By John D. Perry, PhD
How tragic it is that the various professions seldom speak to each other, nor read each other’s literature. While urologists discuss “prostatitis”, physical therapists talk about “Levator Ani Syndrome”.
Are these just two different perspectives on the same disease? Or are we dealing with two distinctly different diseases? And, if different, is there any overlap between “prostatitis” and “levator ani”? Is this another classic “chicken vs. egg” question? And, why should men’s diseases be any different from women’s?
These questions are provoked by a recent article by four urologists [Zermann et al, 1999] which asks “whether chronic pelvic pain syndrome may be a consequence of functional disease within the pelvis”. They studied clinic patients with “chronic abacterial prostatitis”; It turns out that for 88 percent of 103 patients, “myofascial tenderness” in the rectal area was “always associated with the inability to relax the pelvic floor efficiently”; “rarely did these patients learn to relax and control pelvic muscles.” Measured with urodynamic instruments, they found 92.2% of patients had “dysfunction of the pelvic floor muscles.”
That’s the good news. The bad news is that the rest of us have known that since at least 1987, and we have been treating levator ani syndrome with EMG biofeedback ever since. Today there are several clinicians in major cities who devote their entire practice to the treatment of this otherwise fairly intractable and debilitating condition. Levator syndrome is the single most common reason that people write letters to the InContiNet website — usually 2 or 3 times a week. Many patients have been incapacitated for ten to twenty years or longer without relief.
Chronic Pelvic Pain Syndrome or “CPPS” refers to a common condition which appears to resemble a bacterial infection of the prostate gland — but it is unresponsive to antibiotic treatment, and urologists are unable to cultivate any bacterial agent which “cause” the apparent “infection” and, therefore, the pelvic pain. “Hypertonicity” of the pelvic floor muscles has long been acknowledged, but it is assumed — in urology at least — to be merely an involuntary reaction to the pain of the “underlying” infection.
The traditional urological view is that there “must be” a underlying infection, an “organic cause”, even if the work up and lab tests were unable to find it. What is new about the present research is the postulation of a “functional” muscle disorder which itself might be the cause of the CPPS pain. These authors, at the University of Colorado, observed that many of these patients responded to “modulation-based therapies, such as biofeedback, alpha-blockers, or sacral nerve [electrical] stimulation”, despite having failed at “antibiotics and analgesics”. They blame “unregulated sacral reflexes” in the central nervous system as the underlying cause. But that has been the prevailing hypothesis in the field of biofeedback for more than a decade. What they describe as an “unregulated sacral reflex” is what we have been calling a “viscous cycle” of pain, tension, and then more pain. Which comes first, the chicken or the egg?
According to these urologists, prior pelvic surgery is considered a potential triggering event for the out-of-control reflexes — as demonstrated in nearly 40% of their patients. For the remaining 60%, those with no significant medical history, “long-standing pelvic floor dysfunction . . . could predispose them over time to chronic pain and urinary tract dysfunction because of compromised local immunity related to altered peptide pools.”
The postulation of a functional cause for CPPS in males is radical — and ironic. What has been and still is missing is any extrapolation from comparable CPPS conditions in females. Ironically, it was the early research of the fourth author of the present study that inspired the contemporary biofeedback treatment of chronic pelvic pain.
In 1981 (at the 75th meeting of the American Urological Association), Richard Schmidt and Emil Tanagho presented a paper that was quickly published in the prestigious journal Urology a few months later, called “Urethral Syndrome or Urinary Tract Infection?”. These authors reported:
“…women with frequent urinary tract infections uniformly had hyperactive urethral striated muscle, those with the most severe form of urge showing varying resting tension . . . discomfort or urge was proportional to the elevation . . . not all symptoms of infections were documented by culture, hence [pain symptoms] could have been related to tension in the pelvic floor rather than bacteriuria.” [Emphasis added.]
The authors conclude that: “Urethral symptoms result from physiologic imbalance in urethral [EMG] activity and may predispose to urinary tract infection.” In other words, excessive EMG activity may either be the source of pain (“Urethral Syndrome”), or it may lead to UTI (“Urinary Tract Infection”), which would be an additional source of pain. In either case, they advise, “physicians treating urge complaints in young women should be aware that both entities have to be treated.” [Emphasis added.]
