There are many practical psychiatric, social, and ethical problems which accompany heart transplantation. These include pre- and postoperative anxiety and depressive conditions, postoperative delirium, and social and family dysfunctional syndromes. This paper reviews the literature critically in the following five areas: pre-transplant evaluation, coping with surgery, postoperative sequelae, rehabilitation, and management. Although most recipients have a good outcome from the physical and psychiatric points of view, a substantial minority experience family conflicts and sexual dysfunction after surgery. An average of 45% of patients from all studies returned to full-time employment. The distinctive role and contribution of the psychiatrist on the transplant team is discussed and important areas for future research are outlined.

A large number of rating scales have been devised to assess the clinical construct of ‘depression’. These scales have been universally used in research with little consideration of their content, or how they relate to accepted definitions of depressive disorder. The scales are often arbitrarily selected and used for the study on the assumption that all measure the same construct. The item analysis of a number of the most widely used depression scales reveals a variation in the areas of psychopathology they cover; some scales place greater emphasis upon the assessment of anxiety than upon depressed mood. Since disturbance in neurobiological systems is manifest by specific aspects of affective and behavioural malfunction, and since psychodynamic factors lead to particular cognitive sets, the advancement of research will depend upon the construction and validation of more refined measures than are provided by the present approach.

The history of psychiatric research on genotypes, phenotypes, and the brain reveals much about the role of these concepts in our past and current understanding of schizophrenia and other psychiatric illnesses. Although interest in each topic is old by the standards of our young science, all have waxed and waned in their influence during our brief history. By ‘genotype’ I mean the hereditary constitution consisting of the genetic code, and by ‘phenotype’ I mean the physical expression of those genes throughout the life cycle of the individual. The relevance of the genotype to our field was recognised during the time of Charles Darwin, and reflected in the views of Henry Maudsley. Early optimism about the role that genetics would play in our understanding of mental disorder was tempered by the failure to find patterns of inheritance that corresponded to those described by Mendel. Enthusiasm about the study of genetic influences on human attributes was further attenuated when pseudo-genetics was embraced as a rationale for the horror of genocide. There has been a long and honourable history of genetic research in psychiatry, sustained by individuals such as Dr Eliot Slater (the 35th Maudsley lecturer and then Director of the Medical Research Council Psychiatric Genetics Research Unit at the Maudsley Hospital), but a renewal of the early excitement about genetic research has been engendered largely by recent developments in molecular biology.

Current overemphasis on nosological diagnosis has led to a neglect of the process of symptom recognition. There is evidence, however, that the perception of the symptom alone does not guarantee symptom ascertainment since a decision-making component is also involved. To achieve the latter, additional information must be provided by the contextual cues implicit in the ongoing diagnostic hypothesis. Current diagnostic systems, however, still assume a two-stage model according to which symptom and disease recognition are independent cognitive events. This paper suggests that this model is inadequate and that descriptive psychopathology is not transparent. It then describes a neural network simulation to make various aspects of the problem explicit. This takes into account the multidimensional and probabilistic aspects of symptom recognition and is, from this point of view, superior to traditional algorithmic models. It also has the capacity to represent the different cognitive styles involved in symptom recognition.

Patients with chronic, refractory irritable bowel syndrome (n =102) were entered into a randomised controlled trial of psychotherapy versus supportive listening. Independent physical and psychological assessments were carried out at the beginning and end of the 12-week trial. For women, psychotherapy was found to be superior to supportive listening, in terms of an improvement in both physical and psychological symptoms. There was a similar trend for men, but this did not reach significance. Following completion of the trial, patients in the control group were offered psychotherapy; 33 accepted and following treatment experienced a marked improvement in their symptoms; ten declined. At follow-up one year later, those patients who had received psychotherapy remained well, patients who had dropped out of the trial were unwell with severe symptoms, and most of the controls who declined psychotherapy had relapsed. This study shows that psychotherapy is feasible and effective in the majority of irritable bowel syndrome patients with chronic symptoms unresponsive to medical treatment.

Among a large workplace population interviewed over a year, current symptoms were assessed using the Hopkins Symptom Checklist (HSCL). Variation in symptoms by date of assessment was observed among the 314 women but not the 1556 men. Among women, symptoms were greatest during late autumn and winter, and significant inverse correlations were found between available daylight at the time of assessment and standard symptom dimensions of anxiety and somatisation, as well as an expanded mood scale more inclusive of depressive symptoms within the check-list. The amplitude of the seasonal effect was such that the prevalence of female ‘cases', as defined by HSCL criteria, was twice as high during winter than during the rest of the year. The data are consistent with a role for light-dark exposure in eliciting or synchronising annual mood rhythms. The sex-by-season interactions may contribute to the sex differences in overall prevalence of depression.

