A number of factors have been proposed as being linked to schizophrenia: genetic, psychological, endocrinological, metabolic, environmental, virological, and auto-immunological factors, as well as neurotransmitter systems and structural disorders of the brain. All may act as predisposing, triggering, or functionally modulating factors in what is probably a condition composed of several types of disorder with varying aetiology. Neuroanatomical and neuromorphological data have revealed ventricular enlargement and diminished frontal and temporal lobe volume in some patients. These changes are concentrated particularly in the hippocampus/parahippocampal gyrus/amygdala, but are relatively small and span some overlap with healthy subjects. Twin studies suggest that at least some of these changes may result from other than genetic factors. Functional disturbances of the brain have also been connected with frontal and temporal structures in some schizophrenic patients. Of the single neurotransmitter substances, dopamine and serotonin appear to represent some of the central restitutive mechanisms whose function is to maintain mental stability; the understanding of their interplay with other neurotransmitters such as noradrenaline, acetylcholine, GABA, and glutamate, should provide a more integrated view of both normal and disturbed brain function.

The excess of winter–spring births among individuals suffering from schizophrenia provides strong evidence for the existence of some prenatally occurring factors in the pathogenesis of schizophrenia. Recent epidemiological findings suggest that maternal viral infections during the second trimester of pregnancy may play a crucial role in the aetiology of adult schizophrenia. A ‘two-hit window’ hypothesis of the mechanism of action of prenatal factors in the pathogenesis of schizophrenia suggests at least two time-specific prenatal aetiological events. The observed association between prenatal viral infection and increased incidence of adult schizophrenia need not be a direct cytotoxic result of the viral infection, but may be caused indirectly, for example from foetal minor cerebral haemorrhages produced by the anticoagulant effects of aspirin.

The evidence for a genetic contribution to schizophrenia is compelling. However, the pattern of inheritance is complex and it is usually assumed that environmental factors also have a role that will eventually be identified. We argue that this is not necessarily the case. While a hypothesis combining genetic diathesis with environmental stress cannot be disproved, it is also possible that ‘non-genetic’ factors consist entirely of stochastic events affecting gene expression or structure.

We reviewed follow-up studies of adults with depressive disorders seen in psychiatric settings, and noted outcomes in terms of recovery, recurrence, and persistent depression, at six months, one year, two to five years, and ten or more years after an index episode of depression. Recovery increased with time: about half recovered at least briefly by six months, and a large majority did so in the long term. Only about a quarter recovered from an index episode and remained well more than ten years thereafter. A quarter of patients suffered recurrence of depression within a year of an index episode, and three-quarters did so at least once during follow-up periods lasting more than ten years. For more than one in ten patients, the depression proved persistent, the proportion affected remaining relatively stable over time. The review highlighted a relative paucity of conclusive investigations on the outcome of the commonest psychiatric disorder in clinical settings.

As grief is both an individual and shared experience, adopting a systemic perspective is most appropriate for health-care professionals seeking to assist the bereaved. Within this framework, the family virtually always constitutes the most significant social group in which grief is experienced. In this paper we review the literature on family grief, covering clinical case reports, the observations of family therapists, systematic family bereavement research and family intervention studies. An understanding of patterns of family grief and vulnerability factors for morbid grief is pivotal to both preventive intervention and treatment of an established disorder.

Five aspects of the diagnosis and treatment of multiple personality disorder (MPD) were examined. The following five conclusions were made: the contemporary diagnostic criteria are vague and overinclusive; the recent alleged increase in prevalence of the disorder is almost certainly artefactual; legal proceedings involving MPD patients raise disturbing questions about personal responsibility; there is little literature support for the theory that MPD results from childhood trauma; and many of the techniques used to diagnose and treat the condition reinforce its symptoms. A careful revision of diagnostic criteria for the disorder is recommended.

The efficacy of lithium prophylaxis for recurrent mood disorders is well established. Despite concern that the later efficacy studies have shown poorer results, these studies (after 1980) are equally confirmatory of lithium's efficacy. However, questions have been raised with regards to the effectiveness of lithium prophylaxis under ‘ordinary’ clinical conditions. Part of the confusion stems from the failure to distinguish clearly efficacy (the potential of a treatment) from effectiveness (the results obtained under clinical conditions). Studies of effectiveness or naturalistic studies show poorer results than efficacy studies in all areas of medicine. The major reason for this discrepancy with lithium prophylaxis is poor compliance. Estimations of the efficiency (cost benefits) of lithium prophylaxis are flawed by the failure to consider such issues. It is proposed that specialised lithium or mood disorders clinics have the potential to narrow the gap between efficacy and effectiveness – efficiency.

To facilitate the introduction of this new section, designed to shed light on the peer review process, the Editor has used the review of a paper of which he is a co-author. The referees for this paper were originally anonymous, but they both agreed to be named for the purposes of this article. The original article was twice the length of the published version. The effect of the assessment should be readily apparent. Editorial decisions were undertaken by members of the Editorial Board other than the current Editor.

