Prostatodynia o painful male urethral syndrome?

UIIC?OYNA:YIICS

PROSTATODYNIA OR PAINFUL MALE URETHRAL SYNDROME?

GEORGE A, BAH13ALIAS, M .D . From the Department of Urology, University of Patras School of Medicine, Patras, Greece

ABSTRACT--A prospective video-pressure flow-EMG urodynamic evaluation in two group patients was undertaken to show possible differences in the prostatodynia versus non .prostalo group regarding their urodynamic characteristics . There was no statistically significant differe and the main characteristic in both groups was the increased maximum. urethral closure p (MUCP) recorded at the distal prostatic and membranous urethral segments . During voiding was a distal urethral narrowing along with a proximal one seen in several patients and a syn nous decrease in urinary flow rate (peak and average flow) in the majority of patients . This tional urethral obstruction should be named "painful urethral syndrome" and not prostato and may be only a step in a chain. of events leading finally to chronic nonspecific prostatitis .

Symptoms of inflammation of the prostate and disease status have been given various nomenclature . Prostatosis, prostatodynia, prostatitis syndromes are several diagnoses inclusive but not conclusive of a cause and effect relationship between etiology, pathophysiologic mechanism, and clinical complaints . Drach et al . i have classified prostatitis syndromes as bacterial, abacterial, and prostatodynia, terminology which represents the most widely recognized classification of these disorders, This study was undertaken to continue and expand previous experience- with patients fulfilling the criteria of prostatodynia and especially to include a subset of patients with "inflammatory findings" in the prostate . A full urodynamic evaluation was undertaken to study any differences characteristic of or pertaining to each group of patients . Material and Methods Sixty consecutive patients were prospectively studied with video-pressure-flow studies and synchronous recording of the electromyographic activity of the external urethral sphincter as described previously.z a Two subgroups of patients were studied . One group with less than 10 white blood cells (WBC) per high-power

146

field (hpf), negative urine and prostatic tares, and no history of documented un tract infections, and another group with si symptoms but with more than 10 WBC/hp history of one positive urine culture in the (more than 6 months prior to this study negative (sterile) culture at the time of dynamic evaluation (Table 1) . The first group of patients with noninf rnatory prostate included 40 patients and defined as the prostatodynia group, and the and group (20 patients) with the inflamma

TALL I .

Clinical complaints

Symptoms

% Pa

Penile pain Perineal discomfort Suprapubic discomfort Urinary frequency Testicular pain Painful ejaculation Urethral pain with or without urination Scrotal pain Burning with urination Painful erection Decrease in volume of ejaculate

UROLOGY

/

AUGUST 1000

; VOLUME xXXVi, NQ

4



ate was the nonprostatodynia group of paAll patients were compared to a control of individuals matched in age and sex (20 nts) . The medical history was recorded special emphasis on urologic complaints . a complete neurologic examination a 10F e-lumen catheter was introduced into the der transurethrally, and postvoiding residr ne was measured . The catheter permitsimultaneous but independent measureis of bladder and urethral pressures . One n was used for bladder filling with 14 per:meglumine diatrizoate at room temperaat a rate of 50 mL per minute . An opening ted 1 cm proximal to the catheter tip was to record intravesical pressure through a ad lumen . Urethral pressures were monivia the third lumen through 2 .1 mm side located 8 cm proximal to the tip of the eter. The position of the side holes was tified by radiopaque markers on the cathethus permitting accurate fluoroscopic localon of the pressure recording . Normal saline 'infused at a constant rate of 1 .9 mL per ute through the urethral lumen via a Y-conor. Intra-abdominal pressures were reed via a rectal tube that was held in place a water-filled balloon . All pressures reed were transduced electronically and reed on a DANTEC 6-channel strip chart reer . -lectromyography of the external urethral ucter was performed using a coaxial or opolar needle electrode, and was monitored an oscilloscope and audio signal . Pressure sducers were zeroed at the level of the pu,Lsymphysis with the patient in an oblique, ne position. Urethral pressure profile was rmed during slow manual withdrawal of ;catheter after minimal bladder filling (50 to mL) . Stabilization of pressures was 'eved by stopping withdrawal of the catheor five seconds at 1 cm intervals starting at -,bladder neck . The bladder and urethra e observed fluoroscopically, and selected s were recorded on videotape during the dy. n the basis of oscilloscopic and auditory dings electromyographie activity was gnosed as normal or consistent with an upmotor neuron, lower motor neuron, or ed lesion . The Student t-test was used to pare the maximum urethral closure presin the study groups with that in an agesex-matched control group (20 patients) .

