Among the myths that are often cited about suicide is that ‘people who talk about killing themselves rarely die by suicide’, but the evidence seems to contradict this statement. The aim of this study was to conduct a meta-analysis of studies reporting a prevalence of suicide communication (SC), and to examine the diagnostic accuracy of SC towards suicide in case-control reports.

Eligible studies had to examine data relative to completed suicides and report the prevalence of SC. Data relative to sample characteristics, study definition, modality and recipient of the SC were coded.

We included 36 studies, conducted on a total of 14 601 completed suicides. The overall proportion of SC was 44.5% [95% confidence interval (CI) 35.4–53.8], with large heterogeneity (I2 = 98.8%) and significant publication bias. The prevalence of SC was negatively associated with the detection of verbal communication as the sole means of SC and, positively, with study methodological quality. Based on seven case-control studies, SC was associated with an odds ratio of 4.66 for suicide (95% CI 3.00–7.25) and was characterized by sufficient diagnostic accuracy only if studies on adolescents were removed.

Available data suggest that SC occurs in nearly half of subjects who go on to die by suicide, but this figure is likely to be an underestimate given the operational definitions of SC. At present, SC seems associated with overall insufficient accuracy towards subsequent suicide, although further rigorous studies are warranted to draw definite conclusions on this issue.

We have previously shown that the selective serotonergic reuptake inhibitor, citalopram, reduces the neural response to reward and aversion in healthy volunteers. We suggest that this inhibitory effect might underlie the emotional blunting reported by patients on these medications. Bupropion is a dopaminergic and noradrenergic reuptake inhibitor and has been suggested to have more therapeutic effects on reward-related deficits. However, how bupropion affects the neural responses to reward and aversion is unclear.

Seventeen healthy volunteers (9 female, 8 male) received 7 days bupropion (150 mg/day) and 7 days placebo treatment, in a double-blind crossover design. Our functional magnetic resonance imaging task consisted of three phases; an anticipatory phase (pleasant or unpleasant cue), an effort phase (button presses to achieve a pleasant taste or to avoid an unpleasant taste) and a consummatory phase (pleasant or unpleasant tastes). Volunteers also rated wanting, pleasantness and intensity of the tastes.

Relative to placebo, bupropion increased activity during the anticipation phase in the ventral medial prefrontal cortex (vmPFC) and caudate. During the effort phase, bupropion increased activity in the vmPFC, striatum, dorsal anterior cingulate cortex and primary motor cortex. Bupropion also increased medial orbitofrontal cortex, amygdala and ventral striatum activity during the consummatory phase.

Our results are the first to show that bupropion can increase neural responses during the anticipation, effort and consummation of rewarding and aversive stimuli. This supports the notion that bupropion might be beneficial for depressed patients with reward-related deficits and blunted affect.

Data on gender-specific profiles of cognitive functions in patients with Parkinson's disease (PD) are rare and inconsistent, and possible disease-confounding factors have been insufficiently considered.

The LANDSCAPE study on cognition in PD enrolled 656 PD patients (267 without cognitive impairment, 66% male; 292 with mild cognitive impairment, 69% male; 97 with PD dementia, 69% male). Raw values and age-, education-, and gender-corrected Z scores of a neuropsychological test battery (CERAD-Plus) were compared between genders. Motor symptoms, disease duration, l-dopa equivalent daily dose, depression - and additionally age and education for the raw value analysis - were taken as covariates.

Raw-score analysis replicated results of previous studies in that female PD patients were superior in verbal memory (word list learning, p = 0.02; recall, p = 0.03), while men outperformed women in visuoconstruction (p = 0.002) and figural memory (p = 0.005). In contrast, gender-corrected Z scores showed that men were superior in verbal memory (word list learning, p = 0.02; recall, p = 0.02; recognition, p = 0.04), while no difference was found for visuospatial tests. This picture could be observed both in the overall analysis of PD patients as well as in a differentiated group analysis.

Normative data corrected for gender and other sociodemographic variables are relevant, since they may elucidate a markedly different cognitive profile compared to raw scores. Our study also suggests that verbal memory decline is stronger in women than in men with PD. Future studies are needed to replicate these findings, examine the progression of gender-specific cognitive decline in PD and define different underlying mechanisms of this dysfunction.

To date no comprehensive evaluation has appraised the likelihood of bias or the strength of the evidence of peripheral biomarkers for bipolar disorder (BD). Here we performed an umbrella review of meta-analyses of peripheral non-genetic biomarkers for BD.

