Kirchberger K, Schmitt H, Hummel C, Peinemann A, Pauli E, Kettenmann B, Stefan H
Department of Neurology, University of Erlangen-Nuernberg, Erlangen, Germany.
Epilepsia. 1998 Aug;39(8):841-9. doi: 10.1111/j.1528-1157.1998.tb01178.x.
During presurgical evaluation, 14 patients with medically intractable focal epilepsies underwent magnetoencephalographic (MEG) recordings for focus localization. To increase the number of epileptic discharges required for MEG analysis, we administered methohexital (MHT), a short-acting barbiturate known to provoke epileptic activity. We also investigated the spike-provoking properties of clonidine in comparison with MHT.
Patients were briefly anesthetized with intravenously administered MHT after being premedicated orally with clonidine. Numbers and locations of epileptic MEG discharges were assessed after clonidine premedication as well as during MHT anesthesia. Results were compared with baseline MEG recordings.
MHT increased the frequency of focal epileptic discharges in 8 of 13 patients ( of the 14 patients did not receive MHT after premedication with clonidine). Premedication with clonidine also increased focal epileptic discharges in 9 of 14 patients. The numbers of epileptic signals and numbers of spikes contributing to MEG source localizations were significantly increased in MEG recordings under both treatment conditions (clonidine premedication and MHT anesthesia) as compared with baseline MEG recordings.
Our results confirmed the selective proconvulsive effects of MHT on the epileptic focus, as previously suggested by EEG and electrocorticographic (ECoG) investigations. However, our present data establish for the first time that clonidine increases epileptic activity in patients with seizure disorders and indicate that clonidine is suitable as an activating agent for localization of epileptogenic foci by MEG. This effect of clonidine on specific epileptic activity also indicates that specific care must be taken when clonidine is used as an antihypertensive drug in patients with seizure disorders.
在术前评估期间，14例药物治疗无效的局灶性癫痫患者接受了脑磁图（MEG）记录以进行病灶定位。为了增加MEG分析所需的癫痫放电次数，我们给予了美索比妥（MHT），一种已知可诱发癫痫活动的短效巴比妥酸盐。我们还比较了可乐定与MHT诱发棘波的特性。
患者在口服可乐定进行预处理后，静脉注射MHT进行短暂麻醉。在可乐定预处理后以及MHT麻醉期间评估癫痫MEG放电的数量和位置。将结果与基线MEG记录进行比较。
13例患者中有8例（14例患者中1例在可乐定预处理后未接受MHT）的MHT增加了局灶性癫痫放电的频率。可乐定预处理也使14例患者中的9例局灶性癫痫放电增加。与基线MEG记录相比，在两种治疗条件下（可乐定预处理和MHT麻醉）的MEG记录中，癫痫信号数量和对MEG源定位有贡献的棘波数量均显著增加。
我们的结果证实了MHT对癫痫病灶的选择性促惊厥作用，正如先前脑电图和皮质脑电图（ECoG）研究所表明的那样。然而，我们目前的数据首次证实可乐定可增加癫痫患者的癫痫活动，并表明可乐定适合作为通过MEG定位癫痫病灶的激活剂。可乐定对特定癫痫活动的这种作用还表明，在癫痫患者中使用可乐定作为抗高血压药物时必须特别小心。
