Individuals with autism spectrum disorders (ASDs) are characterized by social communication difficulties and behavioural rigidity. Difficulties in learning from others are one of the most devastating features of this group of conditions. Nevertheless, the nature of learning difficulties in ASDs is still unclear. Given the relevance of implicit learning for social and communicative functioning, a link has been hypothesized between ASDs and implicit learning deficit. However, studies that have employed formal testing of implicit learning in ASDs provided mixed results.

We undertook a systematic search of studies that examined implicit learning in ASDs using serial reaction time (SRT), alternating serial reaction time (ASRT), pursuit rotor (PR), and contextual cueing (CC) tasks, and synthesized the data using meta-analysis. A total of 11 studies were identified, representing data from 407 individuals with ASDs and typically developing comparison participants.

The results indicate that individuals with ASDs do not differ in any task considered [SRT and ASRT task: standardized mean difference (SMD) −0.18, 95% confidence interval (CI) −0.71 to 0.36; PR task: SMD −0.34, 95% CI −1.04 to 0.36; CC task: SMD 0.27, 95% CI −0.07 to 0.60].

Based on our synthesis of the existing literature, we conclude that individuals with ASDs can learn implicitly, supporting the hypothesis that implicit learning deficits do not represent a core feature in ASDs.

Suicide and self-harm are prevalent in individuals diagnosed with psychotic disorders. However, less is known about the level of self-injurious thinking and behaviour in those individuals deemed to be at ultra-high risk (UHR) of developing psychosis, despite growing clinical interest in this population. This review provides a synthesis of the extant literature concerning the prevalence of self-harm and suicidality in the UHR population, and the predictors and correlates associated with these events.

A search of electronic databases was undertaken by two independent reviewers. A meta-analysis of prevalence was undertaken for self-harm, suicidal ideation and behaviour. A narrative review was also undertaken of analyses examining predictors and correlates of self-harm and suicidality.

Twenty-one eligible studies were identified. The meta-analyses suggested a high prevalence of recent suicidal ideation (66%), lifetime self-harm (49%) and lifetime suicide attempts (18%). Co-morbid psychiatric problems, mood variability and a family history of psychiatric problems were among the factors associated with self-harm and suicide risk.

Results suggest that self-harm and suicidality are highly prevalent in the UHR population, with rates similar to those observed in samples with diagnosed psychotic disorders. Appropriate monitoring and managing of suicide risk will be important for services working with the UHR population. Further research in this area is urgently needed considering the high rates identified.

Compassion-focused therapy (CFT) is a relatively novel form of psychotherapy that was developed for people who have mental health problems primarily linked to high shame and self-criticism. The aim of this early systematic review was to draw together the current research evidence of the effectiveness of CFT as a psychotherapeutic intervention, and to provide recommendations that may inform the development of further trials.

A comprehensive search of electronic databases was undertaken to systematically identify literature relating to the effectiveness of CFT as a psychotherapeutic intervention. Reference lists of key journals were hand searched and contact with experts in the field was made to identify unpublished data.

Fourteen studies were included in the review, including three randomized controlled studies. The findings from the included studies were, in the most part, favourable to CFT, and in particular seemed to be effective for people who were high in self-criticism.

CFT shows promise as an intervention for mood disorders, particularly those high in self-criticism. However, more large-scale, high-quality trials are needed before it can be considered evidence-based practice. The review highlights issues from the current evidence that may be used to inform such trials.

Schizotypy is a complex concept, commonly defined as a genetic vulnerability to schizophrenia that falls on a continuum between healthy variation and severe mental illness. There is a growing body of evidence supporting an association between childhood trauma and increased psychotic experiences and disorders. However, the evidence as to whether there is a similar association with schizotypy has yet to be systematically synthesized and assessed.

We conducted a systematic search of published articles on the association between childhood trauma and schizotypy in four major databases. The search covered articles from 1806 to 1 March 2013 and resulted in 17 003 articles in total. Twenty-five original research studies met the eligibility criteria and were included in this review.

All 25 studies supported the association between at least one type of trauma and schizotypy, with odds ratios (ORs) ranging between 2.01 and 4.15. There was evidence supporting the association for all types of trauma, with no differential effects. However, there was some variability in the quality of the studies, with most using cross-sectional designs. Individuals who reported adverse experiences in childhood scored significantly higher on positive and negative/disorganized schizotypy compared to those who did not report such experiences.

