The Prostatitis Foundation

1999 Selected Abstracts from American Urological Association annual meeting
Chronic Prostatitis: A Myofascial Pain Syndrome?


Dirk-Henrik Zermann, MD, Manabu Ishigooka, MD, Ragi Doggweiler, MD, Richard A. Schmidt, MD
University of Colorado Health Sciences Center, Denver.

[Infect Urol 12(3):84-88, 92, 1999. ]

Chronic abacterial prostatitis with associated pain remains a diagnostic and therapeutic challenge. Although the focus is most commonly a bacterial etiology, given the often unsuccessful results of antimicrobial therapy to relieve symptoms, it is reasonable to ask whether chronic pelvic pain syndrome may be a consequence of a functional disease within the pelvis. An analysis of clinical and urodynamic findings in 103 men with a complaint of chronic prostatitis-chronic pelvic pain was carried out with a neurourologic focus to evaluate the role of pelvic floor dysfunction as a cause of symptoms. All patients included in this study had negative microbiologic tests before entering the study group. A significant number of the men had neurologic dysfunction.

Men with pain in the genitourinary tract, a common problem, are generally given a descriptive diagnosis such as orchialgia, chronic abacterial prostatitis, or prostatodynia. The latter 2 terms have historically been used to classify benign prostatic disorders.[1] These classifications have helped to provide guidelines for antibiotic therapy in prostatic diseases. However, these same classifications have not adequately explained neurologic pain mechanisms or defined potential therapies to relieve symptoms in men with pelvic pain syndromes. Thus, the National Institutes of Health (NIH) recently redefined the categories of prostatitis (Table I).[2]

Male voiding dysfunction is often associated with discomfort or pain in the suprapubic or perineal region, testes, tip of the penis, and low back area. Neural dysregulation of the lower urinary tract could manifest as symptoms of frequency and urgency.

Much of the research regarding prostatitis syndromes has centered around microbiology as an etiology. Investigations have focused on cultures of prostatic secretions and polymerase chain reaction to identify various organisms responsible for inflammation in the prostate.[3-5] Most patients continue to be treated with repeated antibiotic regimens without significant relief.[6-8]

In recent years, alpha-blockers, because they act on smooth muscle of the bladder neck and prostate, have been found to be therapeutically useful in prostatitis syndromes.[9] Furthermore, investigations show a correlation between symptoms of prostatitis and those of bladder dysfunction.[10,11] Additionally, although infection is not a prerequisite for symptoms, it is possible that the presence of an infectious organism results in an immune reaction causing inflammation and subsequent pain and other symptoms.

Chronic prostatitis-chronic pelvic pain syndrome (CPPS) remains a diagnostic and therapeutic enigma. Thus, other approaches have been utilized to explain and treat this condition. A neurobehavioral perspective is emerging as a plausible basis for diagnosing and treating some patients with CPPS. The current study was conducted to evaluate voiding dysfunction and pelvic pain in 103 men through a retrospective review of symptoms, physical examination, and urodynamic findings.

Patients and Methods
Patients who had been treated at the University of Colorado Health Sciences Center Clinic in Denver for voiding dysfunction and pelvic pain were the subjects of this retrospective review. The clinic functions primarily as a tertiary care center for patients referred with functional disorders of the lower urinary tract. The clinic utilizes a standardized approach with all new patients, including evaluating past medical history with a focus on previous infection or inflammation, surgery, and traumatic events; documenting current pain and dysfunctional voiding behavior; and evaluating other conditions that are potentially related to somatic and autonomic dysregulation.

The clinical examination includes a neurourologic investigation that evaluates the pelvic floor muscles via rectal examination. Voluntary contraction and, by implication, control of the pelvic muscles are assessed. Urodynamic studies are also performed. Sphincter function profiles (microtip catheter) are performed in a staged fashion to record the reflex reactivity of the sphincter to light touch. Sensation experienced by the patient to catheter withdrawal is noted. Hypersensitivity is scored as none, mild, or significant. Basal sphincter tone and behavior are recorded continuously during bladder filling and voiding by keeping the pressure transducer within the external urethral sphincter region. Overall pelvic floor activity is monitored via an intra-anal surface electrode (Dantec, Denmark).

The urodynamic database includes a cystometrogram; uroflow measurement; and measurement of sphincter sensitivity and closure pressures at rest and during active filling; urethral functional length with a full and empty bladder; and the ability of the patient to voluntarily contract and relax the sphincter with a "hold" command.

All study patients had been screened with a urine analysis and culture to exclude a microbiologic basis for symptoms, and cystoscopy or uroradiology to exclude significant morphologic changes within the lower urinary tract.

Between August 1994 and August 1997, 103 patients with the main complaint of pelvic pain of at least 12 months' duration were evaluated (Table II). All patients had undergone extensive urologic and microbiologic evaluation -- as well as several therapeutic attempts without relief of pain -- before being seen at the clinic. All patients were considered to have NIH category IIIb noninflammatory chronic pel-vic pain syndrome. The majority of patients had pain within the perineum and testicular regions.

