24802
Neurophysiological Substrates and Developmental Sequelae of Sensory Seeking in Infants at High Risk for Autism Spectrum Disorder
Children with autism spectrum disorder (ASD) show a broad range of unusual responses to sensory stimuli and experiences. It has been proposed that early differences in sensory responsiveness may arise from atypical neural function and produce “cascading effects” on development across a number of domains. A primary challenge to confirming these hypotheses is that ASD cannot always be definitely diagnosed in the earliest stages of development (i.e., infancy). A potential solution is to prospectively follow infants at heightened risk for ASD based on their status as infant siblings of children who are diagnosed. The present study examined the developmental sequelae and possible neurophysiological substrates of a specific sensory response pattern: unusually intense interest in nonsocial sensory stimuli or “sensory seeking.” Infants at high risk (HR) for ASD were compared to a control group of infants at relatively lower risk for ASD (LR; siblings of children with typical developmental histories).
Objectives:
Research questions included: a) Do HR infants differ from LR infants in sensory seeking behavior?, b) Does sensory seeking predict concurrent social orienting and future socialization?, and c) Is sensory seeking predicted by early frontal alpha asymmetry?
Methods:
To answer these research questions, we carried out a longitudinal correlational investigation in which 20 HR infants and 20 LR controls were followed over 18 months. At entry to the study, sensory seeking and social orienting were measured in 18-month-old infants using the Sensory Processing Assessment, and alpha asymmetry was measured via resting state EEG. Eighteen months later, social symptomatology was evaluated in a comprehensive diagnostic evaluation.
Results:
HR infants showed elevated sensory seeking relative to LR controls (t(38)=2.26, p = .029), and increased sensory seeking predicted reduced social orienting across groups, concurrently (β=.570, t=2.822, p < .0001) at eighteen months. Seeking behavior additionally predicted future social symptomatology across groups (β=.376, t = 2.78, p = .008), but this effect varied by group (seeking*risk group interaction β=.672, t=4.448, p =.008), such that higher seeking at 18 months predicted increased social symptoms in the HR group, but decreased social symptoms in the LR group. A mediation analysis indicated that social orienting mediates the relation between sensory seeking and social deficits, and that this effect is moderated by risk group. The relation between frontal asymmetry and sensory seeking at 18 months also varied according to risk group (seeking*risk group interaction β=-2.458, t=-3.38, p = .002), such that increased sensory seeking was associated with greater right asymmetry in the HR group, but with greater left asymmetry in the LR group.
Conclusions:
Findings suggest that sensory seeking may produce cascading effects on social development in infants at heightened risk for ASD by impeding social orienting early in life. Atypical frontal alpha asymmetry may underlie this atypical behavioral pattern of sensory responsiveness.