eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions

Chronic Pelvic Pain Syndrome and Prostatodynia

Author: Richard A Watson, MD, Chief of Ambulatory Urology, HUMC Department of Urology, Professor of Surgery (Urology), Department of Surgery, Division of Urology, UMDNJ New Jersey Medical School, Hackensack University Medical Center
Coauthor(s): Robert J Irwin, Jr, MD, Chair, Harris L Willits Professor, Department of Surgery, Division of Urology, University Hospital, University of Medicine and Dentistry of New Jersey
Contributor Information and Disclosures

Updated: Jul 17, 2009

Introduction

Background

The term prostatodynia, or chronic pelvic pain syndrome (CPPS), is used to designate unexplained pelvic pain in men; this pain is associated with irritative voiding symptoms and/or pain located in the groin, genitalia, or perineum in the absence of pyuria and bacteriuria (no pus cells or bacteria seen on microscopic analysis of the urine). However, excess WBCs or bacteria seen on Gram stain and culture of expressed prostatic secretions (EPS) may be found.

The use of the term prostatodynia is not encouraged in current practice. This term carries the negative historical connotation of being a "wastebasket" designation for a melange of psychosomatic symptoms and suggests that the source of the patient's symptoms invariably lies within the prostate gland itself. Current research has provided evidence of numerous extraprostatic considerations, including neuropathic and other systemic pathologies.

An academic distinction is currently made between (1) patients with excess WBCs in their prostatic secretions (chronic nonbacterial prostatitis, class IIIa) and (2) those with normal prostatic secretions (prostatodynia, class IIIb). However, the clinical value of this distinction is now being challenged. The sole parameter is the number of WBCs seen within a smear of prostatic secretions. However, this number may vary widely within the same specimen and even more so from sample to sample taken from the same patient. Furthermore, asymptomatic control patients devoid of any evidence of pelvic pathology have also been found to have a significant number of WBCs in their prostatic secretions. At present, the distinction seems to provide no meaningful differential with respect to either etiology or treatment options.

Pathophysiology

Pontari and Ruggieri's comprehensive 2004 update reviews the numerous pathophysiologic mechanisms implicated as the potential etiology of CPPS. After surveying all of the relevant articles on this topic published from 1966-2003, these researchers reached the following conclusions:¹

• The etiology (or etiologies) of CPPS remains unknown.
• The number of WBCs (pus cells) found in the prostatic fluid under microscopic examination—long considered the hallmark of this disease process—does not correlate with the degree of pain or with other symptoms experienced by patients with CPPS. Histological signs of inflammation were found in only one third of all patients diagnosed with CPPS who underwent prostatic biopsy, further suggesting an extraprostatic etiology for CPPS. Perhaps CPPS—so-called chronic prostatitis (CP)—is not directly associated with the prostate or with inflammation within it, at least in some cases.
• Special signaling molecules called cytokines, which are produced by WBCs (and by other cells), may play a role. While certain cytokines stimulate an inflammatory reaction, others inhibit inflammation. Moreover, the same cytokine may act as either an inciting influence or an inhibiting influence at different sites under varying conditions. Tissue necrosis factors, interleukins, interferons, and epithelial neutrophil-activating factors are but a few of these cytokines. To complicate matters, each of these terms indicates a whole, separate family of closely related molecules, not a single agent. An imbalance in this complex network of cytokines (ie, of proinflammatory cytokines and endogenous cytokine inhibitors) has been linked to the development of pelvic inflammation and pain in patients with CPPS.
• Genetic predisposition to CPPS may be the result of differences in DNA sequences at chromosomal sites that regulate the production and action of these various cytokines.
• Autoimmunity, the abnormal tendency of the body to react against itself, has long been thought to play a role in the development of CPPS. In this context, immunity refers to the body's ability to reject foreign material, such as bacteria or toxins. This process can sometimes turn on itself and lead to rejection of the body's own healthy tissues. In CPPS, the body may be attempting to reject its own prostate.
• Testosterone has been shown to protect against inflammation within the prostate. Perhaps a low testosterone level (or, more likely, a breakdown in the mechanism whereby testosterone inhibits prostatic inflammation) may be at work in some men with CPPS.
• Abnormal functioning of the nervous system, at the local level and/or within the CNS, may also play a role in the development of CPPS. For example, a substance known as nerve growth factor (NGF) can cause an increase in the number and the sensitivity of the pelvic nerves that transmit pain. An increase in NGF has been correlated with the development of CPPS symptoms.
• Each of the above factors has been individually identified as a culprit in the causation of CPPS; additionally, at least in some cases, they may interact with each other to cause CPPS. For instance, cytokines may adversely affect the suppression of NGF, which, in turn, leads to a flare of CPPS symptoms.
• Psychological stress and depression have long been associated with CPPS flare-ups. This observation has led some researchers to mistakenly conclude that CPPS is "all in your head” or that such mental stress results in a lower psychological threshold for the same objective degree of pain. More recent data, however, suggest that psychological stress and depression may measurably influence the local production of cytokines (eg, interleukin 10, interleukin 6) in the pelvis, thus directly exacerbating CPPS inflammation.
• Some cases of "abacterial" prostatitis may not actually be abacterial. Recent data suggest that gram-positive bacteria, which have traditionally been dismissed as normal florae in prostatic fluid cultures, may not be so normal in men with CPPS. Normal defense mechanisms allow healthy men to render these bacteria harmless as mere microbial "hitchhikers." However, these defense mechanisms may be defective in men with CPPS. This theory helps explain why prolonged courses of antibiotics sometimes provide symptomatic relief for men with CPPS despite the absence of bacteria that are traditionally considered pathogenic.

