DEMYELINATION IN CHRONIC COMPRESSION MYELOPATHY

在慢性压迫性脊髓病中，可以通过手术减压来恢复长束的功能。这一临床事实表明，主要病变在白质是可逆的。然而，以前没有做过精确的组织学检查。因此，我们做了以下的实验来研究慢性压迫性脊髓病的白质组织学变化。每只近交系Fisher-344大鼠胸椎板骨膜下移植一小块经口服DMBA（7,12-二甲基苯(A)炭疽）诱导的乳腺癌（F癌）。截瘫大鼠全身麻醉后经耳灌注固定。在光镜和电镜下观察脊髓后柱。第一阶段在截瘫后尽可能长时间饲养，使压迫损伤持续时间尽可能长。然而，在本组中，由于严重压迫导致脊髓灌注不足，我们未能固定脊髓。第二组在大鼠截瘫后数日内经耳灌注。癌症移植后，大鼠瘫痪需要6到10周的时间。镜下检查，脊髓被硬膜外肿块严重压迫，但未见硬膜下癌细胞浸润。H-E和髓磷脂染色除脊髓畸变外，未见吞噬等明显改变。电镜检查，除一只动物的小范围外，未见明显的轴突肿胀和沃勒氏变性。大部分轴突似乎正常。最突出和普遍的发现是髓磷脂层的破坏。有一些裸露的大直径纤维。这种破坏似乎是由于髓鞘层之间水肿液的收集，少突胶质细胞的细胞质也含有水肿液。这种髓鞘的破坏在Ranvier淋巴结不明显，但在压迫下的任何地方。破坏区未见吞噬细胞和星形胶质细胞增生。综上所述，该动物模型适合观察早期慢性压迫性脊髓病，主要组织学改变为少突胶质细胞水肿和脊髓白质部分脱髓鞘。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