Multiple studies have found a reduced reward positivity (RewP) among individuals with major depressive disorder (MDD). Event-related potential studies have also reported blunted neural responses to pleasant pictures in MDD as reflected by the late positive potential (LPP). These deficits have been interpreted broadly in terms of anhedonia and decreased emotional engagement characteristic of depression.

In the current study, a community-based sample of 83 participants with current MDD and 45 healthy individuals performed both a guessing task and a picture viewing paradigm with neutral and pleasant pictures to assess the RewP and the LPP, respectively.

We found that both RewP and LPP to pleasant pictures were reduced in the MDD group; moreover, RewP and LPP were both independent predictors of MDD status. Within the MDD group, a smaller RewP predicted impaired mood reactivity in younger but not older participants. Smaller LPP amplitudes were associated with increased anhedonia severity in the MDD group.

These data replicate and merge separate previous lines of research, and suggest that a blunted RewP and LPP reflect independent neural deficits in MDD – which could be used in conjunction to improve the classification of depression.

There is controversy over the extent to which the new International Classification of Diseases (ICD-11) diagnosis of complex posttraumatic stress disorder (CPTSD) is distinct from posttraumatic stress disorder (PTSD). This study aimed to conduct the first investigation of distinctive neural processes during threat processing in CPTSD relative to PTSD.

This cross-sectional functional magnetic resonance study included 99 participants who met criteria for PTSD (PTSD = 32, CPTSD = 28) and 39 trauma-exposed controls. PTSD was assessed with the Clinician-Administered PTSD Scale (CAPS). CPTSD was assessed with an adapted version of the International Trauma Questionnaire. Neural responses were measured across the brain while threat or neutral faces were presented at both supraliminal and subliminal levels.

During supraliminal presentations of threat stimuli, there was greater bilateral insula and right amygdala activation in CPTSD participants relative to PTSD. Reduced supraliminal right dorsolateral prefrontal cortex activation and increased subliminal amygdala and insula activation were observed as common dysfunction for both CPTSD and PTSD groups relative to trauma controls. There were no significant differences in terms of subliminal presentations and no differences in functional connectivity. Dissociative responses were positively associated with right insula activation (r = 0.347, p < 0.01).

These results provide the first evidence of distinct neural profiles of CPTSD and PTSD during threat processing. The observation of increased insula and right amygdala activation in CPTSD accords with the proposal that CPTSD is distinguished from PTSD by disturbances in emotion regulation and self-concept.

Executive dysfunction is one of the main cognitive theories of autism spectrum disorder (ASD). Despite evidence of deficits in executive functions in individuals with ASD, little is known about executive dysfunctions as candidate cognitive endophenotypes for ASD. In this study, we investigated executive functions in youths with ASD, their unaffected siblings and typically developing controls (TDC).

We recruited 240 youths with a clinical diagnosis of ASD (aged 6–18 years), 147 unaffected siblings of ASD youths, and 240 TDC youths. TDC youths were recruited based on the age and sex distribution of the ASD youths. Participants were assessed using the verbal Digit Span test and four executive function tasks from the Cambridge Neuropsychological Test Automated Battery, including Intra-dimensional/Extra-dimensional Shift (I/ED), Spatial Span (SSP), Spatial Working Memory (SWM), and Stocking of Cambridge (SoC).

ASD youths, relative to TDC, performed significantly worse in executive function tasks assessing verbal working memory (forward and backward digit span), set-shifting (I/ED), visuospatial working memory (SSP, SWM), and planning/problem solving (SoC). Furthermore, unaffected siblings, relative to TDC, performed worse in forward and backward digit recalls and made more errors in SWM. These results were independent of the effects of age, sex, IQ, and symptoms of attention-deficit/hyperactivity disorder.

Our findings support impaired executive functions in youths with ASD. However, unaffected siblings were mostly unimpaired except in the areas of verbal and spatial working memory, which may be potential cognitive endophenotypes for ASD.

