Dynamic Testing - International Continence Society · 2015. 12. 14. · This chapter on “Dynamic...

ABBREVIATIONSBOO bladder outlet obstructionBOOI bladder outlet obstruction index, previously

known as AG numberBPE benign prostatic enlargementBPO benign prostatic obstructionDHIC detrusor hyperactivity with impaired

contractile functionDO detrusor overactivityDOI detrusor overactivity incontinenceEMG electromyogram/electromyographyFDV first desire to voidFSF first sensation of fillingICS International Continence SocietyIPSS International Prostate Symptom ScoreISD intrinsic sphincter deficiencyLPP leak point pressureLUT lower urinary tractLUTS lower urinary tract symptomsMax Cap maximum cystometric capacityMRI magnetic resonance imagingMUP maximum urethral closure pressureNDV normal desire to voidNPV negative predictive value (see section C.IV.1)OAB overactive bladder syndrome/symptomsPOP pelvic organ prolapsePPV positive predictive value (see section C.IV.1)PVR post-void residual urine (volume)SD standard deviationSDV strong desire to voidSEM standard error of the meanSPECT single photon emission computed tomographySPT specificity (see section C.IV.1)STV sensitivity (see section C.IV.1)TURP transurethral resection of the prostateTVT tension-free vaginal tapeUSI urodynamic stress incontinenceVLPP Valsalva leak point pressure

REFERENCES

F. CONCLUSION

E. DYNAMIC TESTING FORFAECAL INCONTINENCE

D. CLINICAL APPLICATIONSOF URODYNAMIC STUDIES

C. URODYNAMICS: NORMALVALUES, RELIABILITY, AND

DIAGNOSTIC AND THERAPEUTIC

PERFORMANCE

B. MECHANISMS OF URINARYCONTINENCE AND

INCONTINENCE

A. INTRODUCTION

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CONTENTS

This chapter on “Dynamic Testing” is the successorto the chapters on “Urodynamic Testing” in the twoprevious consultations. [1,2] The name changereflects the inclusion of a new topic, faecal (or anal)incontinence. In the section on faecal incontinence,the available functional tests, their applications invarious groups of patients and types of faecal incon-tinence, and the evidence for their clinical utility, arereviewed in as much detail as is practicable. For uri-nary incontinence, reviews of this sort appeared inthe two previous consultations. [1,2] In this 3rd

consultation we have updated the evidence for thereproducibility and reliability of urodynamic measu-rements, and the evidence for their clinical utility.The primary aim of the chapter however is to reas-sess the functional and anatomic mechanisms of uri-nary continence, to discuss what urodynamic testsought to be performed to elucidate these mecha-nisms; and to make recommendations for what testsshould be performed and when. Thus we have triedto present a critical view of the role of urodynamics,the current state of urodynamic assessment, andrecommendations for the future.

In this chapter, therefore, faecal (anal) and urinaryincontinence are addressed rather differently. Yet infact the 2 topics clearly have much in common, inregard to both pathophysiological mechanisms andclinical application. In future consultations weexpect a more integrated approach to emerge andyield fruitful insights.

Following this introduction, and an explanation ofthe definitions of the various types of urinary incon-tinence and their corresponding urodynamic obser-vations, the chapter contains a fundamental discus-sion of the two main types of urinary incontinence(stress and urge), a review of data about normalvalues and reliability of urodynamic parameters,reviews of the literature regarding clinical urodyna-mic evaluation of different patient groups with uri-nary incontinence (women, men, children, neuroge-nic dysfunction, and the frail elderly), a section ondynamic testing in faecal incontinence, and finallythe committee’s recommendations regarding dyna-mic testing.

