Voiding Dysfunction Associated with Pudendal Nerve Entrapment

The pudendal nerve is a sensory and somatic nerve which originates from the ventral rami of the second, third, and fourth (and occasionally the fifth) sacral nerves roots. After branching from the sacral plexus, the PN leaves the pelvis through the less sciatic foramen and travels three main regions: the gluteal region, the pudendal canal, and the perineum. It accompanies the internal pudendal vessels upward and forward along the lateral wall of the ischiorectal fossa, being contained in a sheath of the obturator fascia termed the pudendal canal (= Alcock’s canal). The pudendal nerve gives off three distal branches, the inferior rectal nerve, the perineal nerve and the dorsal nerve of the penis in males, corresponding to the dorsal nerve of the clitoris in females.

The PN innervates the external genitalia of both sexes, as well as sphincters for the bladder and the rectum. As the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve results in contraction of the external urethral sphincter. Contraction of the external sphincter, coupled with that of the internal sphincter, maintains urethral pressure (resistance) higher than normal bladder pressure. The storage phase of the urinary bladder can be switched to the voiding phase either involuntarily (reflexively) or voluntarily. The pudendal nerve then causes relaxation of the levator ani so that the pelvic floor muscle relaxes. The pudendal nerve also signals the external sphincter to open. The sympathetic nerves send a message to the internal sphincter to relax and open, resulting in a lower urethral resistance. The PN is also known to have a potential modulative effect on bladder function. Somatic afferent fibers of the pudendal nerve are supposed to project on sympathetic thoracolumbar neurons to the bladder neck and modulate their function. This neuromodulative effect works exclusively at the spinal level and appears to be at least partly responsible for bladder neck competence and at least continence [1].

Therefore, if a problem occurs within the nervous system, the entire voiding cycle is affected.

The diagnosis of pudendal neuralgia is reserved for patients who have allodynia in the entire distribution of the pudendal nerve - vulvar, perineal and perianal area – without any irradiation in other lumbosacral dermatomes and with typically severe pain on sitting, relieved in contrary by standing, and absent when recumbent or when sitting on a toilet seat. Various other symptoms may occur in some cases, for example urinary hesitancy (difficulty starting the flow of urine), frequency (frequent need to pass urine), urgency (sudden sensation to pass urine), constipation/painful bowel movements, reduced awareness of defecation (the process of passing bowel motions), sexual dysfunction including loss of libido, recurrent numbness of the penis and/or scrotum after prolonged cycling, altered sensation of ejaculation and impotence in men.

Symptoms of prostatitis-like pain are conducted through pudenal afferents and occur in 11 % of American men, and approximately 95 % of the patients diagnosed with chronic prostatitis have no evidence of bacterial infection or inflammatory cells in the prostatic fluid [2].

Further possible symptoms include burning, loss of sensation or numbness, increased sensitivity, electric shock or stabbing pain, knife-like or aching pain, feeling of a lump or foreign body, twisting or pinching, abnormal temperature sensations, constipation, pain and straining with bowel movements, straining or burning when urinating, painful intercourse, and sexual dysfunction – including hyperarousal or decreased sensitivity.

Neurological examination is then extremely important for diagnosis of nerve damages. Extrinsic lesions (PN entrapment) do not include any loss of sensation or feeling of numbness in pudendal dermatomes but on the contrary imply hyperesthesia without troubles of micturition or continence. In neurogenic PN damages, loss of sensation or numbness selectively is usually combined with contralateral anal deviation due to homolateral perineal/perianal myoatrophia; urodynamic testing can show bladder overactivity [3] but may also be normal. Urethral incontinence occurs only in bilateral neurogenic PN damages.

For diagnosis, behind the anamnesis, the more commonly used tests are the PN motor latency test (PNMLT), electromyography (EMG), diagnostic nerve blocks, and magnetic resonance neurography (MRN). EMG studies of the pudendal nerve, often touted as a diagnostic tool, are unreliable since they can be abnormal after vaginal delivery or vaginal hysterectomy and do not define the neurologic level of the pathology. Transvaginal, or in men transrectal palpation of the pudendal nerve at the sacrospinal ligament is the key to the diagnosis: patients have exquisite tenderness when digital pressure is applied over the pudendal nerve and produce a typically Tinel’s sign (sensation of tingling or “pins and needles” in the distribution of the PN). A selective PN block by transvaginal or perineal approach – a technique of anesthesia well known in obstetrics - is then crucial for the diagnosis and treatment of pudendal neuralgia.

