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Published on: April 27, 2014
Overactive bladder inhibition in response to pelvic floor muscle exercises
Ahmed Shafik1, Ismail A Shafik
1Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo, Egypt. ashafik@ahmedshafik.org
Abstract:
A recent study by the senior author demonstrated that striated urethral sphincter contraction effected the inhibition of vesical contraction and suppression of the desire to micturate, an action suggested to be mediated through the "voluntary urinary inhibition reflex". We hypothesized that the effect of pelvic floor muscle (PFM) exercises on the overactive bladder was mediated through this reflex action. The current communication investigates this hypothesis. A total of 28 patients (mean age 44.8+/-10.2 years, 18 men, 10 women) with overactive bladder and 17 healthy volunteers (mean age 42.6+/-9.8 years, 12 men, 5 women) were enrolled in the study. The vesical and posterior urethral pressures were determined before and after vesical filling reached the volume at which urge in control subjects, and involuntary voiding in the patients, occurred. Intra-abdominal pressure was recorded to obtain detrusor pressure readings. The bladder was refilled to the above volume and the subject asked to hold PFM contractions for 10 s during which the vesical and posterior urethral pressures were recorded. In healthy volunteers, the mean detrusor and posterior urethral pressures at urge to void were 30.6+/-4.8 SD and 18.7+/-3.3 cm H(2)O, respectively. On PFM contraction, the detrusor pressure declined to 11.6+/-1.4 cm H(2)O (P<0.01) and urethral pressure increased to 139.8+/-17.4 cm H(2)O (P<0.001). In patients, the mean detrusor and posterior urethral pressure readings when the bladder was filled to the volume which induced involuntary incontinence, were 28.2+/-4.2 and 17.3+/-3.4 cm H(2)O, respectively; on PFM contractions, the detrusor pressure decreased to 10.6+/-2.1 cm H(2)O (P<0.01), while urethral pressure increased to 86.6+/-7.9 cm H(2)O (P<0.001) and voiding did not occur. In conclusion, PFM contractions led to a decline of detrusor and increase of urethral pressures and suppressed the micturition reflex. These contractions appear to induce their effect by preventing internal sphincter relaxation produced by the micturition reflex. Failure of the internal sphincter to relax seems to cause reflex detrusor relaxation, an action presumably mediated through the "voluntary urinary inhibition reflex". The results of the current study encourage the treatment of overactive bladder with PFM contractions.
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