Ferraz M L, Gabbai A A, Oliveira A S, Ferrari A P, Miszputen S J, Ferreira Neto A, Castelo Filho A, Schmidt B
Disciplina de Neurologia, Escola Paulista de Medicina, São Paulo, Brasil.
Arq Neuropsiquiatr. 1989 Jun;47(2):139-49. doi: 10.1590/s0004-282x1989000200003.
Twenty-two chronic alcoholic patients were assessed by neurologic examination and muscle biopsy. The patients manifested proximal muscular weakness to a variable extent. One case presented as an acute bout of myopathy, according to the Manual Muscle Test, MMT. The most prominent histologic feature observed was muscle atrophy (95.3%) better evidenced through the ATPase stain with the predominance of type II A fibers (71.4%). Lack of the mosaic pattern (type grouping) seen in 76% of the cases and an important mitochondrial proliferation with intrasarcoplasmatic lipid accumulation in 63% of the patients. In case of acute presentation of muscle weakness the pathological substrate is quite different, i.e. presence of myositis mainly interstitial characterized by lymphoplasmocytic infiltrate and several spots of necrosis like Zencker degeneration. Based on histologic criteria, our data suggest that: the main determinant of muscle weakness seen in chronic alcoholic patients is neurogenic in origin (alcoholic polyneuropathy); the direct toxic action of ethanol under the skeletal muscle is closely related to the mitochondrial metabolism; the so-called acute alcoholic myopathy has probably viral etiology.
通过神经学检查和肌肉活检对22名慢性酒精中毒患者进行了评估。患者均表现出不同程度的近端肌无力。根据徒手肌力测试(MMT),有1例表现为急性肌病发作。观察到的最突出的组织学特征是肌肉萎缩(95.3%),通过ATP酶染色能更好地证实,其中以II A型纤维为主(71.4%)。76%的病例未见镶嵌模式(类型分组),63%的患者存在重要的线粒体增殖并伴有肌浆内脂质蓄积。在急性肌无力表现的病例中,病理基础有很大不同,即主要为间质性肌炎,其特征为淋巴细胞和浆细胞浸润以及几个类似Zencker变性的坏死灶。基于组织学标准,我们的数据表明:慢性酒精中毒患者所见肌无力的主要决定因素起源于神经源性(酒精性多发性神经病);乙醇对骨骼肌的直接毒性作用与线粒体代谢密切相关;所谓的急性酒精性肌病可能由病毒引起。