Attenuation of social-communication and language impairments is possible with very early identification and intervention in infancy. Yet reliable detection of these impairments remains limited to the toddler years, and little is known about their pathogenesis in the neonatal period. Identification of the earliest neural and behavioral determinants of social communication and language hinges on prospective, longitudinal study of at-risk infants from birth. The prevalence of social-communication and language impairments, as well as autism spectrum disorder (ASD), for preterm infants (HR-PT) and infant siblings of children with ASD (HR-SIB) greatly exceeds that of the general population. Yet the key mechanistic pathways underlying deficits in social communication and language remain largely unknown. Language emerges in the context of rich social interactions, which begin in the neonatal period, and are made possible by a set of necessary hierarchical conditions (collectively called neonatal neurobehavior). This hierarchy begins with the most basic task of the newborn?autonomic and physiologic stability, and advances to controlled motor movements, adaptive self-soothing strategies, sustained periods of calm alertness, and attention to people and objects. Once this last step is achieved, neonates are primed and ready for social attention and interaction. We hypothesize that disruption at any point in the neurobehavioral hierarchy will prevent the infant from establishing readiness for social interaction, resulting in altered early social experiences, diminished frequency and quality of contingent social interactions, and reduced social and language learning opportunities. The current study will directly test the hypothesis that disrupted neurobehavioral development (e.g., autonomic dysregulation, poor motor organization, decreased self-soothing, and abnormal attention) during the critical neurodevelopmental period between birth and 4 months will have downstream, negative consequences on the development of social communication and language.
Aim 1 will characterize trajectories of neurobehavioral and social-communication development across low-risk, HR-PT, and HR-SIB infants.
Aim 2 will identify neurobehavioral determinants of the emergence of social-communication skills and the acquisition of language. Neonatal neurobehavior will be measured longitudinally from 1-4 months, social communication will be measured at 5 time points from 9 months to 2 years, and language outcome will be measured at 24 months. Critically, this study will extend early detection research down to the first month of life, when neurological organization is undergoing significant transformation. The innovative use of clinical measures in the context of dense, longitudinal sampling across two groups of at-risk infants will identify specific, mechanistic links between early neurobehavioral development and the emergence of social-communication and language impairments.
The current study will identify the earliest neurobehavioral determinants of social-communication and language impairment across two groups of at-risk infants ? high-risk preterm infants and high-risk infant siblings of children with ASD. Findings from this study will provide precise information about the timing and specificity of neurobehavioral disruption that leads to specific social-communication and language impairments at key points in development from 9 to 24 months of age. Identification of early neurobehavioral trajectories that determine the emergence of social communication and language disorders will ultimately lead to novel conceptual frameworks for very early intervention, capitalizing on neuroplasticity that peaks in the infant months and diminishes significantly thereafter.
