The effects of aortic occlusion on transcranially induced evoked potentials in the dog.

Evoked potentials were produced by anodal stimulation over the motor cortex in six dogs. Potentials were recovered from the cranial thoracic and caudal lumbar portions of the spinal cord, and the radial and sciatic nerves. Evoked potential averages were recorded every 1.5 minutes during 40 minutes of aortic occlusion and during 40 minutes of reperfusion. Mean amplitudes of evoked potentials recovered from the caudal lumbar spinal cord decreased to 50% of original values at minute 12.2. Upon release of occlusion, the evoked potentials returned to baseline levels and remained there throughout the period of reperfusion. Sciatic nerve amplitudes decreased to 50% of original values at minute 4.5. In no subject could wave forms be recovered after minute 9.0. Upon release of occlusion, the evoked potentials returned to baseline levels and above, then deteriorated to 29 +/- 12% after 40 minutes of reperfusion. We concluded that transcranially induced evoked potentials were highly sensitive to spinal cord ischemia. Evoked potentials recovered from the sciatic nerve were consistent with functional grey matter immediately upon reperfusion, but deteriorated during reperfusion.