Pontari and Ruggieri conclude that "To what degree these factors interact in a given patient and to what degree there is a common pathway or several pathways that lead to the end point of pelvic pain remains to be determined." Clearly, the final answer (or answers) is not yet determined. Opportunities abound for clinical and basic science research in this area.¹

Frequency

United States

CP is the most common urological diagnosis in men older than 50 years and is the third most common diagnosis in men younger than 50 years. This diagnosis results in at least 2 million office visits per year. The average urologist sees approximately 10 patients with prostatitis per month, 30% of whom are new patients. Specific urinary pathogens are detected infrequently after culture. The vast majority of these patients are categorized as having chronic nonbacterial prostatitis or prostatodynia, otherwise known as CPPS in the male.

Age

CP most commonly affects men older than 50 years. It is only slightly less common in men younger than 50 years.

Clinical

History

• Symptoms parallel those experienced by persons with chronic bacterial and nonbacterial prostatitis.
• The typical patient is a young–to–middle-aged man with variable symptoms of chronic, irritative, and/or obstructive voiding accompanied by moderate to severe pain in the pelvis, lower back, perineum, and/or genitalia.
• Erectile dysfunction is the symptom that initially brings many men to seek medical attention; however, the patient often waits until the end of the interview to mention the problem or he may avoid mentioning it at all unless the physician specifically inquires.
• To facilitate history taking and to establish a more uniform standard, a US National Institutes of Health (NIH) collaborative panel has proposed the Chronic Prostatitis Symptom Index (NIH-CPSI). This index is calculated using a series of 9 questions that contain 21 items used to assess patient history in a standardized and quantifiable format.
  • Pain symptoms (4 questions)
    • In the past week, have you experienced any pain (1) between your rectum and testicles, (2) in the testicles, (3) in the tip of the penis, or (4) below your waist?
    • In the past week, have you experienced pain or burning upon urination or pain or discomfort during or after sexual intercourse?
    • How often have you had pain in any of the above areas over the last week?
    • Over the last week, which number (1-10) best describes your average pain or discomfort on the days that you had it?
  • Urinary symptoms (2 questions)
    • Over the last week, how often have you had the sensation of not emptying your bladder completely after you finished urinating?
    • Over the last week, how often have you had to urinate again less than 2 hours after you finished urinating?
  • Impact of symptoms (2 questions)
    • Over the last week, how much have your symptoms kept you from doing the kinds of things you would usually do?
    • Over the last week, how much did you think about your symptoms?
  • Quality of life: If you were to spend the rest of your life with your symptoms just the way they have been during the last week, how would you feel about that?
• The NIH describes 4 categories of prostatitis, as follows:
  • Type I - Acute bacterial prostatitis
  • Type II - Chronic bacterial prostatitis
  • Type III - Chronic abacterial prostatitis, ie, chronic pelvic pain syndrome (CPPS) categorized as either type IIIa (inflammatory CPPS) or type IIIb (noninflammatory CPPS)
  • Type IV - Asymptomatic inflammatory prostatitis

