Abstracts

Rationale: Generalized tonic-clonic seizures (GTCS) are a major risk factor for sudden unexpected death in epilepsy (SUDEP). Postictal EEG suppression, arrhythmia, and hypoventilation are often observed in patients with GTCS. Nocturnal supervision seems to protect against SUDEP independent of seizure control. Here we characterize postictal EEG recovery, heart rate, and respiratory rate in relation to seizure management in patients with primary or secondarily GTCS. The findings may further delineate the role of ictal hypoxia and postictal hypoventilation in SUDEP. Methods: We reviewed the medical records and video EEG of patients who underwent long-term monitoring at the University of Chicago medical center. We included 14 patients (4 men, 10 women) who had 1 to 2 GTCS. Mean age at evaluation was 39 years (20 to 78 years). Seizure duration ranged from 60 to 300 seconds. Five patients had primary GTCS and 9 patients had secondarily GTCS. We evaluated the EEG rhythm, heart rate, respiratory rate, and seizure management including oral suctioning and supplemental oxygen up to 2 minutes after seizure cessation. Results: Thirteen of 14 patients (93%) demonstrated immediate postictal EEG suppression. Eleven of 14 patients (79%) had postictal tachycardia. Ten of 14 patients (71%) had postictal tachypnea. Twelve of the 13 patients (92%) with EEG suppression showed delta or theta slowing 5 to 80 seconds after receiving suctioning or supplemental oxygen. One patient had theta slowing regardless of seizure management. Two patients without seizure management had prolonged EEG suppression, tachycardia, and tachypnea. One of these 2 patients had an unwitnessed GTCS in prone position leading to SUDEP. Conclusions: Postictal EEG suppression, tachycardia, and tachypnea are common features after GTCS. Postictal hypoventilation secondary to partial airway obstruction or pulmonary edema is postulated as one of the causes. Here we show that immediate seizure management facilitates the recovery of postictal EEG suppression, tachycardia, and tachypnea. Our findings suggest that the convergence of ictal hypoxia and postictal hypoventilation is a potential mechanism of SUDEP.