Relapse rates among individuals with psychotic disorders are high. In addition to the financial burden placed on clinical services, relapse is associated with worse long-term prognosis and poorer quality of life. Robust evidence indicates that stressful life events commonly precede the onset of the first psychotic episode; however, the extent to which they are associated with relapse remains unclear. The aim of this systematic review is to summarize available research investigating the association between recent stressful life events and psychotic relapse or relapse of bipolar disorder if the diagnosis included psychotic symptoms. PsycINFO, Medline and EMBASE were searched for cross-sectional, retrospective and prospective studies published between 01/01/1970 and 08/01/2020 that investigated the association between adult stressful life events and relapse of psychosis. Study quality was assessed using the Effective Public Health Practice Project guidelines. Twenty-three studies met eligibility criteria (prospective studies: 14; retrospective studies: 6; cross-sectional: 3) providing data on 2046 participants in total (sample size range: 14–240 participants). Relapse was defined as a return of psychotic symptoms (n = 20), a return of symptoms requiring hospitalization (n = 2) and a return of symptoms or hospitalization (n = 1). Adult stressful life events were defined as life events occurring after the onset of psychosis. Stressful life events included but were not limited to adult trauma, bereavement, financial problems and conflict. Eighteen studies found a significant positive association between adult stressful life events and psychotic relapse and five studies found a non-significant association. We conclude that adult stressful life events, occurring after psychosis onset, appear to be associated with psychotic relapse.

In the context of an ongoing WHO research programme in depression, a total of 573 patients consulting psychiatrists in Canada, Iran, Japan and Switzerland were assessed with the WHO/SADD schedule which proved to be a simple and reliable instrument for standardized recording of clinical data. The results indicated that the ‘average’ depressive patients seeking care in culturally different settings have many clinical features in common. A screening instrument, developed in the same study, has been shown to be effective in selecting depressive patients among in- and out-patient populations.

Rates and methods of suicide during 1961–70 of migrants in Australia were compared with native born Australians. Large differences in both rates and methods of suicide were found in individual migrant groups. The rates were more akin to those in the country of origin than of the Australian-born, no matter how long the migrants had lived in Australia. By contrast, methods of suicide used by migrants approached more closely those of the Australian-born the longer they had lived in Australia. The change in methods used was greatest in those migrant groups coming from countries with a language and culture more akin to those in Australia. A discussion follows of various possible sociological and cultural factors, both within the countries of origin and within Australia, which could have contributed to these results.

Background. The median age at first childbirth has increased dramatically in many high-income countries during the past decades. The psychiatric consequences of this demographic change are insufficiently described on a population level. This study aimed to investigate whether parental age at childbearing is related to psychiatric morbidity among Swedish youths.

Method. This was a cohort study based on Swedish national registers. A national cohort of 292129 children born to primiparas women during 1973–1979 was followed prospectively from 1987 to 2002 in registers. Multivariate Cox analyses of proportional hazards were used to estimate the relative risk of hospital admission for schizophrenia, alcohol and illicit drug abuse, suicide attempts and deaths.

Results. Youths born of teenage mothers had a high risk for suicide death [relative risk (RR) 1·9, 95% confidence interval (CI) 1·3–2·7] and hospital admissions because of suicide attempt (RR 2·0, 95% CI 1·7–2·3) and substance abuse (alcohol: RR 1·6, 95% CI 1·4–1·8; illicit drug: RR 2·2, 95% CI 1·9–2·5) after adjustments for major sociodemographic confounders, compared with children of mothers aged 25–29 years. Offspring of older parents (>34 years) had the highest risk for schizophrenia (RR 1·8, 95% CI 1·0–3·0).

Conclusions. Parental age is related to psychiatric morbidity.

The relationship was examined between symptoms rated in a sample of out-patient depressives, and measures of life stress derived from a separate interview. There was an association between symptoms reflecting the endogenous–neurotic distinction and life stress. However, the association was relatively weak, and was mainly with total social problems at the time of presentation, rather than with life events at onset. These findings are consistent with other studies which indicate that the absence of prior life events and the presence of the endogenous symptom pattern are only weakly related.

