Suppr超能文献

创伤后癫痫。

Posttraumatic epilepsy.

机构信息

Epilepsy Research Laboratory, Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, Finland.

出版信息

Curr Opin Neurol. 2010 Apr;23(2):183-8. doi: 10.1097/WCO.0b013e32833749e4.

Abstract

PURPOSE OF REVIEW

The purpose of this study is to focus on recent advances in understanding of the genetic and epidemiologic risk factors, development, modeling, and prevention of epilepsy after traumatic brain injury (TBI).

RECENT FINDINGS

Epidemiologic data suggest that the epileptogenic period after TBI in humans may last longer than previously thought. Depression was found to be an important risk factor for posttraumatic epilepsy (PTE). Once PTE has developed, it remits less often than previously reported. Moreover, patients with PTE appear to have a higher mortality rate than patients with TBI without epilepsy. In animal models it was reported that in addition to rats, also mice develop PTE. Furthermore, the immature rat brain is sensitive to TBI-induced epileptogenesis. The development of a lowered seizure threshold after TBI can be alleviated by pharmacotherapy in rats.

SUMMARY

These observations provide small but encouraging steps towards a better understanding of the mechanisms of posttraumatic epileptogenesis, which is a key to developing a cure for this condition.

摘要

目的综述

本研究旨在重点关注创伤性脑损伤 (TBI) 后癫痫发生的遗传和流行病学风险因素、发病机制、模型建立和预防方面的最新进展。

最近的发现

流行病学数据表明,人类 TBI 后的致痫期可能比以前认为的要长。抑郁被认为是外伤性癫痫 (PTE) 的一个重要危险因素。一旦发生 PTE,其缓解频率比以前报道的要低。此外,PTE 患者的死亡率似乎高于无癫痫的 TBI 患者。在动物模型中,据报道,除了大鼠外,小鼠也会发生 PTE。此外,未成熟大鼠的大脑对 TBI 诱导的癫痫发生敏感。TBI 后发作阈值降低可通过药物治疗在大鼠中得到缓解。

总结

这些观察结果为更好地理解外伤性癫痫发生的机制提供了一些小但令人鼓舞的进展,这是开发该疾病治疗方法的关键。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验