A hypothesis for anatomical pathways of chronic pelvic pain "of unknown origin".

Background Interstitial cystitis/bladder pain syndrome (IC/BPS) is a disabling bladder condition. ESSIC, the IC/BPS society defines two types of IC/BPS: with Hunner's lesion (HL) and without. Pathogenesis is stated as unknown, with no cure possible. Scheffler in 2021 reported cystoscopically validated cure of HL IC/BPS by repair of uterosacral ligaments (USL) and in 2022, Goeschen reported non-HL IC/BPS cure in 198 women following USL repair. Both Scheffler and Goeschen hypothesized IC/BPS may be a phenotype of the Integral Theory's Posterior Fornix Syndrome "PFS" (chronic pelvic pain, OAB and emptying dysfunctions) and therefore potentially curable. Summary The hypothesis explores whether visceral plexuses (VP), due to weakened uterosacral ligaments support, serve as a primary source of pelvic pain impulses, leading to development of an inflammatory condition - for example, Interstitial Cystitis/Bladder Pain Syndrome, a chronic inflammatory condition, which shares similarities with vulvodynia and Complex Regional Pain Syndrome (CRPS). According to our hypothesis, such conditions involve axon reflexes. Stimuli such as gravity applied to unsupported nerve branches within the visceral pelvic plexus, trigger centrally propagating impulses, which then progress antidromally to influence innervated tissues through cytokine release and nociceptor stimulation, perpetuating inflammatory processes at the end organs, and pain perception. Key messages The hypothesis raises the question, "are IC/BPS, vulvodynia, other pain sites, even non-bacterial "chronic prostatitis" in the male, different phenotypes of the chronic pelvic pain syndrome which includes PFS. If so, the hypothesis opens several new research directions, and would predict inflammatory findings in tender endorgan pain sites.

Conceptualizing stress urinary incontinence surgery beyond midurethral slings: Very early results from simplified ligament repair without tapes.

AIMS AND METHODS: To find a simpler cure for stress urinary incontinence (SUI) without tapes. Proposed is a paraurethral operation with incisions in both sulci to plicate pubourethral ligaments (PUL) with thick polyester sutures. RESULTS: VIDEO and ultrasound experiments showed the main cause of SUI was weak PULs extending on effort, allowing the posterior pelvic muscles to open out posterior urethral wall, so urine was lost on effort. Midurethral sling (MUS) tapes prevent PUL extension and SUI. The research question: "Would PUL plication by 0.5 or 0.25 mm polyester tapes create sufficient new collagen to cure SUI in the longer term?" Instron-testing of collagen from a rejected polyester aortic graft indicated sufficient potential collagen strength. Five surgeons unrelated to the authors who tested the new operation, reported negative cough tests on 30/31 women before patient discharge; these data were encouraging, but not conclusive. CONCLUSIONS: PUL ligament repair by large polyester sutures, like the MUS, appears to prevent PUL elongation and cure SUI in the very short term, thereby validating the predictions of the Integral Theory as regards the role of ligaments in continence. If successful long term, this operation could avoid many problems associated with MUS operations. 1. Simplicity: less surgical skill is required; the local anesthetic methodology makes the operation widely scalable especially in poor countries with few health facilities. 2. Built-in safety: there is no tape to compress urethra, no applicators to damage bladder, nerves, blood vessels, bowel. 3. Cost: a polyester suture.

Overactive bladder (OAB): a failed concept needing revision to accommodate an external anatomical control system.

THESIS AND AIMS: In 45 years, the definitions and practice of the urodynamically based overactive bladder (OAB)/detrusor overactivity (DO) system have failed to adequately address pathogenesis and cure of urinary urge incontinence, frequency and nocturia. METHODS: We analysed the OAB syndrome with reference to the Integral Theory paradigm's (ITS) binary feedback system, where OAB in the female is viewed as a prematurely activated, but otherwise normal micturition caused mainly, but not entirely, by ligament damage/laxity. The ITS Clinical Assessment Pathway which details the relationships between structural damage (prolapse), ligaments and dysfunction (symptoms) is introduced. RESULTS: The ITS was able to "better explain" OAB pathophysiology in anatomical terms with reference to the binary model. The phasic patterns diagnostic of "detrusor overactivity" are explained as a struggle for control by the closure and micturition reflexes. The exponentially determined relationship between urethral diameter and flow explains why obstructive patterns occur, why they do not and why urine may leak with no recorded pressure. Mechanically supporting ligaments ("simulated operations") during urodynamic testing can improve low urethral pressure, negative pressure during coughing with SUI and diminish urge sensation or even DO patterns, transforming urodynamics from non-predictive test to accurate predictor of continence surgery results. High cure rates for OAB by daycare repair of damaged ligaments is a definitive test of the binary system's validity. CONCLUSION: Conceptual progression of OAB to the Integral Theory paradigms's prematurely activated micturition validates OAB component symptoms as a syndrome, explains pathogenesis, and unlocks a new way of understanding, diagnosing, treating and researching OAB.