All forms of childhood trauma and other stressful events (e.g. bullying) were found to be associated with schizotypy, with especially strong associations with positive schizotypy. However, because of the methodological limitations of several studies and a lack of further exploration of different possible mechanistic pathways underlying this association, more research is required.

Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are two common childhood disorders that exhibit genetic and behavioural overlap and have abnormalities in similar brain systems, in particular in frontal and cerebellar regions. This study compared the two neurodevelopmental disorders to investigate shared and disorder-specific structural brain abnormalities.

Forty-four predominantly medication-naïve male adolescents with ADHD, 19 medication-naïve male adolescents with ASD and 33 age-matched healthy male controls were scanned using high-resolution T1-weighted volumetric imaging in a 3-T magnetic resonance imaging (MRI) scanner. Voxel-based morphometry (VBM) was used to test for group-level differences in structural grey matter (GM) and white matter (WM) volumes.

There was a significant group difference in the GM of the right posterior cerebellum and left middle/superior temporal gyrus (MTG/STG). Post-hoc analyses revealed that this was due to ADHD boys having a significantly smaller right posterior cerebellar GM volume compared to healthy controls and ASD boys, who did not differ from each other. ASD boys had a larger left MTG/STG GM volume relative to healthy controls and at a more lenient threshold relative to ADHD boys.

The study shows for the first time that the GM reduction in the cerebellum in ADHD is disorder specific relative to ASD whereas GM enlargement in the MTG/STG in ASD may be disorder specific relative to ADHD. This study is a first step towards elucidating disorder-specific structural biomarkers for these two related childhood disorders.

Although the association between attention-deficit/hyperactivity disorder (ADHD) and drug use disorder (DUD) is well documented, it is unclear whether it is causal or results from familial confounding.

In this study we included all 551 164 individuals born in Sweden between 1991 and 1995 and used linked data from multiple nationwide registries to identify those with ADHD prior to age 15 years (1.71%). We used Cox proportional hazards models to investigate the future risk for DUD as a function of an ADHD registration and then compared the results from the entire population with the results from a co-relative design. Using the Swedish Multi-Generation Register, we identified all full-sibling, half-sibling and first-cousin pairs discordant for ADHD.

In the population sample, ADHD had a substantially increased risk for future DUD with a hazard ratio (HR) of 3.34 after accounting for gender and parental education. Examining discordant cousin pairs, discordant half-siblings and discordant siblings, those with ADHD had HRs for DUD of 3.09, 2.10 and 2.38 respectively. Controlling for the number of ADHD registrations, ADHD patients with and without stimulant treatment were similarly associated with later DUD risk.

ADHD diagnosed before 15 years of age was strongly related to future risk for DUD. The magnitude of this association was modestly reduced in relative pairs discordant for ADHD, suggesting that the ADHD–DUD association is partly causal and partly a result of familial confounding. We found no evidence to suggest that this association resulted from stimulant treatment.

Late preterm births constitute the majority of preterm births. However, most evidence suggesting that preterm birth predicts the risk of mental disorders comes from studies on earlier preterm births. We examined if late preterm birth predicts the risks of severe mental disorders from early to late adulthood. We also studied whether adulthood mental disorders are associated with post-term birth or with being born small (SGA) or large (LGA) for gestational age, which have been previously associated with psychopathology risk in younger ages.

Of 12 597 Helsinki Birth Cohort Study participants, born 1934–1944, 664 were born late preterm, 1221 post-term, 287 SGA, and 301 LGA. The diagnoses of mental disorders were identified from national hospital discharge and cause of death registers from 1969 to 2010. In total, 1660 (13.2%) participants had severe mental disorders.

Individuals born late preterm did not differ from term-born individuals in their risk of any severe mental disorder. However, men born late preterm had a significantly increased risk of suicide. Post-term birth predicted significantly increased risks of any mental disorder in general and particularly of substance use and anxiety disorders. Individuals born SGA had significantly increased risks of any mental and substance use disorders. Women born LGA had an increased risk of psychotic disorders.

Although men born late preterm had an increased suicide risk, late preterm birth did not exert widespread effects on adult psychopathology. In contrast, the risks of severe mental disorders across adulthood were increased among individuals born SGA and individuals born post-term.

