Copy number variants are small chromosomal deletions and duplications. When they alter the dose of genes critical for normal brain development and adult brain functioning they may cause severe disorders such as autism and schizophrenia. Numerous such loci have recently been identified. They are offering amazing leads for neuropsychiatric research.

Bebbington (1986) draws attention to a possible cause for concern regarding the comparability of recent epidemiological research utilising the PSE-ID-CATEGO system of psychiatric caseness deter mination. In taking issue with our observation that cases in our recent community survey (Brown et al, 1985) were broadly similar in terms of severity to those reported in a recent series of out-patients (Sashidharan, 1985), he makes the point that such conclusions are only justifiable when it can be con fidently assumed that thresholds for symptom in clusion are applied uniformly between research centres. He argues that this assumption may well be invalid and marshalls two arguments to suggest that the Bedford team may have adopted less stringent rating thresholds. Firstly, he draws attention to the very different population prevalences of disorder reported in recent surveys, contrasting one-year prevalence figures for the Bedford College survey in Islington (Brown elal, 1985) withthelowerrates reported for other investigations in Edinburgh (Dean eta!, 1983) and Camberwell (Bebbington et al, 1981). Secondly, he reminds us of the body of evidence which suggests that psychiatrists operate stricter criteria for PSE symptoms than their lay colleagues (Wing et al, 1977a; Sturt et al, 1981).

Psychotic episodes and epilepsy can occur without mental retardation in tuberous sclerosis. The diagnosis may depend on elucidating the family history since physical signs may not be obvious. Establishing the diagnosis makes genetic counselling possible.

The Hungarian psychiatrist Laszlo Meduna was the first who induced epileptic fits to influence the course of mental illness. The following account, based on a review of Meduna's recently unearthed files and his writings, traces the beginnings of convulsive therapy.

According to the experience of people with schizophrenia, their psychiatrists' attitude towards the outcome of their illness is lacking in hope, which directly affects mutual faith in treatment. Here we discuss the scientific basis of hope and show its instrumental role in optimising the best treatment strategies for schizophrenia.

Thirty-six consecutively admitted patients with schizophrenia and 20 with mania were studied for the morbid risk of psychosis in their first-degree relatives. Using the family history method of ascertainment, the morbid risk for schizophrenia in the relatives of schizophrenic probands was 4.12% compared with 1.42% in the relatives of manic probands. While this difference was not statistically significant, that between the morbid risk for affective psychoses in the relatives of manic patients (7.81%) was significantly higher than for the relatives of schizophrenic patients (0%).

Since 1948 the World Health Organization has had the challenging task of trying to achieve ‘the attainment by all peoples of the highest possible level of health’ (World Health Organization, 1946). A central part of this work has involved assessing the extent of health-related problems in different parts of the world and advocating for the implementation of effective strategies to address these problems. For many years the World Health Organization has expressed concerns about the relatively low level of funding assigned to mental health services in many countries. Estimates based on data collected in 2000 show that in most of sub-Saharan Africa and South-East Asia there are fewer than one mental health nurse and one psychiatrist per 100 000 people (World Health Organization, 2001). Two papers produced with the support of the World Health Organization and published in this issue of the Journal strengthen the argument for additional funding for mental health services. In the first paper, üstün and colleagues (2004, this issue) summarise data on the relative impact of common health-related problems in different regions of the world, and in an accompanying paper Chisholm and others (2004, this issue) estimate the cost-effectiveness of different interventions for depression in these different areas.

This paper describes treatment with cortisone and A.C.T.H. of two patients in whom Alzheimer's Disease (A.D.) had been confirmed histologically by cerebral biopsy.

A.D. is a progressive dementia which usually occurs between the ages of 40 and 60 years, and there is no known specific treatment. Intellectual deterioration, which progresses insidiously over a period of 2–10 years, leads to gross dementia, and the inevitable problems of care and supervision often necessitate removal to an institution. Histologically the disease is characterized by atrophy of cortical nerve cells and the presence within the cortex of argentophile plaques which are demonstrable by the silver impregnation techniques of Bielschowsky or von Braunmühl (see Fig. 1); these plaques have a mixed granular and fibrillary structure. The same silver methods also show irregular thickening and disorientation of the nerve cell fibrils, which form “tangles” and “loops” (see Fig. 2). Identical plaques and neurofibrillary changes are also seen in senile dementia, the term “senile plaque” being used in both diseases.

