Department of Neurology, Division of Pulmonary and Critical Care Medicine, University of California, Davis, California, USA.
Epilepsia. 2010 Aug;51(8):1359-64. doi: 10.1111/j.1528-1167.2009.02518.x. Epub 2010 Feb 12.
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 CO(2) , allowing a precise evaluation of seizure-related respiratory disturbances.
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.
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 ETCO(2) 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.
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.
在耐药性癫痫患者中,癫痫猝死(SUDEP)的发生率接近每 1000 患者年 9 例。呼吸原因与 SUDEP 有关。我们报告说,在与定位相关的癫痫发作中,三分之一的发作会出现发作性低氧血症。现在我们报告了发作期和发作后期的呼吸变化,包括与肺泡 CO₂(ETCO₂)直接相关的终末 CO₂(ETCO₂)变化,这可以精确评估与发作相关的呼吸障碍。
对 33 名患有与定位相关的癫痫患者(伴有或不伴有继发性全身惊厥)进行了视频-脑电图(EEG)遥测,并记录了呼吸数据,共记录了 187 次发作。
发作后/发作后 ETCO₂ 从基线增加 14 ± 11 mm Hg(11,-1 至 50)[平均值 ± 标准差(SD)(中位数,范围)]。35 次发作中,60 mm Hg 时有 15 次,70 mm Hg 时有 5 次,ETCO₂ 峰值达到或高于 50 mm Hg。33 名患者中有 11 名患者的 ETCO₂ 升高超过 50 mm Hg。发作后/发作后 ETCO₂升高超过基线的持续时间为 424 ± 807 s(154,4 至 6225)。发作性呼吸暂停的持续时间为 49 ± 46 s(31,6-222);大多数发作性呼吸暂停事件为中枢性的。10 次发作时出现氧饱和度降至 60%或更低,其中 5 次未进展为全身惊厥。发作后呼吸频率和幅度增加。峰 ETCO₂变化和变化持续时间与呼吸暂停持续时间或癫痫持续时间无关。峰 ETCO₂变化与对侧癫痫扩散显著相关。
癫痫发作时会出现严重和持续的 ETCO₂升高。发作后,呼吸肌功能不受影响。可能是由于肺分流或短暂的神经性肺水肿引起的通气-灌注失衡导致了这些发现。