QLOCy

The competence of the bladder neck was tested by cough, straining, and Crede maneuver at rest or with minimal bladder filling (50 to 100 mL) and with a full bladder . The bladder neck was defined as incompetent when radiopaque contrast material appeared in the proximal urethra during early bladder filling in the absence of a synchronous detrusor contraction . 3 Prostatic biopsy was performed in several cases to rule out granulomatous prostatitis or other abnormalities . Patients underwent cystoscopy to exclude organic urethral obstruction or other pathologic conditions when indicated . Detailed psychiatric evaluation or personality profile were not part of this study. Results Patients' ages ranged from twenty-six to forty-nine years (average 35 .2 years) . The duration of symptoms before urodynamic evaluation ranged from six months to sixteen years (mean duration 4 .10 yrs) . The most frequent symptoms were perineal discomfort and penile pain with or without voiding (Table I) . Localization cultures by the Meares-Stamey technique prior to urodynamic study were sterile in all patients . 4 Microscopic examination of the prostatic expressate showed < 10 WBC/hpf in the prostatodynia patients and >10 WBC/hpf in the nonprostatodynia patients . Neurologic examination did not disclose any abnormalities . Involuntary detrusor contractions were seen in 3 patients (7 .5 %) in the prostatodynia group and in none of the nonprostatodynia group . In all patients of both groups who were able to void during urodynamic evaluation, electromyography confirmed synchronous relaxation of the external urethral sphincter that is synergetic voiding . The magnitude of detrusor contractions ranged from 20 to 70 cm water with a mean of 30 ± 7 cm water (± standard error) . The functional bladder capacity ranged from 250 to 800 mL, with a mean of 420, 30 ± 36 .25 mL . All the aforementioned urodynamic parameters were not statistically significantly different in the two groups of patients (P > 0 .05) . No statistical difference was found also in the urinary flow rates between the two groups regarding the peak or the average flows (P > 0 .05) . Peak urinary flow rates ranged from 4 to 33 ml,/see with a mean of 10 .5 mL/sec and a standard error of 1 .50 . Mean urinary flow rates ranged from 3 to 16 mL/sec with a mean of 6 .6 mL/sec and a standard error of 1 .2 .

AUGUST 1990 / VOLUME XXXVI, NUMBKH 2

147



FIGURE 1 . (A) Voidij

cystoarethrograph~ during urinary flo there is proximal rt' rowing (upper arrow), level of preprostat sphincter and distal 21 rowing (lower arrow)' level of distal prosta or membranous urethr segment, and (B) dti4 gramrnatic depicts showing two steno" (functional urethral n struction) .

Maximum urethral closure pressure (MUCP) was 122 ± 7 .2 cm water in the prostatodynia group and 115 ± 4 .4 cm water in the nonprostatodynia group . MUCP was not significantly higher in either group (P > .005), but when compared with the control group MUCP was higher in both groups (P < 0 .05) which was also reported previously . Urethral profilometry showed a gradual increase in pressure starting immediately at the bladder neck and reaching its maximum at the external urethral sphincter level . The postvoid residual ranged from 0 to 410 mL (92 .34 ± 20 .42 mL) . The prostate was not tender on palpation, and in 10 of 60 patients urethral catheterization was difficult, obviously owing to transient spasm of the external urethral sphincter . Voiding cystourethrography revealed incomplete funneling of the bladder neck in the majority of patients (84%) who voided during the study and a distal narrowing of the prostatic urethra approximately at 4 .5 to 5 em distance from the bladder neck (Fig . 1A and B) . There was a higher incidence of posterior urethral pain at the end of voiding in the nonprostatodynia group of patients, but this finding did not reach statistical significance (P > 0 .05) . Electromyography of the external urethral sphincter showed normal motor unit potentials in the majority of patients, and abnormal potentials were recorded only in 5 patients (3 in nonprostatodynia and 2 in prostatodynia groups), mostly in the form of increased percentage of polyphasics (per screen) and in 2 patients as intermittent bursts of electromyographic activity that could not be suppressed voluntarily. The latter activity was recorded during the filling (storage) phase of the cystometrogram but not during the expulsion phase

