Abstracts

Rationale: Sudden unexpected death in epilepsy (SUDEP) is a feared complication of seizures. Its exact pathophysiology is not known. Various factors have been implicated including cardiac arrhythmias, neurogenic pulmonary edema, and respiratory suppression. There are multiple reports of ictal cardiac asystole, some with associated apnea or hypoxia. None have documented a normal oxygen saturation at the time of asystole. We present the case of a patient with medically refractory epilepsy and seizure induced cardiac asystole with documented normal oxygen saturation at the time of cardiac arrest. Methods: In May 2010, we began continuously monitoring oxygen saturation via pulse oximeter and cardiac telemetry in all patients admitted for video electroencephalographic (EEG) monitoring in order to identify cardiac arrhythmias. Scalp EEG was recorded using the standard International 10-20 system, including T1 and T2 electrodes. All EEGs were reviewed by an epileptologist with assistance from EEG technologists. Cardiac telemetry and oxygen saturation were continuously monitored by nurses. Results: A single patient with seizure induced asystole was identified. She is a 36 year old right handed woman with epilepsy since age 10 and no known cardiovascular disease. Seizures consist of generalized tonic-clonic activity without preceding aura. She reported 1-28 seizures per month. Past medical history is significant for premature birth, depression, obesity, smoking, and asthma. There is no family history of seizures or cardiovascular disease. Magnetic resonance imaging was remarkable for abnormal signal change in the left medial temporal lobe. At the time of evaluation her antiepileptic medications were levetiracetam, gabapentin and lamotrigine. They were not reduced. Interictal EEG revealed bilateral independent temporal sharp waves without definite lateralization. One focal onset seizure with rapid secondary generalization was captured. Initial ictal EEG rhythm and clinical semiology were non-lateralizing. Sixty-one seconds after seizure onset there was brief progressive sinus bradycardia leading to 12 seconds of asystole. Bradyarrhythmia began almost immediately after the clinical convulsion ended, but while EEG still showed an ictal rhythm over the temporal regions. Asystole was associated with background suppression on EEG. There was spontaneous return to sinus bradycardia, then normal sinus rhythm. Oxygen saturation at the time of asystole was 95% as documented on cardiac telemetry strip. Cardiology was consulted. Cardiovascular risk factors were assessed. Moderate pulmonary hypertension was found on transthoracic echocardiogram. The patient declined pacemaker implantation. Conclusions: We present the first case of seizure induced cardiac asystole with clearly documented normal oxygen saturation at onset of cardiac arrest. This indicates that asystole, and likely other ictal cardiac dysrhythmias, are not necessarily a secondary effect of hypoxia. Further research is needed to better understand the causes of ictal asystole and its connection to SUDEP.