Changes in Early Aperiodic EEG Activity Are Linked to Autism Diagnosis and Language Development in Infants With Family History of Autism.
Carol L Wilkinson, Haerin Chung, Amy Dave and 2 others
PMID 40420626WHAT IT FOUND
Infants with a family history of autism showed reduced brain activity at 3 months.
Greater increases in this activity by 12 months linked to later autism diagnosis and lower language scores at 18 months, independent of cognitive ability.
Key findings
01At 3 months, infants with elevated familial likelihood of autism had significantly reduced total aperiodic EEG activity compared to low-likelihood infants.
02Infants later diagnosed with autism showed greater developmental increases in aperiodic activity from 3 to 12 months compared to those without a diagnosis.
03In infants with elevated familial likelihood, greater changes in aperiodic offset and slope from 3 to 12 months were associated with lower verbal developmental quotients at 18 months.
STILL TO COME
How it was doneWhat they foundWhat it means for SLPs
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What it does not show
The sample size for the longitudinal EEG analysis was small, with only 73 infants providing data at both 3 and 12 months. The study population was largely composed of White families with higher incomes, which limits generalizability. Language assessments were conducted at 18 months, a time when many toddlers with delays naturally catch up, so the findings may not predict persistent language disorders. The study did not have sufficient power to assess EEG associations with language development beyond 18 months. Equipment changes during the study (switching from 64-channel to 128-channel nets) required sensitivity analyses, though no significant differences were found.
Declared interests
The authors declare that they have no conflict of interest. The study was supported by NIH funding.
The easy way to misread this
Do not interpret these EEG findings as a diagnostic tool or a cause of language delay. The study shows an association between brain activity changes and language outcomes in a specific high-risk group, but it does not prove that the brain activity causes the delay, nor can it be used to diagnose individual patients.