTIN
ROTHand NICKARGYLE
The major study in Klein’s group (ZITRIN et al., 1981) conveyed a different picture. They compared the results of treatment with imipramine and behaviour therapy, imipramine with supportive psychotherapy, and placebo with behaviour therapy administered over 26 weeks. Significant improvements were recorded both in the therapists’ and patient’s self ratings in respect to each treatment program that included imipramine. The results were interpreted as due to the beneficial effects of imipramine on “spontaneous panic”, thus reducing anticipatory anxiety and avoidance behaviour. Surprisingly, imipramine with behaviour therapy was no more effective than imipramine with supportive therapy. It is to be noted, however, that the dropout rate ranged from 20 to 26% in the agoraphobic and mixed phobic cases, and at the end of one year, about 22% of agoraphobics were in relapse. Here again, end of trial ratings show the patient to be well above a symptomatic baseline, but residual disabilities are not well delineated. The interpretation of MARKS (1981a, b), that antidepressant medication exerts its benefits in agoraphobia through its influence on concomitant depression, remains to be explored. KLEIN(1964) reported that panic attacks predicted response to tricyclic antidepressants, whereas generalised anxiety alone responded better to benzodiazepines. Since then, imipramine has been used increasingly in the treatment of panic attacks in doses up to 300 mg a day particularly in America. M.A.O.I.‘s have also been found to be effective (SHEEHANet al., 1980). Alprazolam, a triazobenzodiazepine, is currently being used in a large multicenter trial, and the first phase shows its efficacy in the treatment of panic disorder (SWINSON, 1985). For the present, the claims of behaviour therapy appear to be supported by a stronger body of follow-up observations than those of drug treatment. In a 5-10 yr follow-up study of 32 patients with panic disorder who had been treated with drugs (tricyclic compounds in two-thirds of the cases), CLONINGERet al. (1981) judged them to have made very little impression on the course of illness-all six severely phobic patients remained severely disabled. But it is clear that the validity of the claims advanced for the two forms of treatment can only be settled by controlled studies in which (1) behaviour therapy, (2) pharmacological treatment either with tricyclic compounds or M.A.O.I.‘s (SHEEHANet al., 1980), or (3) a combination of both forms of treatment are compared. Moreover, although psychotherapy has for the present proved inferior to behavioural treatment in agoraphobia, it cannot be assumed, that employed as an adjunct, it would add nothing of substance to the results achieved by other forms of treatment. CONCLUDINGREMARKS Agoraphobia may be regarded as a paradigm of the disorders that were, before the introduction of DSM-III, classified under the heading of “Neuroses” in all countries. Recent progress in relation to the etiology and treatment of this disorder may, therefore, prove to be germane for a wide range of problems in psychiatry. The excess mortality for circulatory system disease in men with panic disorder (CORYELLet al., 1982) carries the implications into general medicine. There is a growing body of evidence that the emotional state of the individual influences life expectation in a number of somatic diseases and following surgical procedures (PETTYand NOYES,1981; LOWNet al., 1980; DERACWTI~ et al.,
ANXIETY, PANIC ANDPHOBICDISORDERS
51
1976; ROTH, 1983). Perhaps neurochemical discoveries in relation to anxiety, phobias, panic, and depersonalisation might make clinical description redundant, much as knowledge of the sequence of nucleotides in DNA molecules with the amino acids they sort and assemble into proteins, has rendered much of the older language of cellular biology and genetics redundant. Appropriate biological treatment would rapidly evolve, and the clinician could omit from consideration the patient’s life situation, premorbid personality, and the historical record of the development, adjustment, and interpersonal relationships. Such an achievement is not within sight even with the major psychoses, and in relation to the group of disorders considered here, it is even less likely to materialise in the foreseeable future. Agoraphobic and anxiety states do not spring fully fledged as Minerva did from the head of Zeus. They arise within the context of certain personalities and patterns of life history and development. Unless the psychiatrist looks before and after and seeks to relate the illness to the premorbid personality and the stresses that have impinged on its Achilles’ heels, his understanding will be too shallow to ensure adequate rapport and communication or effective treatment. For an indefinite time, the disorders in this field will need both the observational and descriptive tools and insight of psychopathology and psychodynamics and the methods and languages of neurobiology that strive to delineate clinical phenomena in terms of the activity of neurones, their transmitters, and modulators. I have travelled the perilous path between doubt and certainty (with what success, I cannot judge) attempting (to invert an aphorism of A. E. Housman) to use such lamp-posts as there are, not like a drunkard to dissimulate instability, but to light us on our way. REFERENCES AGRAS,W. S., SYLVESTER, D. and OLTVERAU, D. (1969) The epidemiology of common fears and phobias. Comp. Psychiat. 10,151-156. BECK,A. T. (1976) Cognitive Therapy and the Emotional Disorders. International Universities Press, New York. BENEDICT,V. (1870) Uber Platzschwindel. Alg. Wiener med. Ztg 15, 488. BERGMANN,K. (1971) The neuroses of old age. In Recent Developments in Psychogeriatrics (Edited by KAY, D. W. and WALK, A.), pp. 39-50. Headley Bros, Ashford. BUGLASS, D., CLARKE,J., HENDERSON, A. S., KREITMAN,N. and PRESLEY,A. S. (1977). A study of agoraphobic housewives. Psychol. Med. 7, 73-86. CBTANO, D. (1980) Enquiries into the classification of affective disorders. Ph.D. Thesis, Trinity College, University of Cambridge. CLONINOER,C. R., MARTS, R. L., CLAYTON,P. and GUZE, S. B. (1981) A blind follow-up and family study of anxiety neurosis: preliminary analysis of the St Louis 500. In Anxiety: New Research and Changing Concepts (Edited by Krm~, D. E. and RABKIN,J. G.), pp. 137-154. Raven Press, New York. CORNELL,W., Novas, R. and CLANCY,J. (1982) Excess mortality in Panic Disorder. A comparison with primary unipolar depression. Archs gen. Psychiat. 39, 701-703. CROWE,M. J., MARKS,I. M., AGRAS,W. S. and LEITENBERG, H. (1972) Time-limited desensitization, implosion and shaping for phobic patients: a crossover study. Behav. Res. Ther. 10,319-328. CROWE, R. R., NOYES,R., PAULS,D. L. and SLYMAN,D. A. (1983) A family study of panic disorder. Archs gen. Psychiat. 40, 1065-1069. DARU~IN,C. (1872) The Expression of the Emotions in Man and Animals. J. Murray, London. DELTITO,J. A., PERUGI,G., MARE=, I., IMIGNANI, V. and CASSANO,G. (1986) The importance of separation anxiety in the differentiation of panic anxiety from agoraphobia. Psychiat. Devel. 4, 227-236. DEROGATIS, L. R., ABELOFF, M. D. and MCBETH,C. D. (1976) Cancer patients and their physicians in the perception of psychological symptoms. Psychosomatics 17, 197-201. AMERICANPs~c~~~rmc ASSOCIATION (1980) Diagnostic and Statistical Manual pf Mental Disorders> 3rd Edn (DSM-III) (1980). American Psychiatric Association, Washington, D.C.
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