Major depressive disorder (MDD) and chronic pain are highly comorbid, and pain symptoms are associated with a poorer response to antidepressant medication treatment. It is unclear whether comorbid pain also is associated with a poorer response to treatment with repetitive transcranial magnetic stimulation (rTMS).

162 MDD subjects received 30 sessions of 10 Hz rTMS treatment administered to the left dorsolateral prefrontal cortex (DLPFC) with depression and pain symptoms measured before and after treatment. For a subset of 96 patients, a resting-state electroencephalogram (EEG) was recorded at baseline. Clinical outcome was compared between subjects with and without comorbid pain, and the relationships among outcome, pain severity, individual peak alpha frequency (PAF), and PAF phase-coherence in the EEG were examined.

64.8% of all subjects reported pain, and both depressive and pain symptoms were significantly reduced after rTMS treatment, irrespective of age or gender. Patients with severe pain were 27% less likely to respond to MDD treatment than pain-free individuals. PAF was positively associated with pain severity. PAF phase-coherence in the somatosensory and default mode networks was significantly lower for MDD subjects with pain who failed to respond to MDD treatment.

Pain symptoms improved after rTMS to left DLPFC in MDD irrespective of age or gender, although the presence of chronic pain symptoms reduced the likelihood of treatment response. Individual PAF and baseline phase-coherence in the sensorimotor and midline regions may represent predictors of rTMS treatment outcome in comorbid pain and MDD.

Despite a wide range of proposed risk factors and theoretical models, prediction of eating disorder (ED) onset remains poor. This study undertook the first comparison of two machine learning (ML) approaches [penalised logistic regression (LASSO), and prediction rule ensembles (PREs)] to conventional logistic regression (LR) models to enhance prediction of ED onset and differential ED diagnoses from a range of putative risk factors.

Data were part of a European Project and comprised 1402 participants, 642 ED patients [52% with anorexia nervosa (AN) and 40% with bulimia nervosa (BN)] and 760 controls. The Cross-Cultural Risk Factor Questionnaire, which assesses retrospectively a range of sociocultural and psychological ED risk factors occurring before the age of 12 years (46 predictors in total), was used.

All three statistical approaches had satisfactory model accuracy, with an average area under the curve (AUC) of 86% for predicting ED onset and 70% for predicting AN v. BN. Predictive performance was greatest for the two regression methods (LR and LASSO), although the PRE technique relied on fewer predictors with comparable accuracy. The individual risk factors differed depending on the outcome classification (EDs v. non-EDs and AN v. BN).

Even though the conventional LR performed comparably to the ML approaches in terms of predictive accuracy, the ML methods produced more parsimonious predictive models. ML approaches offer a viable way to modify screening practices for ED risk that balance accuracy against participant burden.

Children from low-socioeconomic backgrounds exhibit more behavioural difficulties than those from more affluent families. Influential theoretical models specify family stress and child characteristics as mediating this effect. These accounts, however, have often been based on cross-sectional data or longitudinal analyses that do not capture all potential pathways, and therefore may not provide good policy guidance.

In a UK representative sample of 2399 children aged 5–15, we tested mediation of the effect of household income on parent and teacher reports of conduct problems (CP) via unhealthy family functioning, poor parental mental health, stressful life events, child physical health and reading ability. We applied cross-lagged longitudinal mediation models which allowed for testing of reciprocal effects whereby the hypothesised mediators were modelled as outcomes as well as predictors of CP.

We found the predicted significant longitudinal effect of income on CP, but no evidence that it was mediated by the child and family factors included in the study. Instead, we found significant indirect paths from income to parental mental health, child physical health and stressful life events that were transmitted via child CP.

The results confirm that income is associated with change in CP but do not support models that suggest this effect is transmitted via unhealthy family functioning, parental mental health, child physical health, stressful life events or reading difficulties. Instead, the results highlight that child CP may be a mediator of social inequalities in family psychosocial functioning.

The UK Biobank is a large middle-aged cohort recruited in 2006–2010. We used data from its participants to analyze mortality, survival, and causes of death associated with mental disorders.

