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Poster #10 - Neural Responses and Sensory Responsivity in Infants with Fragile X Syndrome and Familial Autism Risk

Sat, March 25, 12:30 to 1:15pm, Salt Palace Convention Center, Floor: 1, Hall A-B

Abstract

Background: Atypical sensory processing and sensory responsivity is widely reported in research on autism spectrum disorder (ASD) and fragile X syndrome (FXS) and may result from atypical neural processing, signal integration, or gating (Sinclair et al., 2017). Examination of sensory processing in infancy could provide insight into the development of atypical sensory responsivity within these disorders. Event-related potentials (ERPs) are valuable for investigating relations between neural correlates of sensory processing and emerging behavioral sensory responsivity. In particular, the infant P1 ERP component is associated with visual sensory orienting, providing a sensitive index to examine early occurring neural responses in relation to observed behavioral sensory responsivity.
Objective: To investigate neural correlates of sensory processing in 12-month-old infants at high-risk for ASD in relation to clinical measures of sensory responsivity concurrently and as a predictor of sensory responsivity in early childhood.
Methods: Twelve-month-old infants with FXS (n=15), siblings of children with ASD (i.e., ASIBs; n=21), and low-risk control (LRC) infants (n=21) participated in an ERP study including presentations of familiar and novel faces and toys (Guy et al., 2018). Group differences in P1 amplitude were investigated. The Sensory Experiences Questionnaire (SEQ) total score was used to assess sensory responsivity in participants at 12 months and early childhood (M = 43.15 months). SEQ scores were analyzed in relation to P1 responses.
Results: The groups differed on P1 amplitude, F(2, 972) = 55.97, p < .001, np2 = .10. Amplitude was greater among participants with FXS, M = 18.39µV, than ASIBs, M = 10.71µV, or LRC participants, M = 11.01µV. At 12 months of age, there was an interaction of SEQ score and participant group on P1 amplitude, F(2, 864) = 5.16, p = .006, np2 = .01. Higher SEQ scores at 12 months were associated with greater concurrent P1 amplitude responses for ASIBs, however, the opposite pattern was observed in LRC infants, and no relation was seen for infants with FXS. In predicting SEQ scores during early childhood from 12-month-olds’ ERPs, there was an interaction of SEQ score, group, and stimulus type, F(4, 882) = 2.45, p = .045, np2 = .01. Among participants with FXS, greater amplitude P1 was associated with higher SEQ scores across stimulus type, while LRC participants showed relations between P1 amplitude and SEQ varied based on stimulus type. There were no significant effects of SEQ scores in early childhood for ASIBs.
Conclusions: High-risk infant groups demonstrated unique patterns of P1 activation, which were uniquely associated with sensory responsivity concurrently during infancy and as a predictor during early childhood. Although infants with FXS demonstrated greater P1 amplitude responses than ASIBs or LRC infants, greater SEQ scores were observed only as a predictor of elevated sensory responsivity in early childhood. In contrast, elevated sensory responsivity was associated with greater P1 amplitude during infancy for ASIBs, despite not displaying elevated atypical P1 responses. Results indicate that P1 amplitude is associated with sensory responsivity, but that the nature and developmental timing at which these relations are observed varies based on risk group.

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