There are numerous possible causes for pudendal neuropathy. Some of the possible causes are an inflammatory or autoimmune illness, frequently interpreted as infection. After iatrogenic nerve damages, which are frequent in obstetrics and gynecology pudendal neuralgia is common, with etiologies such as compression of the nerve through a postpartal haematoma, fibrosis of the ischiorectal fossa, stretching of the nerve during delivery or surgical damages during transvaginal sacrospinous colpopexy [4]. More recent interventions using mesh material for sacrospinal fixation [5], sacro-colpopexy or rectopexy may also expose patients to risk for pudendal nerves damages [6].

There are many treatment options depending on the cause of the pudendal neuropathy. One must keep in mind, that reduction or stopping association of medical pain treatment may be the first step in recovery of urinary functions, since most pain killers present side effects on bladder and sphincters control.

Because excessive tension (spasm) in the striated muscles of the pelvic floor appears to be common to most of the pelvic pain syndromes, treatment options always include pelvic floor physical therapy to relax pelvic floor muscles and pain medications. Trial of pudendal nerve blocks with botulinum toxine A is a real option [9], but bilateral infiltration must be done carefully to avoid urinary and fecal incontinence.

Where medical treatments are not successful in relieving symptoms, surgical treatments may be tried. In refractory pain situation, surgical treatment is a well know option. Robert has described the transgluteal approach for neurolysis of the PN at the infrapiriform canal and transection of the sacrospinal ligament [10]. Shafik on the other hand attempted to decompress the PN by following a perineal para-anal pathway. His dissection follows the inferior rectal nerve to the Alcock’s canal [11] and focused on the Alcock’s canal itself. The laparoscopic transperitoneal approach to the PN focuses mainly on the proximal portion of the PN but at the same time of the sacral nerves roots [12].

However surgical decompression of the nerve may not be effective in case of irreversible damage to the nerve, as may be seen in longstanding poorly controlled diabetes mellitus, or surgical damage or even destruction of the PN. Neurectomy is a possible option, but induces systematical numbness in corresponding nerve(s) distribution and exposes the patient to risk for incontinence if performed bilaterally and to risk for neuromas while duplicating the pre-existing pain level. Taking into consideration the underlying cause, location, and type of pain, attempts at conservative procedure should almost always be considered before moving to destructive procedures. It is well accepted that the actual state of the art neurosurgical treatment of peripheral neuropathic pain is neuromodulation that is an important part of the continuum of managing chronic intractable pain. It is hard to imagine contemporary pain management without this modality of treatment. Neuromodulation procedures are particularly attractive because they are nondestructive and reversible. The idea of achieving pain relief by electrically stimulating the dorsal columns of the spinal cord (spinal cord stimulation - SCS) was derived from the gate control theory by Melzack and Wall in 1965 [13].

Because sacral nerve stimulation does not permit neuromodulation of all pudendal afferent fibers together, it has not been considered to be a real therapeutic option for pudendal neuralgia in the international medical literature [14, 15]. To permit stimulation of the PN itself, the Bion® microstimulator was developed and designed to be implanted by perineal access adjacent to the pudendal nerve using a custom blunt dissector and cannula [16]. The main disadvantage of this device is the high risk for migration since implantation does not secure the device to any fixed anatomical structures. Spinelli has also reported about the technique of implantation of a tined lead near the PN by perineal or posterior approach [17], but with the same high risk for lead migration, dislocation or even cable breakage. The laparoscopic technique of implantation called “LION procedure” [18], enable a safe and reproducible implantation of a multiple channel electrode in direct contact to the PN within the protection of the pelvis. Fixation of the lead to neighbor endopelvic structures may prevents electrode dislocation, migration or cable breakage, but required general anesthesia and surgery. Neuromodulation of the SNR #2-4/5 has major advantage to permit simultaneously a pain control as a bladder control, especially for bladder overactivity.