Curr Urol Rep (2010) 11:261–264 DOI 10.1007/s11934-010-0111-y
Chronic Prostatitis/Chronic Pelvic Pain Syndrome and Pelvic Floor Spasm: Can We Diagnose and Treat? Karin E. Westesson & Daniel A. Shoskes
Published online: 20 May 2010 # Springer Science+Business Media, LLC 2010
Abstract National Institutes of Health category III prostatitis, also known as chronic prostatitis/chronic pelvic pain syndrome, is a common condition with significant impact on quality of life. This clinically defined syndrome has a multifactorial etiology and seems to respond best to multimodal therapy. At least half of these patients have pelvic floor spasm. There are several approaches to therapy including biofeedback, acupuncture, and myofascial release physical therapy. However, the only multicenter study of pelvic floor physical therapy for pelvic floor spasm in men failed to show an advantage over conventional Western massage. We have proposed a clinical phenotyping system called UPOINT to classify patients with urologic chronic pelvic pain and subsequently direct appropriate therapy. Here, we review the current approach to category III prostatitis and describe how clinical phenotyping with UPOINT may improve therapy outcomes. Keywords Prostatitis . Chronic pelvic pain syndrome . Pelvic spasm . Myofascial release
Introduction Prostatitis is a common condition accounting for 2 million outpatient visits per year costing $84 million for its treatment [1]. The community standard of care for this condition is abysmal, with considerable frustration amongst both primary care physicians and urologists [2]. Based on a consensus K. E. Westesson : D. A. Shoskes (*) Glickman Urological and Kidney Institute, Cleveland Clinic Foundation, The Cleveland Clinic, 9500 Euclid Avenue, Desk Q10-1, Cleveland, OH 44195, USA e-mail: dshoskes@gmail.com
conference, a National Institutes of Health (NIH) panel proposed a syndrome-based classification of the disorder [3]. Category I is acute bacterial prostatitis, typically presenting with a febrile urinary tract infection (UTI). Category II, the old chronic bacterial prostatitis, is defined as recurrent UTI in which the causative bacteria can be recovered from the prostate fluid between symptomatic episodes. Category III is chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), defined as having characteristic symptoms of pain, lower urinary tract symptoms (LUTS), and often erectile dysfunction, but without evidence of UTI. Category IV is asymptomatic, with inflammation found on biopsy of the prostate or semen analysis for other indications. Much research over the past 15 years has focused on CP/ CPPS, which is both the most common symptomatic form of prostatitis and the most challenging to treat. Unfortunately, therapy is invariably prolonged multiple courses of antibiotics without cultures or consideration of prior response [4]. The common failure of this approach has prompted examination of other possible etiologies to explain the symptoms of CP/ CPPS and to direct therapy. Such etiologies may include autoimmunity [5], dysfunctional voiding [6], stress [7], and neurologic changes typical for a systemic chronic pain syndrome [8]. A significant extraprostatic factor in generating pain in many men with CP/CPPS is pelvic floor spasm. This muscular spasm alone can produce and mimic the pain and LUTS of CP/CPPS. We will review the role of pelvic floor spasm in patients with CP/CPPS, including its incidence, diagnosis, and possible therapy.
Pelvic Floor Spasm and CP/CPPS In 1979, Segura et al. [9] raised the question whether some patients with “prostatosis” actually had pelvic floor tension
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myalgia. In the 1980s, myofascial pain syndromes, which had the features of skeletal muscle spasm and trigger points, hyperirritable, sensitive, tender spots within a tight band of skeletal muscle or fascia, were recognized [10]. Importantly, the location of the trigger point may be different from the location of the pain that it triggers [11]. Common treatments for myofascial pain and trigger points include analgesics, anti-inflammatories, physical therapy, biofeedback, muscle relaxants, direct anesthetic injection, and acupuncture [12]. In the late 1990s, the possibility that pelvic muscle spasm and trigger points may be involved in the symptom generation of CP/CPPS was explored by several groups; in particular, by Dr. Berger at the University of Washington and Dr. Anderson at Stanford University. Kaplan et al. [13] demonstrated that contraction of the external sphincter during voiding could explain the urinary symptoms in some men with CP/CPPS, and that symptoms could improve with biofeedback. Berger et al. [14] compared muscle tender points in 62 patients with CP/CPPS with 98 control men. They found patients with CP/ CPPS to have more extensive tender points and that these were not specific to the prostate [14]. Anderson et al. [15••] mapped the relationship between muscular trigger points and the location of pain symptoms in 72 men with CP/CPPS [15••]. They found that internal and external muscle trigger points in the pelvis and abdomen reproduced pain in the penis, perineum, rectum, testicle, and groin [15••]. In the only multicenter study of muscle tenderness and CP/CPPS, 384 men with symptomatic CP/CPPS were compared with 121 pain-free controls in seven clinical centers [16•]. Overall, 51% of patients with CP/CPPS and 7% of controls had tenderness at any tested