Problems with eye contact represent one of the most pervasive and early manifesting symptoms of autism spectrum disorders (ASDs). Prior electrophysiological research in gaze perception in ASD has focused primarily on passive observation of social information, failing to address the interactive nature of eye contact. Our preliminary work in typical development (TD) revealed two event-related potential (ERP) indices of detection of shared gaze in real time during reciprocal interactions: the N170, measured at occipitotemporal electrodes, and the P300, measured at central electrodes. The temporal dynamics of brain activity during reciprocal social interactions in ASD remain largely unexplored.
Objectives:
By applying experimental paradigms in which on-screen faces responded to participant gaze, this study investigated brain activity evoked by reciprocal eye contact. Our objective was to evaluate the characteristics of ERP markers of shared gaze in individuals with ASD and to explore their relationship to social behavior. We predicted that individuals with ASD would not differentiate changes in responsive gaze at early or late ERP components and that the N170 would be less sensitive to point of gaze in individuals with ASD versus TD.
Methods:
ERPs were recorded from 20 high-functioning adolescents with ASD and 20 matched TD controls using a 128 electrode Geodesic Hydrocel Net. Eye movements were recorded from high-speed remote eye-tracking system (SR-Research Eyelink 1000) integrated with a stimulus presentation computer and EEG recording. Through co-registered ET and EEG, the experimental paradigm was controlled by participant gaze. Trials began with a peripherally-presented fixation crosshair followed by a centrally-presented face displaying either direct or averted gaze. Contingent upon participant fixation, the face responded by either looking at the participant (eye contact) or looking away from the participant (averted gaze). ERPs were time-locked to face movement; the N170 was extracted from occipital electrodes and the P300 was extracted at central electrodes.
Results: Preliminary results show an enhanced P300 to eye contact in typically developing individuals that was attenuated in ASD (mean amplitude TD 1.7µV, mean amplitude ASD -.41µV). Among typically developing individuals 73% of fixations were to eye-regions of the face, and the N170 to responsive eye contact was attenuated on trials in which participants fixated to non-eye regions of the face (mean difference in amplitude = 1.94µV). Analyses in progress investigate the relationship between point of gaze and neural response to eye contact in individuals with ASD.
Conclusions:
We demonstrate an electrophysiological marker of shared gaze that is absent in individuals with ASD. We interpret this finding to indicate that individuals with ASD are less sensitive to socially-relevant changes in gaze even when these changes are contingent on their own behavior. That these individuals differentially respond to the outcomes of their own gaze shifts suggests a potentially different approach to learning about their environment and others during development. By exploring brain response to shared gaze in a context driven by participant behavior we gain a more nuanced profile of social brain dysfunction and a potential mechanism for defining subgroups based on performance during interactive assessment.