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[内源性惊厥性犬尿氨酸在酗酒者癫痫发作发展机制中的致病作用]

[Pathogenic role of the endogenous convulsant kynurenine in the mechanisms of development of epileptic attacks in alcoholics].

作者信息

Gromov S A, Eryshev O F, Kartasheva E V, Ryzhov I V

出版信息

Zh Nevropatol Psikhiatr Im S S Korsakova. 1991;91(6):38-41.

PMID:1664582
Abstract

The role of the endogenous convulsant kynurenine (K) in the mechanisms of the development of epileptic seizures in alcoholic persons was studied on a clinical material of 63 patients suffering from alcoholism with the presence on the EEG of paroxysmal alterations without epileptic fits (n = 28) and alcoholic epilepsy (n = 35), epileptic patients not abusing alcohol (n = 20), and practically healthy subjects (n = 10). There was a significant increase of the K concentration in alcoholic patients with paroxysmal disturbances on the EEG or convulsive seizures. That increase directly correlated with the rate of convulsive epileptic fits. The rise of K in patients with alcoholic epilepsy was lower than in epileptic patients, being, however, significantly higher than in practically healthy subjects abusing alcohol and having but paroxysmal alterations on the EEG (without seizures).

摘要

以内源性惊厥性犬尿氨酸(K)在酒精中毒者癫痫发作机制中的作用为研究对象,选取了63例酒精中毒患者作为临床资料,其中28例脑电图有阵发性改变但无癫痫发作,35例为酒精性癫痫;另选20例不酗酒的癫痫患者及10例实际健康受试者作为对照。脑电图有阵发性紊乱或惊厥发作的酒精中毒患者体内K浓度显著升高,且该升高与惊厥性癫痫发作频率直接相关。酒精性癫痫患者体内K的升高幅度低于癫痫患者,但显著高于酗酒且脑电图仅有阵发性改变(无发作)的实际健康受试者。

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