Pelvic Pain Syndromes

Several organic and functional disorders of the urinary bladder, reproductive tract, anorectum, and the pelvic floor musculature cause pelvic pain. This article describes functional disorders in which chronic pelvic and anorectal pain cannot be explained by a specified pathology. Currently, these functional disorders are classified into urogynecologic conditions (ie, chronic prostatitis and chronic pelvic pain syndrome [CP-CPPS] or interstitial cystitis and painful bladder syndrome [IC-PBS]); anorectal disorders (ie, proctalgia fugax); and the levator ani syndrome. Although these disorders are defined by predominant pain, they can be associated with functional disturbances (ie, disordered voiding or defecation).  Although this nomenclature suggests that these conditions are distinct, there is considerable overlap of their symptoms, which is perhaps inevitable because the urogenital tract and anorectum are in proximity and intimately related to the levator ani, because visceral discomfort is poorly localized, and because pelvic floor dysfunctions can impair urogenital and anorectal functioning. Indeed, these disorders have much in common.

“Neurogenic” Pelvic Pain Syndrome

It is through the culmination of an accumulating body of scientific literature, failures in traditional treatments, and improved dialogue between health care professionals frustrated with treating mysterious chronic pelvic syndromes not amenable to allopathic care that the term “Neurogenic” Pelvic Pain Syndrome derives its name. This article will postulate a common neurological or neuromusculoskeletal etiology for a grouping of chronic pelvic pain syndromes.  These syndromes are traditionally considered to be separate entities to which no identifiable pathology exits. The term “Neurogenic” as a grouping for these conditions is pointed to in the growing body of literature that these syndromes may essentially share a common neurological etiology.

PNE, an abbreviation for pudendal nerve entrapment may also represent an abbreviation for a diagnosis Probably Not Entertained. The reason that it is not commonly diagnosed is that it is the mother of all masqueraders. I believe that this diagnostic deception, in the eyes most medical practitioners, stems from two causes. The first is that it is a relatively new diagnosis that was first described by Amarenco in 1987 as the Alcock’s Canal or Cyclists Syndrome, and therefore is a relatively unfamiliar entity. And secondly, the symptoms that it produces fall into the domain of many medical specialists who falsely recognize them as more familiar problems and therefore give them a knee jerk diagnosis-treatment response.

The uninformed are easily deceived because PNE throws out a camouflage screen operating on two levels. The primary level represents the pain created by the nerve compression itself and the second levels are the symptoms created by the muscles dysfunction brought about by the compressed and damaged nerve. And it is this secondary muscle dysfunction that adds to the source of the diagnostic confusion. Since the pudendal nerve innervates the muscles of the pelvic floor which includes the urinary and anal sphincters, nerve compression not only causes pain, but also causes increased muscle tension which is transferred to the penetrating organs i.e. the urethra, vagina, and rectum. This increased muscle tension causes symptoms in the organs, as well as the muscles themselves. When this muscle tension exceeds a certain threshold, the muscles develop myofascial trigger points. Complicating the matter even more is that these local trigger points refer the pain to more distant areas.

Now you can begin to understand the practitioner’s dilemma. They are presented with the same symptom complexes as seen with myofascial dysfunction in its disguise as visceral disease i.e. urinary hesitancy, urgency and frequency, interstitial cystitis, prostatodynia, anal pain, scrotal pain, orgasmic pain, and pain with sitting. However, even if the disguised muscle component is recognized, the underlying and driving force is different than that usually seen with myofascial trigger points.

Fortunately, this dilemma can easily be solved by asking some simple questions. Is the pain initiated or worsened with sitting and lying on the affected side? Is the pain improved with standing and when sitting on a toilet seat?

