Abstract

The extent of neurologic deficit in spinal cord injury (SCI) is dependent on the primary injury, biologic responses to injury, including inflammation, edema, and scar formation, and neural restructuring. During the recovery phase of SCI, which follows a period of spinal shock lasting weeks to up to 2 years, uninhibited spinal reflexes result in detrusor overactivity with dyssynergia of the urethral sphincter, associated with progressive lower urinary tract dysfunction and potentially upper tract deterioration. Minimization of secondary injury following acute SCI and optimization of nerve regeneration may maximize functional recovery and limit end organ dysfunction, including of the lower urinary tract. Early administration of neuromodulation via electrical or electromagnetic stimulation has been shown to limit secondary injury and potentially restore function. Low-frequency electrical stimulation accelerates axonal growth in the peripheral nervous system and may have a similar benefit in the central nervous system. Limited evidence suggests that sacral neuromodulation has the potential to limit or even prevent maladaptive neural restructuring of the lower urinary tract when administered during the spinal shock phase, when the bladder is areflexic. Herein, we review the pathophysiology of voiding dysfunction following acute injury, existing evidence for the benefit of early SNM in SCI, and possible mechanisms of action, including neural regeneration.

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