Abstracts

Rationale: Ictal asystole is a likely underreported feature in focal epilepsy. The mechanisms and potential relationship with sudden death in epilepsy (SUDEP) are not well understood. Although several proposed mechanisms for ictal asystole exist, the particular structural and related risk factors deserve further exploration.Methods: Report of two cases of ictal asystole. The first patient was monitored in the epilepsy unit on video electroencephalogram (VEEG). The second patient was monitored in the coronary care unit. Neither patient had baseline cardiac problems. Magnetic resonance imaging (MRI) of the brain was performed for both patients.Results: Case 1: A 37 year-old male with history of apparently mild blunt impact to the right occiput area presented for VEEG monitoring for further characterization. A captured episode began with a feeling of d j vu followed by loss of awareness and bilateral tonic extensor posturing. On EEG, electrographic ictus emerged and remained restricted to the right temporal region. Electrocardiogram (ECG) showed bradycardia followed by asystole for 22 seconds, during which EEG became markedly suppressed. After his heart rate resumed, the EEG background activity quickly returned to normal. Postictally he was nauseated and vomited. MRI brain one month prior showed a minute focus of diffusion restriction in the right paramedian cervicomedullary junction (from questionable hypoperfusive ischemia). He was started on lamotrigine and underwent dual chamber pacemaker placement. Case 2: A 60 year-old female with primary CNS lymphoma presented with two new episodes of staring and loss of awareness followed by left arm and left leg shaking for 20 to 30 seconds with simultaneous emergence of ictal bradycardia followed by asystole for 10 to 15 seconds. MRI brain showed an enhancing lesion that extended along the right lateral ventricle and into the right frontal and temporal lobes, insula, thalamus, hypothalamus, right cerebral peduncle and pons. Brain biopsy was consistent with primary CNS lymphoma. Based on her clinical presentation and imaging findings, her ictal bradycardia and asystole were thought to originate mostly from the right insula. She was started on levetiracetam, phenytoin and dexamethasone with control of her seizures and decrease in cerebral edema. A transcutaneous pacemaker was also placed.Conclusions: There are different hypotheses regarding mechanisms for ictal bradycardia and asystole. Per the lateralization hypothesis, seizures with a left-sided epileptic focus result in bradycardia and a right-sided focus result in tachycardia. A second hypothesis considers activation of parasympathetic or sympathetic centers during seizures, with prior studies showing stimulation of the left insular cortex resulting in bradycardia but right insular cortex stimulation inducing tachycardia. In contrast to both hypotheses, these two cases of ictal asystole occurred with right-sided foci. Thus the structural pathology or mechanism may not be strictly unilateral.