The amygdala and subgenual anterior cingulate cortex (sACC) are key brain regions for the generation of negative affect. In this longitudinal fMRI study of adolescents we investigated how amygdala–sACC connectivity was correlated with negative affectivity (NA) both cross-sectionally and longitudinally, and examined its relationship to the onset of first-episode depression.

Fifty-six adolescents who were part of a larger longitudinal study of adolescent development were included. They had no history of mental illness at the time of their baseline scan (mean age 16.5 years) and had a follow-up scan 2 years later (mean age 18.8 years). We used resting-state functional-connectivity MRI to investigate whether cross-sectional and change measures of amygdala–sACC connectivity were (i) correlated with NA and its change over time, and (ii) related to the onset of first-episode depression.

The magnitude of amygdala connectivity with sACC showed significant positive correlation with NA at both time-points. Further analysis confirmed that change in amygdala–sACC connectivity between assessments was correlated with change in NA. Eight participants developed a first episode of depression between the baseline and follow-up assessments: they showed increased amygdala–sACC connectivity at follow-up.

Amygdala–sACC connectivity is associated with NA in adolescence, with change in connectivity between these regions showing positive correlation with change in NA. Our observation that the onset of depression was associated with an increase in connectivity between the regions provides support for the neurobiological ‘scar’ hypothesis of depression.

Military training is a chronic stressful period that often induces stress-related psychopathology. Stress vulnerability and resilience depend on personality trait anxiety, attentional threat bias and prefrontal–limbic dysfunction. However, how these neurobehavioral elements interact with regard to the development of symptoms following stress remains unclear.

Fifty-five healthy combat soldiers undergoing intensive military training completed functional magnetic resonance imaging (fMRI) testing while performing the dot-probe task (DPT) composed of angry (threat) and neutral faces. Participants were then stratified according to their bias tendency to avoidance (n = 25) or vigilance (n = 30) groups, categorized as high or low trait anxiety and assessed for post-stress symptom severity.

Avoidance compared to vigilance tendency was associated with fewer post-trauma symptoms and increased hippocampal response to threat among high anxious but not low anxious individuals. Importantly, mediation analysis revealed that only among high anxious individuals did hippocampal activity lead to lower levels of symptoms through avoidance bias tendency. However, in the whole group, avoidance bias was modulated by the interplay between the hippocampus and the dorsal anterior cingulate cortex (dACC).

Our results provide a neurobehavioral model to explain the resilience to post-trauma symptoms following chronic exposure. The model points to the importance of considering threat bias tendency in addition to personality traits when investigating the brain response and symptoms of trauma. Such a multi-parametric approach that accounts for individual behavioral sensitivities may also improve brain-driven treatments of anxiety, possibly by targeting the interplay between the hippocampus and the dACC.

The aetiological pathways to borderline personality disorder (BPD) remain only partly elucidated. Retrospective research indicates that prenatal adversity may be an important early risk factor in the development of BPD. This requires corroboration with prospective longitudinal studies.

A community sample of 6050 mothers and their children (born between April 1991 and December 1992) were assessed. Maternal anxiety and depression and maternal alcohol and tobacco consumption were assessed during pregnancy (18 and 32 weeks gestation). Postnatal risks, including maladaptive parenting (suboptimal parenting and parent conflict), family adversity, maternal anxiety and depression and maternal alcohol and tobacco consumption, were assessed during early childhood. Internalizing and externalizing symptoms were assessed in late childhood. Trained psychologists interviewed children in late childhood to ascertain the presence of BPD (at least five probable/definite symptoms).

In unadjusted analyses, all prenatal risk factors (i.e. maternal alcohol and tobacco consumption and maternal anxiety and depression) were significantly associated with BPD. Following adjustment for sex, birthweight and postnatal exposure to anxiety and depression respectively, maladaptive parenting, family adversity and child's internalizing and externalizing symptoms, prenatal anxiety at 18 weeks gestation [odds ratio (OR) 1.57, 95% confidence interval (CI) 1.18–2.09] and depression at 18 weeks (OR 1.59, 95% CI 1.08–2.32) and 32 weeks (OR 1.57, 95% CI 1.14–2.18) gestation remained significantly associated with BPD.

