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Children's early language environments are related to later development. Little is known about this association in siblings of children with autism spectrum disorder (ASD), who often experience language delays or have ASD. Fifty-nine 9-month-old infants at high or low familial risk for ASD contributed full-day in-home language recordings. High-risk infants produced more vocalizations than low-risk peers; conversational turns and adult words did not differ by group. Vocalization differences were driven by a subgroup of "hypervocal" infants. Despite more vocalizations overall, these infants engaged in less social babbling during a standardized clinic assessment, and they experienced fewer conversational turns relative to their rate of vocalizations. Two ways in which these individual and environmental differences may relate to subsequent development are discussed.

Context Brain enlargement has been observed in 2-year-old children with autism, but the underlying mechanisms are unknown. Objective To investigate early growth trajectories in brain volume and cortical thickness. Design Longitudinal magnetic resonance imaging study. Setting Academic medical centers. Participants Fifty-nine children with autism spectrum disorder (ASD) and 38 control children. Intervention Children were examined at approximately 2 years of age. Magnetic resonance imaging was repeated approximately 24 months later (when aged 4-5 years; 38 children with ASD; 21 controls). Main Outcome Measures Cerebral gray and white matter volumes and cortical thickness. Results We observed generalized cerebral cortical enlargement in individuals with ASD at both 2 and 4 to 5 years of age. Rate of cerebral cortical growth across multiple brain regions and tissue compartments in children with ASD was parallel to that seen in the controls, indicating that there was no increase in rate of cerebral cortical growth during this interval. No cerebellar differences were observed in children with ASD. After controlling for total brain volume, a disproportionate enlargement in temporal lobe white matter was observed in the ASD group. We found no significant differences in cortical thickness but observed an increase in an estimate of surface area in the ASD group compared with controls for all cortical regions measured (temporal, frontal, and parieto-occipital lobes). Conclusions Our longitudinal magnetic resonance imaging study found generalized cerebral cortical enlargement in children with ASD, with a disproportionate enlargement in temporal lobe white matter. There was no significant difference from controls in the rate of brain growth for this age interval, indicating that brain enlargement in ASD results from an increased rate of brain growth before age 2 years. The presence of increased cortical volume, but not cortical thickness, suggests that early brain enlargement may be associated with increased cortical surface area. Cortical surface area overgrowth in ASD may underlie brain enlargement and implicates a distinct set of pathogenic mechanisms.