An anatomical classification - a new paradigm for management of urinary dysfunction in the female

Author
PE PAPA PETROS* Dr Med Sc FRCOG FRACOG CU
Dept of Gynaecology
Royal Perth Hospital
Perth, Western Australia

and U ULMSTEN MD PhD
Professor and Head
Dept of of Obstetrics and Gynaecology
Academic Hospital
University of Uppsala,
Uppsala
Sweden

* Correspondence: PE PAPA PETROS
Suite 14 A Surgicentre
38 Ranelagh Cres.
South Perth
WA 6151
Australia

Tel No : 61-89-474 1966
Fax : 61-89-474 3766

Running title Anatomical classification
No of words = 2831 (excludes abstract, legends and references).
Synopsis An anatomical classification links bladder dysfunction to laxity in three zones of vagina.
Key words incontinence classification; vagina; ligaments; stress; bladder instability; bladder emptying; pelvic floor.

An anatomical classification - a new paradigm for management of urinary dysfunction

Abstract
A new anatomical classification specifies anatomical defects in the anterior, middle and posterior zones of the vagina as causing urinary dysfunction. An external musculoelastic mechanism stretches the vagina to open and close the outflow tract. The same pelvic floor muscles provide a peripheral control mechanism for micturition . The stretched vagina prevents the filling bladder from activating the stretch receptors. Vaginal laxity may weaken transmission of muscle forces, interfering with opening and closure, a mechanical process. Laxity may also destabilize the peripheral control mechanism, a neurological process, causing bladder control to swing between the open and closed modes, bladder instability. Specific symptoms, signs, and urodynamic tests were arranged into a pictorial algorithm. This acts as a practical guide for locating the three zones of anatomical defects. It was possible to reinterpret almost all the definitions and descriptions of the International Continence Society in terms of this classification, and to explain how vaginal laxity may cause premature activation of the micturition reflex (detrusor instability) stress incontinence and abnormal emptying (dribble, overflow). This convergence in anatomical and urodynamic (ICS) concepts explains many previously unexplained phenomena, and potentially opens up an entirely new approach to management, nonsurgical strengthening of specific ligaments, or surgical reinforcement thereof with ambulatory "keyhole" methods which do not require catheterization.

INTRODUCTION
The ICS paradigm In 1976, the First Report of the International Continence Society (ICS) introduced the first modern paradigm for classification of urinary dysfunction (1), based on urodynamics. The ICS classified urinary incontinence (2) as denoting a symptom of urine loss, a sign (objective demonstration of urine loss), or a condition (objective demonstration of urine loss in the absence of detrusor instability). "Detrusor instability" described a phasic pattern found during subtracted cystometry, and "genuine stress incontinence" described urine loss coincident with stress in the absence of "detrusor instability". It was stated specifically that the classification depended on the results of objective urodynamic investigations, because symptoms were unreliable. However, it was also specified that urodynamic investigations should correlate with symptoms and signs, because detrusor instability could occur in entirely normal patients (2). Similar contradictions exist as concerns management. It is recommended that the stress incontinence component should be treated surgically, and the detrusor instability component nonsurgically. Yet most incontinent patients are afflicted with both conditions. Such internal contradictions have created considerable confusion in understanding the ICS classification and recommendations. Such recommendations may not, in fact, be correct. A large multicentre trial has demonstrated that urodynamics were not predictive of surgical failure, neither was surgery contraindicated in the presence of an unstable bladder (3).

Surgical paradigms have a limited life cycle (4). Though we believe, for the reasons stated above, that the ICS paradigm is now inadequate, our anatomical classification does not seek to discard the whole body of work on which the ICS paradigm is based. Rather, we seek to demonstrate that all these contradictions can be resolved by reinterpreting existing ICS descriptions as being secondary to anatomical defects in the vagina.

An anatomical paradigm for normal function The existing ICS classification (2) for lower urinary tract dysfunction is predicated on the bladder and urethra interacting as a functional unit. In 1990, the Integral Theory added an extrinsic mechanism to this concept activated by specific pelvic floor muscles(5). Further to this theory (5,6), we hypothesize that the normal bladder has only 2 stable modes, open and closed. At rest, tissue elasticity of the vagina mechanically maintains urethral closure. As the bladder fills, three directional muscle forces (arrows, figure 1), stretch the vagina to maintain closure, and to counteract the hydrostatic pressure on the stretch receptors "N", figure 1 (7,8), thus preventing their premature activation (bladder instability(5,6)). To go from closed to open mode, energy is required to stretch the elastic tissues of vagina to their elastic limit. Relaxation of the forward arrows permits the two posterior forces, figure 1, to mechanically stretch open the outflow tract. All these events were confirmed by radiological studies (7,8).