This study provides prospective evidence of associations between prenatal adversities and BPD at 11–12 years. Prenatal anxiety and depression were independently associated with BPD, suggesting that they may exert direct effects on BPD during the prenatal period. This highlights the importance of programmes to reduce maternal stress during pregnancy.

The influence of genetic factors on major depressive disorder is lower than on other psychiatric disorders. Heritability estimates mainly derive from cross-sectional studies, and knowledge on the longitudinal aetiology of symptoms of anxiety and depression (SxAnxDep) across the lifespan is limited. We aimed to assess phenotypic, genetic and environmental stability in SxAnxDep between ages 3 and 63 years.

We used a cohort-sequential design combining data from 49 524 twins followed from birth to age ⩾20 years, and from adolescence into adulthood. SxAnxDep were assessed repeatedly with a maximum of eight assessments over a 25-year period. Data were ordered in 30 age groups and analysed with longitudinal genetic models.

Over age, there was a significant increase during adolescence in mean scores with sex differences (women>men) emerging. Heritability was high in childhood and decreased to 30–40% during adulthood. This decrease in heritability was due to an increase in environmental variance. Phenotypic stability was moderate in children (correlations across ages ~0.5) and high in adolescents (r = 0.6), young adults (r = 0.7), and adults (r = 0.8). Longitudinal stability was mostly attributable to genetic factors. During childhood and adolescence there was also significant genetic innovation, which was absent in adults. Environmental effects contributed to short-term stability.

The substantial stability in SxAnxDep is mainly due to genetic effects. The importance of environmental effects increases with age and explains the relatively low heritability of depression in adults. The environmental effects are transient, but the contribution to stability increases with age.

To investigate trajectories of cognitive decline in patients with different types of dementia compared to controls in a longitudinal study.

In 199 patients with Alzheimer's disease (AD), 10 with vascular dementia (VaD), 26 with dementia with Lewy bodies (DLB), 20 with behavioural variant frontotemporal dementia (bvFTD), 15 with language variant frontotemporal dementia (lvFTD) and 112 controls we assessed five cognitive domains: memory, language, attention, executive and visuospatial functioning, and global cognition (Mini-Mental State Examination, MMSE). All subjects had at least two neuropsychological assessments (median 2, range 2–7). Neuropsychological data were standardized into z scores using baseline performance of controls as reference. Linear mixed models (LMMs) were used to estimate baseline cognitive functioning and cognitive decline over time for each group, adjusted for age, gender and education.

At baseline, patients with dementia performed worse than controls in all cognitive domains (p < 0.05) except visuospatial functioning, which was only impaired in patients with AD and DLB (p < 0.001). During follow-up, patients with AD declined in all cognitive domains (p < 0.001). DLB showed decline in every cognitive domain except language and global cognition. bvFTD showed rapid decline in memory, language, attention and executive functioning (all p < 0.01) whereas visuospatial functioning remained fairly stable. lvFTD declined mostly in attention and executive functioning (p < 0.01). VaD showed decline in attention and executive functioning.

We show cognitive trajectories of different types of dementia. These estimations of natural disease course have important value for the design of clinical trials as neuropsychological measures are increasingly being used as outcome measures.

To clarify the role of genetic and environmental risk factors in alcohol use disorders (AUDs), we performed a meta-analysis of twin and adoption studies and explored the impact of sex, assessment method (interview v. hospital/population records), and study design (twin v. adoption study) on heritability estimates.

The literature was searched for all unique twin and adoption studies of AUD and identified 12 twin and five adoption studies. The data were then reconstructed and analyzed using ordinal data full information maximum likelihood in the OpenMx program. Heterogeneity was tested with likelihood ratio tests by equating the parameters across studies.

There was no evidence for heterogeneity by study design, sex or assessment method. The best-fit estimate of the heritability of AUD was 0.49 [95% confidence interval (CI) 0.43–0.53], and the proportion of shared environmental variance was 0.10 (95% CI 0.03–0.16). Estimates of unique environmental proportions of variance differed significantly across studies.

AUD is approximately 50% heritable. The multiple genetically informative studies of this syndrome have produced consistent results that support the validity of this heritability estimate, especially given the different potential methodological weaknesses of twin and adoption designs, and of assessments of AUD based on personal interviews v. official records. We also found evidence for modest shared environmental effects suggesting that environmental factors also contribute to the familial aggregation of AUDs.

