Abstract
It has been proposed that early differences in sensory responsiveness arise from atypical neural function and produce cascading effects on development across domains. This longitudinal study prospectively followed infants at heightened risk for autism spectrum disorder (ASD) based on their status as younger siblings of children diagnosed with ASD (Sibs-ASD) and infants at relatively lower risk for ASD (siblings of typically developing children; Sibs-TD) to examine the developmental sequelae and possible neurophysiological substrates of a specific sensory response pattern: unusually intense interest in nonsocial sensory stimuli or “sensory seeking.” At 18 months, sensory seeking and social orienting were measured with the Sensory Processing Assessment, and a potential neural signature for sensory seeking (i.e., frontal alpha asymmetry) was measured via resting state electroencephalography. At 36 months, infants’ social symptomatology was assessed in a comprehensive diagnostic evaluation. Sibs-ASD showed elevated sensory seeking relative to Sibs-TD, and increased sensory seeking was concurrently associated with reduced social orienting across groups and resting frontal asymmetry in Sibs-ASD. Sensory seeking also predicted later social symptomatology. Findings suggest that sensory seeking may produce cascading effects on social development in infants at risk for ASD and that atypical frontal asymmetry may underlie this atypical pattern of sensory responsiveness.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 41-53 |
| Number of pages | 13 |
| Journal | Developmental Cognitive Neuroscience |
| Volume | 29 |
| DOIs | |
| State | Published - Jan 2018 |
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Keywords
- Autism
- EEG
- Frontal asymmetry
- Infant siblings
- Longitudinal
- Sensory
ASJC Scopus subject areas
- Cognitive Neuroscience
Cite this
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Developmental sequelae and neurophysiologic substrates of sensory seeking in infant siblings of children with autism spectrum disorder. / Damiano-Goodwin, Cara R.; Woynaroski, Tiffany G.; Simon, David M.; Ibañez, Lisa V.; Murias, Michael Andrew; Kirby, Anne; Newsom, Cassandra R.; Wallace, Mark T.; Stone, Wendy L.; Cascio, Carissa J.
In: Developmental Cognitive Neuroscience, Vol. 29, 01.2018, p. 41-53.Research output: Contribution to journal › Article
TY - JOUR
T1 - Developmental sequelae and neurophysiologic substrates of sensory seeking in infant siblings of children with autism spectrum disorder
AU - Damiano-Goodwin, Cara R.
AU - Woynaroski, Tiffany G.
AU - Simon, David M.
AU - Ibañez, Lisa V.
AU - Murias, Michael Andrew
AU - Kirby, Anne
AU - Newsom, Cassandra R.
AU - Wallace, Mark T.
AU - Stone, Wendy L.
AU - Cascio, Carissa J.
PY - 2018/1
Y1 - 2018/1
N2 - It has been proposed that early differences in sensory responsiveness arise from atypical neural function and produce cascading effects on development across domains. This longitudinal study prospectively followed infants at heightened risk for autism spectrum disorder (ASD) based on their status as younger siblings of children diagnosed with ASD (Sibs-ASD) and infants at relatively lower risk for ASD (siblings of typically developing children; Sibs-TD) to examine the developmental sequelae and possible neurophysiological substrates of a specific sensory response pattern: unusually intense interest in nonsocial sensory stimuli or “sensory seeking.” At 18 months, sensory seeking and social orienting were measured with the Sensory Processing Assessment, and a potential neural signature for sensory seeking (i.e., frontal alpha asymmetry) was measured via resting state electroencephalography. At 36 months, infants’ social symptomatology was assessed in a comprehensive diagnostic evaluation. Sibs-ASD showed elevated sensory seeking relative to Sibs-TD, and increased sensory seeking was concurrently associated with reduced social orienting across groups and resting frontal asymmetry in Sibs-ASD. Sensory seeking also predicted later social symptomatology. Findings suggest that sensory seeking may produce cascading effects on social development in infants at risk for ASD and that atypical frontal asymmetry may underlie this atypical pattern of sensory responsiveness.
AB - It has been proposed that early differences in sensory responsiveness arise from atypical neural function and produce cascading effects on development across domains. This longitudinal study prospectively followed infants at heightened risk for autism spectrum disorder (ASD) based on their status as younger siblings of children diagnosed with ASD (Sibs-ASD) and infants at relatively lower risk for ASD (siblings of typically developing children; Sibs-TD) to examine the developmental sequelae and possible neurophysiological substrates of a specific sensory response pattern: unusually intense interest in nonsocial sensory stimuli or “sensory seeking.” At 18 months, sensory seeking and social orienting were measured with the Sensory Processing Assessment, and a potential neural signature for sensory seeking (i.e., frontal alpha asymmetry) was measured via resting state electroencephalography. At 36 months, infants’ social symptomatology was assessed in a comprehensive diagnostic evaluation. Sibs-ASD showed elevated sensory seeking relative to Sibs-TD, and increased sensory seeking was concurrently associated with reduced social orienting across groups and resting frontal asymmetry in Sibs-ASD. Sensory seeking also predicted later social symptomatology. Findings suggest that sensory seeking may produce cascading effects on social development in infants at risk for ASD and that atypical frontal asymmetry may underlie this atypical pattern of sensory responsiveness.
KW - Autism
KW - EEG
KW - Frontal asymmetry
KW - Infant siblings
KW - Longitudinal
KW - Sensory
UR - http://www.scopus.com/inward/record.url?scp=85031031294&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85031031294&partnerID=8YFLogxK
U2 - 10.1016/j.dcn.2017.08.005
DO - 10.1016/j.dcn.2017.08.005
M3 - Article
C2 - 28889988
AN - SCOPUS:85031031294
VL - 29
SP - 41
EP - 53
JO - Developmental Cognitive Neuroscience
JF - Developmental Cognitive Neuroscience
SN - 1878-9293
ER -