Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants|
|Research Institution||KITASATO UNIVERSITY|
TACHIBANA Shigekuni Kitasato Univ.School of Medicine, Associate Professor, 医学部, 助教授 (60104535)
TAKANO Makoto Kitasato Univ.School of Medicine, Research Associate, 医学部, 助手 (60216687)
YAMAZAKI Yoshinori Kitasato Univ.School of Medicine, Research Associate, 医学部, 助手 (20210403)
KITAHARA Yukio Kitasato Univ.School of Medicine, Assistant Professor, 医学部, 講師 (40177861)
IIDA Hideo Kitasato Univ.School of Medicine, Assistant Professor, 医学部, 講師 (20159560)
三枝 宏伊 北里大学, 医学部, 助手 (60235017)
太田 顕成 北里大学, 医学部, 講師 (10050569)
|Project Period (FY)
1994 – 1996
Completed(Fiscal Year 1996)
|Budget Amount *help
¥2,200,000 (Direct Cost : ¥2,200,000)
Fiscal Year 1996 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1995 : ¥800,000 (Direct Cost : ¥800,000)
Fiscal Year 1994 : ¥700,000 (Direct Cost : ¥700,000)
|Keywords||chronic compression myelopathy / epidural compression / cancer / partial demyelination / oligodendroglia / nakid axon / spinal cord / posterior column / partial demyelination / oligodendroglia / posterior colunen / 圧迫性脊髄障害 / 脊髄白質 / 髄鞘 / 脱髄 / 脊髄圧迫 / 脱髄病変 / 胸椎 / 腫瘍 / ラット|
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
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