Physical

• No finding is pathognomonic.
  • Examination of the genitalia reveals normal results.
  • Digital rectal examination may reveal a tight anal sphincter. When the anal sphincter tone is hyperactive, a verifiable spastic neuropathy must be excluded. The hyperactivity may otherwise indicate a spasmodic hyperirritability of the pelvic floor musculature, which may be amenable to medical and biofeedback therapies.
  • The prostate and adjacent tissues may be moderately to severely tender, and the gland itself may be slightly congested or boggy. However, the presence of a small, relatively firm gland does not exclude the possibility of CPPS type III. Extreme tenderness upon gentle palpation of the prostate should raise suspicion for acute bacterial prostatitis or even a prostatic abscess.
• The value of this examination is to exclude other diagnoses, such as prostate cancer, chronic urethritis/meatitis, and granulomatous prostatitis.

Causes

• Bacteria
  • An informative review of the possible role for fastidious bacteria (ie, bacteria that cannot be isolated on standard culture media) in the development of chronic prostatitis (CP)/CPPS has recently been presented by a leader in this field, Professor John N. Krieger at the University of Washington.² Among the fastidious organisms that have been implicated are Chlamydia trachomatis, the genital mycoplasmas (ie, Ureaplasma urealyticum, Mycoplasma hominis, Mycoplasma genitalium), a protozoan (ie, Trichomonas vaginalis), Neisseria gonorrhoeae, genital tract viruses (eg, herpes simplex virus types 1 and 2, cytomegalovirus), fungi, anaerobic bacteria, and gram-positive bacteria.
  • Only 10 (8%) of 135 patients with CP/CPPS in this series tested positive for fastidious organisms. However, in another series, 79 (47%) of 170 specimens from patients with CP/CPPS exhibited gene sequencing (16S rDNA) positive for the presence of microbes, while only 21 (20%) of 117 control specimens from patients undergoing radical prostatectomy were positive (P <.01). These observations support a potential role for uncommon organisms in CP/CPPS.²
• Bacteriologic breakthroughs
  • Propionibacterium acnes
    • Intriguing findings from collaborating investigators in Australia and California now suggest that persistent microbial infection with an indolent but persistent organism that is difficult to detect and difficult for the host to eradicate may act as an etiologic agent for CP and for the subsequent development of prostate cancer.³ The presence of this organism, P acnes, could be detected only via sophisticated gene-sequencing and polymerase chain reaction technology. P acnes could not be identified using routine histology, Gram stain, or routine culture techniques.
    • These preliminary findings suggest that chronic abacterial prostatitis may, in certain cases, actually be due to an occult, chronic, bacterial infection. Further, persistence of this smoldering infection may lead to the development of prostate cancer.
    • Confirmation of these findings, along with the identification of effective methods to eradicate these bacteria, could lead to cure and prevention, at least in some cases, of both CP and prostate cancer.
  • Escherichia coli
    • E coli infection is a common cause of acute bacterial prostatitis. However, these bacteria cannot be cultured in patients with chronic abacterial prostatitis. Certain strains of these bacteria may have developed a cloaking defense that allows them to conceal their activity and to resist antibiotic therapy.
    • Biofilms develop when large numbers of bacteria embed in a microscopic slime layer called an exopolysaccharide matrix. Entrenched within this biofilm layer, the bacteria may resist antibacterial treatment, counter the human body's natural defenses, and defy detection by routine culture techniques. By forming these biofilms within the prostate, E coli and related bacterial pathogens may cause chronic, treatment-resistant prostatitis. In some cases, they may also be the cause of chronic abacterial prostatitis. Prolonged (6-wk) courses of effective antibiotics (eg, one of the quinolones), when used to treat the first bout of acute prostatitis, may prevent the bacteria from forming a biofilm. Early vigorous treatment of the first case of prostatitis using this method may help prevent the inflammation from progressing into the chronic phase of bacterial or abacterial prostatitis.⁴
• Neuropathy
  • Findings of spastic hyperactivity in the absence of a definable underlying neuropathy from videourodynamic studies suggest the presence of either an occult neural etiology or an acquired functional voiding disorder.
  • Myofascial pain syndrome has been postulated as a cause for CPPS/CP. Even in the face of clinical inflammation, a reflex triggering of spasm in the musculature of the pelvic floor can be a secondary, but clinically significant, source of much of the symptomatology.⁵

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