Our exposures were mental disorders identified using (1) symptom-based outcomes derived from an online Mental Health Questionnaire (n = 157 329), including lifetime/current depression, lifetime/current generalized anxiety disorder, lifetime/recent psychotic experience, lifetime bipolar disorder, current alcohol use disorder, and current posttraumatic stress disorder and (2) hospital data linkage of diagnoses within the International Classification of Diseases, 10th revision (ICD-10) (n = 502 422), including (A) selected diagnoses or groups of diagnoses corresponding to symptom-based outcomes and (B) all psychiatric diagnoses, grouped by ICD-10 section. For all exposures, we estimated age-adjusted mortality rates and hazard ratios, as well as proportions of deaths by cause.

We found significantly increased mortality risk associated with all mental disorders identified by symptom-based outcomes, except for lifetime generalized anxiety disorder (with hazard ratios in the range of 1.08–3.0). We also found significantly increased mortality risk associated with all conditions identified by hospital data linkage, including selected ICD-10 diagnoses or groups of diagnoses (2.15–7.87) and ICD-10 diagnoses grouped by section (2.02–5.44). Causes of death associated with mental disorders were heterogeneous and mostly natural.

In a middle-aged cohort, we found a higher mortality risk associated with most mental disorders identified by symptom-based outcomes and with all disorders or groups of disorders identified by hospital data linkage of ICD-10 diagnoses. The majority of deaths associated with mental disorders were natural.

Several previous studies have identified a continuity between childhood anxiety/withdrawal and anxiety disorder (AD) in later life. However, not all children with anxiety/withdrawal problems will experience an AD in later life. Previous studies have shown that the severity of childhood anxiety/withdrawal accounts for some of the variability in AD outcomes. However, no studies to date have investigated how variation in features of anxiety/withdrawal may relate to continuity prognoses. The present research addresses this gap.

Data were gathered as part of the Christchurch Health and Development Study, a 40-year population birth cohort of 1265 children born in Christchurch, New Zealand. Fifteen childhood anxiety/withdrawal items were measured at 7–9 years and AD outcomes were measured at various interviews from 15 to 40 years. Six network models were estimated. Two models estimated the network structure of childhood anxiety/withdrawal items independently for males and females. Four models estimated childhood anxiety/withdrawal items predicting adolescent AD (14–21 years) and adult AD (21–40 years) in both males and females.

Approximately 40% of participants met the diagnostic criteria for an AD during both the adolescent (14–21 years) and adult (21–40 years) outcome periods. Outcome networks showed that items measuring social and emotional anxious/withdrawn behaviours most frequently predicted AD outcomes. Items measuring situation-based fears and authority figure-specific anxious/withdrawn behaviour did not consistently predict AD outcomes. This applied across both the male and female subsamples.

Social and emotional anxious/withdrawn behaviours in middle childhood appear to carry increased risk for AD outcomes in both adolescence and adulthood.

Cognitive reserve (CR) has been associated with the development and prognosis of psychosis. Different proxies have been used to estimate CR among individuals. A composite score of these proxies could elucidate the role of CR at illness onset on the variability of clinical and neurocognitive outcomes.

Premorbid intelligence quotient (IQ), years of education and premorbid adjustment were explored as proxies of CR in a large sample (N = 424) of first-episode psychosis (FEP) non-affective patients. Clusters of patients were identified and compared based on premorbid, clinical and neurocognitive variables at baseline. Additionally, the clusters were compared at 3-year (N = 362) and 10-year (N = 150) follow-ups.

The FEP patients were grouped into five CR clusters: C1 (low premorbid IQ, low education and poor premorbid) 14%; C2 (low premorbid IQ, low education and good premorbid adjustment) 29%; C3 (normal premorbid IQ, low education and poor premorbid adjustment) 17%; C4 (normal premorbid IQ, medium education and good premorbid adjustment) 25%; and C5 (normal premorbid IQ, higher education and good premorbid adjustment) 15%. In general, positive and negative symptoms were more severe in the FEP patients with the lowest CR at baseline and follow-up assessments, while those with high CR presented and maintained higher levels of cognitive functioning.

