Electrophysiology of focal clonic seizures in humans:: a study using subdural and depth electrodes
Electrophysiology of focal clonic seizures in humans:: a study using subdural and depth electrodes
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DOI：
10.1093/brain/awg051
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发表时间：
2003-03-01
期刊：
影响因子：
14.5
通讯作者：
Rosenow, F
中科院分区：
文献类型：
--
作者：
Hamer, HM;Lüders, HO;Rosenow, F
局灶性阵挛发作是一种常见的癫痫现象。然而，关于其发病机制的数据很少。本研究纳入了11例在长时间视频EEG监测期间发生局灶性阵挛发作的局灶性癫痫患者。9名患者在中央前回上有硬膜下电极，1名患者有额外的双侧丘脑底核（STN）深度电极。在5例患者中，EEG与参与阵挛发作的肌肉的EMG共同记录。分析了发作期EEG的频率、模式和演变，并研究了它们与EEG和EMG活动的关系。局灶性阵挛发作总是与多棘波模式的主要运动区的脑电图（频率范围1.6-3.4赫兹），而相邻的电极不覆盖中央前回表现出不同的脑电图模式。在癫痫发作时，来自中央前回的发作EEG包括重复的尖峰放电8-28 s（中位数19.5 s），伴随着肌张力的持续增加。这演变成与临床阵挛相关的多棘波复合波模式，持续14-202 s（中位数30.5 s）。阵挛性肌肉收缩由复合肌肉动作电位（CMAP）的爆发组成，该复合肌肉动作电位（CMAP）同时发生在激动肌和拮抗肌中，并被完全肌肉松弛的时期分开。每一系列的CMAP遵循的多棘波在EEG的潜伏期为17-50 ms。肌肉松弛的时期发生在EEG慢波。只有部分皮层棘波之后是同侧海马棘波。CMAP遵循皮质多棘波，与是否观察到多棘波无关。提示局灶性阵挛性发作为局灶性强直-阵挛性发作。癫痫性阵挛由激动肌和拮抗肌以规则的间隔同时收缩组成，由皮层初级运动区的局部多棘波活动产生。海马的激活似乎不是阵挛性癫痫发作的重要组成部分。
Focal clonic seizures are a frequent epileptic phenomenon. However, there are few data about their pathogenesis. Eleven patients with focal epilepsy who experienced focal clonic seizures during prolonged video-EEG monitoring were included in this study. Nine patients had subdural electrodes on the precentral gyrus and one patient had additional bilateral subthalamic nucleus (STN) depth electrodes. In five patients, the EEG was co-registered with the EMG of muscles which were involved in the clonic seizures. The frequency, pattern and evolution of the ictal EEG were analysed and their relationship to STN and EMG activity was studied. Focal clonic seizures were always associated with a polyspike-wave pattern in the EEG of the primary motor area (frequency range 1.6-3.4 Hz), while neighbouring electrodes not overlying the precentral gyrus showed different EEG patterns. At seizure onset, the ictal EEG derived from the precentral gyrus consisted of repetitive spiking for 8-28 s (median 19.5 s), accompanied by a continuous increase in muscle tone. This evolved to a pattern of polyspike-wave complexes which were associated with clinical clonus and lasted for 14-202 s (median 30.5 s). The clonic muscle contractions consisted of bursts of compound muscle action potentials (CMAPs) which occurred synchronously in agonistic and antagonistic muscles and were separated by periods of complete muscle relaxation. Each series of CMAPs followed the polyspikes in the EEG with a latency of 17-50 ms. The periods of muscle relaxation occurred during the EEG slow waves. Only some of the cortical spikes were followed by ipsilateral STN spikes. CMAPs followed the cortical polyspikes independently of whether or not STN spikes were seen. The study suggests that focal clonic seizures are focal tonic-clonic seizures. The epileptic clonus consisted of simultaneous contractions of agonistic and antagonistic muscles at regular intervals and was generated by localized polyspike-wave activity in cortical primary motor areas. Activation of the STN did not appear to be an essential component of clonic seizures.