Previous meta-analyses of psychotherapies for children and adolescents with post-traumatic stress disorder (PTSD) did not investigate whether treatment efficacy is diminished when patients report multiple (versus single) traumas.

To examine whether efficacy of psychological interventions for paediatric PTSD is diminished when patients report multiple (versus single) traumas.

We systematically searched PsycInfo, MEDLINE, Web of Science and PTSDpubs on 21 April 2022 and included randomised controlled trials (RCTs) meeting the following criteria: (a) random allocation; (b) all participants presented with partial or full PTSD; (c) PTSD is the primary treatment focus; (d) sample mean age <19 years; (e) sample size n ≥ 20. Trauma frequency was analysed as a dichotomous (single versus ≥2 traumas) and continuous (mean number of exposures) potential moderator of efficacy.

Of the 57 eligible RCTs (n = 4295), 51 RCTs were included in quantitative analyses. Relative to passive control conditions, interventions were found effective for single-trauma-related PTSD (Hedges’ g = 1.09; 95% CI 0.70–1.48; k = 8 trials) and multiple-trauma-related PTSD (g = 1.11; 95% CI 0.74–1.47; k = 12). Psychotherapies were also more effective than active control conditions in reducing multiple-trauma-related PTSD. Comparison with active control conditions regarding single-event PTSD was not possible owing to scarcity (k = 1) of available trials. Efficacy did not differ with trauma exposure frequency irrespective of its operationalisation and subgroup analyses (e.g. trauma-focused cognitive–behavioural therapy only).

The current evidence base suggests that psychological interventions for paediatric PTSD can effectively treat PTSD in populations reporting single and multiple traumas. Future trials for PTSD following single-event trauma need to involve active control conditions.

Understanding the evolution of negative symptoms in first-episode psychosis (FEP) requires long-term longitudinal study designs that capture the progression of this condition and the associated brain changes.

To explore the factors underlying negative symptoms and their association with long-term abnormal brain trajectories.

We followed up 357 people with FEP over a 10-year period. Factor analyses were conducted to explore negative symptom dimensionality. Latent growth mixture modelling (LGMM) was used to identify the latent classes. Analysis of variance (ANOVA) was conducted to investigate developmental trajectories of cortical thickness. Finally, the resulting ANOVA maps were correlated with a wide set of regional molecular profiles derived from public databases.

Three trajectories (stable, decreasing and increasing) were found in each of the three factors (expressivity, experiential and attention) identified by the factor analyses. Patients with an increasing trajectory in the expressivity factor showed cortical thinning in caudal middle frontal, pars triangularis, rostral middle frontal and superior frontal regions from the third to the tenth year after the onset of the psychotic disorder. The F-statistic map of cortical thickness expressivity differences was associated with a receptor density map derived from positron emission tomography data.

Stable and decreasing were the most common trajectories. Additionally, cortical thickness abnormalities found at relatively late stages of FEP onset could be exploited as a biomarker of poor symptom outcome in the expressivity dimension. Finally, the brain areas with less density of receptors spatially overlap areas that discriminate the trajectories of the expressivity dimension.

Reward processing has been proposed to underpin the atypical social feature of autism spectrum disorder (ASD). However, previous neuroimaging studies have yielded inconsistent results regarding the specificity of atypicalities for social reward processing in ASD.

Utilising a large sample, we aimed to assess reward processing in response to reward type (social, monetary) and reward phase (anticipation, delivery) in ASD.

Functional magnetic resonance imaging during social and monetary reward anticipation and delivery was performed in 212 individuals with ASD (7.6–30.6 years of age) and 181 typically developing participants (7.6–30.8 years of age).

Across social and monetary reward anticipation, whole-brain analyses showed hypoactivation of the right ventral striatum in participants with ASD compared with typically developing participants. Further, region of interest analysis across both reward types yielded ASD-related hypoactivation in both the left and right ventral striatum. Across delivery of social and monetary reward, hyperactivation of the ventral striatum in individuals with ASD did not survive correction for multiple comparisons. Dimensional analyses of autism and attention-deficit hyperactivity disorder (ADHD) scores were not significant. In categorical analyses, post hoc comparisons showed that ASD effects were most pronounced in participants with ASD without co-occurring ADHD.

Our results do not support current theories linking atypical social interaction in ASD to specific alterations in social reward processing. Instead, they point towards a generalised hypoactivity of ventral striatum in ASD during anticipation of both social and monetary rewards. We suggest this indicates attenuated reward seeking in ASD independent of social content and that elevated ADHD symptoms may attenuate altered reward seeking in ASD.