1 48

(voiding) . A coordinated function of the det' sor and the external urethral sphincter was s in all patients who voided during the study._ Comment In a previous report we have described t clinical and urodynamic characteristics of pr' tatodynia . 2 Prostatodynia is a syndrome dl has been linked to a form of detrusor-sphinc, dyssynergia or tension myalgia of the pel floors Nilsson, Colleen, and Mardhr ha= found evidence of psychotic trends or defects_. sex identification in several of these patie with prostatodynia . Sinaki, Merritt, a . Stillwell' have evaluated individuals wit diagnosis of pyriformis syndrome, levator spasm syndrome, proctalgia fugax, rectal pa, or coecygodynia, and proposed that all patio had "tension myalgia of the pelvic floor," Pei floor myalgia was attributed to habitual c° traction and spasms of the pelvic floor mus by Segura, Opitz, and Greenc . 7 The latter order is usually related to local inflammator , painful conditions . These patients complai' pain associated with running, sitting, or ac ties causing perineal .muscle fatigue and do complain of symptoms associated with voidi In this, as in our previous presentation, r examination with palpation of the prostate the pelvic floor musculature did not reprod the pain . Pain produced by palpation of the pal floor musculature is characteristic of pel floor tension myalgia which we believe is a . ferent entity regarding the striated musculat of this area . During voiding there was a e plete relaxation of the striated urethral sphi ter proved by complete absence of its elec, myographic activity . Despite this sphinct

UROLOGY

/

AUGUST 1990

1

VOLUME XXXVI, NUM1,

Lion the urinary flow was decreased probwing to distal urethral narrowing (Fig . ad and Downie' have attributed a distal gal narrowing to "sympathetic dyssynerpatients with known neurologic lesions . patients findings on neurologic examinaore negative, and in several there was roximal urethral narrowing (Fig . 1) at lust centimeter of the urethra . Voluntary pt o interrupt voiding or synchronous abI straining that may have produced the ethral narrowing were not documented se electromyography showed there was a ]etc relaxation and a simultaneous inintra-abdominal pressure did not ocexclusion of the striated sphincter as use of this urethral narrowing and the fae clinical response to a-blockers observed esc patients led to the proposal by Baret al .' of a sympathetically mediated al spasm synchronous with voiding . ooth muscle structures and autonomic ination in the area of the external urethral cter have been demonstrated by various tigators,9-11 and Elbadawi and Schenk 12 claimed that the striated external urethral er receives an autonomic innervation noradrcnergic and cholinergic nerves . ergic innervation and structures seem to an important role in this area . The ejacuy ducts and the seminal vesicles have a priadrenergic irmervation . Also the first al segment immediately distal to the der neck (1-1 .5 cm) is an area rich in nergic innervation and is the preprostatic ,ter.9 13 The distal end of this urethral segis located proximal to all of the prostatic orifices of the glandular zone of the proseluding central and peripheral zones) . prostatic urethra, immediately distal to the ostatic sphincter is 3 . .4 cm in length, and verumontanurn is found at about the midof the prostatic urethra receiving the openo the ejaculatory ducts . Smooth muscle fiare found in this entire part of the urethra, are continuous proximally with the fiextending into the preprostatic segment lore cephalad to the trigone . Distally the tatic urethra contains an outer layer of ated muscle which is continuous with the exal urethral sphincter. om this description it is seen that the pres atic and prostatic and membranous 1 segments are invested internally by a er continuous layer rich in adrenergic in-

