Pudendal Canal Decompression Research Articles

Role of Pudendal Canal Syndrome in the Pathogenesis of Interstitial Cystitis and Its Treatment by Pudendal Canal Decompression

Objective: Pudendal canal syndrome (PCS) which is comprised of pudendal nerve compression in the pudendal canal occurs commonly in females and presents with pelvic, pubic, suprapubic, anal, and perianal pain, as well as dysuria and dyspareunia. These manifestations are similar to those of interstitial cystitis (IC). We investigated the hypothesis that IC is a manifestation of PCS and may thus respond favorably to similar treatment. Patients and Methods: Sixty-six patients (59 women, age 41.6 ± 4.2 years) complained of suprapubic, pubic, perineal, anal, and vaginal pain, dyspareunia, dysuria, and urinary frequency. Neurologic examination showed perianal and perivulvar hypoesthesia and an absent anal reflex. There were subnormal anal pressure and diminished electromyography of the external urethral sphincter and puborectalis and levator ani muscles as well as an increase of pudendal nerve terminal motor latency. These results pointed to the manifestations being possibly due to pudendal neuropathy. A pudendal nerve block improved the symptoms and pudendal nerve decompression was performed. Results: In 54/66 patients, pain disappeared with improvement of anal pressure, electromyography of external urethral sphincter, puborectalis and levator ani muscles and nerve terminal motor latency. Perianal and perivulvular hypoesthesia was normalized. Twelve patients did not improve either clinically or in terms of investigative results. Conclusion: A simple, easy, and cost effective technique is presented for the treatment of IC. It was based on the symptomatic and investigative similarities between IC and PCS. Pudendal canal decompression affected a cure of IC in most of the patients. Further studies are required to reproduce these results.

Intra-abdominal laparoscopic pudendal canal decompression – A feasibility study

Pudendal canal syndrome (PCS) is induced by the compression or the stretching of the pudendal nerve within Alcock's canal. Considering the difficulty and possible complications involved in exposing the pudendal canal and nerve by either transperineal, transgluteal or transischiorectal approaches, an intra-abdominal laparoscopic pudendal canal decompression (ILPCD) was employed. For this technique, 30 male adult human cadavers were examined. Measurements revealed an adequate working space in 16 (80%) of the 20 cadavers, while in four specimens the ischiococcygeus muscle was too large to be mobilized sufficiently. The mean working space was 24 mm with a range of 18 to 31 mm. It was considered that a working space of less than 20 mm would not be sufficient for manipulation of the instruments. With regards to pudendal nerve compression, it was observed that 7 (35%) of the 20 cadavers exhibited anatomic signs of PCS. In five (25%) specimens, the compression was observed between the sacrospinous and sacrotuberous ligaments, while the other two (10%) exhibited a broader compression, by the falciform portion of the sacrotuberous ligament. Under the guidance of a laparoscope, the peritoneum was cut laterally to the bladder, and fascia pelvis was identified. The latter was split and the internal iliac vein was traced to the opening of the pudendal canal allowing clear visualization of its contents. Subsequently, either the sacrospinous or sacrotuberous ligament was cut. Considering that none of the surgical procedures currently used are known to completely improve all the symptoms of PCS, ILPCD could theoretically reduce stretching of the pudendal nerve.

Alcock's canal releasing for pudendal artery syndrome resulting from gunshot injury

A 21-y-old man applied to hospital with a complaint of erectile dysfunction, which started soon after a gunshot injury. The entry of the bullet was at the middle right gluteal region without any exit hole. A pelvic X-ray revealed the bullet and the scattered particles. On penile Doppler ultrasonography, the peak systolic velocities (PCV) of the right and the left cavernosal arteries were 19 and 29 cm/s, respectively. Pudendal angiography revealed poor visualization of the right pudendal artery below the level of the bullet. The patient underwent a right-sided Alcock's canal releasing surgery. After the operation, on control penile Doppler ultrasonography, PCV on the right and the left cavernosal arteries were 53 and 35 cm/s, respectively. The control angiography revealed a normal right pudendal artery. The patient was fully potent 2 y after the operation. Not only the entrapment of pudendal nerve but also the pudendal artery may cause Pudendal canal syndrome. A gunshot injury may cause such a condition due to the reaction caused by the bullet. Pudendal canal decompression is a simple and effective treatment for pudendal canal syndrome.

Neuronal innervation of urethral and anal sphincters: surgical anatomy and clinical implications.

The present review describes the neuronal innervation of the external urethral and anal sphincters. A knowledge of this innervation helps in understanding the clinical symptoms of urinary and anorectal pathology, and in choosing the appropriate technique of nerve localization or block. An ability to locate the pudendal nerve, on the basis of surgically documented anatomy, has important diagnostic and therapeutic advantages. It can be used to study the integrity of pelvic floor muscles, in biofeedback training, nerve blocks, pudendal canal decompression, chronic stimulation trials to treat urinary or faecal incontinence, and in nerve conduction studies or evoked potential recordings. Furthermore, the superficial location of the sphincteric innervation in the perineum and ischiorectal fossa renders the nerve branches susceptible to injury during operative correction of urinary or faecal incontinence. Supported by a knowledge of anatomy, we can make firm recommendations on which to base safe surgical techniques that avoid damage to urethral and anal sphincteric innervation.

