Increasing evidence suggests that autism is associated with abnormal white-matter (WM) anatomy and impaired brain ‘connectivity’. While myelin plays a critical role in synchronized brain communication, its aetiological role in autistic symptoms has only been indirectly addressed by WM volumetric, relaxometry and diffusion tensor imaging studies. A potentially more specific measure of myelin content, termed myelin water fraction (MWF), could provide improved sensitivity to myelin alteration in autism.

We performed a cross-sectional imaging study that compared 14 individuals with autism and 14 age- and IQ-matched controls. T1 relaxation times (T1), T2 relaxation times (T2) and MWF values were compared between autistic subjects, diagnosed using the Autism Diagnostic Interview – Revised (ADI-R), with current symptoms assessed using the Autism Diagnostic Observation Schedule (ADOS) and typical healthy controls. Correlations between T1, T2 and MWF values with clinical measures [ADI-R, ADOS, and the Autism Quotient (AQ)] were also assessed.

Individuals with autism showed widespread WM T1 and MWF differences compared to typical controls. Within autistic individuals, worse current social interaction skill as measured by the ADOS was related to reduced MWF although not T1. No significant differences or correlations with symptoms were observed with respect to T2.

Autistic individuals have significantly lower global MWF and higher T1, suggesting widespread alteration in tissue microstructure and biochemistry. Areas of difference, including thalamic projections, cerebellum and cingulum, have previously been implicated in the disorder; however, this is the first study to specifically indicate myelin alteration in these regions.

Self-harm is a common reason for Emergency Department (ED) attendance. We aimed to develop a clinical tool to help identify patients at higher risk of repeat self-harm, or suicide, within 6 months of an ED self-harm presentation.

The tool, the ReACT Self-Harm Rule, was derived using multicentre data from a prospective cohort study. Binary recursive partitioning was applied to data from two centres, and data from a separate centre were used to test the tool. There were 29 571 self-harm presentations to five hospital EDs between January 2003 and June 2007, involving 18 680 adults aged ⩾16 years. We estimated sensitivity, specificity and positive and negative predictive values to measure the performance of the tool.

A self-harm presentation was classified as higher risk if at least one of the following factors was present: recent self-harm (in the past year), living alone or homelessness, cutting as a method of harm and treatment for a current psychiatric disorder. The rule performed with 95% sensitivity [95% confidence interval (CI) 94–95] and 21% specificity (95% CI 21–22), and had a positive predictive value of 30% (95% CI 30–31) and a negative predictive value of 91% (95% CI 90–92) in the derivation centres; it identified 83/92 of all subsequent suicides.

The ReACT Self-Harm Rule might be used as a screening tool to inform the process of assessing self-harm presentations to ED. The four risk factors could also be used as an adjunct to in-depth psychosocial assessment to help guide risk formulation. The use of multicentre data helped to maximize the generalizability of the tool, but we need to further verify its external validity in other localities.

Being physically assaulted is known to increase the risk of the occurrence of post-traumatic stress disorder (PTSD) symptoms but it may also skew judgements about the intentions of other people. The objectives of the study were to assess paranoia and PTSD after an assault and to test whether theory-derived cognitive factors predicted the persistence of these problems.

At 4 weeks after hospital attendance due to an assault, 106 people were assessed on multiple symptom measures (including virtual reality) and cognitive factors from models of paranoia and PTSD. The symptom measures were repeated 3 and 6 months later.

Factor analysis indicated that paranoia and PTSD were distinct experiences, though positively correlated. At 4 weeks, 33% of participants met diagnostic criteria for PTSD, falling to 16% at follow-up. Of the group at the first assessment, 80% reported that since the assault they were excessively fearful of other people, which over time fell to 66%. Almost all the cognitive factors (including information-processing style during the trauma, mental defeat, qualities of unwanted memories, self-blame, negative thoughts about self, worry, safety behaviours, anomalous internal experiences and cognitive inflexibility) predicted later paranoia and PTSD, but there was little evidence of differential prediction.

Paranoia after an assault may be common and distinguishable from PTSD but predicted by a strikingly similar range of factors.

In previous studies an association between deployment to Iraq or Afghanistan and an overall increased risk for post-traumatic stress disorder (PTSD) in UK armed forces has not been found. The lack of a deployment effect might be explained by including, in the comparison group, personnel deployed on other operations or who have experienced traumatic stressors unrelated to deployment.

