Abstracts

Rationale: Seizures of childhood absence epilepsy (CAE) cause brief impairments of consciousness and are seen as 3-4 Hz spike-and-wave discharges on EEG. Previous neuroimaging studies show that absence seizures involve widespread cortical and subcortical attentional and default mode networks. We hypothesize that seizures impair task performance by selectively disrupting attentional networks and areas involved in primary information processing.Methods: We measured behavior on two attentional tasks in CAE patients during simultaneous EEG-fMRI with 32 EEG channels in 26 patients, and high-density 256 lead out-of-magnet EEG acquisitions in 15 patients. During the continuous performance task (CPT), patients selectively pressed a button to the letter X as a viewed letters on a screen at 1 Hz. During the repetitive tapping task (RTT), patients viewed letters on a screen as in CPT but pressed a button in response to every letter. Power in EEG leads was correlated to task performance during seizures. Results: Performance on CPT was more impaired than performance on RTT during seizures. However, ictal performance for both tasks showed variability across subjects and across seizures. For both CPT and RTT, longer duration was correlated to worse task performance. For the high-density EEG, spectral analysis for the seizure frequency band at 2.5-4 Hz revealed frontal predominance of seizure amplitude. Power in this frequency band was higher for seizures with poor performance (<25% correct) compared to good performance (>75% correct) in RTT independent of seizure duration (P < 0.0001).Conclusions: These results suggest that higher amplitude seizures cause greater impairments of task performance, possibly due to their effects on antero-medial brain regions important in attention networks. Elucidating neuroimaging signals during absence seizures and their relation to behavioral impairments can improve our understanding of the mechanism of loss of consciousness during absence seizures and lead to development of better therapeutics for CAE.