Unprecedented numbers of cases of MPD have been diagnosed, mainly in North America, since 1957. Widespread publicity for the concept makes it uncertain whether any case can now arise without being promoted by suggestion or prior preparation. In order to determine if there is any evidence that MPD was ever a spontaneous phenomenon, a series of cases of MPD from the earlier literature has been examined, with particular attention given to alternative diagnoses which could account for the phenomena reported and to the way in which the first alternate personality emerged. The earlier cases involved amnesia, striking fluctuations in mood, and sometimes cerebral organic disorder. The secondary personalities frequently appeared with hypnosis. Several amnesic patients were trained with new identities. Others showed overt iatrogenesis. No report fully excluded the possibility of artificial production. This indicates that the concept has been elaborated from the study of consciousness and its relation to the idea of the self. The diagnosis of MPD represents a misdirection of effort which hinders the resolution of serious psychological problems in the lives of patients.

Many kinds of stress stimulate the neuroendocrine systems controlling catecholamine and glucocorticoid secretion. Stress-induced stimulation of CRF-containing neurons appears to be mediated by serotonergic, noradrenergic, and possibly other neuronal pathways. Stress can alter various neurobiological and endocrine functions, two essential components of the neuroendocrine responses being release of adrenalin from chromaffin cells of the adrenal medulla and secretion of glucocorticoids from adrenocortical cells. Activation of adrenal steroid secretion is mainly by a reflex activation of hypothalamic neurons, which stimulate ACTH secretion from the anterior pituitary. While the neuropeptide CRF plays a major role in the neuroendocrine response to stress, the neuronal signals which are responsible for the regulation of CRF neurons have not been completely elucidated. A number of other regulatory substances may also participate, alone or with CRF, in the control of ACTH secretion by pituitary corticotrophs, and there is increasing evidence that classical neurotransmitters or neuropeptides may act directly on adrenocortical cells to modulate corticosteroid secretion. We review the neuronal, neuroendocrine, and humoral pathways which participate in the regulation of stress-induced corticosteroid secretion, and present preliminary data on the effect of the tricyclic antidepressant, tianeptine in the response of the HPA axis to stress.

This paper concerns certain questions which arose during the analysis of a trial showing positive effects of tacrine in Alzheimer's disease. Cognitive improvement occurred during the first two weeks, reached a maximum at one month and was maintained during the rest of the three-month treatment period. Rebound effects were not detected in any of the key outcome variables, but were suggested by one of the supporting cognitive tests and other measures. Practice effects occurred on tests which were repeated at short intervals or too frequently. The paper discusses the significance of these findings for the interpretation of other trials and for practical management.

In-vitro spectrometric measures were made of spin-lattice (T1) and spin-spin (T2) relaxation times of samples of grey and white matter from the brains of 15 patients with a pathological diagnosis of Alzheimer's disease, 5 with multi-infarct dementia, and 11 non-demented subjects. Relaxation times were significantly greater in the parietal white matter and temporal white matter of patients with Alzheimer's disease compared with that of the other subjects. This was associated with an increase in tissue water content. These findings confirm measures obtained in some imaging studies.

The aetiology of psychiatric morbidity associated with education in Africa was explored using two different screening methods (as described in paper III, this supplement). The interactive effect of psychosocial variables was examined by Log linear analysis which demonstrated five independent factors: (a) the financial implications of education which represented the change from subsistence to cash economy; (b) fear of envy and bewitchment which represented the intense cultural response to education; (c) parenting in the pre-school years which was the independent family variable; (d) academic ability; (e) attributes of the school. Age of starting school and birth rank had a marginal effect. Current family adversity in terms of unstable parental union, paternal use of alcohol, polygamy and sibship size operated by interactive or additive effect. Gender and social status had no effect. The brain fag syndrome can be related to the complex social changes during rapid social transition where education is a major agent of change.

D1 and D2 dopamine (DA) receptor occupancy was determined by PET in the basal ganglia of drug-treated schizophrenic patients. In 22 patients treated with classical neuroleptics at conventional doses, the average D2 occupancy was 78% (s.d. 6%). In five patients treated with the prototype atypical antipsychotic drug clozapine, a lower D2 occupancy of 48% (s.d. 11%, P<0.01) was found. Accordingly, clozapine is ‘atypical’ with respect to the striatal D2 DA receptor occupancy induced in patients. No obvious D1 DA receptor occupancy was induced by the classical neuroleptics haloperidol or sulpiride. The thioxanthene flupenthixol induced a 36-44% D1 occupancy in individual patients. In four patients treated with clozapine the D1 occupancy was 38-52%.

In DSM–III–R, pica, with anorexia nervosa, bulimia nervosa and rumination disorder of infancy, is accorded the status of a separate eating disorder. However, in the Draft of ICD–10, only anorexia nervosa and bulimia nervosa are listed under eating disorders. Pica in children, and feeding disorder in infancy and childhood, are incorporated with enuresis, encopresis, and feeding, movement and speech disorders in a separate “heterogeneous group of disorders”. Extensive research on the history and terminology of eating disorders from the 16th to the 20th century suggests that, historically, pica was regarded as a symptom of other disorders rather than a separate entity. This paper aimed to locate and assess chronologically significant definitions and accounts of pica, to provide a fuller clinical description of a condition which, despite its current relevance, has received little detailed historical examination, and to give some consideration to the multiple aetiological theories which have been put forward. The historical findings are related to the descriptive criteria for pica in DSM–III–R and Draft ICD–10.

Samples of ventricular CSF were taken from 52 consecutive patients admitted for psychosurgery for intractable depression. Concentrations of asparagine, aspartate, glutamine, glutamic acid, and serine were determined. Glutamate and aspartate concentrations, implicated in excitotoxic brain damage, were not affected by various types of psychotropic drug treatment. Serine, a modulator of glutamate responses, was significantly elevated in samples from subjects receiving antidepressants. These subjects responded poorly to the operation. Psychotropic drugs are unlikely to be neurotoxic. Nevertheless, antidepressants may influence excitatory neurotransmission.

