脊髓空洞症发病机制的实验研究

Experimental study on pathogenesis of syringomyefia

目的建立兔sM动物模型，并探讨其发病机制。方法16只兔，随机分为实验组和对照组，氯胺酮麻醉下枕后正中入路显微手术，暴露脊髓中央管开口，实验组将直径0．5mm、长6mm铅笔替芯经开口置人脊髓中央管内，对照组不植入，术前与术后2、4、6、8周行MRI检查，8周处死动物，行脊髓组织学检查。结果组织学测量颈段脊髓中央管直径：实验组（0．505±0．046）mm，对照组（0．304±0．045）mm，二者差异有统计学意义（t=8．787，P〈0．05）；MRI检查在他加权像显示实验组术后2—4周颈髓中央管开始出现线状高信号，至6—8周线状高信号增粗增长。结论脊髓中央管开口端机械阻塞可成功制成兔SM模型，各种原因引起的脊髓中央管开口梗阻可能是临床上SM发生的原因。

Objective To establish an animal model of SM in rabbits and research it＇s pathogenesis. Methods 16 rabbits were randomly divided into experimental group and control group, all animals were perfomed microsurgery via suboccipital midline approach. The core of pencil （ diameter 0. 5 mm, length 6 mm） was planted into spinal central canal via its opening in experimental group. MRI were carried out preoperation and 2,4, 6,8 weeks after operation. All rabbits were executed after 8 weeks and spinal cord histological examinations were perfomed. Results The diameter of cervical spinal central canal were （0. 505 ±0. 046）ram in experimental group and （0. 304 ±0. 045） mm in control group, which have significance difference （ t = 8. 787, P 〈 0. 05）. The MRI T2 weighted sagittal films showed the linear high signal shadow at middle of cervical spinal cord 2 ~ 4 weeks after operation in experimental group and the linear high signal shadow became wider and longer in 6-8 weeks. Conclusion The SM model in rabbits were established suceessftdly via mechanical obstruction of the opening of spinal central canal. The pathogenesis of SM pitients may be obstruction of the opening of spinal central canal caused by defferent kinds of elements.