Background: Deficits in social cognition are well-recognized in both schizophrenia and autism spectrum disorders (ASD). However, it is less clear how social cognition deficits differ between both disorders and what distinct mechanisms may underlie such differences. We aimed at reviewing available evidence from studies directly comparing social cognitive performance between individuals with schizophrenia and ASD.Methods: We performed a systematic review of literature up to May 22, 2018 on Pubmed, Web of Science, and Scopus. Search terms included combinations of the keywords “social cognition,” “theory of mind,” “autism,” “Asperger,” “psychosis,” and “schizophrenia.” Two researchers independently selected and extracted data according to PRISMA guidelines. Random-effects meta-analyses were conducted for performance on social cognitive tasks evaluating: (1) emotion perception; (2) theory of mind (ToM); (3) emotional intelligence (managing emotions score of the Mayer-Salovey-Caruso Emotional Intelligence Test); and (4) social skills.Results: We identified 19 eligible studies for meta-analysis including a total of 1,040 patients (558 with schizophrenia and 482 with ASD). Eight studies provided data on facial emotion perception that evidenced a better performance by participants with schizophrenia compared to those with ASD (Hedges' g = 0.43; p = 0.031). No significant differences were found between groups in the Reading the Mind in the Eyes Test (8 studies; Hedges' g = 0.22; p = 0.351), other ToM tasks (9 studies; Hedges' g = −0.03; p = 0.903), emotional intelligence (3 studies; Hedges' g = −0.17; p = 0.490), and social skills (3 studies; Hedges' g = 0.86; p = 0.056). Participants' age was a significant moderator of effect size in emotion perception and RMET analyzes, with larger differences favoring patients with schizophrenia being observed in studies with younger participants.Conclusions: The instruments that are currently available to evaluate social cognition poorly differentiate between individuals with schizophrenia and ASD. Combining behavioral tasks with neurophysiologic assessments may better characterize the differences in social cognition between both disorders.
Background: Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder manifesting as lifelong deficits in social communication and interaction, as well as restricted repetitive behaviors, interests and activities. While there are no specific pharmacological or other physical treatments for autism, in recent years repetitive Transcranial Magnetic Stimulation (rTMS), a technique for non-invasive neuromodulation, has attracted interest due to potential therapeutic value. Here we report the results of a systematic literature review and meta-analysis on the use of rTMS to treat ASD.Methods: We performed a systematic literature search on PubMed, Web of Science, Science Direct, Bielefeld Academic Search, and Educational Resources Information Clearinghouse. Search terms reflected diagnoses and treatment modalities of interest. Studies reporting use of rTMS to treat core ASD or cognitive symptoms in ASD were eligible. Two researchers performed article selection and data extraction independently, according to PRISMA guidelines. Changes in ASD clinical scores or in cognitive performance were the main outcomes. Random effects meta-analysis models were performed.Results: We found 23 eligible reports, comprising 4 case-reports, 7 non-controlled clinical trials, and 12 controlled clinical trials, comparing the effects of real TMS with waiting-list controls (n = 6) or sham-treatment (n = 6). Meta-analyses showed a significant, but moderate, effect on repetitive and stereotyped behaviors, social behavior, and number of errors in executive function tasks, but not other outcomes. Most studies had a moderate to high risk of bias, mostly due to lack of subject- and evaluator-blinding to treatment allocation. Only 5 studies reported stability of these gains for periods of up 6 months, with descriptions that improvements were sustained over time.Conclusions: Existing evidence supports that TMS could be useful to treat some dimensions of ASD. However, such evidence must be regarded with care, as most studies did not adequately control for placebo effects. Moreover, little is known regarding the most effective stimulation parameters, targets, and schedules. There is an urgent need for further randomized, double-blind, sham-controlled trials, with adequate follow-up periods, to test the efficacy of transcranial magnetic stimulation to treat these disorders. Available evidence must be regarded as preliminary and insufficient, at present, to support offering TMS to treat ASD.
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