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

Abstract

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.

Association between voiding lower urinary tract symptoms and findings on dynamic magnetic resonance imaging with regard to pelvic organs and their supportive structures

“…In addition, the point of C during straining also had a more ventral location in patients with vLUTS than in those without vLUTS, which was associated with longer iUSL and iCL during straining. Consequently, C, which is thought to be a keystone of the pelvic organs, 15,16 and with PUVA >140 (no marked urethral kinking) when BN descended more than 2 cm. 17 They concluded that BOO caused urethral kinking in these cases.…”

“…In addition, the point of C during straining also had a more ventral location in patients with vLUTS than in those without vLUTS, which was associated with longer iUSL and iCL during straining. Consequently, C, which is thought to be a keystone of the pelvic organs, 15,16 might prevent BN and B from being displaced more dorsally during straining and might even play some role in more ventral BN movement during straining. These positions/movements might be partially associated with a more ventral position of AR in patients with vLUTS than in those without vLUTS because the vertical length of the urogenital hiatus (H‐line) was moderately correlated to ARx during straining ( r = 0.511, p < .0001), which suggested that subtle differences in pelvic floor muscle impairment may contribute to the presence or absence of vLUTS.…”

Corrigendum

“…In the article by Petros et al, 1 Figure 8 and its caption contained error. The corrected Figure and caption appear below:…”

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

“…What is meant by “urethral failure”? If “urethral failure” means the detrimental effect on urethral resistance to flow, Figure 5, by muscle or ligament weakness, 9 then the ITS, “three theory paradigm” and “urethral failure” proposals may (possibly) all be “on the same page,” if the “urethral failure” concept accords with ITS for function 9,11 and dysfunction 52 …”