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. In answer to, "Now what?," Petros presents the Integral Theory System. SUI and UUI are dysfunctions of the bladder's binary control mechanism, mainly ligament laxity because of defective collagen/elastin. The urethra is an emptying tube. Pelvic muscle forces reflexly contract against ligaments to close urethra, open it (micturition) and stretch the vagina underlying urethelial stretch receptors to mechanically support them, preventing premature activation of micturition (UUI). High validated cure rates for SUI and UUI by repair of weakened ligaments question viability of the "urethral failure" concept. CONCLUSIONS: The major achievement of this debate (both sides) is not what causes UUI or SUI, or what doesn't, though clearly, this is important. It is calling out a 50-year ossification of the whole construct of UUI, ranging from flawed definitions to systematic denial of known cures, all of which have stalled treatment of the one billion women who suffer with incontinence. The time has come for change.

Late-occurring pain/other dysfunctions in midurethral sling class actions are likely caused by uterosacral ligament weakness, not implant or surgeon.

BACKGROUND: Large sums of money have been awarded against manufacturers of midurethral slings (MUS) because of complaints of pain and other complications, even though pelvic pain is rarely seen at the 6-12 weeks review. HYPOTHESIS AND AIMS: Pain/other posterior fornix symptoms (urge, frequency, nocturia, and abnormal emptying) may appear weeks or months after MUS surgery due to dislocation of already weakened uterosacral ligaments (USL), a consequence of diversion of pelvic forces from pubourethral ligaments strengthened by the sling. METHODS: Review for prevalence, pathogenic pathway from damaged USLs to pain, OAB, emptying, and other late complications by reference to data from functional anatomy imaging, mechanical support of USLs (speculum test), and post-USL surgical repair. RESULTS: Pelvic pain and other pelvic symptoms frequently co-exist pre-operatively with SUI, but are not volunteered because patients complain of one main pelvic symptom, others being "under the surface" (Pescatori Iceberg). Late de novo occurrence of symptom complications beyond perioperative MUS surgery may occur: pain (5.7%), retention (5.4%), UTI (9.3%), and OAB (10.2%). Xray/ultrasound evidence of pelvic forces acting on USLs support the hypothesis of diversion of forces. Improvement of pain and urgency by the "speculum test" indicates USL causation, as do cure of pain and other pelvic symptoms by USL slings. CONCLUSIONS: Late-occurring PFS symptoms are the fault of neither implant, nor surgeon, but more likely consequences of pelvic forces acting on USLs already weakened by childbirth/age. Bladder/bowel/pain symptoms need to be sought out preoperatively and discussed before MUS surgery. BRIEF SUMMARY: Late MUS complications, OAB, pain, retention subject to class actions, may be caused by uterosacral dislocation from pre-existing structural weakness, not surgeon or device.

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.e., 16 times). For example, if the radius doubles in size, the bladder pressure required for urine to flow out decreases by a factor of 16, from say, 160 to 10 cm H2 O. A midurethral sling reinforces PUL to prevent the urethra opening out, thereby restoring both the distal urethral and bladder neck closure mechanisms.

Defining urge as an uncontrolled micturition explains pathogenesis, informs cure and helps solve the burgeoning OAB crisis.

