Although research has shown that exposure to potentially traumatic and morally injurious events is associated with psychological symptoms among veterans, knowledge regarding functioning impacts remains limited.

A population-based sample of post-9/11 veterans completed measures of intimate relationship, health, and work functioning at approximately 9, 15, 21, and 27 months after leaving service. Moral injury, posttraumatic stress, and depression were assessed at ~9 months post-separation. We used Latent Growth Mixture Models to identify discrete classes characterized by unique trajectories of change in functioning over time and to examine predictors of class membership.

Veterans were assigned to one of four functioning trajectories: high and stable, high and decreasing, moderate and increasing, and moderate and stable. Whereas posttraumatic stress, depression, and moral injury associated with perpetration and betrayal predicted worse outcomes at baseline across multiple functioning domains, moral injury associated with perpetration and depression most reliably predicted assignment to trajectories characterized by relatively poor or declining functioning.

Moral injury contributes to functional problems beyond what is explained by posttraumatic stress and depression, and moral injury due to perpetration and depression most reliably predicted assignment to trajectories characterized by functional impairment over time.

Undertreatment of depression in primary care is common. Efforts to address this tend to overlook the role of patient attitudes. Our aim was to validate and describe responses to a questionnaire about attitudes to depression and its treatment in a sample with experience of moderate and severe depressive episodes.

Cross-sectional survey of 866 individuals with a confirmed history of an ICD-10 depressive episode in the 12 months preceding interview, recruited from 7271 consecutive general practitioner (GP) attendees in 36 general practices in England and Wales. Attitudes to and beliefs about depression were assessed using a 19-item self-report questionnaire.

Factor analysis resulted in a three-factor solution: factor 1, depression as a disabling, permanent state; factor 2, depression as a medical condition responsive to support; and factor 3, antidepressants are addictive and ineffective. Participants who received and adhered to antidepressant medication and disclosed their depression to family and friends had significantly lower scores on factors 1 and 3 but higher scores on factor 2.

People with moderate or severe depressive episodes have subtle and divergent views about this condition, its outcome, and appropriate help. Such beliefs should be considered in primary care as they may significantly impact on help seeking and adherence to treatment.

Pre- and perinatal adversities may increase the risk for schizophrenia and bipolar disorder. Hypoxia-related obstetric complications (OCs) are associated with brain anatomical abnormalities in schizophrenia, but their association with brain anatomy variation in bipolar disorder is unknown.

Magnetic resonance imaging brain scans, clinical examinations and data from the Medical Birth Registry of Norway were obtained for 219 adults, including 79 patients with a DSM-IV diagnosis of bipolar disorder (age 29.4 years, s.d. = 11.8 years, 39% male) and 140 healthy controls (age 30.8 years, s.d. = 12.0 years, 53% male). Severe hypoxia-related OCs throughout pregnancy/birth and perinatal asphyxia were each studied in relation to a priori selected brain volumes (hippocampus, lateral ventricles and amygdala, obtained with FreeSurfer), using linear regression models covarying for age, sex, medication use and intracranial volume. Multiple comparison adjustment was applied.

Perinatal asphyxia was associated with smaller left amygdala volume (t = −2.59, p = 0.012) in bipolar disorder patients, but not in healthy controls. Patients with psychotic bipolar disorder showed distinct associations between perinatal asphyxia and smaller left amygdala volume (t = −2.69, p = 0.010), whereas patients with non-psychotic bipolar disorder showed smaller right hippocampal volumes related to both perinatal asphyxia (t = −2.60, p = 0.015) and severe OCs (t = −3.25, p = 0.003). No associations between asphyxia or severe OCs and the lateral ventricles were found.

Pre- and perinatal hypoxia-related OCs are related to brain morphometry in bipolar disorder in adulthood, with specific patterns in patients with psychotic versus non-psychotic illness.

Theta cordance is a novel quantitative electroencephalography (QEEG) measure that correlates with cerebral perfusion. A series of clinical studies has demonstrated that the prefrontal theta cordance value decreases after 1 week of treatment in responders to antidepressants and that this effect precedes clinical improvement. Ketamine, a non-competitive antagonist of N-methyl-d-aspartate (NMDA) receptors, has a unique rapid antidepressant effect but its influence on theta cordance is unknown.

In a double-blind, cross-over, placebo-controlled experiment we studied the acute effect of ketamine (0.54 mg/kg within 30 min) on theta cordance in a group of 20 healthy volunteers.

Ketamine infusion induced a decrease in prefrontal theta cordance and an increase in the central region theta cordance after 10 and 30 min. The change in prefrontal theta cordance correlated with ketamine and norketamine blood levels after 10 min of ketamine infusion.

Our data indicate that ketamine infusion immediately induces changes similar to those that monoamineric-based antidepressants induce gradually. The reduction in theta cordance could be a marker and a predictor of the fast-acting antidepressant effect of ketamine, a hypothesis that could be tested in depressive patients treated with ketamine.

This random-effects model meta-analysis of double-blind, randomized placebo-controlled trials compared recurrence rates in bipolar disorder (BD) patients between antipsychotic/mood stabilizer discontinuation and maintenance groups.

We conducted systematic literature search of Embase, PubMed, and CENTRAL databases without language restriction from inception until 22 May 2020. Independent investigators assessed studies and extracted data. We calculated risk ratios (RRs) and numbers needed to benefit or harm (NNTB/NNTH). Primary outcome was the recurrence rate of any mood episode at 6 months. Secondary outcomes were recurrence rates of depressive episodes and manic/hypomanic/mixed episodes and all-cause discontinuation at 6 months. We also investigated these outcomes at 1, 3, 9, 12, 18, and 24 months.

