Changes of evoked action potentials and histology of the spinal cord, and hind limb dysfunction in spinal cord ischemia of cats.

The electrophysiological, neurological, and neuropathological correlates of the spinal cord ischemia induced by the aortic cross-clamping of cats were studied with the goal of developing the reliable evoked spinal cord potentials (ESCPs) for the monitoring of spinal cord ischemia. The five types of ESCPs were elicited as follows; descending ESCPs recorded from the L2 and L5 vertebral levels, vertex motor evoked potential from the L2 vertebral level, ascending ESCP from the T1 vertebral level, and segmental ESCP after sciatic nerve stimulation. The late negative waves of both descending ESCP from L5 and segmental ESCP were susceptible to ischemia. The descending ESCP from L5 was not influenced by peripheral nerve ischemia or reflected ischemia in the whole spinal cord. Therefore, the late negative wave of the descending ESCP from L5 served as the most reliable index for spinal cord ischemia. When aortic clamping was continued for > or = 30 min after the disappearance of the late negative wave of descending ESCP from L5, the amplitude recovery of this wave decreased to 25%, resulting in paraplegia. Histologically, the posterior horn of the gray matter in the lumbar enlargement was the most vulnerable to ischemia.