BACKGROUND: Parallel with the demographic ageing crisis, is a disabling overactive bladder (OAB) crisis (urgency/frequency/nocturia), 30% prevalence in older women, pathogenesis stated as unknown and, according to some learned societies, incurable. HYPOTHESIS/AIMS: To review International Continence Society and Integral System paradigms to test our thesis that OAB per se is not a pathological condition, rather, a prematurely activated uncontrolled micturition; pathogenesis being anatomical damage in a nonlinear feedback control system comprising cortical and peripheral (muscle/ligament) components. METHODS: We examined studies from basic science, anatomy, urodynamics, ultrasonic and video xrays, ligament repairs, from which we created a nonlinear binary model of bladder function. We applied a Chaos Theory feedback equation, Xnext = Xc(1 - X) to test our hypothesis against existing concepts and hypotheses for OAB pathogenesis. RESULTS: The bladder has ONLY two modes, EITHER closed OR open (micturition). Closure is reflexly controlled cortically and peripherally: muscles contracting against ligaments stretch the vagina to suppress afferent signals to micturate from urothelial stretch receptors. "OAB" can be caused by anatomical damage anywhere in the model, by childbirth or age-weakened ligaments, which can be repaired to cure all three OAB symptoms. Urodynamic "DO" graphs are interpreted anatomically and by the feedback equation. CONCLUSION: OAB is in crisis. Our thesis of OAB as an uncontrolled micturition from anatomical defects in the bladder control system provides fresh directions for further development of new treatments, nonsurgical and surgical, to help break the crisis and bring hope and cure to 600 million women sufferers.

An anatomical pathogenesis of lower urinary tract definitions from the 2002 ICS report symptoms, conditions, syndromes, urodynamics.

AIM: To present an anatomical pathogenesis parallel with the 2002 International Continence Society Lower Urinary Tract (LUTS) definitions standardization Report 2002. METHODS: Each LUTS section is discussed using the same numbers as the Report. RESULTS: Normal function Bladder control is binary, with two reflexes alternating, either closure (dominant) or open (micturition), with the same cortical and peripheral components: three directional muscle forces contracting against pubourethral (PUL) and uterosacral (USL) ligaments for closure, two against uterosacral ligaments for micturition. Dysfunction OAB symptoms reflect a prematurely activated micturition; PUL/USL weakness prevents muscle forces from controlling afferent urothelial emptying signals. Stress urinary incontinence is a consequence of weak PULs allowing posterior muscle forces to open the urethra during effort. Lax USLs weaken contractile force of the posterior urethral opening vectors, so detrusor has to contract against an unopened urethra. This is experienced as "obstructive micturition." CONCLUSIONS: Anatomical analysis indicates the ICS definitions are fundamentally sound, except for "OAB" which implies detrusor causation. Minor changes, OAB to "overactivated" bladder allow causation outside of bladder. This construct supports OAB and its component symptoms as a syndrome, as intuited by the Committee, (albeit as a prematurely activated micturition), retains the acronym, explains OAB cure by ligament repair, and incontinence pathogenesis from two post-2002 syndromes which need an addition to the definitions, Posterior Fornix Syndrome (of which OAB is a component) and Tethered Vagina Syndrome, which is the basis for skin-grafting cure of the 30%-50% of women who continue leaking urine massively after successful obstetric fistula closure.

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. Yet, surgical cure of OAB has been known since 1997, when this journal published the first urodynamically controlled study with 20-month data: 86% cure for UUI, 85% for frequency, 80% for nocturia following pubourethral ligament (PUL) and uterosacral ligament (USL) sling repair in 85 women. This study was followed by many other publications over the years recording OAB cure. It is not that even a small fraction of the 600 million women on the planet will now undergo surgery, or that damaged ligaments are the only cause of OAB. However, knowing OAB can be cured opens the door for young creative minds to bring hope and relief to these women non-surgically, as well as surgically.

Retropubic TFS Minisling for Postprostatectomy Male Incontinence: First Report.

HYPOTHESIS: A structurally sound puboprostatic ligament (PPL), like the pubourethral ligament in the female, is the core structure for control of stress urinary incontinence (SUI) in males. METHODS: The hypothesis was tested at several levels. Twelve transperineal ultrasound examinations were performed to confirm reflex directional closure vectors around the PPL, with digital support for the PPL rectally and cadaveric testing with a tissue fixation system (TFS) minisling, and finally, 22 cases of postprostatectomy incontinence were addressed only with retropubic insertion of a 7-mm TFS sling between the bladder neck and perineal membrane to reinforce the PPL. RESULTS: On ultrasound testing, 3 urethral closure muscles were confirmed to act reflexively around the PPL to close the urethra distally and at the bladder neck. A finger was inserted rectally, pressed against the symphysis only on one side of the urethra at the origin of the PPL that controlled urine loss on coughing. The mean pre-op pad loss was 3.8 pads at 9 months; the mean post-op loss was 0.7 pads; 13/22 (59%) patients were 100% improved; 7/22 (31%) improved >50% but <100%; 2/22 (9.1%) improved <50%. CONCLUSIONS: The 7-mm-wide TFS minisling is the first retropubic minisling for postprostatectomy urinary incontinence. It differs significantly from transobturator male operations surgically and in modus operandi. As in the female, reconstruction of the PPL alone was sufficient to cure/improve SUI, suggesting that preservation of the PPL is of critical importance during retropubic radical prostatectomy.

