Social cognition as a mediator variable between neurocognition and functional outcome in schizophrenia: empirical review and new results by structural equation modeling.

University Hospital of Psychiatry, University of Bern, Bolligenstrasse 111, 3000 Bern 60, Switzerland.
Schizophrenia Bulletin (Impact Factor: 8.61). 09/2011; 37 Suppl 2:S41-54. DOI: 10.1093/schbul/sbr079
Source: PubMed

ABSTRACT Cognitive impairments are currently regarded as important determinants of functional domains and are promising treatment goals in schizophrenia. Nevertheless, the exact nature of the interdependent relationship between neurocognition and social cognition as well as the relative contribution of each of these factors to adequate functioning remains unclear. The purpose of this article is to systematically review the findings and methodology of studies that have investigated social cognition as a mediator variable between neurocognitive performance and functional outcome in schizophrenia. Moreover, we carried out a study to evaluate this mediation hypothesis by the means of structural equation modeling in a large sample of 148 schizophrenia patients. The review comprised 15 studies. All but one study provided evidence for the mediating role of social cognition both in cross-sectional and in longitudinal designs. Other variables like motivation and social competence additionally mediated the relationship between social cognition and functional outcome. The mean effect size of the indirect effect was 0.20. However, social cognitive domains were differentially effective mediators. On average, 25% of the variance in functional outcome could be explained in the mediation model. The results of our own statistical analysis are in line with these conclusions: Social cognition mediated a significant indirect relationship between neurocognition and functional outcome. These results suggest that research should focus on differential mediation pathways. Future studies should also consider the interaction with other prognostic factors, additional mediators, and moderators in order to increase the predictive power and to target those factors relevant for optimizing therapy effects.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: There is substantial evidence regarding a social cognitive deficit in schizophrenia, and it has been suggested to be a trait-marker of this disorder. However, a domain-by-domain analysis of social cognitive deficits in individuals at clinical high risk (CHR) for psychosis has not been performed. Electronic databases were searched for studies regarding social cognitive performance in individuals at CHR. The included social cognitive domains, which were classified based on the Social Cognition Psychometric Evaluation (SCOPE) initiative of the National Institute of Mental Health (NIMH), were as follows: theory of mind (ToM), social perception (SP), attributional bias (AB), and emotion processing (EP). Twenty studies that included 1229 individuals at CHR and 825 healthy controls met the inclusion criteria. The overall effect size for social cognition was medium (g=-0.477). The largest effect size was identified for AB (g=-0.708). A medium effect size was identified for EP (g=-0.446) and ToM (g=-0.425), and small effects were identified for SP (g=-0.383). This is the first quantitative domain-by-domain social cognitive meta-analysis regarding CHR individuals. The present study indicated that individuals at CHR exhibited significant impairments in all domains of social cognition compared with healthy controls, with the largest effect size identified for AB. The identification of social cognitive domains that reflect an increased risk for impending psychosis and of predictors of the conversion to psychosis via a longitudinal follow-up study is required. Copyright © 2015 Elsevier B.V. All rights reserved.
    Schizophrenia Research 03/2015; 164(1-3):28-34. DOI:10.1016/j.schres.2015.02.008 · 4.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Social cognition may be critical to the impoverished social functioning seen in serious mental illness. However, although social-cognitive deficits are consistently demonstrated in schizophrenia spectrum disorders (SSD), studies in bipolar disorder (BD) have produced inconsistent results. This inconsistency may relate to symptom profiles of patients studied, particularly the presence or absence of psychotic features. Thus, we examined social cognition in bipolar disorder with psychotic features (BD +) versus without psychotic features (BD −) relative to SSD and controls.
    02/2015; 32. DOI:10.1016/j.scog.2014.12.003
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Social dysfunction is common in patients with psychotic disorders. Oxytocin is a neuropeptide with a central role in social behavior. This study aims to explore the relationship between oxytocin pathway genes and symptoms related to social dysfunction in patients with psychotic disorders. We performed association analyses between four oxytocin pathway genes (OXT, OXTR, AVP, and CD38) and four areas of social behavior-related psychopathology as measured by Positive and Negative Syndrome Scale. For this purpose, we used both a polygenic risk score (PGRS) and single OXTR candidate single nucleotide polymorphism previously reported in the literature (rs53576, rs237902, and rs2254298). A total of 734 subjects with DSM-IV psychotic spectrum disorders and 420 healthy controls were included. Oxytocin pathway PGRSs were calculated based on the independent Psychiatric Genomics Consortium study sample. There was a significant association between symptom of Emotional Withdrawal and the previously reported OXTR risk allele A in rs53576. No significant associations between oxytocin pathway gene variants and a diagnosis of psychotic disorder were found. Our findings indicate that while oxytocin pathway genes do not appear to contribute to the susceptibility to psychotic disorders, variations in the OXTR gene might play a role in the development of impaired social behavior.
    Frontiers in Human Neuroscience 01/2015; 9:9. DOI:10.3389/fnhum.2015.00009 · 2.90 Impact Factor


1 Download
Available from