Maternal depression is negatively associated with cognitive development across childhood and adolescence, with mixed evidence on whether this association differs in boys and girls. Herein, we performed a systematic review and meta-analysis of sex-specific estimates of the association between maternal depression and offspring cognitive outcomes.

Seven databases (PubMed, EMBASE, PsycINFO, ERIC, CINAHL, Scopus, ProQuest) were searched for studies examining the longitudinal association between maternal depression and offspring (up to 18 years) cognitive outcomes. Studies were screened and included based on predetermined criteria by two independent reviewers (Cohen's κ = 0.76). We used random-effects models to conduct a meta-analysis and used meta-regression for subgroup analyses. The PROSPERO record for the study is CRD42020161001.

Twelve studies met inclusion criteria. Maternal depression was associated with poorer cognitive outcomes in boys [Hedges’ g = –0.36 (95% CI −0.60 to −0.11)], but not in girls [−0.17 (–0.41 to 0.07)]. The association in boys varied as a function of the measure of depression used (b = –0.70, p = 0.005): when maternal depression was assessed via a diagnostic interview, boys [−0.84 (–1.23 to −0.44)] had poorer cognitive outcomes than when a rating scale was used [−0.16 (–0.36 to 0.04)].

This review and meta-analysis indicates that maternal depression is only significantly associated with cognitive outcomes in boys. Understanding the role of sex differences in the underlying mechanisms of this association can inform the development of targeted interventions to mitigate the negative effects of maternal depression on offspring cognitive outcomes.

Consistent with pathophysiological models of psychosis, temporal disturbances in schizophrenia spectrum populations may reflect abnormal cortical (e.g. prefrontal cortex) and subcortical (e.g. striatum) cerebellar connectivity. However, few studies have examined associations between cerebellar connectivity and timing dysfunction in psychosis populations, and none have been conducted in youth at clinical high-risk (CHR) for psychosis. Thus, it is currently unknown if impairments in temporal processes are present in CHR youth or how they may be associated with cerebellar connectivity and worsening of symptoms.

A total of 108 (56 CHR/52 controls) youth were administered an auditory temporal bisection task along with a resting state imaging scan to examine cerebellar resting state connectivity. Positive and negative symptoms at baseline and 12 months later were also quantified.

Controlling for alcohol and cannabis use, CHR youth exhibited poorer temporal accuracy compared to controls, and temporal accuracy deficits were associated with abnormal connectivity between the bilateral anterior cerebellum and a right caudate/nucleus accumbens striatal cluster. Poor temporal accuracy accounted for 11% of the variance in worsening of negative symptoms over 12 months.

Behavioral findings suggest CHR youth perceive durations of auditory tones as shortened compared to objective time, which may indicate a slower internal clock. Poorer temporal accuracy in CHR youth was associated with abnormalities in brain regions involved in an important cerebellar network implicated in prominent pathophysiological models of psychosis. Lastly, temporal accuracy was associated with worsening of negative symptoms across 12 months, suggesting temporal dysfunction may be sensitive to illness progression.

Prolonged grief disorder (PGD) has recently been recognized as a separate psychiatric diagnosis, despite controversy over the extent to which it is distinctive from posttraumatic stress disorder (PTSD) and major depressive disorder (MDD).

This study investigated distinctive neural processes underpinning emotion processing in participants with PGD, PTSD, and MDD with functional magnetic resonance study of 117 participants that included PGD (n = 21), PTSD (n = 45), MDD (n = 26), and bereaved controls (BC) (n = 25). Neural responses were measured across the brain while sad, happy, or neutral faces were presented at both supraliminal and subliminal levels.

PGD had greater activation in the pregenual anterior cingulate cortex (pgACC), bilateral insula, bilateral dorsolateral prefrontal cortices and right caudate and also greater pgACC–right pallidum connectivity relative to BC during subliminal processing of happy faces. PGD was distinct relative to both PTSD and MDD groups with greater recruitment of the medial orbitofrontal cortex during supraliminal processing of sad faces. PGD were also distinct relative to MDD (but not PTSD) with greater activation in the left amygdala, caudate, and putamen during subliminal presentation of sad faces. There was no distinction between PGD, PTSD, and MDD during processing of happy faces.