The Pubmed/Medline, EMBASE and PsycInfo electronic databases were searched up to May 2015. Two independent authors conducted searches, examined references for eligibility, and extracted data. Meta-analyses in any language examining peripheral non-genetic biomarkers in participants with BD (across different mood states) compared to unaffected controls were included.

Six references, which examined 13 biomarkers across 20 meta-analyses (5474 BD cases and 4823 healthy controls) met inclusion criteria. Evidence for excess of significance bias (i.e. bias favoring publication of ‘positive’ nominally significant results) was observed in 11 meta-analyses. Heterogeneity was high for (I2 ⩾ 50%) 16 meta-analyses. Only two biomarkers met criteria for suggestive evidence namely the soluble IL-2 receptor and morning cortisol. The median power of included studies, using the effect size of the largest dataset as the plausible true effect size of each meta-analysis, was 15.3%.

Our findings suggest that there is an excess of statistically significant results in the literature of peripheral biomarkers for BD. Selective publication of ‘positive’ results and selective reporting of outcomes are possible mechanisms.

Patients with a deletion at chromosome 22q11.2 (22q11DS) have 30% lifetime risk of developing a psychosis. People fulfilling clinical criteria for ultra-high risk (UHR) for psychosis have 30% risk of developing a psychosis within 2 years. Both high-risk groups show white-matter (WM) abnormalities in microstructure and volume compared to healthy controls (HC), which have been related to psychotic symptoms. Comparisons of WM pathology between these two groups may specify WM markers related to genetic and clinical risk factors.

Fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD) and mean diffusivity (MD) were assessed using diffusion tensor magnetic resonance imaging (MRI), and WM volume with structural MRI, in 23 UHR patients, 21 22q11DS patients, and 33 HC.

Compared to UHR patients 22q11DS patients had (1) lower AD and RD in corpus callosum (CC), cortical fasciculi, and anterior thalamic radiation (ATR), (2) higher FA in CC and ATR, and (3) lower occipital and superior temporal gyrus WM volume. Compared to HC, 22q11DS patients had (1) lower AD and RD throughout cortical fasciculi and (2) higher FA in ATR, CC and inferior fronto-occipital fasciculus. Compared to HC, UHR patients had (1) higher mean MD, RD, and AD in CC, ATR and cortical fasciculi, (2) no differences in FA.

UHR and 22q11DS patients share a susceptibility for developing psychosis yet were characterized by distinct patterns of WM alterations relative to HC. While UHR patients were typified by signs suggestive of aberrant myelination, 22q11DS subjects showed signs suggestive of lower axonal integrity.

Cognitive impairments are an important feature of both remitted and depressed major depressive disorder (MDD) and bipolar disorder (BD). In particular, deficits in executive functioning may hamper everyday functioning. Identifying the neural substrates of impaired executive functioning would improve our understanding of the pathophysiology underlying these disorders, and may eventually aid in discriminating between MDD and BD, which is often difficult during depression and remission. To date, mostly medicated MDD and BD subjects have been investigated, which may have influenced results. Therefore, we investigated executive functioning in medication-free depressed and remitted MDD and BD subjects.

We used the Tower of London (ToL) visuospatial planning task to assess behavioural performance and blood oxygen-level dependent responses in 35 healthy controls, 21 remitted MDD, 23 remitted BD, 19 depressed MDD and nine depressed BD subjects.

Visuospatial planning per se was associated with increased frontostriatal activity in depressed BD compared to depressed MDD. In addition, post-hoc analyses indicated that visuospatial planning load was associated with increased parietal activity in depressed compared to remitted subjects, and BD compared to MDD subjects. Task performance did not significantly differ between groups.

More severely affected, medication-free mood disorder patients require greater parietal activity to perform in visuospatial planning, which may be compensatory to maintain relatively normal performance. State-dependent frontostriatal hyperactivity during planning may be a specific BD characteristic, providing clues for further characterization of differential pathophysiology in MDD v. BD. This could potentially provide a biomarker to aid in the differentiation of these disorders.

There is little knowledge about the psychosocial distress of children affected by human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS) in Ghana, to aid the planning of services. This study investigated mental health problems among children affected by HIV/AIDS, compared with control groups of children orphaned by other causes, and non-orphans.

The study employed a cross-sectional survey that interviewed 291 children and their caregivers. Both children and caregivers completed the Strengths and Difficulties Questionnaire that measured children's psychosocial wellbeing. Verbal autopsy was used to identify whether children lost one or both parents from AIDS.