1. WHAT IS URODYNAMICS?

The conventional view – implicitly adopted in theprevious consultations – is that urodynamics is aseries of more or less agreed-upon clinical tests, suchas filling cystometry and pressure-flow studies, andthat all that remains to be done is to establish whichtests have clinical utility and in what circumstances.Urodynamics is defined by the International Conti-nence Society (ICS) however as the study of thefunction and dysfunction of the urinary tract by anyappropriate method [emphasis added]. [3] Accor-ding to this definition, urodynamics is the only wayof understanding why people are continent or incon-tinent, because the attempt to gain that understandingis what constitutes urodynamics. Therefore urodyna-mics occupies a central place in this consultation. Itis the pivotal link between basic science on the onehand and clinical reality on the other. It can answerquestions such as: How does the normal person stay

II. HISTORICAL BACKGROUND

I. GENERAL REMARKS

A. INTRODUCTION

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Dynamic Testing D. GRIFFITHS, A. KONDO

S. BAUER, N. DIAMANT, LIMIN LIAO, G. LOSE, W. SCHÄFER, N. YOSHIMURA

H. PALMTAG

continent? What really goes wrong when they beco-me incontinent? These questions can be posed as partof clinical or animal research, but they are importantin individual patients too. Conventional urodynamictesting may not be necessary in every patient, butmaking the appropriate measurements remains theonly way of knowing what urinary tract function is.Treatment that is not carried out blindfolded but isbased on knowledge requires urodynamics.

2. WHAT HAS URODYNAMICS ACCOMPLISHED?

Since urodynamics entered clinical consciousness 40years ago, its main achievement has been to focusattention on neuromuscular function and dysfunc-tion, especially as embodied in the concept of detru-sor overactivity. To a considerable extent this hasbeen useful. For example, it is now universally reco-gnized that stress incontinence is not the only pos-sible reason for urine loss in an otherwise healthymiddle-aged female, and that surgery is not the onlytreatment. Drug and behavioral treatments, aimed atcorrection of function, have been greatly enhanced,as demonstrated in the chapters on pharmacotherapyand conservative management in this book. A lessdesirable consequence has been that attention hasbeen directed away from gross anatomy and structu-ral issues, so that understanding of the anatomicaland mechanical basis of stress incontinence hasadvanced very slowly. In spite of the deeper unders-tanding of dysfunction provided by urodynamics,numerous studies have demonstrated only weak cor-relations between symptoms and urodynamic fin-dings, and there has been little objective evidencethat doing urodynamics – and selecting treatmentoptions on this basis – improves clinical outcomes. Inthe previous consultation, accordingly, the evidencefor clinical utility was judged not particularly cogent,and a rather limited clinical place was suggested forurodynamic testing, especially in women. [1]

3. WHAT SHOULD BE THE ROLE OF URODYNA-MICS IN CLINICAL PRACTICE?

There is general agreement among experts that theimmediate aim of urodynamic testing is to reproducethe symptom(s) of the patient under controlled andmeasurable conditions, so that the cause of the symp-toms can be determined. Certainly, if the symptom isnot reproduced the test can be regarded as a failure(although failure to understand the symptoms mayalso contribute). Conceptually, reproduction of thesymptom allows diagnosis, helps inform treatmentchoice, and improves treatment outcome.

Urodynamic studies provide an objective descriptionof lower urinary tract function and dysfunction interms of qualitative and quantitative variables. Thusideally they should provide objective informationuseful for the clinician:

a) to identify or to rule out factors contributing to theincontinence and assess their relative importance

b) to obtain information about other aspects of lowerurinary tract dysfunction

c) to predict the consequences of lower urinary tractdysfunction for the upper urinary tract

d) to predict the outcome, including undesirable sideeffects, of a contemplated treatment

e) to confirm the effects of intervention or unders-tand the mode of action of a particular type of treat-ment, especially a new one

f) to understand the reasons for failure of previoustreatments for incontinence

Urodynamic studies should be performed and repor-ted in accordance with the standards of the Interna-tional Continence Society [4] to optimize interpreta-tion and facilitate comparison between different stu-dies.

The conventional view is that urodynamic investiga-tion ought to provide a gold standard for assessingincontinence. However there is still a pressing needscientifically to conceptualize continence function interms which can be measured urodynamically. Ideal-ly the chosen variables should fulfill several require-ments: 1) measurements should be standardized; 2)results should be reproducible; 3) parameters forhealth and disease should be specific and sensitivewith clear cut-off levels and without too much over-lap, so as to give clinical useable predictive values;4) parameters should contribute to choice of therapy;and 5) parameters should be correlated with the out-

Main recommendations for urodynamics in cli-nical practice according to the previousConsultation (ICI 2000) [1]:

• Investigation should only be performed inwomen if voiding difficulty or neuropathy issuspected, if previous surgical or non-surgicaltreatments have failed, or if invasive or surgicaltreatments are considered.