These results provide initial evidence of distinct neural profiles of PGD relative to related psychopathological conditions, and highlight activation of neural regions implicated in reward networks. This pattern of findings validates current models of PGD that emphasize the roles of yearning and appetitive processes in PGD.

There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene–environment correlation.

The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0–17 years; ALSPAC) and at age 8 years (MoBa).

Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure.

Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment.

Performance monitoring entails rapid error detection to maintain task performance. Impaired performance monitoring is a candidate pathophysiological process in psychotic disorders, which may explain the broader deficit in executive function and its known associations with negative symptoms and poor functioning. The current study models cross-sectional pathways bridging neurophysiological measures of performance monitoring with executive function, symptoms, and functioning.

Data were from the 20-year assessment of the Suffolk County Mental Health Project. Individuals with psychotic disorders (N = 181) were originally recruited from inpatient psychiatric facilities. Data were also collected from a geographically and demographically matched group with no psychosis history (N = 242). Neural measures were the error-related negativity (ERN) and error positivity (Pe). Structural equation modeling tested mediation pathways.

Blunted ERN and Pe in the clinical cohort related to impaired executive function (r = 0.26–0.35), negative symptom severity (r = 0.17–0.25), and poor real-world functioning (r = 0.17–0.19). Associations with executive function were consistent across groups. Multiple potential pathways were identified in the clinical cohort: reduced ERN to inexpressivity was mediated by executive function (β = 0.10); reduced Pe to global functioning was mediated by executive function and avolition (β = 0.10).

This supports a transdiagnostic model of psychotic disorders by which poor performance monitoring contributes to impaired executive function, which contributes to negative symptoms and poor real-world functioning. If supported by future longitudinal research, these pathways could inform the development of targeted interventions to address cognitive and functional deficits that are central to psychotic disorders.

There is substantial variability in involuntary psychiatric admission rates across countries and sub-regions within countries that are not fully explained by patient-level factors. We sought to examine whether in a government-funded health care system, physician payments for filling forms related to an involuntary psychiatric hospitalization were associated with the likelihood of an involuntary admission.

This is a population-based, cross-sectional study in Ontario, Canada of all adult psychiatric inpatients in Ontario (2009–2015, n = 122 851). We examined the association between the proportion of standardized forms for involuntary admissions that were financially compensated and the odds of a patient being involuntarily admitted. We controlled for socio-demographic characteristics, clinical severity, past-health care system utilization and system resource factors.

Involuntary admission rates increased from the lowest (Q1, 70.8%) to the highest (Q5, 81.4%) emergency department (ED) quintiles of payment, with the odds of involuntary admission in Q5 being nearly significantly higher than the odds of involuntary admission in Q1 after adjustment (aOR 1.73, 95% CI 0.99–3.01). With payment proportion measured as a continuous variable, the odds of involuntary admission increased by 1.14 (95% CI 1.03–1.27) for each 10% absolute increase in the proportion of financially compensated forms at that ED.

We found that involuntary admission was more likely to occur at EDs with increasing likelihood of financial compensation for invoking involuntary status. This highlights the need to better understand how physician compensation relates to the ethical balance between the right to safety and autonomy for some of the world's most vulnerable patients.

The etiology of depression remains poorly understood. Changes in blood lipid levels were reported to be associated with depression and suicide, however study findings were mixed.

We performed a two-sample Mendelian randomisation (MR) analysis to investigate the causal relationship between blood lipids and depression phenotypes, based on large-scale GWAS summary statistics (N = 188 577/480 359 for lipid/depression traits respectively). Five depression-related phenotypes were included, namely major depression (MD; from PGC), depressive symptoms (DS; from SSGAC), longest duration and number of episodes of low mood, and history of deliberate self-harm (DSH)/suicide (from UK Biobank). MR was conducted with inverse-variance weighted (MR-IVW), Egger and Generalised Summary-data-based MR (GSMR) methods.

