An experimental model of the spinal epidural neoplasm was produced in rats by injecting Walker 256 carcinoma cell suspension anterior to the T-12/13 vertebral body. Using this animal model, regional spinal cord blood flow (rSCBF) and its response to CO2 inhalation (CO2 R) were estimated by 14C-antipyrine autoradiography and the hydrogen clearance method. In the early stage of weakness of the hind limbs, axonal swelling and edema of the white matter were revealed by histopathological

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... while both rSCBF and CO2-R remained nor mal. In the middle stage of weakness, the tumor invaded the spinal canal and compressed the spinal cord epidurally, and edema of white matter progressed although the gray matter was scarcely affected. The rSCBF decreased gradually at the compressed and caudal levels. Disturbance of CO,-R was also noted at the compressed and caudal levels, and appeared to preceed the rSCBF decrease. The disturbances of rSCBF and CO2-R were remarkable at the compressed level than at the caudal level. No disturbances were observed at the rostral level. In the end stage of weakness, disturbances of rSCBF and CO2-R progressed rapidly and microangiography revealed obstruction of the vertebral venous plexus at the level of compression, while the greater vessels (radicular arteries, anterior spinal artery, posterior spinal arteries and posterior median vein) were patent even in this stage. From the data collected, the pathophysiology in the spinal epidural neoplasm is considered as follows : 1) the vertebral venous plexus is stenosed or obstructed by the epidural tumor in the early stage of weakness and vasogenic edema starts in the spinal cord; 2) as the tumor grows, mechanical compression of the spinal cord occurs in addition to obstruction of the vertebral venous plexus, and the edema progresses further; and 3) rSCBF decreases rapidly to the critical flow level in the end stage and the cord function becomes irreversible.