Kuba R, Rektor I, Brázdil M
Epilepsy Centre, First Department of Neurology, St Anne's University Hospital, Brno, Czech Republic.
Eur J Neurol. 2003 Nov;10(6):641-9. doi: 10.1046/j.1468-1331.2003.00684.x.
The aim of the investigation was to evaluate the ictal EEG in the putamen and the temporal and frontal lobes during contralateral ictal limb dystonia (ID). Ten epilepsy surgery candidates participated in the study. All of them were investigated using intracerebral and/or subdural electrodes. In four of the patients, the putamen was investigated with diagonal depth electrodes (patients 1-4), in six of the patients, both the temporal and frontal lobes were investigated (patients 5-10). All of the investigated contacts were located contralateral to the side of the ictal dystonia. All of the patients suffered from temporal lobe epilepsy (TLE); in patient 10, both temporal and frontal seizure types were recorded. A total of 20 complex partial seizures (CPS) were analysed. ID was never an early symptom in the course of CPS. Slow activity was recorded in the putamen in all 10 seizures of the four patients in whom the putamen was investigated (patients 1-4). In five of these seizures, there was a time-locked change in the ictal EEG in relation to the ID (slowing of activity in three seizures; acceleration in two seizures). At the time of the onset of ID, several cortical regions were involved in the ictal discharge, within both the contralateral temporal and frontal lobes. In all 10 seizures of the six patients in whom both the temporal and frontal lobes on the contralateral side were evaluated (patients 5-10), the ictal paroxysmal discharge was noted in both lobes (i.e. frontal and temporal) at the time of ID onset. We can conclude that ID is a late symptom in TLE. Widespread activation of the contralateral temporal and frontal lobes is needed for the appearance of ID; however, the critical region responsible for the genesis of ID was not revealed. Although there are some non-specific changes in the putamen contralateral to ID, the changes were never epileptic in type. The putamen probably collaborates in the genesis of ID, but it does not generate the epileptic discharge during its course.
该研究的目的是评估对侧发作期肢体肌张力障碍（ID）期间壳核以及颞叶和额叶的发作期脑电图。10名癫痫手术候选者参与了该研究。他们均接受了脑内和/或硬膜下电极检查。其中4例患者使用对角深部电极对壳核进行了检查（患者1 - 4），6例患者对颞叶和额叶均进行了检查（患者5 - 10）。所有检查触点均位于发作期肌张力障碍侧的对侧。所有患者均患有颞叶癫痫（TLE）；在患者10中，记录到了颞叶和额叶两种发作类型。共分析了20次复杂部分性发作（CPS）。ID在CPS过程中从未作为早期症状出现。在对壳核进行检查的4例患者的所有10次发作中（患者1 - 4），壳核均记录到慢波活动。在其中5次发作中，发作期脑电图与ID存在时间锁定变化（3次发作活动减慢；2次发作活动加速）。在ID发作时，对侧颞叶和额叶的几个皮质区域均参与了发作期放电。在对6例对侧颞叶和额叶均进行评估的患者的所有10次发作中（患者5 - 10），在ID发作时双侧叶（即额叶和颞叶）均记录到发作期阵发性放电。我们可以得出结论，ID是TLE中的晚期症状。ID出现需要对侧颞叶和额叶广泛激活；然而，尚未发现负责ID发生的关键区域。尽管ID对侧的壳核存在一些非特异性变化，但这些变化在类型上从未表现为癫痫性。壳核可能参与了ID的发生，但在其过程中并不产生癫痫放电。
