Barkhof Frederik, Bruck Wolfgang, De Groot Corline J A, Bergers Elisabeth, Hulshof Sandra, Geurts Jeroen, Polman Chris H, van der Valk Paul
Dutch MR-MS Center, and Department of Radiology, Vrije Universiteit Medical Center, PO Box 7057, 1007 MB Amsterdam, the Netherlands.
Arch Neurol. 2003 Aug;60(8):1073-81. doi: 10.1001/archneur.60.8.1073.
Various types of pathologic mechanisms in multiple sclerosis (MS) can alter magnetic resonance imaging (MRI) signals, and the appearance of remyelinated lesions on MRI is largely unknown.
To describe the MRI appearance of remyelinated lesions in MS.
Comparison of postmortem MRI findings with histopathologic findings.
Brain donations from a general community. Patients Magnetic resonance images from 36 rapid autopsies yielded 161 areas that could be matched with histologic characteristics, including 149 focal T2-weighted abnormalities, with a range of signal intensities on T1-weighted images. In a subset of 49 lesions, magnetization transfer ratio could be determined.
An observer blinded to the MRI findings assessed the presence of remyelination using light microscopic criteria; in 25 areas, in situ hybridization was used to assess the presence of oligodendrocytes expressing proteolipid protein messenger RNA.
Remyelinated areas were found in 67 lesions (42%): partial remyelination was present in 30 lesions (19%), whereas 37 lesions (23%) were fully remyelinated. Remyelinated lesions contained enhanced numbers of oligodendrocytes containing proteolipid protein messenger RNA. All areas with remyelination shown histopathologically were hyperintense on T2-weighted images. Strong hypointensity on T1-weighted images was significantly associated (chi2 = 29.8, P<.001) with demyelinated and partially remyelinated lesions compared with fully remyelinated lesions. The magnetization transfer ratio of remyelinated lesions (mean [SD], 27.6% [41%]) differed (F = 46.3, P<.001) from both normal-appearing white matter (35.2% [32%]) and demyelinated lesions (22.3% [48%]).
Remyelinated lesions return an abnormal signal on T2-weighted images. Both T1-weighted images and magnetization transfer ratio may have (limited) additional value in separating lesions with and without remyelination.
多发性硬化症（MS）的多种病理机制可改变磁共振成像（MRI）信号，而MRI上再髓鞘化病变的表现 largely unknown。
描述MS中再髓鞘化病变的MRI表现。
死后MRI结果与组织病理学结果的比较。
来自普通社区的脑捐赠。患者 36例快速尸检的磁共振图像产生了161个可与组织学特征匹配的区域，包括149个局灶性T2加权异常，在T1加权图像上具有一系列信号强度。在49个病变的子集中，可以确定磁化传递率。
一名对MRI结果不知情的观察者使用光学显微镜标准评估再髓鞘化的存在；在25个区域，使用原位杂交评估表达蛋白脂蛋白信使RNA的少突胶质细胞的存在。
在67个病变（42%）中发现了再髓鞘化区域：30个病变（19%）存在部分再髓鞘化，而37个病变（23%）完全再髓鞘化。再髓鞘化病变中含有蛋白脂蛋白信使RNA的少突胶质细胞数量增加。组织病理学显示有再髓鞘化的所有区域在T2加权图像上均为高信号。与完全再髓鞘化病变相比，T1加权图像上的强低信号与脱髓鞘和部分再髓鞘化病变显著相关（χ2 = 29.8，P <.001）。再髓鞘化病变的磁化传递率（平均值[标准差]，27.6%[41%]）与正常外观的白质（35.2%[32%]）和脱髓鞘病变（22.3%[48%]）均不同（F = 46.3，P <.001）。
再髓鞘化病变在T2加权图像上呈现异常信号。T1加权图像和磁化传递率在区分有无再髓鞘化的病变方面可能具有（有限的）附加价值。
