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棘波-慢波癫痫发作的细胞和网络机制。

Cellular and network mechanisms of spike-wave seizures.

作者信息

Blumenfeld Hal

机构信息

Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520-8018, USA.

出版信息

Epilepsia. 2005;46 Suppl 9:21-33. doi: 10.1111/j.1528-1167.2005.00311.x.

Abstract

Spike-wave seizures are often considered a relatively "pure" form of epilepsy, with a uniform defect present in all patients and involvement of the whole brain homogeneously. Here, we present evidence against these common misconceptions. Rather than a uniform disorder, spike-wave rhythms arise from the normal inherent network properties of brain excitatory and inhibitory circuits, where they can be provoked by many different insults in several different brain networks. Here we discuss several different cellular and molecular mechanisms that may contribute to the generation of spike-wave seizures, particularly in idiopathic generalized epilepsy. In addition, we discuss growing evidence that electrical, neuroimaging, and molecular changes in spike-wave seizures do not involve the entire brain homogeneously. Rather, spike-wave discharges occur selectively in some thalamocortical networks, while sparing others. It is hoped that improved understanding of the heterogeneous defects and selective brain regions involved will ultimately lead to more effective treatments for spike-wave seizures.

摘要

棘波-慢波癫痫发作通常被认为是一种相对“纯粹”的癫痫形式,所有患者均存在一致的缺陷且全脑均一性受累。在此,我们提出证据反驳这些常见的误解。棘波-慢波节律并非一种一致的疾病,而是源自大脑兴奋性和抑制性回路的正常固有网络特性,在多个不同的脑网络中,它们可由许多不同的损伤诱发。在此我们讨论几种不同的细胞和分子机制,这些机制可能有助于棘波-慢波癫痫发作的产生,尤其是在特发性全身性癫痫中。此外,我们讨论越来越多的证据表明,棘波-慢波癫痫发作中的电、神经影像学和分子变化并非全脑均一性受累。相反,棘波-慢波放电选择性地出现在一些丘脑皮质网络中,而其他网络则不受影响。希望对所涉及的异质性缺陷和选择性脑区的更好理解最终将导致对棘波-慢波癫痫发作更有效的治疗。

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