Certain migrant groups are at an increased risk of psychotic disorders compared to the native-born population; however, research to date has mainly been conducted in Europe. Less is known about whether migrants to other countries, with different histories and patterns of migration, such as Australia, are at an increased risk for developing a psychotic disorder. We tested this for first-generation migrants in Melbourne, Victoria.

This study included all young people aged 15–24 years, residing in a geographically-defined catchment area of north western Melbourne who presented with a first episode of psychosis (FEP) to the Early Psychosis Prevention and Intervention Centre (EPPIC) between 1 January 2011 and 31 December 2016. Data pertaining to the at-risk population were obtained from the Australian 2011 Census and incidence rate ratios were calculated and adjusted for age, sex and social deprivation.

In total, 1220 young people presented with an FEP during the 6-year study period, of whom 24.5% were first-generation migrants. We found an increased risk for developing psychotic disorder in migrants from the following regions: Central and West Africa (adjusted incidence rate ratio [aIRR] = 3.53, 95% CI 1.58–7.92), Southern and Eastern Africa (aIRR = 3.06, 95% CI 1.99–4.70) and North Africa (aIRR = 5.03, 95% CI 3.26–7.76). Migrants from maritime South East Asia (aIRR = 0.39, 95% CI 0.23–0.65), China (aIRR = 0.25, 95% CI 0.13–0.48) and Southern Asia (aIRR = 0.44, 95% CI 0.26–0.76) had a decreased risk for developing a psychotic disorder.

This clear health inequality needs to be addressed by sufficient funding and accessible mental health services for more vulnerable groups. Further research is needed to determine why migrants have an increased risk for developing psychotic disorders.

Clinicians routinely use impressions of speech as an element of mental status examination. In schizophrenia-spectrum disorders, descriptions of speech are used to assess the severity of psychotic symptoms. In the current study, we assessed the diagnostic value of acoustic speech parameters in schizophrenia-spectrum disorders, as well as its value in recognizing positive and negative symptoms.

Speech was obtained from 142 patients with a schizophrenia-spectrum disorder and 142 matched controls during a semi-structured interview on neutral topics. Patients were categorized as having predominantly positive or negative symptoms using the Positive and Negative Syndrome Scale (PANSS). Acoustic parameters were extracted with OpenSMILE, employing the extended Geneva Acoustic Minimalistic Parameter Set, which includes standardized analyses of pitch (F0), speech quality and pauses. Speech parameters were fed into a random forest algorithm with leave-ten-out cross-validation to assess their value for a schizophrenia-spectrum diagnosis, and PANSS subtype recognition.

The machine-learning speech classifier attained an accuracy of 86.2% in classifying patients with a schizophrenia-spectrum disorder and controls on speech parameters alone. Patients with predominantly positive v. negative symptoms could be classified with an accuracy of 74.2%.

Our results show that automatically extracted speech parameters can be used to accurately classify patients with a schizophrenia-spectrum disorder and healthy controls, as well as differentiate between patients with predominantly positive v. negatives symptoms. Thus, the field of speech technology has provided a standardized, powerful tool that has high potential for clinical applications in diagnosis and differentiation, given its ease of comparison and replication across samples.

Methodological and ethical constraints have hampered studies into long-term lasting outcomes of stimulant treatment in individuals with attention-deficit/hyperactivity disorder (ADHD). Lasting effects may be beneficial (i.e. improved functioning even when treatment is temporarily ceased) or detrimental (i.e. worse functioning while off medication), but both hypotheses currently lack empirical support. Here we investigate whether stimulant treatment history predicts long-term development of ADHD symptoms, social–emotional functioning or cognition, measured after medication wash-out.

ADHD symptoms, social–emotional functioning and cognitive test performance were measured twice, 6 years apart, in two ADHD groups (stimulant-treated versus not stimulant-treated between baseline and follow-up). Groups were closely matched on baseline clinical and demographic variables (n = 148, 58% male, age = 11.1). A matched healthy control group was included for reference.

All but two outcome measures (emotional problems and prosocial behaviour) improved between baseline and follow-up. Improvement over time in the stimulant-treated group did not differ from improvement in the not stimulant-treated group on any outcome measure.

