Effect of urinary diversion on the recovery of micturition reflexes after spinal cord injury in the rat.

Patients with suprasacral spinal cord injury usually exhibit severe lower urinary tract dysfunction, which is generally attributed to loss of supraspinal input to the spinal micturition centers. However, some of the dysfunction may also arise secondary to bladder overdistension during the initial period of bladder areflexia. This study evaluated the consequences of bladder overdistension by performing urinary diversion in spinalized (T8-T10) rats. Bladder function was evaluated in urethane-anesthetized control and spinalized animals approximately 24 days after diversion. Chronically spinalized diverted and nondiverted rats exhibited similar micturition dysfunction: bladder/sphincter dyssynergia, incomplete voiding and ineffective (nonvoiding) bladder contractions. These data indicate that neither the condition of the bladder (such as chronic overdistension or bladder hypertrophy) nor afferent input from the bladder to the spinal cord dictates the development of reflex micturition and micturition dysfunction after spinal cord injury, suggesting that the dysfunction is intrinsic to spinal micturition reflex pathways.