利多卡因点燃不会引起癫痫。

V Voiculescu, D Haţegan, E Manole, A Ulmeanu
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引用次数: 0

摘要

40只Wistar大鼠每周5天注射利多卡因溶液(90 mg/kg s.c),连续30-40天。在36只动物中,出现了僵硬发作。经过一段时间的无序运动后,动物们完全一动不动,后肢僵硬地伸展着。僵硬的发作持续了10到60分钟。胸段脊髓半切抑制了同侧腿的刚性。将电极置于大脑皮层或植入颞叶深处的电记录无法显示出发作性活动。这些数据不能证实其他作者报告的利多卡因点燃后典型癫痫发作的结果。尽管存在本质差异,癫痫点燃和利多卡因点燃的僵硬发作都是中枢神经系统可塑性的表现。因此,药物诱导的可塑性似乎是一个比癫痫点燃更普遍的过程。
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Lidocaine kindling does not generate epilepsy.

Forty Wistar rats were injected with a solution of lidocaine (90 mg/kg s.c.) 5 days per week for 30-40 days. In 36 of the animals, attacks of stiffness were obtained. After a period of disordered movements, the animals, remained completely immobile with the hindlimbs rigidly extended. The attacks of stiffness lasted from 10 to 60 minutes. The hemisection of the spinal cord at the thoracic level suppressed the rigidity of the ipsilateral leg. Electrical recording with electrodes applied to the cortex or implanted in the depth of the temporal lobe failed to reveal paroxysmal activity. These data could not confirm the results of other authors reporting typical epileptic seizures after lidocaine kindling. Despite essential differences, epileptic kindling and lidocaine-kindled stiffness attacks are both manifestations of the central nervous system plasticity. Therefore it appears that pharmacologically induced plasticity is a more general process than epileptic kindling.

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