Little is known about the mental health of partners of survivors of high levels of trauma in post-conflict countries.

We studied 677 spouse dyads (n = 1354) drawn from a community survey (response 82.4%) in post-conflict Timor-Leste. We used culturally adapted measures of post-traumatic stress disorder (PTSD), psychological distress, explosive anger and grief.

Latent class analysis identified three classes of couples: class 1, comprising women with higher trauma events (TEs), men with intermediate TEs (19%); class 2, including men with higher TEs, women with lower TEs (23%); and class 3, comprising couples in which men and women had lower TE exposure (58%) (the reference group). Men and women partners of survivors of higher TE exposure (classes 1 and 2) had increased symptoms of explosive anger and grief compared with the reference class (class 3). Women partners of survivors of higher TE exposure (class 2) had a 20-fold increased rate of PTSD symptoms compared with the reference class, a pattern that was not evident for men living with women exposed to higher levels of trauma (class 1).

Men and women living with survivors of higher levels of trauma showed an increase in symptoms of grief and explosive anger. The manifold higher rate of PTSD symptoms amongst women living with men exposed to high levels of trauma requires replication. It is important to assess the mental health of partners when treating survivors of high levels of trauma in post-conflict settings.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use.

A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype.

Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency.

There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

Cognitive behaviour therapy (CBT) for chronic fatigue syndrome (CFS) leads to a significant decrease in CFS-related symptoms and disability. The primary objective of this study was to explore whether partners’ solicitous responses and patients’ and partners’ perceived relationship satisfaction had an effect on treatment outcome.

The treatment outcome of a cohort of 204 consecutively referred patients treated with CBT was analysed. At baseline, CFS patients completed the Maudsley Marital Questionnaire. The Checklist Individual Strength subscale Fatigue and the Sickness Impact Profile total scores completed by CFS patients post-treatment were used as measures of clinically significant improvement. Partners completed the Family Response Questionnaire, the Maudsley Marital Questionnaire, the Brief Illness Perception Questionnaire, and the Causal Attribution List. Logistic regression analyses were performed with clinically significant improvement in fatigue and disability as dependent variables and scores on questionnaires at baseline as predictors.

Solicitous responses of the partner were associated with less clinically significant improvement in fatigue and disability. Partners more often reported solicitous responses when they perceived CFS as a severe condition. Patients’ relationship dissatisfaction was negatively associated with clinically significant improvement in fatigue.

Partners’ solicitous responses and illness perceptions at the start of the therapy can negatively affect the outcome of CBT for CFS. We emphasize the importance of addressing this in therapy.

Lower intelligence quotient (IQ) has frequently been reported in patients with schizophrenia. However, it is unclear whether IQ declines (further) after illness onset and what the familial contribution is to this change. Therefore, we investigate IQ changes during the course of illness in patients with non-affective psychosis, their siblings and controls.

Data are part of the longitudinal Genetic Risk and Outcome of Psychosis (GROUP) study in the Netherlands and Belgium. Participants underwent three measurements, each approximately 3 years apart. A total of 1022 patients with non-affective psychosis [illness duration: 4.34 (s.d. = 4.50) years], 977 of their siblings, and 565 controls had at least one measure of IQ (estimated from four subtests of the WAIS-III).

At baseline, IQ was significantly lower in patients (IQ = 97.8) and siblings (IQ = 108.2; p < 0.0001) than in controls (IQ = 113.0; p < 0.0001), and in patients as compared with siblings (p < 0.0001). Over time, IQ increased in all groups. In siblings, improvement in IQ was significantly more pronounced (+0.7 points/year) than in patients (+0.5 points/year; p < 0.0001) and controls (+0.3 points/year; p < 0.0001). IQ increase was not significantly correlated with improvement in (sub)clinical outcome in any of the groups.

During the first 10 years of the illness, IQ increases to a similar (and subtle) extent in a relatively high-functioning group of schizophrenia patients and controls, despite the lower IQ in patients at baseline. In addition, the siblings’ IQ was intermediate at baseline, but over time the increase in IQ was more pronounced.