The results indicated that controlling for relevant sociodemographic factors, both children's self-reports and caregivers’ reports indicate that both children living with HIV/AIDS-infected caregivers and children orphaned by AIDS were at heightened risk for mental health problems than both children orphaned by other causes and non-orphans. The findings further indicated that a significant proportion of orphaned and vulnerable children exhibited symptoms for depression and other psychiatric disorders (approximately 63%) compared with 7% among the non-orphaned group. Caregivers gave higher ratings for children on externalizing problems and lower on internalizing problems, and vice versa when the children's self-reports were analysed.

The findings suggest that both children and their informants have diverse yet complementary perspectives on psychological outcomes. The study discusses the theoretical and practical implications of these findings and urgently calls for necessary intervention programmes that target all children affected by HIV/AIDS to effectively alleviate psychological distress and enhance the mental health of these children.

Depressive and anxiety disorders are associated with shorter leukocyte telomere length (LTL), an indicator of cellular aging. It is, however, unknown which pathways underlie this association. This study examined the extent to which lifestyle factors and physiological changes such as inflammatory or metabolic alterations mediate the relationship.

We applied mediation analysis techniques to data from 2750 participants of the Netherlands Study of Depression and Anxiety. LTL was assessed using quantitative polymerase chain reaction. Independent variables were current depressive (30-item Inventory of Depressive Symptoms – Self Report) and anxiety (21-item Beck's Anxiety Inventory) symptoms and presence of a depressive or anxiety disorder diagnosis based on DSM-IV; mediator variables included physiological stress systems, metabolic syndrome components and lifestyle factors.

Short LTL was associated with higher symptom severity (B = −2.4, p = 0.002) and current psychiatric diagnosis (B = −63.3, p = 0.024). C-reactive protein, interleukin-6, waist circumference, triglycerides, high-density lipoprotein cholesterol and cigarette smoking were significant mediators in the relationship between psychopathology and LTL. When all significant mediators were included in one model, the effect sizes of the relationships between LTL and symptom severity and current diagnosis were reduced by 36.7 and 32.7%, respectively, and the remaining direct effects were no longer significant.

Pro-inflammatory cytokines, metabolic alterations and cigarette smoking are important mediators of the association between depressive and anxiety disorders and LTL. This calls for future research on intervention programs that take into account lifestyle changes in mental health care settings.

Previous neuroimaging studies indicate abnormalities in cortico-limbic circuitry in mood disorder. Here we employ prospective longitudinal voxel-based morphometry to examine the trajectory of these abnormalities during early stages of illness development.

Unaffected individuals (16–25 years) at high and low familial risk of mood disorder underwent structural brain imaging on two occasions 2 years apart. Further clinical assessment was conducted 2 years after the second scan (time 3). Clinical outcome data at time 3 was used to categorize individuals: (i) healthy controls (‘low risk’, n = 48); (ii) high-risk individuals who remained well (HR well, n = 53); and (iii) high-risk individuals who developed a major depressive disorder (HR MDD, n = 30). Groups were compared using longitudinal voxel-based morphometry. We also examined whether progress to illness was associated with changes in other potential risk markers (personality traits, symptoms scores and baseline measures of childhood trauma), and whether any changes in brain structure could be indexed using these measures.

Significant decreases in right amygdala grey matter were found in HR MDD v. controls (p = 0.001) and v. HR well (p = 0.005). This structural change was not related to measures of childhood trauma, symptom severity or measures of sub-diagnostic anxiety, neuroticism or extraversion, although cross-sectionally these measures significantly differentiated the groups at baseline.

These longitudinal findings implicate structural amygdala changes in the neurobiology of mood disorder. They also provide a potential biomarker for risk stratification capturing additional information beyond clinically ascertained measures.

When children have marked problems with motor coordination, they often have problems with attention and impulse control. Here, we map the neuroanatomic substrate of motor coordination in childhood and ask whether this substrate differs in the presence of concurrent symptoms of attention-deficit/hyperactivity disorder (ADHD).

Participants were 226 children. All completed Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5)-based assessment of ADHD symptoms and standardized tests of motor coordination skills assessing aiming/catching, manual dexterity and balance. Symptoms of developmental coordination disorder (DCD) were determined using parental questionnaires. Using 3 Tesla magnetic resonance data, four latent neuroanatomic variables (for the cerebral cortex, cerebellum, basal ganglia and thalamus) were extracted and mapped onto each motor coordination skill using partial least squares pathway modeling.

