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γ-氨基丁酸(GABA)功能受损导致的肌肉痉挛——一项电生理与药理学观察

Muscle cramp as the result of impaired GABA function--an electrophysiological and pharmacological observation.

作者信息

Obi T, Mizoguchi K, Matsuoka H, Takatsu M, Nishimura Y

机构信息

Department of Neurology, National Shizuoka Hospital, Japan.

出版信息

Muscle Nerve. 1993 Nov;16(11):1228-31. doi: 10.1002/mus.880161113.

Abstract

We investigated the mechanism of cramps in 2 patients: a 48-year-old man with bulbospinal neuronopathy, and a 46-year-old man with amyotrophic lateral sclerosis. Cramps were quite easily induced by volitional exertion and high-frequency stimulation of the peripheral nerves. When an ulnar nerve was blocked with lidocaine at the elbow, no cramp was induced despite the application of high-frequency stimulation at the wrist. Diazepam (GABAA agonist) was effective in the first patient and baclofen (GABAB agonist) in the second, with no cramps induced in spite of increasing stimulation intensity. Impairment of interneurons mediated by GABA as the neurotransmitter is thought to be involved in the mechanism of the cramps.

摘要

我们研究了2例患者抽筋的机制:1例48岁患有延髓脊髓神经元病的男性,以及1例46岁患有肌萎缩侧索硬化症的男性。随意运动和外周神经的高频刺激很容易诱发抽筋。当在肘部用利多卡因阻断尺神经时,尽管在腕部施加了高频刺激,但并未诱发抽筋。地西泮(GABAA激动剂)对首例患者有效,巴氯芬(GABAB激动剂)对第二例患者有效,尽管刺激强度增加,但均未诱发抽筋。由γ-氨基丁酸作为神经递质介导的中间神经元功能障碍被认为与抽筋机制有关。

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