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Six months of intensive rehabilitative exercise intervention can lead to a significant improvement in symptoms [31]. However, as with any rehabilitation protocol, motivation of the patient is paramount. Animal studies could be useful for preclinical testing of adjuvant agents to facilitate the effects of rehabilitation exercises.

Despite the differences between animals and humans, rats have been used to demonstrate that nerve injury occurs during vaginal distension [10,33] and that the pudendal nerve is particularly vulnerable to damage during vaginal delivery [10], similar to the clinical situation. A variety of behavioral and functional outcomes have been used to demonstrate urethral dysfunction after either vaginal distension or pudendal nerve injury, since animals will not sneeze or cough on command. Voiding behavior studies [8], a sneeze test [], LPP testing [,35], modified LPP testing [], maximum urethral closure pressure [38], and a vertical tilt table test [39] all have been used to demonstrate urinary function or behavior after vaginal distension or pudendal nerve injury.

The results of these studies are consistent [10,40] and demonstrate symptoms consistent with development of SUI after either pudendal nerve injury or vaginal distension. Rats are a useful model to use because many animals can be studied in a short period of time, the urologic anatomy and physiology of the rat are well described reviewed by Steers [41] , and techniques can be easily transferred to mice for use in functional genomics studies.

Nonetheless, no animal is a perfect representation of a clinical situation, particularly one such as SUI that is a function of injury, endocrine influences, neural activity, interaction of multiple muscle groups, and the effects of gravity. In addition, no animal has the baby's head-to-birth canal ratio of the human [42] that is thought to cause the traumatic injuries that lead to eventual development of SUI.

Rat neural control of voiding is somewhat different than that of humans: unlike in humans, the urethra contracts during voiding in rats [43]. This effect is minimized by the use of LPP as a urethral functional measure, since it is measured in the absence of voiding. Therefore, while not a perfect representation of human voiding, female rats are a reasonable choice as one of several animal models in which to conduct preclinical testing of potential interventions. This study determined the time course and extent of incontinence symptoms and recovery after bilateral pudendal nerve injury using LPP testing.

LPP was significantly decreased at all four time points studied after pudendal nerve injury. Although we found no statistically significant differences between LPPs at any time point after nerve crush, we did find an increasing trend after a minimum of 4 days after nerve crush. P abd was significantly decreased compared to controls only 4 and 7 days after nerve crush, suggesting that nerve function may begin recovering by 2 weeks after injury or that compensatory events might occur in the urethra. We have previously shown that voiding behavior returns to normal 2 weeks and 3 months after pudendal nerve injury [].

In contrast to these previous results, data from this study demonstrate that LPP remains decreased 2 weeks after nerve injury. Two weeks is probably not enough time for the regenerating pudendal nerve to complete functional connections with the EUS. Since LPP is a more sensitive measure than voiding behavior, it probably better represents the state of urethral functional recovery.

Normalization of voiding behavior by 2 weeks after injury may be due to compensatory effects at the urethra other than those due to pudendal nerve regeneration. The trend to increasing LPP and P abd after the minimum 4 days after nerve crush suggests that the pudendal nerve will reinnervate the EUS and urethral resistance will recover.

We have previously demonstrated a return to normal voiding behavior 3 months after pudendal nerve crush, even though only approximately 50 percent of the pudendal motoneurons had regenerated to the EUS [8]. Future experiments will be aimed at documenting functional changes and examining the natural recovery after pudendal nerve injury over a longer time period, as well as studying the effects of interventions. This study characterizes the short-term time course of urinary functional outcomes after pudendal nerve injury in the female rat. This animal model could be useful for preclinical testing of pharmacologic agents and other protocols aimed at rehabilitation of the injuries incurred in vaginal delivery and prevention of SUI onset.

Further functional, anatomical, and molecular characterization of the animal model is necessary prior to its use for preclinical testing. Short-term timecourse of bilateral pudendal nerve injury on leak-point pressure in female rats. This experiment was designed to study the time course of functional changes in the urethra after pudendal nerve crush in rats. Leak-point pressure LPP was measured 2, 4, 7, or 14 days after bilateral pudendal nerve crush and was compared to that of a control group. LPP at all four time points after nerve injury was significantly decreased compared to control values.

