Anoxia-ischemia: A mechanism of seizure termination in ictal asystole

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Schuele SU, Bermeo AC, Alexopoulos AV, and Burgess RC (2009) Anoxia-ischemia: A mechanism of seizure termination in ictal asystole.

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Abstract: Cerebral anoxia-ischemia (CAI) is a potent inhibitor of cerebral hyperactivity and a potential mechanism of seizure self-termination. Prolonged ictal asystole (IA) invariably leads to CAI and has been implicated as a potential cause of sudden unexplained death in epilepsy (SUDEP). IA was seen in eight consecutive patients (0.12% of all patients monitored). Ten of their seizures with IA had evidence of CAI on electroencephalography (EEG), manifested by bilateral hypersynchronous slowing (BHS), and were compared to 18 seizures without signs of CAI. The ictal EEG pattern resolved in all 10 CAI events with onset of the BHS. The period from IA onset to seizure end was reduced in events with BHS compared to events without BHS (10.5 s vs. 28.3 s, respectively; p = 0.005), and the total seizure duration tended to be shorter. Anoxia-ischemia as a result of IA may represent an effective endogenous mechanism for seizure termination and may explain why the hearts of patients with ictal asystole reported to date in the literature resumed beating spontaneously.

Keywords: Ictal asystole, Seizure termination, Sudden unexplained death in epilepsy, SUDEP.


  • Study of 8 patients who experienced asystole during seizures (10 instances) while undergoing EEG monitoring. Asystole preceded, and appeared to cause, the EEG pattern of bilateral hypersynchronous slowing (BHS), which in turn may have hastened the end of the seizure, as the time from onset of asystole to end of seizure was considerably shorter when BHS occurred. Cases were previously reported in Schuele et al.


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