There was consistent evidence that triglyceride (TG) is causally associated with DS (MR-IVW β for one-s.d. increase in TG = 0.0346, 95% CI 0.0114–0.0578), supported by MR-IVW and GSMR and multiple r2 clumping thresholds. We also observed relatively consistent associations of TG with DSH/suicide (MR-Egger OR = 2.514, CI 1.579–4.003). There was moderate evidence for positive associations of TG with MD and the number of episodes of low mood. For HDL-c, we observed moderate evidence for causal associations with DS and MD. LDL-c and TC did not show robust causal relationships with depression phenotypes, except for weak evidence that LDL-c is inversely related to DSH/suicide. We did not detect significant associations when depression phenotypes were treated as exposures.

This study provides evidence to a causal relationship between TG, and to a lesser extent, altered cholesterol levels with depression phenotypes. Further studies on its mechanistic basis and the effects of lipid-lowering therapies are warranted.

Several studies have reported diminished learning from non-social outcomes in depressed individuals. However, it is not clear how depression impacts learning from social feedback. Notably, mood disorders are commonly associated with deficits in social functioning, which raises the possibility that potential impairments in social learning may negatively affect real-life social experiences in depressed subjects.

Ninety-two participants with high (HD; N = 40) and low (LD; N = 52) depression scores were recruited. Subjects performed a learning task, during which they received monetary outcomes or social feedback which they were told came from other people. Additionally, participants answered questions about their everyday social experiences. Computational models were fit to the data and model parameters were related to social experience measures.

HD subjects reported a reduced quality and quantity of social experiences compared to LD controls, including an increase in the amount of time spent in negative social situations. Moreover, HD participants showed lower learning rates than LD subjects in the social condition of the task. Interestingly, across all participants, reduced social learning rates predicted higher amounts of time spent in negative social situations, even when depression scores were controlled for.

These findings indicate that deficits in social learning may affect the quality of everyday social experiences. Specifically, the impaired ability to use social feedback to appropriately update future actions, which was observed in HD subjects, may lead to suboptimal interpersonal behavior in real life. This, in turn, may evoke negative feedback from others, thus bringing about more unpleasant social encounters.

Although alcohol use disorder (AUD) runs strongly within families, studies examining the impact of rearing environment, unconfounded by genetic effects, are rare and, to date, contradictory. We here seek to conduct such a study using an adoptive co-sib control design.

Defining high-risk as having ⩾1 biological parent with an externalizing syndrome (AUD, drug abuse or crime), we identified 1316 high-risk full-sibships and 4623 high-risk half-sibships containing at least one member who was home-reared and one who was adopted-away. Adoptive families are carefully screened in Sweden to provide high-quality rearing environment for adoptees. AUD was assessed from national medical, criminal and pharmacy registries.

Controlling for sex, parental age at birth, and, for half-siblings, affection status of the non-shared parent, hazard ratios (±95% CI) for AUD in the matched adopted v. home-reared full- and half-siblings were, respectively, 0.76 (0.65–0.89) and 0.77 (0.70–0.84). The protective effect of adoption on AUD risk was stronger in the full- and half-sibling pairs with very high familial liability (two high-risk parents) and significantly weaker when the adoptive family was broken by death or divorce or contained a high-risk adoptive parent.

In both full- and half-sibling pairs, we found evidence that the rearing environment substantially impacts on the risk for AUD. High-quality rearing environments can meaningfully reduce the risk for AUD, especially in those at high familial risk.

Research exploring the longitudinal course of posttraumatic stress disorder (PTSD) symptoms has documented four modal trajectories (low, remitting, high, and delayed), with proportions varying across studies. Heterogeneity could be due to differences in trauma types and patient demographic characteristics.

This analysis pooled data from six longitudinal studies of adult survivors of civilian-related injuries admitted to general hospital emergency departments (EDs) in six countries (pooled N = 3083). Each study included at least three assessments of the clinician-administered PTSD scale in the first post-trauma year. Latent class growth analysis determined the proportion of participants exhibiting various PTSD symptom trajectories within and across the datasets. Multinomial logistic regression analyses examined demographic characteristics, type of event leading to the injury, and trauma history as predictors of trajectories differentiated by their initial severity and course.