Impairments of contextual processing and theory of mind (ToM) have both been offered as accounts of the deviant language characterising formal thought disorder (FTD) in schizophrenia. This study investigated these processes in patients' dialogue. We predicted that FTD patients would show a decrement in linguistic alignment, associated with impaired ToM in dialogue.

Speech samples were elicited via participation in an interactive computer-based task and a semi-structured interview to assess contextual processing abilities and ToM skills in dialogue, respectively, and from an interactive card-sorting task to measure syntactic alignment. Degree of alignment in dialogue and the syntactic task, and evidence of ToM in (i) dialogue and (ii) a traditional ToM task were compared across schizophrenia patients with FTD (n = 21), non-FTD patients (n = 22) and healthy controls (n = 21).

FTD patients showed less alignment than the other two groups in dialogue, and than healthy controls on the syntactic task. FTD patients showed poorer performance on the ToM task than the other two groups, but only compared to the healthy controls in dialogue. The FTD group's degree of alignment in dialogue was correlated with ToM performance in dialogue but not with the traditional ToM task or with syntactic alignment.

In dialogue, FTD patients demonstrate an impairment in employing available contextual information to facilitate their own subsequent production, which is associated with a ToM deficit. These findings indicate that a contextual processing deficit impacts on exploiting representations via the production system impoverishing the ability to make predictions about upcoming utterances in dialogue.

In schizophrenia, relative stability in the magnitude of cognitive deficits across age and illness duration is inconsistent with the evidence of accelerated deterioration in brain regions known to support these functions. These discrepant brain–cognition outcomes may be explained by variability in cognitive reserve (CR), which in neurological disorders has been shown to buffer against brain pathology and minimize its impact on cognitive or clinical indicators of illness.

Age-related change in fluid reasoning, working memory and frontal brain volume, area and thickness were mapped using regression analysis in 214 individuals with schizophrenia or schizoaffective disorder and 168 healthy controls. In patients, these changes were modelled as a function of CR.

Patients showed exaggerated age-related decline in brain structure, but not fluid reasoning compared to controls. In the patient group, no moderation of age-related brain structural change by CR was evident. However, age-related cognitive change was moderated by CR, such that only patients with low CR showed evidence of exaggerated fluid reasoning decline that paralleled the exaggerated age-related deterioration of underpinning brain structures seen in all patients.

In schizophrenia-spectrum illness, CR may negate ageing effects on fluid reasoning by buffering against pathologically exaggerated structural brain deterioration through some form of compensation. CR may represent an important modifier that could explain inconsistencies in brain structure – cognition outcomes in the extant literature.

Life stress and blunted reward processing each have been associated with the onset and maintenance of major depressive disorder. However, much of this work has been cross-sectional, conducted in separate lines of inquiry, and focused on recent life stressor exposure, despite the fact that theories of depression posit that stressors can have cumulative effects over the lifespan. To address these limitations, we investigated whether acute and chronic stressors occurring over the lifespan interacted with blunted reward processing to predict increases in depression over time in healthy youth.

Participants were 245 adolescent girls aged 8–14 years old (Mage = 12.4, s.d. = 1.8) who were evaluated at baseline and two years later. The reward positivity (RewP), an event-related potential measure of reward responsiveness, was assessed at baseline using the doors task. Cumulative lifetime exposure to acute and chronic stressors was assessed two years later using the Stress and Adversity Inventory for Adolescents (Adolescent STRAIN). Finally, depressive symptoms were assessed at both baseline and follow-up using the Children's Depression Inventory.

As hypothesized, greater lifetime acute stressor exposure predicted increases in depressive symptoms over two years, but only for youth exhibiting a blunted RewP. This interaction, however, was not found for chronic stressors.

Lifetime acute stressor exposure may be particularly depressogenic for youth exhibiting a blunted RewP. Conversely, a robust RewP may be protective in the presence of greater acute lifetime stressor exposure.