The motor coordination skill of aiming/catching was significantly linked to latent variables for both the cerebral cortex (t = 4.31, p < 0.0001) and the cerebellum (t = 2.31, p = 0.02). This effect was driven by the premotor/motor cortical regions and the superior cerebellar lobules. These links were not moderated by the severity of symptoms of inattention, hyperactivity and impulsivity. In categorical analyses, the DCD group showed atypical reduction in the volumes of these regions. However, the group with DCD alone did not differ significantly from those with DCD and co-morbid ADHD.

The superior cerebellar lobules and the premotor/motor cortex emerged as pivotal neural substrates of motor coordination in children. The dimensions of these motor coordination regions did not differ significantly between those who had DCD, with or without co-morbid ADHD.

An association between low levels of physical activity and impaired cognitive performance in schizophrenia has been proposed, but most studies have relied on self-report measures of activity. This study examined the association between actigraphy-derived physical activity and cognitive performance adjusting for multiple covariates in patients with schizophrenia.

Patients with schizophrenia (n = 199) were recruited from chronic psychiatric wards, and 60 age-, sex- and body mass index-matched comparison participants were recruited from the staff of two hospitals and universities. Physical activity was assessed objectively for 7 days using an ActiGraph. Cognitive performance was assessed with the Cognitrone test from the Vienna Test System and the Grooved Pegboard Test. Demographic variables, metabolic parameters, positive and negative symptoms, duration of illness and hospitalization, and medication use were included as covariates. Pearson correlations and multivariable linear regressions were conducted to examine the associations between physical activity levels and cognitive performance.

Patients with schizophrenia were less physically active and had poorer performance on attention/concentration and speed of processing than the comparison group. Patients with schizophrenia who spent more time in light physical activity showed better performance on attention/concentration (β = 0.198, p = 0.020) and speed of processing (β= −0.169, p = 0.048) tasks than those who were less active. Cognitive performance was also associated with moderate-vigorous physical activity, but the effect was no longer significant once light physical activity had been taken into account.

This study provides evidence for a positive association between objectively measured light physical activity and cognitive performance in people with schizophrenia, after adjustment for multiple confounders.

White matter (WM) impairments have been reported in patients with bipolar disorder (BD) and those at high familial risk of developing BD. However, the distribution of these impairments has not been well characterized. Few studies have examined WM integrity in young people early in the course of illness and in individuals at familial risk who have not yet passed the peak age of onset.

WM integrity was examined in 63 BD subjects, 150 high-risk (HR) individuals and 111 participants with no family history of mental illness (CON). All subjects were aged 12 to 30 years.

This young BD group had significantly lower fractional anisotropy within the genu of the corpus callosum (CC) compared with the CON and HR groups. Moreover, the abnormality in the genu of the CC was also present in HR participants with recurrent major depressive disorder (MDD) (n = 16) compared with CON participants.

Our findings provide important validation of interhemispheric abnormalities in BD patients. The novel finding in HR subjects with recurrent MDD – a group at particular risk of future hypo/manic episodes – suggests that this may potentially represent a trait marker for BD, though this will need to be confirmed in longitudinal follow-up studies.

Adults with major depressive disorder (MDD) demonstrate increased susceptibility to interfering effects of anxiety on cognitive control; although under certain conditions adults with MDD are able to compensate for these effects. The brain mechanisms that may facilitate the ability to compensate for anxiety either via the recruitment of additional cognitive resources or via the regulation of interference from anxiety remain largely unknown. To clarify these mechanisms, we examined the effects of anxiety on brain activity and amygdala–prefrontal functional connectivity in adults diagnosed with MDD.

A total of 22 unmedicated adults with MDD and 18 healthy controls (HCs) performed the Tower of London task under conditions designed to induce anxiety, while undergoing a functional magnetic resonance imaging assessment.

During the easy condition, the MDD group demonstrated equivalent planning accuracy, longer planning times, elevated amygdala activity and left rostrolateral prefrontal cortex (RLPFC) hyperactivity relative to HCs. Anxiety mediated observed group differences in planning times, as well as differences in amygdala activation, which subsequently mediated observed differences in RLPFC activation. During the easy condition, the MDD group also demonstrated increased negative amygdala–dorsolateral prefrontal cortex (DLPFC) connectivity which correlated with improved planning accuracy. During the hard condition, HCs demonstrated greater DLPFC activation and stronger negative amygdala–DLPFC connectivity, which was unrelated to planning accuracy.

Our results suggest that persons with MDD compensate for anxiety-related limbic activation during low-load cognitive tasks by recruiting additional RLPFC activation and through increased inhibitory amygdala–DLPFC communication. Targeting these neural mechanisms directly may improve cognitive functioning in MDD.

