Sixty years ago the distinguished epidemiologist Joseph Goldberger, following his outstanding achievements in clarifying the causes of pellagra, was offered a large research grant to investigate schizophrenia. He responded to the proposal by studying the available evidence concerning the schizophrenic syndrome and then politely declined to take up the challenge. ‘In five or more years’, he wrote, ‘I could probably find out nothing. Much work will be needed on the physiology of the central nervous system and on many collateral problems before dementia praecox can be understood’ (Parsons, 1943).

Schizophrenic subjects (N = 30) performed less well than controls (N = 30) on neuropsychological tests sensitive to frontal and temporal lobe impairment and showed prolonged latency of the P300 event-related potential. Relatives of schizophrenic probands were also tested. Relatives with an abnormal P300 had a similar range of neuropsychological deficits as were found in the schizophrenic group and relatives with a normal P300 response performed as well as the normal control group. The results suggest that neurophysiological and neuropsychological testing of relatives may help to clarify the mode of inheritance of schizophrenia in some families.

Serum concentrations of the third and fourth components of the complement system and total complement haemolytic activity were measured in 167 psychiatric patients. Total complement haemolytic activity was decreased in chronic schizophrenic patients as compared to healthy controls and bipolar patients. The relatively diminished total haemolytic activity was not attributable to drug treatment. It is not clear if the reduced total haemolytic activity is an epiphenomenon or related to the involvement of an autoimmune process in the pathophysiology of schizophrenia.

Many structural brain abnormalities have been described in schizophrenia, consistent with a neurodevelopmental model for this disease. We report here a study of the cavum septum pellucidum (CSP) in schizophrenia compared to control groups, as well as the clinical correlates of this congenital anomaly in schizophrenia. We conducted a magnetic resonance imaging (MRI) study to compare rates of CSP in schizophrenia (N = 67) v. psychiatric controls (bipolar and schizoaffective, N = 60) and healthy controls (N = 37). Of the controls 18·9 %, and of all psychotic subjects 18·1 % had a CSP of any size and there was no difference in the frequency of large CSP among the groups. Males had higher rates of CSP than females (25% v. 9·7%, P = 0·01) in all groups. Schizophrenics had higher CSP rates than affective patients (25%, v. 10%, P = 0·02). No clinical difference was found between schizophrenics with or without CSP.

Elevation of serum creatine kinase (CK) concentrations occurs almost invariably in neuroleptic malignant syndrome (NMS). However, the role of CK levels in the diagnosis of the syndrome remains controversial. This study measured CK levels in patients who became pyrexial while on psychotropic medication and thereby mimicked some of the features of NMS. In all of these cases a diagnosis of infectious illness was made and patients responded to appropriate antibiotic therapy without alteration in psychotropic medication. Two other groups were studied for comparison – patients on psychotropics who were apyrexial and patients who became pyrexial but were not on psychotropics. Significant, unexpected elevations of CK were documented in 70% of those patients who became pyrexial while on psychotropics – in three cases elevation of concentrations to more than 1000 IU/1 (ten times reference value) were found. Thirty per cent of patients who became pyrexial but were not on psychotropics also developed elevation of CK but this was of a much smaller magnitude (lt; 200 IU/1 in five out of six cases). The results of the study suggest that elevation of CK is a non-specific finding, particularly in patients who become pyrexial on psychotropics. Use of CK as a diagnostic criterion may lead to overdiagnosis of NMS.

The goal of this study was to examine the familial resemblance of schizotypic traits, and to explore whether different schizotypic traits are familially related to one another. Several of the Chapmans' psychosis proneness scales were administered to a group of college students and their families. Evidence of at least some familial resemblance was found for both physical anhedonia and perceptual aberration, though it was stronger for anhedonia. Anhedonia and perceptual aberration appeared to be familially influenced independently of one another. Finally, the results indicated that offspring resembled their mothers more than they resembled their fathers on both anhedonia and perceptual aberration.

Parental representation was assessed with the Parental Bonding Instrument (PBI) in 12 monozygotic (MZ) and 19 dizygotic (DZ) same-sexed twin pairs discordant for DSM-III-R schizophrenia. The schizophrenic twins reported less care and more overprotection from both parents than the non-schizophrenic co-twins. Multiple regression analysis disclosed that the results were independent of sex and age. Furthermore, the analysis demonstrated that whether the twins were monozygotic or dizygotic had no impact on the results. A stepwise discriminant analysis showed that difference in perceived paternal protection was the most important variable distinguishing between schizophrenic probands and their non-schizophrenic co-twins.

