Bateman Lisa M, Li Chin-Shang, Seyal Masud
Clinical Neurophysiology, UCDMC, Sacramento, CA 95817, USA.
Brain. 2008 Dec;131(Pt 12):3239-45. doi: 10.1093/brain/awn277. Epub 2008 Oct 24.
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; 6-327). The mean oxygen saturation nadir following secondary generalization was 75.4% +/- 11.4% (77%; 42-100%). 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; 2.8-77.8). 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.
在少数病例系列中曾报告过发作期低氧血症,其可能导致癫痫性猝死(SUDEP)。我们试图确定接受住院视频脑电图遥测的局灶性相关性癫痫患者发作期低氧血症的发生率和严重程度。我们研究了与癫痫发作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侧别、发作持续时间、发作的对侧扩散、发作起始时患者的体位和体重指数等因素是否会影响发作期相关的低氧血症。连续56例难治性局灶性相关性癫痫患者共记录到304次伴有氧饱和度数据的发作;304次发作中有51次进展为全面性惊厥。脉搏血氧饱和度测定显示,在所有发作中,无论是否继发全面性发作,有101次(33.2%)发作的氧饱和度下降至90%以下,其中31次(10.2%)发作的氧饱和度下降至80%以下,11次(3.6%)发作的氧饱和度下降至70%以下。氧饱和度下降至90%以下的平均持续时间为69.2±65.2秒(47;6 - 327)。继发全面性发作后的最低平均氧饱和度为75.4%±11.4%(77%;42 - 100%)。氧饱和度下降至90%以下与癫痫发作定位显著相关[P = 0.005;颞叶发作与颞外发作的比值比(OR)= 5.202;95%置信区间=(1.665,16.257)]、发作侧别[P = 0.001;右侧发作与左侧发作的OR = 2.098;95%置信区间=(1.078,4.085)]、发作的对侧扩散[P = 0.028;有对侧扩散与无对侧扩散的OR = 2.591;95%置信区间=(1.112,6.039)]以及性别[P = 0.048;女性发作与男性发作的OR = 0.422;95%置信区间=(0.179,0.994)]。在253次无继发全面性惊厥的部分性发作亚组中,34.8%的发作氧饱和度下降至90%以下,31.8%的发作氧饱和度下降至80%以下,12.5%的发作氧饱和度下降至70%以下。氧饱和度下降程度与发作持续时间显著相关(P = 0.001),与发作扩散至对侧半球的脑电图证据也显著相关(P = 0.003)。100次发作中有50%出现中枢性呼吸暂停或呼吸浅慢。这些发作中有9%出现混合性或阻塞性呼吸暂停。对7例患者(19次发作)记录了呼气末二氧化碳(ETCO2)。发作期ETCO2相对于发作前基线的平均升高值为18.6±17.7 mmHg(13.2;2.8 - 77.8)。在这19次发作中,所有氧饱和度下降至85%以下的情况均伴有ETCO2升高。发作期低氧血症在局灶性相关性癫痫患者中经常发生,可能较为明显且持续时间较长;即使是未进展为全面性惊厥的发作。氧饱和度下降伴有ETCO2升高,支持发作期氧饱和度下降是通气不足所致的假设。发作期低氧血症和高碳酸血症可能导致癫痫性猝死。