The sample comprised 8261 regular UK armed forces personnel who deployed to Iraq, Afghanistan or other operational areas or were not deployed. Participants completed the PTSD CheckList – Civilian Version (PCL-C) and provided information about deployment history, demographic and service factors, serious accidents and childhood experiences.

Deployment to Iraq or Afghanistan [odds ratio (OR) 1.2, 95% confidence interval (CI) 0.6–2.2] or elsewhere (OR 1.1, 95% CI 0.6–2.0) was unrelated to PTSD although holding a combat role was associated with PTSD if deployed to Iraq or Afghanistan (OR 2.7, 95% CI 1.9–3.9). Childhood adversity (OR 3.3, 95% CI 2.1–5.0), having left service (OR 2.7, 95% CI 1.9–4.0) and serious accident (OR 2.1, 95% CI 1.4–3.0) were associated with PTSD whereas higher rank was protective (OR 0.3, 95% CI 0.12–0.76).

For the majority of UK armed forces personnel, deployment whether to Iraq, Afghanistan or elsewhere confers no greater risk for PTSD than service in the armed forces per se but holding a combat role in those deployed to Iraq or Afghanistan is associated with PTSD. Vulnerability factors such as lower rank, childhood adversity and leaving service, and having had a serious accident, may be at least as important as holding a combat role in predicting PTSD in UK armed forces personnel.

Maternal depression in the pre- and postpartum period may set women on a course of chronic depressive symptoms. Little is known about predictors of persistently elevated depressive symptoms in mothers from pregnancy onwards. The aims of this study are to determine maternal depression trajectories from pregnancy to the child's fifth birthday and identify associated risk factors.

Mothers (N = 1807) from the EDEN mother–child birth cohort study based in France (2003–2011) were followed from 24–28 weeks of pregnancy to their child's fifth birthday. Maternal depression trajectories were determined with a semi-parametric group-based modelling strategy. Sociodemographic, psychosocial and psychiatric predictors were explored for their association with trajectory class membership.

Five trajectories of maternal symptoms of depression from pregnancy onwards were identified: no symptoms (60.2%); persistent intermediate-level depressive symptoms (25.2%); persistent high depressive symptoms (5.0%); high symptoms in pregnancy only (4.7%); high symptoms in the child's preschool period only (4.9%). Socio-demographic predictors associated with persistent depression were non-French origin; psychosocial predictors were childhood adversities, life events during pregnancy and work overinvestment; psychiatric predictors were previous mental health problems, psychological help, and high anxiety during pregnancy.

Persistent depression in mothers of young children is associated to several risk factors present prior to or during pregnancy, notably anxiety. These characteristics precede depression trajectories and offer a possible entry point to enhance mother's mental health and reduce its burden on children.

Although DSM-IV attention deficit hyperactivity disorder (ADHD) is known to be associated with numerous adverse outcomes, uncertainties exist about how much these associations are mediated temporally by secondary co-morbid disorders.

The US National Comorbidity Survey Replication Adolescent Supplement (NCS-A), a national survey of adolescents aged 13–17 years (n = 6483 adolescent–parent pairs), assessed DSM-IV disorders with the World Health Organization (WHO) Composite International Diagnostic Interview (CIDI). Statistical decomposition was used to compare direct effects of ADHD with indirect effects of ADHD through temporally secondary mental disorders (anxiety, mood, disruptive behavior, substance disorders) in predicting poor educational performance (suspension, repeating a grade, below-average grades), suicidality (ideation, plans, attempts) and parent perceptions of adolescent functioning (physical and mental health, interference with role functioning and distress due to emotional problems).

ADHD had significant gross associations with all outcomes. Direct effects of ADHD explained most (51.9–67.6%) of these associations with repeating a grade in school, perceived physical and mental health (only girls), interference with role functioning and distress, and significant components (34.5–44.6%) of the associations with school suspension and perceived mental health (only boys). Indirect effects of ADHD on educational outcomes were predominantly through disruptive behavior disorders (26.9–52.5%) whereas indirect effects on suicidality were predominantly through mood disorders (42.8–59.1%). Indirect effects on most other outcomes were through both mood (19.8–31.2%) and disruptive behavior (20.1–24.5%) disorders, with anxiety and substance disorders less consistently important. Most associations were comparable for girls and boys.

Interventions aimed at reducing the adverse effects of ADHD might profitably target prevention or treatment of temporally secondary co-morbid disorders.

