Functional plasticity following spinal cord lesions.

Spinal cord injury results in marked modification and reorganization of several reflex pathways caudal to the injury. The sudden loss or disruption of descending input engenders substantial changes at the level of primary afferents, interneurons, and motoneurons thus dramatically influencing sensorimotor interactions in the spinal cord. As a general rule reflexes are initially depressed following spinal cord injury due to severe reductions in motoneuron excitability but recover and in some instances become exaggerated. It is thought that modified inhibitory connections and/or altered transmission in some of these reflex pathways after spinal injury as well as the recovery and enhancement of membrane properties in motoneurons underlie several symptoms such as spasticity and may explain some characteristics of spinal locomotion observed in spinally transected animals. Indeed, after partial or complete spinal lesions at the last thoracic vertebra cats recover locomotion when the hindlimbs are placed on a treadmill. Although some deficits in spinal locomotion are related to lesion of specific descending motor pathways, other characteristics can also be explained by changes in the excitability of reflex pathways mentioned above. Consequently it may be the case that to reestablish a stable walking pattern that modified afferent inflow to the spinal cord incurred after injury must be normalized to enable a more normal re-expression of locomotor rhythm generating networks. Indeed, recent evidence demonstrates that step training, which has extensively been shown to facilitate and ameliorate locomotor recovery in spinal animals, directly influences transmission in simple reflex pathways after complete spinal lesions.