There exists the view that ischemia in the spinal cord accounts for the paralysis caused by cervical spondylotic myelopathy (CSM), but little work has been done to study the change of spinal cord blood flow (SCBF) in CSM. To clarify this situation, the experimental model designed by Tanaka (1978) was used as a model of CSM (Fig. 1). Among 27 cats in which the spinal canal was narrowed between C4 and C6, 13 cats developed delayed paralysis 33 weeks after operation in an average. Spinal cord blood flow was measured by the reference sample method using isotopelabeled microspheres of 15 +/- 3 mu in diameter. The mean SCBF values for each spinal segments in normal animals ranged from 23.0 g/min . 100 g in T11 to 40.2 g/min . 100 g in C8, resulting in that blood flow in the cervical and lumbar enlargements was constantly higher than that in the other regions of the cord (Fig. 3). The mean blood flow values for the gray matter, ventral white matter, lateral white matter, and dorsal white matter in cervical region were 99.1, 5.0, 5.9, and 11.4 g/min . 100 g respectively, without significant difference between each spinal segments (Fig. 4). In an animal with acute spinal cord compression, the SCBF decreased significantly 15 minutes after spinal cord compression was induced (Figs. 5, 6). On the other hand, in two delayed paralysis animals SCBF in the narrowed segments was within normal limits (Figs. 5, 6). These results suggest that paralysis as seen in CSM may develop without ischemia of the spinal cord.