Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors
Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors
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DOI：
10.1093/brain/awn277
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发表时间：
2008-12-01
期刊：
影响因子：
14.5
通讯作者：
Seyal, Masud
中科院分区：
文献类型：
--
作者：
Bateman, Lisa M.;Li, Chin-Shang;Seyal, Masud
在小系列病例中报告了发作性低氧血症，并可能导致癫痫猝死（SUDEP）。我们试图确定发作低氧血症的发病率和严重程度与定位相关的癫痫患者进行住院视频脑电图遥测。我们研究了癫痫相关的氧饱和度下降是否是通气不足的结果，以及癫痫发作的定位和定侧、癫痫发作持续时间、癫痫发作的对侧传播、癫痫发作时患者的体位和体重指数等因素是否影响癫痫相关的低氧血症。在56例连续的难治性定位相关癫痫患者中，共记录了304次伴随血氧饱和度数据的癫痫发作; 304次癫痫发作中有51次进展为全身性惊厥。脉搏血氧饱和度测定显示，在101（33.2）次癫痫发作中，氧饱和度低于90，伴或不伴继发性全身化，31（10.2）次癫痫发作伴氧饱和度低于80，11（3.6）次癫痫发作低于70。低于90的平均去饱和持续时间为69.2 ± 65.2 s（47; 6327）。二次泛化后的平均血氧饱和度最低值为75.4 ± 11.4（77; 42100）。低于90的去饱和度与癫痫发作定位显著相关[P 0.005;颞叶与颞叶外的比值比（OR）为5.202; 95 CI（1.665，16.257）]，癫痫发作偏侧化[P 0.001;右侧与左侧的OR 2.098; 95 CI（1.078，4.085）]，癫痫发作对侧扩散[P 0.028;对侧扩散vs无扩散的OR 2.591; 95 CI（1.112，6.039）]和性别[P 0.048;女性与男性的OR为0.422; 95 CI（0.179，0.994）]。在253例部分性癫痫发作而无继发性全身性惊厥的亚组中，34.8例癫痫发作的去饱和度低于90，31.8例去饱和度低于80，12.5例去饱和度低于70。去饱和程度与癫痫发作持续时间（P 0.001）和癫痫发作蔓延至对侧半球的电图证据（P 0.003）显著相关。100次癫痫发作中有50次发生中枢性呼吸暂停或呼吸不足。其中9次癫痫发作发生混合性或阻塞性呼吸暂停。7例患者（19次癫痫发作）记录了呼气末二氧化碳（ETCO 2）。ETCO 2较发作前基线平均增加18.6 ± 17.7 mm Hg（13.2; 2.877.8）。在这19次癫痫发作中，所有低于85的氧饱和度下降均伴有ETCO 2增加。发作性低氧血症常发生在局部相关性癫痫患者中，并且可能明显和延长;即使癫痫发作没有进展为全身性惊厥。氧饱和度下降伴随ETCO 2增加，支持发作期氧饱和度下降是通气不足的结果的假设。发作性低氧血症和高碳酸血症可能导致SUDEP。
Ictal hypoxemia has been reported in small series of cases and may contribute to sudden unexpected death in epilepsy (SUDEP). We sought to determine the incidence and severity of ictal hypoxemia in patients with localization-related epilepsy undergoing in-patient video-EEG telemetry. We examined whether seizure-associated oxygen desaturation was a consequence of hypoventilation and whether factors such as seizure localization and lateralization, seizure duration, contralateral spread of seizures, patient position at seizure onset and body mass index influenced ictal-related hypoxemia. A total of 304 seizures with accompanying oxygen saturation data were recorded in 56 consecutive patients with intractable localization-related epilepsy; 51 of 304 seizures progressed to generalized convulsions. Pulse oximetry showed oxygen desaturations below 90 in 101 (33.2) of all seizures with or without secondary generalization, with 31 (10.2) seizures accompanied by desaturations below 80 and 11 (3.6) seizures below 70. The mean duration of desaturation below 90 was 69.2 65.2 s (47; 6327). The mean oxygen saturation nadir following secondary generalization was 75.4 11.4 (77; 42100). Desaturations below 90 were significantly correlated with seizure localization [P 0.005; odds ratio (OR) of temporal versus extratemporal 5.202; 95 CI (1.665, 16.257)], seizure lateralization [P 0.001; OR of right versus left 2.098; 95 CI (1.078, 4.085)], contralateral spread of seizures [P 0.028; OR of contralateral spread versus no spread 2.591; 95 CI (1.112, 6.039)] and gender [P 0.048; OR of female versus male 0.422; 95 CI (0.179, 0.994)]. In the subset of 253 partial seizures without secondary generalized convulsions, 34.8 of seizures had desaturations below 90, 31.8 had desaturations below 80 and 12.5 had desaturations below 70. The degree of desaturation was significantly correlated with seizure duration (P 0.001) and with electrographic evidence of seizure spread to the contralateral hemisphere (P 0.003). Central apnoeas or hypopnoeas occurred with 50 of 100 seizures. Mixed or obstructive apnoeas occurred with 9 of these seizures. End-tidal carbon dioxide (ETCO2) was recorded in seven patients (19 seizures). The mean increase in ETCO2 from preictal baseline was 18.6 17.7 mm Hg (13.2; 2.877.8). In these 19 seizures, all oxygen desaturations below 85 were accompanied by an increase in ETCO2. Ictal hypoxemia occurs often in patients with localization-related epilepsy and may be pronounced and prolonged; even with seizures that do not progress to generalized convulsions. Oxygen desaturations are accompanied by increases in ETCO2, supporting the assumption that ictal oxygen desaturation is a consequence of hypoventilation. Ictal hypoxemia and hypercapnia may contribute to SUDEP.