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基底神经节对癫痫发作的控制?实验数据综述。

The control of seizures by the basal ganglia? A review of experimental data.

作者信息

Deransart Colin, Depaulis Antoine

机构信息

Klinikum der Albert-Ludwigs-Universität, Neurologische Universitätsklinik, Sektion Klinische Neuropharmakologie, Neurozentrum, Freiburg im Breisgau, Germany.

出版信息

Epileptic Disord. 2002 Dec;4 Suppl 3:S61-72.

Abstract

Over the past few years, the role of the basal ganglia in epilepsy has been widely debated, the debate being mainly based on experimental data obtained from several animal models. In the present review, the possibility that basal ganglia circuits can generate some forms of seizure or participate to their initiation will first be addressed. In the second part of this chapter, recent data suggesting the involvement of the basal ganglia in the control of seizures will be discussed. Although it is clear that basal ganglia circuits cannot generate seizures and are unlikely to be involved in their initiation, numerous experimental data have revealed that seizures modify the activity of this system. More recently, the collection of pharmacological and electrophysiological data in animal models of epilepsy has led to the emergence of the basal ganglia as a possible control circuit for the seizures. These experimental data have already led to initial clinical trials in epileptic patients. The preliminary clinical data encourage the further development of experimental research in chronic models of epilepsy to better determine the exact output circuits involved in seizure interruption, the mechanisms participating in seizure control and whether the same circuits are involved in the control of different types of seizures. These studies may allow the identification of crucial structures and the types of epilepsy likely to benefit from this new therapeutic approach.

摘要

在过去几年中,基底神经节在癫痫中的作用一直备受争议,这场争论主要基于从多个动物模型获得的实验数据。在本综述中,首先将探讨基底神经节回路是否能够产生某些形式的癫痫发作或参与其起始过程。在本章的第二部分,将讨论近期表明基底神经节参与癫痫控制的数据。虽然很明显基底神经节回路不能产生癫痫发作,也不太可能参与其起始过程,但大量实验数据表明癫痫发作会改变该系统的活动。最近,在癫痫动物模型中收集的药理学和电生理学数据使得基底神经节成为癫痫可能的控制回路。这些实验数据已经引发了针对癫痫患者的初步临床试验。初步临床数据鼓励在慢性癫痫模型中进一步开展实验研究,以更好地确定参与癫痫发作中断的确切输出回路、参与癫痫控制的机制以及相同回路是否参与不同类型癫痫的控制。这些研究可能有助于识别关键结构以及可能从这种新治疗方法中获益的癫痫类型。

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