Researchers at Albert Einstein College of Medicine, Bronx, NY report a 17-year-old boy with chronic intractable epilepsy and vagus nerve stimulator who developed ictal asystole many years after the onset of epilepsy. The boy had severe mental retardation, autism, and refractory epilepsy throughout childhood. MRI showed symmetric posterior cortical polymicrogyria. A first episode of supraventricular tachycardia occurred at 11 years old, and a vagus nerve stimulator inserted at age 12 years. On long-term video-EEG monitoring and cardiac telemetry, tonic arm extension seizures with head deviation to either side were accompanied by a 3-9 second period of asystole, simultaneous with attenuation of the EEG. The EEG indicated frequent electrographic seizures confined to the right posterior hemisphere quadrant. Persistent baseline bradycardia 50-65 beats per min and occasional sinus pauses lasting 1-2 sees were not associated with clinical or EEG seizures. The asystole was not linked to the vagus nerve stimulator, and ultimately necessitated placement of a cardiac pacemaker, with no interaction of the two devices. Repeated seizures may injure the brain parasympathetic or cardiac centers, leading to asystole. [1]

COMMENT. Cardiac abnormalities associated with epilepsy include tachycardia or bradycardia, T-wave flattening, AV block, atrial fibrillation, long QT, torsades de pointe (paroxysmal ventricular tachycardia), and ictal asystole. Asystole has a role in sudden unexplained death in epilepsy.

Ictal asystole and anti-NMDAR antibody encephalitis. Ictal asystole is recently reported as a complication of anti-NMDAR encephalitis. In this 15-year-old girl, seizures with asystole developed 26 days after initial presentation of symptoms and temporal lobe seizures that were associated with bradycardia. After insertion of a demand pacemaker on day 46, there were no further cardiac events [2]. In this case, asystole occurred at the onset of the illness and was not explained by a prolonged recurrence of seizures.