Vaginal denervation of the bladder nerve supply.

Eleven patients with incontinence of urine owing to detrusor contractions have been treated by partial denervation of the bladder. Seven have substantially improved.

The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine. A neurophysiological study.

Single-fibre electromyography of the pubococcygeus muscle of the pelvic floor was performed in 69 asymptomatic women and 105 women with stress incontinence of urine or genitourinary prolapse or both. The results suggest that partial denervation of the pelvic floor with subsequent reinnervation is a normal accompaniment of ageing and is increased by childbirth. Women with stress incontinence of urine or genitourinary prolapse or both have a significant increase in denervation of the pelvic floor compared with asymptomatic women.

The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women.

Conduction was studied in the terminal branches of the pudendal nerve in 42 women with normal urinary control and 87 women with stress incontinence of urine, genitourinary prolapse, or both. Women with stress incontinence of urine had delayed conduction to both the striated urethral muscle and the pelvic floor muscle, indicative of denervation injury. Women with normal urinary control and genitourinary prolapse had similar conduction times to the urethral sphincter striated muscle as normal women but clear evidence of denervation damage to the pelvic floor.

The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histological and histochemical study.

Histological and histochemical analysis of biopsy samples of pubococcygeus muscle obtained from asymptomatic women and from women with stress incontinence of urine, with or without genitourinary prolapse, have been compared. In the asymptomatic women both age and parity appeared to be related to the morphological features of the samples and in particular those obtained from the posterior part of the pubococcygeus. In the symptomatic women there was a significant increase in the number of muscle fibres showing pathological damage which were obtained from the posterior part of the pelvic floor. The range of diameters of both Type I and Type II fibres obtained from this region was significantly different between symptomatic and asymptomatic women. These findings may be attributable to partial denervation of the pelvic floor in patients with urinary stress incontinence with or without genital tract prolapse.

Pelvic floor damage and childbirth: a neurophysiological study.

Ninety six nulliparous women were investigated to establish whether childbirth causes damage to the striated muscles and nerve supply of the pelvic floor. The techniques used were concentric needle electromyography (EMG), pudendal nerve conduction tests and assessment of pelvic floor contraction using a perineometer. There was EMG evidence of re-innervation in the pelvic floor muscles after vaginal delivery in 80% of those studied. Women who had a long active second stage of labour and heavier babies showed the most EMG evidence of nerve damage. Forceps delivery and perineal tears did not affect the degree of nerve damage seen. We conclude that vaginal delivery causes partial denervation of the pelvic floor (with consequent re-innervation) in most women having their first baby. In a few this is severe and is associated with urinary and faecal incontinence. For some it is likely to be the first step along a path leading to prolapse and/or stress incontinence.