Pudendal Canal: Surgical Anatomy and Clinical Implications

The anatomy of the pudendal canal (PC) was studied in 26 cadavers: 10 stillborn and 16 adults (mean age, 48.2 years). Two approaches were used to expose the PC: gluteal and perineal. The PC was an obliquely lying tube with a mean length of 0.8 cm in the stillborn and 1.6 cm in the adult cadavers. It started at a mean distance of 0.8 cm from the ischial spine in the stillborn and of 1.6 cm in the adult cadavers, and ended at a mean distance of 0.7 cm and 2.6 cm, respectively, from the lower border of the symphysis pubis. The PC wall was formed by the splitting of the obturator fascia and not by the lunate fascia. The PC contained the pudendal nerve and vessels embedded in loose areolar tissue. The three branches of the neurovascular bundle arose inside the canal in all but three cadavers. The wall of the PC consisted of collagen and elastic fibers, whereas that of the obturator fascia consisted of collagen only. The PC seems to be structurally adapted to serve certain functions. The criss-cross textile arrangement of collagen fibers in its wall allows the canal to change its shape in response to changes in pudendal vessels that occur during sexual activity. The elastic recoil may not only help to "pump" the blood up the pudendal vein, but also to prevent PC subluxation. The PC may, furthermore, act as a "pulley" for the neurovascular bundle. The pulley action may be disrupted by disordered pelvic floor muscles or defecation. Knowledge of the precise anatomy of the PC is necessary to carry out PC decompression in the treatment of PC syndrome.

Endoscopic pudendal canal decompression for the treatment of fecal incontinence due to pudendal canal syndrome.

Fecal incontinence resulting from pudendal canal syndrome has been treated by pudendal canal decompression (PCD) with satisfactory results. Considering the possible difficulty in exposing the pudendal canal and nerve by the open method, laparoscopic PCD was practiced in 9 women aged between 37 and 52 years. They were complaining of fecal incontinence; urinary stress incontinence was an additional complaint in 4/9 women. Neurologic, manometric, and EMG studies confirmed the diagnosis of pudendal canal syndrome. For laparoscopic PCD a 1-cm incision lateral to the anal orifice was performed. A balloon dilator was introduced in the ischiorectal fossa (IRF) to create a working space, and CO2 was insufflated. Under the guidance of a laparoscope, the IRF was entered and the inferior rectal nerve identified and followed to the pudendal canal. The latter was split open, releasing the pudendal nerve into the IRF. Fecal control was achieved in 7/9 patients and urinary control in 2/4. Fecal and urinary control were associated with improvement in perianal sensation, rectal neck pressure, EMG of external anal sphincter and levator ani muscle as well as in pudendal nerve terminal motor latency. Two women showed no improvement. Failure is suggested to be due to an advanced pudendal neuropathy. In conclusion, laparoscopic PCD is a simple, easy, and safe procedure. It allows for better exposure of the contents of the IRF than the open procedure, thus avoiding injury of the pudendal nerve and its branches during the performance of the PCD.

Pudendal Artery Syndrome Presenting as Ischemic Proctitis: Report of 3 Cases

Ischemic proctitis due to pudendal artery syndrome is described in 3 cases. The patients showed common clinical and investigative findings which included: anal pain and bleeding; strainodynia; tender, edematous and ulcerated rectal neck, as well as obliterated distal internal pudendal artery. Manifestations of pudendal neuropathy were also present. The inflammatory process was localized to the rectal neck. Bilateral internal pudendal artery obliteration with non visualization of the inferior rectal arteries is suggested to define proctitis as ischemic. Pudendal artery obstruction seems to result from levator subluxation and sagging which pulls on the pudendal vessels and nerve resulting in pudendal canal syndrome. Pudendal canal decompression achieved elimination of the symptoms and healing of the rectal neck lesions in the 3 cases. To our knowledge, the first 3 cases of ischemic proctitis caused by pudendal artery syndrome are reported here.

Pudendal artery syndrome with erectile dysfunction: treatment by pudendal canal decompression.