A retrospective survey was undertaken of the clinical EEG in a series of consecutive admissions to Broadmoor Special Hospital (N = 265). Following reporting of the records by visual inspection, the EEGs were classified according to 4 descriptive categories: predominantly monorhythmic; low voltage fast, ‘choppy’ dysrhythmic with excess theta; and dysrhythmic with paroxysmal features. The last 3 categories constituted EEG patterns with atypical or anomalous features. The EEGs of patients with high scores on Welsh's MMPI Anxiety scale (‘withdrawers’) were compared with those of patients with low scores (‘approachers’). Lateralization of paroxysmal EEG features was studied with reference to MMPI personality measures (Blackburn's Impulsivity and Sociability and Welsh's Anxiety), legal diagnosis, type of offence, and relationship to victim. The EEGs were studied in a further sample of 29 admissions who had been assessed, using Hare's Research Scale for the Assessment of Psychopathy (Hare, 1980). While the overall incidence of atypical EEG features reported in the present study (around 60% of cases) was comparable with that reported previously for offender populations, they occurred significantly more frequently in ‘withdrawers’ than in ‘approachers’. This suggests that the high frequency of atypical EEG features in abnormal offenders may be due to the preponderance of ‘withdrawers’ in this population. Patients who had committed violent offences against strangers, as opposed to people known to them, tended to have bilateral paroxysmal features in their EEG. High scores on Hare's Psychopathy scale were significantly associated with prominent Posterior Temporal Slow Activity. The study offers some prospect that the combined use of EEG and personality assessments may be of potential value in the assessment of dangerousness.

Background. Sustained attention has been found to be impaired in individuals suffering from schizophrenia and their close relatives. This has led to the hypothesis that impaired sustained attention is an indicator of vulnerability to schizophrenia.

Methods. The Edinburgh High Risk Study used the Continuous Performance Test-Identical Pairs version (CPT-IP) to assess sustained attention in 127 high risk participants, 30 controls and 15 first-episode schizophrenic patients. A second assessment was completed by 59 high risk and 18 control participants 18 months to 2 years after the first.

Results. No differences in attentional capacity were found between the high risk and control groups and there was no association between genetic liability to schizophrenia and poor performance on the CPT-IP. Additionally, no association between occurrence of psychotic symptoms in the high risk group and impaired attentional capacity was found.

Conclusions. The results suggest that deficits in sustained attention are not indicative of a genetic vulnerability to schizophrenia, and are not associated with the occurrence of psychotic symptoms.

Background. Diverse forms of thought disorder, as measured by the Thought Disorder Index (TDI), are found in many conditions other than schizophrenia. Certain thought disorder categories are primarily manifest during psychotic schizophrenic episodes. The present study examined whether forms of thought disorder qualify as trait indicators of vulnerability to schizophrenia in persons who are not clinically ill, and whether these features could be linked to genetic or environmental risk or to genotype–environment interactions. The Finnish Adoptive Study of Schizophrenia provided an opportunity to disentangle these issues.

Methods. Rorschach records of Finnish adoptees at genetic high risk but without schizophrenia-related clinical diagnoses (N = 56) and control adoptees at low genetic risk (N = 95) were blindly and reliably scored for the Thought Disorder Index (TDI). Communication deviance (CD), a measure of the rearing environment, was independently obtained from the adoptive parents.

Results. The differences in total TDI between high-risk and control adoptees were not statistically significant. However, TDI subscales for Fluid Thinking and Idiosyncratic Verbalization were more frequent in high-risk adoptees. When Rorschach CD of the adoptive rearing parents was introduced as a continuous predictor variable, the odds ratio for the Idiosyncratic Verbalization component of the TDI of the high-risk adoptees was significantly higher than for the control adoptees.

Conclusions. Specific categories of subsyndromal thought disorder appear to qualify as vulnerability indicators for schizophrenia. Genetic risk and rearing-parent communication patterns significantly interact as a joint effect that differentiates adopted-away offspring of schizophrenic mothers from control adopted-away offspring.

L-tryptophan 50 mg/kg was administered orally to patients suffering from either unipolar or bipolar affective illness, and the concentration of 5-hydroxyindol-acetic acid estimated in their cerebrospinal fluid eight hours later. There was no significant difference between the patient groups or between these and patients with neurological disease. These findings suggest a reduced neuronal activity in the 5-hydroxytryptaminergic system in some depressed patients rather than an absolute deficiency of tryptophan-5-hydroxylase. The synthesis of 5-HIAA in response to tryptophan varied with age.

