Emotions may be rooted in biology but the process of cultural construction gives those emotions form and a language for their expression. The changing construction of jealousy in Western societies has transformed a socially sanctioned response to infidelity into a form of personal pathology which is the mere outward expression of immaturity, possessiveness and insecurity. This is a history of the stripping away of social, ethical and finally interpersonal meanings from an experience, to leave it as a piece of individual psychopathology. Fidelity and jealousy are constructed as they are because of the nature of the social and economic realities which drive our culture. The erosion of the area of human experience which could be identified with normal jealousy leaves the boundary between the pathological jealousy of psychiatry and normal experience increasingly problematic.

Research supported by the Medical Research Council (MRC) is in part initiated in response to proposals from research workers and in part identified by the Council undertaking regular reviews of its portfolio, to identify areas of particular promise, and to ensure that they are adequately supported. One such review, carried out by a group chaired by Professor J. K. Wing, on research in schizophrenia has been published (Schizophrenia and Allied Conditions Committee, 1987), and in the intervening years has been influential in shaping the Council's policy in the field. The report highlighted the molecular genetics of schizophrenia as an example of the ever-increasing number of areas in which an interdisciplinary approach is essential and in which advances in one field can be exploited in another.

Most authorities now agree that a genetic contribution is the best established aetiological factor in manic-depressive illness (McGuffin & Katz, 1989) and schizophrenia (Gottesman & Shields, 1982). In both cases the size of the genetic contribution is substantial, as reflected in estimates of broad heritability (the proportion of total phenotypic variance accounted for by genes) of 60–80%. However, the evidence in favour of a genetic contribution from family, twin and adoption studies tells us that we are dealing with complex conditions which do not have simple Mendelian modes of transmission and in which environmental influences almost certainly play a part. The main debate about mode of transmission has centred upon whether it is entirely polygenic (i.e. dependent upon the action of many different genes, each of small effect) or whether for each of the major psychoses there is a gene of major effect.

The major psychoses remain an enigma. Affective and schizophrenic psychoses are apparently present (probably at about the same lifetime prevalence of approximately 2%) in all human societies. Yet their aetiology is obscure. While a genetic contribution is acknowledged by most authorities, few accept that genes are a sufficient explanation of causation because: onset is in adult life; psychosis – particularly schizophrenia – is associated with a substantial fertility disadvantage; and most cases lack a family history of illness. But genetic determination has to be considered because onset is determined by chronological age rather than environmental insult (Crow & Done, 1986), adoption away from a family with schizophrenia does not reduce risk of illness, and no plausible environmental precipitant of psychosis has been identified. The fact that psychosis occurs across widely differing climatic, industrial, and social environments without obvious variations in incidence suggests that the disease is relatively independent of the external milieu. The suggestion that birth injury is relevant has been tested in a prospective study (the National Child Development Study) and found wanting (Done et al, 1991).

Genes are now accepted as being important in the aetiology of schizophrenia (Gottesman & Shields, 1982; McGuffin et al, 1987), and over the past decade the emphasis in genetic research has shifted away from genetic epidemiology to searching the chromosomal DNA for the genes themselves. Despite this increasing technical sophistication, the application of linkage analysis to families multiply affected by schizophrenia has been accompanied by the familiar controversy over the exact borders of the adult clinical phenotype (Sherrington et al, 1988; St Clair et al, 1989). Indeed, the preoccupation of researchers with the vagaries of the clinical definition has resulted in repeated attempts to use genetic studies to determine the relative validity of different operational definitions of schizophrenia (McGuffin et al, 1984; Farmer et al, 1987). To us, such studies beg the question of how precisely genes are involved in the aetiology of schizophrenia; after all, genes code for proteins, not for auditory hallucinations in the third person.

A susceptibility locus for schizophrenia in the ‘pseudo-autosomal’ region has been proposed on the basis of the reported excess of sex-chromosome aneuploidies (e.g. XXY and XXX) among patients with schizophrenia and the finding that schizophrenic sib-pairs are more often of the same than of the opposite sex. This hypothesis has been tested in 83 sibships with two or more siblings fulfilling Research Diagnostic Criteria for schizophrenia or schizoaffective disorder. Alleles at the pseudo-autosomal telomeric locus DXYS14, which is unlinked with sex, were analysed using the method of affected sib-pairs. Affected sibs shared alleles at DXYS14 more frequently than expected by random Mendelian assortment, supporting genetic linkage between DXYS14 and schizophrenia.