nervation . Could local factors, i.e ., local inflammation, be involved in the causation of increased stimulation and/or incomplete relaxation of sympathetics? The urodynamic characteristics of prostatodynia and nonprostatodynia groups of patients were essentially similar, and we would propose that the "urodynamic profile" in prostatodynia described in a previous report2 should not be limited only to patients with absent inflammatory findings in the prostate . In the nonprostatodynia group of patients perhaps local inflammation may irritate adrenergic endings and result in high MCUP . Certainly treatment with a-blockers has resulted in alleviation or disappearance of the symptoms which have recurred when the ablocker was discontinued. Since prostatodynia literally means painful prostate, a better term to use is "painful male urethral syndrome," because the increased urethral tone (MUCP) causes a painful urethra and not pain in the prostate which in the overwhelming majority of these cases is nontender on palpation . This increased urethral pressure may push bacteria into the prostatic ducts in a retrograde fashion and cause irritative symptoms or pain and discomfort with the known variable radiation, and later this may result in inflammation . McNeal 13 found that inflammation in the peripheral zone of the prostate occurred more frequently than in the central zone . Furthermore, all of the ducts from the peripheral zone terminate into the distal part of the prostatic urethra beyond the verumontanum . This urethral segment corresponds to the site of the distal urethral narrowing in our video studies . The distinction between nonbacterial prostatitis and prostatodynia has been based on the presence or absence of inflammatory cells in the prostatic expressate . Various reports 1 h-1H have concluded that the actual number of WBC/hpf is of critical significance, and 95 percent of healthy controls should have less than 12 WBC/ hpf . Schaeffer et al . 17 have estimated this upper limit to be 2 WBC/hpf . In a previous report'- we have described clinical and urodynamie parameters in prostatodynia patients with < 10 WBCI hpf in the prostatic expressate . From this and in view of our findings, we question the importance of defining an absolute upper limit of WB /hpf . McNeal'L has demonstrated that prostatitis is usually focal and inflammatory cells may or may not be present in the duct lumens, and in chronic prostatitis, severe

AUGUST 1990 / VOI TJM/E XXXV1, NUMBER 2

149



periductal inflammation may be accompanied by few or no leukocytes within the lumen of the prostatic ducts . Thus the absence of WBC in the expressed prostatic secretions is not an absolute criterion to rule out a prostatic infection . Chronic nonspecific prostatitis as a pathologic (morphologic) entity is seen in up to 50 percent of all autopsies on patients who mostly have been asymptomatic during their lives . In those cases prostatitis has been usually confined to the peripheral zone of the prostate. Isolated microscopic foci or more extensive prostatic involvement in nonspecific chronic prostatitis have also been found in transurethral resection specimens of the prostate ." It is interesting to note that this "prostatitis" involvement was restricted to the tissue fragments excised from the peripheral zone of the prostate . This focal prostatic involvement has been localized to a single major or minor prostatic duct along with its branches to the prostatic acinus . This segmental localization of the inflammatory process denotes either an ascending infection or a reaction to intraluminal material or possibly an autoirnmune reaction directed against epithelium ." In this study we have found increased urethral pressures at rest, e., i, without voiding, in an area corresponding to the distal urethral and or the membranous urethral segment . Interestingly this was also the site of the distal urethral narrowing observed on video study during voiding . This increased urethral pressure may play an important role in the pathogenesis not only of prostatodynia but also of prostatitis . Furthermore, this increased pressure may explain the characteristic anatomic distribution of chronic nonspecific prostatitis . Urinary flow rate (UFR) was decreased in the majority of patients (both maximum and mean) but not in all . The video study of micturition showed a distal narrowing of the prostatic urethra, and in several patients there was also a proximal urethral stenosis (incomplete funneling) at the first centimeter of the prostatic urethra (i .e ., preprostatic segment) . It is noteworthy that the UFR was decreased in all patients with both proximal and distal stenoses . In the patients with normal UFR only a distal stenosis was found . The hydrodynamic significance of this observation can he explained perhaps by the increased urethral resistance to flow caused by the combined stenoses cornpared with the single distal stenosis . Painful male urethral syndrome is characterized primarily by increased maximum urethral

