Community care has lost its innocence. Critics and evangelists vie for television space and newspaper headlines. The Chief Medical Officer had to beg for clarification of a term that had developed too many meanings and an “ethos of virtue” (Acheson, 1985). How should it be defined? Can a hospital be part of the community? Does it mean care ‘in’ ‘by’ the community? The Department of Health and Social Security (DHSS) definition seems to be “the provision of alternatives to long-term institutional care for the chronically sick or those suffering from long-term handicaps or disabilities” (Hunt, 1985). Lord Trefgarne (1984) put the policy aim, more simply, as “to move out of hospital those people who do not really need to be there”.

The effectiveness of specialised work in any branch of medicine cannot depend alone on the personal and professional qualities of the entrant into the field. It demands extended and systematic training, not only in the clinical speciality itself, but also in those many disciplines that bear upon it. In the course of his or her studies, the trainee psychiatrist is expected to further his acquaintance with the relevant basic medical sciences (especially neuroscience), and with organic medicine (particularly neurology), and with the application of these to his field of study. His understanding of these and many other subjects, including genetics, biochemistry, sociology, epidemiology, and statistics, is indispensable to his professional development. Extended clinical experience will teach him something of the day-to-day applications of these studies to psychiatric practice in a wide variety of circumstances. He may also acquire knowledge of such specialised areas of work as mental retardation and forensic psychiatry. Although he will be aware of his many limitations, the well-trained consultant will draw, in his general clinical practice, upon these various fields of knowledge with a justifiable measure of confidence.

Despite the relatively high incidence of therapy-resistant depression, there is little clinical evidence to suggest that there are significant biochemical differences between therapy-resistant and therapy-responsive patients. A major problem for investigators is the lack of an internationally recognised definition of resistant depression. Also, it is possible that depressed patients with delusional symptoms or rapidly cycling affective disorders form subgroups that are more likely to be resistant to tricylic antidepressant treatment and are therefore classified as therapy-resistant. Evidence is presented to show that an abnormality in serotonergic function may characterise some therapy-resistant depressed patients.

The hypothesis that cognitive impairment in Alzheimer's disease is related to cholinergic degeneration in the brain is still, a decade after its formulation, subject to critical evaluation. In marked contrast to the monoamine hypotheses of affective disorders or schizophrenia – based primarily on the mechanisms of action of therapeutic drugs, and yet lacking convincing pathological data on the human brain itself – the cholinergic hypothesis of Alzheimer's disease currently rests largely on evidence of neurochemical pathology in affected tissue, but still depends on effective therapy for its ultimate validation. The urgent need for a means of countering cognitive impairment in degenerative dementias such as Alzheimer's disease (probably the most important cause of intellectual decline in old age) hardly needs emphasising. In this annotation, a number of key questions specifically relating to the cholinergic involvement in Alzheimer's disease are considered. These questions are already being answered both within and, as so often in the history of biological psychiatry, outside the immediate area of investigation.

The development of the British response to ‘the drugs problem’ since the 1960s does not lend itself readily to any optimistic interpretation. The initial wave of enthusiasm for clinics during the latter years of the 1960s soon faded. The clinic system was deprived of sufficient support, and many staff became disillusioned and burnt out. Treatment and responses gradually changed, not as the result of any clearly thought-out policy, but as the result of a vague drift of views.

Ten years ago, specific high-affinity binding sites for benzodiazepines (BDZs) were found in the brain (Mohler & Okada, 1977; Squires & Braestrup, 1977). These binding sites are believed to be the primary site of action of BDZs and are found on the same protein as GABA receptors. GABA is the main inhibitory neurotransmitter in the brain.

Techniques of molecular genetics, including recombinant-DNA technology, are likely to have a key role in modern psychiatric research and practice. This article reviews some methods of DNA analysis and their applications to clinical science: specifically, how these methods can be used to localise, identify, isolate, and clone clinically important genes, and how this should enable us to elucidate the molecular pathology of most inherited (psychiatric) disorders. The implications of these developments for prevention and treatment of genetic disease are discussed.

