Gradually, with changing the electrode placement from a subdural to epidural location and with technological advancements, SCS became widely used. Norman Shealy tested this idea experimentally in 1967 by applying electrical stimulation subdurally to the posterior columns in cats, followed by the first human application of SCS to manage temporarily severe pain in a patient with cancer. For the relief of diffuse pain, it seemed reasonable to stimulate the posterior columns of the spinal cord white matter, where ascending continuations of cutaneous fibers related to multiple dermatomes are compactly arranged. The first application of SCS was for the treatment of chronic intractable pain, motivated by neurophysiological studies suggesting that it was possible to inhibit input from pain fibers into the spinal cord by the stimulation of large-diameter sensory fibers. Epidural spinal cord stimulation (SCS) has been found to be particularly effective for this purpose in humans, probably because it can provide an excitatory drive to several spinal cord segments simultaneously. One approach to improving recovery is to reactivate the intrinsic capacity of the spared lumbar motor circuitry distal to the lesion using externally applied stimulation. While contemporary clinical standards are successfully applied to deal with emergency and secondary complications, and the understanding of spinal cord biology is continuously growing, SCI still cannot be cured and the prognosis for the recovery of meaningful voluntary motor control and locomotion after a clinically complete lesion is very limited. Severe spinal cord injury (SCI) is a catastrophic condition, causing disability of vital body functions below the lesion level. Technological developments that allow dynamic control of stimulation parameters and the potential for activity-dependent beneficial plasticity may further unveil the remarkable capacity of spinal motor processing that remains even after severe spinal cord injuries. The induced change in responsiveness of this spinal motor circuitry to any residual supraspinal input via clinically silent translesional neural connections that have survived the injury may be a likely explanation for rudimentary volitional control enabled by epidural stimulation in otherwise paralyzed muscles. Those fibers then trans-synaptically activate various spinal reflex circuits and plurisegmentally organized interneuronal networks that control more complex contraction and relaxation patterns involving multiple muscles. Current understanding is that such stimulation activates large-to-medium-diameter sensory fibers within the posterior roots. Early work revealed that the spinal circuitry involved in lower-limb motor control can be accessed by stimulating through electrodes placed epidurally over the posterior aspect of the lumbar spinal cord below a paralyzing injury. This review focuses on its resurgence following the progress made in understanding the underlying neurophysiological mechanisms and on recent reports of its augmentative effects upon otherwise subfunctional volitional motor control. Epidural spinal cord stimulation has a long history of application for improving motor control in spinal cord injury.
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