site. The most common site was prostate (41% CP/CPPS; 5% controls), followed by external and internal pelvic floor (13% and 14% CP/CPPS, respectively; 0 controls) and suprapubic area (9% CP/CPPS; 0 controls). Tenderness did not correlate with inflammation or bacterial infection in the prostate fluid. Patients with CP/CPPS with any tenderness had significantly higher symptom severity at baseline and 1 year later. While these studies demonstrate an association between CP/CPPS and muscle tenderness, they do not prove causality in either direction. It is possible that some patients have primary muscle spasm as their first and only etiology, and that trigger points lead to referred pain throughout the genitourinary system. It is also possible that local prostate tenderness, whether through infection or inflammation, causes reactive secondary muscle spasm. In the first circumstance, relieving the muscle spasm should resolve the symptoms. In the second, muscle spasm therapy could give some relief, but ongoing prostatic pathology would maintain baseline symptoms and lead to recurrence once therapy stopped. To use an extreme analogy, muscle relaxants and physical therapy can improve neck muscle spasm, but not if it is caused by meningitis.
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Therapy of Muscle Spasm in CP/CPPS Several approaches directed at pelvic and abdominal muscle spasm have been used to improve the symptoms of CP/CPPS, although most are small, single-center, and not placebo- or sham-controlled. Biofeedback has been used to improve both pain and voiding. In a pilot study, Nadler et al. [17], using biofeedback and bladder retraining, found pain reduction in 8 of 11 patients with CP/CPPS. Cornel et al. [18] showed a reduction in symptom severity and pelvic floor muscle tonus with biofeedback using a rectal electromyographic probe in 33 patients. He et al. [6] showed reduction of symptoms in a study of 21 patients with CP/CPPS following pelvic floor biofeedback. Acupuncture has been used for the treatment of trigger points in myofascial pain syndromes, although it is not clear whether the effect is specific for the muscle spasm or through other pain pathways. Nevertheless, several studies have shown symptom improvement in CP/CPPS following acupuncture. In an open-label study of 97 patients using acupuncture, 92% had a minimum 50% improvement in total symptoms score [19]. Lee et al. [20] reported on a prospective, randomized, sham-controlled trial of twice weekly acupuncture over 10 weeks. They found significant improvement in 73% with active treatment versus 47% in the sham group. In a similar study using electroacupuncture, the active treatment group appeared superior for symptom improvement to sham therapy or supportive measures alone [21]. Myofascial release is a technique of direct stretching, lengthening, and massage of trigger points and muscle spasm. Anderson et al. [22] examined myofascial trigger point release and paradoxical relaxation training as treatment for men with CP/CPPS. Myofascial trigger point release was performed by a physiotherapist. Each trigger point was palpated and pressure was held for 60 s. Voluntary contractions and release/hold-relax/contract-relax/reciprocal inhibition were also used. These therapy sessions were given weekly for 4 weeks and biweekly for 8 weeks. Paradoxical relaxation training, a way of autonomic self-regulation, was given at weekly intervals for 8 weeks. Treatment with these two methods was considered a success in 72% of patients, with success being defined as patients reporting moderate to marked improvement in symptoms. Success was even seen in patients with long-standing disease refractory to other modes of therapy. In a separate report using the same technique, sexual dysfunction, which is common in CP/ CPPS patients despite the relatively young age of prevalence, improved significantly with myofascial release therapy [23]. A major barrier for the scientific study of this technique is bias caused by the operator-dependent nature of both diagnosis and therapy, which can be eliminated through sham therapy and participant blinding. As a pilot to address these issues, an NIH-sponsored study compared myofascial release physical
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therapy to global therapeutic massage in 48 patients with either CP/CPPS (23 men) or interstitial cystitis (24 women) in six clinical centers [24••]. The study did show that it was feasible to perform a multicenter study with standardized assessment and outcomes; however, there was no clinically or statistically significant difference in outcome for the male patients. Clearly, many men suffering from CP/CPPS have pelvic floor spasm as a contributing factor to their symptoms, and there are several therapeutic approaches aimed at myofascial release and trigger point resolution that can improve pain, LUTS, and erectile dysfunction. Pelvic floor spasm, however, is usually one of several mechanisms contributing to CP/ CPPS, and musclecentric therapies may be insufficient to resolve the problem. Indeed, most large placebo- or shamcontrolled multicenter studies of any form of monotherapy have failed to show clinical and statistical improvement in CP/ CPPS [25]. Given the superior outcomes typically seen with multimodal therapy, it is more likely that treatment of pelvic floor spasm will be most efficacious in conjunction with other therapies that treat the specific phenotype of the patient.