The psychiatrist, the neurologist and the cardiologist all meet with patients who complain of their liability to a certain type of “attack” characterized by alteration of their apprehension of reality, varying degrees of subjective distress, and bodily symptoms of autonomic dysfunction, amongst which the cardiac components are given the most prominence. These attacks are often referred to as “acute anxiety attacks” by the psychiatrist and “vaso-vagal attacks” by the neurologist and the cardiologist, and vary considerably in their features and severity. The neurologist sees the most punched out clinical pattern, and in consequence it was the neurologist, Sir William Gowers, who first drew attention to them in his book, The Borderland of Epilepsy.

The nature of the action of insulin in producing cure in cases of schizophrenia is still quite obscure. One of the most striking features of insulin hypoglycaemia is the occurrence of phenomena pointing to disturbance of the autonomic nervous system, and many authors on this subject have expressed the belief that insulin produces cure by virtue of its action on the autonomic nervous system. There is, however, extensive contradiction in the literature as to what actually are the changes which take place in autonomic functions during hypoglycaemia. Some authors say that hypoglycaemia produces a generalized sympathetic stimulation, some say a generalized parasympathetic activity and others that there is dissociation of action of the two systems. Sakel (1) appears to believe that hypoglycaemia produces a vagotonia which underlies the curative effects of his treatment; Hadorn (2), that small doses of insulin stimulate the vagus, and large doses cause a primary secretion of adrenaline; Beno (3), that changes on the vegetative system cannot be sufficient to allow a reasonable understanding of the results; Pfister (4), that hypoglycaemia produces beneficial effects in schizophrenia because it damps the sympathetic; Wespi (5), that dissociation appears to prevail in the autonomic regulation; Gellhorn (6), that the treatment is successful because it leads to excitation of the sympathetico-adrenal apparatus through hypoglycaemia of the brain; and lastly, Heilbrunn (7), that his experiments are in favour of a sympatheticotonia.

The Tunbridge Report on Rehabilitation (1972, para 71) comments on ‘the paucity of research on the requirements of rehabilitation and the evaluation of rehabilitative treatment and techniques.’ An unusual way of evaluating the effectiveness of rehabilitation is to study its cost.

The importance of diagnosis, both in rendering available the knowledge accumulated in the past and in providing a guide to future developments, has long been emphasized in British psychiatry. Thirteen years ago, Mayer Gross, Slater and Roth (5) observed in the first edition of their textbook that diagnosis “has never been only naming and labelling. Ideally it implies judgment of causation, and even if this is impossible for lack of knowledge it always includes a plan of action, i.e. of treatment. …” The authors contrasted this approach with a derogation of the value of diagnosis which they felt had become extant in certain schools of psychiatry, and they deplored this tendency, stating unequivocally “the contemptuous attitude to diagnosis which is so prominent a feature of many contemporary schools runs counter to the entire spirit of medicine”. The pendulum now appears to be swinging back and, whilst several centres have remained preoccupied with socio-cultural and psychodynamic approaches to psychiatric illness, interest in psychiatric diagnosis has redeveloped both in Great Britain and in the United States (Kreitman, 1961; Kreitman et al., 1961; Ward et al., 1962; Sandifer et al., 1964, 1966, 1968). The phenomenon is probably related to a current tendency to exchange ideas across the Atlantic, and to the need for a common diagnostic code emphasized by cross-national epidemiological data, mental hospital population movement statistics, and studies of the efficacy of treatment. Clearly adherence to universally accepted diagnostic criteria is mandatory if meaningful comparisons are to be drawn from these and other psychiatric statistics obtained from different national settings.

Beck's original book on cognitive therapy was published in the USA in 1976 but not reviewed in the Journal until December 1979 (139, 582–583). The review was favourable. A second book (Beck et al, 1979) was not reviewed, although by then there was a substantial and growing literature on cognitive approaches to treatment.