Repetitive exposure of multi-segmental sensory-motor networks to the dynamics of task-specific sensory input as occurs with repetitive training can functionally reshape spinal and supraspinal connectivity thus re-enabling one to perform complex motor tasks, even years post injury.Ī number of observations demonstrate the presence of potentially functioning fibers travelling across the lesion in the majority (84%) of people with clinically diagnosed complete spinal cord injury (SCI) ( Sherwood et al., 1992, Dimitrijevic et al., 1984, Dimitrijevic et al., 1983). Real-time proprioceptive input to spinal networks provides the template for reorganization of spinal networks that play a leading role in the level of coordination of motor pools required to perform a given functional task. In particular, we substantiate the hypotheses that: (1) in the majority of spinal lesions, a critical number and type of neurons in the region of the injury survive, but cannot conduct action potentials, and thus are electrically non-responsive (2) these neuronal networks within the lesioned area can be neuromodulated to a transformed state of electrical competency (3) these two factors enable the potential for extensive activity-dependent reorganization of neuronal networks in the spinal cord and brain, and (4) propriospinal networks play a critical role in driving this activity-dependent reorganization after injury. This review addresses some of the systems-level physiological mechanisms that might explain the effects of electrical modulation and how repetitive training facilitates the recovery of volitional motor control. This key factor can be triggered by neuromodulation of these networks with electrical and pharmacological interventions. The key factor in this recovery is largely activity-dependent plasticity of spinal and supraspinal networks. Preclinical and clinical neurophysiological and neurorehabilitation research has generated rather surprising levels of recovery of volitional sensory-motor function in persons with chronic motor paralysis following a spinal cord injury.
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