Purpose: The rate of sudden unexpected death in epilepsy (SUDEP) approaches 9 per 1,000 patient-years in patients with refractory epilepsy. Respiratory causes are implicated in SUDEP. We reported that ictal hypoxemia occurs in one-third of seizures in localization-related epilepsy. We now report on respiratory changes in the ictal/postictal period including changes in end-tidal CO2 (ETCO2) that correlate directly with alveolar CO2, allowing a precise evaluation of seizure-related respiratory disturbances.
Methods: One hundred eighty-seven seizures were recorded in 33 patients with localization-related epilepsy, with or without secondarily generalized convulsions, undergoing video-electroencephalography (EEG) telemetry with recording of respiratory data.
Results: The ictal/postictal ETCO2 increase from baseline was 14 ± 11 mm Hg (11, −1 to 50) [mean ± standard deviation (SD) (median, range)]. ETCO2 peak was at or above 50 mm Hg with 35 of 94 seizures, 60 mm Hg with 15, and 70 mm Hg with five seizures. Eleven of the 33 patients had seizures with ETCO2 elevation above 50 mm Hg. The duration of ictal/postictal ETCO2 increase above baseline was 424 ± 807 s (154, 4 to 6225). The duration of ictal apnea was 49 ± 46 s (31, 6–222); most ictal apneic events were central. Oxygen desaturation to 60% or less occurred with 10 seizures, including five that did not progress to generalized convulsions. Respiratory rate and amplitude increased postictally. The peak ictal ETCO2 change and duration of change were not associated with apnea duration or seizure duration. Peak ETCO2 change was significantly associated with contralateral seizure spread.
Conclusions: Severe and prolonged increases in ETCO2 occur with seizures. Postictally, respiratory effort is not impaired. Ictally triggered ventilation–perfusion inequality from pulmonary shunting or transient neurogenic pulmonary edema may account for these findings.