A relatively normal 16-year-old Chinese woman with a six-month history of compulsive water drinking resulting in a comatose state is reported. The drinking was perpetuated by an enjoyable altered state of consciousness after ingestion of an average of 20 litres of water per day. Treatment by fluid restriction and, later, simple education was successful. The subjective dimension of an altered state of consciousness may provide an important explanation for the obscure aetiology.

In 1963 Coppen and Shaw reported that patients with manic-depressive psychosis showed, on clinical recovery, a significant decrease in exchangeable sodium, and in residual sodium (exchangeable minus extracellular sodium), presumed intracellular, per litre of body water. Coppen, Shaw, Malleson and Costain (1966) found a similar type of shift in mania but the deviation from normal was, on average, more extreme. Although low and high sodium diets had no effects on the distribution of sodium in manic-depressive psychotics, the administration of spironolactone resulted in a significant reduction of residual sodium (Coppen, 1970). The possible involvement of aldosterone in these changes led Jenner et al. (1967) to examine aldosterone excretion in a 48-hour cycle patient and Murphy, Goodwin and Bunney (1969) to examine groups of manic and depressed patients. Murphy et al. found lower rates of excretion of aldosterone in depression than in mania, but Jenner et al. found the opposite.

Many of the links in the chain of circumstances leading to anorexia nervosa are still not clear. Ever since Sir William Gull in 1868 first described and in, 874 named the condition, investigators have put most of the blame for it on psychological circumstances, such as an adverse relationship between mother and daughter. Tolstrup (1967), after reviewing the observations of a long list of authors, concluded that no physical explanation of note was forth-coming. Another of the many adherents of the psychogenetic school is Thomä (1961).

In a previous study (Drewery and Rae, 1969), using the Interpersonal Perception Technique (I.P.T.) (Drewery, 1969), it was found that while the husbands and wives of the non-patient marriages had a clear concept of masculinity which they shared, the partners in the alcoholic marriages lacked this consensus; they were confused about the male socio-sexual role, and this confusion expressed itself in a conflictful interplay of dependence and independence needs. The conclusions then reported were applied to alcoholic marriages as if they formed a homogeneous group. The present study was designed to test the hypothesis that when alcoholic marriages are dichotomized in terms of the wives' Pd characteristics, two qualitatively and quantitatively distinct marital patterns would be revealed.

Last December I received one of the most surprising letters of my life—an invitation to give the next Maudsley Lecture before this Association. I am deeply grateful for this honour, all the more so since I stand in considerable debt to the hospital which Henry Maudsley founded and which bears his name, having spent two fruitful years there as a research student.

Genital exhibitionism is a disorder without a satisfactory explanation; many views have been put forward as to its nature but although fragments of some of these theories appear to be relevant to the problems of some individuals, for others they are incongruent with the clinical data. At the present time we must conclude that the behavioural act does not signify a homogeneous population and that in every parameter so far studied, be it personality structure, attitude to women, erotic gratification from the act, other deviant behaviour or whatever, there is no single unifying characteristic which is always to be found. The intention in this paper is not to make a broad survey of the disorder for that has been undertaken within the last fifteen years by, inter alia, Evans (1970) and Rooth (1971, 1980); the purpose is to draw attention to some of the more recent studies in order to dispel stereotyped views and thereby to avoid the pitfalls in deriving the formulation of each individual case.

Hitherto two methods have been commonly used to measure dementia—by means of numerical measures of scatter, and by means of the discrepancy between scores on vocabulary and other tests. In the present investigation the value of the most popular techniques with both methods was examined, and a new short measure of dementia was evolved.

Subjects taking the Stanford Binet and similar tests rarely pass abruptly from complete success at and below a certain M.A. level to complete failure at the next and subsequent levels. For example, a subject with a total M.A. of eleven years may succeed in all the subtests at and below the VIII year level and fail all the subtests above the XIV year level, while between these two levels he succeeds in some and fails others. The range of partial success and failure is called the “scatter.” Many psychometrists believe that unusually wide scatter indicates psychopathy or intellectual deterioration. The various methods for measuring scatter are conveniently summarized by Harris and Shakow (1937).

A long-standing observation on the results of intelligence tests in dementia is that vocabulary ability remains comparatively unimpaired until a late stage when the subject is unable to solve other tests. Therefore, it has been claimed, vocabulary score may be taken as a measure of the subject's pre-morbid intelligence, and the discrepancy between his vocabulary ability and ability on other tests as a reflection of the difference between his former and present intelligence, thus providing a measure of his dementia. The Babcock test is the best known of several techniques, based on this principle, for the measurement of dementia.

To many minds there can be but little change in the treatment of depression since Johnson prescribed these remedies in 1776. Indeed the place of chemistry is now prominent, although its application is apparently more important to the patient than its study. It is believed that an enzyme, mono-amine oxidase, found in cerebral tissues, plays a part in the genesis of depression. Amphetamine inhibits the destruction of adrenaline by amine oxidase (McIlwain, 6) and amphetamine is of value in the treatment of mild depression (Guttmann and Sargant, 5). Another substance is 5-hydroxytryptamine, or serotonin, which is said to excite cerebral neurones briefly between its liberation and destruction; it is a cerebral vasoconstrictor and is destroyed rapidly by amine oxidase (McIlwain, 6). Iproniazid (Marsilid) is a drug which inhibits amine oxidase and has been used in the treatment of depression (West and Dally, 10). Its central actions are considered to be similar to those of 5-hydroxytryptamine. Recently, Chessin (3) has described yet another amine oxidase inhibitor, phenelzine, which is the study of this paper.