Traits of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are strongly associated in children and adolescents, largely due to genetic factors. Less is known about the phenotypic and aetiological overlap between ADHD and ASD traits in adults.

We studied 6866 individuals aged 20–28 years from the Swedish Study of Young Adult Twins. Inattention (IA) and hyperactivity/impulsivity (HI) were assessed using the WHO Adult ADHD Self-Report Scale-V1.1. Repetitive and restricted behaviours (RRB) and social interaction and communication (SIC) were assessed using the Autism-Tics, ADHD, and other Comorbidities inventory. We used structural equation modelling to decompose covariance between these ADHD and ASD trait dimensions into genetic and shared/non-shared environmental components.

At the phenotypic level, IA was similarly correlated with RRB (r = 0.33; 95% Confidence Interval (CI) 0.31–0.36) and with SIC (r = 0.32; 95% CI 0.29–0.34), whereas HI was more strongly associated with RRB (r = 0.38; 95% CI 0.35–0.40) than with SIC (r = 0.24; 95% CI 0.21–0.26). Genetic and non-shared environmental effects accounted for similar proportions of the phenotypic correlations, whereas shared environmental effects were of minimal importance. The highest genetic correlation was between HI and RRB (r = 0.56; 95% 0.46–0.65), and the lowest was between HI and SIC (r = 0.33; 95% CI 0.23–0.43).

We found evidence for dimension-specific phenotypic and aetiological overlap between ADHD and ASD traits in adults. Future studies investigating mechanisms underlying comorbidity between ADHD and ASD may benefit from exploring several symptom-dimensions, rather than considering only broad diagnostic categories.

Research has long noted higher prevalence rates of suicidal thoughts and behaviors among individuals with psychotic symptoms. Major theories have proposed several explanations to account for this association. Given the differences in the literature regarding the operationalization of psychosis and sample characteristics, a quantitative review is needed to determine to what extent and how psychosis confers risk for suicidality.

We searched PsycInfo, PubMed, and GoogleScholar for studies published before 1 January 2016. To be included in the analysis, studies must have used at least one psychosis-related factor to longitudinally predict suicide ideation, attempt, or death. The initial search yielded 2541 studies. Fifty studies were retained for analysis, yielding 128 statistical tests.

Suicide death was the most commonly studied outcome (43.0%), followed by attempt (39.1%) and ideation (18.0%). The median follow-up length was 7.5 years. Overall, psychosis significantly conferred risk across three outcomes, with weighted mean ORs of 1.70 (1.39–2.08) for ideation, 1.36 (1.25–1.48) for attempt, and 1.40 (1.14–1.72) for death. Detailed analyses indicated that positive symptoms consistently conferred risk across outcomes; negative symptoms were not significantly associated with ideation, and were protective against death. Some small moderator effects were detected for sample characteristics.

Psychosis is a significant risk factor for suicide ideation, attempt, and death. The finding that positive symptoms increased suicide risk and negative symptoms seemed to decrease risk sheds light on the potential mechanisms for the association between psychosis and suicidality. We note several limitations of the literature and offer suggestions for future directions.

With regard to current neurobiological theories, the aim of our study was to examine possible alterations of temporal and frontal lobe volume in panic disorder (PD).

Seventeen in-patients with PD and a group of healthy control subjects (HC) matched for age and gender were investigated by quantitative volumetric magnetic resonance imaging (MRI). Structures of interest were: the temporal lobe, the amygdala–hippocampus complex (AHC) and the frontal lobe. In addition, a voxel-based morphometry (VBM) analysis implemented in Statistical Parametric Mapping 5 (SPM5) was used for a more detailed assessment of possible volume alterations. Modulated grey matter (GM) images were used to test our a priori hypotheses and to present the volumetric results.

Quantitative volumetric MRI revealed a bilateral reduction in temporal lobe volume in patients with PD compared to HC subjects. The AHC was normal. The right frontal lobe volume was also decreased. Using VBM we detected a significant GM volume reduction in the right middle temporal gyrus [Brodmann area (BA) 21] in patients with PD. In addition, there was a reduction in GM volume in the medial part of the orbitofrontal cortex (BA 11).

Our results of reduced temporal and frontal lobe volume in PD are in agreement with prior studies. By using a recent VBM approach we were able to assess the abnormalities more precisely. The location of GM volume reduction in the right middle temporal gyrus and medial orbitofrontal cortex lends further support to recent aetiological models of PD.