The hypothesis that at least a subgroup of familial cases of schizophrenia could be due to a genetic defect on the X chromosome is supported by the observation of an excess of X-chromosome aneuploidies (XXX and XXY) among populations of patients with psychosis. The distal long arm, Xq27–q28, is a candidate region where linkage has been claimed to manic-depressive disorder and a fragile site has been associated with schizophrenia spectrum disorders. The present study excluded linkage to a large part of this region using four polymorphic probes and multipoint lod-score analysis in 10 families with multiple members with schizophrenia.

Recent reports of cytogenetic abnormalities linked to psychiatric illness and the localisations of the genes for the dopamine (D2) receptor and tyrosinase on the long arm of chromosome 11 have suggested that susceptibility loci for schizophrenia and manic depression might be situated in this region. We could find no evidence for linkage in five Icelandic pedigrees between manic depression and markers in this region, and we have excluded candidate genes coding for the D2 receptor and tyrosinase. We conclude that mutations at loci in this region are not a common cause of manic depression in the population studied.

Changes in relatives' affective attitudes are important contributors to the impact of family psychoeducational programmes on the course of schizophrenia. It remains unclear whether similar changes occur in the interactional style of schizophrenic patients participating in psychoeducational treatment. This study examined changes in the interactional style (coping style) of 33 schizophrenic patients in individual or family treatment. Significant changes were seen in the interactional style of the patients participating in the individual treatment. Similar changes were evident, but not significant, in the family treatment group. The quality of patient interactional style before or after treatment did not predict relapse in either group. Changes in relatives' interactional style early in family treatment are necessary to affect the short-term course of schizophrenia. Modification in patient behaviour during the early phase does not have similar predictive value.

Young married couples, with or without a depressed wife, were divided into three groups according to marital quality. Negative modes of relating were assessed by self-rating and partner-rating questionnaires. The intercorrelation of scores for different modes of relating was higher on partner-rating than on self-rating scales. There was a significant gradient of mean negative-relating scores across the three levels of marital quality. The partner-ratings of depressives and their husbands were higher on all negative-relating scales than those of non-depressed women and their husbands. The self-ratings of the depressives corresponded with these negative ratings while those of their husbands did not. The partner-rating scores differentiated between the depressives with poor marriages and those with better marriages.

The levels of fluphenazine and fluphenazine sulphoxide in schizophrenic patients who were randomly assigned to receive either 5 mg or 25 mg of fluphenazine decanoate every two weeks were monitored. Patients treated with 25 mg of fluphenazine decanoate required three months to reach a steady-state plasma level, indicating that those patients who are being converted from oral to depot fluphenazine should continue to receive oral supplementation during the first three months of treatment with fluphenazine decanoate. Plasma levels of fluphenazine sulphoxide were lower than levels of fluphenazine. At six and nine months following randomisation, there was a statistically significant relationship between lower fluphenazine plasma levels and an increased risk of psychotic exacerbations. A relatively weak relationship was found between fluphenazine plasma levels and akinesia, but non-significant relationships between fluphenazine levels and other neurological side-effects including akathisia, retardation, and tardive dyskinesia. Monitoring the plasma levels may be helpful to clinicians who are attempting to treat stabilised patients with the lowest effective dose of fluphenazine decanoate.

Meta-analysis was used to establish the efficacy of lithium in acute treatment and prophylaxis of depressive illness from existing published clinical trials. Effect sizes were measured by the odds ratio using the Mantel–Haenszel method and the Pearson product-moment correlation coefficient. Some benefit from lithium, compared with other treatments, emerged from trials of acute treatment. Lithium was clearly superior to placebo in the acute treatment of bipolar depressed patients. In controlled studies of lithium prophylaxis over five months to three years, an impressive effect was found for lithium when compared with placebo. For uncontrolled studies there was a similar-sized effect, corresponding to an improvement in the rate of favourable outcome from 35% for placebo to 70% with lithium treatment. The comparison of lithium with other antidepressants in prophylaxis showed no conclusive advantage for lithium in unipolar illness. There is no reason to doubt the efficacy of lithium in the prophylaxis of unipolar depressive illness.