• In men and children, detailed urodynamicinvestigation should be undertaken.

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come of therapy for the disease. [5] To what extentthese ideal requirements can in fact be fulfilled isconsidered in this chapter.

Evidence-based medicine is founded on the assess-ment of evidence for and against the efficacy of par-ticular types of therapeutic intervention. Obviouslythere is a temptation to try to apply the same rules ofevidence to clinical tests such as urodynamics,because evidence that testing improves outcome(through treatment choice and patient selection)would provide a strong basis for its use. However,testing and therapeutic intervention are differentconcepts, and urodynamic testing has another impor-tant objective, which is not applicable to interven-tions and lies outside the scope of evidence-basedmedicine. It is to generate knowledge about thecondition(s) to be treated in a given patient, so thatthe practitioner can formulate rational treatmentoptions based on knowledge rather than work blind-fold; that is, he or she can practice “knowledge-based medicine”.

To judge the importance of this second objective dif-ferent criteria are needed. Indeed, reproduction of thesymptom is too narrow and too limited an aim forurodynamic testing if this objective is to be fulfilled.Particularly in the referral setting, the physician isconfronted with complicated cases in whom theunderlying pathophysiology is uncertain, and what isrequired is not just to reproduce the symptom, but toidentify all the factors that may be contributing. Thusa comprehensive evaluation of the function and dys-function of the lower urinary tract is needed. Urody-namics in children with congenital urinary tract pro-blems provides a good example: pathophysiology isvariable and unpredictable, and some type of treat-ment is mandatory, yet often irreversible. Any avai-lable information about the baseline dysfunctionbefore treatment decisions are made is helpful, and itwould be unethical to neglect to gather it. Urodyna-mics is necessary because it contributes to “know-ledge-based medicine”, whether or not there is nar-rowly-defined “evidence” that it improves outcomes.

Of course, it remains true that we should seek evi-dence of the conventional kind for and against tes-ting. The co-sponsor of this consultation (the ICUD)recommends that, as a minimum, any test should besubjected to three questions:

1. Does the test have good technical performance, forexample, do three aliquots of the same urinesample give the same result when subjected to‘stix’ testing?

2. Does the test have good diagnostic performance,ideally against a “gold standard” measure?

3. Does the test have good therapeutic performance,that is, does the use of the test alter clinical mana-gement, does the use of the test improve outcome?

It is revealing that the example chosen for question 1is a particularly simple one where the result can bechecked against other methods of measuring thesame thing. Question 2 begs a deeper question: Inmeasuring urethral/vesical function, how can therebe any gold standard other than the measurementsthemselves? Question 3 is relevant in the context ofevidence-based medicine, and in this chapter weshall address it.

A recent Cochrane review [6] attempted to test thehypotheses that:

• Urodynamic investigations improve the clinicaloutcomes of incontinence management

• Urodynamic investigations alter clinical decision-making

• One type of urodynamic test is better than anotherin improving the outcomes of incontinence mana-gement and/or influencing clinical decisions.

The authors found only 2 relatively small randomi-zed trials (both in women) that tested one or more ofthese hypotheses. [7,8] They concluded that therewas not enough evidence to show whether womenwith incontinence who underwent urodynamics wereless likely to be incontinent after treatment thanwomen who did not undergo urodynamic testing.They recommended further randomized trials in alltypes of patients whose incontinence might be inves-tigated with urodynamics, estimating that such trialswould need about 400 patients in each arm to provi-de 80% power to detect a 10% difference in inconti-nence rates at a significance level of 5%.

At present therefore there is limited objective evi-dence for the clinical utility of urodynamics, and apressing need to examine this question. If future stu-dies confirm that urodynamics has limited effect onoutcomes or decision-making, however, this wouldimply that it is not important to understand how thelower urinary tract works in order to treat it with cur-rent methods. Such a surprising conclusion couldhave only a few possible explanations:

III. THIS CHAPTER

589

a. All the patients in any given symptom group (e.g.women with stress incontinence) have similarunderlying pathophysiology requiring similartreatment, and so urodynamics cannot classifythem any better than the symptoms alone.

b. Conventional urodynamics does not address theimportant pathophysiological differences thataffect treatment success – i.e., we are doing thewrong tests.

c. We are doing the right tests, but we are doing themso poorly (technically) that the results are unre-liable.

d. Current treatments are so non-specific and non-quantitative that the underlying dysfunction isunimportant: treatment works equally well orpoorly in any case.

