Abstracts

Rationale: Sudden unexplained death in epilepsy (SUDEP) has an annual incidence of 0.09-9.3 per 1000 person years. Cardiac and respiratory mechanisms have been implicated. We have shown that one-third of seizures in patients with localization-related epilepsy, undergoing video-EEG telemetry (VET) have ictal/postictal oxygen desaturation below 90%. Desaturation nadirs were below 70% in 11% of these seizures (Bateman et al. Brain (2008)131:3235-3249). The duration, severity and characteristics of respiratory changes during and following seizures need to be better defined. Methods: We now report on changes in respiratory parameters in another 189 seizures in 33 patients with localization-related epilepsy undergoing VET. All patients had concomitant monitoring of oxygen saturation with pulse oximetry (SAO2); end-tidal CO2 (ETCO2); nasal airflow recorded using a pressure transducer; abdominal excursions recorded with inductance plethysmography; and a single channel electrocardiogram. The mean age was 32 years (range 18-66 years). The mean body mass index was 25±5. Results: Data are reported as mean ± standard deviation (median, range). With partial seizures that did not generalize, the mean SAO2 nadir was 88% ± 11(92, 43-100); following generalization the nadir was 74% ± 11(75, 50-91). The ETCO2 peak increase above preictal baseline was 14mmHg ± 11(11, -1-50). The highest absolute peak ETCO2 recorded was 94 mmHg. ETCO2 return to preictal baseline occurred 438 seconds ±84 (150, 4-6225) after the peak ETCO2. The ictal/postictal duration of oxygen desaturation below 90% was 80 seconds ± 89 (59, 4-712). Recovery of SAO2 to preictal baseline was further delayed to 176 ± 281 seconds (103, 13-2036). The duration of ictal apnea was 49 seconds ± 46 (31, 6-222). There was a postictal increase in respiratory rate (RR) of 7 breaths-per-minute ± 9.2 (6, -6-46). The peak ETCO2 was delayed 56 seconds ± 111 (27,-318-552) and the SAO2 nadir was delayed 111 seconds ± 70 (96, 22-469) following seizure end. The seizure duration was 111 ± 95 seconds (84, 17-724). The heart rate increased from a preictal rate of 85 bpm ± 19 (84, 54-192) to a peak of 131 ± 27 (126, 72-210) with the seizures. The ictal/postictal increase in heart rate persisted for 329 seconds ± 737 (80, 10-4251). Conclusions: There can be persistent and severe elevations in ETCO2 and concomitant drops in oxygen saturation following partial onset seizures despite postictal increases in RR. These changes occur both with partial seizures that do not generalize as well as with secondarily generalized convulsions. Ictal apnea and postictal hypoventilation despite increased RR or a ventilation-perfusion mismatch may account for these changes in SAO2 and ETCO2. Severe ictal/postictal acute hypercapnia with associated acidosis and hypoxemia may contribute to SUDEP in some cases.