Abstracts

Rationale: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of mortality in patients with chronic uncontrolled epilepsy, and its etiologies are still largely unresolved. Here we report that a 35 year-old woman suffered SUDEP after having a generalized seizure in the prone position. The cause of her death was asphyxia from the convergence of post-ictal coma and positional airway obstruction and hypoventilation, rather than the commonly suspected peri-ictal cardiac arrhythmia or central apnea. Methods: A 35-year-old woman with medically intractable complex partial epilepsy admitted for inpatient long-term video-EEG monitoring as part of a pre-surgical evaluation. She was taking oxycarbazepine 2400mg and topiramate 200mg daily that were gradually withdrawn. In the early morning of hospital day four, she was found unresponsive in bed. Immediate attempts at cardiopulmonary resuscitation and cardioversion were unsuccessful. Results: Review of video-EEG recordings revealed that she was sleeping in the prone position with her face partially in a pillow before her seizure. While she was in her sleep, a partial seizure began in her right temporal lobe and subsequently evolved into a secondarily generalized tonic-clonic seizure. The seizure lasted approximately two minutes. Postictally, her EEG background was initially suppressed in amplitude. Two minutes after the seizure, it flattened further and demonstrated only prominent ECG artifacts for the remaining course of SUDEP. ECG showed a sinus tachycardia with a HR 120/min immediately after the seizure. The heart rate gradually slowed to 68/min with wide QRS complexes. Asystole began two minute after the seizure and lasted for approximately one minute. Surprisingly, the ECG activity reappeared with a slow HR of 30-50/min and lasted for almost 10 min. Respiratory body movements were clearly observed on the video immediately after the seizure. Rhythmic muscle artifacts on EEG were synchronized with respiratory movements. Postictally she was tachypneic with a respiratory rate at ~30/min initially. These soon increased to ~45/min for two minutes along with greater respiratory efforts. The patient subsequently became apneic for one minute. However, respiratory effort then reappeared along with ECG activity. Irregular and slow gasping respiratory efforts between 5-15/min lasted for almost 10 min. Arrest of all respiratory efforts occurred at approximately the same time as cardiac arrest 13 min after the seizure. Conclusions: The presence of enduring cardiac activity and respiratory effort for the first two minutes after the seizure suggests that neither peri-ictal cardiac arrhythmia nor central apnea was the likely mechanism of the SUDEP. Postictally,the presence of respiratory effort at an increased rate and intensity strongly suggests that asphyxia secondary to airway obstruction and hypoventilation was the main cause of death. SUDEP may share the similar etilogy to sudden infant death syndrome (SIDS) and is likely preventable.