Stimulant treatment is not associated with the long-term developmental course of ADHD symptoms, social–emotional functioning, motor control, timing or verbal working memory. Adolescence is characterised by clinical improvement regardless of stimulant treatment during that time. These findings are an important source to inform the scientific and public debate.

Major depressive disorder (MDD) is a leading cause of disability worldwide and influenced by both environmental and genetic factors. Genetic studies of MDD have focused on common variants and have been constrained by the heterogeneity of clinical symptoms.

We sequenced the exome of 77 cases and 245 controls of Han Chinese ancestry and scanned their brain. Burden tests of rare variants were performed first to explore the association between genes/pathways and MDD. Secondly, parallel Independent Component Analysis was conducted to investigate genetic underpinnings of gray matter volume (GMV) changes of MDD.

Two genes (CSMD1, p = 5.32×10−6; CNTNAP5, p = 1.32×10−6) and one pathway (Neuroactive Ligand Receptor Interactive, p = 1.29×10−5) achieved significance in burden test. In addition, we identified one pair of imaging-genetic components of significant correlation (r = 0.38, p = 9.92×10−6). The imaging component reflected decreased GMV in cases and correlated with intelligence quotient (IQ). IQ mediated the effects of GMV on MDD. The genetic component enriched in two gene sets, namely Singling by G-protein coupled receptors [false discovery rate (FDR) q = 3.23×10−4) and Alzheimer Disease Up (FDR q = 6.12×10−4).

Both rare variants analysis and imaging–genetic analysis found evidence corresponding with the neuroinflammation and synaptic plasticity hypotheses of MDD. The mediation of IQ indicates that genetic component may act on MDD through GMV alteration and cognitive impairment.

Psychotic experiences (PEs) are reported by a significant minority of adolescents and are associated with the development of psychiatric disorders. The aims of this study were to examine associations between PEs and a range of factors including psychopathology, adversity and lifestyle, and to investigate mediating effects of coping style and parental support on associations between adversity and PEs in a general population adolescent sample.

Cross-sectional data were drawn from the Irish centre of the Saving and Empowering Young Lives in Europe study. Students completed a self-report questionnaire and 973 adolescents, of whom 522 (53.6%) were boys, participated. PEs were assessed using the 7-item Adolescent Psychotic Symptom Screener.

Of the total sample, 81 (8.7%) of the sample were found to be at risk of PEs. In multivariate analysis, associations were found between PEs and number of adverse events reported (OR 4.48, CI 1.41–14.25; p < 0.011), maladaptive/pathological internet use (OR 2.70, CI 1.30–5.58; p = 0.007), alcohol intoxication (OR 2.12, CI 1.10–4.12; p = 0.025) and anxiety symptoms (OR 4.03, CI 1.57–10.33; p = 0.004). There were small mediating effects of parental supervision, parental support and maladaptive coping on associations between adversity and PEs.

We have identified potential risk factors for PEs from multiple domains including adversity, mental health and lifestyle factors. The mediating effect of parental support on associations between adversity and PEs suggests that poor family relationships may account for some of this mechanism. These findings can inform the development of interventions for adolescents at risk.

Detecting genetic factors involved in attention deficit hyperactivity disorder (ADHD) is complicated because of their small effect sizes and complex interactions. The endophenotype approach eases this by coming closer to the relevant genes. Different aspects of temporal information processing are known to be affected in ADHD. Thus, some of these aspects could represent candidate endophenotypes for ADHD.

Fifty-four sib-pairs with at least one child with ADHD and 40 control children aged 6–18 years were recruited and asked to perform two duration discrimination tasks, one with a base duration of 50 ms on automatic timing and one with a base duration of 1000 ms on cognitively controlled timing.

Whereas children with ADHD, but not their unaffected siblings, were impaired in discrimination of longer intervals, both groups were impaired in discriminating brief intervals. Furthermore, a significant within-family correlation was found for discrimination of brief intervals. Task performances of subjects of the control group correlated with individual levels of hyperactivity/impulsivity for discrimination of brief intervals, but not of longer intervals.

