We examined the extent to which trait anger and psychopathic traits predicted post-discharge self-directed violence (SDV) and other-directed violence (ODV) among psychiatric patients.

Participants were 851 psychiatric patients sampled from in-patient hospitals for the MacArthur Violence Risk Assessment Study (MVRAS). Participants were administered baseline interviews at the hospital and five follow-up interviews in the community at approximately 10-week intervals. Psychopathy and trait anger were assessed with the Psychopathy Checklist: Screening Version (PSC:SV) and the Novaco Anger Scale (NAS) respectively. SDV was assessed during follow-ups with participants and ODV was assessed during interviews with participants and collateral informants. Psychopathy facets and anger were entered in logistic regression models to predict membership in one of four groups indicating violence status during follow-up: (1) SDV, (2) ODV, (3) co-occurring violence (COV), and (4) no violence.

Anger predicted membership in all three violence groups relative to a non-violent reference group. In unadjusted models, all psychopathy facets predicted ODV and COV during follow-up. In adjusted models, interpersonal and antisocial traits of psychopathy predicted membership in the ODV group whereas only antisocial traits predicted membership in the COV group.

Although our results provide evidence for a broad role for trait anger in predicting SDV and ODV among discharged psychiatric patients, they suggest that unique patterns of psychopathic traits differentially predict violence toward self and others. The measurement of anger and facets of psychopathy during discharge planning for psychiatric patients may provide clinicians with information regarding risk for specific types of violence.

Although repeatedly associated with white matter microstructural alterations, bipolar disorder (BD) has been relatively unexplored using complex network analysis. This method combines structural and diffusion magnetic resonance imaging (MRI) to model the brain as a network and evaluate its topological properties. A group of highly interconnected high-density structures, termed the ‘rich-club’, represents an important network for integration of brain functioning. This study aimed to assess structural and rich-club connectivity properties in BD through graph theory analyses.

We obtained structural and diffusion MRI scans from 42 euthymic patients with BD type I and 43 age- and gender-matched healthy volunteers. Weighted fractional anisotropy connections mapped between cortical and subcortical structures defined the neuroanatomical networks. Next, we examined between-group differences in features of graph properties and sub-networks.

Patients exhibited significantly reduced clustering coefficient and global efficiency, compared with controls globally and regionally in frontal and occipital regions. Additionally, patients displayed weaker sub-network connectivity in distributed regions. Rich-club analysis revealed subtly reduced density in patients, which did not withstand multiple comparison correction. However, hub identification in most participants indicated differentially affected rich-club membership in the BD group, with two hubs absent when compared with controls, namely the superior frontal gyrus and thalamus.

This graph theory analysis presents a thorough investigation of topological features of connectivity in euthymic BD. Abnormalities of global and local measures and network components provide further neuroanatomically specific evidence for distributed dysconnectivity as a trait feature of BD.

We do not know how primary care treatment of depression varies by age across both psychotropic medication and psychological therapies.

Cohort study including 19 710 people aged 55+ with GP recorded depression diagnoses and 26 276 people with recorded depression symptoms during the period 2009–2013, from 373 General Practices in The Health Improvement Network (THIN) database in England. Main outcomes were initiation of treatment with anti-depressants, anxiolytics, hypnotics, anti-psychotic drugs, referrals to psychological therapies within 6 months of onset.

Treatment rates with antidepressants are high for those recorded with new depression diagnoses (87.1%) or symptoms of depression (58.7%). Treatment in those with depression diagnoses varies little by age. In those with depressive symptoms there was a J-shaped pattern with reduced antidepressant treatment in those in their 60s and 70s followed by increased treatment in the oldest age groups (85+ years), compared with those aged 55–59 years. Other psychotropic drug prescribing (hypnotics/anxiolytics, antipsychotics) all increase with increasing age. Recorded referrals for psychological therapies were low, and decreased steadily with increasing age, such that women aged 75–79 years with depression diagnoses had around six times lower odds of referral (OR 0.17, 95% CI 0.1–0.29) than those aged 55–59 years, and men aged 80–84 years had around seven times lower (OR 0.14, 95% CI 0.05–0.36).

