Ashok P P, Katiyar B C, Dube B, Shukla P K, Tripathi V N
Acta Neurol Scand. 1979 Apr;59(4):200-10. doi: 10.1111/j.1600-0404.1979.tb02930.x.
Twenty unselected consecutive patients of filarial chyluria were evaluated clinically, electromyographically, and histopathologically for neuromuscular dysfunction. None of the patients showed clinical evidence of muscle wasting or weakness suggesting myopathy, although generalized muscle weakness was complained by all of them particularly while climbing the stairs or on getting up or during lifting heavy weights. Electromyographic abnormalities were found in nine patients and slight histopathological abnormalities in two. The average duration of motor unit potentials and the mean amplitude were reduced, compatible with myopathy. There were no fibrillation potentials. Histological abnormalities consisted of a marked variation in muscle fibre size, sarcolemmal nuclear proliferation, and mild interstitial fatty infiltration. None of the patients showed evidence of clinical neuropathy, abnormalities in conduction velocity along the nerves or signs of segmental demyelination in the biopsy of the nerve. Our data suggest that muscle weakness in these patients is myopathic in nature without peripheral nerve involvement, and is possible due to hypoproteinaemia and hypolipidaemia, as these patients lose excessive amounts of protein and fat in their urine.
对20例未经挑选的连续性丝虫性乳糜尿患者进行了临床、肌电图及组织病理学评估,以确定其神经肌肉功能障碍情况。尽管所有患者均主诉有全身肌肉无力,尤其是在爬楼梯、起床或举重物时,但无一例患者有提示肌病的肌肉萎缩或无力的临床证据。9例患者存在肌电图异常,2例有轻微组织病理学异常。运动单位电位的平均时限和平均波幅降低,符合肌病表现。未见纤颤电位。组织学异常包括肌纤维大小明显不一、肌膜核增殖及轻度间质脂肪浸润。所有患者均无临床神经病变证据、神经传导速度异常或神经活检中的节段性脱髓鞘体征。我们的数据表明,这些患者的肌肉无力本质上是肌病性的,无周围神经受累,可能是由于低蛋白血症和低脂血症,因为这些患者尿液中丢失了过量的蛋白质和脂肪。