Neurogenic aspects of stress urinary incontinence

Kamran Sajadi, Bradley C. Gill, Margot S. Damaser

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

PURPOSE OF REVIEW: Vaginal childbirth is a significant risk factor for stress urinary incontinence (SUI). Women with SUI demonstrate dysfunction of the pelvic floor and pudendal nerve. Animal models of SUI have been developed to investigate its pathophysiology and for preclinical testing of potential treatments. RECENT FINDINGS: Vaginal distension, a method of simulating childbirth injury in animals, produces a reliable decrease in leak point pressure (LPP), a measure of urethral resistance to leakage and quantification of SUI severity in animals. In addition to ischemia and direct tissue damage, vaginal distension causes denervation of the external urethral sphincter (EUS). Pudendal nerve crush produces a similar decrease in LPP, whereas combined PNC and vaginal distension injury delays recovery of LPP compared with either single injury alone. Neurophysiologic studies have elucidated the results of each injury and their combination on pudendal nerve and EUS function. Urethrolysis, electrocautery, and pudendal nerve transection produce more durable functional impairment via both structural damage and denervation. Pubourethral ligament injury eliminates the structural support of the urethra, but its neurologic effects are unknown. SUMMARY: Animal models demonstrate a complex interplay between tissue damage and pudendal nerve dysfunction, and provide insight into the importance of neuroregeneration in the recovery of continence.

Original languageEnglish (US)
Pages (from-to)425-429
Number of pages5
JournalCurrent Opinion in Obstetrics and Gynecology
Volume22
Issue number5
DOIs
Publication statusPublished - Oct 2010
Externally publishedYes

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Keywords

  • animal
  • childbirth injury
  • disease models
  • pudendal nerve
  • stress
  • urinary incontinence

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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