In patients with psychotic disorders, the effects of psychological post-traumatic stress disorder (PTSD) treatment on symptoms of psychosis, depression and social functioning are largely unknown

In a single-blind randomized controlled trial (RCT) 155 outpatients in treatment for psychosis (61.3% schizophrenic disorder, 29% schizoaffective disorder) were randomized to eight sessions prolonged exposure (PE; n = 53) or eye movement desensitization and reprocessing (EMDR) (n = 55), or a waiting-list condition (WL, n = 47) for treatment of their co-morbid PTSD. Measures were performed on (1) psychosis: severity of delusions (PSYRATS-DRS), paranoid thoughts (GPTS), auditory verbal hallucinations (PSYRATS-AHRS), and remission from psychotic disorder (SCI-SR-PANSS); (2) depression (BDI-II); (3) social functioning (PSP). Outcomes were compared at baseline, post-treatment, 6-month follow-up and over all data points.

Both PE and EMDR were significantly associated with less severe paranoid thoughts post-treatment and at 6-month follow-up, and with more patients remitting from schizophrenia, at post-treatment (PE and EMDR) and over time (PE). Moreover, PE was significantly associated with a greater reduction of depression at post-treatment and at 6-month follow-up. Auditory verbal hallucinations and social functioning remained unchanged.

In patients with chronic psychotic disorders PE and EMDR not only reduced PTSD symptoms, but also paranoid thoughts. Importantly, in PE and EMDR more patients accomplished the status of their psychotic disorder in remission. Clinically, these effects are highly relevant and provide empirical support to the notion that delivering PTSD treatment to patients with psychotic disorders and PTSD deserves increasing recognition and acceptance among clinicians.

An increasing number of studies have investigated delay discounting (DD) in relation to obesity, but with mixed findings. This meta-analysis synthesized the literature on the relationship between monetary and food DD and obesity, with three objectives: (1) to characterize the relationship between DD and obesity in both case–control comparisons and continuous designs; (2) to examine potential moderators, including case–control v. continuous design, money v. food rewards, sample sex distribution, and sample age (<18 v. >18 years); and (3) to evaluate publication bias.

From 134 candidate articles, 39 independent investigations yielded 29 case–control and 30 continuous comparisons (total n = 10 278). Random-effects meta-analysis was conducted using Cohen's d as the effect size. Publication bias was evaluated using fail-safe N, Begg–Mazumdar and Egger tests, meta-regression of publication year and effect size, and imputation of missing studies.

The primary analysis revealed a medium effect size across studies that was highly statistically significant (d = 0.43, p < 10−14). None of the moderators examined yielded statistically significant differences, although notably larger effect sizes were found for studies with case–control designs, food rewards and child/adolescent samples. Limited evidence of publication bias was present, although the Begg–Mazumdar test and meta-regression suggested a slightly diminishing effect size over time.

Steep DD of food and money appears to be a robust feature of obesity that is relatively consistent across the DD assessment methodologies and study designs examined. These findings are discussed in the context of research on DD in drug addiction, the neural bases of DD in obesity, and potential clinical applications.

Relapse is distressingly common after the first episode of psychosis, yet it is poorly understood and difficult to predict. Investigating changes in cognitive function preceding relapse may provide new insights into the underlying mechanism of relapse in psychosis. We hypothesized that relapse in fully remitted first-episode psychosis patients was preceded by working memory deterioration.

Visual memory and verbal working memory were monitored prospectively in a 1-year randomized controlled trial of remitted first-episode psychosis patients assigned to medication continuation (quetiapine 400 mg/day) or discontinuation (placebo). Relapse (recurrence of positive symptoms of psychosis), visual (Visual Patterns Test) and verbal (Letter–Number span test) working memory and stressful life events were assessed monthly.

Remitted first-episode patients (n = 102) participated in the study. Relapsers (n = 53) and non-relapsers (n = 49) had similar baseline demographic and clinical profiles. Logistic regression analyses indicated relapse was associated with visual working memory deterioration 2 months before relapse [odds ratio (OR) 3.07, 95% confidence interval (CI) 1.19–7.92, P = 0.02], more stressful life events 1 month before relapse (OR 2.11, 95% CI 1.20–3.72, P = 0.01) and medication discontinuation (OR 5.52, 95% CI 2.08–14.62, P = 0.001).

Visual working memory deterioration beginning 2 months before relapse in remitted first-episode psychosis patients (not baseline predictor) may reflect early brain dysfunction that heralds a psychotic relapse. The deterioration was found to be unrelated to a worsening of psychotic symptoms preceding relapse. Testable predictors offer insight into the brain processes underlying relapse in psychosis.