A peripheral feedback mechanism modulated by central control The peripheral striated muscle mechanism for opening and closure (Om,Cm, figure 2) interacts closely with the central inhibitory and facilitatory mechanisms,"C", "O" (7). The afferent mechanism (Oa) is processed at facilitatory ("O") and inhibitory ("C") centres in the brain. If convenient to micturate, the cortical centre "CTX" inhibits "C" and instructs "O" to acclerate Oa. The efferent signals (Oe), in turn, proceed to relax the striated urethral sphincter (Ou), relax the forward contractile muscle force (Cm), stimulate detrusor contraction (Od), and contract the backward and downward opening muscles (Om), figure 2. In this way, the outflow tract is opened out, and the bladder contracts to empty. This same system permits bladder emptying with increased intraabdominal pressure, but without detrusor contraction (Od). If inconvenient to empty, CTX, (figure2), suppresses all opening channels ("O"), and stimulates all closure channels ("C" ). 

How vaginal laxity may destabilize the peripheral mechanism and cause urinary dysfunction

NOTE ICS classification and descriptions are identified by italics .Figure 3 indicates how childbirth may damage the connective tissue of the vagina and its supporting ligaments to cause both uterovaginal prolapse and urinary dysfunction. It is possible to extrapolate from figure 3 that damaged connective tissue would form a continuum with greater and lesser degrees of damage along the length of the vagina. Vaginal laxity in all three zones may prevent the peripheral control mechanism (Cm) from supporting the urine column, so that "N", figure 2, fires off prematurely, "bladder instability"resulting in more frequent micturition (frequency) , and therefore smaller volumes(low bladder capacity ). This event is perceived by the cortex (CTX) as symptoms of frequency, nocturia and urgency (FNU)

Detrusor instability (DI) Laxity in all 3 zones may activate"Oa"the afferent limb of the micturition reflex (sensory urgency). CTX, figure 2, may respond by activating the neurological closure circuit "C". The suppression circuit "C" struggles for supremacy with the micturition circuit "O". Because of the time lag associated with feedback circuits, the detrusor instability graph characteristically demonstrates a phasic (bell shaped) pattern "Y" figure 4. Seen simplistically, as the micturition reflex "O" predominates, the detrusor contracts, and detrusor pressure rises. As "C" gradually wrests control of the neural pathways, the detrusor pressure falls back to the baseline. The spikes superimposed on the bell-shaped graph of detrusor instability represent the striated muscles of the external sphincter (Cm) contracting rapidly to try and close the urethra (9) against the "open" phase. The time lag factor was demonstrated during a handwashing test involving 115 patients with a history of urge incontinence (10). The manifestations of the micturition reflex were, in order of temporal occurrence (10): a sensation of urgency (n=109) (sensory urgency), fall in urethral pressure (n=91)(urethral instability), rise in detrusor pressure (n=56)(detrusor instability), and urine loss (n=52)(urge incontinence). The decreasing yield, and time delay between each manifestation cause us to hypothesize that there may be at least 4 passes in the feedback loop, figure2, before urine is lost: sensory urgency (Oa), urethral relaxation (Ou), detrusor contraction (Od,) and finally, stretching open of the outflow tract by the pelvic floor muscles (Om). The underlying process may be similar for DI and normal micturition (11). A major anatomical defect preventing the action of Cm, figure 2, may allow the backward opening forces (Om) to act as an accelerator (motor detrusor instability). Note the time lag between urethral relaxation (Ou) and detrusor contraction(Od) , and the sudden acceleration in closure pressure fall at Om.(middle graph), figure 4. We know from video micturition studies (7,8) that the urethra is always actively stretched open by pelvic floor contraction prior to urine loss, and we consider that in patients with DI, the same external muscle force acts as an accelerator for the micturition reflex (Om, figure 4). The detrusor contraction"Y" in the bottom graph "B", figure 4, has the classical bell-shaped curve of a feedback system; Om and urine loss were controlled at an early stage by "C", middle graph. As the detrusor continued to contract beyond the zone of urine loss (shaded area,bottom graph), we assume that control of urine loss was achieved by early activation of the peripheral control mechanism (Cm, figure 2). This constricted the urethra, raised urethral resistance, and therefore, detrusor pressure (12). At the same time, the stretched vagina supported the urine column, decreasing the afferent stimulus from the stretch receptors, allowing the closure reflex "C" to predominate over "O", resulting in cessation of detrusor activity. 