Cognitively controlled and also automatic processes of temporal information processing are impaired in children with ADHD. Discrimination of longer intervals appears as a typical ‘disease marker’ whereas discrimination of brief intervals shows up as a ‘vulnerability marker’. Discrimination of brief intervals was found to be familial and linked to levels of hyperactivity/impulsivity. Taken together, discrimination of brief intervals represents a candidate endophenotype of ADHD.

It remains unclear whether the topological deficits of the white matter network documented in cross-sectional studies of chronic schizophrenia patients are due to chronic illness or to other factors such as antipsychotic treatment effects. To answer this question, we evaluated the white matter network in medication-naive first-episode schizophrenia patients (FESP) before and after a course of treatment.

We performed a longitudinal diffusion tensor imaging study in 42 drug-naive FESP at baseline and then after 8 weeks of risperidone monotherapy, and compared them with 38 healthy volunteers. Graph theory was utilized to calculate the topological characteristics of brain anatomical network. Patients’ clinical state was evaluated using the Positive and Negative Syndrome Scale (PANSS) before and after treatment.

Pretreatment, patients had relatively intact overall topological organizations, and deficient nodal topological properties primarily in prefrontal gyrus and limbic system components such as the bilateral anterior and posterior cingulate. Treatment with risperidone normalized topological parameters in the limbic system, and the enhancement positively correlated with the reduction in PANSS-positive symptoms. Prefrontal topological impairments persisted following treatment and negative symptoms did not improve.

During the early phase of antipsychotic medication treatment there are region-specific alterations in white matter topological measures. Limbic white matter topological dysfunction improves with positive symptom reduction. Prefrontal deficits and negative symptoms are unresponsive to medication intervention, and prefrontal deficits are potential trait biomarkers and targets for negative symptom treatment development.

A few previous studies suggest that a large number of individuals do not present at hospital following a suicide attempt, complicating recurrence prevention and prevalence estimation.

Data were extracted from a regular phone survey in representative samples of the French population aged 18–75 years old. Five surveys between 2000 and 2017 collected data about the occurrence of a previous suicide attempt and subsequent care contacts. A total of 102,729 individuals were surveyed. Among them, 6,500 (6.4%) reported a lifetime history of suicide attempt.

Following their last suicide attempt, 39.3% reported they did not present to hospital (53.4% in 18–24 year-olds), with limited changes in rates with time. Risk factors for non-presentation were being male [adjusted odds ratio = 1.3, 95% confidence interval (1.1–1.5)], living with someone [1.2 (1.0–1.4)], being a non-smoker [1.4 (1.2–1.6)], and being younger at time of attempt [0.97 (0.96–0.98) per year]. Of those who did not present to hospital, only 37.7% reported visiting a doctor or a psychiatrist/psychologist after their act v. 67.1% in those who presented to hospital (as a second health contact). In both cases, half disclosed their act to someone else. Prevalence rates of suicide attempts reported in community were 4.6 times higher than those in hospital administrative databases.

This survey at a national level confirmed that a large proportion of individuals does not go to the hospital and does not meet any health care professionals following a suicidal act. Assessment of unmet needs is necessary.

In adults, attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BD) have certain overlapping symptoms, which can lead to uncertainty regarding the boundaries of the two disorders. Despite evidence of cognitive impairments in both disorders separately, such as in attentional and inhibitory processes, data on direct comparisons across ADHD and BD on cognitive–neurophysiological measures are as yet limited.

We directly compared cognitive performance and event-related potential measures from a cued continuous performance test in 20 women with ADHD, 20 women with BD (currently euthymic) and 20 control women.

The NoGo-N2 was attenuated in women with BD, reflecting reduced conflict monitoring, compared with women with ADHD and controls (both p < 0.05). Both ADHD and BD groups showed a reduced NoGo-P3, reflecting inhibitory control, compared with controls (both p < 0.05). In addition, the contingent negative variation was significantly reduced in the ADHD group (p = 0.05), with a trend in the BD group (p = 0.07), compared with controls.

These findings indicate potential disorder-specific (conflict monitoring) and overlapping (inhibitory control, and potentially response preparation) neurophysiological impairments in women with ADHD and women with BD. The identified neurophysiological parameters further our understanding of neurophysiological impairments in women with ADHD and BD, and are candidate biomarkers that may aid in the identification of the diagnostic boundaries of the two disorders.