CR could be considered a key factor at illness onset and a moderator of outcomes in FEP patients. A high CR could function as a protective factor against cognitive impairment and severe symptomatology. Clinical interventions focused on increasing CR and documenting long-term benefits are interesting and desirable.

Deficits in goal-directed behavior (i.e. behavior conducted to achieve a specific goal or outcome) are core to schizophrenia, difficult to treat, and associated with poor functional outcomes. Factors such as negative symptoms, effort-cost decision-making, cognition, and functional skills have all been associated with goal-directed behavior in schizophrenia as indexed by clinical interviews or laboratory-based tasks. However, little work has examined whether these factors relate to the real-world pursuit of goal-directed activities in this population.

This study aimed to fill this gap by using Ecological Momentary Assessment (four survey prompts per day for 1 week) to test hypotheses about symptom, effort allocation, cognitive, and functional measures associated with planned and completed goal-directed behavior in the daily lives of 63 individuals with schizophrenia.

Individuals with schizophrenia completed more goal-directed activities than they planned [t(62) = −4.01, p < 0.001]. Motivation and pleasure (i.e. experiential) negative symptoms, controlling for depressive symptoms, negatively related to planned goal-directed behavior [odds ratio (OR) 0.92, p = 0.005]. Increased effort expenditure for high probability rewards (planned: OR 1.01, p = 0.034, completed: OR 1.01, p = 0.034) along with performance on a daily functional skills task (planned: OR 1.04, p = 0.002, completed: OR 1.03, p = 0.047) negatively related to both planned and completed goal-directed activity.

Our results present correlates of real-world goal-directed behavior that largely align with impaired ability to make future estimations in schizophrenia. This insight could help identify targeted treatments for the elusive motivated behavior deficits in this population.

Obsessive-compulsive personality disorder (OCPD) is a high-prevalence personality disorder characterized by subtle but stable interpersonal dysfunction. There have been only limited studies addressing the behavioral patterns and cognitive features of OCPD in interpersonal contexts. The purpose of this study was to investigate how behaviors differ between OCPD individuals and healthy controls (HCs) in the context of guilt-related interpersonal responses.

A total of 113 participants were recruited, including 46 who were identified as having OCPD and 67 HCs. Guilt-related interpersonal responses were manipulated and measured with two social interactive tasks: the Guilt Aversion Task, to assess how anticipatory guilt motivates cooperation; and the Guilt Compensation Task, to assess how experienced guilt induces compensation behaviors. The guilt aversion model and Fehr–Schmidt inequity aversion model were adopted to analyze decision-making in the Guilt Aversion Task and the Guilt Compensation Task, respectively.

Computational model-based results demonstrated that, compared with HCs, the OCPD group exhibited less guilt aversion when making cooperative decisions as well as less guilt-induced compensation after harming others.

Our findings indicate that individuals with OCPD tend to be less affected by guilt than HCs. These impairments in guilt-related responses may prevent adjustments in behaviors toward compliance with social norms and thus result in interpersonal dysfunctions.

This confirmatory study aimed to examine whether we can foresee recurrence of depressive symptoms using personalized modeling of rises in restlessness.

Participants were formerly depressed patients (N = 41) in remission who (gradually) discontinued antidepressants. Participants completed five smartphone-based Ecological Momentary Assessments (EMA) a day, for a period of 4 months, yielding a total of 21 180 observations. Statistical Process Control by means of Exponentially Weighted Moving Average (EWMA) control charts was used to detect rises in the EMA item ‘I feel restless’, for each individual separately.

An increase in restlessness was detected in 68.3% of the participants with recurring depressive symptoms, and in 26.3% of those who stayed in remission (Fisher's exact test p = 0.01, sensitivity was 68.3%, specificity was 73.7%). In the participants with a recurrence and an increase in restlessness, this increase could be detected in the prodromal phase of depression in 93.3% of the cases and at least a month before the onset of the core symptoms of depression in 66.7% of the cases.

Restlessness is a common prodromal symptom of depression. The sensitivity and specificity of the EWMA charts was at least as good as prognostic models based on cross-sectional patient characteristics. An advantage of the current idiographic method is that the EWMA charts provide real-time personalized insight in a within-person increase in early signs of depression, which is key to alert the right patient at the right time.