Magnetic seizure therapy (MST), despite being in an early phase of clinical research, has been demonstrated to be associated with antidepressant efficacy. However, safety, tolerability and efficacy data in connection with functional brain activity from larger samples are lacking. The aim of this study was to determine clinical and cognitive effects of MST and the influence of MST on regional brain glucose metabolism.

Twenty-six patients suffering from treatment-resistant depression (TRD) underwent MST. Ten patients underwent a randomized trial and 16 patients an open-label study design. The primary outcome criterion was the severity of depressive symptoms assessed with the Hamilton Depression Rating Scale (HAMD). Depressive symptoms, tolerability and cognitive safety, along with social functioning and quality of life parameters, were assessed using various rating scales. A clinical follow-up visit 6 months following the completion of a course of MST and [18F]-fluorodeoxyglucose positron emission tomography (FDG-PET) scans of 12 patients were analysed.

A significant response to MST was demonstrated by 69% of the patient sample, with 46% meeting remission criteria. Anxiety ratings were significantly reduced in responders and their quality of life was improved. Half of the responders relapsed within 6 months. No cognitive side-effects were observed. FDG-PET scans showed a metabolic increase in the frontal cortex bilaterally and a decrease in the left striatum.

Robust antidepressant and anti-anxiety efficacy of MST was demonstrated, and found to be associated with localized metabolic changes in brain areas that are strongly implicated in depression. Thus, MST presents an effective, well-tolerated and safe treatment option for patients unable to respond to other forms of therapy for depression.

While children of parents with criminal behavior (CB) are at increased risk for CB, we have limited knowledge about the causes of this cross-generational transmission.

We examined intergenerational continuity in CB in the Swedish population ascertained from the national conviction registers in three family types: intact (n = 21 11 074), ‘not-lived-with’ (n = 16 53 15 where biological parents never lived with their offspring) and ‘step’ (n = 1 24 800 offspring) which reflected, respectively, the effects of genes + rearing, genes only and rearing only. We also examined three criminal conviction subtypes: violent CB (VCB), property CB (PCB) and white-collar CB (WCCB).

Combined across mothers and fathers, the hazard ratio (HR) for CB in offspring given parental CB was 1.95 in intact, 1.56 in ‘not-lived-with’ and 1.28 in stepfamilies. In all three family types, all forms of CB in parents (VCB, PCB and WCCB) significantly predicted risk for all forms of CB in offspring. However, VCB in offspring was most strongly predicted by VCB in parents in intact, not-lived-with and stepfamilies. In intact families only, some specific parent–offspring transmission was also seen for WCCB.

Both genetic and environmental factors contribute substantially to parent–offspring resemblance for CB. With respect to criminal subtypes, much of parent–offspring transmission appears to be non-specific. However, specific genetic and environmental risk factors for VCB are transmitted across generations. A limitation of these analyses is that CB was assessed only via official criminal convictions.

Co-morbidity among use of different substances can be explained by a shared underlying dimensional factor. What remains unknown is whether the relationship between substance use and various co-morbid mental disorders can be explained solely by the general factor or whether there remain unique contributions of specific substances.

Data were from the 2007 Australian National Survey of Mental Health and Wellbeing (NSMHWB). A unidimensional latent factor was constructed that represented general substance use. The shared and specific relationships between lifetime substance use indicators and internalizing disorders, suicidality and psychotic-like experiences (PLEs) were examined using Multiple Indicators Multiple Causes (MIMIC) models in the total sample. Additional analyses then examined the shared and specific relationships associated with substance dependence diagnoses as indicators of the latent trait focusing on a subsample of substance users.

General levels of latent substance use were significantly and positively related to internalizing disorders, suicidality and psychotic-like experiences. Similar results were found when examining general levels of latent substance dependence in a sample of substance users. There were several direct effects between specific substance use/dependence indicators and the mental health correlates that significantly improved the overall model fit but they were small in magnitude and had relatively little impact on the general relationship.

The majority of pairwise co-morbid relationships between substance use/dependence and mental health correlates can be explained through a general latent factor. Researchers should focus on investigating the commonalities across all substance use and dependence indicators when studying mental health co-morbidity.