Videotaped social interactions were shown to a population of schizophrenics and controls who were asked to comment on the emotional state of the principal protagonist. Their free responses were subjected to a content analysis to examine which of three possible explanations of known schizophrenic inaccuracies on this task were responsible: formal thought disorder, selective avoidance of psychological factors, or perceptual/attentional deficits. Neither selective avoidance nor marked thought disorder were found to explain these errors. The schizophrenics as a group rated much the same, irrespective of clinical profile. Their judgements of personality were less clear-cut than the controls.

Stressors induce behavioural disturbances and neurochemical changes in animals, some of which are reminiscent of the symptoms and presumed neurochemical concomitants of depression in humans. Just as in humans, where considerable inter-individual variability is evident in the symptom profile of depression, there is marked inter-individual and inter-strain variability in the behavioural effects of stressors in animals. It is proposed that stressors induce adaptive neurochemical changes, failure of which may engender behavioural disturbances. Variability in the symptoms of depression and in the efficacy of its pharmacological treatment may reflect the biochemical heterogeneity of the illness. Inter-individual differences in vulnerability to stressor-provoked neurochemical changes may contribute to the behavioural profiles observed.

The Cross-National Collaborative Panic Study, Phase Two, compared alprazolam with imipramine and with placebo in a sample of 1168 randomly assigned subjects. The study, conducted at 12 centres, assessed clinical change over eight weeks of double-blind drug treatment. Improvement occurred with alprazolam by week 1 and 2, and with imipramine by week 4. By the end of week 8, however, the effects of the two active drugs were similar to each other, and both were superior to placebo for most outcome measures.

During a six-month period, 306 psychiatric assessments were recorded prospectively on specifically designed schedules. There was a skewed distribution towards younger patients, and 78% were male. Just over half were seen for a court report, one-third of cases came from solicitors, and in two-thirds the request was merely for advice. Secure care was only sought in 15%. In nearly two-thirds an offence had precipitated the referral. Half were seen in prison. The majority had a history of dangerous behaviour and one-fifth were regarded as a sexual risk to others. Only one-third had not previously seen a psychiatrist. A personality disorder was diagnosed in 41%, but only 6% were considered to be psychopaths. These and other findings are discussed to help give an insight into the service.

The treatment of severely disturbed patients is strengthened in an important way by listening closely to them and by attempting to understand their experience in the depth that is made possible by the use of psychoanalytic concepts. It follows that the practice of clinical psychiatry in the UK would be greatly improved by the introduction of a psychoanalytic and psychotherapeutic perspective into the acute ward. This paper reviews the work done on a ward at the Maudsley Hospital in which this approach was the practice.

This paper describes the results obtained by combining data from the Northwick Park and Leicester randomised controlled trials of ECT. Patients who suffered from depression in which retardation and delusions were features and who received real ECT had a significantly improved outcome at the end of four weeks of treatment (as measured by improvement in the HRSD) in comparison with those who received simulated ECT. However, this treatment effect was not detectable at six-month follow-up. Patients who were neither retarded nor deluded did not benefit significantly from real as opposed to simulated ECT.

We report a series of 15 patients with delusional (paranoid) disorder as defined in DSM–III–R. All were supervised by a forensic psychiatry service after violent or threatening acts. We hypothesised that delusions and actions in these patients would be congruent with an abnormal mood characterised by fear and anger. Informants and the patients indicated a pervasive and persistent abnormality of mood (fear and defensive anger), with delusions and actions that were congruent with this mood during the offence and for over a month before. Other behaviours, such as fleeing or barricading to avoid delusional persecutors, were also consistent with congruence of mood and delusions. In all cases, violent acts and mood were congruent, but in three cases the violent act was unrelated to delusions. Although a study such as this does not demonstrate that the mood abnormality is primary, we believe moods of fear and anger in delusional disorder are not sufficiently recognised as part of the disorder.

Using a neuroendocrine probe we studied nine male’ offenders in a forensic hospital, convicted of murder, with a diagnosis of antisocial personality disorder, who had been behaviourally ‘quiescent’ for varying periods and who had not recently been abusing drugs. Nine healthy age-matched men also participated. All subjects received 30 mg d-fenfluramine (d-FEN), a 5–HT releasing agent, orally, after an overnight fast, and serial samples for prolactin estimation were taken hourly for five hours. Responses were significantly impaired in the patients, suggesting a subsensitivity of certain 5–HT systems in antisocial personality disorder, regardless of recent or ongoing behavioural disturbance.

Nearly half of those seen in a forensic service were offered some form of help, but it did not reliably match that requested. In 63% of court reports there was no specific treatment recommendation, but where there was, it was likely to be accepted. Only one-third of all outpatients completed the treatment offered – 40% of the lapses were due to imprisonment. One-third of out-patient treatments were conducted under conditions of probation orders, and this form of compulsion was associated with a significantly higher number of completed treatment plans. Personality disorder was also associated with more treatment completions. These and other findings are discussed to assist in an understanding of the service.

Sixty agoraphobics were treated by behavioural therapy (self-exposure in vivo) either with their partner involved in all aspects of treatment or without their partner. The two treatment formats were about equally effective. Behavioural treatment directed at the agoraphobia resulted in improvement irrespective of marital quality and partner involvement in the therapy. The effects of treatment led neither to a deterioration of the marriage nor to adjustment problems in the partner. Avoidance behaviour, intropunitivity and overprotection were found to predict treatment response. The partners of agoraphobics were not found to have psychological problems themselves.