Postictal generalized EEG suppression is linked to seizure-associated respiratory dysfunction but not postictal apnea

Summary Purpose: The relationship of postictal generalized electroencephalography (EEG) suppression (PGES) with sudden unexpected death in epilepsy (SUDEP) is controversial. It has been suggested that PGES is associated with respiratory inhibition leading to SUDEP, but the relationship between PGES and respiratory depression is unknown. Respiratory rate and amplitude of airflow increase following seizures but there is persistent hypercapnia and hypoxemia. To determine whether seizures with PGES result in respiratory dysfunction, we analyzed respiratory parameters recorded during video‐EEG telemetry in patients with localization‐related epilepsy. Methods: Secondarily generalized convulsive seizures (GC) with PGES on scalp EEG or bilateral postictal attenuation (BA) on intracranial recordings were compared to GC without PGES/BA. Oxygen desaturation nadir and duration, end‐tidal CO2 (ETCO2), apnea duration, and duration of the seizure and of the convulsive component were compared in GC with or without PGES/BA. Key Findings: There was no significant difference between GC with (n = 30) or without PGES/BA (n = 72) for total seizure duration or duration of the convulsion. GC with PGES/BA had a mean oxygen desaturation nadir of 68.8 ± 11.8% (71.5, 43–88) (mean ± standard deviation [median, range]) that was lower (p = 0.002) than seizures without PGES/BA (76.31 ± 10.17% [79, 42–93]). The duration of desaturation was significantly longer and peak ETCO2 higher in GC with PGES/BA. There was no difference in apnea duration. Apnea did not start during PGES/BA and did not typically extend into the postictal period in GC with or without PGES/BA. Significance: PGES is not associated with postictal central apnea but is more likely related to the severity of seizure‐associated intrinsic pulmonary dysfunction.