This paper is concerned with steadily developing knowledge of the epidemiology of some psychiatric disorders in sub-Saharan Africa. The diversity of ‘Black Africa’ is noted, and preconceptions about African psychiatry briefly discussed. Problems of sociological versus clinical philosophies are also mentioned. Early estimates of prevalence of psychiatric disorder in black Africa were universally low, being based on hospital data. More recent studies, sampling diverse populations, suggest a burden of psychiatric morbidity in black Africa which is not dissimilar to that found in more developed countries, and some studies suggest that rates in Africa may even be higher than in developed countries.

Aspects of clinical psychiatric syndromes described in Africa which are discussed include the issue of schizophrenic disorders having a better prognosis in developing countries; controversy over this is by no means at an end. There is an increasing realisation as to the frequency of affective disorders in Africa; while somatisation is common, cherished beliefs, such as the absence of guilt, have not been confirmed by more recent research. Nor is suicide as infrequent as has been suggested. The relationship of background physiological abnormalities of cerebral functioning may be relevant to some of the clinical issues that are currently under discussion in African psychiatry.

To illustrate the contribution anthropology can make to cross-cultural and international research in psychiatry, four questions have been put to the cross-cultural research literature and discussed from an anthropological point of view: ‘To what extent do psychiatric disorders differ in different societies?’ ‘Does the tacit model of pathogenicity/pathoplasticity exaggerate the biological aspects of cross-cultural findings and blur their cultural dimensions?’ ‘What is the place of translation in cross-cultural studies?’ and ‘Does the standard format for conducting cross-cultural studies in psychiatry create a category fallacy?’ Anthropology contributes to each of these concerns an insistence that the problem of cross-cultural validity be given the same attention as the question of reliability, that the concept of culture be operationalised as a research variable, and that cultural analysis be applied to psychiatry's own taxonomies and methods rather than just to indigenous illness beliefs of native populations.

Neuroleptics are structurally a heterogenous group of compounds which possess antipsychotic activity. They increase dopamine metabolites by blocking dopamine receptors and enhancing presynaptic turnover. This forms the cornerstone of the dopamine hypothesis of neuroleptic action, which is supported by wide-ranging behavioural, physiological and biochemical studies. It is, however, clear that neuroleptics are far less specific for the dopamine receptor than was previously considered. They influence a range of neuronal activities, including calcium-activated potassium conductance, which governs the rate of action potential generation by many neurones. Recent physiological studies indicate that all commonly used neuroleptics alter calcium-activated potassium conductance in central neurones, in concentrations similar to those achieved clinically. An adaptive increase in calcium-activated potassium conductance mechanisms in key sensory processing neurones would render the psychotic patient less susceptible to bombardment by environmental stimuli. This action may explain in part the therapeutic effect of neuroleptics.

Dinan's paper seeks to question the validity of the now widely accepted hypothesis that neuroleptic drugs of various different chemical categories all act by a common mechanism, namely by blockade of dopamine receptors of the D2 type in brain (for review see Creese et al, 1978, 1983; Iversen, 1985). While it is always refreshing to re-examine existing scientific dogma, his criticisms did not appear to me to be very substantial. Having quite fairly reviewed the evidence in favour of the “dopamine hypothesis” for neuroleptic drug action, Dinan summarises his reasons for questioning it. He points out that many neuroleptic drugs have potent actions on a number of other targets, apart from the dopamine receptors in brain. This is indeed so, and the archetypal compound, chlorpromazine, has a particularly rich spectrum of pharmacological activity, being a potent antagonist of serotonin (5-HT2) receptors, ?-adrenoceptors, and histamine (HI) receptors in brain and other tissues. Other neuroleptics also have potent actions on a number of other systems. Indeed, if one were to have studied only chlorpromazine, it is doubtful whether the “dopamine hypothesis” could ever have been developed. The strength of this hypothesis lies in the fact that of all the diverse pharmacological actions which different neuroleptic drugs exhibit, this is the only action that is common to all neuroleptic compounds. Furthermore, in a large group of neuroleptics, which differ widely in potency (doses in man ranging from 1 mg/day to almost 1000 mg/day), the potencies of these drugs as dopamine (D2) antagonists correlate significantly with their clinical potencies. Attempts to make such correlations with any other known pharmacological properties of these drugs fail to show significance (Creese et al, 1978, 1983).