Low compliance we regard as a partial but stable suppression of the micturition reflex "O" during filling. Od , figure 2, is contained in perfect balance by the central and peripheral control mechanisms "C". Cm contracts sufficiently to increase the urethral resistance. This, in turn, causes rise in detrusor pressure (12),( low compliance). 

How neurological lesions may cause urinary dysfunction With reference to figure 2, a neurological lesion anywhere along the spinal cord or brain may interfere with the feedback loop. Thus MS lesions in the spinal cord may interfere with the inhibitory signal "C". This allows the afferent impulses Oa to pass through the brain more freely. The bladder is far more frequently in "open" mode (reflex incontinence). Transection of the spinal cord will not allow Cm to relax, or Om to open out the urethra. The patient remains in "closed" mode, with urinary retention. Diabetic neuropathy may affect Oa or Oe , causing urinary retention . 

Irritative lesions Inflammation , tumours of the bladder base area, and perhaps even the pathogenic processes causing interstitial cystitis may stimulate the stretch receptors "N", figure 2, to fire off at a lower threshold. This concept may be extrapolated to include isolated irritative foci. Our clinical experience indicates the latter may represent a small minority of cases only. 

A connective tissue pathogenesis for female urinary dysfunction We have hypothesized (5,6), that mechanical problems (stress, emptying problems) and symptoms of an unstable bladder, have, in the main, a common origin, laxity in the vagina or its supporting ligaments. Connective tissue damage, may be birth related, figure 3, or congenital. At least for stress incontinence this is obvious. All surgical operations stretch (and therefore tighten) the vagina in some way. 

How vaginal laxity may cause mechanical problems Laxity in the anterior zone may prevent the twin forward forces, figure 1, from stretching the vaginal hammock to create water-tight closure of the urethra (genuine stress incontinence, insensible loss). Laxity in the middle or posterior zones may prevent the backward forces (Om, figure 2,) (backward/downward arrows, figure 1) from stretching open the outflow tract. This concept explains the conundrum of apparent urethral obstruction on urodynamic testing, with no urethral narrowing to be found at surgery. Urethral resistance to emptying is inversely proportional to the 4th power of the radius (15). If, for example, the lax vagina can only stretch the lax urethra to half(1/2) its fully opened diameter by applying Om figure 2 , then the resistance to urine outlow is 16 times greater (1/2x1/2x1/2x1/2) than it should be, and this is interpreted urodynamically as obstructive flow, raised residual urine, and symptomatically as difficulty in initiation of flow, slow flow, interrupted flow, and a feeling of not having emptied. 

EXPLANATION OF THE DIAGNOSTIC ALGORITHM We recommend that the algorithm be copied, and each parameter ticked if positive. The anatomical defects are then confirmed by vaginal examination and recorded. Following this, the diagnosis becomes pictorially evident. The anterior zone is distal to the transverse sulcus of bladder neck, the midzone between this and the cervix, and the posterior zone behind the cervix. 

NOTE: even a 1st degree of prolapse may cause symptoms; the amount of prolapse is not linearly related to the quantum of symptoms. 

Anterior zone defects 

The three directional closure forces which mechanically close the outflow tract effectively act against the anterior ligamentous supports of the vagina (7,8), figure 1. Therefore stress incontinence (genuine stress incontinence) is the main manifestation of anterior zone defect. Anything preventing watertight closure of the vaginal hammock may inactivate the forward closure force (continuous leakage, unconscious incontinence). FNU may occur because of failure of the forward forces to stretch the vagina sufficiently to support "N", figure 1. Faecal incontinence is included because it was cured in almost 100% of cases following IVS operation (13). 

A cough transmission ratio (CTR) above 100% in the proximal urethra changing to less than 100% in the distal urethra may signify excessive stretching and narrowing of the proximal urethra by the backward forces, figure 1, induced by pubourethral ligament laxity. CTR <100% in the distal urethra may signify hammock laxity (5). No explanation is offered by the ICS to explain such changes in pressure transmission ratios. 

