LAUSR

INTRODUCTION In patients with ictal asystole (IA) both cardioinhibition and vasodepression may contribute to syncopal loss of consciousness. We investigated the temporal relationship between onset of asystole and development of syncope in IA, in order to estimate the frequency with which pacemaker therapy, by preventing severe bradycardia, may diminish syncope risk. METHODS In this retrospective cohort study we searched video-EEG databases for individuals with focal seizures and IA (asystole ≥3 seconds preceded by heart rate deceleration) and assessed the durations of asystole and syncope and their temporal relationship. Syncope was evaluated using both video observations (loss of muscle tone) and EEG (generalized slowing/flattening). We assumed that asystole starting ≤3 seconds before syncope onset, or after syncope began, could not have been the dominant cause. RESULTS We identified 38 seizures with IA from 29 individuals (17 males; median age 41 years). Syncope occurred in 22/38 seizures with IA and was more frequent in those with longer IA duration (median duration 20 [range 5-32] seconds versus 5 [range 3-9] seconds; p<0.001) and those with the patient seated versus supine (79% versus 46%; p=0.049). IA onset always preceded syncope. In 20/22 seizures (91%), IA preceded syncope by >3 sec. Thus, in only two instances was vasodepression rather than cardioinhibition the dominant presumptive syncope triggering mechanism. CONCLUSIONS In IA, cardioinhibition played an important role in most seizure-induced syncopal events, thereby favouring the potential utility of pacemaker implantation in patients with difficult to suppress IA. This article is protected by copyright. All rights reserved.