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

Stephan U. Schuele, Adriana C. Bermeo, Andreas V. Alexopoulos, Richard C. Burgess

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)170-173
Number of pages4
JournalEpilepsia
Volume51
Issue number1
DOIs
StatePublished - 2010

Keywords

  • Ictal asystole
  • SUDEP
  • Seizure termination
  • Sudden unexplained death in epilepsy

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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