A twofold increase in the prevalence of depression among women has been consistently observed. Several possible explanations, including methodological, endocrine, psychosocial, and genetic factors, have been proposed for the increased rates of depression among women. This paper describes the analysis of data from a family-genetic study of depressed probands to examine whether genetic factors can explain the preponderance of depressed females. Our data indicate that the excess of females with major depression cannot be attributed to increased genetic loading for depression in women. Other factors which may explain increased rates of major depression in women are discussed.

Twenty-five patients with anorexia nervosa were compared with 17 normal healthy control subjects in terms of their cerebral computed tomographic (CT) scan appearances. The patients displayed significantly greater ventricular and sulcal enlargement when compared to control subjects. There were no relationships between the CT scan appearance and clinical indices of illness severity or weight loss in the patient group. In 14 patients who had repeat scans after attaining normal body weight, no significant change was observed in the ventricular appearance, but there was a significant lessening in the degree of sulcal widening.

The Focus Group Discussions (FGD) described in this paper are the first step of a study aiming to develop an ‘emic’ case-finding instrument. In keeping with the realities of primary care in Zimbabwe, nine FGD were held with 76 care providers including 30 village community workers, 22 traditional and faith healers (collectively referred to as traditional healers in this paper), 15 relatives of patients and 9 community psychiatric nurses. In addition to the general facets of concepts of mental illness, three ‘etic’ case vignettes were also presented.

A change in behaviour or ability to care for oneself emerged as the central definition of mental illness. Both the head and the heart were regarded as playing an important role in the mediation of emotions. The types of mental illness described were intimately related to beliefs about spiritual causation. Angered ancestral spirits, evil spirits and witchcraft were seen as potent causes of mental illness. Families not only bore the burden of caring for the patient and all financial expenses involved, but were also ostracized and isolated. Both biomedical and traditional healers could help mentally ill persons by resolving different issues relating to the same illness episode. All case vignettes were recognized by the care providers in their communities though many felt that the descriptions did not reflect ‘illnesses’ but social problems and that accordingly, the treatment for these was social, rather than medical.

The data enabled us to develop screening criteria for mental illness to be used by traditional healers and primary care nurses in the next stage of the study in which patients selected by these care providers on the grounds of suspicion of suffering from mental illness will be interviewed to elicit their explanatory models of illness and phenomenology.

In a community-based study of patients with a first-ever stroke, intellectual impairment (as denned by scores on a common screening test for dementia, the Mini-Mental State Examination) was found in 26% at 1 month post-stroke, and in 21% at 6 and 12 month follow-up. Low scores on the screening test were associated with greater age, physical disability before the stroke, larger stroke lesion volumes as measured on CT scan, and non-stroke changes such as atrophy and white matter low attenuation on the CT scan. There was a negative correlation between scores on the Mini-Mental State Examination and symptom levels on two measures of mood disorder. However, there was no evidence of a specific relationship between major depression and low scores on the Mini-Mental State. We examined various aspects of the relationship between mood symptoms and low scores on the Mini-Mental State, but found no evidence to support the suggestion that this relationship represented an example of depressive pseudodementia. We discuss the significance of our findings for clinical psychiatry and neuropsychology.

Background. Olfactory identification ability has been associated with processing in the orbitofrontal cortex (OFC), an area that has been implicated in the pathophysiology of obsessive–compulsive disorder (OCD). Although olfactory sensitivity is normal in patients with OCD, no study has investigated olfactory identification in this disorder.

Methods. A group of 20 subjects with OCD and 23 age- and education-matched controls performed a standardized test of olfactory identification. They also performed computerized tests of spatial memory span, spatial working memory and spatial recognition memory that have been shown previously to be sensitive to cognitive deficits in patients with OCD.

Results. Performance on the olfactory identification task, spatial recognition task and spatial span task was significantly worse in the OCD group than controls.

Conclusions. While impairment in spatial cognition is consistent with previous studies of OCD, its significance for brain-behaviour models of OCD is unclear. However, the finding of abnormal olfactory identification in patients with OCD is consistent with the hypothesis that there is a disruption to processing at the level of the OFC in the disorder.

