Do Children with ASD Show An Abnormal Neural Response to Faces At 12 Months of Age?

Background:  To date, the effort to understand early development in children with ASD has predominantly focused on behavioral symptoms in the first years of life.  However, emerging research points to the importance of exploring a broader endophenotype, including a consideration of neural measures of atypical responses to visual stimuli.

Objectives: To determine whether children with ASD show in neural response to faces early in life; in particular, are there neural markers of atypical response by 12-months?

Methods:  Infants were enrolled in a longitudinal study of children at high- and low- risk for ASD (based on family history).  High density EEG/ERP data were collected at 12-months in response to images of the infant’s mother and a stranger.  The components of interest were the face-sensitive N290/P400 complex, measured over the right occipito-temporal region (N290:150-450ms; P400:260-600ms) and the Nc, a negative-going fronto-central deflection (350-700ms).  A single electrode was chosen for each component of interest.  Mean amplitude in microvolts was calculated for all components; latency in milliseconds was extracted for N290/P400 but not for the Nc due to its diffuse morphology.

Analyses focus on 15 children across three groups; classification to these three groups was based on a follow-up visit at 24-or 36-months and was as follows: (1) children classified as having ASD (‘outcome’); (2) children at high-risk for ASD but who have been classified as typically developing (‘HRA-‘); (3) children at low-risk for ASD and who have been confirmed to be typically developing (‘LRC-‘).  Each child in the outcome group was matched to a child in the HRA- and LRC- group based on initial cognitive ability.

Results:  Results comprise a preliminary set of analyses; 10-20 additional children will soon ‘age in’ to these analyses.  For ease of interpretation, analyses focus on infants’ responses to mothers.  Due to the limited sample size, results will be presented in a descriptive fashion.  Mean amplitude of the Nc was similar across groups (ranging from -7.77 to -8.81).  However, mean amplitude of the N290 in the outcome group (M=4.42,SD=11.30) contrasted with that of the HRA- and LRC- groups (respectively: M=11.51,SD=10.51;M=13.94,SD=2.48).  Similarly, mean amplitude of the P400 was smallest in the outcome group (M=5.81,SD=16.43), followed by the HRA- group (M=10.76,SD=11.33) and the LRC- group (M=16.42,SD=3.61).  Finally, whereas the HRA- and LRC- groups showed similar latencies for the N290 (respectively: M=218.40,SD=62.26;M=216.80,SD=20.27), the response was slower in the outcome group (M=312.80,SD=83.44).  P400 latency results paralleled those observed in amplitude: the outcome group had the slowest response (M=426.40,SD=73.41), followed by the HRA- (M=400.00,SD=27.13) and the LRC- groups (M=391.20,SD=28.76).

Conclusions:  There may be differences in neural response to faces for children later diagnosed with ASD. In particular, by 12-months, response may be smaller and slower than in comparison children.  Moreover, there is some indication that there is a combined effect of risk status and eventual outcome: children at high-risk with negative outcomes may show less pronounced but similar patterns of response to high-risk, positive outcome children.