Characterizing Social Cognitive Deficits in High-Functioning Autism Spectrum Disorders and Schizophrenia

Background:   Traditionally, Autism Spectrum Disorders (ASDs) and Schizophrenia (SZ) are considered separate clinical entities.  However, recent evidence suggests that both are neurodevelopmental disorders characterized by core deficits in social cognitive processes independent of other cognitive impairments. It is not yet clear if the groups differentiate on the specific social cognitive deficit (e.g. theory of mind, affect recognition, empathy processes) they exhibit.

Objectives:   To compare performance on tasks probing theory of mind (ToM) and affect recognition in individuals with ASDs, individuals with SZ and matched healthy controls (HC).

Methods:   Eighteen high functioning individuals with ASDs, sixteen individuals with SZ and twenty-eight HC, ages 18 to 30 were recruited to date. The groups matched on age, gender and race but not on an IQ estimate (as measured by WAIS-III vocabulary and block design subtests). We administered a battery of social cognition tasks, including the Hinting task and the Social Attribution task (SAT) to measure ToM, as well as the Reading the Mind in the Eyes test (RMET) and the Bell Lysaker Emotion Recognition test (BLERT) to asses affect recognition. A repeated measure ANCOVA was performed with group as a between-subject factor and social task as within-subject factor, while controlling for IQ.

Results:  Results demonstrated a main effect of group (F=7.64, p=0.001) with no main effect of task or a group by task interaction. Follow-up ttests demonstrated that both SZ and ASD groups showed impaired performance compared to controls on all 4 tasks. Notably, the ToM tasks tended to show a differentiation between the patient groups, such that ASD performed worse than SZ, while they were equally impaired on the affect recognition tasks.

Conclusions:  Our data support overall social cognitive deficits in individuals with high-functioning ASD and SZ compared to matched controls. Moreover, our results suggest similar deficits on affect recognition but potentially more severe ToM deficits in ASD.   These results have implication for future research on the neurobiology mechanism, endophenotypes and treatment of ASD and SZ.