Pudendal Nerve Entrapment
The basic idea here is that compression of the pudendal nerve in the Alcock's canal (by impact trauma, an operation in the immediate area, or congenital malformations) can lead to a syndrome of pelvic pain.
This is an extremely rare disorder. It was described by a 2010 paper as " an uncommon cause of pain in the pelvic floor". Please read our warning about surgery offered for this condition. The surgery to alleviate it should not be entered into lightly. Many people who have "decompression of the pudendal nerve" surgery are still in great pain years later. Some are in worse pain than before the operation, and a significant percentage develop Sacroiliac Joint Dysfunction (SIJD) and pelvic instability due to the severing of the sacrotuberous and sacrospinous ligaments (leaving them unable to play sport, lift weights etc). Only a small handful of doctors in the world will do this operation. It is not mainstream medicine. The operation can cost tens of thousands of US dollars, and most insurances will not cover it. Our recommendation is that unless you have pain that comes on only when and immediately upon sitting, combined with episodes of penile numbness, and/or urinary or fecal incontinence, do not consider this option before thoroughly investigating the far more common causes of pelvic pain.
Anatomical Basis of Chronic Pelvic Pain Syndrome: the Ischial Spine and Pudendal Nerve Entrapment
Stanley J. Antolak, Jr., M.D., David M. Hough, M.D., Wojciech Pawlina, M.D., Robert J. Spinner, M.D.
Department of Urology, Department of Radiology, Department of Anatomy, and Department of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota.
Chronic pelvic pain syndrome is a conundrum that may be explained partly by pudendal nerve entrapment (PNE), which causes neuropathic pain. In men with PNE, aberrant development and subsequent malpositioning of the ischial spine appear to be associated with athletic activities during their youth. The changes occur during the period of development and ossification of the spinous process of the ischium.
Chronic perineal pain may be caused by pudendal nerve entrapment (PNE). Patients with PNE typically present with pain in the penis, scrotum, labia, perineum, or anorectal region that is aggravated by sitting, relieved by standing, and absent when recumbent or when sitting on a toilet seat. PNE is a clinical diagnosis of conditions in patients with the typical history. Robert et al. (1) and Shafik (2) described how the pudendal nerve is entrapped between the sacrotuberous (ST) and sacrospinous (SSp) ligaments and may engage the falciform process of the ST ligament. Stretching of the pudendal nerve from chronic constipation causes neuropathy (3). Normal vaginal delivery causes measurable neuropathy lasting approximately 3 months (4).
Prostatitis-like urogenital pain and voiding and sexual dysfunction are the hallmark of pudendal neuropathy. Symptoms of prostatitis-like pain occur in 11% of American men, and approximately 95% of the men whose conditions are diagnosed as chronic prostatitis have no evidence of bacterial infection or inflammatory cells in the prostatic fluid (5).
Misdiagnosis begets expensive testing, serious misapplication of surgical procedures, and prolongation of nerve trauma. Treatment response is better in men who receive an early diagnosis and who meticulously avoid traumatic activities. In our practice, many of these men have PNE. At surgical treatment of PNE, Robert noted that 11% of patients required excision of an elongated ischial spine that was interpreted by the surgeon as conflicting with the pudendal nerve. Frequently, in male patients operated on for pudendal neuropathy at Mayo Clinic, the ischial spine is elongated with a posterior orientation, occasionally shaped like a scimitar. In men, the typical ischial spine is a low-lying spike. Magnetic resonance imaging (MRI) studies of the pudendal nerve, especially at the ischial spine, have been attempted at Mayo Clinic, but MRI is not adequate for diagnosis of PNE. Mayo Clinic radiologists have reviewed MRI scans from other institutions and cannot confirm purported pudendal nerve compression (Maus T: Personal communication, June 2001). Our paper discusses the clinical syndrome of chronic pelvic pain syndrome, how it may be explained by PNE in men, and the etiology and suspected pathophysiology.
CLINICAL EVALUATION AND OBSERVATION
Men with urogenital pain or rectal pain or both, with or without voiding symptoms and with or with out ejaculatory pain, may have chronic pelvic pain syndrome. Prostatitis (reproductive tract infection) is ruled out by the absence of infection or inflammatory cells in the prostatic secretions (voided bladder 3 urinalysis, as described by Meares and Stamey) and the seminal fluid. These patients have National Institutes of Health (NIH) category IIIB chronic prostatitis and chronic pelvic pain syndrome (6) (Table 1).