Non-Hunner's Interstitial Cystitis Is Different from Hunner's Interstitial Cystitis and May Be Curable by Uterosacral Ligament Repair.

BACKGROUND: The posterior fornix syndrome (PFS) was first described in 1993 as a predictably occurring group of symptoms: chronic pelvic pain (CPP), urge, frequency, nocturia, emptying difficulties/urinary retention, caused by uterosacral ligament (USL) laxity, and cured by repair thereof. SUMMARY: Our hypothesis was that non-Hunner's interstitial cystitis (IC) and PFS are substantially equivalent conditions. The primary objective was to determine if there was a causal relationship between IC and pelvic organ prolapse (POP). The secondary objective was to assess whether other pelvic symptoms were present in patients with POP-related IC and if so, which ones? How often did they occur? A retrospective study was performed in 198 women who presented with CPP, uterine/apical prolapse (varying degrees), and PFS symptoms, all of whom had been treated by posterior USL sling repair. We compared their PFS symptoms with known definitions of IC, CPP, and bladder symptoms. To check our hypothesis for truth or falsity, we used a validated questionnaire, "simulated operations" (mechanically supporting USLs with a vaginal speculum test to test for reduction of urge and pain), transperineal ultrasound and urodynamics. KEY MESSAGES: 198 patients had CPP and 313 had urinary symptoms which conformed to the definition for non-Hunner's IC. The cure rate after USL sling repair was CPP 74%, urge incontinence 80%, frequency 79.6%, abnormal emptying 53%, nocturia 79%, obstructive defecation 80%. Our findings seem to support our hypothesis that non-Hunner's IC and PFS may be similar conditions; also, non-Hunner IC/BPS may be a separate or lesser disease entity from "Hunner lesion disease". More rigorous scientific investigation, preferably by RCT, will be required.

Vulvodynia: a neuroinflammatory pain syndrome originating in pelvic visceral nerve plexuses due to mechanical factors.

This short opinion aimed to present the evidence to support our hypothesis that vulvodynia is a neuroinflammatory pain syndrome originating in the pelvic visceral nerve plexuses caused by the failure of weakened uterosacral ligaments (USLs) to support the pelvic visceral nerve plexuses, i.e., T11-L2 sympathetic and S2-4 parasympathetic plexuses. These are supported by the USLs, 2 cm from their insertion to the cervix. They innervate the pelvic organs, glands, and muscles. If the USLs are weak or lax, gravitational force or even the muscles may distort and stimulate the unsupported plexuses. Inappropriate afferent signals could then be interpreted as originating from an end-organ site. Activation of sensory visceral nerves causes a neuro-inflammatory response in the affected tissues, leading to neuroproliferation of small peripheral sensory nerve fibers, which may cause hyperalgesia and allodynia in the territory of the damaged innervation. Repair of the primary abnormality of USL laxity, responsible for mechanical stimulation of the pelvic sensory plexus, may lead to resolution of the pain syndrome.

Understanding the mechanics of closure is key to optimal midurethral sling technique.

The animal experiments and prototype midurethral sling operations demonstrated that the sling provided new collagen to reinforce weak pubourethral ligaments (PUL). The now strengthened PULs were able to restore the contractile power of the 3 oppositely-acting directional closure forces. By contraction, these three forces exponentially altered the intraurethral resistance to flow when they closed the urethra to sustain continence. Relaxation of the forward force allowed the two posterior forces to uninhibitedly open the posterior urethral wall just prior to detrusor contraction, to facilitate evacuation of urine. The aim of this work is to examine the mechanics of the component anatomical structures which contribute to these functions, to analyse how subtle details impact on the actual surgical technique of the midurethral sling operations to optimize success, contribute to complications and how to prevent and fix them.