150

closure pressure in the area corresponding the external (striated) urethral sphincter b" also in the entire prostatic urethra (displament of the urethral profile curve to the ri and upward) .' , " It is conceivable that sevee patients may be found with no urinary co' plaints or inflammatory cells in their prosta expressate despite an increased MUCPs' MUCP of the same magnitude as in the pati reported in this study. A critical level of maximum urethral pros is needed to cause reflux of the urethral conte into the prostatic ducts and produce clini" symptoms . This level of pressure may vary patients and in others a lower sensitiv threshold of the afferent urethral sensors m be present . In contrast to this proposed uret hyposensitivity, Parsons and Turton" have fined "urethral hypersensitivity" to cireulatt catccholamines in order to explain the incre MUCP observed in several patients with` known neuropathy. Certainly reflux should necessarily be related to clinical complai Urethral hypertonia by itself is an objective measurable finding associated with the tient's symptomatology (Fig . 2) . This asso tion of urethral hypertonia with clinical c' plaints is necessary to diagnose painful m urethral syndrome (Table I) . The decrea UFR and the demonstration of proximal distal urethral narrowings are other import' features of this syndrome but are not of prim significance . Incomplete involuntary sm muscle relaxation during voiding despite pletc relaxation of the striated musculature`' explain this functional urethral obstruct" which was completely reversible after tr' ment with a-blockers . This response was observed in the majori our patients . Increased stimulation adrenergic innervation may explain urethral hypertonia at rest which was treated successfully with a-blockers . The jective (i .e ., alleviation of symptoms) and, jective (i .e ., increased UFR and normalize' of MUCP) responses to the administration 0 blockers may serve as an indirect rnctho diagnose painful male urethral syndrome-, especially if this favorable clinical and objea, response is reversed on the discontinuation blockers . This was repeatedly shown in ourtients . In several patients fulfilling the diagn, criteria of painful male urethral syndrome;'_ ministration of a-blockers is not followed by

UROLOGY / AUGUST 1990 / VOLUME XXXV], NUl1



NON SPECIFIC PROSTATITIS

URETHRAL SYNDROME r

I

(

P M U S

)

stress, psychogenic causes etc .)

2 . Urethral hypertonia may lead to or may be caused by chronic nonspecific prostatitis . Painful urethral syndrome may be only one step in a chain of events . Painful male urethral syndrome is the al entity of urethral hypertonia . It is conceivable that a subclinical form of urethral hypertonia may hat can still cause chronic prostatitis without any clinical complaints .

improvement in symptoms and the relief functional urethral obstruction . In those orable cases we may be faced either with of adrenergic receptor sensitivity or with severe or extensive intraprostatic inflamy involvement . Further research effort e needed to elucidate the exact etiology of esponse to a-blockadc . e mean intrinsic detrusor pressure at the voiding in these patients was 30 cm wa7 SE which is low, and as suggested by 2° these patients may have "low-pressure ow pattern ." In our patients the detrusor es were not increased but were considrof adequate magnitude . We believe that -pressure low-flow syndrome is not too only found, and in those cases a-blockers d not be expected to increase a previously i ary flow or correct a videoscopieally urethral narrowing (as seen in our paersibility of the urethral hypertonia, the omatology, and the decreased flow were ed after stopping the a-blockers in our tits which should not be characteristic of essure low-flow syndrome, Why then the etrusor pressures despite the obvious ral narrowings during voiding? Perhaps ary urethral hypertonia may inversely afadder contractility. en and Blaivas 20 have described patients proximal (only) urethral obstruction and bladder trabeculation in the majority of of severe grade), one third of these pa-

Y

tients had unstable detrusors, and in several radiographs there is a uniformly narrow prostatic urethra characteristically due to benign prostatic hypertrophy . We are presenting an entirely different group of patients . Norlen and Blaivas are referring to patients with "organic" bladder neck obstruction with significantly increased detrusor pressure and severe bladder trabeculation . We report on a group of patients with low (but adequate) mean detrusor pressure, and absent are both bladder trabeculation and involuntary detrusor contractions with a distal and a proximal urethral narrowing during voiding . Also patients with BPH were not included . It is emphasized that incision of the bladder neck is not the appropriate treatment . Hellstrom et a1 . 21 have recently referred to patients with similar clinical complaints, and we note that they are Coming to similar conclusions as to the significance of the increased urethral pressure . Furthermore, they are referring to demonstrable spasticity of the external urethral sphincter which was not found in the patients included in this presentation . We agree with the demonstration of intraprostatic reflux in paraplegics, but we have seen it most commonly in quadriplegics with prominent detrusor external sphincter dyssyuergia (unpublished data) . Siroky, Goldstein, and Krane 28 in their investigation of men with "functional voiding disorders" have included patients with (1) bladder areflexia and increased perineal muscle spasticity, (2) bladder hyperreflexia with normal EMG, and (3) normal bladder with normal