Within our patient population, we have identified 5 symptom groups:
- I. Short-term pain, preceded by voiding complaints; usual onset is after 2 to 5 months of identifiable trauma.
- II. Insidious, long-standing symptoms with many past consultations and treatments or surgical procedures.
- III. Sudden onset of pain while squatting and lifting. Often this pain precipitates a visit to an emergency department, but no pathologic features are identified (the pain is often treated, however, as epididymitis or testicular torsion).
- IV. Pain after pelvic radiation therapy, typically for carcinoma of the prostate. (This group is estimated to be less than 1% of all men with urogenital pain.)
- V. Pain from inflammatory processes after perineal surgery or drainage of phlegmon. (This group is estimated to be less than 1% of all men with urogenital pain.)
ANATOMY AND PATHOPHYSIOLOGY OF EXERCISE-INDUCED REPETITIVE MICROTRAUMA
The striking common feature in all patients is that flexion activities of the hip (sitting, climbing, squatting, cycling, and exercising) induce or aggravate urogenital pain, chronic pelvic pain, or prostatitis-like pain. Many of the men played American football, lifted weights, and wrestled as teenagers and young adults.
Our primary hypothesis is that hypertrophy of the muscles of the pelvic floor during the years of youthful athleticism causes elongation and posterior remodeling of the ischial spine. The SSp ligament then rotates, causing the ST and SSp ligaments to overlie one another. The ligaments act like a lobster claw, with the pudendal nerve traversing the interligamentous space where it can be crushed (Robert RR: Personal communication, March 2000). In addition, in this position the pudendal nerve travels a longer course because it is posterior or dorsal to the SSp ligament. In this course it may stretch over the SSp ligament or the ischial spine during squatting or during sitting or standing from a seated position. We surmise that the gluteus muscle, intimately attached to the ST ligament, exerts a shearing effect as it extends the hip while the pelvic floor is forced inferiorly during the Valsalva maneuver.
The greater sciatic notch provides egress for the piriformis muscle. The pudendal nerve exits the pelvis at the inferior aspect of this muscle. In the athlete, flexion and abduction of the thigh are common motions, and they may lead to hypertrophy of the piriformis muscle. If the sciatic notch is narrowed because of the posterior orientation of the ischial spine, the cross-sectional area of the greater sciatic notch is reduced. Concomitant hypertrophy of the piriformis muscle may cause compression of the pudendal nerve against the posterior edge of the SSp ligament. Pain that suggests this process includes the pain that is induced during sports activity such as that of a baseball catcher (squatting and rising to throw the ball—motions that require extension of the gluteus muscle and abduction and extension of the hip). Another graphic example is a Canadian skater no longer able to turn (a motion requiring bending, squatting with 1 leg flexed while extending, rotating, abducting, and then adducting the crossing leg). Remodeling of the border of the sacrum, a broadening of that structure, also narrows the aperture of the greater sciatic notch (Fig. 1).
ISCHIAL SPINE: ONTOGENY, DEVELOPMENT, AND PATHOLOGY
The ischial spine is absent in quadrupeds, and it is largest in hominids (7). The progression to upright posture in bipeds requires increasing development of the musculature of the pelvic floor to assist the sphincters and to prevent evisceration in the erect position. All pelvic floor muscles have a direct or indirect attachment to the ischial spine: 1) The SSp ligament has muscular attachments. 2) The tendinous arch rises from the ischial spine, traverses the fascia of the obturator internus, and attaches to the pubis. 3) The coccygeus muscle may affect the posterior remodeling of the ischial spine during development. The enormous forces required to appose the 2 sides of the pelvic floor during the Valsalva maneuver could well lead to malformation and malpositioning of the ischial spine with dire outcomes leading to PNE syndrome.
The ischial spine develops from a separate ossification center that arises between the ages of 13 and 15 years (8). Ossification is complete between the ages of 23 and 25 years. This interval of development is when youth are involved with athletic pursuits that induce hypertrophy of the pelvic floor muscles and the extenders and rotators of the hip. Palpation of levator ani muscles during digital rectal examination in young athletes reveals thick musculature. (Note that hypertrophy of the pelvic floor muscles can be measured with use of ultrasonography in women performing Kegel exercises.) Thus, in young athletes anatomical changes are established for future chronic pelvic pain syndrome.