People with severe mental ill health (SMI) experience some of the largest health inequalities of any sector within society. For these inequalities to be reduced, an understanding of the behavioural determinants of health in this population is needed.

Utilising data from the Closing the Gap Health Study, we aimed to assess the extent to which people with SMI report health-risk factors and behaviours, their interest in modifying them, and the factors associated with being motivated to modify these behaviours.

Adult (≥18 years old) participants were recruited via primary and secondary care in the English National Health Service. To be eligible, participants needed to have a documented diagnosis of schizophrenia, psychotic disorders or bipolar disorder. Data were collected by survey on demographics, general physical health, diet, physical activity, alcohol, smoking and body mass index.

Between April 2016 and March 2020, n = 9914 participants were recruited. Among people with SMI, high rates of obesity (37.5%), infrequent physical activity (62.0%), not meeting current guidelines (≥5) for the consumption of fruit and vegetables (85.0%) and smoking (42.2%) were observed. However, most participants were motivated to reduce health-risk behaviours. Perceiving the importance of health-promoting behaviours, being of poorer general health and being female were significantly associated with being motivated to modify health-risk behaviours.

Despite experiencing poor physical and mental health outcomes compared with the general population, and contrary to popular misconceptions, people with SMI perceive health as important and are motivated to make behavioural changes to improve health.

Case studies have linked SARS-CoV-2 infection to suicidal behaviour. However, conclusive evidence is lacking.

To examine whether a history of SARS-CoV-2 infection or SARS-CoV-2-related hospital admission was associated with self-harm in the general population and in high-risk groups.

A cohort design was applied to nationwide data on all people aged ≥15 years and living in Denmark between 27 February 2020 and 15 October 2021. Exposure was identified as having had a positive SARS-CoV-2 PCR test, and further assessed as SARS-CoV-2-related hospital admission. Rates of probable self-harm were examined using adjusted incidence rate ratios (aIRRs). The following subgroups were identified: (a) lower educational level, (b) chronic medical conditions, (c) disability pension, (d) mental disorders, (e) substance use disorders, and history of (f) homelessness and (g) imprisonment.

Among 4 412 248 included individuals, 260 663 (5.9%) had tested positive for SARS-CoV-2. Out of 5453 individuals presenting with self-harm, 131 (2.4%) had been infected. Individuals with a history of a positive SARS-CoV-2 test result had an aIRR for self-harm of 0.86 (95% CI 0.72–1.03) compared with those without. High rates were found after a SARS-CoV-2-related hospital admission (aIRR = 7.68; 95% CI 5.61–10.51) or a non-SARS-CoV-2-related admission (aIRR = 10.27; 95% CI 9.65–10.93) versus non-infected and not admitted. In sensitivity analyses with a more restrictive definition of self-harm, a positive PCR test was associated with lower rates of self-harm.

Individuals with a PCR-confirmed SARS-CoV-2 infection did not have higher rates of self-harm than those without. Hospital admission in general, rather than being SARS-CoV-2 positive. seemed to be linked to elevated rates of self-harm.

Recent developments in computational psychiatry have led to the hypothesis that mood represents an expectation (prior belief) on the likely interoceptive consequences of action (i.e. emotion). This stems from ideas about how the brain navigates its external world by minimising an upper bound on surprisal (free energy) of sensory information and echoes developments in other perceptual domains.

In this paper we aim to present a simple partial observable Markov decision process that models mood updating in response to stressful or non-stressful environmental fluctuations while seeking to minimise surprisal in relation to prior beliefs about the likely interoceptive signals experienced with specific actions (attenuating or amplifying stress and pleasure signals).

We examine how, by altering these prior beliefs we can model mood updating in depression, mania and anxiety.

We discuss how these models provide a computational account of mood and its related psychopathology and relate it to previous research in reward processing.

Models such as this can provide hypotheses for experimental work and also open up the potential modelling of predicted disease trajectories in individual patients.

Psychotic disorders and schizotypal traits aggregate in the relatives of probands with schizophrenia. It is currently unclear how variability in symptom dimensions in schizophrenia probands and their relatives is associated with polygenic liability to psychiatric disorders.

To investigate whether polygenic risk scores (PRSs) can predict symptom dimensions in members of multiplex families with schizophrenia.

The largest genome-wide data-sets for schizophrenia, bipolar disorder and major depressive disorder were used to construct PRSs in 861 participants from the Irish Study of High-Density Multiplex Schizophrenia Families. Symptom dimensions were derived using the Operational Criteria Checklist for Psychotic Disorders in participants with a history of a psychotic episode, and the Structured Interview for Schizotypy in participants without a history of a psychotic episode. Mixed-effects linear regression models were used to assess the relationship between PRS and symptom dimensions across the psychosis spectrum.

