Abstracts

RATIONALE: The presence of spike or other epileptiform activity in sleep has been described even in the absence of clinical seizures in patients with autistic spectrum disorders (ASD). Overnight ambulatory or video EEG results show 20-60% of these children have epileptiform EEG abnormalities, yet the frequency in normal age-matched controls is unknown. In addition, genetic factors may play a significant role in the frequency of epilepsy. Therefore we studied overnight ambulatory EEG in non-epileptic, non-autistic children between 2-6 years of age who had a sibling with ASD and an abnormal 24 hour EEG. We hypothesized that the normal siblings would not have the types of EEG abnormalities seen in their autistic siblings.
METHODS: Twelve siblings without autistic spectrum disorders (average age 5.5 years, 6M/6F) were selected for study by digital 24 hour EEG monitoring. All children had siblings with ASD and an abnormal EEG (7 male, 5 female, average sibling age 4.6 years). EEG studies were coded by number and read independently by 2 board certified pediatric epileptologists blinded to the identity of the patients. Interpretation of the EEGs were compared for agreement between the readers. Frequency and type of EEG abnormalities were described. All subjects were paid for participation and the study was approved by the Lake Forest Hospital IRB.
RESULTS: Independent readings were exactly the same for both epileptologists. Two of the 12 siblings showed evidence of epileptiform discharges. One was read as borderline abnormal, and the 9 others had normal studies. The abnormal EEGs showed one patient with triphasic benign focal epilepsy type discharge, and one patient with generalized polyspike-wave discharges.
CONCLUSIONS: The lack of similarity between sibling EEGs suggests that genetics alone do not explain the higher frequency of EEG abnormalities reported in ASD. Of the abnormal EEG findings, one showed benign focal epilepsy of childhood, and the other abnormal EEG showed a suspected primary generalized epileptiform potential. Since these findings may be seen fairly commonly in childhood, and occurrence in our study population was infrequent and lower than the spike incidence in the ASD patients, we conclude that siblings have less frequent epileptiform activity than seen in the ASD population. It remains to be studied whether or not the general childhood population exhibits the same frequency of typicality in routine or prolonged EEG.