Hai-Hong Jiang

Dual Simulated Childbirth Injuries Result in Slowed Recovery of Pudendal Nerve and Urethral Function

Pelvic floor muscle trauma and pudendal nerve injury have been implicated in stress urinary incontinence (SUI) development after childbirth. In this study, we investigated how combinations of these injuries affect recovery.

Electrical Stimulation of the Pudendal Nerve Promotes Neuroregeneration and Functional Recovery from Stress Urinary Incontinence in a Rat Model

The pudendal nerve can be injured during vaginal delivery of children, and slowed pudendal nerve regeneration has been correlated with development of stress urinary incontinence (SUI). Simultaneous injury to the pudendal nerve and its target muscle, the external urethral sphincter (EUS), during delivery likely leads to slowed neuroregeneration. The goal of this study was to determine if repeat electrical stimulation of the pudendal nerve improves SUI recovery and promotes neuroregeneration in a dual muscle and nerve injury rat model of SUI. Rats received electrical stimulation or sham stimulation of the pudendal nerve twice weekly for up to 2 wk after injury. A separate cohort of rats received sham injury and sham stimulation. Expression of brain-derived neurotrophic factor (BDNF) and βII-tubulin expression in Onufs nucleus were measured 2, 7, and 14 days after injury. Urodynamics, leak point pressure (LPP), and EUS electromyography (EMG) were recorded 14 days after injury. Electrical stimulation significantly increased expression of BDNF at all time points and βII-tubulin 1 and 2 wk after injury. Two weeks after injury, LPP and EUS EMG during voiding and LPP testing were significantly decreased compared with sham-injured animals. Electrical stimulation significantly increased EUS activity during voiding, although LPP did not fully recover. Repeat pudendal nerve stimulation promotes neuromuscular continence mechanism recovery possibly via a neuroregenerative response through BDNF upregulation in the pudendal motoneurons in this model of SUI. Electrical stimulation of the pudendal nerve may therefore improve recovery after childbirth and ameliorate symptoms of SUI by promoting neuroregeneration after injury.

1648 SPINAL CORD REGENERATION IMPROVES LOWER URINARY TRACT FUNCTOIN AFTER A COMPLETE SPINAL CORD TRANSECTION IN RATS

increase in intermicturition interval, explainable by an increase in voiding efficiency (as evidenced by a 2X increase in voided volume together with a decrease in post-void intravesical pressure), together with an increase in compliance. Importantly, the number of non-voiding contractions decreased dramatically (to 26% of control values). CONCLUSIONS: The effect of acute ROS inhibition at the LSSC produces a favorable response in chronic SCI rats, reducing many hallmark indices of neurogenic hyperreflexia secondary to traumatic suprasacral spinal cord injury. These results suggest that an ongoing activation of ROS production, likely due to central sensitization following suprasacral SCI, contributes significantly to the aberrant reflex activity associated with neurogenic bladder.