B. S. Mietto, P. Andrade, M. Jardim, S. Antunes, E. Sarno
{"title":"Demyelination in Peripheral Nerves: Much to Learn from Leprosy Neuropathy","authors":"B. S. Mietto, P. Andrade, M. Jardim, S. Antunes, E. Sarno","doi":"10.4172/2376-0389.1000174","DOIUrl":null,"url":null,"abstract":"Copyright: © 2016 Mietto BS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Leprosy is a chronic infectious disorder of the peripheral nervous system (PNS) caused by the infection of non-neuronal nerve cells, preferentially Schwann cells and resident macrophages, by Mycobacyerium leprae (ML) [1]. There is growing evidence suggesting that damage to the myelin sheath is due to a disturbed Schwann cell response in conjunction with immune cell participation [2-4]. Although demyelination is not easily found in neuropathic leprosy nerve biopsies (Figure 1), nerve conduction studies routinely used in leprosy referral centers indicate that demyelination occurs during most leprosy reactional episodes [5]. Moreover, nerve conduction analyses show that part of these patients recover from previous lesions after 6-month corticosteroid treatment (Jardim MR personal communication). Other drugs that favor re-myelination are worth being investigated (Figure 1).","PeriodicalId":16369,"journal":{"name":"Journal of multiple sclerosis","volume":"22 1","pages":"1-2"},"PeriodicalIF":0.0000,"publicationDate":"2016-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of multiple sclerosis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4172/2376-0389.1000174","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
周围神经脱髓鞘:从麻风病神经病学到了很多
版权所有:©2016 Mietto BS, et al。这是一篇根据知识共享署名许可协议发布的开放获取文章,该协议允许在任何媒体上不受限制地使用、分发和复制,前提是要注明原作者和来源。麻风是一种慢性外周神经系统(PNS)感染性疾病,由麻风分枝杆菌(Mycobacyerium leprae, ML)[1]感染非神经元神经细胞,尤其是雪旺细胞和巨噬细胞引起。越来越多的证据表明,髓鞘损伤是由于施旺细胞反应紊乱以及免疫细胞参与所致[2-4]。虽然在神经性麻风病神经活检中不容易发现脱髓鞘(图1),但在麻风病转诊中心常规使用的神经传导研究表明,脱髓鞘发生在大多数麻风病反应性发作[5]。此外,神经传导分析显示,这些患者中的一部分在6个月的皮质类固醇治疗后从先前的病变中恢复(Jardim MR个人通讯)。其他有利于髓鞘再生的药物值得研究(图1)。
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