Circulatory disturbance of rat spinal cord induced by occluding ligation of the dorsal spinal vein

Spinal cord infarction can be caused by venous disturbances due to trauma or cancer invasion. However, the precise mechanism of venous infarction is not fully understood. To characterize disorders associated with spinal venous occlusion, we performed time-kinetic pathological analyses of rat spinal cord infarction induced by transdural ligation of the dorsal spinal vein at the levels of the T10-T13 vertebrae. One day after ligation congestion, edema and hemorrhage were observed mainly in the dorsal funiculus. Axons were well preserved, but on the 3rd day axonal degeneration became evident. On the 7th day, the necrotic lesion was confined to the dorsal funiculus and was round in shape with foamy macrophage infiltration and astrocytic gliosis. On the 14th day, the involved cord became atrophic, and infiltration of foamy macrophages and astrocytosis became more prominent. After 21-28 days, the infarction focus decreased in size due to gliosis, and residual macrophages were observed. The main lesion was confined to the dorsal funiculus at all times. However, the severity of the softening varied among rats. Thus, we conclude that the disturbance of venous drainage actually results in spinal cord softening. The variability in the lesions is probably due to the presence of unexpected anastomoses of the spinal venous system.