4.3 Article

EEG power at 3 months in infants at high familial risk for autism

Journal

Publisher

BMC
DOI: 10.1186/s11689-017-9214-9

Keywords

Autism; Electroencephalography; Early development; Infant siblings; Biomarker

Funding

  1. National Institutes of Health [R01DC010290, R21 DC 08637]
  2. Autism Speaks [1323]
  3. Simons Foundation [137186]
  4. American Brain Foundation
  5. Autism Science Foundation
  6. Nancy Lurie Marks Family Foundation
  7. American Australian Association

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Background: Alterations in brain development during infancy may precede the behavioral manifestation of developmental disorders. Infants at increased risk for autism are also at increased risk for other developmental disorders, including, quite commonly, language disorders. Here we assess the extent to which electroencephalographic (EEG) differences in infants at high versus low familial risk for autism are present by 3 months of age, and elucidate the functional significance of EEG power at 3 months in predicting later development. Methods: EEG data were acquired at 3 months in infant siblings of children with autism (high risk; n = 29) and infant siblings of typically developing children (low risk; n = 19) as part of a prospective, longitudinal investigation. Development across multiple domains was assessed at 6, 9, 12, 18, 24, and 36 months. Diagnosis of autism was determined at 18-36 months. We assessed relationships between 3-month-olds' frontal EEG power and autism risk, autism outcome, language development, and development in other domains. Results: Infants at high familial risk for autism had reduced frontal power at 3 months compared to infants at low familial risk for autism, across several frequency bands. Reduced frontal high-alpha power at 3 months was robustly associated with poorer expressive language at 12 months. Conclusions: Reduced frontal power at 3 months may indicate increased risk for reduced expressive language skills at 12 months. This finding aligns with prior studies suggesting reduced power is a marker for atypical brain function, and infants at familial risk for autism are also at increased risk for altered developmental functioning in non-autism-specific domains.

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