Abstract
Spinal cord injury (SCI) often results in life-long sensorimotor impairment. Spontaneous recovery from SCI is limited, as supraspinal fibers cannot spontaneously regenerate to form functional networks below the level of injury. Despite this, animal models and humans exhibit many motor behaviors indicative of recovery when electrical stimulation is applied epidurally to the dorsal aspect of the lumbar spinal cord. In 1976, epidural stimulation was introduced to alleviate spasticity in Multiple Sclerosis. Since then, epidural electrical stimulation (EES) has been demonstrated to improve voluntary mobility across the knee and/or ankle in several SCI patients, highlighting its utility in enhancing motor activation. The mechanisms that EES induces to drive these improvements in sensorimotor function remain largely unknown. In this review, we discuss several sensorimotor plasticity mechanisms that we hypothesize may enable epidural stimulation to promote recovery, including changes in local lumbar circuitry, propriospinal interneurons, and the internal model. Finally, we discuss genetic tools for afferent modulation as an emerging method to facilitate the search for the mechanisms of action.
Highlights
Spinal cord injury (SCI) often results in life-long sensorimotor dysfunction
We refer to the entirety of this endogenous system as the descending supraspinal control, and we propose that it is a contributory mechanism involved in recovery from SCI both with and without spinal cord stimulation
This review identifies several plasticity mechanisms that may be evoked by electrical stimulation (EES) through the activation of peripheral afferents
Summary
Spinal cord injury (SCI) often results in life-long sensorimotor dysfunction. Regeneration within the adult spinal cord is limited, some spontaneous or activity-dependent sensorimotor recovery still occurs, mostly mediated by localized sprouting and plasticity of axon terminals (Waters et al, 1996; Burns et al, 1997). Substantial recovery after trauma is challenging because of the poor ability of supraspinal axons to regenerate and form functional networks below the level of injury. The loss of these vital inputs reduces the generation, regulation, and patterning of motor outputs. Improvements in motor function can be achieved with locomotor training, rehabilitation, and/or increased neuronal activity
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