Schizophrenia PRS is significantly associated with the negative/disorganised symptom dimension in participants with a history of a psychotic episode (P = 2.31 × 10−4) and negative dimension in participants without a history of a psychotic episode (P = 1.42 × 10−3). Bipolar disorder PRS is significantly associated with the manic symptom dimension in participants with a history of a psychotic episode (P = 3.70 × 10−4). No association with major depressive disorder PRS was observed.

Polygenic liability to schizophrenia is associated with higher negative/disorganised symptoms in participants with a history of a psychotic episode and negative symptoms in participants without a history of a psychotic episode in multiplex families with schizophrenia. These results provide genetic evidence in support of the spectrum model of schizophrenia, and support the view that negative and disorganised symptoms may have greater genetic basis than positive symptoms, making them better indices of familial liability to schizophrenia.

Prior research has solely focused on the association between handgrip strength and risk of depression in single countries or general populations, but more knowledge is required from wider-spread cohorts and target populations.

This study aimed to investigate the association between handgrip strength and risk of depression using repeated measures in adults aged 50 years and over.

Data on handgrip strength and risk of depression were retrieved from the Survey of Health, Ageing and Retirement in Europe (SHARE) waves 1, 2, 4, 5, 6 and 7, using a hand dynamometer (Smedley, S Dynamometer, TTM) and the EURO-D 12-item scale, respectively. Time-varying exposure and covariates were modelled using both Cox regression and restricted cubic splines.

A total of 115 601 participants (mean age 64.3 years (s.d. = 9.9), 54.3% women) were followed-up for a median of 7.3 years (interquartile range: 3.9–11.8) and 792 459 person-years. During this period, 30 208 (26.1%) participants experienced a risk of depression. When modelled as a continuous variable, we observed an inverse significant association for each kg increase of handgrip strength and depression up to 40 kg in men and up to 27 kg in women.

Being physically strong may serve as a preventive factor for depression in older adults, but this is limited up to a maximum specific threshold for men and women.

In February 2022, Russia began its invasion of Ukraine. War increases the demand for mental healthcare among affected populations, but with devastating losses across the nation, it is unclear if Ukrainian mental health services are able to meet the needs of the people.

We aimed to evaluate the state of Ukrainian in-patient mental health services, which remains the backbone of the nation's psychiatric services, early in the 2022 Russian invasion.

We conducted a nationwide cross-sectional study on Ukrainian in-patient mental health facilities during the 2022 Russian invasion. Using an online questionnaire, we obtained responses from the heads of 32 in-patient mental health facilities across Ukraine, representing 52.5% of all in-patient mental health facilities in the nation. We gathered information on hospital admissions, staff, humanitarian aid received and the additional needs of each facility.

Hospital admissions were reduced by 23.5% during the war (April 2022) compared with before the war (January 2022). Across facilities, 9.6% of hospital admissions in April 2022 were related to war trauma, with facilities reporting percentages as high as 30.0%. Facilities reported reductions in staff, with 9.1% of total medical workers displaced and 0.5% injured across facilities. One facility reported that 45.6% of their total medical workers were injured. Although facilities across Ukraine have received humanitarian aid (such as medical supplies, food, volunteers), they reported additionally needing equipment as well as more staff.

The mental health service structure in Ukraine has been severely damaged during the 2022 invasion, with staff shortages despite a significant number of hospital admissions related to war trauma.

There is a growing global awareness of the psychological consequences of long COVID, supported by emerging empirical evidence. However, the emergence and long-term trajectories of psychological symptoms following the infection are still unclear.

To examine when psychological symptoms first emerge following infection with SARS-CoV-2 and the long-term trajectories of psychological symptoms comparing long- and short-COVID groups.

We analysed longitudinal data from the UCL COVID-19 Social Study (March 2020 to November 2021). We included data from adults living in England who reported contracting SARS-CoV-2 by November 2021 (n = 3115). Of these, 15.9% reported having had long COVID (n = 495). They were matched to participants who had short COVID using propensity score matching on a variety of demographic, socioeconomic and health covariates (n = 962 individuals with 13 325 observations) and data were further analysed using growth curve modelling.

Depressive and anxiety symptoms increased immediately following the onset of infection in both long- and short-COVID groups. But the long-COVID group had substantially greater initial increases in depressive symptoms and heightened levels over 22 months follow-up. Initial increases in anxiety were not significantly different between groups, but only the short-COVID group experienced an improvement in anxiety over follow-up, leading to widening differences between groups.

