20007
Dissociating Neural Response to Gaze Cues in ASD and Schizophrenia Using Simulated Face-to-Face Interaction
Deficits in maintaining and interpreting social gaze are hallmark features of autism spectrum disorder (ASD). Individuals with ASD show reduced attention to direct gaze, attenuated sensitivity to gaze changes, and less use of gaze cues to facilitate facial communication. Atypical gaze processing is not unique to ASD and is evident in other disorders, including schizophrenia. It is unknown whether specific abnormalities in gaze processing differ by diagnostic category, or whether they are general indicators of social dysfunction across neurodevelopmental disorders.
The N170 is a negative-going event-related potential (ERP) that is recorded over occipitotemporal scalp and indexes the earliest stages of face processing. It is sensitive to point of gaze on the face and is atypical in both ASD and schizophrenia. In addition, N170 variability is associated with empathy, social competence, anxiety, and withdrawal across clinical populations. Previous studies of N170 response to gaze-related cues are limited by their use of static faces, which have questionable ecological validity. This study utilizes 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 schizophrenia.
Objectives:
This study aimed to (i) evaluate N170 response to direct and averted gaze in adults with ASD, schizophrenia, and typical development to determine between-group differences in neural processes associated with face decoding and (ii) examine transdiagnostic associations between neural response and social difficulties.
Methods:
Participants included 7 adults with ASD, 8 with SCZ, and 7 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 N170 was extracted from electrodes over right occipitotemporal scalp. Participants completed the Social Responsiveness Scale (SRS) and the Broader Autism Phenotype Questionnaire (BAPQ). Between-group differences were examined with repeated measures ANOVAs; transdiagnostic associations between neural response to gaze shift and self-report of social difficulties were explored with bivariate correlations.
Results:
Between-group analyses revealed no main effects of group or gaze direction, and no group by gaze direction interaction for N170 amplitude (Fig.1). Instead, across groups, N170 amplitude was significantly negatively correlated with social aloofness (BAPQ) and social motivation (SRS) (Fig.2). N170 latency, however, showed between-group differences: there was a main effect of group, driven by a significant latency delay in schizophrenia relative to both ASD and controls (Fig.1). There was no main effect of gaze direction or group by gaze direction interaction for N170 latency.
Conclusions:
Results revealed that efficiency of face-decoding neural mechanisms during simulated face-to-face interactions differentiates ASD from other disorders characterized by social dysfunction. In contrast, strength of these mechanisms relates to social competency transdiagnostically, rather than varying by diagnostic category. These findings support a dimensional approach to understanding gaze processing differences in ASD and related disorders.