However when these questions are not asked and the diagnosis is not entertained patients begin to receive the “standard treatments’ for (a) nonbacterial /bacterial prostatitis, prostatodynia, or orchialgia with long term antibiotics, anti-inflammatory medication or surgery. (b)Vulvar pain with antifungals, laser surgery, laproscopy to rule out endometriosis, or a hysterectomy. (c) Or for a diagnosis of levator ani syndrome, coccygodynia and proctalgia a treatment course of high voltage galvanic stimulation,
hemmorhoidectomy, anal sphincterotomy, coccygectomy, or Botox injections.

Therefore, it is no wonder that the time to the diagnosis of PNE is a mean of 4 years (1-15 yrs); have seen 10-30 M.D.s; and have suffered innumerable invasive and noninvasive procedures; and have developed significant central and peripheral sensitization with the concomitant allodynia, hyperalgesia ; and have developed an attitude of hopelessness and have become markedly depressed to the point of committing suicide.

Why does PNE occur? In general, it is the result of our pelvic floor anatomy in which the pudendal nerve both follows a tortuous course that leaves it exposed to damage by ligaments, fascia, and muscles, and has a position inside of the ischial tuberosities that leave it vulnerable to direct trauma. However, there must be more specific reasons otherwise every bicycle rider would develop PNE. Possibilities that increase the likelihood of developing PNE are (1) the wider pelvis seen in women who have a 3:1 incidence over men. (2) genetic variations in the nerve course and pelvic muscle structure (3) or developmental changes in the muscles and pelvic bones.

Dr. Stanley Antolak attributes many cases of entrapment, especially in athletes, to the remodeling of the ischial spine. Flexion exercises of the hip from such activities as cycling and squats in early years can result in a pull on the ischial spine by the hypertrophied pelvic floor muscles. These forces will cause a rotation of the sacrospinous ligament causing it to override the sacrotuberous ligament, thus acting like a “lobster claw” which pinches the traversing pudendal nerve. The remodeling also causes the pudendal nerve to traverse a longer course making it more vulnerable to squats, sitting, or standing from a seated position. This results in an additional site for repetitive micro trauma of the pudendal nerve as it curls around the ischial spine.

Why the Bladder/Prostate/Visceral Symptoms?

The visceral branches arise from S3 and S4 and occasionally S2 and go to the bladder, rectum, and vagina and communicate with the sympathetic plexus. Muscle branches S4 supply the levator ani, coccygeus, and external anal sphincter. Injuries to the nerve supply to these areas causes symptomatology that resembles infective or inflammatory processes of pelvic viscera, thus is often misdiagnosed as Chronic Prostatitis and Interstitial Cystitis. Thus, by the time we treat these patients, they have often received many rounds of antibiotics and anti-inflammatories.  Furthermore, altered innervation to the sympathetic and somatic sphincter of bladder can cause incomplete emptying, which is a common cause of infection.  Perhaps this nerve entrapment creates an environment which allows the infective process to take hold.  And it is these secondary infective processes that are mere manifestations and reinforcing contributors to a primary functional and anatomical impairment or pathology.

A changed inflammatory local environment and pelvic muscular dysfunction could explain some symptoms observed in CP/CPPS patients. Indeed, urodynamic studies have confirmed that most of the lower urinary tract symptoms are highly related to pelvic muscular disorders, which could be associated with local inflammation.

The prevalence of prostatitis is extremely high, with vast majority belongs to National Institutes of Health Category III: Chronic Prostatitis (CP)/Chronic Pelvic Pain Syndromes (CPPS). The etiology of CP/CPPS is noninfectious, with no precise mechanisms has been elucidated to date.

There is no sufficiently validated therapy for chronic pelvic pain syndrome (CPPS). The functional CPPS-like symptoms, such as disturbances of micturition and erectile function (EF), can have a crucial diminishing effect on quality of life (QoL) that may be even greater than the pain itself. The pathophysiology is almost entirely unknown. Previous infections, pelvic floor hypertension, local chemical alterations, and perfusion disturbances are under discussion. Even the role of the prostate in CPPS is questionable. because women can also develop CPPS-like symptoms.


