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.
Subject(s)
Brain/physiopathology , Electroencephalography/statistics & numerical data , Epilepsy/complications , Heart Arrest/complications , Hypoxia-Ischemia, Brain/physiopathology , Autonomic Nervous System/physiopathology , Bradycardia/complications , Bradycardia/physiopathology , Cause of Death , Cortical Synchronization/statistics & numerical data , Death, Sudden/etiology , Electrocardiography/statistics & numerical data , Epilepsy/mortality , Epilepsy/physiopathology , Epilepsy, Temporal Lobe/physiopathology , Functional Laterality/physiology , Heart/physiopathology , Heart Arrest/diagnosis , Heart Arrest/physiopathology , Humans , Hypoxia-Ischemia, Brain/etiology , Remission, Spontaneous , Risk Factors , Seizures , Time FactorsABSTRACT
Ictal asystole (IA) has been implicated as a preventable cause of sudden unexplained death in epilepsy presumably provoked by a direct autonomic effect of the electrical stimulus on the heart. An electronic database search of patients with IA was performed comparing heart rate (HR) characteristics to a group of patients with vasovagal asystole. IA was seen in eight patients, all with temporal lobe epilepsy. No statistical difference was found in duration of asystole, bradycardia, and baseline HR characteristics except of a higher HR acceleration postasystole in the controls. None of the six patients with IA who underwent pacemaker implantation had recurrence of asystolic events during mean follow-up of 5 years. This study in a small group of patients suggests that the epileptic activation leading to IA is possibly mediated through a transient increase in vagal tone and not by a direct autonomic effect on the heart.
