Behse F, Buchthal F, Carlsen F
J Neurol Neurosurg Psychiatry. 1977 Nov;40(11):1072-82. doi: 10.1136/jnnp.40.11.1072.
Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symmetrical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.
对12例糖尿病性神经病患者腓肠神经的形态学研究结果与神经传导相关,其中5例主要是感觉受累,4例有严重的对称性感觉运动性多发性神经病,3例有多发性单神经病。所有患者均有大、小髓鞘纤维及无髓鞘纤维的丢失,即使在疾病早期也是如此;节段性髓鞘再生是 teased 纤维中最显著的髓鞘改变,仅在少数纤维中发现节段性脱髓鞘。轴突退变和施万细胞损伤似乎相互独立进展。记录的传导速度与根据最大纤维直径预期的传导速度之间的关系表明,20%至30%的减慢是由纤维丢失以外的原因引起的;传导速度严重降低主要是由纤维丢失所致。腓肠神经的电生理结果在很大程度上代表了其他神经的结果,尽管正中神经的异常不太明显。在糖尿病性神经病的半数神经内膜血管中,血管周围间隙增厚或含有比正常更多层的基膜。在其他获得性神经病的四分之一神经内膜血管中也发现了同样的异常。