The perinatal or early life environment may influence the development of mental illness in adulthood. It is not clear how, or when, any such influences might be mediated. Foetal exposure to maternal stress in the intrauterine environment has been suggested as a possible mediator of foetal origins of mental illness but the postnatal environment may also be of importance. This study aimed to test the foetal origins hypothesis by using retrograde and antegrade interbirth intervals (time to mother's most recent and next deliveries respectively) as proxy measures of antenatal and postnatal maternal stress.

Linked datasets of the Scottish Morbidity Record (SMR) were used to identify a birth cohort. Where applicable, the dates of each mother's most recent previous and/or next subsequent delivery were noted, allowing birth intervals to be calculated. The cohort was followed up into young adulthood, using self-harm, substance misuse, psychotic disorder and affective disorder as outcome measures. Data were analysed using Cox regression.

No significant relationship was observed between affective disorders and interbirth interval, neither retrograde nor antegrade. Short (<18-month) antegrade birth intervals were independently associated with increased risk of psychotic disorder and self-harm. Long (>72-month) retrograde intervals were associated with increased risk of self-harm and substance misuse.

The data do not provide evidence for the foetal origins of mental disorders but, in the cases of psychotic disorders, and of self-harm, suggest that the early postnatal rather than the antenatal environment may be of greater importance.

The impact of different levels of depression severity on quality of life (QoL) is not well studied, particularly regarding ICD-10 criteria. The ICD classification of depressive episodes in three levels of severity is also controversial and the less severe category, mild, has been considered as unnecessary and not clearly distinguishable from non-clinical states. The present work aimed to test the relationship between depression severity according to ICD-10 criteria and several dimensions of functioning as assessed by Medical Outcome Study (MOS) 36-item Short Form general health survey (SF-36) at the population level.

A sample of 551 participants from the second phase of the Outcome of Depression International Network (ODIN) study (228 controls without depression and 313 persons fulfilling ICD criteria for depressive episode) was selected for a further assessment of several variables, including QoL related to physical and mental health as measured with the SF-36.

Statistically significant differences between controls and the depression group were found in both physical and mental markers of health, regardless of the level of depression severity; however, there were very few differences in QoL between levels of depression as defined by ICD-10. Regardless of the presence of depression, disability, widowed status, being a woman and older age were associated with worse QoL in a structural equation analysis with covariates. Likewise, there were no differences according to the type of depression (single-episode versus recurrent).

These results cast doubt on the adequacy of the current ICD classification of depression in three levels of severity.

This study integrated an experimental medicine approach and a randomized cross-over clinical trial design following CONSORT recommendations to evaluate a cognitive training (CT) intervention for attention deficit hyperactivity disorder (ADHD). The experimental medicine approach was adopted because of documented pathophysiological heterogeneity within the diagnosis of ADHD. The cross-over design was adopted to provide the intervention for all participants and make maximum use of data.

Children (n = 93, mean age 7.3 +/− 1.1 years) with or sub-threshold for ADHD were randomly assigned to CT exercises over 15 weeks, before or after 15 weeks of treatment-as-usual (TAU). Fifteen dropped out of the CT/TAU group and 12 out of the TAU/CT group, leaving 66 for cross-over analysis. Seven in the CT/TAU group completed CT before dropping out making 73 available for experimental medicine analyses. Attention, response inhibition, and working memory were assessed before and after CT and TAU.

Children were more likely to improve with CT than TAU (27/66 v. 13/66, McNemar p = 0.02). Consistent with the experimental medicine hypotheses, responders improved on all tests of executive function (p = 0.009–0.01) while non-responders improved on none (p = 0.27–0.81). The degree of clinical improvement was predicted by baseline and change scores in focused attention and working memory (p = 0.008). The response rate was higher in inattentive and combined subtypes than hyperactive-impulsive subtype (p = 0.003).

Targeting cognitive dysfunction decreases clinical symptoms in proportion to improvement in cognition. Inattentive and combined subtypes were more likely to respond, consistent with targeted pathology and clinically relevant heterogeneity within ADHD.