It is suggested that schizophrenic thought disorder comprises four relatively independent components: delusion; intrinsic thinking disturbance; formal thought disorder; and deficient real-world knowledge – a new concept. Schizophrenic and neurotic control subjects were given tests of thinking, perception, appreciation of conversational discourse, and social and practical knowledge. Not all deluded schizophrenics had intrinsic thinking disturbance. Those that did tended to have overinclusive categorisation as the most apparent deficit. Formal thought disorder was associated with a poor performance on the test of conversational discourse. The most striking result was that 75% of schizophrenic patients were markedly deficient, relative to neurotic patients, on their knowledge of everyday social issues.

The publication of DSM-III introduced the diagnosis Post-Traumatic Stress Disorder (PTSD), thus providing, for the first time, a framework for studying the consequences of extremely stressful events. Previously, traumatic neuroses had attracted a wide variety of labels – as wide as the experiences that produced them. Competing explanations in psychological and biological terms have characterised the approach to these disorders, and social and legal issues have added to the confusion. In recent years, psychosocial issues have tended to dominate the literature in relation to PTSD. While acknowledging the importance of such phenomenological and psychosocial approaches, this paper seeks to redress the balance by focusing on a biological perspective.

The possibility of a rise in rates of depression among adolescents and young adults was first reported in the 1970s. Particular note was taken of the emergence of childhood depression and the increase in suicide attempts and death among adolescents and young adults. Data from large-sample family studies and community epidemiological surveys have been reviewed and reanalysed, using life-table statistical methodology. Evidence for secular trends are presented, and the problems of disentangling period and cohort effect are discussed. It appears that the ‘baby boomers' -those born in the years after World War II- have had increased rates of depression and other related illnesses, including drug abuse and alcoholism. The theoretical aspects of this are discussed, particularly for gene-environment interactions.

The purpose of this collection of papers is to describe the present state of development of Chapter V (F) of the Tenth Revision of the International Classification of Diseases (ICD-10) (to be published by the World Health Organization, Geneva), and to discuss some related issues concerning psychiatric classification in an international setting.

Depression in childhood and adolescence has become a topic of considerable research interest in the last decade. A number of studies ranging over the last half-century provide information about the prevalence of depressive symptoms and syndromes in non-referred populations. These studies are critically reviewed in the light of an analysis of the various meanings that the term ‘depression’ may carry, and a variety of methodological issues. The sparse evidence for the involvement of a number of potential risk factors for depressive disorders is then considered and suggestions for future work in this area are outlined.

The association between the familial risk for schizophrenia and season of birth was studied in 88 schizophrenic patients. An increased risk for schizophrenia and ‘spectrum’ disorders was demonstrated among the first-degree relatives of winter and spring-born schizophrenic patients. However, patients with a family history of schizophrenia and ‘spectrum’ disorders did not differ from patients with no family history with respect to season of birth. Season of birth was unrelated to the sex of the patient, birth order, age at onset, or clinical subtypes (paranoid vs non-paranoid, as defined by the RDC, and ‘narrow’ vs ‘broad’, as defined by Taylor & Abrams' 1975 criteria). The morbid-risk data support a ‘stress-diathesis' hypothesis whereby environmental factors (in this case a seasonally varying viral insult may be implicated) interact with genetic vulnerability to increase the risk for schizophrenia.

Recent surveys indicate that the frequency of assaults on psychiatric staff by in-patients has increased substantially over the past decade. With patient assaultiveness becoming of greater concern, the need to predict, anticipate, and avoid confrontations with potentially assaultive patients has grown. Regrettably, the vast majority of studies examining the nature, correlates, and predictors of in-patient assaultiveness suffer from methodological problems that limit the validity of their findings.

The prospective monitoring of two separate groups of chronically schizophrenic patients on regular depot maintenance therapy suggests that depression developing after an interval of 1 year from recovery from an acute relapse indicates a significant increase in the risk of a further relapse within 2 years, compared with depression within the first year, or no depression. Patients with such depression were more prone to relapses than other patients, despite regular medication within normal dose ranges. The results suggest that the aetiology of depression occurring in patients after 1 year in a stable mental state is different from that of depression within the first year, and in many patients, the former represents underlying schizophrenic activity prior to an early relapse.