Background. We have used proton magnetic resonance imaging and spectroscopy to measure hippocampus/amygdala volumes and anterior hippocampal metabolite concentrations (N-acetyl aspartate (NAA), creatine/phosphocreatine and choline) in subjects with temporal lobe epilepsy (TLE), schizophrenia and in normal controls.

Method. Four groups of right-handed patients were selected: 12 with TLE and psychosis (EP), 12 with TLE and no psychosis (ENP), 26 with schizophrenia, and 38 normal controls. Imaging and spectroscopy were performed with a 1.5T Signa GE scanner.

Results. The schizophrenia group showed a significant left-sided reduction in all metabolites. In the epilepsy groups NAA was reduced bilaterally. The NAA reduction in the EP group was greater than in the ENP group, especially on the left, although the result did not reach significance. Total hippocampus/amygdala volumes showed no significant differences in any of the groups when compared with normal controls. When compared with controls significant, specific regional volume reductions were present bilaterally in the EP group and in the left hippocampus/amygdala in schizophrenia. The regional volume reduction found in schizophrenia was also present in EP but not in ENP.

Conclusion. Spectroscopic abnormalities were more pronounced in the epilepsy groups and were bilateral, and abnormalities in schizophrenia were left sided. Specific regional hippocampus/amygdala volume reductions were more marked in the EP group and were bilateral. Left-sided regional volume reduction identified in the dominant hemisphere of schizophrenics was also present in EP patients, but not in ENP, suggesting that this region in the left temporal lobe may be significant in the aetiology of psychosis. This is further supported by the predominantly left-sided NAA reduction in schizophrenia. High resolution morphometric studies may identify specific regions of the brain associated with the development of psychosis.

Background. Numerous nosological decisions are made when moving from the common human symptom of unusual fatigue to the rare chronic fatigue syndrome (CFS). These decisions have infrequently been subjected to rigorous evaluation.

Method. We obtained telephone interview data on fatiguing symptoms from 31406 individuals twins in the Swedish Twin Registry aged 42–64 years; 5330 subjects who endorsed fatigue and possessed no exclusionary condition formed the analytic group. We evaluated the definition and classification of CFS-like illness using graphical methods, regression models, and latent class analysis.

Results. Our results raise fundamental questions about the 1994 Centers for Disease Control criteria as (1) there was no empirical support for the requirement of four of eight cardinal CFS symptoms; (2) these eight symptoms were not equivalent in their capacity to predict fatigue; and (3) no combination of symptoms was markedly more heritable. Critically, latent class analysis identified a syndrome strongly resembling CFS-like illness.

Conclusions. Our data are consistent with the ‘existence’ of CFS-like illness although the dominant nosological approach captures population-level variation poorly. We suggest that studying a more parsimonious case definition – impairing chronic fatigue not due to a known cause – would represent a way forward.

Background. We test the hypothesis that the neuregulin 1 (NRG1) gene at chromosome 8p22-p12, which has been implicated as a susceptibility gene to schizophrenia, is associated with variations in schizotypal personality in non-clinical populations.

Method. A randomly selected sample of 905 adolescents were assessed for their personality features using the Perceptual Aberration Scale (PAS) and the Schizotypal Personality Questionnaire (SPQ) and genotyped for three single nucleotide polymorphisms (SNP8NRG221533, rs3924999, and rs2954041) at the NRG1 gene. Relations between the three genetic variants and continuous schizotypal personality scores were evaluated using ANOVA for single-locus analyses and haplotype trend regression test for multi-locus analyses.

Results. Single locus analysis showed that the A allele of rs3924999, a functional polymorphism in exon 2, had the largest effect size and exhibited a prominent allele–dose trend effect for the PAS score. Haplotype analyses using the haplotype trend regression test indicated that the A allele of rs3924999 was mainly responsible for the association with the PAS but not with the SPQ or its three factors, and the magnitude of significance was not strengthened by the combination of this allele with adjacent locus.

Conclusions. Our study provides the first evidence for the association of NRG1 with schizotypal personality and indicates a possible role of NRG1 in the genetic etiology of schizophrenia through perceptual aberrations.