This study was designed to test the hypothesis that patients with SAD have significantly different physiological responses to light than healthy age- and sex-matched controls. We studied retinal contrast sensitivity, visual evoked EEG responses, and melatonin suppression by, and cerebral blood flow response to, full-spectrum artificial daylight. There was no significant difference between 10 patients and 11 controls in retinal contrast sensitivity, or amplitude or latency of N2, P2, P100 or P300 on EEG. We compared melatonin suppression in 12 SAD patients and 12 controls. During exposure to 500 lux and 1500 lux artificial daylight both the SAD patients and controls had a significant melatonin percentage suppression; however, the percentage suppression did not differ significantly between the SAD patients and the controls. In addition, we carried out a small pilot study into the effect of light on cerebral blood flow in four SAD patients and four controls. Before exposure to 1500 lux artificial daylight there was no significant difference between patients and controls in global, regional or cerebral hemispheric blood flow. After light exposure the SAD patients and controls had a significantly different percentage change in cerebral blood flow. We suggest that patients with SAD do not have significantly physiological responses to light than controls, except perhaps in cerebral blood flow. Furthermore, mechanisms other than supersensitivity of melatonin suppression must explain both the pathophysiology of the disorder and its response to treatment with light.

We examined 24-hour melatonin rhythms from 20 patients with seasonal affective disorder (SAD) and 20 healthy volunteers. Patients and controls were individually matched for age, sex, and month of study. Plasma samples were taken at hourly intervals, and were assayed for melatonin by radio-immunoassay. The 24-hourly melatonin estimations for each individual were fitted to a cosine curve, and the significance of the curve fits was calculated. Two analyses were performed. In analysis 1 the following were calculated: (a) cosine fit, (b) significance of fits, (c) mean amplitude and acrophase (peak) and (d) mean melatonin levels. The curve fits were highly significant for all but three subjects (two patients, one control), but there were no significant differences in any measure between the two groups. In analysis 2 the comparisons were repeated and restricted to the 18 patients and 19 controls in whom there was a statistically significant melatonin rhythm. Again there were no significant differences between groups. These results suggest that the circadian rhythm of melatonin is not abnormal in SAD, and that the therapeutic effect of light in SAD is not mediated by phase shifts in melatonin secretion.

Eleven patients with seasonal affective disorder (SAD) and ten controls matched for age, IQ, and education were tested on a number of computerised tests designed to assess attention, memory, and learning. When depressed, patients showed no deficit in attention but were impaired on spatial memory and learning. They were also significantly slower to respond than controls, with a pattern that suggested slowed information processing centrally, rather than simple sensory or motor slowing. On recovery from depression, improvement was seen in most tests, although impairment remained in latency to respond on a test of spatial memory. This continuing impairment correlated with residual depressive symptoms but not with ventricular brain ratio (VBR).

The use of items from the Schedule for Affective Disorders and Schizophrenia and from the Present State Examination scales for assessing positive and negative symptoms in schizophrenia was examined using factor analysis. The factorial structure of the items which putatively assess positive and negative symptoms was examined. A three-factor solution was obtained with factors identified as: a negative symptom factor (factor 1); a positive symptom factor (factor 2); a ‘disorganisation’ factor (factor 3), consisting primarily of items related to disordered thinking. A solution which was highly similar in important loadings was obtained with an independent sample of patients. High correlations of the rotated factors with the external criteria supported the interpretations of the factors. The results indicate that symptoms generally classified as negative or positive are factorially independent. Furthermore, a disorganisation factor, consisting of items previously included in positive and negative symptoms factors, is necessary for a full representation of the factor structure.

The presence or absence of 22 schizophrenic symptoms was recorded with the age at onset of illness in 470 patients with non-affective, non-organic psychoses. Positive and negative formal thought disorder, affective symptoms, inappropriate affect, delusions of grandiosity or passivity, primary delusions other than delusional perception, and thought insertion and withdrawal were all more common in early-onset cases (age at onset 44 years or less; n = 336). Persecutory delusions with and without hallucinations, organised delusions, and third-person, running commentary and accusatory or abusive auditory hallucinations were all more common in late-onset cases (age at onset 45 years or more; n = 134). There was no difference between cases of early and late onset in the prevalence of delusions of reference, bizarre delusions, delusional perception, or lack of insight. We conclude that although there are clinical similarities between cases of schizophrenia with early and late onset, there are sufficient differences between them to suggest that they are not phenotypically homogeneous.

Neuropsychological and psychiatric evaluations were made of 39 subjects with possible Alzheimer's disease and a history of excessive alcohol consumption (AD + ETOH), who had been abstinent or had drunk minimally for at least three months before evaluation, and 225 patients with probable Alzheimer's disease (PAD) of comparable age, years of education, and baseline global impairment. At baseline, there were no significant differences between the groups in terms of age of onset of dementia, neuropsychological test scores, or current behavioural or psychiatric symptoms. One year later, no differences in rates of decline between 20 abstinent AD + ETOH patients and 88 PAD subjects could be shown. Thus, past heavy alcohol consumption does not appear to modify the presentation of dementia of the Alzheimer's type, nor does it modify progression over a one-year interval.

