DEMYELINATION IN CHRONIC COMPRESSION MYELOPATHY

在慢性压迫性脊髓病中，通过手术减压可以预期长脊髓束的功能恢复。这一临床事实表明，白色物质中的主要病变是可逆的。然而，以前没有进行过精确的组织学检查。本研究通过将7，12-dimethylbenz（a）anthracen（DMBA）诱发的乳腺癌（F癌）移植于每只近交系Fisher-344大鼠胸椎椎板骨膜下，观察慢性压迫性脊髓病白色物质的组织学变化。致大鼠截瘫后，在全麻下进行经耳灌注固定。在第一阶段，大鼠截瘫后尽可能长时间的饲养，以获得尽可能长时间的压迫性损伤。然而，在这一组中，我们未能 ...更多信息 通过严重压迫固定由于低灌注的脊髓。在第二组中，在大鼠截瘫后的几天内进行经耳灌注。术后6 ~ 10周大鼠出现截瘫，光镜下见硬膜外肿块压迫脊髓，但硬膜下未见癌细胞浸润。电镜检查除1只动物的小范围内外，未见明显的轴突肿胀和Wallerian变性。大部分轴突似乎是正常的。最突出和普遍的发现是髓鞘层的破坏。有一些裸露的大直径纤维。这种破坏可能是由于髓鞘板层间水肿液的聚集，少突胶质细胞的细胞质中也含有水肿液。这种髓鞘的破坏在朗维尔结处并不明显，但在受压的任何地方都是如此。结论：该动物模型适用于观察慢性压迫性脊髓病的早期阶段，其主要组织学改变为脊髓少突胶质细胞水肿和部分白色物质脱髓鞘。少

In chronic compression myelopathy, functional recovery of the long tract can be expected by surgical decompression. This clinical fact indicates that the main lesion in the white matter being reversible. However, precise histological examination has not been previously done. Therefore, the following experiments were done to investigate histological changes in the white matter in chronic compression myelopathy.A small piece of breast cancer (F cancer) induced by oral administration of DMBA (7,12-dimetylbenz (a) anthracen) was transplanted each inbred Fisher-344 rat at sub periosteum of the thoracic lamina. After the rats being paraplegic, trans-auricular perfusion fixation was performed under general anesthesia. The posterior column of the spinal cord was examined under photo and eletron microscope.In the first stage, the rats were brought up as long as possible after having become paraplegic to obtain compression lesion as long duration as possible. However, in this group, we failed to … More fix the spinal cord due to low perfusion by severe compression. Then in the second group, trans-auricular perfusion was done within a few days after the rat became paraplegic. It took 6 to 10 weeks for the rat became paraplegic after the cancer transplantation.On photo-microscopic examination, the spinal cord was severely comressed by extradural mass, though no invasion of the carcinomatous cells beneath the dura was observed. No obvious chages including phagocytosis can be seen on H-E and myelin staining except distortion of the cord.On electron-microscopic examination, except in a small area in one animal, no obvious axonal swelling and Wallerian degeneration can be seen. Most of the axon seemed to be normal. The most prominent and universal finding was destruction of the myelin lamina. There were some naked large diameter fibers. This destruction seems due to collection of edema fluid between myelin lamina, and the cytoplasm of the oligodendroglia also contain edema fluid. Such a destruction of the myelin sheath was not prominent at the node of Ranvier but anywhere under compression. No phagocytic cell or hyperplasia of the astrocyte was observed in the destructed area.In conclusion, this animal model is suitable to observe an early stage of chronic compression myelopathy, and the main histological change is edema of the oligodendroglia and partial demyelination of the white matter of the spinal cord. Less