A substantial proportion of the burden of depression arises from its recurrent nature. The risk of relapse after antidepressant medication (ADM) discontinuation is high but not uniform. Predictors of individual relapse risk after antidepressant discontinuation could help to guide treatment and mitigate the long-term course of depression. We conducted a systematic literature search in PubMed to identify relapse predictors using the search terms ‘(depress* OR MDD*) AND (relapse* OR recurren*) AND (predict* OR risk) AND (discontinu* OR withdraw* OR maintenance OR maintain or continu*) AND (antidepress* OR medication OR drug)’ for published studies until November 2014. Studies investigating predictors of relapse in patients aged between 18 and 65 years with a main diagnosis of major depressive disorder (MDD), who remitted from a depressive episode while treated with ADM and were followed up for at least 6 months to assess relapse after part of the sample discontinued their ADM, were included in the review. Although relevant information is present in many studies, only 13 studies based on nine separate samples investigated predictors for relapse after ADM discontinuation. There are multiple promising predictors, including markers of true treatment response and the number of prior episodes. However, the existing evidence is weak and there are no established, validated markers of individual relapse risk after antidepressant cessation. There is little evidence to guide discontinuation decisions in an individualized manner beyond overall recurrence risk. Thus, there is a pressing need to investigate neurobiological markers of individual relapse risk, focusing on treatment discontinuation.

The official definition of post-traumatic stress disorder (PTSD) in DSM-III and is subsequent DSM editions is based on a conceptual model that brackets traumatic or catastrophic events from less severe stressors and links them with a specific syndrome. The diagnosis of PTSD requires an identifiable stressor and the content of the defining symptoms refers to the stressor, for example, re-experiencing the stressor and avoidance of stimuli that symbolize the stressor. Temporal ordering is also required: when sleep problems and other symptoms of hyperarousal are part of the clinical picture, they must not have been present before the stressor occurred. The ICD-10 definition of PTSD follows the same model. The defining symptoms alone, without a connection to the stressor, are not regarded as PTSD (Green et al. 1995). Since the introduction of PTSD in DSM-III, the official definition has been adopted in most studies, although discussions about the validity of the definition has continued (Breslau & Davis, 1987; Davidson & Foa, 1993; Green et al. 1995). Although it is widely believed that other disorders (e.g. major depression) can be precipitated by external events, these disorders can occur independent of stressors and do not require a link with a traumatic event in their diagnostic criteria. Previous classifications that separated major depression into stress-related (reactive) or endogenous have been abandoned in newer versions of the DSM, because of lack of evidence of the validity of this distinction.

Unnatural causes of death due to traffic accidents (TA) and suicide attempts (SA) constitute a major burden on global health, which remained stable in the last decade despite widespread efforts of prevention. Recently, latent infection with Toxoplasma gondii (T. gondii) has been suggested to be a biological risk factor for both TA and SA. Therefore, a systematic search concerning the relationship of T. gondii infection with TA and/or SA according to PRISMA guidelines in Medline, Pubmed and PsychInfo was conducted collecting papers up to 11 February 2019 (PROSPERO #CRD42018090206). The random-effect model was applied and sensitivity analyses were subsequently performed. Lastly, the population attributable fraction (PAF) was calculated. We found a significant association for antibodies against T. gondii with TA [odds ratio (OR) = 1.69; 95% confidence interval (CI) 1.20–2.38, p = 0.003] and SA (OR = 1.39; 95% CI 1.10–1.76, p = 0006). Indication of publication bias was found for TA, but statistical adjustment for this bias did not change the OR. Heterogeneity between studies on SA was partly explained by type of control population used (ORhealthy controls = 1.9, p < 0.001 v. ORpsychiatric controls = 1.06, p = 0.87) and whether subjects with schizophrenia only were analysed (ORschizophrenia = 0.87, p = 0.62 v. ORvarious = 1.8, p < 0.001). The association was significantly stronger with higher antibody titres in TA and in studies that did not focus on schizophrenia subjects concerning SA. PAF of a T. gondii infection was 17% for TA and 10% for SA. This indicates that preventing T. gondii infection may play a role in the prevention of TA or SA, although uncertainty remains whether infection and outcome are truly causally related.