Epilepsy Center, Department of Neurology, University Hospital Erlangen, Erlangen, Germany.
Department of Anesthesiology, University Hospital Erlangen, Erlangen, Germany.
Clin Neurophysiol. 2014 Feb;125(2):223-30. doi: 10.1016/j.clinph.2013.07.006. Epub 2013 Aug 2.
The short acting anesthetic etomidate has been shown to provoke epileptic spikes and rarely seizures. Influence of etomidate on the occurrence of epileptic HFO (high frequency oscillations) however is unknown. An HFO inducing effect of etomidate would allow further validation of the substance as a provocation measure in presurgical evaluation as well as provide insights into the common mechanisms of HFO, spike and seizure generation.
We retrospectively analyzed EEG data from four patients who underwent etomidate activation during invasive video-EEG monitoring with subdural strip electrodes. Spikes were manually selected in raw data, HFO in band pass filtered data (80-250Hz). Rate and spatial distribution of HFO and spikes in three segments were compared: immediately after etomidate administration, as well as during slow wave sleep and while awake.
Rates of HFO and spikes increased significantly after etomidate administration: Overall average rates of spikes were 9.7/min during sleep, 10/min while awake and 61.4/min after etomidate. Average HFO rates were 9.5/min during sleep, 8.3/min while awake and 24.4/min after etomidate (p<0.001, non-parametric ANOVA). Spatial distributions of HFO and spikes after administration of etomidate were consistent with the seizure onset zone (SOZ) and area of resection when available (SOZ: two patients; resection: one patient; no information: one patient). Except for spurious events, no additional HFO and spike foci were seen with activation.
Etomidate administration activates spikes and HFO. Spatial distributions do not extend beyond electrodes showing spikes and HFO without Etomidate and seem consistent with the epileptic network.
Etomidate activation is a safe procedure to provoke not only epileptic spikes but also HFO, which were shown to have a high specificity for the SOZ.
短效麻醉药依托咪酯已被证明会引发癫痫棘波，且罕见地导致癫痫发作。然而，依托咪酯对癫痫高频振荡（HFO）发生的影响尚不清楚。依托咪酯诱导 HFO 的作用将进一步验证其作为术前评估激发手段的合理性，同时为 HFO、棘波和癫痫发作产生的共同机制提供深入见解。
我们回顾性分析了 4 名患者在接受硬膜下条带电极侵入性视频脑电图监测期间接受依托咪酯激活时的脑电图数据。在原始数据中手动选择棘波，在带通滤波数据（80-250Hz）中选择 HFO。比较了三个时间段内 HFO 和棘波的频率和空间分布：依托咪酯给药后即刻，慢波睡眠期间和清醒时。
依托咪酯给药后，HFO 和棘波的频率显著增加：睡眠时棘波的总体平均频率为 9.7/min，清醒时为 10/min，依托咪酯后为 61.4/min。睡眠时 HFO 的平均频率为 9.5/min，清醒时为 8.3/min，依托咪酯后为 24.4/min（p<0.001，非参数 ANOVA）。依托咪酯给药后 HFO 和棘波的空间分布与致痫区（SOZ）和切除区域一致（SOZ：2 名患者；切除：1 名患者；无信息：1 名患者）。除了假阳性事件外，激活时没有发现额外的 HFO 和棘波焦点。
依托咪酯给药会激活棘波和 HFO。其空间分布不会超出未用依托咪酯时显示棘波和 HFO 的电极范围，并且与癫痫网络一致。
依托咪酯激活不仅可以诱发癫痫棘波，还可以诱发 HFO，这对 SOZ 具有高度特异性，是一种安全的激发程序。
