Abstracts

Rationale: Many seizures are associated with significant ictal tachycardia, which has been associated with increased risk of SUDEP. Prior studies using scalp EEG have suggested that the site and lateralization of seizure onset influences the degree of ictal HR changes, but precise anatomical localization of these regions is poorly understood. We retrospectively examined the relationship between the seizure onset location and spread and ictal tachycardia in patients undergoing intracranial EEG monitoring as part of their evaluation for epilepsy surgery. Methods: We reviewed the NYU Comprehensive Epilepsy Center database to identify patients who underwent bilateral intracranial EEG recordings between January 2010 and June 2011. Children below 12 years of age and patients with prior brain resection, uninterpretable EKG at seizure onset, and those post brain radiation therapy or in status epilepticus were excluded. Nineteen patients were identified. Three consecutive, electrographically similar seizures were reviewed for each patient. For patients with fewer than 3 similar seizures and if more seizure types were present, those were also included for a total of 3-4 seizures per person. HR was calculated based on the computer detected R-R interval (CareFusion Nicolet, Madison, WI) and the EKG was visually reviewed for accuracy. Only parts of seizures correlating to accurate HR readings were included. Ictal tachycardia was defined as an elevation for HR > 20% of pre-ictal baseline. Ictal localization was divided into frontal (F), orbito-frontal (O-F), temporal (T), mesial temporal (MT), parietal (P) and occipital (O) regions for each second of the seizure. Comparisons were made using Chi-square or Fischer's exact test. Results: Fifty-nine seizures were reviewed from 19 patients (mean age 29.7, range 15-51) and 9 seizures were excluded due to uninterpretable EKG. Of the remaining seizures, 40 (80%) were associated with ictal tachycardia. Lateralization of the seizure onset zone did not predict occurrence of ictal tachycardia (p=0.17). However, bilateral seizure onsets were associated with early (< 10 sec) ictal tachycardia (p=0.021). Among seizures that were unilateral at ictal onset (28), 46% developed tachycardia only upon spread to the contralateral hemisphere. There was no association seen between lobar onset zone (F, O-F, T, MT, P, O) and development of tachycardia (p=0.35). There was no difference seen in development of tachycardia between genders (p=1.0). Conclusions: Neither the localization or lateralization of the seizure onset zone predicts the occurrence of ictal tachycardia. However, bilateral involvement at seizure onset is associated with early ictal tachycardia (<10 secs). These findings suggest that ictal tachycardia is probably linked to the ictal spread and possible involvement of subcortical networks, rather than the seizure onset zone.