Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan.
J Neuroimmunol. 2020 Apr 15;341:577170. doi: 10.1016/j.jneuroim.2020.577170. Epub 2020 Jan 24.
In demyelinating polyneuropathies, distribution patterns of demyelination reflect underlying pathogenesis. Median and ulnar nerve conduction studies were reviewed in 85 typical chronic inflammatory demyelinating polyneuropathy (CIDP) patients and 29 multifocal acquired demyelinating sensory and motor neuropathy (MADSAM). Distal latencies were prolonged in typical CIDP and near normal in MADSAM. Abnormal amplitude reductions in the nerve trunks were more frequent in MADSAM than typical CIDP. Presumably because the blood-nerve barrier is anatomically deficient at the distal nerve terminals, antibody-mediated demyelination is a major pathophysiology in typical CIDP. In contrast, blood-nerve barrier breakdown is likely to be predominant in MADSAM.
在脱髓鞘性多发性神经病中，脱髓鞘的分布模式反映了潜在的发病机制。回顾了 85 例典型的慢性炎症性脱髓鞘性多发性神经病（CIDP）患者和 29 例多发性获得性感觉运动性脱髓鞘神经病（MADSAM）的正中神经和尺神经传导研究。典型 CIDP 患者的远端潜伏期延长，而 MADSAM 患者的远端潜伏期接近正常。在 MADSAM 中，神经干的异常幅度降低比典型 CIDP 更为常见。推测是因为血-神经屏障在远端神经末梢解剖上存在缺陷，抗体介导的脱髓鞘是典型 CIDP 的主要病理生理学改变。相比之下，血-神经屏障的破坏在 MADSAM 中可能更为突出。