Findings from a total of 103 men (mean age, 47 years, range, 23-89) were included in the review. The most common lower urinary tract symptoms reported by patients included a slow, weak urinary stream (n=65) and hesitancy and frequency (n=16). Incontinence (n=4) and retention (n=5) were rare. A small percentage of patients reported headache (n=11) and bowel (n=8) and erectile (n=6) dysfunction. One individual reported pain in both feet, the onset and severity of which paralleled symptoms of dysfunctional voiding. Four patients had a history of preexisting neurologic problems: myelomeningocele (n=1), spinal cord malformation (n=2), and Persian Gulf syndrome (n=1). A history of previous surgery was reported in 37 patients (35.9%) (Table III), 25 of whom had no pain before surgery. In these cases, pain began as a consequence of elective or accident-related surgery. Twelve patients underwent surgery specifically to relieve pain (orchiectomy for orchialgia, cystectomy for uncontrollable bladder pain) without success.

Evaluation of the pelvic floor via rectal examination revealed tenderness of the striated muscle in 91 men (88.3%). This myofascial tenderness was always associated with the inability to relax the pelvic floor efficiently either as a single or repetitive effort. Follow-up evaluations confirmed these findings. Although improvements were noted in some patients, rarely did these patients learn to relax and control pelvic muscles.

Eighty-four patients (81.6%) underwent a urodynamic workup. The remaining 19 patients refused a urodynamic evaluation. The principal findings in nearly all patients were: (1) hypersensitivity of the urethra or tenderness in the external sphincter region, (2) a hypertonic sphincter, and (3) dyssynergic behavior with voiding. These findings were scored individually to quantify the degree of muscular dysfunction and hyperalgesia.

The average maximum bladder capacity was 395 mL. Cystometry showed abnormal compliance in 5 patients. Normal compliance was evident in 95% of all patients. Sphincter sensitivity, as evaluated by catheter insertion and movement within the urethra during urethral evaluation, revealed that 10 patients had normal sensitivity, 40 had minimally increased sensitivity, and 34 had markedly increased sensitivity. This was scored using a linear analog scale.

The average functional sphincter length with an empty bladder was 45.7 mm (range, 25-65 mm), and with a full bladder, it was 44.6 mm (range, 24-65 mm). The urethral profile was normal in 12 men (11.7%); 44 (52.4%) showed a dysfunctional/dyssynergic pattern, 10 (11.9%) had an obstructive behavior, and 18 (21.4%) had a combined functional and obstructive pattern. The average urethral sphincter pressure was 81.9 cm H2O (range, 44-117 cm H2O) with the bladder less than 50% filled and 93.6 cm H2O (range, 44-157 cm H2O) with the bladder more than 50% filled.

Uroflow measurements revealed, in general, a decrease of maximum and average uroflow. Peak uroflow was 14.4 mL/sec (range, 4-21 mL/sec; normal = >25 mL/sec). Average uroflow was 8.0 mL/sec (range, 2-15 mL/sec; normal = >11-13 mL/sec).

Conventional approaches to diagnosis and treatment of chronic abacterial prostatitis/CPPS have not adequately relieved the suffering of many men with this condition. Clearly there is a need to investigate other factors that may be involved in or contribute to the generation and maintenance of chronic pain in the male pelvis.[12]

The pelvic organs are uniquely linked to and organized by the nervous system, involving sympathetic, parasympathetic, and somatic innervation.[13] It has been suggested that chronic nociceptive bombardment of central regulatory (micturition) circuits via somatic (pelvic floor) afferents could trigger a cascade of neural events, culminating in neurogenically mediated inflammation.[14] Function of the pelvic floor (striated muscle) directly affects that of the pelvic viscera. It is not surprising, therefore, that chronic pelvic floor dysfunction is often combined with smooth muscle dysfunction of the lower urinary tract, and both may be maintained by upregulated sacral reflexes.

A more complete understanding of the pathophysiologic relationship between chronic pain and striated muscle behavior could lead to prevention and/or more effective therapy for CPPS. Indeed, a review of these data showed that 92.2% of men who presented to the tertiary care center for pelvic pain had dysfunction of pelvic floor muscles. This finding was true regardless of evidence of inflammation (prostatitis, cystitis). It should be noted, however, that this patient population was a selected patient pool and therefore may not reflect the typical patient with CPPS.

Many of these patients responded to modulation-based therapy, such as biofeedback, alpha-blockers, or sacral nerve stimulation[15] after failing therapy with antibiotics and analgesics. This observation would suggest a role for the nervous system in generating and maintaining symptoms of prostatitis and pain.