Comments:

• The studies that show that symptoms and urody-namic findings do not correspond very well [1]make possibility “a” unlikely, because they showthat similar symptoms have different underlyingpathophysiology as revealed by urodynamics.Moreover, we think we know that detrusor ove-ractivity and urge and stress incontinence eachcome in multiple types.

• There is strong suspicion, based on expert opi-nion, that possibility “c” is correct – that urodyna-mics is often done poorly; the International Conti-nence Society and other bodies are improving thissituation by establishing standards for proper trai-ning and certificate programs in urodynamics. [9]

• Possibility “b” is a likely explanation: the conven-tional urodynamic testing that we do is inadequa-te by itself to unravel the pathophysiologicalbehavior we are interested in.

• Possibility “d” is also likely to be correct: becau-se of our lack of understanding, current treatmentsare not aimed accurately at the right target.

Some of the mismatch between symptoms and uro-dynamic findings is due to inherent physiologicalvariability in the function of the lower urinary tract,which is reflected in the urodynamics (as well as inthe variability of symptoms). For example, post-voidresidual urine in the elderly [10] shows a diurnalvariation that implies that there are systematicchanges in some unknown controlling parameter.Similarly, analysis of the variability of voiding stu-dies in adult males reveals an unknown source ofvariation that affects detrusor contractility and ure-thral resistance simultaneously. [11] Even more

revealingly, normal subjects and near-normalpatients often find it difficult to reproduce their usualbehavior – for example to void, or demonstrateincontinence – under the artificial circumstances of aurodynamic test, or they require a particular type ofprovocation such as hearing running water, to elicitit. This physiological variability of urodynamicresults shows that – in neurologically intact subjects– they are not just measurements of the fixed proper-ties of a mechanical system. Physiological variabili-ty is not an indication of unreliability; it is a promisethat there are neurological or cortical sources ofcontrol that we have hardly begun to imagine. Iden-tification of these sources offers the prospect of enti-rely new therapies.

Possibilities “b” and “d” both imply that the mismat-ch between urodynamic findings on the one hand andsymptoms, treatment selection, and outcomes on theother reflects gaps in our understanding of what iswrong and how it should be corrected. In fact, thereare obvious omissions in conventional urodynamics.Attention is focused on the accessible end organs(the bladder and urethra) and the easy measurements(pressure, volume and flow rate), leaving large gapsin what is studied:

a. The urethra and pelvic floor form a complicatedstructure whose mechanics is critical to continen-ce under stress conditions, yet it is currentlyunderstood in only a most rudimentary way. [12]

b. The bladder and urethra are just the tip of the ice-berg of a complicated nervous control system thatcan go wrong at any level. Any abnormality, fromcerebral cortex to brainstem, to spinal cord, rightdown to the end organs, may lead to symptomssuch as urgency, frequency or incontinence.Impairment of cortical control is obviously impor-tant but almost entirely ignored.

Filling in these gaps will deepen our understandingof the pathophysiology of urinary incontinence,improve our understanding of patients’ symptoms,and possibly lead to new treatments. However, it willalso require new or improved types of urodynamicstudy. One of the aims of this chapter is to discusswhat types of study ought to be done in this new uro-dynamics.

Finally, evidence-based medicine as currentlyconceived is only one aspect of good medicine. Ano-ther aspect is understanding of function and dysfunc-tion – knowledge-based medicine – and it dependson urodynamics. In each patient group the relativeimportance of evidence-based and knowledge-basedmedicine differs and must be established.

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One of the main aims of a urodynamic test –although not the only aim – is to reproduce the symp-tom. Standards have been set out to define symptomsand to define urodynamic observations, but it notalways clear what urodynamic observation repro-duces what symptom. Here we attempt to clarify thesituation.

1. DEFINITIONS

The following definitions are taken from the standar-dized terminology of the International ContinenceSociety. [4] Comments are bulleted. The standardisa-tion reports of the International Continence Societyshould be consulted for definitions not included here.[3,4]

Urinary incontinence is the complaint of any invo-luntary leakage of urine.