These anatomical changes can be evaluated by use of various methods. Judet views of the pelvis highlight the ischial spine and the greater sciatic notch. In symptomatic patients with PNE (chronic pelvic pain syndrome and NIH Category IIIB chronic prostatitis), Judet views of the pelvis show interesting variations. Normative data are being obtained for comparison with these variations. For example, the diameter of the sciatic notch has been measured. The Thoms method is a classic means of pelvimetry in women, and comparative studies in men are available (9). Review of the bony structure of the male pelvis in teaching specimens from medical school anatomy laboratories shows a wide variation (age and weight of decedents are not available) (Pawlina W: Personal communication, May 2001). This variation is consistent with the wide variation of bony pelvic measurements in published literature (9).
Imaging techniques that permit 3-dimensional reconstruction of the pelvis have been used to evaluate pudendal artery abnormalities (10). With 3-dimensional reconstruction, one may be able to measure the positional variation of the ischial spine over the ischial tuberosity and the distance between the ischial spine and the sacrococcygeal notch.
The radiographs in Figures 1 through 3 are representative of those of many of the patients in our study group. Figure 1 is a radiograph of the pelvis of a man with unilateral symptoms of PNE. Note the “normal” ischial on the right and the elongated, broad ischial spine on the symptomatic left side. The radiograph in Figure 2 is from a patient with exstrophy of the bladder and diastasis of the pubic rami who presented with severe symptoms of pelvic pain due to malignancy.
Significant abnormalities of each ischial spine relate to the requirements of pelvic floor musculature to respond to congenital or acquired deformities, resulting in the remodeling of the bones in the absence of athletic activities. For example, a businessman presented with 12 years of severe penile pain originally induced by straining during bowel movements. He had a history of 55 years of chronic constipation. A radiograph of his pelvis (Fig. 3) shows broad, stubby ischial spines similar to those in the man with exstrophy of the bladder (Fig. 2).
A female dancer and dance instructor, age 73 years, had severe pain after a 1,300-km automobile trip. She has abnormal ischial spines (not illustrated) similar to those in Figure 3, which are thought to be associated with repetitive flexion and extension of the hip joint and associated pelvic floor contraction required in her artistic endeavors.
Chronic pelvic pain is often caused by a compression neuropathy of the pudendal nerve. The bony remodeling as a result of the activity of pelvic floor muscles leads to juxtaposition of the SSp and ST ligaments which compress the pudendal nerve in the narrowed interligamentous space. Elongation of the ischial spine in response to the same muscular forces presents an additional site for repetitive microtrauma of the pudendal nerve.
Future attention must be paid to 1) the transverse diameter of the ST and SP ligaments which compress the pudendal nerve 2) the dimensions of the greater sciatic notch (diameter and depth), correlated to age, weight, and body habitus; 3) the cross-sectional area of the greater sciatic notch and the piriformis muscle; and 4) sequential pelvis x-rays in youthful and maturing athletes to measure changes in position and appearance of the ischial spine.
Development of this information should aid in the definition and proper treatment of chronic pelvic pain syndrome, which affects a significant percentage of men, is a medical economics drain, and is a personal tragedy with occasional fatal outcomes due to suicide. Chronic pelvic pain syndrome in women should be studied in a similar manner. Application of the same principles in women is of paramount importance lest vulvodynia and other syndromes continue to be misdiagnosed and inappropriately treated.
1. Robert R, Prat-Pradal D, Labat JJ, et al: Anatomic basis of chronic perineal pain: role of the pudendal nerve. Surg Radiol Anat 20: 93-98, 1998
2. Shafik A: Pudendal canal syndrome: a new etiological factor in prostatodynia and its treatment by pudendal canal compression. Pain Digest 8: 32-36, 1998
3. Amarenco G, Lanoe Y, Perrigot M, Goudal H: A new canal syndrome: compression of the pudendal nerve in Alcock’s canal or perineal paralysis of cyclists [French]. Presse Med 16: 399, 1987
4. Tetzschner T, Sorensen M, Lose G, Christiansen J: Pudendal nerve function during pregnancy and after delivery. Int Urogynecol J Pelvic Floor Dysfunct 8: 66-68, 1997
5. Roberts RO, Lieber MM, Bostwick DG, Jacobsen SJ: A review of clinical and pathological prostatitis syndromes. Urology 49: 809-821, 1997
6. Krieger JN, Nyberg L Jr, Nickel JC: NIH consensus definition and classification of prostatitis. JAMA 282: 236-237, 1999
7. Elftman HO: The evolution of the pelvic floor of primates. Am J Anat 51: 307-346, 1932
8. Abitbol MM: Evolution of the ischial spine and of the pelvic floor in the Hominoidea. Am J Phys Anthropol 75: 53-67, 1988
9. Letterman GS: The greater sciatic notch in American whites and negroes. Am J Phys Anthropol 28: 99-116, 1941
10. Kawanishi Y, Lee KS, Kimura K, Kojima K, Yamamoto A, Numata A: Feasibility of multi-slice computed tomography in the diagnosis of arteriogenic erectile dysfunction. BJU International 88, 390-395, 2001
Abstract accepted for presentation (poster): Western Section AUA October 2002.
