An Electrophysiological Study of Visual Function in Infants At Risk for An ASD

Background: Differences in face processing and attentional mechanisms have been found among infants who will later develop autism when compared to typically developing comparison populations (Luyster, et al 2011). Despite these differences it is difficult to determine the precise neural processes that underpin them. While infant studies have investigated later processing (N290/P400 and Nc), it is unknown if differences found in these studies is driven by earlier low-level visual processing differences in high-risk groups. The P1 component reflects the visual processing stream and visual cortex, and is used clinically as a measure of visual function.

Objectives: To date we focused on examining the P1 component, the first positive deflection in the visual ERP, in a population of infants with a known single gene defect who are at elevated risk for developing an ASD– specifically, those diagnosed with Tuberous Sclerosis Complex (TSC) with 40-50% receiving an ASD diagnosis.  In the next set of analyses we look to expand our analysis of the PI component to another at-risk group of infants who are high-risk for developing autism by proxy of having an older sibling diagnosed with an autism spectrum disorder. These infants are expected to have a positive ASD diagnosis at a rate of 1:5.The objective is to investigate the functional significance of the P1 in two groups of high-risk infants.

Methods: Infants were presented with visual stimuli of faces (mother/stranger). For the existing analysis we evaluated the P1 data from 45 infants, aged 12-36 months and age-matched between 3 groups [control; TSC- (no comorbid ASD diagnosis); TSC+ (comorbid ASD diagnosis)]. For our further analyses we will evaluate the data from infants, aged 12-36 months who participate in the Infant Sibling Project taking place at Boston University and Children’s Hospital.

Results: For the TSC analyses, a repeated measures analysis of P1 amplitude and diagnosis group revealed that the P1 amplitude was larger for infants with TSC who have a comorbid ASD diagnosis than infants with TSC with no comorbid diagnosis, or controls. This finding suggests that early visual function may be impaired in children who go on to develop ASD.

Conclusions: Based upon the differentiation of the P1 between the TSC at-risk group with a positive outcome and those without, we anticipate similar findings among our high-risk infant sibling population. If the high risk infant sibling groups [HRA- (no ASD diagnosis at outcome age); HRA+ (positive ASD diagnosis at outcome age)] show similar findings to the previous analysis, a greater P1 response in the HRA+ group, this will further the evidence that early visual processing may be impaired in at-risk infants who go on to develop ASD.