Midzone defects may prevent the backward and downward forces from mechanically stretching open the urethra, and may invalidate the bladder neck closure mechanism, figure 1. 

Therefore emptying symptoms (underactivity, overflow incontinence, postmicturition dribble) and urodynamic indicators such as slow peak or mean flow rate, prolonged emptying time, raised residual urine etc. are also an important component of mid zone defects, figure1. FNU may occur because of failure of the backward forces to stretch the vagina sufficiently to support "N", figure 1, and stress incontinence, (albeit less frequently), because of their failure to pretension the vaginal hammock(6). 

Posterior zone defects The downward force is a key component in mechanically stretching open the bladder base during micturition, but also during closure (7,8). 

Therefore emptying symptoms (underactivity, overflow incontinence, postmicturition dribble) and urodynamic indicators such as slow peak or mean flow rate, prolonged emptying time, raised residual urine etc. are an important component of posterior zone defects, figure1.

 A positive Valsalva PTR in the presence of stress incontinence has been described as an important objective sign in posterior zone laxity (6). Restoration of the posterior ligaments, the insertion point of the downward force, frequently improves genuine stress incontinence, urge incontinence, nocturia ,detrusor instability, sensory urgency, (6,14) , especially in patients with prior hysterectomy. Hysterectomy would predispose to middle and posterior zone laxity. We therefore advise uterine conservation where possible. Though nocturia may occur with laxity in all 3 zones, we have found empirically that nocturia occurs more frequently with posterior zone defects, perhaps in a ratio of 4 to 1. We hypothesize that in the supine patient, lax posterior ligaments may not adequately support the distending bladder base, allowing the stretch receptors to fire off prematurely, so that the urge symptoms cause the patient to wake and go to the toilet, nocturia. This concept is better understood by rotating figure 1 clockwise at 90 degrees. Non-urinary symptoms caused by vaginal laxity confer greater accuracy upon the algorithm. Pelvic pain of otherwise unknown origin has been cured by repairing laxity in the posterior ligaments of vagina (16). 

Direct testing of the anatomical classification 

Laxity in the 3 zones of vagina, figure 3, can be confirmed directly by vaginal examination. Application of an artery forcep on one side exactly at midurethra (midurethral one-sided Bonney test) almost invariably controls supine urine loss with coughing (6). This same maneouvre during perineal ultrasound observation (unpublished data), may prevent abnormal descent and funnelling of bladder base. Support of bladder base with sponge-holding forceps generally reverses urge symptoms in patients examined with a full bladder. Significant improvements in urine leakage on insertion of The Continence Guard for both stress (17) and urge incontinence (18) appears to confirm our hypothesis of vaginal laxity being a principal cause of urinary dysfunction. The Continence Guard stretches the middle zone of the vagina (17). This would tighten the hammock and enhance the action of the posterior force on the urethra. Palpation of the prolapsed cervix or vaginal vault in patients with pelvic pain of otherwise unknown origin, figure 1, generally reproduces that pain. It is frequently possible to control symptoms attributed to posterior laxity with a ring pessary (6). 

Surgical proofs of the anatomical classification 

The hypothesis of vaginal laxity causing urinary dysfunction was directly tested by prospectively repairing specific ligamentous laxity in the 3 zones of vagina according to the pictorial algorithm (14,19,20). These operations gave a high cure rate for stress, urge, frequency, nocturia, and abnormal emptying. Urodynamically diagnosed "detrusor instability" was not a negative prognostic factor (14). The problem of iatrogenic scar tissue at the midzone, figure 1, (excessive vaginal tightness) has been previously described as the "tethered vagina syndrome" (5,6) We believe this condition is generally equivalent to the "pipestem" urethra. The scar tissue "tethers" the forward and backward forces, (arrows, figure 1), causing the backward force to pull open the urethra on being given the signal to close. The cardinal symptom of this condition, therefore, is uncontrolled emptying of the bladder immediately the patient's foot touches the floor on getting out of bed in the morning. The cardinal sign is excessive tightness in the anterior vaginal wall in the area of bladder neck. Cure may be achieved by insertion of a full thickness skin graft in the midzone (6), or Martius plasty, both of which may restore midzone elasticity. Adequate elasticity is needed in the midsection so as to allow separate functioning of the urethral closure mechanism (forward arrows, figure 1) and the bladder neck closure mechanism (backward arrows). 

