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.

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.

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.

Among 29 multiply affected pedigrees, age of onset among parents and offspring was examined for evidence of both anticipation and genomic imprinting. The results do not suggest that either mechanism is operating in schizophrenia, but only very large effects can be confidently excluded.

Numerous studies have found that male schizophrenic patients have earlier ages at onset than females. However, none of these studies have corrected the observed ages for known gender differences in the age distribution of the population. Using a pre-existing data set, we applied a non-parametric method to correct the male and female distributions of observed age at onset for sex-specific age distributions. The distributions of observed age at onset indicated earlier onset among males. After correction, the age-at-onset distributions shifted toward older ages, but the difference between males and females remained statistically significant. Thus, gender differences in the age at onset of schizophrenia are not artefactual.

In the context of a prevalence survey of schizophrenia in South Westminster, a questionnaire was administered to 271 patients to assess alcohol-related morbidity. In this epidemiologically based sample, the lifetime prevalence of alcohol abuse was 22.1 %. Compared with control patients matched for age and sex, these index cases had a significantly shorter duration of illness. A possible explanation is that drinking may mask the onset of schizophrenia, leading to a delay in diagnosis. The index cases also had significantly higher ratings for hallucinations and for hostility, anxiety and depression, and a greater number of disturbed types of behaviour. The highest levels of alcohol consumption were associated with more severe orofacial dyskinesia, suggesting that alcohol use may be an added risk factor for the development of tardive dyskinesia in some patients. The severity of akathisia was also related to alcohol use, and there were significant relationships between the subjective distress related to akathisia and the level of abuse. A possible interpretation is that alcohol had been used by patients with akathisia to alleviate the associated agitation and dysphoria.

Abnormalities of ‘social’ reasoning were investigated in patients suffering from persecutory delusions and in matched depressed and normal controls using transparent (obvious) and opaque (unobvious) tests of attributional style. Whereas depressed and normal subjects yielded similar causal inferences for both attributional measures, the deluded subjects showed a marked shift in internality, attributing negative outcomes to external causes on the transparent Attributional Style Questionnaire but, on the more opaque Pragmatic Inference Task, attributing negative outcomes to internal causes and thus showing a cognitive style resembling that of the depressed group. This finding, interpreted in terms of explicit versus implicit judgements, supports the hypothesis that delusions function as a defence against underlying feelings of low self-esteem.

In a controlled trial of alprazolam and exposure in 154 patients with panic disorder with agoraphobia, relations between panic, anticipatory anxiety, and phobic avoidance were examined. The three symptoms were independent of one another at baseline and improved largely independently during treatment; only early improvement in avoidance predicted global improvement after treatment. Global improvement was more related to reduction of avoidance than a decrease in panics. Panic was not a valuable outcome measure in panic disorder with agoraphobia.

Patients with panic disorder plus agoraphobia had 8 weeks of drug treatment (alprazolam or placebo) plus psychological treatment (exposure or relaxation). At the end of treatment at week 8, 40 patients who had become much/very much improved rated how much their gains were attributable to medication or to their own efforts. During the tapering-off to week 16, and treatment-free follow-up to week 43, patients who at week 8 had attributed their gains to medication and felt less confident in coping without tablets had more severe withdrawal symptoms and greater loss of gains than did patients who at week 8 had attributed their gains to their own efforts during treatment. Baseline illness severity, greater age, higher expectations from drug treatment, and more side-effects of drugs during treatment all predicted more external attributions (i.e. to the effect of drugs) but did not independently predict relapse. Patients on alprazolam compared with placebo had more drug attributions. Though drug attributions predicted relapse in both alprazolam and placebo groups, predictions were stronger in the alprazolam group.

We contacted and interviewed 150 cocaine users in south London community settings. Most were taking cocaine regularly, but not daily, and in substantial doses. Three main routes of administration were used: smoking (40%), intranasal (32%), and injecting (24%). Injectors reported having used cocaine more frequently, in higher doses and for longer periods of time. Despite their frequent and extensive use of cocaine, the overall level of dependence was low for the great majority of the sample. Two-thirds (66%) of the full sample (and two-thirds (65%) of the crack smokers) reported only minor signs of dependence during the year prior to interview. Route of drug administration was related to severity of dependence. Cocaine taken by injection was associated with the highest levels of dependence; intranasal use was associated with the lowest levels, and crack smoking was intermediate between the two. There had been substantial changes in the initial route by which cocaine was used, with a clear trend away from injection on the first occasion of use. Those who first used cocaine before 1986 were more likely to have used the drug either intranasally or by injection. Cocaine users who first tried the drug after 1987 were increasingly likely to take it by smoking crack. Women and black (predominantly Afro-Caribbean) subjects were more evident in this sample of cocaine users than has previously been reported in many UK studies.

The purpose of this study was twofold: to measure the overall direct costs of depression for 1990 in the UK, and to develop a model to illustrate issues in the evaluation of the relative cost-effectiveness of the pharmacological treatment of depression. We compared a tricyclic antidepressant, imipramine, with paroxetine, a newer antidepressant. For assessing the cost of illness, we used a top-down approach. We calculated direct but not indirect costs. Cost-effectiveness was evaluated by developing a simulation model based on the theory of clinical decision analysis to compare the costs and outcome of each treatment. From this we estimated the expected cost per patient and the cost per successfully treated patient. The total cost to the nation of depressive illness was estimated to be £222 million. The expected costs per patient were found to be similar for paroxetine and imipramine (£430 v. £424). The costs per successfully treated patient were found to be lower for paroxetine (£824) than for imipramine (£1024). The results were stable when a sensitivity analysis was applied to the variables employed in the model. The most sensitive variable was the cost of treatment failure. Our model thus reveals that medication that appears expensive in terms of cost per day may not be so when patient compliance and the total costs of treatment are taken into account.

We tested the hypothesis that second-trimester exposure to influenza is a risk factor for schizophrenia in the child. The dates of birth of Dutch schizophrenic in-patients were examined for any effect of the 1957 A2 influenza epidemic. Individuals who were in their second trimester of foetal life at the peak of the epidemic were at no greater risk of developing schizophrenia than controls. As the present study has a larger sample size than all previous European studies, and is supported by a large study in the USA, it provides strong evidence against the hypothesis that second-trimester exposure to influenza is a risk factor for schizophrenia.

This paper presents an approach to estimating the prevalence of cocaine use, based upon a new ratio estimation technique. This method can be applied to random samples of overlapping populations for which no sampling frames exist. When the ratio estimation method is applied to the two study samples (drawn from populations of people using cocaine and people using heroin) the ratio of cocaine users to heroin users (C/H) was 1.55, with a 95% confidence interval of ±0.48. Such estimates should be applied with caution. However, if used with reference to national estimates of about 75 000 heroin users, application of the present estimate suggests that there may be about 116 000 cocaine users in the UK.

Data were analysed from 62 schizophrenic patients between 18 and 30 years of age, treated at the community mental health centres in Navarra, who had relapsed and then completed a one-year follow-up study. Factors influencing the course of illness during follow-up were: continuing cannabis consumption; previous cannabis intake; non-compliance with treatment; and stress.

It is usually assumed that psychiatric disturbance cannot be caused by SLE alone. We report two cases of ANA-negative SLE presenting with psychiatric features.

In two adults, both schizophrenia and hydrocephalus were associated with aqueduct stenosis. The prevalence is argued to be above chance, and may contribute to the neurodevelopmental hypothesis of the causality of schizophrenia.

We report a case in which clozapine caused a marked and disabling exacerbation of obsessive–compulsive rituals in a patient with schizophrenia.