Therapeutic injections of the pudendal nerve define the symptoms of noninflammatory chronic pelvic pain syndrome.
Antolak SJ, Hough D, King Maus T, Vrtiska Pawlina W.
Trauma to the pudendal nerve by friction, compression, and direct blunt trauma causes protean complaints including somatic and autonomic sensory and motor dysfunction. Robert describes pudendal neuralgia/entrapment as perineal pain aggravated by sitting, reduced when standing, not present recumbent and relieved sitting on a toilet seat. Pelvic pain is a “boundary disease” addressed by different specialties as proctalgia, vulvodynia, coccydynia, “prostatitis-like pains”, etc. Adventuresome treatments of suspected “organ disease” fail to address a possible neuritic basis for pelvic pain. Symptomatic responses to pudendal nerve perineural injections (PNPI) are the basis for this report. PNPI is the second intervention in a planned three-phase program that includes self-care (perineal hyperprotection) and decompression of the pudendal nerve.
Inflammatory / bacterial prostatitis is ruled out. The males have noninflammatory prostatitis—NIH category IIB chronic prostatitis/chronic pelvic pain syndrome (CPPS). All patients have had normal MRI of the spine and CT or MRI of the pelvis. Urodynamic study and cystoscopy were performed as indicated. EMG of the ischiocavernosus and bulbocavernosus muscle is recommended. Pudendal nerve terminal motor latency testing is no longer available (lack of normative data). History of youthful athletics and review of sitting, cycling and exercise flexion trauma is recorded. Bladder, erectile, ejaculatory and rectal symptoms are sought. Examination includes pinprick testing of three pudendal nerve sites bilaterally and compression of the pudendal nerve at two sites bilaterally (Tinnel’s sign). A series of three PNPI of bupivacaine and dexamethasone are performed at six-week intervals using CT guidance. NIH Chronic Prostatitis Symptom Index is used for recording pain levels. Skin sensation is measured 1-2 hours after injection.
Most patients have a history of active high school sports, adult jogging, cycling and gymnasium workouts requiring repetitive hip flexion. Symptom onset is usually insidious, difficult to identify and occurs 1-2 months after initiation of trauma. A single precipitating event such as squatting to lift a heavy object or prolonged cycling may be identified. Irritable bladder complaints precede pain. Primary and secondary pain sites vary according to which branch(es) is affected. The sites in order of prevalence are: scrotum, perineum, penis/urethra, anus, and coccyx. Sensory abnormalities are identified in 55.8% of men. EMG abnormalities are found in 14/41 (34%) of men.(data on females not available). Autonomic dysfunction, manifested by erectile and ejaculatory problems, and voiding and rectal dysfunction in both sexes may improve dramatically. Responses to PNPI vary but confirm the role of pudendal neuralgia. Reduction of pain correlates with the adequacy of anesthesia response. Self-catheterization for urinary retention is discontinued when voiding normalizes.
“ … During this age the ischial spine (IS) is forming. Because of action of the pelvic floor muscles, bone remodeling occurs, resulting in elongation and posterior orientation of the IS. Members of the Western Section have demonstrated the effects of pudendal nerve anesthetic dating back to the work of Comar and Bors and later Tanagho and more recently Doctor R.A. Schmidt. Review of the work of these physicians indicates that anesthesia in the pudendal distribution is obtained with perineural injections that the injecting needle touching the pudendal nerve will induce “radiculopathies in the pudendal distribution” and a clamp like contraction of the anal sphincter is demonstrative of adequate placement of the needle.
Doctor John Bascom, a colorectal surgeon in Oregon, and a group
of radiologists used a TENS unit with an insulated needle to stimulate
the pudendal nerve prior to PNPI in a small number of patients.
The marked anatomical variation of the pudendal nerve noted by Austrian
researchers will explain the difficulty of consistent patient response
and will also explain the variability of patient complaints. “