CONCLUSIONS 

The anatomical paradigm interprets female urinary dysfunction in terms of anatomical defects in 3 zones of the vagina. It was possible to reinterpret almost all the definitions and descriptions of the International Continence Society in terms of this anatomical classification, and to explain how connective tissue laxity in these zones may cause premature activation of the micturition reflex (detrusor instability) stress incontinence and abnormal emptying (dribble, overflow), by weakening the contractile forces of the opening and closure muscles of the pelvic floor. This convergence in anatomical and urodynamic (ICS) concepts explains many previously unexplained phenomena, and potentially opens up an entirely new approach to management, nonsurgical strengthening of specific zones of weakness, or surgical reinforcement using ambulatory "keyhole" methods which do not require catheterization. Both methods are being successfully applied. 

Resource Units for this paradigm, comprise a 120 page handbook, a video on functional pelvic floor anatomy, and pathogenesis, diagnostic triage. A 2nd video demonstrates the operations themselves, and explains the rationale therof . These are available from Dept of Media, Edith Cowan University, Churchlands Campus, Pearson St, Churchlands WA. FAX +61-8- 92738029. 

LEGENDS Figure 1 Diagnostic pictorial algorithm This is a schematic 3 dimensional view of bladder supported by vagina. The arrows represent directional striated muscle forces. 'N' = stretch receptors at bladder base. 

 

ANTERIOR DEFECT  (xs laxity)	MIDDLE DEFECT  (xs laxity)	POSTERIOR DEFECT  (xs laxity)
Principal symptoms  SI (severe)  Ur loss on standing  post-stress instability  'always damp' faecal incontinence (FI)  noct enuresis /cured at puberty or 'wet since childhood'    Principal signs  lax hammock  +ve pad test (SI)  +ve midurethral Bonney  'funnelling' on U/S  UVJ prolapse (strain)  Urodynamics  +ve CTR with SI stress related DI	Principal symptoms  emptying  FI persisting after IVS  Principal signs  cystocoele  ATFP defect  Urodynamics  raised residual slow emptying time +ve PTR (Valsalva) with SI  xs tightness 'tethered vagina'  uncommon(5%), iatro genic,  may occur years after vag surg/ BNE  'motor' DI getting out of bed  often no major SI	Principal symptoms  incont symptoms worse 1 week before period  pain - low abdo          - low sacral           - deep dyspareunia  emptying  nocturia  Principal signs  1.excitation pain - cervical or vaginal  2. prolapse  uterus or vagina (enterocoele)    Urodynamics  raised residual slow emptying time  +ve PTR (Valsalva) with SI

NOTE 

1) FNU (frequency, nocturia, urgency) may occur with all defects 

2) not all criteria may be present in a particular defect 

Figure 2 Schematic outline of central and peripheral control of the micturition reflex. 

This is a sagittal simplified schematic representation of bladder, urethra, vagina, spinal cord (SC) and brain. "N"= nerve endings at bladder base, SM = intraurethral striated muscle sphincter. The broken lines represent the paths for closure"C". The unbroken lines "O" represent the paths of the micturition reflex - afferent outflow(Oa) from "N" to spinal cord and brain, and efferent flow(Oe) to detrusor(Od),urethra (Ou)and pelvic muscles (Om). . CTX = cortex. The two directional arrows below vagina (V) represent the muscle forces acting during the micturition (Om) and closure (Cm) reflexes. 

Figure 3 

Damage to vagina at childbirth 

The circles represent the foetal head overstretching the connective tissue of vagina and its supporting ligaments as it descends through the birth canal. 

1 hammock and pubourethral ligament (PUL) laxity 

2 cystocoele and arcus tendineus fasciae pelvis (ATFP) laxity 

3 uterosacral/cardinal(USL) ligament laxity (uterine prolapse and enterocoele) 

4 rectocoele 

Figure 4 

Manifestations of the micturition reflex during a handwashing test 

U=urethral pressure; B=bladder pressure; CP = closure pressure; C=closing reflex . O=opening (micturition) reflex. X=commencement of urethral relaxation. Y=commencement of detrusor contraction. 

Upper graph (U) Note the time delay between the effects of O" and "C"on urethral pressure. 

