• A Shafik.
• Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Egypt.
• Eur. J. Obstet. Gynecol. Reprod. Biol. 1998 Oct 1;80(2):215-20.

AbstractNotwithstanding many established causes of vulvodynia there still remains an idiopathic group with unknown etiology and variable results of treatment. We present 11 women with idiopathic vulvodynia in whom the etiology could be defined and who were successfully treated. Age varied from 28-53 years. The vulvar pain was associated with stress urinary incontinence in 6/11 patients and all had constipation. Perineal and vulvar hypoesthesia occurred in 6, weak anal reflex in 7 and diminished EMG activity of the external anal sphincter in 3, of the external urethral sphincter in 6 and of the levator ani muscle in 11. There was significant increase (P<0.05) of the pudendal nerve terminal motor latency (PNTML) in all. The motor and sensory change as well as the increased PNTML point to pudendal canal syndrome. Pudendal nerve block, as a diagnostic and therapeutic test, effected temporary pain relief. Pudendal nerve decompression was performed. The inferior rectal nerve was exposed through a para-anal incision, and followed to the pudendal nerve in the pudendal canal. Pudendal canal fasciotomy was done to release the pudendal nerve in the ischiorectal fossa. Vulvar pain disappeared in 9/11 women and stress urinary incontinence in 4/6. Anal reflex was normalized in 5/7 women, and vulvar and perineal hypoesthesia in 4/6. The EMG activity of the external urethral sphincter improved in 4/6, of the external anal sphincter in 2/3 and of the levator ani in 9/11 women. The PNTML was normalized in 9/11 women. In conclusion, pudendal nerve decompression effected relief and improvement in the sensory and motor manifestations of the pudendal nerve in 9/11 women. Two women did not improve due probably to an irreversible damage of the pudendal nerve, or to incomplete pudendal nerve decompression.

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