Table 2. The new NIH consensus classification of prostatitis (Krieger et al. 1999)
Category   Clinical findings
I   Acute bacterial prostatitis
II   Chronic bacterial prostatitis
III   Chronic prostatitis/chronic pelvic pain syndrome
    A Inflammatory
    B Noninflammatory
IV   Asymptomatic inflammatory prostatitis

We postulate that category III B is a symptomatic manifestation of another specific entity; PNE and/or other myofascial mechanical dysfunction of the pelvic floor and lumbopelvic region. It is this somatovisceral and visceral-somatic interaction may be the primary culprit to chronic pelvic pain syndromes, to which no other defined or identifiable pathological etiology exists. We submit the term “neurogenic prostatitis” is an appropriate terminology. Furthermore, the term “neurogenic” could be applied to other pelvic pain syndromes of similar etiology (with neuromuscular and biomechanical origins), such as Interstitial Cystitis (IC).



There is no sufficiently validated therapy for chronic pelvic pain syndrome (CPPS). The functional CPPS-like symptoms, such as disturbances of micturition and erectile function (EF), can have a crucial diminishing effect on quality of life (QoL) that may be even greater than the pain itself. The pathophysiology is almost entirely unknown. Previous infections, pelvic floor hypertension, local chemical alterations, and perfusion disturbances are under discussion. Even the role of the prostate in CPPS is questionable, because women can also develop CPPS symptoms.

Treatment:

Physiotherapy, trigger-point massage, electromagnetic treatment, and acupuncture have already been used for CPPS with varying success. Orthopaedic pain syndromes, fractures, and wound healing disorders are successfully treated by low-energy extracorporeal shock wave therapy (ESWT). Shock waves could reduce passive muscle tone and improve the range of movement in upper-arm contractures caused by stroke. Ischaemic dysfunctional myocardial areas could be reperfused by local application of shock waves]. In an initial feasibility study, we were able to show that shock waves are easily applicable by perineal approach without side-effects, achieving significant improvement of CPPS-related symptoms, particularly with regard to pain.

Generally, the effects of extracorporeal shock waves on living tissue consist of transformation of mechanical signals into biochemical or molecular-biologic signals that again induce particular alterations within cells (mechanotransduction).
Many possible ESWT effects are currently under discussion: Hyperstimulation of nociceptors and interrupting the flow of nerve impulses could lead to pain alleviation. ESWT is able to increase local microvascularisation as well as reduce muscle tone and spasticity.

Shock waves can possibly influence the neuroplasticity of thehumanpainmemory: The prolonged lack of effective pain therapy could lead to a reinforcement of negative impulses (pain) in the brain. Long-term fixation of these impulses could result in the development of a particular pain memory. By triggering minimal pain impulses, ESWT could break this negative-conditioned pain memory by resetting the pain- an approach based on the neuron-holographic brain model. It defines the healing effects of ESWT by selective erasing of pathologic reflex patterns and might explain the possibility of influencing areas of pain localised at a distance from the treatment locus.

There is a relatively long history of ESWT for painful illnesses of different origins, particularly for chronic plantar fasciitis, which is at present probably the best-evaluated ESWT indication. ESWT could be of significant importance in the treatment of CPPS (type IIIB prostatitis) and PNE because of the straightforwardness of its application and the lack of any appreciable sideeffects. Reults of randomized control trials for CPPS and PNE have demonstrated subjective urination conditions improved significantly for the entire follow-up period of 12 wk.  All patients completed outpatient treatments and follow-ups without any problems. All patients in the ESWT group showed statistically (highly) significant improvement of pain, QoL, and voiding conditions following ESWT in comparison to the placebo group, which experienced a continuous deterioration of the same parameters during the follow-up period. Perineal ESWT was easy and safe to perform without anaesthesia or any side-effects. Improvements in all Quality of Life (QOL) measures were demonstrated in ESWT patients compared to placebo.

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