A practical ligament-based diagnostic system for cure of pelvic symptoms and prolapse.

The Integral Theory Paradigm (ITP) has a 25-year track record of successfully treating bladder/bowel/pain symptoms caused by laxity in specific ligaments, even when the prolapse is minimal. The ITP-based treatment involves ligament support and can be nonsurgical or daycare surgical. An accurate diagnostic protocol is required. The Integral Theory Diagnostic system is performed in an outpatient setting. It a step-by-step "how to" resource for clinicians who wish to learn a practical anatomical diagnostic method which can quickly and accurately identify a ligament cause for bladder/bowel/pain symptoms, and therefore, potentially cure them. The structured ITP diagnosis flow chart uses symptoms to diagnose anatomical defects. It comprises 4 related steps. The ITP is holistic, and bladder, bowel, pain symptoms co-occur. The first step, therefore, is to establish all possible symptoms for transfer to the Diagnostic Algorithm which is the second step. Because patients complain of one main symptom, other symptoms must be located by direct questioning, using the Diagnostic Algorithm as an aide memoire, or a questionnaire to locate bladder, bowel, pain symptoms. Second step: symptoms are placed into 3 anatomical zones: anterior zone, pubourethral ligament (PUL) [stress urinary incontinence (SUI)]; middle zone, cardinal ligament (CL) (transverse defect cystocele); posterior zone, uterosacral ligament (USL) (uterine prolapse and enterocele). The third step is a vaginal examination to confirm the ligament damage (prolapses) in the three zones predicted by the algorithm. The fourth step is "simulated operations" (mechanical support of specific ligaments per vaginam) to validate the particular ligament indicated by the diagnostic algorithm, is indeed causing that symptom. For SUI, a hemostat test at midurethra supports PUL vaginally to stop urine loss on coughing; the lower blade of a bivalve speculum gently inserted into the vagina can relieve urge and pain.

Further developments of pubourethral ligament surgery for stress urinary incontinence.

Midurethral slings (MUS) have revolutionized the treatment of stress urinary incontinence (SUI). MUS operations work by creating a collagenous pubourethral ligament (PUL). Since 1996, more than 10 million operations have been performed worldwide. Early complications with the MUS included bowel perforations, massive retropubic hemorrhages, nerve injuries, even death. Though the invention of the transobturator tape (TOT) operation, and later, minislings, has eliminated many such complications, the most frequent complication, post-operative urinary retention, remains. MUS operations are unavailable in many countries because of expense. Low-cost surgical options discussed include the tension-free artisan minisling which uses a 10 cm × 1 cm tape inserted as a "U" below the urethra; 91% cure was achieved at 5.7 years in a study of 90 women, though it was accompanied by a 4.2% erosion rate. The more recent urethral ligament plication (ULP) is based on transperineal ultrasound studies which showed that the main cause of the SUI was elongation of weak PULs. This allowed the posterior pelvic muscles to open out the posterior urethral wall to cause SUI. Basic science collagen studies indicated that suturing PULs with No. 2 wide-bore polyester sutures would provide sufficient collagen to repair weakened PULs. Cure of SUI, when it occurred, was immediate. Reference to the original experimental animal studies indicated that collagen 1, the key structural support of PUL, had formed by 3 months. This is an optimistic sign for longer term cure, substantiated by very little deterioration after 3 months over a 12-month period in the first surgical trial (unpublished data). In conclusion, the ULP operation can be performed under local anesthesia/sedation. If it fulfils its promise for longer-term cure, SUI cure will be available for hundreds of millions of women in underdeveloped countries for a few dollars per case.

Chronic pelvic pain of "unknown origin" in the female.

