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.
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.
A postal survey of all practising psychiatrists in Australia, conducted in 1980 with the purpose of establishing psychiatric manpower requirements for 1980-91, is described. It is estimated that in 1980 there was one Whole Time Equivalent psychiatrist, aged 65 years or less, per 19,400 population in Australia. The relativity of manpower requirements is emphasised. A number of different models of estimating future requirements is proposed. The two models most favoured estimate a shortfall for the whole of Australia of 294 and 349 psychiatrists, respectively, in 1980, and a need for an additional 621 or 692 by 1991. A major maldistribution of psychiatrists is identified, viz between states, between capital cities and country areas, and between general psychiatry and specialised areas. The two issues of the number of trainees required and of how to train psychiatrists in special areas of expertise are discussed.
Summary: Inherited deficiency of acetaldehyde dehydrogenase type I (ALDH‐I) was found in 43% (50/117) of normals, 33% (27/82) of schizophrenics, but only 4% (5/113) of alcoholics among Japanese. The ALDH‐I deficiency was never found, however, in 146 mostly schizophrenic subjects from Europe (Basel, Moscow, Zagreb), Australia (Nedlands), India (Lucknow), Morocco (Casablanca) and Mexico (Mexico City). It was demonstrated that ALDH‐I deficiency produces the flushing syndrome which inhibits the development of drinking habit and alcohol dependence syndrome.
Averaged cortical evoked potentials from single clicks were recorded from 51 patients and controls. The patient group consisted of 40 subjects with a diagnosis of 'nuclear' schizophrenia, and 11 subjects with diagnoses including mania, anxiety neurosis and personality disorder. Changes in auditory evoked cortical responses (AECR's) were most marked in clinically stable, dysphoric, chronic schizophrenics. These subjects showed reproducible, low amplitude, 'untidy' responses in which the amplitude of the primary peak was lower than the amplitude of later peaks. Chronic schizophrenics who were rated as being depressed, showed a more 'normal' AECR. AECR changes during the memorising of nonsense syllables demonstrated a functional separation between early and later peaks of the AECR. It was postulated that the AECR changes in schizophrenia and during memorising result from pathological patterns of cortical desynchronisation produced by altered mid-brain activity different from that of anxious arousal, and that the clinical 'steady-state' of chronic schizophrenia is reflected in the 'steady-state' desynchronisation changes in the AECR.
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