✓ An experimental model of spinal epidural neoplasm was produced in rats by injecting Walker 256 carcinoma cell suspension anterior to the T12–13 vertebral body. With this model, spinal cord blood flow (SCBF) and its response to CO2 inhalation were estimated by the carbon-14-antipyrine autoradiography and the hydrogen clearance methods. In the early stages after tumor implantation, weakness, axonal swelling, and edema of the white matter were observed, while both SCBF and its response to CO2 inhalation remained normal. In the next stage, the tumor invaded the spinal canal and compressed the spinal cord epidurally. The edema of the white matter progressed, while the gray matter was morphologically intact. The SCBF and its response to CO2 inhalation were altered at both the compression area and caudally in the spinal cord. Changes in response to CO2 inhalation appeared earlier than the SCBF decrease. In the last stage, the SCBF decreased rapidly to the critical level, producing irreversible nervous tissue damage. Microangiographic studies revealed extensive obliteration of the spinal epidural venous plexus and patency of the larger nutritional vessels. From the data obtained, the progressive vascular pathophysiology related to spinal epidural neoplasm is as follows: 1) the vertebral venous plexus is compressed and obliterated in the early stages of the disease, and vasogenic edema appears in the spinal cord; 2) as the tumor grows, mechanical compression of the spinal cord is added and the circulatory disturbance increases; and 3) in the last stage, SCBF decreases rapidly to a critical flow level, and the loss of cord function becomes irreversible.
Cervical laminectomy and micro resection of the posterior venous plexus in Hirayama disease
