Jiang Chuan, Wang Xinyu, Lu Chunli, Li Qian, Ma Longbing, Li Wei, Cui Shengyu, Li Kang, Wang Xiang, Feng Yuxin, Jian Fengzeng
Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Spine Center, China International Neuroscience Institute (CHINA-INI), Beijing, China.
Neurospine. 2023 Dec;20(4):1346-1357. doi: 10.14245/ns.2346834.417. Epub 2023 Dec 31.
Syringomyelia is a common central nervous system disease characterized by the dilation of the central canal (CC). Regarding the pathogenesis of syringomyelia, cerebrospinal fluid (CSF) circulation obstruction in the subarachnoid space (SAS) of the spinal cord has been widely accepted. However, clinical and animal studies on obstructing the CSF in SAS failed to form syringomyelia, challenging the theory of SAS obstruction. The precise pathogenesis remains unknown.
We utilized an extradural compression rat model to investigate the pathogenesis underlying syringomyelia. Magnetic resonance imaging enabled detection of syringomyelia formation. To assess CSF flow within the SAS, Evans blue was infused into the cisterna magna. Histological analysis allowed morphological examination of the CC. Furthermore, CSF flow through the CC was traced using Ovalbumin Alexa-Flour 647 conjugate (OAF-647). Scanning electron microscopy (SEM) enabled visualization of ependymal cilia.
The findings showed that the dura mater below the compression segment exhibited lighter coloration relative to the region above the compression, indicative of partial obstruction within the SAS. However, the degree of SAS occlusion did not significantly differ between syringomyelia (SM-Y group) and those without (SM-N group). Intriguingly, hematoxylin and eosin staining and CSF tracing revealed occlusion of the CC accompanied by reduced CSF flow in the SM-Y group compared to SM-N and control groups. SEM images uncovered impairment of ependymal cilia inside the syringomyelia.
CC occlusion may represent a physiological prerequisite for syringomyelia formation, while SAS obstruction serves to initiate disease onset. The impairment of ependymal cilia appears to facilitate progression of syringomyelia.
脊髓空洞症是一种常见的中枢神经系统疾病，其特征为中央管扩张。关于脊髓空洞症的发病机制，脊髓蛛网膜下腔脑脊液循环梗阻已被广泛认可。然而，在脊髓蛛网膜下腔阻塞脑脊液的临床和动物研究未能形成脊髓空洞症，这对蛛网膜下腔梗阻理论提出了挑战。确切的发病机制仍然未知。
我们利用硬膜外压迫大鼠模型来研究脊髓空洞症的发病机制。磁共振成像能够检测脊髓空洞症的形成。为了评估蛛网膜下腔内的脑脊液流动，将伊文思蓝注入枕大池。组织学分析可对中央管进行形态学检查。此外，使用卵清蛋白Alexa-Flour 647共轭物（OAF-647）追踪通过中央管的脑脊液流动。扫描电子显微镜（SEM）能够观察室管膜纤毛。
研究结果表明，压迫节段下方的硬脑膜相对于压迫上方区域颜色较浅，表明蛛网膜下腔内存在部分梗阻。然而，脊髓空洞症组（SM-Y组）和无脊髓空洞症组（SM-N组）之间蛛网膜下腔阻塞程度无显著差异。有趣的是，苏木精-伊红染色和脑脊液追踪显示，与SM-N组和对照组相比，SM-Y组中央管阻塞并伴有脑脊液流动减少。扫描电子显微镜图像显示脊髓空洞症内部室管膜纤毛受损。
中央管阻塞可能是脊髓空洞症形成的生理前提，而蛛网膜下腔梗阻则引发疾病发作。室管膜纤毛的损伤似乎促进了脊髓空洞症的进展。