The findings support work on the psychobiological pathways involved in the development of psychological symptoms relating to long COVID. The results highlight the need for monitoring of mental health and provision of adequate support to be interwoven with diagnosis and treatment of the physical consequences of long COVID.

Individuals with physical comorbidities and polypharmacy may be at higher risk of depression relapse, however, they are not included in the ‘high risk of relapse’ group for whom longer antidepressant treatment durations are recommended.

In individuals with comorbid depression and type 2 diabetes (T2DM), we aimed to investigate the association and interaction between depression relapse and (a) polypharmacy, (b) previous duration of antidepressant treatment.

This was a cohort study using primary care data from the UK Clinical Practice Research Datalink (CPRD) from years 2000 to 2018. We used Cox regression models with penalised B-splines to describe the association between restarting antidepressants and our two exposures.

We identified 48 001 individuals with comorbid depression and T2DM, who started and discontinued antidepressant treatment during follow-up. Within 1 year of antidepressant discontinuation, 35% of participants restarted treatment indicating depression relapse. As polypharmacy increased, the rate of restarting antidepressants increased until a maximum of 18 concurrent medications, where individuals were more than twice as likely to restart antidepressants (hazard ratio (HR) = 2.15, 95% CI 1.32–3.51). As the duration of previous antidepressant treatment increased, the rate of restarting antidepressants increased – individuals with a previous duration of ≥25 months were more than twice as likely to restart antidepressants than those who previously discontinued in <7 months (HR = 2.36, 95% CI 2.25–2.48). We found no interaction between polypharmacy and previous antidepressant duration.

Polypharmacy and longer durations of previous antidepressant treatment may be associated with depression relapse following the discontinuation of antidepressant treatment.

Studies show ethnic inequalities in rates of involuntary admission and types of clinical care (such as psychological therapies). However, few studies have investigated if there is a relationship between clinical care practices and ethnic inequalities in involuntary admission.

This study investigated the impact of ethnicity and clinical care on involuntary admission and the potential mediation effects of prior clinical care.

In this retrospective cohort study, we used data from the electronic records of the South London and Maudsley NHS Foundation Trust and identified patients with a first hospital admission between January 2008 and May 2021. Logistic regression and mediation analyses were used to investigate the association between ethnicity and involuntary admission, and whether clinical care, in the 12 months preceding admission, mediates the association.

Compared with White British people, higher odds of involuntary admission were observed among 10 of 14 minority ethnic groups; with more than twice the odds observed among people of Asian Chinese, of Asian Bangladeshi and of any Black background. There were some ethnic differences in clinical care prior to admission, but these had a minimal impact on the inequalities in involuntary admission. More out-patient appointments and home treatment were associated with higher odds of involuntary admission, whereas psychological therapies and having a care plan were associated with reduced odds of involuntary admission.

Ethnic inequalities in involuntary admission persist after accounting for potential mediating effects of several types and frequencies of clinical care. Promoting access to psychological therapies and ensuring that care plans are in place may reduce involuntary admissions.

Evidence on the role of co-occurring psychiatric disorders in mortality associated with psychotic depression is limited.

To estimate the risk of cause-specific mortality in psychotic depression compared with severe non-psychotic depression while controlling for comorbid psychiatric disorders.

This cohort study used routine data from nationwide health registers in Finland. Eligible participants had their first diagnosis for psychotic depression or for severe non-psychotic depression between the years 2000 and 2018, had no pre-existing diagnoses for schizophrenia spectrum disorders or bipolar disorder, and were aged 18–65 years at the index diagnosis. Causes of death were defined by ICD-10 codes. The follow-up time was up to 18 years.

We included 19 064 individuals with incident psychotic depression and 90 877 individuals with incident non-psychotic depression. Half (1199/2188) of the deaths in those with psychotic depression occurred within 5 years from the index diagnosis and the highest relative risk was during the first year after the diagnosis. Compared with individuals with non-psychotic depression, those with psychotic depression had a higher risk of all-cause mortality (adjusted hazard ratio, aHR = 1.59, 95% CI 1.48–1.70), suicides (aHR = 2.36, 95% CI 2.11–2.64) and fatal accidents (aHR 1.63, 95% CI 1.26–2.10) during the subsequent 5-year period after the index diagnosis.

Psychotic symptoms markedly added to the mortality risk associated with severe depression after controlling for psychiatric comorbidity. Prompt treatment and enhanced monitoring for psychotic symptoms is warranted in all patients with severe depression to prevent deaths because of suicides and other external causes.

