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Testing of potential therapies for spinal cord injury has been significantly hampered by the unavailability of a standardized, reproducible animal model with predictable outcome at a given force of injury (dose-response). The rat was selected in the development of this model in preference to larger animals for economy and availability; this permits use of large numbers of animals to increase statistical validity. In the experiments reported in this article, a static load method (weight placed gently on cord) of inducing cord injury was evaluated. A total of 198 Sprague-Dawley rats were used. Under general anesthesia, a one-level laminectomy was carried out at T-12 with the dura mater intact. Weights varying from 80 to 150 g were lowered onto the dorsal surface of the intact dura mater for durations of 0 to 300 seconds. Recovery of motor function was assessed for up to 8 weeks using two behavioral tests, a modified Tarlov scale and an inclined plane test of hind limb motor function. A statistically significant relationship was found between force of injury and motor recovery as measured by the Tarlov scale, but this did not correlate with inclined plane performance; the duration that the weight rested on the cord did not influence outcome. Pathologically, there was variation in the extent of damage for a given injury load. A semiquantitative pathological assessment of cord injury showed a statistically significant correlation between pathological score and behavioral deficit as measured by the Tarlov scale, but this did not correlate with inclined plane performance. In view of these deficiencies, the static load technique does not seem to be an ideal model for spinal cord injury research.

Computer-averaged evoked potential responses (EPs) to stimulation of the sciatic nerve and cervical spinal cord were recorded from the dura and skin over the causda equina and spinal cord in seven monkeys, three with chronic spinal cord lesions. Sciatic EPs consited of predominantly negative triphasic propagated potentials recorded at all spinal levels and greatest in amplitude over the cauda equina and caudal spinal cord. The conduction velocity of this EP was faster over the cauda equina and rostral spinal cord than over caudal cord segments. Triphasic potentials were succeeded by small negative potentials over the cauda equina and larger negative potentials over the lumbar enlargement. Sciatic EPs over the upper lumbar and thoracic cord were more sensitive to asphyxia than the initial triphasic potentials recorded over cauda equina and caudal cord but resisted changes from increasing the rate of stimulation up to 100 per second. Propagated thoracic EPs were preceded by nonpropagated potentials. The longer latency negative potentials occurring locally over the cauda equina and lower lumbar enlargement were abolished at levels of asphyxia and were attenuated at rates of stimulation that did not affect the preceding triphasic potentials. Following complete spinal cord transection, nonpropagated sciatic EPs were recorded in leads rostral to the section. In preparations with chronic partial cord hemisection involving dorsal and lateral quadrants, ipsilateral sciatic EPs had increased latency, reduced amplitude, and poor definition in the vicinity of and rostral to the lesion. Direct cervical cord stimulation elicited caudally propagated potentials which were followed by large, broad potentials over the number enlargement.