A Critical Examination of Ligamentous Pathogenesis of Bladder Pain/Lower Urinary Tract Symptoms Using the UEDA Criteria.

To critically analyse the relationship of bladder pain syndrome (BPS/IC), as defined, to the posterior fornix syndrome, "PFS" predictably co-occurring bladder urgency, frequency, nocturia, chronic pelvic pain, emptying symptoms/retention, caused by uterosacral ligament (USL) laxity and cured by USL repair. The starting and end points of this paper are the questions, "Are there arguments that BPS/IC can, in some cases, be linked to PFS?" And if so, "To what extent?" We used the criteria required by Ueda for proper diagnosis: "understanding symptoms, detecting abnormal findings and verifying them as a cause of the symptoms." Literature, diagnostic and surgical, indicate that chronic pelvic pain "of unknown origin" can be caused by unsupported visceral pelvic plexuses because of weak USLs; these cause fire of afferent impulses, which the brain mistakenly interprets as coming from the end-organ itself (i.

Comparing urethral closure mechanisms.

The ongoing debate in "International Urogynecology Journal" about urethral closure mechanisms is important, because without a clear understanding of the anatomy of closure and stress urinary incontinence, the surgeon can never understand how corrective surgery works, or how to systematically address complications of such operations. The two dominant mechanisms which explain urethral closure rely either on Enhorning's 'pressure transmission theory', or musculo-elastic closure which relies on structurally sound suspensory ligaments. Pressure transmission hypotheses fail a simple test, "Why does the same raised intrabdominal pressure which 'closes the urethra' not stop micturition when the woman strains downwards?" Rather, it increases urine flow, a consequence of the relaxation of the forward closure muscle, pubococcygeus, which allows the posterior vectors levator plate/longitudinal muscle of the anus, to open out the urethra prior to micturition, while the raised pressure from straining drives the urine out faster.

An anatomical pathway for restoration of bladder neck closure by a midurethral sling, according to the integral theory.

A firm pubourethral ligament (PUL) is required to prevent the reflex posterior pelvic muscle forces forcibly opening out the posterior urethral wall on effort. A weak or loose PUL elongates on effort and this allows the posterior pelvic muscles to stretch open the posterior urethral wall causing urine loss, "stress urinary incontinence." Such forcible opening out of the urethra exponentially reduces the urethral resistance to flow inversely by the fourth power of the radius (i.

THE CASE AGAINST urethral failure is not a critical factor in female urinary incontinence. Now what? The integral theory system.

SUBJECT OF THE DEBATE: "Urethral failure is a critical factor in female urinary incontinence Now what?" The CASE FOR by Hokanson, DeLancey pinpointed inadequacy of bladder causation for urgency urinary incontinence (UUI) and poor urethral support for stress urinary incontinence (SUI) as responsible for long-standing lack of progress in incontinence science. They proposed "Urethral failure" as causation for SUI and UUI. The CASE AGAINST, by Peter Petros agrees "abnormal detrusor function as cause for (UUI) is a failed concept, and SUI surgery results are sometimes suboptimal, but rejects "urethral failure" as cause for UUI and SUI.

Pressure transmission theory-The Rasputin of incontinence.

Background: Enhorning's pressure transmission theory (PTT), though mortally wounded by multiple invalidations from the 1990 Integral Theory of female urinary incontinence (IT), like Rasputin, continues to survive as a theory for continence and incontinence.

Aim: To examine the questions: How has the PTT survived? What is its contribution to knowledge?

Methods: Eleven different invalidations are presented based on images, pressure readings, clinical examples, experiments by the author, and others, for example, flow mechanics, finite element models, and surgical operations.

Results: Each of the 11 invalidations prima facie invalidate the PTTs of enhorning and others.

The emperor has no clothes: OAB can be cured surgically.

The paper by Karjalainen et al., who reviewed 2,933 pelvic organ prolapse surgeries, showed 75% cure for "bothersome" urge urinary incontinence (UUI), is more than an "Aha" moment; it is an "Emperor has no clothes" moment. Since 1976, a convention of "no surgery" for women with UUI (now overactive bladder, OAB) has become almost an article of faith.