"Chronic Prostatitis": part 6

Conclusion

by Ivo Tarfusser, MD (©1996)


In conclusion, in my opinion, our current view of "chronic prostatitis"is too narrow and rigid, the presuppositions are too limited, leading to thepresent incapacity to expand knowledge. Several researchers in the field are nowlooking closely at possible mechanisms causing prostatitis (CBP, NBP) to liveist own life, i e factors resulting from an initial inflammatory process(alterations of micro-membranes in the glands, antigene-antibody-deposits,auto-immune mechanisms, etc) which act as irritant, further enhancing theinflammatory reaction. Others are still busy searching for a hypothetical, yetundiscovered microorganism responsible for NBP. Few, if any, are dealing withthe issue of PDy.

It seems very unlikely that there is one singleorgan or mechanism responsible for the different manifestations of the chronicprostatitis syndrome (or chronic pelvic syndrome). Rather, we should considerthere being many different etiologies leading to the same or similar symptoms,through a variety of different pathogenetic mechanisms. Since the symptoms aresimilar, slovenly labeled "prostatitis", there is a tendency to askfor the cause of prostatitis. I am afraid that we will never get ananswer as long as we, obstinately, think of prostatitis as a disease confined tothe prostate or as one nosologic entity, instead of appreciating these symptomsas being the consequence of one among several potential causes and mechanisms,not necessarily emanating from the prostate or from the prostate alone.

Conventional,generally accepted, assessment methods, like cultures etc, are certainlyindispensable, and will deliver an indication about the possible origin ofcomplaints in a subset of patients. But we cannot limit our efforts to thesetechniques, nor should attention in research be exclusively directed to theprostate. This will, inevitably, lead to having a large number of patientswithout explainable cause of their condition.

One important step inthinking in different tracks has been the effort at some major American centers(Mayo, Stanford) in focusing on the role of the pelvic floor muscles. In myopinion, extending this concept to an understanding of the interaction betweenperiphery (prostate, bladder, seminal tract), pelvic floor musculature and,probably very important, the pudendal nerve (which carries sensibility andmotoric signals to the interested area) will yield a better understanding of thesymptoms in another subset of patients. It seems reasonable that the symptoms inthe pudendal nerve innervation area, in a part of the patients, is generated inthe periphery, by inflammatory/infectious disease of the prostate, irritation ofparts of the seminal tract, etc. But it is also conceivable (and should beinvestigated) that other patients get their symptoms from a primary irritationof the nerve (compression, mechanical irritation), leading to similarmanifestations as in prostatitis. Finally, a dynamic interaction between thesemechanisms could be postulated: patients in whom the process starts in theperiphery, causing reflectory pelvic floor hypertension which in turn starts avicious circle of pudendal nerve irritation, eventually becoming an independentself-perpetuating mechanism, even after remission/cure of the originalperipheral affection. To emphasize the problem, the investigating community isfaced with, one has to remind himself that any combination of pain andurogenital symptoms can, theoretically, be caused both by primary disease in theperiphery as well as primary/secondary neuropathy, with or without myopathy.