AUGUST 1990 / VOLUME XXXV1, NUMBER 2

151

EMG and painful complaints in all three categories . They conclude that symptomatic treatment with anticholinergics should be given to patients with bladder hyperreflexia or Diazepam to patients with nonrelaxing perineal floor muscles . We consider our patients as an entirely different group since in all patients who voided there was an appropriate EMG relaxation of the external urethral sphincter and bladder hyperreflexia was not seen except in only 7 .5 percent of the cases . Conclusions Our urodynamic findings in both the prostatodynia and nonprostatodynia group of patients were not significantly different . In both groups of patients the main characteristic was the increased MUCP compared with the control group (P < 0 .05) . The urinary flow rate (both maximum and mean flows) was decreased in the majority of patients, but not in all patients . The video study of micturition showed a distal narrowing of the prostatic and membranous urethral segment and also a proximal urethral stenosis (i .e ., incomplete funneling) at the preprostatic urethral segment . The observed high pressure in the urethra may explain the variable clinical presentation of this syndrome and also provide a possible link in the pathogenesis of prostatitis . This urodynamic profile was not observed only in patients with absent inflammatory findings in the prostatic expressate but also in the nonprostatodynia group of patients . We believe prostatodynia is not a good term to use . We prefer the term "painful male urethral syndrome" primarily because urethral hypertonia causes a painful urethra and not pain in the prostate which is non tender on palpation . This increased urethral pressure is caused by increased adrcncrgic stimulation and can he clinically evident as painful male urethral syndrome (clinical form of urethral hypertonia) . This increased adrcnergic stimulation can be caused either by local (chronic prostatitis) or distant factors and may eventually cause chronic nonspecific prostatitis (Fig. 2) . In several patients urethral hypertonia may not cause any symptoms (subclinical form) but still result in chronic prostatitis . This subelinical form of urethral hypertonia may explain the extraordinarily high percentage of nonspecific prostatitis findings in autopsies on asyrnptomatic males .

152

Painful male urethral syndrome is a dis° entity dissimilar to detrusor external sphirt dyssynergia or pelvic floor tension myalgiax should respond to a-blockade in most case' The important points made in this pres tion are : (1) to underline the importan" urethral hypertonia in the etiology of this dromc ; (2) to propose a possible cause an feet relationship between urethral hyperand prostatitis ; and (3) to stress the signific"' of the role of a-adrenergic innervation an ' the striated sphincter in the causation of thi$ pertonia . The low-pressure low-flow syndrome is a, ferent entity because administration of a-b' ers should not be expected to cause either of symptoms and flow improvement or re' bility of symptomatology and flow to pret' ment status after discontinuation of a-blo" (as seen in our patients) . The isolated bladder neck obstruction, ganic obstruction) is ruled out because (1) it relieved by a-blockers with video disap' ante of the urethral narrowing, and (2 bladder hypertrophy or irabeculation present radiologically or on cystoscopy. We want to stress the existence of these tients s with the described syndrome and t` vise against an incision or resection of the der neck as a means to treat these patien suggested by several reports . If such a ph'„ phy should prevail, why not incise the urethral narrowing as well, i.e ., do a mod_ sphincterotomy? Incision of the bladder neck should be co ered only as a last resort since most patien' spend to drug therapy, and it should rem l therapeutic option only in organic (perma irreversible stenosis proved by increased d sor pressure, bladder hypertrophy, and'orz' sistence of symptoms and low flows . If the presented pathophysiology is acce coining the term "painful male urethral drome" should not "add to the confusion" ing in the literature, but only help to bette dcrstand and treat these patients . Urethral hypcrtonia present at rest MUCP), i .e ., without urine in the pros urethra, can explain the irritative symp and pain in these patients in the abser, voiding . During voiding this hypertonia d either incomplete sympathetic relaxatioo sympathetically induced spasticity is resp ble for proximal and distal urethral narro and may eventually cause intraprostatic re

UROLOGY / AUGUST 1990

;