We identified 22 studies (n = 5462) receiving aripiprazole, asenapine, divalproex, long-acting injectable (LAI)-aripiprazole, LAI-risperidone, lamotrigine, lithium, olanzapine, paliperidone, or quetiapine. Mean study duration was 64.50 ± 69.35 weeks. The maintenance group demonstrated lower recurrence rates of any mood episode, depressive episodes, and manic/hypomanic/mixed episodes as well as reduced all-cause discontinuation at every observational point. The RRs (95% confidence interval, NNTB/NNTH) of recurrence rate at 6 months were 0.61 (0.54–0.70, 5) for any mood episode, 0.72 (0.60–0.87, 13) for depressive episodes, and 0.45 (0.36–0.57, 6) for manic/hypomanic/mixed episodes. The RR for all-cause discontinuation at 6 months was 0.71 (0.61–0.82, 6).

Maintaining drug treatment during clinically stable BD prevented recurrence for up to 24 months. Discontinuation of medications for ⩾1 month significantly increased recurrence risk. However, 47.3% of patients who discontinued drugs for 6 months did not experience recurrence.

Women suffering from first onset postpartum mental disorders (PPMD) have a highly elevated risk of suicide. The current study aimed to: (1) describe the risk of self-harm among women with PPMD and (2) investigate the extent to which self-harm is associated with later suicide.

We conducted a register-based cohort study linking national Danish registers. This identified women with any recorded first inpatient or outpatient contact to a psychiatric facility within 90 days after giving birth to their first child. The main outcome of interest was defined as the first hospital-registered episode of self-harm. Our cohort consisted of 1 202 292 women representing 24 053 543 person-years at risk.

Among 1554 women with severe first onset PPMD, 64 had a first-ever hospital record of self-harm. Women with PPMD had a hazard ratio (HR) for self-harm of 6.2 (95% CI 4.9–8.0), compared to mothers without mental disorders; but self-harm risk was lower in PPMD women compared to mothers with non-PPMD [HR: 10.1, (95% CI 9.6–10.5)] and childless women with mental disorders [HR: 9.3 (95% CI 8.9–9.7)]. Women with PPMD and records of self-harm had a significantly greater risk for later suicide compared with all other groups of women in the cohort.

Women with PPMD had a high risk of self-harm, although lower than risks observed in other psychiatric patients. However, PPMD women who had self-harmed constituted a vulnerable group at significantly increased risk of later suicide.

Guidelines and mental healthcare models suggest the use of psychological treatment for anxiety disorders in primary care but systematic estimates of the effect sizes in primary care settings are lacking. The aim of this study was to examine the effectiveness of psychological therapies in primary care for anxiety disorders.

The Cochrane Central Register of Controlled Trials (CENTRAL), EMBASE, Medline, PsycINFO and Pubmed databases were searched in July 2010. Manuscripts describing psychological treatment for anxiety disorders/increased level of anxiety symptoms in primary care were included if the research design was a randomized controlled trial (RCT) and if the psychological treatment was compared with a control group.

In total, 1343 abstracts were identified. Of these, 12 manuscripts described an RCT comparing psychological treatment for anxiety with a control group in primary care. The pooled standardized effect size (12 comparisons) for reduced symptoms of anxiety at post-intervention was d = 0.57 [95% confidence interval (CI) 0.29–0.84, p = 0.00, the number needed to treat (NNT) = 3.18]. Heterogeneity was significant among the studies (I2 = 58.55, Q = 26.54, p < 0.01). The quality of studies was not optimal and missing aspects are summarized.

We found a moderate effect size for the psychological treatment of anxiety disorders in primary care. Several aspects of the treatment are related to effect size. More studies are needed to evaluate the long-term effects given the chronicity and recurrent nature of anxiety.

Altered corticostriatothalamic encoding of reinforcement is a core feature of depression. Here we examine reinforcement learning in late-life depression in the theoretical framework of the vascular depression hypothesis. This hypothesis attributes the co-occurrence of late-life depression and poor executive control to prefrontal/cingulate disconnection by vascular lesions.

Our fMRI study compared 31 patients aged ⩾60 years with major depression to 16 controls. Using a computational model, we estimated neural and behavioral responses to reinforcement in an uncertain, changing environment (probabilistic reversal learning).

Poor executive control and depression each explained distinct variance in corticostriatothalamic response to unexpected rewards. Depression, but not poor executive control, predicted disrupted functional connectivity between the striatum and prefrontal cortex. White-matter hyperintensities predicted diminished corticostriatothalamic responses to reinforcement, but did not mediate effects of depression or executive control. In two independent samples, poor executive control predicted a failure to persist with rewarded actions, an effect distinct from depressive oversensitivity to punishment. The findings were unchanged in a subsample of participants with vascular disease. Results were robust to effects of confounders including psychiatric comorbidities, physical illness, depressive severity, and psychotropic exposure.

Contrary to the predictions of the vascular depression hypothesis, altered encoding of rewards in late-life depression is dissociable from impaired contingency learning associated with poor executive control. Functional connectivity and behavioral analyses point to a disruption of ascending mesostriatocortical reward signals in late-life depression and a failure of cortical contingency encoding in elderly with poor executive control.