Exposure to adversities in early childhood is associated with psychotic experiences and disorders in adulthood. We aimed to examine whether early childhood adversities are associated with middle childhood psychotic experiences in a cohort of children at familial high risk of schizophrenia (FHR-SZ), bipolar disorder (FHR-BP) and population-based controls (controls).

Four hundred and forty-six children from The Danish High Risk and Resilience Study – VIA7 and VIA11 participated in this study (FHR-SZ = 170; FHR-BP = 103; controls = 173). Exposure to early childhood adversities and psychotic experiences were assessed using face-to-face interviews. Having childhood adversities assessed at baseline (age 7) was used as predictor. Psychotic experiences assessed at follow-up (age 11) were used as outcome.

Across the sample, exposure to early childhood interpersonal adversities was associated with an increased risk for any middle childhood psychotic experiences and subclinical delusions when adjusting for relevant confounders (OR 1.8, 95% CI 1.0–3.1, p = 0.05; OR 3.0, 95% CI 1.6–5.6, p < 0.001). There was no significant dose–response effect of exposure to multiple types of childhood adversities on any psychotic experiences. There were no interaction effects between early childhood adversities and FHR on middle childhood psychotic experiences. Exploratory analyses revealed that experiencing domestic violence in early childhood was associated with any middle childhood psychotic experiences (OR 2.8, 95% CI 1.5–5.1, p = 0.001).

Exposure to interpersonal adversities during early childhood is associated with an increased risk for middle childhood psychotic experiences including specifically subclinical delusions. Future studies should examine associations between exposure to childhood adversities and conversion to psychosis within this cohort.

In late 2019, a new virus began spreading in Wuhan, China. By the end of 2021, more than 260 million people worldwide had been infected and 5.2 million people had died because of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Various countermeasures have been implemented to contain the infections, depending on the country, infection prevalence, and political and infrastructural resources. The pandemic and the containment measures have induced diverse psychological burdens. Using internet queries as a proxy, this study examines the psychological consequences on a European level of SARS-CoV-2 containment measures.

Using informetric analyses, this study reviews within 32 European countries a total of 28 search parameters derived from the International Statistical Classification of Diseases and Related Health Problems (ICD-10) as aspects of affective disorder.

Our results show that there are several psychological aspects which are significantly emphasized during the pandemic and its containment measures: ‘anxiety’, ‘dejection’, ‘weariness’, ‘listlessness’, ‘loss of appetite’, ‘loss of libido’, ‘panic attack’, and ‘worthlessness’. These terms are significantly more frequently part of a search query during the pandemic than before the outbreak. Furthermore, our results revealed that search parameters such as ‘psychologist’, ‘psychotherapist’, ‘psychotherapy’ have increased highly significantly (p < 0.01) since the pandemic.

The psychological distress caused by the pandemic correlates significantly with the frequency of people searching for psychological and psychotherapeutic support on the Internet.

Persistent cognitive deficits are prevalent in patients with bipolar disorder (BD) and unipolar disorder (UD), but treatments effectively targeting cognition in these mood disorders are lacking. This is partly due to poor insight into the neuronal underpinnings of cognitive deficits.

The aim of this functional magnetic resonance imaging (fMRI) study was to investigate the neuronal underpinnings of working memory (WM)-related deficits in somatically healthy, remitted patients with BD or UD (n = 66) with cognitive and functional impairments compared to 38 healthy controls (HC). The participants underwent neuropsychological testing and fMRI, while performing a visuospatial and a verbal N-back WM paradigm.

Relative to HC, patients exhibited hypo-activity across dorsolateral prefrontal cortex as well as frontal and parietal nodes of the cognitive control network (CCN) and hyper-activity in left orbitofrontal cortex within the default mode network (DMN) during both visuospatial and verbal WM performance. Verbal WM-related response in the left posterior superior frontal gyrus (SFG) within CCN was lower in patients and correlated positively with out-of-scanner executive function performance across all participants.

