Enhancement of aerobic fitness improves social functioning in individuals with schizophrenia.

Individuals with schizophrenia display substantial deficits in social functioning (SF), characterized by chronic, lifelong presentations. Yet, at present there are few effective interventions to enhance SF in this population. Emerging evidence from studies of clinical populations that display similar SF deficits suggests that aerobic exercise (AE) may improve social skills. However, this putative impact has not been investigated in schizophrenia. Employing a single-blind, randomized clinical trial design, 33 individuals with schizophrenia were randomized to receive 12 weeks of Treatment-As-Usual (TAU; n = 17) or TAU + AE (n = 16) utilizing active-play video games (Xbox 360 Kinect) and traditional AE equipment. Participants completed an evaluation of aerobic fitness (VO2max) as well as self-, informant-, and clinician-reported SF measures at baseline and after 12 weeks. Twenty-six participants completed the study (79%; TAU = 13; AE = 13). At follow-up, the AE participants improved their VO2max by 18.0% versus - 0.5% in the controls (group x time interaction, F1,24 = 12.88; p = .002). Hierarchical stepwise regression analyses indicated improvements in VO2max significantly predicted enhancement in SF as indexed by self-, informant-, and clinician-reported measures, predicting 47%, 33%, and 25% of the variance, respectively (controlling for baseline demographics, medications, mood symptoms, and social networks). Compared to the TAU group, AE participants reported significant improvement in SF (23.0% vs. - 4.2%; group × time interaction, F1,24 = 7.48, p = .012). The results indicate that VO2max enhancement leads to improvements in SF in people with schizophrenia. Furthermore, low VO2max represents a modifiable risk factor of SF in people with schizophrenia, for which AE training offers a safe, non-stigmatizing, and nearly side-effect-free intervention.

Habenula-prefrontal resting-state connectivity in reactive aggressive men - A pilot study.

Disproportionate anger and reactive aggression in response to provocation are core symptoms of intermittent-explosive disorder (IED). Previous research shows a link between the propensity for aggression in healthy individuals and altered functioning of prefrontal-limbic and default-mode networks (DMN) at rest when no provocation is present. In a pilot study, we used resting-state functional magnetic resonance imaging to investigate the effects of pronounced reactive aggression in men, exemplified by IED, on the functional organization of resting-state brain networks including subcortical nodes such as the habenula previously implicated in aggression in preclinical models. Graph theory was applied to resting-state networks to determine alterations in global efficiency and clustering in high reactive aggressive men compared to low reactive aggressive men (controls). Further, we computed within-group correlations between trait aggression and graph measures, as well as within-group whole-brain seed-to-voxel regression analyses between trait aggression and habenula resting-state functional connectivity (rsFC). Reactive aggressive men compared to controls showed higher global efficiency in the left habenula, the left pulvinar in the thalamus, the left dorso-lateral prefrontal cortex, and the right temporal pole, as well as a trend for decreased clustering in DMN nodes. In the reactive aggressive group, high levels of trait aggression were linked to lower global efficiency of the left habenula, and to lower rsFC between the left habenula and the left ventro-lateral prefrontal cortex, a core region involved in inhibitory control. Together with preclinical evidence, our findings in men underline the relevance of aberrant habenula-prefrontal connectivity for the severity of aggressive behavior. This article is part of the Special Issue entitled 'Current status of the neurobiology of aggression and impulsivity'.