Phathophysiology of spinal cord blood circulation, biochemical study.

关于脊髓空洞症的发病机制，目前仍存在许多争议。用25%高岭土脑池内注射诱发18只成年家兔脊髓积水模型，用光镜和透射电镜观察脊髓的超微结构变化。在高岭土注射后2周、4周、6周和6个月，通过经心灌注二甲胂酸盐缓冲液中的戊二醛-多聚甲醛溶液，处死所有家兔。取脊髓不同节段约1 mm厚切片，光镜和透射电镜观察，所有动物脊髓空洞均向后延伸于背侧白色柱之间。邻近空洞的白色物质水肿。在灰色和白色物质中均发生了血管周围空间的极度扩大。在空洞附近的一些神经纤维中，髓鞘被分裂、变薄并完全丢失，而轴突本身在许多其他纤维中丢失。在一些裸露的轴突中可见少突胶质细胞突起的髓鞘再形成。星形胶质细胞突起内含有大量胶质纤维，覆盖着许多暴露于空洞的纤维。结膜显微镜下未见伊文思蓝外渗。轴突变性，脱髓鞘，并最终完全丧失，同时星形胶质细胞增殖和髓鞘再生的少突胶质细胞进行了观察。这些超微结构的变化有许多相似之处所看到的脑积水和尸检结果的人类脊髓灰质炎。

There are many controversial issues on the pathogenesis of the syringomyelia. The ultrastructural changes occurring in the spinal cord in a hydrosyringomyelic rabbit model were investigated by light microscopy and transmission electron microscopy.Hydrosyringomyelia was induced into 18 adult rabbits by intracisternal injection of 25% kaolin. All of the rabbits were killed two, four, and six weeks and six months after the kaolin injection by transcardial perfusion of glutaraldehyde-paraformaldehyde solution in cacodylate buffer. About 1 mm thick sections were taken from various levels of spinal cord segments, and processed for the light and transmission electron microscopy.In all animals, the syrinx extended posteriorly between the dorsal white columns. white matter adjacent to the syrinx was edematous. Extreme perivascular space enlargement had occurred both in the gray and white matter. Myelin sheaths were split up, thinned out and completely lost in some nerve fibers near the syrinx, while the axon itself was lost in many other fibers. Remyelination by oligodendrocytic processes was seen in some denuded axons. Astrocytic processes containing huge bundles of glial filaments covered many fibers which were exposed to the syrinx. No extravasation of Evans blue was seen on concal microscopy. Axonal degeneration, demyelination, and final complete loss, and simultaneous astrocytic proliferation and remyelination by oligodendrocytes were observed. These ultrastructural changes have many similarities to those seen in hydrocephalus and autopsy findings of human syringomyelia.