In some quarters schizophrenia has gained the reputation of a graveyard of research. Few findings stand the test of time, most of the pieces of this particular jigsaw seem to be missing, and it is not easy to make sense of those that are available. Even ‘hard’ scientific findings fail to be replicated, an example being the status of D2 receptors in drug-naive schizophrenics (Wong et al, 1986; Farde et al, 1987).

Although delusion remains one of the basic problems in psychopathology, attempts to understand its pathogenesis have been dominated by unsubstantiated speculation. Previous psychodynamic formulations have recently given way to increasing interest in measurement, and testing of models derived from cognitive psychology. However, the formation, elaboration, and persistence of delusional beliefs may be an expression of the convergence of numerous causal influences, each exerting an effect at a different stage in the evolution of the belief. This review takes a structured overview of the literature, placing the numerous part theories and scant experimental findings within a general model of delusional development. It argues for a return to systematic research on symptoms rather than complex diagnostic formulations to facilitate better understanding of the development of delusional disorders and stimulate further interest in therapeutic intervention.

When William Sargant died in 1988 at the age of 81, he had made his mark on British psychiatry. He had exerted considerable influence on US psychiatry as well. This was especially obvious during a time when physical treatments were hardly the fashion in US psychiatry. As The Times (1988) stated at the time of his death, he had made psychiatry more respectable by keeping it close to the medical model. He did a great deal to make depression intelligible to general practitioners and, therefore, to make it a legitimate, respectable illness.

Subtypes of the features of chronic schizophrenia were investigated. As in previous research, three discrete syndromes were found. These were then related to demographic, psychological, and movement-disorder variables. Possible pathophysiological mechanisms are discussed in terms of known neostriatal functions.

Chromosomal aberrations associated with schizophrenic disorders may suggest regions in which to focus a search for genes predisposing to schizophrenia by a linkage strategy. As for other genetic illnesses, chromosomal abnormalities may also provide useful tools for subsequent physical mapping, fine localisation, and isolation of important susceptibility genes. Identification of several chromosomal aberrations may be especially important, given the unknown pathophysiology, the paucity of known brain genes, and the probable genetic heterogeneity of schizophrenia and manic-depression. However, because psychiatric disorders are common and inherited in a complex manner, researchers must use caution when drawing inferences about associations with chromosomal aberrations. Reported abnormalities involving autosomes (chromosomes 1–22) associated with psychotic disorders are reviewed. Their relevance to linkage studies localising genes for schizophrenia was estimated by standardised criteria for specificity, diagnosis, family history, and overall weight of evidence. Four ‘possibly relevant’ chromosomal regions were identified: 5q, 11q, 18q, and 19p. This paper outlines strategies for future studies to detect new chromosomal aberrations associated with major psychotic disorders that may be relevant to isolating the genes for schizophrenia.

A sample of 115 DSM–III–R schizophrenics was studied by means of the SANS and SAPS. A factor analysis from the nine subscales and two symptoms (inappropriate affect and poverty of content) and a review of the previous factor analyses suggest that schizophrenic symptoms cannot be appropriately classified into positive and negative syndromes. The low internal consistency of the SAPS suggests that the positive symptoms are not a homogeneous syndrome. Our results fit better with Liddle's model of three syndromes (negative, delusion-hallucination and disorganisation syndromes). It is argued that we are far from a valid classification of schizophrenic symptoms and the positive-negative dichotomy appears to be an oversimplification.

A modified version of the revised Personality Diagnostic Questionnaire (PDQ–R), based on DSM–III–R personality disorders (PDs), was completed by 60 psychiatric patients. An informant's version was also completed by 60 relatives or friends nominated by each subject. Discrete DSM–III–R PDs were rare; the mean number of PDs per subject was 4.5. Cluster analysis showed that only antisocial PD was a basis for classification of patients, while most patients formed two groups which were mainly distinguished by quantitative differences related to the total scores of positive PD criteria. A shorter version of the questionnaire can be used as a screening test for co-morbid PDs (STCPD) which can predict the number of co-morbid DSM–III–R PDs. The total scores of positive PD criteria from the STCPD were usually (and significantly) higher than the corresponding scores from informants' questionnaires but when an informant's total score exceeded that of the patient, this indicated a subject's under-reporting.

In a double-blind, parallel group trial, 78 subjects with social phobia received moclobemide (a new reversible inhibitor of monoamine oxidase A) phenelzine, or placebo. After eight weeks, both active drugs – phenelzine somewhat more than moclobemide – were clinically and statistically significantly more effective than placebo, as assessed by rating scales. There was some further improvement between weeks 8 and 16, particularly in the moclobemide group; at week 16, 82% of the moclobemide and 91% of the phenelzine-treated patients were almost asymptomatic. Moclobemide was, however, much better tolerated than phenelzine. Patients withdrawn from active drugs had relapsed by week 24, providing additional support for the efficacy of the active drugs.

