Young Adults with ASD Have a Higher Rate of Epileptiform Eegs Than Young Children in a Clinical Sample

Saturday, May 16, 2015: 11:30 AM-1:30 PM
Imperial Ballroom (Grand America Hotel)
D. U. Menon1 and J. B. Ewen2, (1)Kennedy Krieger Institute, Baltimore, MD, (2)Kennedy Krieger Institute/Johns Hopkins School of Medicine, Baltimore, MD
Background: Children with autism spectrum disorders (ASD) have abnormal EEGs more commonly than does the general population, with peaks of onset under 5 years and over 10 years of age. Further, many children with ASD who do not have epilepsy do nevertheless have abnormal EEGs. The significance of these EEG abnormalities is unclear but is a topic of considerable interest due to the potential of revealing mechanistic insights about both disorders as well as potential therapeutic pathways in ASD. The incidence of epileptiform discharges (independent of clinical epilepsy) at difference ages is, however, unknown.

Objectives: In a sample of children referred for EEG, to determine whether individuals with ASD have a different prevalence of abnormal EEGs by ages.

Methods: We reviewed all clinical EEG reports from the Kennedy Krieger Institute Clinical Neurophysiology Laboratory that had the words “autism,” “autistic,” “Asperger,” “ASD,” or “PDD” in the history section. EEGs were recorded between 1984 and 2014 and included routine, extended (1-4 hours) and overnight studies. 429 subjects each contributed one EEG. EEGs were coded as normal or showing epileptiform (focal, multifocal, and generalized) or non-epileptiform abnormalities. We then stratified by age (0-5y, 6-11y, 12-14y, 15-18y, >18y), and a logistical regression compared odds of having epileptiform EEGs between the 0-5y age group and all other age groups separately.

Results: Adults >18 years of age had a far higher chance of having epileptiform discharges on EEG as compared with children aged 0-5 years (OR = 6.3; p = 0.003). No other comparison was significant.

Conclusions: The primary conclusion is that there is a higher rate of epileptiform EEG in young adults with ASD as compared with young children with ASD. Given that random sampling from the overall population of individuals was not performed, the likelihood of sampling bias must be considered in the interpretation. One possibility is that clinicians have a more accurate pre-test assessment of whether the patient has epilepsy in adults than in young children. The adults sample would then be enriched with individuals with epilepsy as compared with the younger children.

Another possible explanation for the results is that the overall population prevalence of epileptiform EEGs is higher in adults than young children with ASD. Future analyses will look at the rates of clinical epilepsy in this sample, to determine to what extent epilepsy mediates the relationship between age and abnormal EEGs.