We used SPECT to examine striatal D2 receptor binding in 20 antipsychotic-free DSM–III–R schizophrenic patients and 20 age- and sex-matched normal controls. Dynamic single-slice SPECT, at a slice chosen to include the basal ganglia, began immediately following intravenous injection of 185 MBq of 123I-IBZM. A semiquantitative approach was used to generate indices of specific D2 receptor binding in the basal ganglia. There was no overall elevation of D2 receptor binding between patients and controls. A male sex-specific left lateralised asymmetry of striatal D2 receptor binding was found in the patient group. Age-dependent decline of striatal D2 receptors was confirmed in controls, but not in patients. These results suggest that alterations in striatal D2 receptor distribution and density do occur in schizophrenia, and possibly reflect wider disruptions in prefrontal-striatal-limbic circuits.

We investigated linkage between schizophrenia and the loci DXYS14, DXYS17, and MIC2 within the pseudoautosomal region in 85 families with two or more siblings suffering from schizophrenia or schizoaffective disorder. A maximum lod score of 2.44 was reached at MIC2, with a dominant model of inheritance at a recombination fraction of 0.367 in females and 0.046 in males (a F: M sex ratio > 1, i.e. opposite to that expected with a pseudoautosomal locus). Evidence consistent with linkage (P = 0.01) was also obtained with a sibling pair analysis at the MIC2 locus. These data do not support (although they do not definitively exclude) a locus within the pseudoautosomal region; they are consistent with the presence of a gene that predisposes to schizophrenia in the sex-specific regions of the X and Y chromosomes.

A nationwide Finnish sample of schizophrenics' offspring given up for adoption was compared blindly with matched controls, who were adopted offspring of non-schizophrenic biological parents. The adoptive families were investigated thoroughly using joint and individual interviews and psychological tests. The biological parents were also interviewed and tested. Among the 155 index offspring, the percentage of both psychoses and other severe diagnoses (borderline syndrome and severe personality disorders) was significantly higher than in the 186 matched control adoptees. This supports a genetic hypothesis. However, notable differences between these two groups only emerged in the families which were rated as disturbed. Thus the genetic effect (i.e. the differences between high and low genetic propensity) was only manifested as a psychiatric disorder in the presence of a disturbed family environment. The impact of disturbed family relations was strongest in the presence of the appropriate genotype.

Individuals affected by mental retardation are a clinically and aetiologically heterogeneous group. This heterogeneity is particularly highlighted when we consider the genetics of mental retardation. Recent advances in molecular genetic techniques have enabled us to understand more about the molecular basis of several genetic syndromes associated with mental retardation. In contrast, where there is no discrete cause, the interplay of genetic and environmental influences remains poorly understood.

Schizophrenics have been repeatedly found to experience more obstetric complications (OCs) at birth. The meaning of such a finding is debated, and the aim of this study is to contribute to the understanding of OCs' aetiological role in schizophrenia. We compared a group of schizophrenic patients with their siblings and controls, on the basis of obstetric files stemming from the same University Hospital Maternity Ward. Schizophrenic patients had more frequent umbilical cord complications and atypical presentations, as well as higher scores on a scale measuring OCs linked to possible neonatal asphyxia.

My involvement with the psychiatry of learning disability began in 1968 when Professor Batchelor, then Professor of Psychiatry at the University of Dundee, suggested that mental illness in people with learning disability was a clinically interesting and under-researched topic which merited further investigation. At that time, mental illness was not usually considered even a part of the medical specialty of learning disability – or at least, not in Scotland. People in mental handicap hospitals who developed signs of mental illness were normally passed on to colleagues in general psychiatry who were considered to have the investigative and treatment expertise. If admission to in-patient care was considered necessary, it was usually to the local general psychiatry service.

Antipsychotic medication is the mainstay of treatment for the functional psychotic illnesses. Such drugs are also referred to as neuroleptics (meaning a drug with both antipsychotic effects and effects on movement) and major tranquillisers. The psychotic illnesses for which they are prescribed include schizophrenia, mania in the course of a bipolar mood disorder, and, more rarely, depression accompanied by psychotic symptoms. These are not uncommon illnesses. At some time during their lives approximately 1% of the population will suffer at least one episode of schizophrenia and a further 1% will suffer at least one episode of mania. During an episode some patients, but by no means all, suffer extreme changes in their thinking, mood and behaviour which can be very distressing to experience and which can make patients a danger to themselves or other people.

Although the prevailing conception of the aetiopathogenesis of schizophrenia assumes the combined effect of a biological predisposition and of environmental stress, genetic factors have recently received more attention than environmental ones. Rather than concentrating on only one of these, Professor Tienari and his team have directed their research efforts to clarifying the joint effects of both. For that purpose, they have gathered a comprehensive body of material, starting from 19 447 schizophrenic women with 291 children given away for adoption; of the latter, 155 index children, with their biological and adoptive parents, were ultimately included in their study. A group of 185 control children was collected for comparison, and their parents (adoptive and biological) were also investigated.