Assessment of lower urinary tract functional deficit in rats with contusive spinal cord injury

Traumatic spinal cord injury (SCI) produces lower urinary tract (LUT) dysfunction that has been studied in surgical transection models. Our aim was to assess LUT functional deficit in a clinically relevant model of incomplete SCI to investigate how partial preservation of supraspinal connections might affect LUT dysfunction. Standardized weight-drop contusion (10 g x 2.5 cm) or complete transection, was produced at T8 in female Sprague-Dawley rats. Behavioral tests were used to assess hind limb sensorimotor function at Day 1 after surgery and weekly thereafter. The urometric experiments were conducted on groups (n = 7) of uninjured rats and on injured rats during Weeks 1 and 2 after SCI (before and after spontaneous voiding was established) as well as Week 2 after a complete transection (n = 3). Under anesthesia, the bladder was continuously perfused with saline. Changes in bladder pressure and external urethral sphincter (EUS) electrical activity were monitored. The bladder was then dissected and weighed and both the bladder and spinal cord were fixed for pathoanatomical analyses. Our results indicate that several aspects of LUT dysfunction after contusive SCI were similar to transection, e.g., reduction of voiding efficiency (approximately 5% of normal value), decrease in inter-contraction interval (47%), increase in bladder capacity (8-fold), and weight (4.6-fold). One aspect appeared different from transection--partial recovery from acute bladder/sphincter dyssynergia. Because the coordination of bladder and EUS function is mediated by brainstem pathways, partial recovery of synergy after SCI was likely due to sparing of some relevant bulbospinal projections as was confirmed by retrograde transneuronal viral tracing.