A minimum was reached 4 days after injury, and LPP appeared to trend upward with increasing time after injury, suggesting that nerve function may begin to recover or compensatory changes in the urethra may occur. Pudendal nerve crush induces decreased LPP in female rats, mimicking the clinical symptoms of stress incontinence.

Mutual influence between vesicourethral and anorectal function in spinal cord injury patients

When fully characterized, this model could be useful for preclinical testing of treatment and rehabilitation protocols. Key words : female, incontinence, leak-point pressure, nerve injury, pudendal nerve, rat, urethra.

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DOI: Pudendal Nerve Crush. Catheter Implantation. Leak-Point Pressure Testing. Data Analysis. The standardization of terminology of lower urinary tract function: report from the standardization sub-committee of the international continence society. Neurourol Urodyn. Urinary incontinence in women. Urinary incontinence in women of reproductive age. Gynecol Obstet Invest.

Neurobiology Of Incontinence Ciba Foundation Symposium

Monitoring pudendal nerve function during labor. Obstet Gynecol. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol. Morphology and neuropathology of the pelvic floor in patients with stress incontinence. Int Urogynecol J. Treatment of stress urinary incontinence in women with urethral hypermobility and intrinsic sphincter deficiency. J Urol. Effects of pudendal nerve injury in the female rat. Neuroregeneration and voiding behavior patterns after pudendal nerve crush in female rats. Functional and neuroanatomical effects of vaginal distension and pudendal nerve crush in the female rat.


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Effects of anesthesia on cystometry and leak-point pressure of the female rat. Life Sci. Alteration by urethane of glutamergic control of micturition. Eur J Pharm. The nonstop transvesical cystometrogram in urethane-anesthetized rats: a simple procedure for quantitative studies on the various phases of the urinary bladder voiding cycle.

J Pharm Methods. Matsuura S, Downie JW. Effect of anesthetics on reflex micturition in the chronic cannula-implanted rat. The standardization of terminology for researchers in female pelvic floor disorders. Delivery and pudendal nerve function.

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Acta Obstet Gynecol Scand. Swash M. The neurogenic hypothesis of stress incontinence. In: Bock G, Whelan J, editors. Neurobiology of incontinence. New York: Wiley; Ciba Foundation Symposium. Injury to innervation of pelvic floor sphincter musculature in childbirth. Follow-up evaluation of the effect of vaginal delivery on the pelvic floor. Dis Colon Rectum. Damage to the innervation of the voluntary anal and periurethral sphincter musculature in incontinence: an electrophysiological study. Collagen injection therapy in elderly women: long-term results and patient satisfaction.

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Long-term outcome and quality of life after modified pubovaginal sling for intrinsic sphincteric deficiency. Five-year results after anti-incontinence operations. Am J Obstet Gynecol. Endoscopic silicone injection for female stress urinary incontinence due to intrinsic sphincter deficiency: impact of coexisting urethral mobility on treatment outcome. Learn more. There are a number of causes of incontinence. The common forms of urinary incontinence, faecal incontinence or double incontinence, are stress related, in that voiding of urine or faeces occurs in response to a sudden increase in pressure in the bladder or anorectum that is not opposed by an adequate pressure increase in the sphincteric region.

This weakness of the sphincter mechanism is due to chronic partial denervation of the striated sphincter muscles of the pelvic floor, comprising the external anal sphincter muscle and puborectalis puboanalis components of the voluntary anal sphincter musculature, and the periurethral and intramural components of the urinary striated sphincter musculature. Weakness of the pelvic floor, and perineal descent during straining, lead to secondary changes in the anatomy of the bladder neck, of the anorectal angle, and of the smooth muscle of the internal urinary and anal sphincters.

The cystometric and anal manometric changes found in patients with stress incontinence are secondary to this neurogenic weakness of the pelvic floor. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account.

If the address matches an existing account you will receive an email with instructions to retrieve your username. Julie Whelan Search for more papers by this author. Tools Request permission Export citation Add to favorites Track citation. Share Give access Share full text access. Share full text access.

Please review our Terms and Conditions of Use and check box below to share full-text version of article. Summary There are a number of causes of incontinence.