The Camberwell Collaborative Depression Study is an investigation of a series of 130 patients (76 female; 54 male) attending the Maudsley Hospital Services with unipolar depression of recent onset (the probands), and of their first-degree relatives. This paper describes the first element of the study, the investigation of the index cases or probands, which was carried out by members of the MRC Social Psychiatry Unit over the period 1982–1985. A description of the methods of the study is followed by an analysis of life events in relation to the symptomatic pattern of the depressive state. An ‘endogenous' group was defined as cases of depression falling within Catego classes D and R, and compared with a ‘neurotic’ group conforming to classes N and A. The hypothesis that the ‘endogenous' group of disorders would be relatively independent of prior life stress was not confirmed. Depressed women were more likely to have experienced life events or difficulties than their male counterparts, and there was some evidence that sex, but not age or social class, influenced the relationship between adversity and the type of depression. Examination of the timing of life events was strongly suggestive of a causal effect, with a pronounced rise in the month before onset. This was not limited to the most severe events. Differences between the ‘endogenous' and ‘neurotic’ groups in the temporal patterning of events before onset are discussed. The findings are interpreted in terms of the literature on the topic.

The measure of expressed emotion (EE) of the relative has been found to be an important predictor of schizophrenic relapse. Electrodermal measures were recorded when the schizophrenic patient was talking to an experimenter, and when the patient was talking to a relative. Although there were no differences during the relative-absent period, patients with a high-EE relative present exhibited significantly higher frequencies of non-specific skin-conductance responses (NS-SCRs) than patients with a low-EE relative present. Patients show a significant decrease in NS-SCRs on the entry of low-EE, but not high-EE relatives. Patients with high-EE relatives show overall higher levels of skin-conductance levels (SCLs) than patients with low-EE relatives. Although patients with high-EE relatives rate themselves significantly more tense and anxious on self-rating scales, there are no significant correlations between self-ratings and electrodermal measures. The use of electrodermal reactivity as an assessment measure of relapse risk is discussed.

The proposals for the chapter dealing with mental, behavioural and developmental disorders in the tenth revision of the International Classification of Diseases (ICD) are in the true sense a product of many minds. In their development WHO has called on and received the generous advice and support of its network of collaborating centres, of the members of Expert Advisory Panels on Mental Health, Neurosciences and Drug Dependence and Alcohol Problems from some 60 countries, and of the non-governmental organizations with whom WHO is in official relations. Among the latter, the collaboration with the World Psychiatric Association has been particularly useful; this Association sent the text of the ICD to all of its member societies, assembled their views and comments and worked closely with WHO in incorporating these comments into the text of the ICD. The WPA has created a special committee under the chairmanship of Professor E. Stromgren which summarised all the views received, and maintained collaboration with WHO throughout the development of the proposals.

Ninety-one subjects diagnosed clinically as having a ‘neurotic depression’ were interviewed and then re-assessed at 6 weeks and 20 weeks. Four symptom profiles of clinical features were derived: ‘negative cognition’, ‘lack of drive’, ‘anxiety’, and ‘arousal’, the last being independent of the other three dimensions and of the severity of depression. Symptom profile scores were then examined against antecedent risk variables and outcome. Links between profile scores and personality variables suggest that personality may colour the clinical presentation of neurotic/reactive depressions, and challenge the assumption that a typology of these depressive disorders based on clinical features is achievable. The break-up of an intimate relationship in the preceding 12 months was a strong predictor of a good outcome. Further analyses suggested, firstly, that there was a distinct subgroup delineated by this life event, with features weighted to the ‘arousal’ symptom profile, including many symptoms often associated with diagnosis of ‘endogenous depression’; and, secondly, that this life event and a good outcome were directly linked, being uninfluenced by personality or other mediating variables.