The remit of this review is confined to the experimental scientific works and surgeries based on the Integral Theory Paradigm (ITP). Chronic pelvic pain (CPP) is a major societal problem which is said to occur in up to 20% of women. The pathogenesis of CPP of "unknown origin" is said to be unknown and CPP is said to be incurable. According to the ITP, however, CPP is said to be mainly caused by the inability of loose or weak uterosacral ligaments (USLs) to mechanically support visceral nerve plexuses (VPs), T11-L2 and S2-4. These fire off de novo impulses, interpreted by the cortex as pain coming from the end organs. CPP, when it occurs simultaneously in multiple pelvic sites, is associated with uterine/apical prolapse (often minimal) and bladder symptoms such as overactive bladder (OAB), nocturia, retention. This combination of symptoms was described in 1993 as the "posterior fornix syndrome" (PFS). As such, CPP when associated with the PFS, is potentially curable by surgical repair of USLs. However, patients with CPP generally complain only of one symptom, CPP. This is known as the "Pescatori iceberg" effect. Other PFS symptoms are "under the surface" and must be sought out by direct questioning. The diagnostic algorithm is helpful in locating other associated symptoms. Definitive diagnosis of CPP, caused by USL laxity, is immediate alleviation of pain by mechanical support of USLs by using the speculum test or by tampons in the posterior fornix. Treatment of CPP can be non-surgical, by strengthening USLs by squatting exercises, supporting USLs mechanically with tampons or USL surgery. Coexisting bladder symptoms are (variously) improved or cured. URL for CPP https://www.pelviperineology.org/volume/36/issue/3.

Pubourethral and uterosacral male analogues suggest parallel male/female pelvic anatomy and symptom pathogenesis.

The thesis that functional/dysfunctional male/female pelvic floor anatomy are parallel, originated from two studies: a successful retropubic perineal male sling for post-prostatectomy stress urinary incontinence (SUI) and discovery of a male uterosacral ligament (USL) analogue, we named "prostatosacral ligament" (PSL). In 25 out of the studied 27 males (92.6%), it starts on both sides of the median sulcus of the prostate the ligament passes lateral to the rectum being fused with the lateral margin of the mesorectum before leaving it as it thins out to be attached posteriorly similar to the USL. The ultrasound data during straining in men and women showed the same three oppositely acting muscle vectors contracting around analogous ligaments, puboprostatic ligament (PPL) (male), and pubourethral ligament (PUL) (female). Further parallels were pubovesical ligaments (PVLs) and arc of Gilvernet as part of the continence and micturition mechanisms. Impressive evidence for parallel anatomy came from the successful cure of 22 males with post-prostatectomy SUI using a perineal retropubic tissue fixation system (TFS) minisling applied to the PPL using a similar methodology to that used in the female for PUL midurethral sling repair for cure of SUI. Laparoscopic evidence confirmed the prostate as a male analogue of the cervix, and PSLs as analogues of USLs: PSL origin from the prostate attached laterally to the mesorectum and inserted into the sacrum. Histologically, PSLs had identical features with USLs: collagen, elastin, smooth muscle, blood vessels and nerves. Virtually identical symptoms for "chronic prostatitis" (CP) and "posterior fornix syndrome" (PFS), such as chronic pelvic pain, overactive bladder (OAB), abnormal emptying, gave birth to the hypothesis, of a common pathogenesis for "CP" and "PFS", USL (or PSL) laxity. If this could be proven by "simulated operations", "CP", at least in theory, may be potentially correctible by PSL repair.

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.

Técnica de reconstrucción de ligamentos pélvicos según la Teoría Integral / Pelvic Ligament Reconstruction Technique According to Integral Theory