Our findings suggest that cognitive impairments across BD and UD are associated with insufficient recruitment of task-relevant regions in the CCN and down-regulation of task-irrelevant orbitofrontal activity within the DMN during task performance. Specifically, a lower recruitment of the left posterior SFG within CCN during verbal WM was associated with lower cognitive performance.

In this study, we examined the relationship between polygenic liability for depression and number of stressful life events (SLEs) as risk factors for early-onset depression treated in inpatient, outpatient or emergency room settings at psychiatric hospitals in Denmark.

Data were drawn from the iPSYCH2012 case-cohort sample, a population-based sample of individuals born in Denmark between 1981 and 2005. The sample included 18 532 individuals who were diagnosed with depression by a psychiatrist by age 31 years, and a comparison group of 20 184 individuals. Information on SLEs was obtained from nationwide registers and operationalized as a time-varying count variable. Hazard ratios and cumulative incidence rates were estimated using Cox regressions.

Risk for depression increased by 35% with each standard deviation increase in polygenic liability (p < 0.0001), and 36% (p < 0.0001) with each additional SLE. There was a small interaction between polygenic liability and SLEs (β = −0.04, p = 0.0009). The probability of being diagnosed with depression in a hospital-based setting between ages 15 and 31 years ranged from 1.5% among males in the lowest quartile of polygenic liability with 0 events by age 15, to 18.8% among females in the highest quartile of polygenic liability with 4+ events by age 15.

These findings suggest that although there is minimal interaction between polygenic liability and SLEs as risk factors for hospital-treated depression, combining information on these two important risk factors could potentially be useful for identifying high-risk individuals.

Sleep disturbance is common in gestational parents during pregnancy and postpartum periods. This study evaluated the feasibility and efficacy of a scalable cognitive behavioural therapy (CBT) sleep intervention tailored for these periods.

This is a two-arm, parallel-group, single-blind, superiority randomised controlled trial. Nulliparous females without severe medical/psychiatric conditions were randomised 1:1 to CBT or attention- and time-matched control. All participants received a 1 h telephone session and automated multimedia emails from the third trimester until 6 months postpartum. Outcomes were assessed with validated instruments at gestation weeks 30 (baseline) and 35 (pregnancy endpoint), and postpartum months 1.5, 3, 6 (postpartum endpoint), 12 and 24.

In total, 163 eligible participants (age M ± s.d. = 33.35 ± 3.42) were randomised. The CBT intervention was well accepted, with no reported adverse effect. Intention-to-treat analyses showed that compared to control, receiving CBT was associated with lower insomnia severity and sleep disturbance (two primary outcomes), and lower sleep-related impairment at the pregnancy endpoint (p values ⩽ 0.001), as well as at 24 months postpartum (p ranges 0.012–0.052). Group differences across the first postpartum year were non-significant. Participants with elevated insomnia symptoms at baseline benefitted substantially more from CBT (v. control), including having significantly lower insomnia symptoms throughout the first postpartum year. Group differences in symptoms of depression or anxiety were non-significant.

A scalable CBT sleep intervention is efficacious in buffering against sleep disturbance during pregnancy and benefitted sleep at 2-year postpartum, especially for individuals with insomnia symptoms during pregnancy. The intervention holds promise for implementation into routine perinatal care.

Adding short-term psychodynamic psychotherapy (STPP) to antidepressants increases treatment efficacy, but it is unclear which patients benefit specifically. This study examined efficacy moderators of combined treatment (STPP + antidepressants) v. antidepressants for adults with depression.

For this systematic review and meta-analysis (PROSPERO registration number: CRD42017056029), we searched PubMed, PsycINFO, Embase.com, and the Cochrane Library from inception to 1 January 2022. We included randomized clinical trials comparing combined treatment (antidepressants + individual outpatient STPP) v. antidepressants in the acute-phase treatment of depression in adults. Individual participant data were requested and analyzed combinedly using mixed-effects models (adding Cochrane risk of bias items as covariates) and an exploratory machine learning technique. The primary outcome was post-treatment depression symptom level.