Middle graph Note the effect on closure pressure as urethral relaxation (Ou), detrusor contraction (Od) and active opening of the urethra (Om), are recruited in turn. The large arrow represents the instant when the patient involuntarily commenced passing urine. C represents the closure force exerted by the pelvic floor. 

Lower graph Note the bell-shaped curve of the detrusor contraction. The shaded column immediately below the large arrow represents the time interval during which urine was lost. The small arrows represent the efforts of the striated urethral muscle attempting closure. 

REFERENCES 

(1) Bates P. Bradley WE. Glen E. et al. First Report On The Standardisation Of Terminology Of Lower Urinary Tract Function. Brit Journ of Urology (1976); 48:39-42 

(2) Abrams P, Blaivas J, Stanton S and Andersen J. Standardisation of Terminology of Lower Urinary Tract Function. Scand J. Urol Nephrol. (1988), Suppl. 114. 

(3) Black N, Griffiths J, Pope C, Bowling A and Abel P, Impact of surgery for stress incontinence on morbidity: cohort study. Brit. Med J (1997),, 315, 1493-8. 

(4) Hall JC, and Platell C,Half-life of truth in surgical literature, The Lancet (1997 ), 350: 9093; 1752 

(5) Petros PE & Ulmsten U. An Integral Theory of female urinary incontinence. Acta Obstetricia et Gynecologica Scandinavica, Supplement 153, Vol 69, (1990), 1-79. 

(6) Petros PE & Ulmsten U. An Integral Theory and its Method for the Diagnosis and Management of Female Urinary Incontinence, Scandinavian Journal of Urology and Nephrology (1993) -Vol 27 Supplement No 153 - 1-93. 

(7)Petros PE and UlmstenU, Role of the pelvic floor in bladder neck opening and closure: II vagina. Int J Urogynecol and Pelvic Floor, (1997) 8: 69-73. 

(8) Petros PE and UlmstenU, Role of the pelvic floor in bladder neck opening and closure: I muscle forces, Int J Urogynecol and Pelvic Floor, (1997), 8:74-80. 

(9) Petros PE & Ulmsten U. Tests for detrusor instability in women These mainly measure the urethral resistance created by pelvic floor contraction acting against a premature activation of thre micturition reflex. Acta Obstetricia et Gynecologica Scandinavica, (1993): 72: 661-667.

(10)Petros PE & Ulmsten U. Bladder instability in women: A premature activation of the micturition reflex. Neurourology and Urodynamics 12, 235-239 (1993).

(11) Petros PE and Ulmsten U ltr Is detrusor instability a prematurely activated (but otherwise normal) micturition reflex? Lancet (1997)No 9050, vol 349, 505. idem 1255-6

(12) Griffiths DJ. Assessment of detrusor contraction strength or contractility. Neurol & Urodynamics, (1991), 10:1-18.

(13) Petros PE, Surgical cure of faecal incontinence in the female by reconstruction of the anterior ligamentous supports of vagina , Abstract, (1994), ICS Meeting, Prague, Czech Republic.

(14) Petros PE, New ambulatory surgical methods based on an anatomical classification of urinary dysfunction improve stress, urge, and abnormal emptying, Int J of Urogynecology (1998) vol8, in press.

(15) Bush MB, Petros PEP, Barrett- Lennard BR, On the flow through the human urethra (1997) Biomechanics 30:9,967-969.

(16) Petros PE Severe chronic pelvic pain in women may be caused by ligamentous laxity in the posterior fornix of the vagina . Aust NZ journal of Obst and Gyanaecol, 1996; 36:3: 349-353.

(17) Thyssen HH and Lose G, Long-term efficacy and ssfety of a disposable vaginal device (Continence Guard) in the treatment of female stress incontinence, Int J urogynecol J (1997) 8; 130-133.

(18) Thyssen HH , Sander P, and Lose G, vaginal device (Continence Guard) in the treatment of urge incontinence in women, Neurourology and Urodynamics,16:,5, 484-486.

(19) Ulmsten U, Henriksson L, Johnson P, and Varhos G, An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence, Int Urogynecol J 7: 81-86 (1996).

(20) Falconer C, Ekman-Orderberg G, Malmstrom A and Ulmsten U, Clinical outcome and changes in connective tissue metabolism after Intravaginal Slingplasty in stress incontinent women, Int Urogynecol J (1996) 7: 133-137.

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