Eighteen patients suffering from Alcoholic Korsakoff's Syndrome participated in a placebo-controlled double-blind cross-over trial of clonidine 0·3 mg b.d. for two weeks versus matched placebo for two weeks. A detailed neuropsychological assessment was carried out at the end of each treatment phase and staff ratings of behaviour were also obtained. Clonidine treatment resulted in no significant improvement over placebo on any of the cognitive measures employed. The results contradict previous smaller studies which had suggested that chronic treatment with clonidine had a memory-enhancing effect in Korsakoff's syndrome.

Fifty-nine patients suffering from a major depressive episode, for whom electroconvulsive therapy (ECT) was clinically indicated, were randomly assigned to one of three electrode placement groups for treatment with brief pulse, threshold-level ECT: bitemporal (BT), right unilateral (RU) or bifrontal (BF). Comparison of these groups in terms of number of treatments, duration of treatment, or incidence of treatment failure, showed that the bilateral placements were superior to the unilateral; comparison of Hamilton, Montgomery–Åsberg, and visual analogue scale scores showed that the bifrontal placement was superior to both bitemporal and unilateral treatment. Bitemporal treatment showed therapeutic results intermediate between BF and RU. Because BF ECT causes fewer cognitive side effects than either RU or BT, and is independently more effective, it should be considered as the first choice of electrode position in ECT.

In a population based sample of 2163 personally interviewed female twins, substantial comorbidity was observed between DSM-III-R defined major depression (MD) and 4 subtypes of phobia: agoraphobia, social phobia, animal phobia and situational phobia. However, the level of comorbidity of MD with agoraphobia was much greater than that found with the other phobic subtypes. We conducted bivariate twin analyses to decompose the genetic and environmental sources of comorbidity between MD and the phobias. Our results suggest that a modest proportion of the genetic vulnerability to MD also influences the risk for all phobic subtypes, with the possible exception of situational phobias. Furthermore, the magnitude of comorbidity resulting from this shared genetic vulnerability is similar across the phobic subtypes. By contrast, the non-familial environmental experiences which predispose to depression substantially increase the vulnerability to agoraphobia, have a modest impact on the risk for social and situational phobias and no effect on the risk for animal phobias. The increased comorbidity between MD and agoraphobia results, nearly entirely, from individual-specific environmental risk factors for MD which also increase the risk for agoraphobia but not for other phobias.

This article examines the effects of depression in the sphere of social functioning. On the basis of previous research, it is hypothesized that a major depressive episode has both concurrent and lingering effects and that these effects are a function of the clinical features associated with the episode. This hypothesis is examined using a large community sample and a non-linear model containing both concurrent and lingering effect parameters. The results corroborate the hypothesized effects. Limitations of the current study are discussed and suggestions are offered regarding appropriate research designs. It is suggested that the most general limitation is theoretical. The existence of lingering effects is a phenomenon which presents a theoretical challenge that may prove strategic in understanding the nature and course of depression.

This paper explores the hypothesis that depression in chronic schizophrenia is in part a psychological response to an apparently uncontrollable life-event, namely the illness and its long-term disabilities. It is suggested that depression is linked to patients' perception of controllability of their illness and absorption of cultural stereotypes of mental illness. Clinically and operationally diagnosed schizophrenic and manic-depressive patients receiving long-term maintenance treatment were studied. The cross-sectional prevalence of depression in schizophrenics was 29% and 11% for patients with bipolar affective illness. The hypothesis was supported. Multivariate analyses revealed that patients' perception of controllability of their illness powerfully discriminated depressed from non-depressed psychotic patients. Although those patients who accepted their diagnosis reported a lower perceived control over illness and an external locus of control, label acceptance was not associated with lowered depression, self-esteem or unemployment. The cross-sectional nature of the study makes the direction of causality and the role of intrinsic illness variables difficult to ascertain; however, the results set the scene for prospective and intervention studies and the various possibilities are discussed.

