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癫痫引起的大脑微观结构变化。

Epilepsy-induced microarchitectural changes in the brain.

作者信息

Armstrong Dawna Duncan

机构信息

Department of Pathology, Texas Children's Hospital & Baylor College of Medicine, 6621 Fannin Street, Houston, TX 77030, USA.

出版信息

Pediatr Dev Pathol. 2005 Nov-Dec;8(6):607-14. doi: 10.1007/s10024-005-0054-3.

Abstract

Our understanding of the pathogenesis of the neuropathology of epilepsy has been challenged by a need to separate the "lesions" that cause epilepsy from the "lesions" that are produced by the epilepsy. Significant clinical, genetic, pathologic, and experimental studies of Ammon horn sclerosis (AHS) suggest that AHS is the result and cause of seizures. The data support the idea that seizures cause alterations in cell numbers, cell shape, and organization of neuronal circuitry, thus setting up an identifiable seizure-genic focus. As such, AHS represents a slowly progressive lesion and a search for the cause of the initiating seizure has led to the identification of ion channel mutations. In this report, the neuropathology of other conditions associated with intractable epilepsy is considered, suggesting that in them similar epilepsy-produced alterations in microarchitecture can be observed. The idea is important to define the optimum time for epilepsy surgery and the underlying etiology of these seizure-genic lesions.

摘要

我们对癫痫神经病理学发病机制的理解受到了挑战,因为需要将导致癫痫的“病变”与由癫痫产生的“病变”区分开来。对海马硬化(AHS)的大量临床、遗传、病理和实验研究表明,AHS既是癫痫发作的结果,也是其病因。这些数据支持这样一种观点,即癫痫发作会导致细胞数量、细胞形态和神经回路组织发生改变,从而形成一个可识别的致痫灶。因此,AHS代表一种缓慢进展的病变,对起始癫痫发作原因的探寻已导致离子通道突变的发现。在本报告中,我们考虑了与难治性癫痫相关的其他病症的神经病理学,这表明在这些病症中可以观察到类似的由癫痫引起的微结构改变。这一观点对于确定癫痫手术的最佳时机以及这些致痫性病变的潜在病因非常重要。

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