BackgroundThere is a broad literature suggesting that cognitive difficulties are associated with violence across a variety of groups. Although neurocognitive and social cognitive deficits are core features of schizophrenia, evidence of a relationship between cognitive impairments and violence within this patient population has been mixed.MethodsWe prospectively examined whether neurocognition and social cognition predicted inpatient violence amongst patients with schizophrenia and schizoaffective disorder (n = 89; 10 violent) over a 12 month period. Neurocognition and social cognition were assessed using the MATRICS Consensus Cognitive Battery (MCCB).ResultsUsing multivariate analysis neurocognition and social cognition variables could account for 34 % of the variance in violent incidents after controlling for age and gender. Scores on a social cognitive reasoning task (MSCEIT) were significantly lower for the violent compared to nonviolent group and produced the largest effect size. Mediation analysis showed that the relationship between neurocognition and violence was completely mediated by each of the following variables independently: social cognition (MSCEIT), symptoms (PANSS Total Score), social functioning (SOFAS) and violence proneness (HCR-20 Total Score). There was no evidence of a serial pathway between neurocognition and multiple mediators and violence, and only social cognition and violence proneness operated in parallel as significant mediators accounting for 46 % of the variance in violent incidents. There was also no evidence that neurocogniton mediated the relationship between any of these variables and violence.ConclusionsOf all the predictors examined, neurocognition was the only variable whose effects on violence consistently showed evidence of mediation. Neurocognition operates as a distal risk factor mediated through more proximal factors. Social cognition in contrast has a direct effect on violence independent of neurocognition, violence proneness and symptom severity. The neurocognitive impairment experienced by patients with schizophrenia spectrum disorders may create the foundation for the emergence of a range of risk factors for violence including deficits in social reasoning, symptoms, social functioning, and HCR-20 risk items, which in turn are causally related to violence.Electronic supplementary materialThe online version of this article (doi:10.1186/s12888-015-0548-0) contains supplementary material, which is available to authorized users.

Most individuals with schizophrenia suffer some cognitive dysfunction: such deficits are predictive of longer-term functioning; and current dopamine-blocking antipsychotics have made little impact on this domain. There is a pressing need to develop novel pharmacological agents to tackle this insidious but most disabling of problems. The acetylcholinergic system is involved in cognitive and attentional processing, and its metabotropic and nicotinic receptors are widespread throughout the brain. Deficits in acetylcholinergic functioning occur in schizophrenia, and high rates of tobacco smoking have been posited to represent a form of self-medication. The nicotinic acetylcholine receptor (nAChR) has emerged as a putative target to improve cognitive deficits in schizophrenia, and this study systematically reviewed the emerging data. Nineteen studies were identified, covering three compound classes: agonists at the α7 and α 4β2 nAChRs, and positive allosteric modulators. Overall data are underwhelming: some studies showed significant improvements in cognition but as many studies had negative findings. It remains unclear if this represents drug limitations or nascent study methodology problems. The literature is particularly hindered by variability in inclusion of smokers, generally small sample sizes, and a lack of consensus on cognitive test batteries. Future work should evaluate longer-term outcomes, and, particularly, the effects of concomitant cognitive training.

IntroductionThis study examines the feasibility of conducting diabetes-focused cognitive–behavioral therapy (CBT) via a secure online real-time instant messaging system intervention to support self-management and improve glycemic control in people with type 1 diabetes.Research design and methodsWe used a pre–post uncontrolled intervention design over 12 months. We recruited adults with type 1 diabetes and suboptimal glycemic control (HbA1c ≥69 mmol/mol (DCCT 8.5%) for 12 months) across four hospitals in London. The intervention comprised 10 sessions of diabetes-focused CBT delivered by diabetes specialist nurses. The primary outcomes were number of eligible patients, rates of recruitment and follow-up, number of sessions completed and SD of the main outcome measure, change in HbA1c over 12 months. We measured the feasibility of collecting secondary outcomes, that is, depression measured using Patient Health Questionnaire-9 (PHQ-9), anxiety measured Generalised Anxiety Disorder (GAD) and the Diabetes Distress Scale (DDS).ResultsWe screened 3177 patients, of whom 638 were potentially eligible, from whom 71 (11.1%) were recruited. The mean age was 28.1 (13.1) years, and the mean HbA1c was 84.6 mmol/mol (17.8), DCCT 9.9%. Forty-six (65%) patients had at least 1 session and 29 (41%) completed all sessions. There was a significant reduction in HbA1c over 12 months (mean difference −6.2 (2.3) mmol/mol, DCCT 0.6%, p=0.038). The change scores in PHQ-9, GAD and DDS also improved.ConclusionsIt would be feasible to conduct a full-scale text-based synchronized real-time diabetes-focused CBT as an efficacy randomized controlled trial.

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