Effect of spinal cord ischemia on compound muscle action potentials and spinal evoked potentials following spinal cord stimulation in the dog.

We recorded the compound muscle action potentials (CMAP) from the soleus muscle and spinal evoked potentials (SpEP) from the caudal spinal cord after stimulation of the rostral spinal cord via epidural electrodes in 18 dogs. We examined the changes of CMAP and SpEP after the cord was made ischemic by clamping the aorta at different levels. Clamping the abdominal aorta below the artery of Adamkiewicz (five dogs) did not change either CMAP or SpEP significantly. When the thoracic aorta was clamped above the radicular and Adamkiewicz arteries (10 dogs), CMAP disappeared entirely within 5-10 min of occlusion, but SpEP showed only minimal latency prolongation limited to the late peaks in seven of 10 dogs. In the remaining three dogs, both CMAP and SpEP disappeared within 30 min of occlusion but with the more rapid deterioration of CMAP than of SpEP. Progressive ligation of lumbar arteries (three dogs) from caudal to rostral levels did not change CMAP until ligation of Adamkiewicz artery. Then CMAP disappeared, but SpEP remained unchanged. These findings suggest that CMAP and SpEP are mediated through different pathways and that CMAP reflect anterior cord function. The described electrophysiologic technique would be useful to monitor spinal cord motor function during surgery of the spine, spinal cord, or thoracoabdominal aorta.