Throughout the history of schizophrenia as a psychiatric concept, opinions have differed sharply over its essential nature and its causes, giving rise to a wide range of explanations that have drawn upon ideas from almost all of the social and biological sciences. Only one fact has truly survived the vicissitudes of argument about the condition: that genetic factors contribute to its aetiology. Even that conclusion, first reached in the very early days of schizophrenia research, sank temporarily out of sight during the radical psychiatry challenges of the 1960s. However, the continuing collection of family, twin, adoption and other data over that period put the genetic hypothesis beyond reasonable doubt (McGuffin, 1988).

In a total of 22 169 parasuicides over 19 years, there was evidence for a seasonal cycle in parasuicide admissions among women, with an increase during the summer and a fall over the winter, including a pronounced December nadir. Further analysis of the winter trough suggests a sociological explanation, the focal point being Christmas. There was no evidence for monthly or seasonal variation among men.

The discovery that tricyclic antidepressants blocked the re-uptake of both noradrenaline and 5-hydroxytryptamine (5-HT) was a significant step on the road to the development of the monoamine hypotheses of depression (Healy, 1987). The subsequent demonstration that the de-aminated metabolites of amitriptyline and imipramine, nortriptyline and desipramine, were antidepressants tilted the balance toward noradrenaline as the pertinent neurotransmitter, as these latter drugs were clearly inhibitors of noradrenergic rather than 5-HT uptake.

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.

There are interesting parallels between sleep disorders and the epilepsies. Firstly, both terms refer to a group of conditions differing in cause, clinical manifestation, natural history and impact on the lives of patients and their relatives. Secondly, the investigation and management of both sets of conditions require a combined physical and psychological approach. Thirdly, neither field is usually covered systematically (if at all) in medical education, although some initiative has been taken in the USA for the introduction of these areas into the curriculum of medical schools (Medical School Curriculum Task Force, 1988). This relative neglect no doubt explains the fourth parallel – that in both sleep disorders and the epilepsies misdiagnosis or inadequate diagnosis appears to be common.

A common denominator can be found permeating thought disorder at various levels – the lack of executive planning and editing. With data available from aphasiology and neuropsychology, certain features of thought disorder can be reinterpreted as being consistent with dysfunction of the frontal lobe. It is hypothesised that thought disorder may reflect a dysfunction of the cortical–subcortical loops that project into the pre-frontal cortex. The hypothesis predicts that thought-disordered patients will have impaired performance on tests of frontal lobe function, regardless of diagnosis.

Child psychiatry in developing countries has recently attained the status of an established specialty. This review looks at available epidemiological data, and factors contributing to similarities and differences in rates of disorder. The relevance of child psychiatry to child health in these countries has service, training and research implications.

Thirty-one patients with schizophrenia and 33 normal control subjects underwent MRI. The BPRS was used to rate clinical symptoms and the NART to estimate premorbid IQ. All were right handed. The temporal lobe was significantly smaller on the left than the right in both the control and schizophrenic groups. The amygdala was smaller on the left than the right in controls but not in schizophrenics. The parahippocampal gyrus was smaller on the left side in the schizophrenic group but not in controls. In the schizophrenic group, ventricular enlargement and cerebral atrophy were significantly related to severity of symptoms. Patients with marked negative symptoms had a bilateral reduction in the size of the head of caudate and the two measures were significantly correlated. Patients with marked positive symptoms had larger VBRs and again the clinical and morphometric changes were significantly correlated. There were no morphometric differences between patients with short duration (two years or less) and chronic symptoms.

The distinction of positive and negative symptoms in describing schizophrenic patients has become popular. It presupposes that symptoms cluster in two dimensions, fitting together not only theoretically but empirically. Factor analysis of three published studies of 93, 62 and 52 schizophrenic patients and a large pooled sample showed that more than two distinct dimensions are required to categorise symptoms in schizophrenia. This result is consistent across methods and samples, and with previous literature. The added dimensionality resulted from a splitting of the positive symptom domain into more distinct factors.

It is probable that all schizophrenics have abnormalities in the medial temporal lobe, which differ in degree but not in kind. The structures of the medial temporal lobe are believed to have a crucial role in the integration and processing of the output from the association cortex. Dysfunction of this system could result in the clinical symptoms that form the core of the schizophrenia syndrome. The structural differences appear to fit the profile of a disturbance in the normal pattern of brain development. The asymmetrical patterns of normal brain development explain how such a disturbance simultaneously affecting both hemispheres could, disproportionately, affect the left (dominant) hemisphere. Epidemiological and pathological evidence points to aberrant genetic mechanisms as being the cause of the developmental anomaly in the majority of cases; environmental factors probably play a minor role. Despite the great progress made in solving the enigma of the structural changes in the brains of schizophrenics, the cause(s) of the changes – the aberrant genetic mechanism controlling brain development – may prove difficult to define.

The spongiform encephalopathies are unusual in several respects. Firstly, they are transmissible, and in some cases inheritable. Secondly, variants of these disorders occur in many species and can be transmitted by consumption of infected material; this has led to concern as to the potential risk from eating contaminated animal products. Thirdly, increasing evidence suggests that a ‘prion’ protein is central to their aetiology and pathogenesis, and that no nucleic acid is involved in the infective process. The role of the prion gene and its protein is outlined and proposed as the basis for an improved classification of the transmissible dementias.

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.

The assessment of catatonic symptoms, unlike that of other schizophrenia symptoms, has not acquired accuracy and phenomenological rigour, and their distinction from extrapyramidal side-effects is not always easy. The Modified Rogers Scale can rate abnormalities in movement, volition, speech, and overall behaviour in schizophrenia. It is detailed, reliable and valid, and permits the isolation of a score for non-extrapyramidal and hence presumably catatonic phenomena.

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.

Of 510 patients consecutively admitted and diagnosed as schizophrenic, 310 who failed to meet research criteria for schizophrenia were labelled as having ‘atypical psychosis'. This heterogeneous group of patients was then subtyped into more homogeneous subgroupings according to their clinical characteristics, independent of their family data. One subgroup resembled schizophrenia, one resembled affective disorders and a third (n = 57), which did not resemble either schizophrenia or affective disorder, was defined as ‘schizoaffective’. Comparing the morbidity risks for schizophrenic and affective disorders in the relatives of this schizoaffective group with those of the relatives of ‘typical’ groups of schizophrenia and affective disorder, showed that this group was different from those with schizophrenic and affective disorders.

Psychoanalytical ideas are used to outline how poor narcissistic development can lead to poor regulation of self-esteem. This in turn often underlies domestic violence, the short-term treatment of which can be aided by psychodynamic understanding.

Age of onset was examined for 139 members of 30 families affected by early-onset AD. Most (77%) of the variance of age of onset derived from differences between rather than within families. The constancy of age of onset within families was also observed in an analysis restricted to families derived from a population-based epidemiological study with complete ascertainment of early-onset AD. Furthermore, we observed clustering of age of onset within those families that support linkage to the predisposing locus on chromosome 21. Our data are compatible with the view that allelic heterogeneity at the AD locus may account for the similarity in age of onset within families. This finding may be of value for scientific studies of AD as well as for genetic counselling.

Ethical principles are influenced by personal values and beliefs, and by societal context. They are not immutable. In medicine, as new technologies have developed and changes in health-care delivery have resulted, historically held views about the responsibilities, obligations and relationships between health-care providers and patients have been challenged.