In a follow-up study of 49 children and adolescents with anxious or depressive disorders up to 50% had not recovered. In the 12 months preceding onset there were no social factors which predicted recovery at follow-up. Between onset and follow-up the children were less likely to be exposed to undesirable life events, and significant improvements in maternal confiding relationships were reported. Neither of these improvements predicted the level of recovery at follow-up. Poor recovery is best predicted by moderate to poor friendships after the onset of disorder, particularly for those with a diagnosis of depression. Further confirmation is provided that direct interviewing of children by trained personnel using semistructured schedules is a valid method for determining mental symptoms and perception of recent friendships.

Ninety-nine neurotic patients from a controlled trial of CPN v. psychiatric out-patient aftercare were followed up seven years later. Of the 92 survivors, 76 were successfully interviewed. Few differences were found between the groups. Chronic mild symptoms and moderate social disability persisted, and tended to worsen a little. Treatment patterns persisted for one to two years beyond the original study; the CPN group had more CPN contacts, fewer psychiatric out-patient contacts and less psychiatric care. Thereafter, more out-patients were discharged from psychiatric care and care patterns for the two groups became similar. Out-patients attended more non-psychiatric out-patient clinics than the CPN group, but it is possible that this reflected pre-existing differences. About a third of patients remained in contact with the psychiatric service during follow-up.

The 109 female survivors of a mental hospital population surveyed in 1965 for facial dyskinesia were followed up 16 years later. The 99 survivors with non-organic brain syndromes were analysed. Prevalence of dyskinesia had risen from 18.4% to 46.5% during follow-up and its development was significantly associated with neuroleptic dosage. Enlarged ventricles on brain scans were significantly associated with dyskinesia, cognitive impairment and neuroleptic prescribing.

This study compares the withdrawal responses of methadone and heroin addicts during a ten-day in-patient detoxification programme with methadone. Contrary to suggestions in the literature, the methadone group reported more severe withdrawal symptoms during both the acute withdrawal phase and the recovery phase. There were no differences between the two groups in onset or duration of symptoms. Whereas there may be reasons to favour methadone as a maintenance drug, its use may lead to difficulties during withdrawal.

An unselected sample of 204 epileptic patients attending a neurological out-patient clinic in Abeokuta, Nigeria, was evaluated for psychiatric morbidity using the CIS. Thirty-seven per cent emerged as psychiatric cases, almost a third of these being cases of psychosis. Patients with partial seizure of temporal lobe origin were the most psychiatrically impaired, while those with partial seizure of non-temporal lobe origin the least. These findings are broadly similar to those reported for epileptic populations in other studies. However, in spite of the relatively high prevalence of major psychiatric disorders among these patients, their impairments were more likely to remain ‘hidden’ and untreated than those in similar patients in developed countries.

The 1980s witnessed the honeymoon between American psychiatry and an enigmatic and mysterious drug complication called neuroleptic malignant syndrome (NMS). I fear that the 1990s are witnessing the same in British psychiatry. Gone is the era when case reports in British literature described the syndrome without identifying it by name (Allan & White, 1972; Moyes, 1973), ostensibly owing to lack of awareness. Probably, no one had bothered to read the original description in the French-language literature (Delay et al, 1960). The pendulum has now swung to the other extreme. Every known drug-related complication is being labelled NMS. In the US, Addonizio et al (1986) suggested a ridiculously high incidence figure of 12.2%. The same trend for overdiagnosis is seen in the recent case report by Dalkin & Lee (1990). The authors of this case report seem to have forgotten that NMS is an idiosyncratic adverse drug reaction which is dose-independent. There is no reason to label every neuroleptic overdose as NMS on grounds of raised creatine phosphokinase (CPK) level.

“To isolate and quantify possible determinants of any increased prevalence of depressive disorders in women we studied a select group of men and women, initially similar in terms of a number of putative social determinants of depression, and reviewed the sample five years later when social role diversity was anticipated. We used the Diagnostic Interview Schedule (DIS) to generate DSM–III and RDC diagnoses to estimate lifetime depressive disorders, and established (via corroborative reports) the likely accuracy of those data. Despite lifetime depression being a relatively common experience, no significant sex differences in depressive episodes were demonstrated, suggesting the possible irrelevance of biological factors in determining any sex difference. As there was not major social role divergence over the five year study, we interpret the lack of a sex difference as a consequence, and suggest that findings support the view that social factors are of key relevance in determining any female preponderance in depression described in general population studies.”