عملکرد شناختی اجتماعی در علائم اولیه روان پریشی: فرا تجزیه و تحلیل
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32001||2015||7 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Schizophrenia Research, Volume 164, Issues 1–3, May 2015, Pages 28–34
Background 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. Method 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). Results 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). Conclusion 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.
Social cognition refers to the mental operations that underlie social interactions, including the processes involved in the perception, interpretation, and generation of responses to the intentions, dispositions, and behaviors of other individuals (Penn et al., 1997 and Green et al., 2005). Social cognition, similar to other aspects of cognition, is a multifaceted concept that comprises several sub-domains and processes. The Social Cognition Psychometric Evaluation (SCOPE) initiative of the National Institute of Mental Health (NIMH) identified four relevant domains, namely, theory of mind (ToM), social perception (SP), attributional bias (AB), and emotion processing (EP) (Green et al., 2004, Green et al., 2008 and Pinkham et al., 2014). Recent meta-analyses have indicated that social cognitive function in patients with schizophrenia was markedly impaired (Savla et al., 2013 and Chung et al., 2014). Deficits in social cognition are associated with the functional outcome of schizophrenia and contribute to the functional outcome beyond neurocognition (Schmidt et al., 2011 and Mehta et al., 2013a). Social cognitive deficits are relatively stable throughout the disease course (Addington et al., 2006 and Horan et al., 2012) given that these deficits are observed during remission (Sprong et al., 2007 and Mehta et al., 2013b), as well as in relatives (Lavoie et al., 2013). These findings suggest that social cognitive deficits represent a trait marker for schizophrenia that is related to a genetic vulnerability associated with the pathology rather than a state-related aspect; however, some inconsistencies exist in each domain (Fiszdon and Reddy, 2012 and Pinkham, 2014). The concepts of ‘clinical high risk’ (CHR) and ‘ultra-high risk’ have been developed over the previous two decades to identify subjects at imminent risk of psychosis (Miller et al., 2002, McGorry et al., 2003 and Fusar-Poli et al., 2013). Similarly, the concept of ‘Basic Symptom’, which is considered to be an earlier state of psychosis, has also been developed complementary to and along with high risk concepts (Schultze-Lutter et al., 2012). The high-risk state for psychosis is also associated with significant and widespread impairments in social cognition and neurocognitive performances (Fusar-Poli et al., 2012a, Bora and Murray, 2014 and Lee et al., 2014a). A recent study demonstrated that ToM was impaired in individuals at CHR, and the performance of this group was intermediate between patients with first-episode psychosis and healthy controls (Bora and Pantelis, 2013). Individuals at CHR who later developed psychosis performed worse in the ToM domain compared with those who did not transition to psychosis (Kim et al., 2011). These results suggest that the ToM performance in individuals at CHR is intermediate between those of the healthy population and patients with schizophrenia. Patients with schizophrenia consistently exhibit deficits in SP (Green et al., 2007 and Couture et al., 2010), and EP (Gur et al., 2002 and Fisher et al., 2008); however, individuals at CHR exhibit mixed findings regarding social cognitive deficits (Pinkham et al., 2007, Couture et al., 2008, Pauly et al., 2010 and Devylder et al., 2013). Therefore, the domains of social cognition that are associated with the largest impairments in individuals at CHR are not clear. Savla et al. (2013) found no significant differences in AB in patients with schizophrenia compared with healthy controls but did demonstrate that performances in other domains were impaired in patients with schizophrenia. However, most studies in individuals at CHR exhibit higher AB compared with healthy controls (An et al., 2010, Hauser et al., 2011, Stowkowy and Addington, 2012 and Thompson et al., 2013). These findings suggest that an abnormality of AB in CHR is the specific feature that distinguishes it from schizophrenia. Previous meta-analyses only investigated a single domain or social cognition as a whole (Fusar-Poli et al., 2012b and Bora and Pantelis, 2013). However, a domain-by-domain quantitative analysis of social cognitive function in individuals at CHR has not been performed. The identification of the domains and the extent of social deficits in individuals at CHR will aid in the determination of specific impairments that are trait markers for schizophrenia, indicate an increased or decreased risk of the transition to psychosis, and identify more specific targets in the development of therapeutic regimens for the high-risk group. The goals of the current meta-analysis are (1) to examine the magnitude of the differences between individuals at CHR and healthy controls across all four domains of social cognition, (2) to evaluate the impact of different moderators on the performance of each domain, and (3) to determine if significant impairments in each component of social cognition are present in CHR individuals who later develop psychosis compared with CHR non-converters.