Abstract
AbstractBackgroundSocial symptomatology quantified by clinical interview (Autism Diagnostic Observation Schedule, ADOS) and self-report (Social Responsiveness Scale, SRS) indicate symptom severity in autism spectrum disorder (ASD). Reluctance to engage in interpersonal eye contact is a frequently observed behavioral hallmark, though neural bases for these difficulties and relation to symptomatology are not understood. We test the hypothesis that eye contact in ASD activates atypical neural mechanisms that are related to individual differences in symptomatology.MethodsNeural activity represented by hemodynamic signals was acquired by functional near-infrared spectroscopy (fNIRS) during real person-to-person eye contact (confirmed by eye-tracking) for 17 adult ASD (3 female, 14 male) and 19 typically-developed (TD) participants (8 female, 11 male). Assessment of social function was based on ADOS scores for ASD participants and SRS scores for the combined group of ASD and TD participants.ResultsIndividual ADOS scores were negatively correlated (r = -0.69) with individual fNIRS beta-values (representing strength of hemodynamic signals) within clusters in the right dorsal stream regions: somatosensory cortices, angular gyrus, and supramarginal gyrus. Hemodynamic responses in the right dorsolateral prefrontal cortex (DLPFC) were also negatively correlated (r = -0.77) with ADOS scores. Similarly, SRS scores for the combined ASD and TD groups were also negatively correlated (r = -0.58) with somatosensory cortices and the supramarginal gyrus.ConclusionsThese findings are consistent with the hypothesis that neural mechanisms in the dorsal stream and DLPFC are related to social symptomatology and implicate high-level interactive face and eye-processing systems as potential neurobiological markers of ASD.
Publisher
Cold Spring Harbor Laboratory