Abstracts

Rationale: Ictal asystole has been implicated as a potential cause of sudden unexpected death in epilepsy patients (SUDEP). Severe bradycardia or asystole occurs in 0.27-0.5% of patients who have seizures during video-EEG monitoring (VEEG). Patients with partial seizures involving the insular, orbito-frontal and anterior-mid temporal regions are at risk. We are reporting the clinical presentation and outcome of two patients with ictal asystole diagnosed during VEEG.Methods: Chart review of two patients with ictal asystole detected during VEEG. Results: Patient 1: A 65 year old woman with history of convulsive seizures that are well controlled on phenytoin with no seizures reported in almost 20 years. One year prior to presentation to us she started experiencing recurrent syncope. Extensive cardiac work up and brain MRI scan were unrevealing. Phenytoin was switched to Levetiracetam for the concern that the syncope episodes were related to epileptic seizures and she was referred for inpatient VEEG. Levetiracetam was discontinued during VEEG and two syncope events were recorded. Both were associated with left mid temporal ictal discharge that was initially associated with bradycardia and progressed into asystole within 5 and 9 seconds after the ictal onset respectively lasting between 22 and 29 seconds respectively (Fig 1). During the asystole she was unresponsive and the EEG showed severe voltage attenuation followed by diffuse delta activity as the cardiac rhythm recovered and she regained consciousness. The following day she underwent a cardiac pacemaker insertion and was discharged on Keppra 500mg orally two times a day. Six months later she had not experienced any further syncope events. Patient 2: A 64 year old woman with one year history of syncope episodes lasting up to 15 minutes for which she underwent an unrevealing cardiac evaluation and brain MRI scan showed mild cerebral atrophy. She was empirically placed on Levetiracetam for presumed seizures. Valproic acid was added when syncope recurred and was referred for inpatient VEEG. A single ictal discharge during sleep was recorded after both Levetiracetam and Valproic acid were discontinued. The ictal onset was from the left mid temporal area and 12 seconds after the ictal onset she developed sinus bradycardia and 28 seconds later cardiac asystole occurred lasting for 9 seconds (Fig 2). The concomitant EEG by that time showed diffuse slowing and voltage attenuation. As the cardiac rhythm recovered the EEG activity normalized. She underwent another unrevealing cardiac work up and cardiology opted not to place a cardiac pacemaker recommending good seizure control. She was discharged on Levetiracetam and Valproic acid. However Four months later she experienced another prolonged syncope and a cardiac pacemaker was inserted. Conclusions: Ictal asystole might be of rare occurrence in patients with epilepsy but healthcare providers must be vigilant in considering it as it carries serious risks for mortality and morbidity. Good seizure control reduces these risks but this might not be an alternative for cardiac pacing to ensure safe outcome in these patients.