ICS 1999, Denver
Read by title abstracts
Pelvic floor
CHRONIC SPASM OF PELVIC FLOOR MUSCLES IN PATIENTS WITH CHRONIC PELVIC PAIN

R. Doggweiler, DH. Zerman, M. Ishigooka, RA. Schmidt
University of Tennessee, Memphis, TN, U.S.A., University of Colorado HSC, Denver, CO, U.S.A.

Introduction the charts of 167 patients affected of GPP were reviewed for toileting factors that may contribute to the onset of pelvic pain.

Methods All CCP patients are required to fill out a questionnaire thus providing information regarding present toileting habite (i.e. urgency, frequency, hesitancy, incontinence, urinary tract infections etc.). Patients subsequently underwent a urodynamic study using a multichannel system with a Micro Transducer Catheter. Parameters recorded included Cystometrogram (CMG), an urethral sphincter pressure profile (UPP). Simultaneous measurement of the detrusor and urethral sphincter pressure during the filling and voiding and a detrusor pressure flow study. Additionally sphincter sensitivity (pain) and reactivity (changes in pressure during retracting catheter) during the UPP were noted, as well as changes in the pressure during voluntary tightening the sphincter.

Results Of the 167 patients all had significant voiding symptoms (urgency, frequency, incontinence of dribbling), urethral hypersensitivity consistent with chronic pain in the perineal area. 74 patients confirmed voiding problems in childhood (enuresis, chronic holding and rigid toilet training). On rectal exam all patients were noted to have tenderness of the levator and/or urethral sphincter, as well as inefficiency in voluntary contraction and relaxation of these muscles. On urodynamics, urethral sphincter pressures were significantly elevated, so and 120 cm H2O with a media of 90 cmH2O, (normal = 70-80 for males and 60-70 for females). Hypersensitivity to catheter movement was present in all 167 patients whereas dynamic urethral hyperactivity during bladder filling was recorded in 134 patients.

Conclusion Outlet hyperactivity, hypersensitivity, and altered void behavior were present, to some degree in all patients presenting for management of chronic pelvic pain. It is known that afferent nerve fibers can when metabolically stressed, upregulate the release of neurogenic inflammatory factors both centrally and peripherally (e.g., induced myositis). This upregulation could also be caused by chronic toileting abuse that starts early in childhood. Chronic pain syndromes evolve over time as the system slowly deteriorates. Longstanding discoordinated behavior of the pelvic floor muscles, a form of repetitive motion stress, might therefore be considered a triggering factor in the evolution of the chronic pain syndrome.