Predicting ASD and Other Developmental Outcomes in the First Year of Life Using EEG in a Diverse Community-Based Sample (Revision)
- Institution
- BOSTON CHILDREN'S HOSPITAL, MA
- Principal investigator
- Charles Alexander Nelson
- Funding
- $625K
- Duration
- 2021–2026
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Abstract
Project Summary Children growing up in disadvantaged, high-stress environments are at a significantly increased risk for developmental delays and autism. Early identification of those at greatest risk is crucial to improving outcomes. There is mounting evidence from our laboratory that there are patterns in the EEG that emerge during the first year of life that are reliably associated with autism outcomes at 2-3 years of age. The primary goals of the parent grant (NS120986) thus extend our previous work (DC010290) by collecting high-dimensional EEG data collection in a large pediatric primary care clinic, thus demonstrating the potential scalability of EEG as a biomarker of autism risk. Importantly, the study is situated in a clinic serving infants who have historically been underserved and understudied: primarily Black and Hispanic infants growing up in low-income homes. The parent study collects EEGs during infant well-child visits at 4, 9, and 12 months, with diagnostic outcomes assessed at 24 months using the Mullen Scales of Early Learning (MSEL), Rapid Interacting Screening Test for Autism in Toddlers, the Autism Diagnostic Observation Schedule (ADOS), and the Vineland Adaptive Behavior Scales. In addition to EEGs, data collected as part of the parent study include parent report of development, temperament, and parental perceived stress, along with demographic information and medical record abstraction. Prior to launching this study, our preliminary data suggested that infants born into low income and high stress households have a higher prevalence of both autism (10%) and developmental delay (20%) at 24 months. However, our preliminary data thus far suggest even higher rates of autism (19%) and developmental delays (41%). These rates are concerning and it is imperative that we further characterize whether the pattern of findings to date persists through 3 years of age. The goal of this competing revision is to extend the parent project to evaluate developmental progress of our enrolled participants, from 24- to 30- to 36-months in order to better characterize the stability of early symptoms of autism and developmental delays. Aim 1a: Evaluate the stability of autism symptoms from 24- to 30- to 36-months in our enrolled sample of children raised in low resource families. Aim 1b: Evaluate the stability of language and developmental delay from 24- to 36-months in our enrolled sample of children raised in low resource families. Aim 2: Exploratory aim to compare EEG features in autistic toddlers who do and do not exhibit substantial improvement in symptoms between 24-36 months. These additional evaluations will be critical to furthering our understanding of biological and environmental factors influencing early development in this underserved, understudied, high risk population.
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