24094
Early Childhood Longitudinal EEG Analysis to Investigate Neural Correlates of Language in Children at Risk for Autism

Friday, May 12, 2017: 5:00 PM-6:30 PM
Golden Gate Ballroom (Marriott Marquis Hotel)
C. L. Wilkinson1, A. R. Levin2, H. M. O'Leary2, H. Tager-Flusberg3 and C. A. Nelson4, (1)Developmental Medicine, Boston Children's Hospital, Boston, MA, (2)Neurology, Boston Children's Hospital, Boston, MA, (3)Psychological and Brain Sciences, Boston University, Boston, MA, (4)Boston Children's Hospital, Boston, MA
Background:  The neural mechanisms of autism spectrum disorders (ASD) are still poorly understood. In part, this is due to the complexity and heterogeneity of the disorder and our limited understanding of typical neural processing in early childhood. Longitudinal studies of infants at increased familial risk for autism are needed to uncover early differences in neural circuitry in ASD and identify which abnormalities impact language and cognitive development.

Rhythmic synchronization of brain activity in the gamma frequency range (~30-50Hz) is thought to be crucial for higher order cognitive processing, including sensory integration and binding of information. Differences in gamma have been observed in older children and adults with ASD. In typical infants, recent EEG studies also support gamma’s association with language processing, with increased gamma power at 2 years of age correlating with better language ability.

Objectives:  To characterize spontaneous gamma power and its correlation with language ability in infants and toddlers at risk for ASD compared to low risk children.

Methods:  This study analyzed EEG data collected as part of the Infant Sibling Project, a longitudinal study comparing infants at high risk of developing ASD with low risk controls. Infants with a sibling with ASD were designated high risk, while infants with least one typically developing sibling and no known first degree relatives with ASD were designated low risk. Each infant was developmentally evaluated at multiple intervals, including 24 and 36 months by the Mullen Scales of Early Learning. Infants were evaluated for ASD at 24 and 36 months. High-density spontaneous EEG recordings conducted at 12, 18 and 24 months of age were analyzed. Spontaneous frontal gamma power at these ages was correlated with language outcomes at 24 and 36 months.

Results:  Spontaneous frontal mean gamma power was not significantly different at 12, 18, or 24 months between low risk (LR) and high risk (HR) groups, including the subgroup of high risk children with ASD (HR/ASD). However, correlation of spontaneous gamma power and language skills at 24 months was directionally opposite and significantly different between LR and HR groups (Fisher z-transform; -1.91, p<0.05; n=36 LR, 33 HR). At 24 months left frontal gamma power was positively correlated with language skills in the LR group (Pearson r = 0.351, p<0.05), but negatively correlated in the HR group (Pearson r = -0.354, p<0.05), and the HR/ASD subgroup (Pearson r = -0.51, p>0.05, n=8).

Conclusions:  Preliminary EEG analyses support differences in the function of spontaneous frontal gamma power in LR and HR children. While LR and HR groups had similar mean frontal gamma power, the correlation between gamma power and language ability is strikingly different. Future analysis of evoked gamma in auditory language tasks will help to further elucidate these differences.