Cognitive impairment is a core feature of schizophrenia, associated with poor functional outcomes. The course of cognitive function in the years following illness onset has remained a subject of debate, with a previous analysis finding no worsening, providing support for the neurodevelopmental model of schizophrenia. Since then, many more studies have reported on longitudinal cognitive performance in early psychosis, with some indicating deterioration, which does not align with this view.

This study aims to quantitatively review the literature on the longitudinal trajectory of cognitive deficits in the years following psychosis onset, in comparison with healthy controls. It is the first to also synthesise longitudinal data on social cognition.

Electronic databases (‘PubMed’, ‘PsycInfo’ and ‘Scopus’) were searched (to end September 2021). Meta-analyses of 25 longitudinal studies of cognition in early psychosis were conducted (1480 patients, 789 health controls). Unlike previous analyses, randomised controlled trials and those with multiple cognitive testing periods within the first year were excluded to minimise bias (PROSPERO, ID: CRD42021241525).

Small improvements were observed for global cognition (g = 0.25, 95% CI 0.17–0.33) and individual cognitive domains, but these were comparable with healthy controls and likely an artefact of practice effects.

There is no evidence of continued cognitive decline or improvement in the early years following psychosis onset, with a need for more studies over longer follow-up periods. Practice effects highlight the importance of including control samples in longitudinal and intervention studies. Further data are needed to evaluate the course of social cognition subdomains.

Healthcare workers (HCWs) have faced considerable pressures during the COVID-19 pandemic. For some, this has resulted in mental health distress and disorder. Although interventions have sought to support HCWs, few have been evaluated.

We aimed to determine the effectiveness of the ‘Foundations’ application (app) on general (non-psychotic) psychiatric morbidity.

We conducted a multicentre randomised controlled trial of HCWs at 16 NHS trusts (trial registration number: EudraCT: 2021-001279-18). Participants were randomly assigned to the app or wait-list control group. Measures were assessed at baseline, after 4 and 8 weeks. The primary outcome was general psychiatric morbidity (using the General Health Questionnaire). Secondary outcomes included: well-being; presenteeism; anxiety; depression and insomnia. The primary analysis used mixed-effects multivariable regression, presented as adjusted mean differences (aMD).

Between 22 March and 3 June 2021, 1002 participants were randomised (500:502), and 894 (89.2%) followed-up. The sample was predominately women (754/894, 84.3%), with a mean age of 44⋅3 years (interquartile range (IQR) 34–53). Participants randomised to the app had a reduction in psychiatric morbidity symptoms (aMD = −1.39, 95% CI −2.05 to −0.74), improvement in well-being (aMD = 0⋅54, 95% CI 0⋅20 to 0⋅89) and reduction in insomnia (adjusted odds ratio (aOR) = 0⋅36, 95% CI 0⋅21 to 0⋅60). No other significant findings were found, or adverse events reported.

The app had an effect in reducing psychiatric morbidity symptoms in a sample of HCWs. Given it is scalable with no adverse effects, the app may be used as part of an organisation's tiered staff support package. Further evidence is needed on long-term effectiveness and cost-effectiveness.

Research on the effectiveness of pharmacotherapies for schizophrenia and comorbid substance use disorder (SUD) is very sparse, and non-existent on the prevention of the development of SUDs in patients with schizophrenia.

To compare the real-world effectiveness of antipsychotics in schizophrenia in decreasing risk of developing an initial SUD, and psychiatric hospital admission and SUD-related hospital admission among patients with an SUD.

Two independent national cohorts including all persons diagnosed with schizophrenia (N = 45 476) were followed up for 22 (Finland: 1996–2017) and 11 (Sweden: 2006–2016) years. Risk of developing an SUD was calculated with between-individual models, and risks of psychiatric and SUD-related hospital admission were calculated with within-individual models, using Cox regression and adjusted hazard ratios (aHRs) for using versus not using certain antipsychotics.

For patients with schizophrenia without an SUD, clozapine use (Finland: aHR 0.20, 95% CI 0.16–0.24, P < 0.001; Sweden: aHR 0.35, 95% CI 0.24–0.50, P < 0.001) was associated with lowest risk of developing an initial SUD in both countries. Antipsychotic polytherapy was associated with second lowest risk (aHR 0.54, 95% CI 0.44–0.66) in Sweden, and third lowest risk (aHR 0.47, 95% CI 0.42–0.53) in Finland. Risk of relapse (psychiatric hospital admission and SUD-related hospital admission) were lowest for clozapine, antipsychotic polytherapy and long-acting injectables in both countries. Results were consistent across both countries.

Clozapine and antipsychotic polytherapy are most strongly associated with reduced risk of developing SUDs among patients with schizophrenia, and with lower relapse rates among patients with both diagnoses.