Data were obtained for all seven trials identified (100%, n = 482, combined: n = 238, antidepressants: n = 244). Adding STPP to antidepressants was more efficacious for patients with high rather than low baseline depression levels [B = −0.49, 95% confidence interval (CI) −0.61 to −0.37, p < 0.0001] and for patients with a depressive episode duration of >2 years rather than <1 year (B = −0.68, 95% CI −1.31 to −0.05, p = 0.03) and than 1–2 years (B = −0.86, 95% CI −1.66 to −0.06, p = 0.04). Heterogeneity was low. Effects were replicated in analyses controlling for risk of bias.

To our knowledge, this is the first study that examines moderators across trials assessing the addition of STPP to antidepressants. These findings need validation but suggest that depression severity and episode duration are factors to consider when adding STPP to antidepressants and might contribute to personalizing treatment selection for depression.

Life stress and blunted reward processing each have been associated with the onset and maintenance of major depressive disorder. However, much of this work has been cross-sectional, conducted in separate lines of inquiry, and focused on recent life stressor exposure, despite the fact that theories of depression posit that stressors can have cumulative effects over the lifespan. To address these limitations, we investigated whether acute and chronic stressors occurring over the lifespan interacted with blunted reward processing to predict increases in depression over time in healthy youth.

Participants were 245 adolescent girls aged 8–14 years old (Mage = 12.4, s.d. = 1.8) who were evaluated at baseline and two years later. The reward positivity (RewP), an event-related potential measure of reward responsiveness, was assessed at baseline using the doors task. Cumulative lifetime exposure to acute and chronic stressors was assessed two years later using the Stress and Adversity Inventory for Adolescents (Adolescent STRAIN). Finally, depressive symptoms were assessed at both baseline and follow-up using the Children's Depression Inventory.

As hypothesized, greater lifetime acute stressor exposure predicted increases in depressive symptoms over two years, but only for youth exhibiting a blunted RewP. This interaction, however, was not found for chronic stressors.

Lifetime acute stressor exposure may be particularly depressogenic for youth exhibiting a blunted RewP. Conversely, a robust RewP may be protective in the presence of greater acute lifetime stressor exposure.

The co-occurrence of stroke and psychosis is a serious neuropsychiatric condition but little is known about the course of this comorbidity. We aimed to estimate longitudinal associations between stroke and psychosis over 10 years.

A 10-year population-based study using data from the English Longitudinal Study of Ageing. A structured health assessment recorded (i) first-occurrence stroke and (ii) psychosis, at each wave. Each were considered exposures and outcomes in separate analyses. Logistic and Cox proportional hazards regression and Kaplan–Meier methods were used. Models were adjusted for demographic and health behaviour covariates, with missing covariates imputed using random forest multiple imputation.

Of 19 808 participants, 24 reported both stroke and psychosis (median Wave 1 age 63, 71% female, 50% lowest quintile of net financial wealth) at any point during follow-up. By 10 years, the probability of an incident first stroke in participants with psychosis was 21.4% [95% confidence interval (CI) 12.1–29.6] compared to 8.3% (95% CI 7.8–8.8) in those without psychosis (absolute difference: 13.1%; 95% CI 20.8–4.3, log rank p < 0.001; fully-adjusted hazard ratio (HR): 3.57; 95% CI 2.18–5.84). The probability of reporting incident psychosis in participants with stroke was 2.3% (95% CI 1.4–3.2) compared to 0.9% (95% CI 0.7–1.1) in those without (absolute difference: 1.4%; 95% CI 0.7–2.1, log rank p < 0.001; fully-adjusted HR: 4.98; 95% CI 2.55–9.72).

Stroke is an independent predictor of psychosis (and vice versa), after adjustment for potential confounders.

Prevention programs that are ‘transdiagnostic’ may be more cost-effective and beneficial, in terms of reducing levels of psychopathology in the general population, than those focused on a specific disorder. This randomized controlled study evaluated the efficacy of one such intervention program called Resilience Training (RT).

College students who reported mildly elevated depressive or subclinical psychotic symptoms (‘psychotic experiences' (PEs)) (n = 107) were randomized to receiving RT (n = 54) or to a waitlist control condition (n = 53). RT consists of a four-session intervention focused on improving resilience through the acquisition of mindfulness, self-compassion, and mentalization skills. Measures of symptoms and these resilience-enhancing skills were collected before and after the 4-week RT/waitlist period, with a follow-up assessment 12-months later.

