Spinal Cord Injury‐Induced Neurogenic Bladder

Abstract

Spinal cord injury (SCI) is one of the most debilitating and devastating injuries to humans. Lower urinary tract dysfunction is of most concern in the management of SCI patients. Proper management depends on understanding the mechanisms underlying the development of neurogenic bladder. Suprasacral SCI induces detrusor areflexia and urine retention initially. The recovery of lower urinary tract function occurs several weeks later, but the voiding function deteriorates and manifests by hyperreflexia and incomplete voiding secondary to the simultaneous contraction of the detrusor and external urethral sphincter (detrusor–sphincter dyssynergia) during voiding. Electrophysiological and pharmacological studies of animals reveal that the recovery of lower urinary tract function relies on the plasticity of bladder afferent pathways. The Aδ afferents convey proprioception and initiate micturition reflex in intact cats and rats. Chronic SCI animals exhibit hyperreflexia during storage and incomplete expulsion during voiding. The Aδ afferent pathway is replaced by capsaicin‐sensitive C‐fiber afferents in chronic SCI cats. In chronic SCI rats, voiding is still mediated thru Aδ afferents. However, C‐fiber afferents modify bladder function and induce bladder hyperreflexia and detrusor–sphincter dyssynergia in chronic SCI rats. Thus, multiple factors have been implicated in the development of neurogenic bladder induced by SCI.