Cure of Interstitial Cystitis and Non-Ulcerating Hunner's Ulcer by Cardinal/Uterosacral Ligament Repair.

A serendipitous cure in a 73-year-old woman of Hunner's ulcer, urge, nocturia, apical prolapse by a tissue fixation system tensioned minisling (TFS) which reinforced the cardinal, and uterosacral ligaments (USLs) led us to analyse the relationship between Hunner's ulcer and known pain conditions associated with USL laxity. The original intention was to cure the "posterior fornix syndrome" (PFS), uterine prolapse, and associated pain and bladder symptoms by USL repair. A speculum inserted preoperatively into the posterior fornix alleviated pain and urge symptoms, by mechanically supporting USLs. Hunner's ulcer, along with pain and other PFS symptoms were cured by USL repair. The concept of USL laxity causing chronic pelvic pain and bladder problems is not new. It was published in the German literature by Heinrich Martius in 1938 and by Petros in the English literature in 1993. These findings raise important questions. As PFS symptoms are identical with those of interstitial cystitis (IC), are PFS and IC similar conditions? If so, then patients with IC who have a positive speculum test are at least theoretically, potentially curable by USL repair. These questions need to be explored.

Passive management of labour may predispose to anal sphincter injury.

INTRODUCTION AND HYPOTHESIS: To compare anal sphincter damage in two groups of primigravid women in Sydney: one passively managed in public hospitals, the other more actively managed in adjacent private hospitals. Data from actively managed labours at the National Women's Hospital, Dublin, served as an independent control. METHODS: We carried out a comparative study of third and fourth degree anal sphincter tears in all primiparas delivering at term in the years 2010-2015 in six Sydney public teaching hospitals with data from patients delivered in six adjacent Sydney private hospitals. A second comparator was published data from the National Women's Hospital, Dublin, where active management is still performed under the direction of midwives. All data was publicly available from www.health.nsw.gov.au/hsnsw . The difference between the two groups: public hospitals were under MANDATORY (NSW DG's upper case emphasis) direction from the Director General of NSW Health (PD 2010-045 File no 09/638-3) for labour to proceed without any augmentation. RESULTS: The study comprised 130,000 women. The mean third and fourth degree anal sphincter tear rate was 8.17% for the public hospitals and 1.52% for the private hospitals in the same period (p < 0.0003). Dublin's rate was 2.6%. There was no significant difference in the emergency Caesarean section rate 2010-2015 (13.7% private vs 12.7% public, 7.9% in National Women's Hospital Dublin) as well as an increase in epidurals, forceps/ventouse and lower Apgar scores. CONCLUSION: Passive management of labour instituted in Sydney public hospitals by government directive seems to be associated with a higher rate of obstetric anal sphincter injuries than was observed with active management. In addition, there were more epidurals, forceps/ventouse, and lower Apgar scores. Our hypothesis of deflexion of the head causing deficient powers is logically appealing, but needs further proof.

A biomechanically based concept for a stronger obstetric anal sphincter repair.

INTRODUCTION AND HYPOTHESIS: This study emanates from the ISPP OASIS and fecal incontinence study group at the 2018 annual meeting of the International Society for Pelviperineology (ISPP) in Bucharest, Romania. The aim was to analyze the biomechanical factors leading to the breakdown of anal sphincter repair and to suggest a more robust technique for external anal sphincter (EAS) repair. METHODS: Our starting point was what happens to the EAS wound repair site during defecation following EAS repair, with special reference to the process of wound healing. RESULTS: We concluded that a graft no more than 1 × 1.5 cm sutured across the EAS tear line would mechanically support the tear line, vastly reduce the internal centrifugal forces acting on it during defecation, thereby giving the wound time to heal. Three different grafts were discussed, autologous, biological, and mesh. Also analyzed were the effects on EAS muscle contractility of overly tight repair and overly loose sphincter repair, the latter occasioned by the tearing out of sutures and repair by secondary intention. CONCLUSIONS: We have analyzed causes of sphincter repair failure, introduced a graft method, preferably autologous, for the prevention thereof and supported ultrasound assessment, rather than the absence of fecal incontinence as the criterion for success of EAS repair. Although based on well-established biomechanical principles, our proposal at this stage remains unproven. Our hope is that these concepts will be challenged, clarified, and tested, preferably in a randomized controlled trial.

