Chen S S, Peng M J, Chen T J
Department of Neurology, Kaohsiung Medical College, Taiwan, Republic of China.
Gaoxiong Yi Xue Ke Xue Za Zhi. 1991 Jun;7(6):296-306.
This study was undertaken to understand the myopathic manifestations as well as the electrophysiological, pathological, and histochemical changes in muscle tissues of chronic alcoholics. Twenty eight cases of chronic alcoholics with neurological complications and confirmed myopathy were included in this study. Of these, 11 cases (39.3%) belonged to the subclinical forms with either Korsakoff-Wernicke encephalopathy or cerebellar atrophy. The remaining 17 cases (60.7%) were clinical forms with various manifestations, such as hypokalemic periodic paralysis, alcoholic rhabdomyolysis, vacuolar myopathy with phosphorylase deficiency, chronic proximal limb-girdle myopathy and neuro-myopathy. Electromyography (EMG) study showed both myopathic and neurogenic changes. The single fiber EMG revealed increased jitter and blocking rate suggesting reinnervation. In muscle biopsy, the histological and histochemical abnormalities included random atrophic fibers, necrotic fibers, fibers with internal nuclei, phagocytosis and moth-eaten fibers. There was selective atrophy of type 2 muscle fibers, particularly of type 2B fiber. Total or partial myophosphorylase deficiency was observed in some cases (33%). All these findings indicate typical myopathic changes, which might be caused by defects in the energy pathways, especially in the glycolytic processes. In some muscle specimens, there were angular atrophic fibers and fiber type groupings suggesting denervation and reinnervation changes. In conclusion, both myopathic and neurogenic alterations were frequently observed in muscles of chronic alcoholics.
本研究旨在了解慢性酒精中毒患者肌肉组织的肌病表现以及电生理、病理和组织化学变化。本研究纳入了28例患有神经并发症且确诊为肌病的慢性酒精中毒患者。其中,11例(39.3%)属于亚临床形式,伴有柯萨科夫-韦尼克脑病或小脑萎缩。其余17例(60.7%)为临床形式,有各种表现,如低钾性周期性麻痹、酒精性横纹肌溶解、磷酸化酶缺乏性空泡性肌病、慢性近端肢体带型肌病和神经肌病。肌电图(EMG)研究显示既有肌病性改变也有神经源性改变。单纤维EMG显示颤抖和阻滞率增加,提示有再支配现象。在肌肉活检中,组织学和组织化学异常包括随机萎缩纤维、坏死纤维、有核内移的纤维、吞噬现象和虫蚀状纤维。2型肌纤维有选择性萎缩,尤其是2B型纤维。在一些病例中(33%)观察到完全或部分肌磷酸化酶缺乏。所有这些发现均表明存在典型的肌病性改变,这可能是由能量代谢途径缺陷,尤其是糖酵解过程中的缺陷所致。在一些肌肉标本中,有角形萎缩纤维和纤维类型分组,提示有失神经和再支配改变。总之,在慢性酒精中毒患者的肌肉中经常观察到肌病性和神经源性改变。