The oldest age groups with new depression diagnoses and symptoms have fewer recorded referrals to psychological therapies, and higher psychotropic drug treatment rates in primary care. This suggests potential inequalities in access to psychological therapies.

A dysfunctional network of prefrontal and (para-)limbic brain region has been suggested to underlie emotional dysregulation in borderline personality disorder (BPD). Abnormal activity in this network may be due to structural alterations in white-matter tracts connecting prefrontal and (para-)limbic brain regions. To test this hypothesis, we investigated the structural integrity of major white-matter tracts connecting these regions in BPD.

Using diffusion tensor imaging, we investigated fractional anisotropy (FA), axonal anisotropy (AD) and radial diffusivity (RD) in the uncinate fasciculus, the major white-matter tract connecting (para-)limbic and prefrontal brain regions, in 26 healthy controls (HC) and 26 BPD participants. To clarify the specificity of possible white-matter alterations among HC and BPD participants, FA, AD and RD were also investigated in the cingulum.

We found distinct structural alterations in the uncinate fasciculus but not in the cingulum of BPD participants. Compared to HC participants, BPD participants showed lower FA and higher RD in the uncinate fasciculus. By contrast, AD did not differ in the uncinate fasciculus of HC and BPD participants.

Our finding of abnormal FA and RD in the uncinate fasciculus indicates distinct white-matter alterations in BPD, presumably due to stress-induced myelin degeneration in the aftermath of stressful life events. Although these alterations may account for abnormal activity in brain regions implicated in emotion dysregulation, such as the amygdala, anterior cingulate cortex and prefrontal cortex, it remains to be determined whether these alterations are specific for BPD.

To evaluate the effectiveness of graded exercise therapy (GET), counselling (COUNS) and usual care plus a cognitive behaviour therapy (CBT) booklet (BUC) for people presenting with chronic fatigue in primary care.

A randomized controlled trial in general practice. The main outcome measure was the change in the Chalder fatigue score between baseline and 6 months. Secondary outcomes included a measure of global outcome, including anxiety and depression, functional impairment and satisfaction.

The reduction in mean Chalder fatigue score at 6 months was 8.1 [95% confidence interval (CI) 6.6–10.4] for BUC, 10.1 (95% CI 7.5–12.6) for GET and 8.6 (95% CI 6.5–10.8) for COUNS. There were no significant differences in change scores between the three groups at the 6- or 12-month assessment. Dissatisfaction with care was high. In relation to the BUC group, the odds of dissatisfaction at the 12-month assessment were less for the GET [odds ratio (OR) 0.11, 95% CI 0.02–0.54, p=0.01] and COUNS groups (OR 0.13, 95% CI 0.03–0.53, p=0.004).

Our evidence suggests that fatigue presented to general practitioners (GPs) tends to remit over 6 months to a greater extent than found previously. Compared to BUC, those treated with graded exercise or counselling therapies were not significantly better with respect to the primary fatigue outcome, although they were less dissatisfied at 1 year. This evidence is generalizable nationally and internationally. We suggest that GPs ask patients to return at 6 months if their fatigue does not remit, when therapy options can be discussed further.

Reward dysfunction is a major dimension of depressive symptomatology, but it remains obscure if that dysfunction varies across different reward types. In this study, we focus on the abnormalities in anticipatory/consummatory processing of monetary and social reward associated with depressive symptoms.

Forty participants with depressive symptoms and forty normal controls completed the monetary incentive delay (MID) and social incentive delay (SID) tasks with event-related potential (ERP) recording.

In the SID but not the MID task, both the behavioral hit rate and the ERP component contingent negative variation (CNV; indicating reward anticipation) were sensitive to the interaction between the grouping factor and reward magnitude; that is, the depressive group showed a lower hit rate and a smaller CNV to large-magnitude (but not small-magnitude) social reward cues compared to the control group. Further, these two indexes were correlated with each other. Meanwhile, the ERP components feedback-related negativity and P3 (indicating reward consumption) were sensitive to the main effect of depression across the MID and SID tasks, though this effect was more prominent in the SID task.

