Post-mortem MRI-guided sampling of multiple sclerosis brain lesions - Increased yield of active demyelinating and (p)reactive lesions
Post-mortem MRI-guided sampling of multiple sclerosis brain lesions - Increased yield of active demyelinating and (p)reactive lesions
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DOI：
10.1093/brain/124.8.1635
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发表时间：
2001-08-01
期刊：
影响因子：
14.5
通讯作者：
van der Valk, P
中科院分区：
文献类型：
--
作者：
De Groot, CJA;Bergers, E;van der Valk, P
对大脑中多发性硬化症病变进行宏观取样往往会发现慢性病变。为了更好地了解多发性硬化症疾病过程的动态，对新的和正在发展的病变的研究非常有意义。由于体内MRI能有效地显示多发性硬化症患者的病变，我们将其应用于未固定的死后脑切片以识别异常，以获得更高的产量。活动性病变。荷兰脑库组织对 29 名多发性硬化症患者进行了快速尸检。将大脑切成1厘米的冠状切片。对一或两个切片进行 T-1 和 T-2 加权 MRI，然后在 MRI 扫描平面上切成 5 毫米厚的相对切片。根据 MRI 结果确定感兴趣区域并进行切除。一半固定在10%福尔马林中并石蜡包埋，相邻一半的相应区域在液氮中速冻。总共 174 个脑组织样本中的 136 个可以与 T-2 加权 MRI 上发现的异常情况相匹配。通过组织化学（免疫）方法确定病变发展阶段。对于 54 个 MRI 可检测样本，记录了它们是否可以宏观检测，即可见和/或可触及。组织病理学分析显示，T2 加权图像上看到的 48% 的高信号区域代表活动性病变，包括位于正常白质的病变，没有明显的髓磷脂损失，但仍显示不同程度的水肿、小胶质细胞簇，具有增强的主要组织相容性复合物 II 类抗原、CD45 和 CD68 抗原表达以及小血管周围不同数量的血管周围淋巴细胞 [指定为 (p) 反应性病变]。从宏观上不可见/不可触及的 MRI 检测到的异常情况来看，58% 是 (p) 反应性病变，21% 包含活动性脱髓鞘病变。相反，可见和/或可触及的脑组织样本主要包含慢性非活动性病变。我们的结论是，MRI 引导下的脑组织取样增加了活动性多发性硬化症病变的产量，包括活动性脱髓鞘和 (p) 反应性病变。
Macroscopic sampling of multiple sclerosis lesions in the brain tends to find chronic lesions. For a better understanding of the dynamics of the multiple sclerosis disease process, research into new and developing lesions is of great interest. As MRI in vivo effectively demonstrates lesions in multiple sclerosis patients, we have applied it to unfixed post-mortem brain slices to identify abnormalities, in order to obtain a higher yield of. active lesions. The Netherlands Brain Bank organized the rapid autopsy of 29 multiple sclerosis patients. The brain was cut in 1 cm coronal slices. One or two slices were subjected to T-1- and T-2-weighted MRI, and then cut at the plane of the MRI scan into 5 mm thick opposing sections. Areas of interest were identified based on the MRI findings and excised. One half was fixed in 10% formalin and paraffin-embedded, and the corresponding area in the adjacent half was snap-frozen in liquid nitrogen. In total, 136 out of 174 brain tissue samples could be matched with the abnormalities seen on T-2-weighted MRIs. The stage of lesional development was determined (immuno) histochemically. For 54 MRI-detectable samples, it was recorded whether they were macroscopically detectable, i.e. visible and/or palpable. Histopathological analysis revealed that 48% of the hyperintense areas seen on T2-weighted images represented active lesions, including lesions localized in the normal appearing white matter, without apparent loss of myelin but nevertheless showing a variable degree of oedema, small clusters of microglial cells with enhanced major histocompatibility complex class II antigen, CD45 and CD68 antigen expression and a variable number of perivascular lymphocytes around small blood vessels [designated as (p)reactive lesions]. From the macroscopically not-visible/not-palpable MRI-detected abnormalities, 58% were (p)reactive lesions and 21% contained active demyelinating lesions. In contrast, visible and/or palpable brain tissue samples mainly contained chronic inactive lesions. We conclude that MRI-guided sampling of brain tissue increases the yield of active multiple sclerosis lesions, including active demyelinating and, (p)reactive lesions.