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通过钆弗塞胺增强磁共振神经成像评估实验性自身免疫性神经炎中的病变演变。

Assessment of lesion evolution in experimental autoimmune neuritis by gadofluorine M-enhanced MR neurography.

作者信息

Stoll Guido, Wessig Carsten, Gold Ralf, Bendszus Martin

机构信息

Department of Neurology, Julius-Maximilians Universität, Josef-Schneider-Str. 11, D-97080 Würzburg, Germany.

出版信息

Exp Neurol. 2006 Jan;197(1):150-6. doi: 10.1016/j.expneurol.2005.09.003. Epub 2005 Sep 30.

DOI:10.1016/j.expneurol.2005.09.003
PMID:16199036
Abstract

Experimental autoimmune neuritis (EAN) represents an animal model of acute inflammatory nerve injury mirroring pathophysiological aspects of the human Guillain-Barré syndrome. In the present study, we for the first time visualized the spatiotemporal evolution of autoimmune nerve injury and recovery by magnetic resonance imaging (MRI) by use of the novel micellar magnetic resonance (MR) contrast agent gadofluorine M (Gf). EAN was induced in Lewis rats by T-cell transfer (AT-EAN) leading to severe axonal damage, and Gf was applied intravenously at various disease stages mostly 24 h before MRI. In naive rats, Gf enhancement was present solely in the vascular compartment. In AT-EAN, clinically asymptomatic rats already showed consistent Gf uptake in spinal nerves on day 3, while sciatic nerves were spared. The cauda equina correspondingly exhibited massive T-cell infiltration. Gf enhancement further extended to the plexus lumbosacralis on day 4. On days 5 and 6, the entire peripheral neuraxis from the cauda equina, along the sciatic down to the tibial and peroneal nerves, showed strong Gf enhancement. Spinal and peripheral nerves now exhibited massive inflammation and axonal injury on parallel histological analysis. Gf enhancement persisted in the afflicted nerves until complete recovery and disappeared with a proximodistal gradient. In conclusion, Gf-enhanced MR neurography opens a new avenue for monitoring nerve damage in-vivo during an immune attack.

摘要

实验性自身免疫性神经炎(EAN)是一种急性炎症性神经损伤的动物模型,反映了人类吉兰-巴雷综合征的病理生理特征。在本研究中,我们首次使用新型胶束磁共振(MR)造影剂钆弗醇(Gf),通过磁共振成像(MRI)可视化自身免疫性神经损伤和恢复的时空演变。通过T细胞转移(AT-EAN)在Lewis大鼠中诱导EAN,导致严重的轴突损伤,并在MRI前大多24小时的不同疾病阶段静脉注射Gf。在未处理的大鼠中,Gf增强仅出现在血管腔。在AT-EAN中,临床无症状的大鼠在第3天脊髓神经中已显示出一致的Gf摄取,而坐骨神经未受累。马尾相应地表现出大量T细胞浸润。Gf增强在第4天进一步扩展至腰骶丛。在第5天和第6天,从马尾开始,沿着坐骨神经直至胫神经和腓总神经的整个外周神经轴均显示出强烈的Gf增强。在平行的组织学分析中,脊髓和外周神经此时表现出大量炎症和轴突损伤。Gf增强在受累神经中持续存在直至完全恢复,并以近端至远端的梯度消失。总之,Gf增强的MR神经造影为在免疫攻击期间体内监测神经损伤开辟了一条新途径。

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