Abstracts

Rationale: The mechanism of seizure termination is not fully understood. Decreased cerebral blood flow associated with asystole produces predictable changes in ion concentration, pH, and cellular function that may lead to seizure termination. To evaluate the effect of cerebral hypoxia-ischemia on seizure termination, we compared seizure duration in syncopal ictal asystole seizures and non-syncopal ictal bradycardia seizures.Methods: All prolonged video-EEG/ECG reports at Mayo Clinic Rochester between January 1990 and May 2007 were reviewed to identify all patients who had asystole or bradycardia during a recorded seizure. Syncopal ictal asystole was defined as an R-R interval greater than 4 seconds and clinical and EEG manifestations consistent with syncope during a seizure. Non-syncopal ictal bradycardia was defined as an R-R interval greater than 2 seconds or activation of a permanent pacemaker during a seizure, without both clinical and EEG features of syncope during the seizure. Durations of seizures associated with syncopal ictal asystole and non-syncopal ictal bradycardia were compared using the Wilcoxon rank-sums test.Results: Syncopal ictal asystole occurred in 11 temporal lobe origin complex partial seizures in seven patients. Mean seizure duration was 34.4 ± 13 seconds. Non-syncopal ictal bradycardia occurred in 16 temporal lobe origin complex partial seizures in seven patients. Mean seizure duration was 64.7 ± 29.5 seconds. The difference in seizure duration in these two groups was statistically significant (p=0.018). In the group with syncopal ictal asystole, the mean asystole duration was 19 ± 11.3 seconds, and the mean asystole onset latency from electrographic seizure onset was 24.2 ± 10.7 seconds. Bilateral high amplitude slowing and/or suppression of the EEG developed during all episodes of syncopal ictal asystole, and were not seen during any non-syncopal ictal bradycardia seizures. Mean latency of these EEG changes from asystole onset was 8 ± 3.7 seconds. In all cases the electrographic seizure activity terminated at the onset of the bilateral high amplitude slowing or EEG suppression. Conclusions: The seizure duration in patients who manifested clinical and EEG evidence for reduced cerebral blood flow during a seizure was significantly less than patients who did not. This suggests that the changes in the neuronal microenvironment, electrophysiologic properties, or both, which occur during transient diffuse cerebral hypoxia-ischemia favor acute seizure termination. Known sequelae of reduced cerebral perfusion which may also lead to seizure termination include: increased intracellular acidity; increased extracellular potassium; and failure of ATP dependent ion pumps. (No source of funding to disclose.)