Compared to the waitlist control group, RT participants reported significantly greater reductions in PEs, distress associated with PEs, depression, and anxiety, as well as significantly greater improvements in resilience, mindfulness, self-compassion, and positive affect, following the 4-week RT/waitlist period (all p < 0.03). Moreover, improvements in resilience-promoting skills were significantly correlated with symptom reductions (all p < 0.05). Lastly, the RT-related reductions in PEs and associated distress were maintained at the 12-month follow-up assessment.

RT is a brief, group-based intervention associated with improved resilience and reduced symptoms of psychopathology, with sustained effects on PEs, in transdiagnostically at-risk young adults. Follow-up studies can further assess the efficacy of RT relative to other interventions and test whether it can reduce the likelihood of developing a serious mental illness.

Little is known about the childhood antecedents and adult correlates of adolescent dual-harm (i.e. co-occurring self- and other-harm). We examine the longitudinal associations between (a) social and psychological risk factors in childhood and adolescent dual-harm and (b) adolescent dual-harm and social and mental health impairments in early adulthood.

Participants (N = 1482) are from a prospective longitudinal community-representative study. Dual-, self-, and other-harm were self-reported at ages 13, 15, and 17. Social and psychological risk factors in childhood were assessed between 7 and 11; early adult correlates at age 20. Groups with dual-harm, self-harm only, other-harm only, and no harm were compared.

Between 13 and 17, 7.2% of adolescents reported dual-harm (self-harm only: 16.2%; other-harm only: 13.3%). Some childhood risk factors (e.g. sensation-seeking, parental divorce, victimization by peers) characterized all harm groups; others were common to the dual- and self-harm (anxiety/depressive symptoms, relational aggression) or dual- and other-harm groups only (low self-control, substance use, delinquency). Adolescents with dual-harm had reported more physical aggression and harsh parenting, and lower school bonding in childhood than any other group. In early adulthood, they reported more anxiety/depressive symptoms, psychopathy symptoms, homicidal ideations, delinquency, and victimization experiences than any other group.

Adolescent dual-harm follows psychological problems and social disconnection in childhood and signals risk of psychopathology and isolation in early adulthood. To curb the burden from dual-harm, interventions must target adolescents, families, peer networks, and school environments. Differentiating youth with dual-harm from those with single-harm is important for developing personalized treatments.

Coordination between the thalamus and cortex is necessary for efficient processing of sensory information and appears disrupted in schizophrenia. The significance of this disrupted coordination (i.e. thalamocortical dysconnectivity) to the symptoms and cognitive deficits of schizophrenia is unclear. It is also unknown whether similar dysconnectivity is observed in other forms of psychotic psychopathology and associated with familial risk for psychosis. Here we examine the relevance of thalamocortical connectivity to the clinical symptoms and cognition of patients with psychotic psychopathology, their first-degree biological relatives, and a group of healthy controls.

Patients with a schizophrenia-spectrum diagnosis (N = 100) or bipolar disorder with a history of psychosis (N = 33), their first-degree relatives (N = 73), and a group of healthy controls (N = 43) underwent resting functional MRI in addition to clinical and cognitive assessments as part of the Psychosis Human Connectome Project. A bilateral mediodorsal thalamus seed-based analysis was used to measure thalamocortical connectivity and test for group differences, as well as associations with symptomatology and cognition.

Reduced connectivity from mediodorsal thalamus to insular, orbitofrontal, and cerebellar regions was seen in schizophrenia. Across groups, greater symptomatology was related to less thalamocortical connectivity to the left middle frontal gyrus, anterior cingulate, right insula, and cerebellum. Poorer cognition was related to less thalamocortical connectivity to bilateral insula. Analyses revealed similar patterns of dysconnectivity across patient groups and their relatives.

Reduced thalamo-prefrontal-cerebellar and thalamo-insular connectivity may contribute to clinical symptomatology and cognitive deficits in patients with psychosis as well as individuals with familial risk for psychotic psychopathology.