VOLUME XXXVI . 9NTI .

it is only reasonable to suggest that I ral hypertonia is the underlying physiologic mechanism causing the symp'at rest and the intraprostatic reflux (and 'aiptoins) during voiding (and at a later and not the reflux itself . The prostate ontender on palpation and prostatodynia `,the term to use . Rio . Patras, Greece References " a ct GV,, Fair WE, Meares EM, and Stamey TA : Classifif benign diseases associated with prostatic pain : prostatitis Jatodynia (Letter to Editor), J Urol 120 : 266 (1978) . jrbalias GA, Mearos EM Jr, and Sant GB : Prostatodynia : and urodynamic characteristics, j Urol 130 . 514 (1983) . 'rbalias GA, and Blaivas JG : Neurologic implications of o logically open bladder neck, J Urol 129 : 780 (1983) . Bares EM, and Stamey TA : Bacteriologic localization pat; bacterial prostatitis and urethritis, Invest Urol 5 : 492 aki M, Merritt JL, and Stillwell GK : Tension myalgia of c floor, Mayo Gin Proc 52 : 717 (1977) . Isson IK, Colleen 5, and Mardh PA : Relationship between o_gical and laboratory findings in patients with symptoms bute prostatitis, in Danlelsson D, Juhlin L. and Mardh PA enital Infections and Their Complications, Stockholm, t and Wiksell Tnt, 1975, pp 133-144 . gura JW. Opitz JL, and Greene LF : ProsLatosis, prostatitis o floor tension myalgia? J Urol 122 : 168 (1979) . ad SA, and Dowuie JW : Sympathetic dyssynergia in the f the external sphincter : a possible source of lower urinary serretion, j Urol 118 : 636 (1977) .

AUGUS'P 1990

/

9 . Gosling JA, et al; The autonomic innetvation of the human male and female bladder neck and proximal urethra, J Un'nl 118 : 302 (1977) . 10 . Critchley HUD, Dixon JS, and Gosling JA : Comparative study of the periurethral and perianal parts of the human le.vator ani muscle, Urol lut 35 : 226 (1980) . 11 . Gosling JA, Dixon IS, Critehley HOD, and Thompson SA : A comparative study of the human external sphincter and periurethral levator ani muscles, Br J Urol 53 : 35 (1981) . 12 . Flhadawi A, and Schenk RA : A new theory of innervation of bladder musculature. Part 4 : Innervation of the vesicourethral junction and external urethral sphincter, J Urol 111 : 613 (1974) . 13 . McNcal JE : The prostate gland morphology and pathobiology, in Stamey TA (Ed) : Mongr Urol 4 : 1 (1983) . 14 . Blacklock NJ, Beavis JP : The response of prostatic fluid pH in inflammation, Br J Urol 46 : 537 (1974) . 15 . Pfau A. Perlherg S, and Shapira A : The fill of the prostatic fluid in health and disease : implications of treatment in chronic bacterial prostatitis, J Urol 119 : 384 (1978) . 16 . Anderson BE, and Wcller C : Prostatic secretion leucocyLe studies in non-bacterial prostatitis (prostatosis), J Urol 121 : 292 (1979) . 17 . Sehaeffer AJ, Wendel EE Dunn JK, and Grayhack JT : Prevalence and significance of prostatic inflammation, j Urol 125 : 215 (1981) . 18 . Meares EM Jr. and Barhalias CA : Prostatits : bacterial, nott-bacterial and prostatodynia, Sendn Urol 1 : 146 (1983) . 19 . Parsons KF and Turton MB : Urethral supersensitivily and occult urethral neoropathy, Br J Urol 52 : t31 (1980) . 20 . Norlen Lj, and Blaivas JG : Unsuspected proximal urethral obstruction in young and middle-aged men, J Urol 135 : 972 (1986) . 21 . Hellstrom WJG, Schmidt RA, Lee TE, and Tanagho EA : Neuromuscular dysfunction in nonbacterial prostatitis, Urology 30 : 183 (1987) . 22 . Siroky MB, Goldstein L, and Krane RJ : Functional voiding disorders in men, J Urol 126 : 200 (1981) .

VO1UME XXXVI, NUMBER 2

1 53