Pudendal artery syndrome (PAS) was studied in 10 patients with erectile dysfunction (ED). Ages ranged from 38 to 55 years. All had chronic constipation and straining at stool, absent nocturnal penile tumescence, low penobrachial pressure index (p < .01), low peak flow velocity (p < .001), and a diameter increase (p < .0001) upon duplex ultrasonography screening. Four of the 10 patients had perineal hypoesthesia, prolonged bulbocavernosus reflex (p < .05), and pudendal nerve terminal motor latency (p < .05), and weak anal reflex and EMG activity of the external anal sphincter. The levator EMG activity was reduced in all patients. Intracavernous papaverine injection induced partial erection after a period longer than normal. Selective pudendal arteriography showed narrowing or obstruction of the distal part of the internal pudendal artery (IPA) on both sides with poorly or non-visualized penile arteries. A generalized arterial disease was excluded and pudendal artery compression in the pudendal canal (PC) was suspected as causing ED. The narrow or obstructed part of the IPA corresponds to the part in the PC. Four of the 10 patients had manifestations of pudendal neuropathy in addition to IPA compression. Pudendal canal decompression (PCD) was performed through a perineal approach. ED improved in 8 of the 10 patients 3-6 months postoperatively. Two of the 4 patients who had pudendal arteriopathy combined with neuropathy did not improve. In conclusion, the 10 patients with ED had common clinical and investigative findings that constitute the pudendal artery syndrome. PCD effected improvement in 80% of the cases.

Surgical anatomy of the pudendal nerve and its clinical implications.

A study of the surgical anatomy of the pudendal nerve (PN) was performed in 13 female and 7 male cadavers. The knowledge of the precise anatomy and anomalies of this important nerve would help in better localization of the nerve and its roots and branches for neurostimulation or for pudendal canal decompression in pudendal canal syndrome. Two routes were used in the dissection: gluteal and perineal. The PN was identified and its course was followed from its roots to its termination. The PN was composed of three roots derived from the 2nd, 3rd, and 4th anterior sacral rami (S 2,3,4). The roots received a contribution from S 1 in five cadavers and from S 5 in one. The three roots formed two cords. The first root continued as the upper cord while the second and third root fused together producing the lower cord. The PN was formed by union of the two cords a short distance proximal to the sacrospinous ligament, and then crossed the back of the ligament. In no specimen did the nerve cross the ischial spine. The inferior rectal nerve arose from the PN in the pudendal canal in 18 cadavers. In two cases it came out proximal to the canal; this would spare the two subjects the anorectal manifestations of the pudendal canal syndrome. As the PN crossed the back of the sacrospinous ligament, it gave origin to a branch that supplied the levator ani muscle. This branch was only found in male cadavers and we call it "accessory rectal nerve"; the levator ani muscle in such cadavers was doubly innervated on its perineal aspect.

Pudendal canal decompression in the treatment of urinary stress incontinence

Twelve women with urinary stress incontinence (USI) due to pudendal canal syndrome (PCS) were treated by pudendal canal decompression. The investigations comprised determination of the EMG activity of the external urethral sphincter (EUS) as well as the straining urethral reflex latency and pudendal nerve terminal motor latency (PNTML). The EMG of the EUS revealed diminished activity at rest and with coughing, with prolonged straining urethral reflex latency and PNTML. There was diminished sensation in the labia majora. These manifestations point to PCS and so pudendal canal decompression was performed. This comprised exposure of the inferior rectal nerve in the ischiorectal fossa through a para-anal incision. The nerve was traced to the pudendal nerve in the pudendal canal, which was split open. The patients were followed for a mean of 17.7 months ±4.2 SD. Three scores were defined: 1, where the patient became dry (6 patients); 2, where the patient unproved (5 patients); and 3, where no change was noted (1 patient). In scores 1 and 2 there was improvement in labia majora sensation and EMG activity of the EUS, as well as a decrease in the straining urethral reflex latency and the PNTML. The technique corrects a basic cause of USI, in contrast to other procedures which deal instead with the effects. The technique is simple, easy and without complications and can be done on an outpatient basis.

Pudendal canal decompression in the treatment of erectile dysfunction.

The results of the treatment of 7 patients with neurogenic erectile dysfunction (ED) by pudendal canal decompression are presented. Ages ranged from 46 to 56 years. Patients had penile, perineal, and scrotal hypoesthesia or anesthesia. EMG of the external urethral sphincter and levator ani muscle revealed diminished activity. There were increased bulbocavernosus and pudendal nerve terminal motor (PNTML) latencies. Patients tested normal for endocrine assays, Doppler examination of the penile arteries penobrachial pressure index, and cavernosometry. Nocturnal penile tumescence activity was absent. These findings pointed to neurogenic ED due to pudendal canal syndrome (PCS). Pudendal canal decompression was done through a para-anal incision. The inferior rectal nerve was followed to the pudendal nerve in the pudendal canal, which was slit open. Mean followup was 19.6 months. No complications were encountered. ED improved in 6 of the 7 patients 2-6 months postoperatively. Sensory and motor changes also improved. It is suggested that chronic straining at stool in these patients led to levator subluxation and sagging, and to pulling on the pudendal nerve with a resulting entrapment in the pudendal canal, pudendal neuropathy, and PCS. ED results from involvement of the penile and perineal branches of the pudendal nerve. To conclude, PCS may cause ED, which improves with pudendal canal decompression.

Pudendal Canal Decompression in the Treatment of Idiopathic Fecal Incontinence

Eleven subjects with pudendal canal syndrome were treated by pudendal canal decompression. All complained of fecal incontinence and 7 of additional urinary stress incontinence. Investigations revealed