Five trajectories were found across the datasets: Low (64.5%), Remitting (16.9%), Moderate (6.7%), High (6.5%), and Delayed (5.5%). Female gender, non-white race, prior interpersonal trauma, and assaultive injuries were associated with increased risk for initial PTSD reactions. Female gender and assaultive injuries were associated with risk for membership in the Delayed (v. Low) trajectory, and lower education, prior interpersonal trauma, and assaultive injuries with risk for membership in the High (v. Remitting) trajectory.

The results suggest that over 30% of civilian-related injury survivors admitted to EDs experience moderate-to-high levels of PTSD symptoms within the first post-trauma year, with those reporting assaultive violence at increased risk of both immediate and longer-term symptoms.

Resting pulse is robustly and inversely associated with the risk for externalizing disorders and may be positively associated with internalizing disorders. We know little about the causal nature of these associations.

We examined resting pulse at conscription examination in 369 301 males born 1960–80 with a mean (s.d.) follow-up of 29.1 (7.7) years. From pulse rates, we predicted, using Cox models, the risk for criminal behavior (CB), drug abuse (DA), alcohol use disorder (AUD), major depression (MD), and anxiety disorders (AD), assessed from medical, criminal, and pharmacy registries. Co-relative analyses were conducted on the general population, cousin, half-sibling, full-sibling, and monozygotic pairs discordant for the outcome. Twin/sibling modeling for pulse was performed using OpenMX.

Familial resemblance for pulse resulted entirely from genetic factors. In the general population, the risk for externalizing disorders (CB, DA, and AUD) and internalizing disorders (MD and AD) were, respectively, significantly associated with low and high resting pulse rate. For CB, DA, and AUD, co-relative analyses showed that the inverse association with pulse resulted entirely from familial common causes (aka ‘confounders’). By contrast, co-relative analyses found that the association between higher pulse and MD and AD resulted from direct causal effects.

Resting pulse has a negative and positive association with, respectively, the risk for externalizing and for internalizing disorders. Co-relative analyses indicate that the nature of these associations differ, suggesting that elevated pulse appears to directly increase the risk for internalizing disorders while the reduced pulse is a risk index for underlying traits that predispose to externalizing disorders.

Accumulating evidence suggests that many psychiatric disorders etiologically represent the extreme end of dimensionally distributed features rather than distinct entities. The extent to which this applies to eating disorders (EDs) is unknown.

We investigated if there is similar etiology in (a) the continuous distribution of the Eating Disorder Inventory-2 (EDI-2), (b) the extremes of EDI-2 score, and (c) registered ED diagnoses, in 1481 female twin pairs at age 18 years (born 1992–1999). EDI-2 scores were self-reported at age 18. ED diagnoses were identified through the Swedish National Patient Register, parent-reported treatment and/or self-reported purging behavior of a frequency and duration consistent with DSM-IV criteria. We differentiated between anorexia nervosa (AN) and other EDs.

The heritability of the EDI-2 score was 0.65 (95% CI 0.61–0.68). The group heritabilities in DeFries–Fulker extremes analyses were consistent over different percentile-based extreme groups [0.59 (95% CI 0.37–0.81) to 0.65 (95% CI 0.55–0.75)]. Similarly, the heritabilities in liability threshold models were consistent over different levels of severity. In joint categorical-continuous models, the twin-based genetic correlation was 0.52 (95% CI 0.39–0.65) between EDI-2 score and diagnoses of other EDs, and 0.26 (95% CI 0.08–0.42) between EDI-2 score and diagnoses of AN. The non-shared environmental correlations were 0.52 (95% CI 0.32–0.70) and 0.60 (95% CI 0.38–0.79), respectively.

Our findings suggest that some EDs can partly be conceptualized as the extreme manifestation of continuously distributed ED features. AN, however, might be more distinctly genetically demarcated from ED features in the general population than other EDs.