La patología de piso pélvico es una entidad multifactorial con un conjunto de síntomas ginecológicos, urinarios, fecales y de sensibilidad pelviperineal. La Teoría Integral de la Continencia propone un tratamiento holístico con la reconstrucción de los ligamentos del piso pélvico. La presente técnica propuesta constituye una alternativa quirúrgica que permite dar respuesta de forma global a los síntomas que refieren las pacientes. Método: Reconstrucción de los ligamentos pubouretrales, cardinales y úterosacros con acortamiento de su longitud y colocación de cinta de malla de polipropileno que permita la formación de colágeno y mejore los resultados a largo plazo. Resultados: Se incluyeron 15 pacientes con prolapso de órganos pélvicos, incontinencia urinaria, vulvodinia, nocturia, alteración del vaciamiento vesical y nocturia. Se realizó seguimiento al 1, 3 y 6 años. Se obtuvo diferencia estadísticamente significativa al año en la incontinencia urinaria de esfuerzo, dolor pélvico, alteración del vaciamiento y nocturia y prolapso ( p = 0,33, 0,033, 0,002 y 0,001 respectivamente). En el seguimiento a 6 años se evaluó el 20 % de la muestra inicial, 2 pacientes con recidiva de la alteración del vaciamiento y la incontinencia urinaria, ninguna con recidiva de prolapso. Vulvodinia: Se incluyeron 2 pacientes las cuales no tuvieron el síntoma a los 3 años de seguimiento. Conclusiones: La técnica propuesta es una alternativa para el tratamiento de la patología del piso pélvico y requiere aumentar el tamaño de la muestra para aumentar el aprendizaje de la técnica y tener mayor evidencia estadística de sus resultados a corto y largo plazo(AU)

Pelvic floor pathology is a multifactorial entity with a set of gynecological, urinary, fecal and pelviperineal sensitivity symptoms. The Integral Theory of Continence proposes a holistic treatment with the reconstruction of the ligaments of the pelvic floor. This proposed technique constitutes a surgical alternative that allows a global response to the symptoms reported by the patients. Method: Reconstruction of the pubourethral, cardinal and uterosacral ligaments with shortening of their length and placement of polypropylene mesh tape that allows collagen formation and improves long-term results. Results: 15 patients with pelvic organ prolapse, urinary incontinence, vulvodynia, nocturia, impaired bladder emptying and nocturia were included. Follow-up was performed at 1, 3 and 6 years. A statistically significant difference was obtained at one year in stress urinary incontinence, pelvic pain, impaired voiding, and nocturia and prolapse (p = 0.33, 0.033, 0.002, and 0.001, respectively). At 6-year follow-up, 20% of the initial sample was evaluated, 2 patients with recurrence of impaired voiding and urinary incontinence, none with recurrence of prolapse. Vulvodynia: 2 patients were included who did not have the symptom at 3 years of follow-up. Conclusions: The proposed technique is an alternative for the treatment of pelvic floor pathology. A larger sample is necessary to improve the learning curve of this technique and achieve greater statistical evidence of its outcomes at short and long term(AU)

Do hiatal expansion and levator avulsion have a role in causation of pelvic organ prolapse?

AIM: To examine whether hiatal expansion and levator avulsion have a role in the causation of pelvic organ prolapse (POP). METHODS: Data from studies which showed a strong association of hiatal expansion and levator avulsion were analysed for causation against an alternative view, POPcausation by ligament/connective tissue damage. RESULTS: Some studies potentially fitted the "Regularity Theory of Causality"; i.e., an apparent cause, occurred with such regularity as to be considered a cause. However, these studies failed the logical requirement of "unconditional": all levator avulsions were to be followed directly by occurrence of POP, if the association were to be considered valid. Two studies which placed a large mesh behind the rectum and around puborectalis muscle greatly diminished levator expansion, but POP recurred in 78% of the women by 12 months. These results invalidated hypotheses of cause (levator expansion) and effect (prolapse). CONCLUSIONS: Levator avulsion/hiatal expansion co-occurs with POP. The cause for both is likely inability of the birth canal to plasticize" sufficiently to prevent simultaneous damage to the hiatal muscles and surrounding fascias and ligaments, which explains the co-occurrence. Greater than 90% cure of POP by site-specific repair of up to 4 pelvic ligaments supported the alternative hypothesis of simultaneous damage to pelvic ligaments to cause prolapse.

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.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.

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.

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.