The central nervous system (CNS) is composed of a balanced (gated) circuitry that appears to be predisposed toward neuronal instability (Fig. 1).[16] Disturbances of the CNS network may cause central dysfunction and dysfunction of peripheral targets -- eg, the lower urinary tract. For example, the relationship between dysfunctional muscle behavior and myalgia has been clearly demonstrated for temporomandibular disorders.[17] These relationships in turn can create changes in central neural circuitry, with resultant permanent change in the way in which nociceptive sensory information is processed (Fig. 2).[18] In the current study, 4 patients had a neurologic disease and pelvic pain. Even if the pelvic floor dysfunction was secondary to neuropathology, the same cascade of changed central processing could be initiated as in a "primary" muscle dysfunction.

Surgical wounding, by its nature, involves an inflammatory reaction as a necessary step toward healing. However, this process is also associated with inappropriate afferent input to the spinal cord. It is known that a large nociceptive barrage of afferent activity delivered to the CNS as a by-product of surgical wounding can be destabilizing to neuronal circuits.[18] This risk increases if the neural regulatory pathways are already in a compromised metabolic state. The mechanisms that determine excitability within CNS circuits, hence the mechanisms that affect the modulation or processing of information (afferent CNS input) on the cellular and molecular level within the CNS, are only partly understood at this time. However, it is an accepted principle that surgery can "wind up" central processing and initiate a chronic pain state.[19] Surgical wounding, as part of therapy, could aggravate symptoms in the long term via these wind-up mechanisms.

Nearly 60% of the study patients had no significant medical history and no apparent anatomic or medical cause that accounted for their chronic pelvic pain. This finding, however, does not exclude the possibility that these patients had a long-standing pelvic floor dysfunction. This could predispose them over time to chronic pain and urinary tract dysfunction because of compromised local immunity related to altered peptide pools (eg, substance P presence or release).[20,21]

The pelvic organs share their innervation with the pelvic floor. Neurons at the level of the spinal cord and the brain stem have broad functions to control and modulate the activity of various pelvic organs. The flooding of nociceptive afferent information (associated with dysfunctional activity within the pelvic floor) into the brain stem nuclei could create a breakdown of normal gating within these centers. A cascade of dysfunctional and autonomic symptoms could follow.

Neuroanatomic studies[22] using the retrograde transneuronal tracer pseudorabies virus have shown a significant overlap of areas within the spinal cord and the brain stem, which are involved in the innervation of perineal muscles of the pelvic floor (ischiocavernosus muscle, bulbospongiosus muscle),[23] external urethral sphincter,[24] urethra,[25] and bladder.[26] Most of the spinal cord labeled neurons belong to areas representing the sympathetic autonomic system. The labeled areas in the brain could be considered to be directly connected with those in the spinal cord. However, it should be emphasized that the premotor autonomic area in the hypothalamus and ventrolateral medulla contains topographically segregated populations of neurons that innervate individual sympathetic preganglionic functional units and control specific patterns of their activity.[27] The periventricular nucleus of the hypothalamus serves as a "master control" for the autonomic nervous system by providing highly specialized innervation to all autonomic relay centers.[28] Pain, once it is established, could be maintained via these central sympathetic pathways.

This thinking is supported by concepts that have emerged from pain research. Changes in central processing, expansion of receptor fields within the CNS, and even cell death have been experimentally induced via noxious inputs to the spinal cord.[29] A compromise of brain stem regulation of micturition (and other pelvic organs) may be possible based on current understanding of neurophysiologic control for structures within the pelvis.[30] The mechanisms that allow for the overfacilitated and permissive communication within the cord and brain stem are not clear, but would be similar to flawed inhibitory gating observed in neuropathic states. This hypothesis is supported by improvement rates of approximately 80% using therapeutic modalities that modulate the pelvic floor function (eg, biofeedback, medication, sacral anterior root stimulation). Spasticity of pelvic muscles could cause urine reflux into prostatic ducts, causing inflammatory reactions.[12] Thus, a neurophysiologic perspective may contribute to our understanding of the pathophysiology of clinical symptoms and supports a modulation-based therapeutic approach.

Given the association of muscle dysfunction and nociception, chronic pelvic pain in some men could be considered a myofascial pain condition that is caused and maintained by central neurogenic mechanisms. The observations reported, as a whole, support the perspective that the bladder and urethral striated muscle, when functionally compromised, are capable of triggering changes within the CNS. These concepts regarding the origin of pelvic pain should be considered when there is dysregulation of pelvic floor activity and traditional clinical approaches fail to explain symptoms. This neurologic perspective requires a more subtle diagnostic evaluation, but can shift emphasis of care toward modulation-based treatments that "wind down" CNS excitability. Based on the possible neuroregulation of CPPS, biofeedback and other modalities of neuromodulation may improve symptoms.

Dr. Zermann is in the Department of Urology, University Hospital at Friedrich-Schiller University in Jena, Germany. Dr. Ishigooka is in the Department of Urology, Yamagata University, Yamagata, Japan. Dr. Doggweiler is in the Department of Urology, University of Tennessee, Memphis. Dr. Schmidt is Professor of Urology at the University of Colorado, Denver.


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