Pelvic Floor Therapy as Part of Multimodal Treatment in CP/CPPS Given the heterogeneous nature of CP/CPPS and the necessity to individualize therapy based upon the patient’s etiology and current pathogenic mechanisms, a clinically relevant classification system is required beyond the current syndrome designation of category III prostatitis. We have proposed a 6-point clinical phenotyping system to classify patients with urologic chronic pelvic pain and subsequently direct appropriate therapy [26]. The clinical domains are urinary symptoms, psychosocial dysfunction, organ specific findings, infection, neurologic/systemic, and tenderness of muscles. These domains produce the mnemonic UPOINT. Each domain is clinically defined, linked to specific mechanisms of symptom production or propagation, and associated with specific therapy. The domains are summarized in Table 1. We have previously shown that the number of UPOINT domains is associated with symptom duration and severity in both CP/CPPS [27] and interstitial cystitis [28]. Others have confirmed a correlation between the NIH Chronic Prostatitis Symptom Index (CPSI) and the number of UPOINT domains in CP/CPPS [29]. In our retrospective study of 90 men with CP/CPPS, the percent of patients positive for each domain was urinary 52%, psychosocial 34%, organ specific 61%, infection 16%, neurologic/systemic 37% and tenderness 53%. There was a significant stepwise increase in total CPSI score as the number of positive domains increased. It is our belief that treatment selection based upon the UPOINT phenotype would have the highest chance of
263 Table 1 Domains of UPOINT Domain
Diagnostic criteria
Urinary CPSI Urinary Subscore > 4, urgency, frequency, nocturia Psychosocial Depression, catastrophizing Organ specific Prostate tenderness, WBC in prostatic fluid, hematospermia, prostatic calcifications Infection Exclude patients with category I and II prostatitis, Gram-negative bacilli, enterococcus localized to prostatic fluid Neuro/systemic Pain beyond abdomen, pelvis, irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome Tenderness Palpable muscle spasm, trigger points in abdomen, pelvic floor CPSI—NIH Chronic Prostatitis Symptom Index; WBC—white blood cells
improving symptoms while not overtreating with unnecessary interventions. In a recently completed prospective study, we treated 100 patients with CP/CPPS with multimodal therapy, offering specific therapy for each positive domain (eg, urinary: α-blocker or antimuscarinic; psychosocial: stress reduction/ psychologic support; organ specific: quercetin; infection: antibiotic; neurologic/systemic: amitriptyline or pregabalin; tenderness: pelvic floor physical therapy) [30]. With a minimum follow-up of 6 months and average follow-up of 50 weeks, 84 patients (84%) reached the primary endpoint of a 6-point or greater improvement in total CPSI. The chance of reaching the primary endpoint was not significantly different regardless of number of positive domains (1 domain 100%; 2 domains 94%; 3 domains 80%; 4 domains 75%; 5 domains 83%; P=0.89). A 50% or greater improvement in total CPSI was found in 51 patients, while 84 patients had at least a 25% or greater improvement. All CPSI subscores were significantly improved from baseline. The improvement seen in all groups was not simply due to regression to the mean of more symptomatic patients, since number of UPOINT domains did not correlate with drop in CPSI (Spearman’s rho=0.034; P=0.74). In addition, drop in CPSI did not correlate with symptom duration or number of therapies. Furthermore, there was no correlation between CPSI drop and the difference between the number of UPOINT domains and number of therapies (P=0.63). While this was not a placebo-controlled study, the incidence and magnitude of improvement was significantly higher than reported in prior large or multicenter studies of comparable duration.
Conclusions CP/CPPS is a common and morbid condition with poor outcome to typical monotherapies. Pelvic floor spasm as evidenced by myofascial tenderness and trigger points is present in at least 50% of patients with CP/CPPS, and
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therapy directed at this spasm can improve all types of CP/ CPPS symptoms. We propose that integration of pelvic floor physical therapy into a multimodal treatment plan driven by the patient’s specific clinical phenotype would have the greatest chance for success.
Disclosure Dr. Daniel Shoskes is an advisory board member for Furr Labs and a clinical trial participant for Pfizer. No other potential conflicts of interest relevant to this article were reported.
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