An 18-item inventory designed by Goldberg et al. (1987) to detect symptoms of anxiety and depression was administered to an elderly general population sample. Latent trait analysis was used to assess the dimensionality of the inventory and the location and discriminatory ability of the symptoms. The items showed different patterns of discrimination in this group compared to the sample of general practice attenders on which the inventory was developed. Overall, the items did define two correlated dimensions of anxiety and depression. In addition, a third dimension of sleep disturbance was detected. Both individual scales and the total symptom scores were sensitive and relatively specific detectors of depressive disorders assessed according to ICD-10 and DSM-III-R criteria. The retention of sleep items on their original scales did not affect the sensitivity of the scales to detect depressive disorders. A two-step administration procedure suggested for use in the administration of the scales was investigated but found to be sensitive to differences between the current sample and the sample on which the inventory was developed. This symptom inventory can be recommended for use in epidemiological investigations as a brief, valid and acceptable method of detecting elevated levels of anxiety and depression in elderly persons.

This issue features groups of papers reporting controlled trials, depression assessment and biological aspects, and disorders in the elderly. The lead editorial reviews recent studies of the effects on cognition of tryptophan depletion, an important probe of serotonin function.

Background. Many studies suggest that pregnancy and birth complications (PBCs) are environmental risk factors for child psychopathology. However, it is not known whether the effects of PBCs occur independently of genetic predisposition. The current study examined the possibility of gene–environment interaction in a twin design.

Method. The East Flanders Prospective Twin Survey prospectively records the births of all twin pairs born in East Flanders, Belgium. The current study included 760 twin pairs aged 6–17 years. Multilevel regression analysis was used to assess the effects of several PBCs collected around the time of birth. Using structural equation modelling, ACE models assuming additive genetic (A), shared environmental (C) and unique environmental (E) influences, were compared in order to examine whether the contribution of genetic factors to parent-rated child problem behaviour varied as a function of exposure to dichotomously and continuously defined PBCs.

Results. A main independent effect of lower birth weight, corrected for gestational age (small for gestational age – SGA), on child problem behaviour was found. In addition, there was an interaction between genetic influence and SGA, in that being smaller for gestational age resulted in less influence of additive genetic factors on individual differences in problem behaviour.

Conclusions. Results are suggestive of negative gene–birth weight interaction. Children who are SGA are less sensitive to the genetic effects, and those with high genetic vulnerability are less sensitive to the effects of being SGA in bringing about post-natal mental health effects.

‘Whether or not it is worthwhile to distinguish between “neurasthenia” and “dysthymic disorders” must depend either on the demonstration that such syndromes have different social covariates, or pursue a different course, or have particular responses to treatment. Until such studies are forthcoming, the distinction seems especially insubstantial.’ (Goldberg & Bridges, 1991)

Epidemiological studies now indicate that fatigue is one of the most common symptoms of ill-health in the community, primary care and other medical settings, and that syndromal diagnoses based on fatigue (including chronic fatigue and neurasthenia) are prevalent and major sources of health care utilization. Such syndromes are characterized by a combination of persistent and disabling fatigue and neuropsychological and neuromuscular symptoms (Lloyd et al. 1990; Angst & Koch, 1991; Sharpe et al. 1991; Fukuda et al. 1994). Essentially, the differences between these syndromes reflect variations in duration criteria rather than symptom constructs. Specifically, the Centers for Disease Control (CDC) defines ‘prolonged fatigue’ as a syndrome of at least 1 month's duration, and chronic fatigue (including idiopathic and chronic fatigue syndrome – CFS) as a fatigue syndrome of at least 6 months duration (Fukuda et al. 1994). The ICD-10 classification system (World Health Organization, 1992) now includes a formal diagnosis of neurasthenia (F48.0) based on mental and physical fatigue of at least 3 months duration. Despite the current international and epidemiological interest in these disorders, DSM-IV has simply included them within the ‘Undifferentiated Somatoform Disorders – 300.81’ category (American Psychiatric Association, 1994).