Overall, we suggest that depressive symptoms are associated with deficits in both the reward anticipation and reward consumption stages, particularly for social rewards. These findings have a potential to characterize the profile of functional impairment that comprises and maintains depression.

Commonly observed distortions in decision-making among patients with major depressive disorder (MDD) may emerge from impaired reward processing and cognitive biases toward negative events. There is substantial theoretical support for the hypothesis that MDD patients overweight potential losses compared with gains, though the neurobiological underpinnings of this bias are uncertain.

Twenty-one unmedicated patients with MDD were compared with 25 healthy controls (HC) using functional magnetic resonance imaging (fMRI) together with an economic decision-making task over mixed lotteries involving probabilistic gains and losses. Region-of-interest analyses evaluated neural signatures of gain and loss coding within a core network of brain areas known to be involved in valuation (anterior insula, caudate nucleus, ventromedial prefrontal cortex).

Usable fMRI data were available for 19 MDD and 23 HC subjects. Anterior insula signal showed negative coding of losses (gain > loss) in HC subjects consistent with previous findings, whereas MDD subjects demonstrated significant reversals in these associations (loss > gain). Moreover, depression severity further enhanced the positive coding of losses in anterior insula, ventromedial prefrontal cortex, and caudate nucleus. The hyper-responsivity to losses displayed by the anterior insula of MDD patients was paralleled by a reduced influence of gain, but not loss, stake size on choice latencies.

Patients with MDD demonstrate a significant shift from negative to positive coding of losses in the anterior insula, revealing the importance of this structure in value-based decision-making in the context of emotional disturbances.

Impaired brain metabolism may be central to schizophrenia pathophysiology, but the magnitude and consistency of metabolic dysfunction is unknown.

We searched MEDLINE, PsychINFO and EMBASE between 01/01/1980 and 13/05/2021 for studies comparing regional brain glucose metabolism using 18FDG-PET, in schizophrenia/first-episode psychosis v. controls. Effect sizes (Hedges g) were pooled using a random-effects model. Primary measures were regional absolute and relative CMRGlu in frontal, temporal, parietal and occipital lobes, basal ganglia and thalamus.

Thirty-six studies (1335 subjects) were included. Frontal absolute glucose metabolism (Hedge's g = −0.74 ± 0.54, p = 0.01; I2 = 67%) and metabolism relative to whole brain (g = −0.44 ± 0.34, p = 0.01; I2 = 55%) were lower in schizophrenia v. controls with moderate heterogeneity. Absolute frontal metabolism was lower in chronic (g = −1.18 ± 0.73) v. first-episode patients (g = −0.09 ± 0.88) and controls. Medicated patients showed frontal hypometabolism relative to controls (−1.04 ± 0.26) while metabolism in drug-free patients did not differ significantly from controls. There were no differences in parietal, temporal or occipital lobe or thalamic metabolism in schizophrenia v. controls. Excluding outliers, absolute basal ganglia metabolism was lower in schizophrenia v. controls (−0.25 ± 0.24, p = 0.049; I2 = 5%). Studies identified reporting voxel-based morphometry measures of absolute 18FDG uptake (eight studies) were also analysed using signed differential mapping analysis, finding lower 18FDG uptake in the left anterior cingulate gyrus (Z = −4.143; p = 0.007) and the left inferior orbital frontal gyrus (Z = −4.239; p = 0.02) in schizophrenia.

We report evidence for hypometabolism with large effect sizes in the frontal cortex in schizophrenia without consistent evidence for alterations in other brain regions. Our findings support the hypothesis of hypofrontality in schizophrenia.

Recent evidence suggests that neurocognitive impairments in remitted patients with bipolar disorder (BD) are heterogeneous. Our study aims to replicate recent findings of neurocognitive subgroups, and further explore whether these are related to impairments in affective cognition, in a large sample of remitted patients recently diagnosed with BD and their unaffected relatives compared to healthy controls (HCs).

Hierarchal cluster analysis was conducted using neurocognitive data from remitted patients with BD (n = 158). Relatives of patients with BD (n = 52) were categorised into groups consistent with their affected relative's cluster assignment. The neurocognitive clusters of patients with BD and relatives, respectively, were compared with HCs (n = 110) in neurocognition and affective cognition (i.e. emotion processing and regulation).