The mechanics of urethral closure, incontinence and midurethral sling repair. Part 2 further experimental validation (1993-2003).

IN: Part 1, The original 1990 science behind the MUS, the hypothesized closure mechanisms, and the prototype MUS itself were presented. The next phase of MUS development began in 1990 in collaboration with the late Ulf Ulmsten. It had two arms Further development of the prototype MUS. Further anatomical, imaging, urodynamic studies to validate the role of PUL in the closure mechanisms. A second series of prototype MUS operations performed under LA/sedation resulted in a permanently implanted polypropylene sling and the MUS as is known today. The tape was elevated until no urine leaked on coughing. This demonstrated that the artificial PUL neoligament needed to be at a specific length to work. Anatomical, EMG and video ultrasound, and X-ray studies confirmed three directional muscles contracted pubourethral (PUL) and uterosacral (USL) ligaments. The contribution of the horseshoe shaped rhabdosphincter (RS) to continence was directly tested with pressure measurements under live surgery conditions. It was concluded that the RS was responsible for pressure generation but not continence. Continence was a consequence of intraurethral resistance to flow created by the distal and proximal urethral closure mechanisms, both governed ultimately by the Law of Poiseuille. CONCLUSIONS: The key element in curing USI is creation of a competent PUL using the collagenous neoligament surgical principle described in Part 1. This creates a firm insertion point for the three directional muscle forces, restoring their contractile strength and closure.

The mechanics of urethral closure, incontinence and midurethral sling repair. Part 1 original experimental studies. (1990).

AIMS: To summarize the mechanics of urethral closure, incontinence, and midurethral sling repair, a work in 3 parts Part 1. Original scientific studies (1990). Part 2. Experimental validation of reliance of the closure mechanisms on a competent PUL (1993-2003). Part 3. Surgery (1990-2016). METHODS: Part1. Two unrelated observations in the mid 1980s led to the discovery of the MUS: a hemostat applied on one side of the midurethral area of the vagina, controlled urine loss on coughing without bladder neck elevation; an implanted Teflon tape cause a collagenous reaction. It was hypothesized that urinary stress incontinence (USI) was caused by collagen loss in the pubourethral ligament (PUL) and a tape implanted in the exact position of PUL would reinforce it and cure USI. A tape removable at 6 weeks was configured as an inverted "U" in the vagina and lowered sequentially. RESULTS: At a certain point, the patient was continent on coughing but was able to pass urine freely. This proved the mechanism for continence was not obstructive. Post-op xrays showed no elevation of bladder neck. This invalidated Enhorning's Theory. Ultrasound showed closure of distal urethra from behind and descent of vaginal fornix on straining. This indicated there were two closure mechanisms, distal urethral, and bladder neck. Three months following sling removal, there was a 50% failure rate. CONCLUSIONS: The 1990 results indicated a permanent sling was required for the MUS. Further proofs were required for the proposed musculoelastic mechanisms.

The mechanics of urethral closure, incontinence, and midurethral sling repair Part 3 surgical applications (1990-2016).

Part 3 briefly summarizes further development in midurethral sling (MUS) instruments and technique following the 1990 prototype operations, then critically examines the whole MUS surgical methodology, 1990 to present day. The aim is to identify positive and negative aspects of these methodologies which can be usefully applied to improve current MUS surgery. ANIMAL EXPERIMENTS: 1987-1988 proved that a collagenous neoligament could be formed by implantation of a tape. There was a wide variation in tissue reaction to implanted tapes. Inflamamatory tissue reaction was very different from bacterial infection and was safe even when a sinus is formed. MUS METHODOLOGY: The key factor in avoiding major vessel and nerve injuries is to penetrate the perianal membrane with scissors, insert the applicator. Importantly, this reveals any bleeding which could otherwise accumulate in the Space of Retzius and only be controlled by digital pressure. The balance between too tight (retention) and too loose (incontinence) is analyzed in terms of the exponential relationship between urethral diameter and urine flow; why elastic tapes are more likely to cause post-operative urinary retention; how to minimize retention by tightening against an indwelling No18 Foley catheter; the importance of routinely repairing the distal closure mechanism with purse string suture to external ligaments, fascial layer of vagina; why minislings avoid most of the serious MUS complication; why a tensioned minisling allows greater precision when tightening the sling and how anchors and individually knitted tapes give hope that tape erosions may decrease.