“Urethral Syndrome”, therefore, is the name given to “Urinary Tract Infections” in which no infectious agent can be found. It is the female equivalent of “Abacterial Prostatitis” in the male. “Urethral Syndrome” is another name for painfully elevated EMG, or what is called “chronic pelvic tension,” in biofeedback.
In 1986-87, Dr. Pat Lariccia set up the first hospital-based incontinence program at Presbyterian Hosptial in Philadelphia. Pat and I discussed several patients with urge incontinence and symptoms of UTI, but in whom no bacterial agents could be cultivated. In general, we found pelvic muscle resting elevations of 5 to 10 microvolts (RMS), two to five times higher than a normal 2 microvolt resting level. The patients responded very quickly to pelvic muscle relaxation using computerized EMG instruments — most within a couple of weeks.
We knew it worked, but “why?” was the question. Then in 1987 Pat discovered the 1981 Schmidt and Tanagho article, and it provided the theoretical foundation for what had already become standard clinical practice in Philadelphia. We confirmed Schmidt and Tanagho’s observation that chronic tension (what they called “physiologic imbalance in urethral activity”) may not only “predispose to urinary tract infection” but this muscle “spasticity” may itself be felt as “pain”.
Fortunately, our EMG biofeedback instruments enabled precise measurement of this resting tension, and showed convincingly the direct and linear connection. The Colorado urologists “monitored” anal sphincter EMG with the “Dantec sponge” electrode, but their urodynamic instruments lack the ability to provide digitally integrated RMS summaries and lack displays useful for biofeedback training.
We also found that previous surgery was frequently implicated in the onset of symptoms. The current study that found that in 36% of patients. Other causes we’ve found include prior local infections and — you guessed it — bad bicycle seats.
So, we’ve come full circle. What started out as an observation in female UTI patients became standard practice in physical therapy and biofeedback, and has now been documented in male prostatitis patients as well.
But then the question arises, whether the observation of elevated pelvic EMG levels in abacterial prostatitis has any implications for understanding “regular”, bacterial prostatitis? After all, if pelvic tension in females can “predispose to urinary tract infections” (Schmidt & Tanagho, 1981), it would seem to follow that the same could happen in males.
Rather than the benignly observed “hypertonicity” of the pelvic floor, chronic pelvic tension may actually cause, or at least contribute to, bacterial prostatitis. If so, merely prescribing a course of antibiotics may not be effective treatment. To use Schmidt & Tanagho’s own words, “both entities have to be treated”. Clearly there is a role for pelvic muscle relaxation, using EMG biofeedback, in these conditions.
By no coincidence, chronically elevated pelvic tension has been implicated in the genesis of vulvodynia and vulvar vestibulitis. Howard Glazer (1975) has shown that a program of drastic pelvic muscle relaxation, based on EMG biofeedback, over a period of several months, led to a substantial improvement in otherwise untreatable patients.
The theory behind Glazer’s therapy is that chronic pelvic tension interferes with blood flow and lymphatic circulation, and thus impedes the body’s own attempts to fight off infection. The same model should be applied to prostatitis. Bacterial infections may well be the result of a myofascial dysfunction in the pelvis.
We owe a debt of gratitude to Dr. Schmidt and his colleagues for establishing the theoretical and urodynamic basis for this form of biofeedback therapy.
Glazer, H.I., Godke, G., Swencionis, C, Hertz, R., & Young, A.W. (1995) Treatment of vulvar vestibulitis syndrome with electromyographic biofeedback of the pelvic floor musculature. Journal of Reproductive Medicine, 40(4):283-290.
Schmidt, R.A. & Tanagho, E.A. (1981) “Urethral Syndrome or Urinary Tract Infection? Urology, 18(4):424-427
Zermann, D.H., Ishigooka, M., Doggweiler, R., Schmidt, R.A. (1999) Chronic Prostatitis: A Myofascial Pain Syndrome? Infect Urol 12(3):84-88, 92