Antidepressant drug treatments increase the processing of positive compared to negative affective information early in treatment. Such effects have been hypothesized to play a key role in the development of later therapeutic responses to treatment. However, it is unknown whether these effects are a common mechanism of action for different treatment modalities. High-density negative ion (HDNI) treatment is an environmental manipulation that has efficacy in randomized clinical trials in seasonal affective disorder (SAD).

The current study investigated whether a single session of HDNI treatment could reverse negative affective biases seen in seasonal depression using a battery of emotional processing tasks in a double-blind, placebo-controlled randomized study.

Under placebo conditions, participants with seasonal mood disturbance showed reduced recognition of happy facial expressions, increased recognition memory for negative personality characteristics and increased vigilance to masked presentation of negative words in a dot-probe task compared to matched healthy controls. Negative ion treatment increased the recognition of positive compared to negative facial expression and improved vigilance to unmasked stimuli across participants with seasonal depression and healthy controls. Negative ion treatment also improved recognition memory for positive information in the SAD group alone. These effects were seen in the absence of changes in subjective state or mood.

These results are consistent with the hypothesis that early change in emotional processing may be an important mechanism for treatment action in depression and suggest that these effects are also apparent with negative ion treatment in seasonal depression.

Patients with schizophrenia have intact ability to experience emotion, but empirical evidence suggests that they fail to translate emotional salience into effortful behaviour. Previous research in patients with chronic schizophrenia suggests that working memory is important in integrating emotion and behaviour. This study aimed to examine avolition and anhedonia in patients with first-episode schizophrenia and clarify the role of working memory in emotion–behaviour coupling.

We recruited 72 participants with first-episode schizophrenia and 61 healthy controls, and used a validated emotion-inducing behavioural paradigm to measure participants' affective experiences and how experienced emotion coupled with behaviour. Participants were given the opportunity to expend effort to increase or decrease their exposure to emotion-inducing photographs. Participants with schizophrenia having poor working memory were compared with those with intact working memory in their liking and emotion–behaviour coupling.

Patients with first-episode schizophrenia experienced intact ‘in-the-moment’ emotion, but their emotion was less predictive of the effort expended, compared with controls. The emotion–behaviour coupling was significantly weaker in patients with schizophrenia with poor working memory than in those with intact working memory. However, compared with controls, patients with intact working also showed substantial emotion–behaviour decoupling.

Our findings provide strong evidence for emotion–behaviour decoupling in first-episode schizophrenia. Although working memory deficits contribute to defective translation of liking into effortful behaviour, schizophrenia alone affects emotion–behaviour coupling.

Accumulating evidence suggests that positive and negative emotions, as well as emotion regulation, play key roles in human health and disease. Recent work has shown the gut microbiome is important in modulating mental and physical health through the gut–brain axis. Yet, its association with emotions and emotion regulation are understudied. Here we examined whether positive and negative emotions, as well as two emotion regulation strategies (i.e. cognitive reappraisal and suppression), were associated with the gut microbiome composition and functional pathways in healthy women.

Participants were from the Mind-Body Study (N = 206, mean age = 61), a sub-study of the Nurses' Health Study II cohort. In 2013, participants completed measures of emotion-related factors. Two pairs of stool samples were collected, 6 months apart, 3 months after emotion-related factors measures were completed. Analyses examined associations of emotion-related factors with gut microbial diversity, overall microbiome structure, and specific species/pathways and adjusted for relevant covariates.

Alpha diversity was negatively associated with suppression. In multivariate analysis, positive emotions were inversely associated with the relative abundance of Firmicutes bacterium CAG 94 and Ruminococcaceae bacterium D16, while negative emotions were directly correlated with the relative abundance of these same species. At the metabolic pathway level, negative emotions were inversely related to the biosynthesis of pantothenate, coenzyme A, and adenosine.

These findings offer human evidence supporting linkages of emotions and related regulatory processes with the gut microbiome and highlight the importance of incorporating the gut microbiome in our understanding of emotion-related factors and their associations with physical health.