Suppr超能文献

酒精性肌病的重新评估。对无肌肉无力或萎缩的慢性酒精中毒患者的临床及活检研究。

Reappraisal of alcoholic myopathy. Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting.

作者信息

Faris A A, Reyes M G

出版信息

J Neurol Neurosurg Psychiatry. 1971 Feb;34(1):86-92. doi: 10.1136/jnnp.34.1.86.

Abstract

To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.

摘要

为了确定导致慢性酒精中毒患者远端肌肉失神经支配的酒精性神经病是否也会导致其近端肌肉出现亚临床肌病,我们研究了11名无肌肉无力或萎缩的慢性酒精中毒患者。6例患者临床检查显示远端反射减退(踝反射)感觉神经病。4例患者,其中1例无症状,腓总运动神经传导速度减慢。2例患者近端肌肉的肌电图显示有神经病变模式。酶组织化学肌肉活检研究表明,8例患者对侧股四头肌存在失神经萎缩和肌病改变。由于存在失神经萎缩,我们得出结论,这些肌病改变代表了这些肌肉失神经支配的影响。因此,我们得出结论,先前我们自己和其他人描述为原发性的近端亚临床酒精性肌病是由众所周知的酒精性神经病导致的失神经支配的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8652/493692/fea6da0ebc3a/jnnpsyc00211-0093-a.jpg

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