Alsoregarding pathologic conditions in the secondary sex glands, themselves, weshould take other mechanisms into consideration than merely trying to detecthypothetical infectious agents. It seems highly unlikely that mechanismsdominating pathogenetics in other organ systems (like the urinary tract,gastro-intestinal tract, etc), e g obstruction, should not be determinant inmany cases in the seminal tract and the prostate, too. I admit, it is difficultto prove scientifically due to the lack of appropriate investigative methods(invasive or, preferably, non-invasive ones), but it should not be too difficultto get indirect evidence. In analogy to similar pathology elsewhere in the body,in a glandular organ system consisting essentially of microtubes and smallchannels, passed by fluid of varying composition and viscosity, obstruction hasto be suspected as one main pathogenetical mechanism until proved otherwise. Andtreatment should be directed to relieve obstruction, even if our diagnostictools are too coarse to allow aquisition of a 100% diagnosis. In many patientswith prostatodynia, I found that pressure on the seminal vesicles can elicit thepain the patients seeks help for. In my opinion, when present, this findingsuggests prostatodynia representing a pathologic condition in the seminal tract,often involving the seminal vesicles. These glands have never got the rightattention, due to their hidden position, usually not reachable by the examiner'sfinger at DRE. In most cases, I found changes in the seminal vesicles suggestiveof obstruction, with the cause of the obstruction lying down-streams, in thenarrow ejaculatory ducts. Like the ureter, these ducts have physiologicalsegments which are even narrower then the rest of the duct (the openings intothe urethra), where stones, inspissated seminal fluid, cellular detritus can getstuck and cause that colicky pain so characteristic for many patients withprostatodynia. This can also happen, if the ejaculatory ducts are compressed ordistorted from out-side (completely or partially, reversibly or permanently) byinflammatory edema, utricular cysts, BPH or cancer. Finally, the inflammatorywall reaction which may ensue can lead to cicatriceal stenoses or obturation ofthe duct. Whether the seminal vesicle and the deferential duct can overcome theincreased resistance by increasing the force of peristaltic contractions or,eventually, decompensate and get dilated from back-pressure, the result is oftenpain (again: compare what happens in the urinary, biliary and intestinal tractin the case of ostruction). The analogies with other organ systems are soevident that it amazes me that they have not yet been translated to the seminaltract, providing ideas for research in this area. As elsewhere in the body,obstructed organs are exquisitely prone to secondary infection and inflammatoryreaction, even if obstruction is not always necessary to startinflammation/infection. On the other hand, inflammation/infection will readilyresolve in a well-drained organ with therapy; if, however, obstruction persists,inflammation/infection will hardly be coped with, even by intensive long-termdrug treatment. Does'nt this make us think of the difficult therapeuticalsituation we are faced with when treating longstanding "prostatitis"?The undeniable therapeutic efficacy of well-performed prostatic massage, in somecases, is probably due to this draining effect. In selected cases, especiallysevere ones, it is my experience that surgical procedures can provide relief orcure, like it does in any other part of the body affected by obstruction and/orfocal chronic inflammatory processes and/or abscesses.

In myexperience, a key to a better diagnosis is the exact analysis of the symptoms.Ejaculatory pain, especially if one-sided, often yields a finding of obstructionin the seminal tract. Burning sensation at micturition combined with painfulejaculation should direct attention to the junction of the urinary and seminaltract (veru). Hematospermia not rarely discloses a utricular cyst. Pain relatedto prolonged sitting, biking, truck-riding, especially in absence of otheruro-genitary symptoms, may suggest a closer investigation/palpation of thepudendal nerve (neuropathy?) and pelvic floor muscles. Crucial in suchinvestigation is a thorough palpation with the finger and the TRUS-probe, and amorphological evaluation (TRUS). Nonetheless, there will still remain a group ofpatients without detectable cause, but in cases with severe pain, chasing thelocation of maximal pain will most often disclose a cause with a reasonabledegree of reliability.

I would like to summarize my postulations and suggestions as follows:

  1. The diagnostic assessment has to includeTRUS. Besides detailed morphologic evaluation, I suggest to use thetransrectal ultrasound probe as palpating finger in order to determine if thereis a site where the discomfort of the patient can be reproduced, and where themaximum tenderness can be elicited. This test is very simple and, still,reliable, reproducable and extremely useful.

  2. I suggest to introduce the termSeminal Vesiculopathy, a condition present if there is a markedtenderness of the seminal vesicles. It should be intended as a descriptive term,which does not imply any pathogenetic mechanism, but it is a very good indicatorthat there is something wrong with the seminal vesicles. Seminal vesiculopathyshould be ruled out as source of pain in all patients with "chronicprostatitis syndrome".

  3. Obstruction is an important factor in many patients with "chronicprostatitis syndrome". It may involve the prostatic acini or the seminalducts, with or without engagement of the seminal vesicles.

  4. Involvment of the Pudendal Nerve or prolonged Tension of thePelvic Floor Muscles should be considered when long-standing pain is amajor symptom and palpation of the accessory sex-glands is not painful.

  5. In severe cases of proved obstruction, the problem might be resolved bysurgery.

In any case, we have to get more distance to and question current concepts,we have to change our big picture radically by introducing elements by nowneglected or underestimated. Without doubt, some elements of conventionaldiagnostic methods and treatment options are still valuable, but they have to bebrought into a wider context and their role has to be re-evalued, in any case,we should question and relativize their central role as "state-of-the-art"methods. Otherwise we'll discover ourselves standing on the same spot foranother twenty years.

Ivo Tarfusser, MD


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