Three discrete neurocognitive clusters were identified in patients with BD: a globally impaired (23.4%), a selectively impaired (31.0%) and a cognitively intact cluster (45.6%). The neurocognitive subgroups differed in affective cognition, with patients categorised as globally impaired exhibited most impairments in facial expression recognition and emotion regulation in social scenarios. First-degree relatives of cognitively impaired patients displayed impaired facial expression recognition but no impairments in non-emotional cognition.

In a clinical sample of remitted patients recently diagnosed with BD 54.4% had either global or selective cognitive impairment, replicating results of previous studies in patients with longer illness duration. The results suggest that patterns of neurocognition are associated with differential impairments in affective cognition. Aberrant affective cognition in relatives of patients categorised as neurocognitively impaired indicates an inherited risk for BD.

Cognitive training (CT) and aerobic exercise both show promising moderate impact on cognition and everyday functioning in schizophrenia. Aerobic exercise is hypothesized to increase brain-derived neurotrophic factor (BDNF) and thereby synaptic plasticity, leading to increased learning capacity. Systematic CT should take advantage of increased learning capacity and be more effective when combined with aerobic exercise.

We examined the impact of a 6-month program of cognitive training & exercise (CT&E) compared to cognitive training alone (CT) in 47 first-episode schizophrenia outpatients. All participants were provided the same Posit Science computerized CT, 4 h/week, using BrainHQ and SocialVille programs. The CT&E group also participated in total body circuit training exercises to enhance aerobic conditioning. Clinic and home-based exercise were combined for a target of 150 min per week.

The MATRICS Consensus Cognitive Battery Overall Composite improved significantly more with CT&E than with CT alone (p = 0.04), particularly in the first 3 months (6.5 v. 2.2 T-score points, p < 0.02). Work/school functioning improved substantially more with CT&E than with CT alone by 6 months (p < 0.001). BDNF gain tended to predict the amount of cognitive gain but did not reach significance. The cognitive gain by 3 months predicted the amount of work/school functioning improvement at 6 months. The amount of exercise completed was strongly associated with the degree of cognitive and work/school functioning improvement.

Aerobic exercise significantly enhances the impact of CT on cognition and functional outcome in first-episode schizophrenia, apparently driven by the amount of exercise completed.

In the present study we investigated whether SCP predicted fatigue and pain over a 14-day period in a sample of 90 CFS patients using a diary method approach. After completing the Depressive Experiences Questionnaire (DEQ) as a measure of SCP, patients were asked each day for 14 days to complete Visual Analogue Scales (VAS) of fatigue, pain and severity of depression. Data were analysed using multilevel analysis.

The results from unconditional models revealed considerable fluctuations in fatigue over the 14 days, suggesting strong temporal variability in fatigue. By contrast, pain was relatively stable over time but showed significant inter-individual differences. Congruent with expectations, fixed-effect models showed that SCP was prospectively associated with higher daily fatigue and pain levels over the 14-day period, even after controlling for levels of depression.

This is the first study to show that SCP predicts both fatigue and pain symptoms in CFS in the daily course of life. Hence, therapeutic interventions aimed at targeting SCP should be considered in the treatment of CFS patients with such features.

Both mental disorders and personality characteristics are associated with impaired work functioning, but these determinants have not yet been studied together. The aim of this paper is to examine the impairing effects that mental disorders and personality characteristics (i.e. neuroticism, locus of control and self-esteem) have on work functioning.

Data for a representative sample of 3570 working people were derived from the first two waves of the Netherlands Mental Health Survey and Incidence Study (NEMESIS), a prospective cohort study in the Dutch adult population.

Higher neuroticism, more external locus of control and lower self-esteem were each significantly associated with subsequent impairment in work functioning, independently of any effects from mental disorders. Associations between mental disorders and subsequent work impairment disappeared once personality traits were taken into account. Personality traits did not moderate the relationships between mental disorders and work functioning.

Working people with vulnerable personalities have a greater risk of impaired work functioning, independent of the risk from any mental disorder they may have.