Plasma melatonin levels were measured at three-hourly intervals over 24 hours in 11 women with untreated anorexia nervosa, and in nine healthy women of normal weight. The circadian rhythm was unaltered but the nocturnal secretion of melatonin was significantly greater in anorectics. It is possible that this was related to nocturnal hypoglycaemia.

Suicide levels in England and Wales during 1979–83 were low among males from the Indian subcontinent (SMR 73) and significantly high in young Indian women (age-specific ratios 273 and 160 at ages 15–24 and 25–34 respectively). Suicide levels were low in Caribbeans (SMRs 81 and 62 in men and women respectively) and high in East Africans (SMRs 128 and 148 in men and women respectively). The excess in East Africans (most of whom are of Indian origin) was largely confined to younger ages. Immigrant groups had significantly higher rates of suicide by burning, with a ninefold excess among women of Indian origin. The pressures leading to higher suicide levels among young women of Indian origin highlight the need for making appropriate forms of support and counselling available to this community.

‘Hysterical conversion’ dates from a century before Freud, from an important attempt to rationalise the nosological status of hysteria. Freud's own concept of ‘conversion’ followed as a quite independent synthesis of 19th-century medical thinking on the subject. Subsequent analytical usage of ‘conversion’ which has influenced the description of hysterical syndromes within mainstream psychiatry, has not been consistent with Freud's own.

The career of the diagnosis of conversion hysteria is reviewed at a time when it is threatened with expulsion from classifications of psychiatric disorder. Criticism of its face validity has not led to adequate diagnostic alternatives, and has been insensitive to its unusual form as a category as well as the contribution it has made to the stability of the classificatory system around it.

Claims have been made that maternal infection with influenza during pregnancy is a cause of schizophrenia in the child. These assertions are based upon some apparently significant associations between the timing of influenza epidemics in the general population and birth rates of people who later suffered from schizophrenia. Such associations have not been present in studies of the 1919 and 1957 epidemics, with sample sizes larger than those on which the claims were made. More decisively, in an investigation of the subsequent psychiatric admissions of people born a few months after the 1957 epidemic, it was found that the children of 945 mothers who actually suffered from influenza during the second trimester of pregnancy were at no greater risk of developing schizophrenia than children of mothers who were not infected. In contrast to the predictions of the influenza hypothesis of 26.5 extra cases by broad diagnostic criteria and 15.8 cases by narrow criteria, the numbers observed in children of mothers exposed to influenza in the second trimester were 3 and 1 cases respectively, close to the expected rate. It is concluded that prenatal influenza and schizophrenia are unrelated.

“The birth dates of schizophrenic inpatients in eight health regions in England and Wales were reviewed for any effect of the 1957 A2 influenza epidemic. 5 months after the peak infection prevalence, the number of births of individuals who later developed schizophrenia was 88% higher than the average number of such births in the corresponding periods of the 2 previous and the next 2 years. This finding is in accordance with a study from Helsinki and with clinical and neuropathological evidence of aberrant fetal brain development in the pathogenesis of schizophrenia.”

Previous studies have suggested that on the Auditory Comprehension Test, a significant proportion of schizophrenics demonstrate a binaural comprehension deficit. To test whether wearing an earplug in their more poorly performing ear would be beneficial, we studied 34 in-patient schizophrenics and noted a binaural deficit in 12 (35%). Of these, eight patients subsequently wore an earplug in each ear for at least one week. We found no effect of the earplug on psychopathology.

Twenty-three adolescents with DSM–III major depressive disorder (endogenous subtype) and 23 normal controls were studied polysomnographically (PSG). The depressed group showed significantly shortened REM latencies (P=0.005) and longer sleep latencies (P=0.04). No other PSG measures differentiated the two groups. The implications of these findings for adolescent depression are discussed.

The association of a recurrent psychosis in the premenstrual period with an increased blink rate is reported. This case adds to evidence supporting a hormonal hypothesis of certain psychotic disorders.

A first episode of psychosis occurred in a young woman of West Indian parentage and one of identical twins following a brief period of high consumption of a drink made from Colubrina plant extract (mabi bark). The course of the psychosis is described and possible underlying mechanisms and the relationship to amphetamine psychosis are discussed.

A patient with a 15-year history of psychiatric illness treated with neuroleptics presented with vomiting, thought alienation, auditory hallucinations and self-neglect. Dopaminergic supersensitivity was diagnosed and increased doses of neuroleptics caused cessation of vomiting. The patient is currently attempting discontinuation of neuroleptics.

A rare case of Charles Bonnet syndrome, which presented in a 38-year-old man, responded to carbamazepine.