The incidence of vegetative symptoms was found to be higher in 61 medication-free patients with anxiety compared to an equal number of age and sex-matched normal controls. Multiple regression analysis identified depression, as rated by Beck Depression Inventory (BDI), as the most highly predictive factor associated with these symptoms. Twenty-two anxious patients who obtained scores less than 5 on BDI (absent or minimal depression) were compared with an equal number of age and sex-matched patients with depression. The depressed patients reported a higher incidence of sleep disturbances, weight loss and appetite loss.

Educational objectives in medical school training used to be stated in global terms, seldom possible to implement and still more difficult to test (Objectives of Medical Education, 1953). The student's training hopefully was required to help him “to respect the rights and dignities of patients”, or towards “expecting to be a student all his life”. How to evaluate the presence or absence of these qualities after training was not conveyed either by the form or by the sometimes frankly inspirational language in which the objectives were stated.

Recent family studies of manic-depressive psychosis have emphasized the role of genetics in the aetiology of this bipolar illness (3, 8). However, the mode of genetic transmission is still unknown, the main controversy being between major gene and polygenic inheritance. Furthermore, it is not yet evident whether bipolar illness constitutes a homogeneous entity or whether it may be subdivided into different genetic subgroups. Mendlewicz, Fieve, Rainer, and Fleiss (1) recently produced some evidence that bipolar psychosis can be differentiated into two subgroups on the basis of family history data. Two matched samples of 30 patients each were studied, distinguished by the presence or absence of bipolar illness in their first degree relatives. The patients with a positive family history (FH+) in first degree relatives showed earlier onset of illness and more psychotic symptoms occurring in the manic phase. Alcoholism, if present, was of an episodic pattern. In patients with a negative family history (FH—), there was a later onset of illness; psychotic symptoms occurred usually in the depressive phase; and alcoholism, when present, tended to be chronic.

The psychological and physiological features of 20 aircrew consecutively referred for treatment of anxiety symptoms when flying were compared with a matched control group of uncomplaining aircrew. There were no significant differences between the two groups on psychometric tests of personality, though there were differences in skin conductance; the phobics had a higher rate of spontaneous fluctuation, and habituated less to a repeated auditory tone. More of the phobic group worried about their wives and acknowledged childhood and other adulthood phobias; more had a family history of an episode perhaps best described as flying trauma. Many were on an overseas posting when symptoms presented. These few features could correctly classify 85 per cent of the subjects into the phobic or control group. This type of ‘phobic aircrew index’ now requires to be validated prospectively for its predictive value.

Reports coming from Central Australia draw attention to mental instability in the Aborigines who live between Hart Range and Lake Nash near the Queensland border (Fig. 1). Well-informed persons—welfare officers, nursing sisters, an aerial medical officer (“flying doctor”) and cattle station managers—are firmly of the opinion that these Aborigines show an undue amount of instability and frank mental illness. Furthermore, South Australian mental hospital records reveal that in recent years, many Aborigines of this region have been referred to Adelaide for treatment of unusual psychoses. Statistics of the sort available in more settled areas are lacking. There is no local psychiatric service to keep a register of disorders occurring in this population. But the local impression of mental instability is strong and the questions it raises are clearly important. Is there a localized instability in Central Australia ? If so, what is its distribution? What is its nature? Is its cause to be found in constitutional peculiarities of the people ? Or in environmental stresses that they are undergoing in their cultural transition ?

The aim of this study was to evaluate changes in selected personality variables following a form of leucotomy described as orbital undercutting (Knight, 1959) and to relate these findings to clinical observations.

Perhaps most clinicians experienced in mental hospital work suspect, at least, that left-handedness and stuttering occur relatively frequently among hospitalized epileptics. However prevalent this impression may be, it remains to be tested systematically. There has been little study of dextrality among the different diagnostic groups. Defects of speech among some groups have been studied considerably, among other groups very little.

Since the initial observations of a relationship between depression and an increase in urinary adrenal glucocorticoids in psychiatric patients by Reiss (1953) and Rizzo et al. (1954), there have been a number of studies confirming this relationship using various chemical techniques (Board et al., 1957; Bunney et al., 1964 and 1965; Gibbons, Gibbons, Maxwell and Wilcox, 1960; Gibbons and McHugh, 1962; Gibbons, 1964; Kurland, 1964a and 1964b; Pryce 1964). One of the questions that immediately comes to mind in reviewing this work has to do with the specificity of this relationship. Perhaps the rise of urine corticoids in depression is a non-specific response to disturbance, as has been demonstrated in various forms of psychological stress (Hamburg, 1962) and in severe psychiatric disturbances such as acute schizophrenic episodes (Sachar et al., 1963). On the other hand it is tempting to hope that there may be a more specific relationship demonstrable between the complex psychobiological phenomenon of depression and some kind of neuroendocrine activation analagous to a syndrome like “periodic hypothalamic discharge” (Wolff et al., 1964). This syndrome is manifested by periodic episodes (lasting several days) of withdrawal and depression associated with marked elevations in 17-hydroxycorticoid excretion. Mandell et al. (1963) have recently demonstrated that subthreshold stimulation of limbic sites intimately related to hypothalamic modulation produces marked changes in plasma 17-hydroxycorticoids in man. Limbic areas have been related to affectual phenomena on a speculative basis since the classical papers of Papez (1937).