Cerebral hemodynamic response to faces and emotions in infants at high risk for autism

Abstract

The incidence of autism spectrum disorders (ASD) has risen alarmingly in the United States, and is now thought to affect approximately 1 in 110 live births. Early diagnosis and intervention is the only treatment proven effective in cases of autism, however the behavioral tests currently available cannot make this diagnosis until at least two years of age. A lack of normal attention to faces and abnormal face processing is a cognitive deficit common to nearly all individuals with autism spectrum disorder, and this deficit is likely present from a very early age. The primary goal of this dissertation is therefore to characterize the specific neural response of face processing in infants with near-infrared spectroscopy (NIRS), and to then apply these measures to the study of abnormal face processing in infants at high risk for autism. In order to achieve these objectives, the work described herein aims to: 1) characterize the hemodynamic response to faces in normal infants at six months of age as measured by the Hitachi ETG-4000 functional Near-Infrared Spectroscopy (fNIRS) system; 2) Simultaneously measure orbitofrontal hemodynamic responses to social/emotional engagement and the response to faces in infants at high risk for autism as compared to low risk controls; and 3) Utilize a novel method of condition-related component selection and classification to identify waveforms associated with face and emotion processing in 6-7-month-old infants at high risk for ASD, and matched low-risk controls. Our results indicate similarities of response waveforms, but differences in both the spatial distribution, magnitude, and timing of oxy-hemoglobin and deoxy-hemoglobin responses between groups. Our findings represent the first identification of neuroimaging markers of a functional endophenotype at six months of age that may be associated with high risk of ASD. These results support a model of altered frontal lobe structure through evidence of altered hemodynamic response and/or functional activity in the high risk infant group, and these changes may, in turn, contribute to the development of ASD in specific individuals.