Torbergsen T, Stålberg E, Bless J K
Department of Neurology, University Hospital, Tromsö, Norway.
Muscle Nerve. 1991 Jan;14(1):35-41. doi: 10.1002/mus.880140107.
Thirteen patients with mitochondrial cytopathy were investigated. They represent different generations, ages, stages, and severities of the disease. All were assumed to have the same metabolic defect. The disease is a multisystem disorder with a metabolic defect located at complex 1 in the respiratory chain. Clinically, the disorder gives symptoms such as hearing loss, retinal pigmental degeneration, ataxia, cardiomyopathy, muscular fatiguability and neuropathy. The patients were investigated with nerve conduction studies, concentric needle EMG, SFEMG, and macro EMG examinations. Neurophysiologic studies revealed signs of myopathy in both the younger members and in those with slight muscular symptoms. In the more advanced stages, neuropathic changes of the axonal type were seen as well. Macro EMG was interpreted as indicating muscle fiber membrane abnormalities in the early stages. Single fiber EMG studies indicate that this metabolic defect does not disturb neuromuscular transmission.
对13例线粒体细胞病患者进行了研究。他们代表了该疾病的不同代际、年龄、阶段和严重程度。所有患者都被认为存在相同的代谢缺陷。该疾病是一种多系统疾病,其代谢缺陷位于呼吸链的复合体I。临床上,该疾病会出现听力丧失、视网膜色素变性、共济失调、心肌病、肌肉疲劳和神经病变等症状。对患者进行了神经传导研究、同心针肌电图、单纤维肌电图和巨肌电图检查。神经生理学研究显示,年轻患者和有轻微肌肉症状的患者均有肌病迹象。在疾病更晚期,还可见轴索性神经病变。巨肌电图在早期被解释为提示肌纤维膜异常。单纤维肌电图研究表明,这种代谢缺陷不会干扰神经肌肉传递。