Karl Popper has taught us that no hypothesis can be regarded as proved-merely as having survived the most stringent tests which have so far been devised. Dinan makes a further attempt to overthrow the dopamine hypothesis of the mechanism of the antipsychotic effect, and provides an alternative suggestion. As one time critic and later advocate of the theory, I think he underestimates its explanatory power and capacity for survival. I doubt that his alternative yet poses a serious challenge. I propose below a second (and perhaps more idiosyncratic) alternative. I do not claim it yet has the explanatory power of the dopamine theory, but I think it generates some new approaches.

A computerised diagnosis, AGECAT, is applied to data from random community samples of the elderly in New York and London in order to examine the prevalence of mental illness in the two cities, especially the result reported from the same study, using a different diagnostic procedure, that the proportion of dementia was higher in New York. The greater proportion of dementia in New York is confirmed for all AGECAT's levels of diagnostic confidence, for both sexes and at all half-decades over 65 years. Provided that this difference is upheld and genetic differences can be discounted, these findings would seem to support a contributory environmental cause for dementia. Proportions of depression as a whole are similar in both cities. Syndrome case and sub-case levels of neurotic disorder are generally higher in London.

The detention of offenders in the legal category ‘psychopathic disorder’ in special hospitals for treatment raises a number of critical issues. There are doubts about the nature of the disorder; what constitutes treatment; who is ‘treatable’; the effectiveness of treatment; and whether evidence of psychological change implies reduced risk of reoffending. In view of these uncertainties, it is argued that indeterminate hospital orders may provide an unrealistic and unjust legal framework for treating ‘psychopaths' in special hospitals, and the use of powers under the Mental Health Act to transfer such patients to hospital during the course of prison sentences is a more appropriate alternative. This provision could be used more frequently, subject to improved safeguards of the right of release at the expiry of sentence.

Results of the sixth quinquennial survey of the resident population of Glenside Hospital, Bristol, are reported. The total population continues to fall, but the rate of decline has slowed; the implications of this are discussed. Many patients live in an emotionally impoverished state, friendless and rarely leaving the hospital. Few in-patients are employed, even within the hospital. Considerable provision is made, however, for the employment of day-patients. To effectively resettle and support in the community those currently remaining in hospital will require increasingly extensive provision.

The extent and factor structure of depressive phenomena were investigated in three primary health care clinics in the city of Calcutta. The Self-Reporting Questionnaire and the Screening for Depression Questionnaire were used as the first-stage instruments, and the Clinical Interview Schedule and the Hamilton Rating Scale for Depression as the second-stage instruments. The implications of the findings are discussed.

Thirty-eight people with a moderate to severe degree of aerophobia self-referred themselves to a course designed to help them travel by air. The course involved three long sessions based on giving information, graded exposure without avoidance, and group support with natural coping models. Measures of self-reported anxiety levels were taken at regular intervals. The results showed that being given information or undergoing a simulated flight had little effect on perceived anxiety. Prolonged exposure to flying had a marked effect on reducing anxiety and anticipated apprehension about future flying. At one-year and three-year follow-up, 40% and 60% of participants had flown commercially, although there was some minor restoration of anticipated anxiety associated with flying; 84% showed less anxiety about flying. Psychological intervention, in collaboration with airlines, may have marked benefits in reducing fear of flying.

Data from two sources-the Edinburgh Psychiatric Case Register and the psychiatric inpatient records of the Scottish Health Service-were used to compare large populations of first-admission schizophrenics born in winter (January to March) and in summer (June to October). Parallel comparisons were carried out for affective psychoses. Comparison of the months of birth of the Scottish patients with those of the general population indicated that there was a 9% excess of schizophrenic births and a 3% excess of affective births in the first 3 months of the year. In the Edinburgh material, winter-born schizophrenics were more likely than the summer-born to receive a diagnosis of paranoid or schizoaffective schizophrenia and less likely to receive diagnoses other than schizophrenia on readmission, but neither of these differences emerged in the much larger Scottish material. There were no differences between winter-and summer-born schizophrenics in age of onset, sex ratio, or prognosis in either data set, nor were any significant differences found between winter- and summer-born affectives. We have therefore failed to demonstrate any convincing differences between winter-and summer-born schizophrenics.

