Dissociating Social Functioning in ASD and Schizophrenia Using Clinical Assessment and Neural Response to Gaze Cues

Thursday, May 12, 2016: 11:30 AM-1:30 PM
Hall A (Baltimore Convention Center)
J. H. Foss-Feig1, A. Naples2, K. Deckert3, E. J. Levy3, K. K. Stavropoulos2, M. Rolison2, N. Santamauro4, U. Kosir5, C. Schleifer5, V. Srihari4, A. Anticevic4 and J. McPartland2, (1)Yale School of Medicine, New Haven, CT, (2)Child Study Center, Yale School of Medicine, New Haven, CT, (3)Yale Child Study Center, New Haven, CT, (4)Yale University School of Medicine, New Haven, CT, (5)Yale University, New Haven, CT

Social difficulties, including deficits in maintaining and interpreting social gaze and in face and emotion processing, are hallmark features of autism spectrum disorder (ASD). Atypical social functioning and gaze processing are not, however, unique to ASD. Both are also impaired in schizophrenia (SCZ), a disorder with genetic, neurobiological, and phenotypic commonalities with ASD. This study utilized novel methods, integrating eye-tracking and electrophysiology (EEG), to study social behavior and brain function during simulated face-to-face interactions in individuals with ASD and SCZ. Specifically, we evaluated P100 and N170 response to direct and averted gaze in adults with ASD, SCZ, and typical development to determine between-group differences in neural processes associated with face decoding. In parallel, we evaluated social functioning on a battery of diagnostic, clinical, and neurocognitive assessments. In this way, we evaluate whether specific abnormalities in gaze processing differ by diagnostic category or are general indicators of social dysfunction across neurodevelopmental disorders.


To evaluate neural markers of gaze processing during simulated face-to-face interactions in individuals with ASD, in comparison to those with SCZ and controls.


Participants included 13 adults with ASD, 14 with SCZ, and 15 controls. EEG data was recorded using a 128-channel sensor net, and eye-tracking data was collected using an Eyelink-1000 remote camera system. Participants were presented with 80 distinct photorealistic, animated faces matched for low-level visual features. Contingent upon participants’ fixating on the face, stimuli responded by shifting eye gaze (either from direct to averted or averted to direct). EEG data was preprocessed off-line, and the P100 and N170 was extracted from electrodes over right occipitotemporal scalp. Participants completed the Social Responsiveness Scale, the Benton Face Recognition task, and the Reading the Mind in the Eyes Test. All were administered gold-standard diagnostic measures of both ASD and SCZ (Autism Diagnostic Observation Schedule; Positive and Negative Symptom Scale). Between-group differences were examined with repeated measures ANOVAs; transdiagnostic associations between neural response to gaze shift and clinical assessment scores were explored with bivariate correlations. 


Between-group analyses revealed amplified P1 response in SCZ, but not ASD, and altered N170 response in ASD, but not SCZ (Fig.1). In contrast to ERP markers, self-report measures of ASD and SCZ symptomatology did not differentiate between diagnostic categories. Across groups, greater P1 response was associated with more positive symptoms of SCZ and with fewer social communication deficits associated with ASD (Fig.2). 


Results revealed that neural efficiency of visual processing and face-decoding during simulated face-to-face interactions differentiates ASD from SCZ. In contrast, signal strength relates to symptom severity transdiagnostically, rather than varying by diagnostic category. These findings support a dimensional approach to understanding gaze processing differences in ASD and related disorders.