Clinico-pathological correlations were examined in 54 patients with neuropathologically verified Alzheimer's disease (AD) who were part of a prospective study. Behavioural disturbance was documented using an expanded version of the Stockton Geriatric Rating Scale (SGRS). The subscores for physical disability (P), apathy (A) and communication failure (C) (summation score PAC) were closely correlated and were high in most patients during the late stages of illness. High PAC scores correlated with an earlier onset and longer duration of illness, lower brain weight, more severe tangle pathology in the parahippocampal gyrus and the frontal and parietal neocortex, and lower neuron counts in the hippocampus and basal nucleus of Meynert. Features of the Klüver-Bucy syndrome (range behaviour and hypermetamorphosis) were significantly associated with lower counts of large neurons in the parahippocampal gyrus and parietal neocortex, but not with more severe plaque or tangle formation or with neuronal loss in the subcortical nuclei. No correction was made for multiple comparisons. These findings may signify decreased cortical inhibition in patients with relatively well preserved subcortical structures who show features suggestive of the Klüver-Bucy syndrome. High PAC scores on the SGRS could reflect more advanced and widespread cerebral pathology in the end stages of AD.

A community study was conducted to determine the prevalence of depressive symptoms and syndromes in 11–16-year-old girls. Girls from three secondary schools (1072 girls in total) were administered questionnaires and 375 were selected for direct interview. The estimated prevalence for current major depressive disorder (within the past month) for the population was 3.6%, and for the past year was 6.0%. Scores on the self-report questionnaire of mood disturbance increased with age, as did the prevalence of depressive disorder. A large proportion of interviewed girls reported depressive symptoms which did not meet the DSM-III-R criteria for major depressive disorder. The estimated prevalence of this ‘partial syndrome’ group was 8.9% for a current episode and 20.7% for the past year.

The clinical characteristics of two subsamples of 11–16-year-old girls were determined from direct interview: those who met DSM-III-R criteria for an episode of major depressive disorder within the past month (n = 28); and those who did not currently meet these criteria but had done so at some time in the previous 12 months (n = 13). The symptom profiles of these cases were compared with a subsample of girls who reported depressive symptoms but did not meet DSM-III-R criteria and were designated as having a ‘partial syndrome’ (n = 93), and a sample of non-depressed controls (n = 129). Phobias and worry about peer acceptance were common in controls suggesting that these symptoms constitute normal adolescent concerns. The symptom profile of depressed cases altered across three age bands (11–12, 13–14, and 15–16 years), suggesting developmental influences on clinical presentation. Comorbidity for anxiety, behavioural, and obsessional disorders was found in 40% of the depressed cases. None of the cases of major depressive disorder was known to the clinical services.

A New Zealand cohort of 58 patients with bipolar affective disorder was studied prospectively with three-monthly interviews in order to determine the relationship between life events and their relapses. Careful attention was paid to dating life events and the earliest signs of relapse and to assessing the independence of life events from the illness. No statistically significant association was found between life events and the likelihood of relapses, either mania or depression, for the 71% of patients who experienced at least one relapse during the two-year study. This finding is at variance with a companion study, with identical methodology, which found a small increase of life events before relapse. These data add further weight to the previous reports that life events are significant precipitants of bipolar illness only for earlier episodes in the course of this chronic disorder.

The fatal toxicity indices of benzodiazepines during the 1980s were calculated from national prescribing data and mortality statistics. The overall rate was 5.9 deaths per million prescriptions for benzodiazepines taken alone or with alcohol only, anxiolytics being less toxic than hypnotics. Diazepam appeared more toxic than average among anxiolytics (P<0.05), and flurazepam and temazepam more toxic than average among hypnotics (both P<0.001). It was shown that the finding for diazepam was probably explained by concurrent use of alcohol, which implies that other anxiolytics may be safer in cases where there is alcohol misuse; but the greater toxicity of flurazepam and temazepam remained unexplained. Benzodiazepines are indeed much less toxic than the barbiturates they superseded, but they are not innocuous and temazepam in particular requires further evaluation.

Current theories suggest that there is a relatively frequent association of self-mutilative behaviour with eating disorders, particularly with the modern binge-purge syndrome, bulimia nervosa. In order to consider this association on a historical dimension. 25 bulimic cases, reported from the late 17th to the late 19th century, were investigated. These were found to include four examples of self-mutilative behaviour, in three males and one female: these cases are described and discussed. The historical evidence lends some support for the suggested connection between eating pathology and self-mutilation.

Disorders of the thyroid gland are associated with disorders of mood (Thomas et al, 1970; Van Uitert & Russakoff, 1979; Folks, 1984; Young, 1984; Jadresic, 1990). Both hypothyroid and hyperthyroid states can be associated with depression, which is sometimes accompanied by psychotic features such as delusions and hallucinations (Wilson & Jefferson, 1986). Similarly, primary affective disorders can be accompanied by changes in thyroid function, with low thyroid-stimulating hormone (TSH) levels and elevated thyroxine (T4) (Kirkegaard & Faber, 1980), and in major depressive illness there is often a blunted TSH response to thyrotrophin releasing hormone (TRH) (Prange et al, 1972; Loosen, 1987).