Twenty chronic male schizophrenic subjects aged 30–50 years were examined by an auditory event-related potential procedure for the evaluation of the P300 component, a CT scan and a neuropsychological test battery. The P300 latency was increased and its amplitude was reduced. CT scan measures showed lateral and third ventricle enlargement, and there was a global neuropsychological impairment. Poor neuropsychological performances were consistently associated with delayed P300 latencies, but not with CT scan measures. Ventricular enlargement was more pronounced among subjects with a negative family history for major psychiatric disorders.

The activities of the A and B forms of the enzyme monoamine oxidase (MAO, E.C. 1.4.3.4) have been assessed with the substrates 5-hydroxytryptamine and benzylamine respectively in seven areas of the brains of 39 patients with schizophrenia and 44 control subjects. Whereas previous studies have found the enzyme unchanged in brain in schizophrenia, in this study there was a modest but significant decrease in the activity of MAO-B in frontal and temporal cortices and in amygdala. This decrease could not be accounted for by neuroleptic medication, age, sex or post-mortem variables. In a series of 22 patients who had been assessed in life, the reduction in MAO-B activity was found to be associated specifically with the presence of negative symptoms (flattening of affect and paucity of speech). The findings are therefore consistent with other evidence for structural and neurochemical change in the temporal lobe that have been associated with the type II (defect state) syndrome of schizophrenia. The change in enzyme activity is unlikely to be related to a change in monoamine metabolism but may reflect a disturbance in glial function. The change in MAO-B activity in brain in this study is confined to particular areas of brain and a subgroup of patients; it is thought to be entirely unrelated to earlier reports of reductions of enzyme activity in platelets, which are probably attributable to prolonged neuroleptic medication.

Twenty-four chronic schizophrenic patients were assessed by the Morningside Rehabilitation Status Scale, the Krawiecka Scale, and the Social Adjustment Scale by Self-Report. Inter-rater correlations suggest that the MRSS can be used by a rater with little previous knowledge of the patient. Between-scale correlations suggest the three scales assess somewhat different dimensions. A standard approach to rehabilitation assessment is suggested.

A three-stage community survey of a representative group of Southampton mothers was carried out. A semi-structured psychiatric interview was administered at 3, 9 and 15 months post-partum. The results of these interviews are presented and used to assess the extent and timing of psychiatric disorders arising in this period. In contrast to previous studies, it was found that the highest incidence of new cases, variously defined, occurred between the third and ninth month post-partum and not immediately following childbirth. These results are discussed in the context of previous studies using the same definition of caseness.

The first-degree relatives of 50 obsessive-compulsive patients and those of matched controls completed the General Health Questionnaire (GHQ) and the Leyton Obsessional Inventory (LOI). Relatives who were identified as possible ‘cases' by their high GHQ scores, or by their own or informant relatives' reports, were interviewed using the Schedule for Affective Disorders and Schizophrenia. Index relatives had a significantly higher lifetime prevalence of mental illness (36%) than had those of controls (17%), due mainly to an excess of depressive and neurotic disorders. However, only one relative from each group was diagnosed as having definite obsessive-compulsive neurosis. In addition, the LOI scores were similar for the index and control relatives.

A preliminary controlled investigation of the effectiveness of Anxiety Management as a treatment for generalised anxiety disorder (GAD) is described. Patients with a primary diagnosis of GAD, in which the current episode had lasted for at least 6 months but not more than 2 years, were included. Anxiety Management, a self-help treatment including procedures for managing somatic and cognitive symptoms, and for dealing with avoidance and low self-confidence, was given either immediately or after a 12-week waiting period. The average length of treatment was 8.7 sessions. Highly significant changes in anxiety, depression, and problem ratings were shown after treatment. These changes were replicated when the waiting list group had also received treatment, and gains were maintained by both groups for 6 months. Similar degrees of improvement and maintenance of change were shown in subgroups with and without minor depressive disorder or recurrent panic attacks.

Suicide was attempted by 1641 people (502 males and 1139 females) in Singapore during 1980. Eleven of these committed suicide during the following three years, giving a suicide rate of 0.67%. Of the eleven suicides, five had schizophrenia and three depression. The risk of suicide in the year following attempted suicide is lower in Singapore (0.5%) than in Britain (1.6%). High risk factors for the Singapore patients were being Chinese, being male, and having a mental illness.

The incidence of schizophrenia among psychiatric and general trained nurses was investigated for the period 1955–1979 in Northern Ireland. No difference was found. These results do not support the hypothesis of schizophrenia as a horizontally transmitted infectious disease.