Previous studies based on probands from clinical samples suggest that panic disorder aggregates strongly in families and may be due to a highly penetrant single major locus. In this study we examine panic disorder as assessed at blind, structured psychiatric interview in 2163 women from a population-based twin registry. DSM-III-R diagnoses were assigned at a narrow and at a broad level both by clinician review and by computer algorithm. The familial aggregation of panic disorder in this sample was only modest. The relatively small number of affected individuals prevented a definitive resolution of competing genetic and non-genetic models of familial transmission. Although there was some inconsistency across diagnostic approaches, most results suggested that the familial aggregation of panic disorder was due largely to genetic factors. Using a multifactorial-threshold model, the best estimates of the heritability of liability ranged from 30 to 40%. From a familial perspective, panic disorder with phobic avoidance appears to represent a more severe form of the syndrome than panic disorder without avoidance. Our results, which suggest that in the general population panic disorder is only a moderately heritable condition, are at variance with results from several previous investigations based on clinically ascertained samples.

Termination of pregnancy for foetal abnormality has become frequent with the increasing sophistication of techniques of antenatal diagnosis. The aim of this study was to obtain quantitative and qualitative information about psychiatric morbidity in women after termination of pregnancy for foetal abnormality.

Two samples of women were compared. The first consisted of 71 women who had had a termination of pregnancy for foetal abnormality (FA group). The second consisted of 26 women who had experienced so-called missed abortion (MA group). Both groups had lost a pregnancy in the mid-trimester of pregnancy, but the MA group had no element of choice.

Standardized psychiatric and social measures were used to assess both groups on three occasions after the termination. In both groups, 4 weeks after the termination psychiatric morbidity was high (four to five times higher than in the general population of women), and social adjustement was impaired. Six months and 12 months after the abortion, levels of psychiatric morbidity were near normal.

Semi-structured interviewing was used to obtain information about the experience of grief after mid-trimester termination. For many women, symptoms of grief persisted throughout the year. These symptoms included typical features of grief as well as grief symptoms specific to pregnancy loss. The findings have implications for the counselling of women after termination for foetal abnormality or after missed abortion.

Behavioural/emotional problems were assessed at least nine years after surgical correction for congenital heart disease (ConHD) in childhood. Parents of 144 10–15-year-old ConHD-children completed the Child Behavior Checklist (CBCL) and 179, 11–17-year-old, ConHD-adolescents completed the Youth Self-Report (YSR). On the CBCL and YSR ConHD-children and adolescents obtained significantly higher problem scores than same-aged peers from normative reference groups. No significant differences were found between problem scores for different cardiac diagnostic groups. A negative correlation was found between CBCL total problem scores and IQ-scores of ConHD-children; for YSR total problem scores no such relationship was found.

The Eating Attitudes Test (EAT) and the Eating Disorder Inventory (EDI) were administered to a female volunteer twin population aged 18 to 45 years. Both members of 147 monozygotic (MZ) and 99 dizygotic (DZ) twin pairs completed the questionnaires. Thirty-five subjects scored over the cut-off point of the EAT-26. Interviews of these high-scoring twins and their co-twins identified three subjects with a past history of anorexia nervosa, and three others with a history of a partial syndrome. A heritability value of 41% was obtained for the overall EAT scores, while factor analysis produced a ‘dieting’ factor with a heritability of 42%. The ‘body dissatisfaction’ and ‘drive for thinness’ subscales of the EDI had heritability values of 52 and 44% respectively. The genetic contribution to the variance in body mass index in the twin sample was estimated at 64%. For all the above phenotypes, an environmental model of transmission with heritability constrained to be zero, could be rejected. Conversely, we were unable to reject a purely additive genetic model with shared environmental variance constrained at zero, suggesting that family environment has little or no effect on the transmission of many of these traits.

Using the 40-item Eating Attitudes Test and other self-report questions, a two-stage screening survey of 1020 (F 646, M 374) Chinese bilingual university students in Hong Kong showed that although female students were ‘underweight’ by Western standard, the majority of them and nearly all female students above a body mass index of 20·5 kg/m2 were cognitively inclined to diet and weigh less, albeit without being driven to actual weight control behaviour. In contrast, most male students and a minority of constitutionally thin female students clearly wished to gain weight. While a number of items were culturally inappropriate, factor analysis supported the overall cross-cultural conceptual validity of the EAT. The principal factor, reflecting dieting concerns, correlated positively with the current body mass index. Among the high scorers, only three female students with partial syndrome bulimia nervosa were identified, yielding a low prevalence of 0·46% for the spectrum of eating disorders. It is argued that the desire for slimness is widespread but its intensity and pathogenic potentiality vary across cultures. In the relative absence of obesity, it may not lead to more eating disorder.