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进行性肌营养不良症是一组遗传性原发性肌病。一般根据病变肌群和临床特点将其分为若干类型,其共同的临床表现为进行性肌无力,严重者最终可致瘫痪。有关本病的生化酶学、组织形态学及肌电图的变化已有广泛研究,本文仅就超微结构变化作初步探讨。1.材料与方法41例进行性肌营养不良症患者,均为西京医院神经内科就诊病人,其中男性32例,女性9例,年龄4～40岁,平均17.1岁。临床分型:假肥大型27例,肢带型8例,面肩肱型3例,肌强直型3例。病程一年以下者1例,2～5年21例,6～10年13例,11年以上6例。肌肉取材部位为股四头肌、腓肠肌、肱二头肌和胫骨前肌,以股四头肌和腓肠肌占多数。
Progressive muscular dystrophy is a group of hereditary primary myopathies. Generally based on the diseased muscle and clinical characteristics will be divided into several types, their common clinical manifestations of progressive weakness, severe cases can eventually lead to paralysis. The biochemical enzymology, histomorphology and EMG changes have been extensively studied in this article, the paper only preliminary study on the ultrastructure changes. 1 Materials and Methods 41 cases of patients with progressive muscular dystrophy were Xijing Hospital neurology patients, including 32 males and 9 females, aged 4 to 40 years, mean 17.1 years. Clinical classification: 27 cases of fake hypertrophy, limb type 8 cases, 3 cases of face and shoulder humerus, 3 cases of muscle rigidity. One case of less than one year duration, 21 cases of 2 to 5 years, 13 cases of 6 to 10 years, 6 cases of more than 11 years. Muscle drawn parts of the quadriceps, gastrocnemius, biceps and tibialis anterior muscle, quadriceps and gastrocnemius muscle majority.