• In each specific circumstance, urinary incontinen-ce should be further described by specifying rele-vant factors such as type, frequency, severity, pre-cipitating factors, social impact, effect on hygieneand quality of life, the measures used to containthe leakage and whether or not the individualseeks or desires help because of urinary inconti-nence. For the purpose of urodynamics, the typeof incontinence is the most relevant factor.

• Each type of incontinence may be described as asymptom, a sign, or a urodynamic observation.

Detrusor overactivity is a urodynamic observationcharacterised by involuntary detrusor contractionsduring the filling phase which may be spontaneousor provoked.

• Although we will use this term, we believe it ismisleading to call detrusor activity observedduring the filling phase “overactivity”, since it isobserved also in healthy volunteers (see sectionB.II, urge incontinence).

“Urethral instability”: Fluctuations in urethralpressure have been defined as the “unstable urethra”.However, the significance of the fluctuations and theterm itself lack clarity and the term is not nowrecommended by the International ContinenceSociety

• If symptoms are seen in association with a decrea-se in urethral pressure a full description should begiven.

• It is misleading to term urethral pressure changesobserved during the filling phase “urethral insta-bility”, since the term seems to imply dysfunctionwhen the behavior may be entirely normal.

Stress urinary incontinence denotes a symptom :the complaint of involuntary leakage of urine oneffort or exertion, or on sneezing or coughing.

The corresponding sign of stress urinary inconti-nence is the observation of involuntary leakage fromthe urethra, synchronous with exertion/effort, orsneezing or coughing, i.e. a positive stress test.

The corresponding urodynamic observation is uro-dynamic stress incontinence, which is the involun-tary leakage of urine during increased abdominalpressure, in the absence of a detrusor contraction,noted during filling cystometry.

• This means the demonstration of leakage onabdominal pressure increase due to moving, strai-ning or coughing, without any effect on the detru-sor pressure signal. This requires careful controlof signal quality.

Urge urinary incontinence is the complaint of invo-luntary leakage accompanied by or immediately pre-ceded by urgency.

The corresponding sign has not been clearly defined.

• This is partly because urge incontinence can pre-sent in different symptomatic forms; for example,frequent small losses between micturitions orcatastrophic, complete bladder emptying; andpartly because urge incontinence is unpredictableand difficult to elicit in a physician’s office.

The corresponding urodynamic observation isdetrusor overactivity incontinence: incontinencedue to an involuntary detrusor contraction.

Urethral relaxation incontinence, defined as leaka-ge due to urethral relaxation in the absence of raisedabdominal pressure or detrusor overactivity, mightalso correspond to the symptom urge incontinence.

• The sensation accompanying detrusor overactivi-ty incontinence or urethral relaxation incontinen-ce should be noted, as if there is none, this couldnot strictly speaking be said to reproduce thesymptom urge incontinence.

Urgency is both a symptom and a urodynamic obser-vation.

The symptom of urgency is the complaint of a sud-den compelling desire to pass urine which is difficultto defer.

IV. DEFINITIONS AND TERMINOLOGY

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• It may accompany urge incontinence (see above),or may occur with other overactive bladder symp-toms (see below) or in isolation.

Urgency as a urodynamic observation is a suddencompelling desire to void, noted during filling cysto-metry.

• Urgency may be associated with leakage (detrusoroveractivity incontinence), or with detrusor ove-ractivity, or with neither. It is frequently observedwithout any demonstrable detrusor overactivity.

• One might expect a relation between urethralpressure changes and the sensation of urgency.However, there seem to be no publications sho-wing such a relation.

• Urgency, with or without urge incontinence, isoften associated with frequency and/or nocturia.The terms overactive bladder syndrome, urgesyndrome or urgency-frequency syndrome des-cribe symptom combinations that are suggestiveof urodynamically demonstrable detrusor overac-tivity but may be due to other forms ofurethral/vesical dysfunction. These terms are usedif there is no proven infection or other obviouspathology.

Mixed urinary incontinence denotes a symptom :the complaint of involuntary leakage associated withurgency and also with exertion, effort, sneezing orcoughing.

• This ICS definition leaves it open as to whetherboth forms of incontinence occur (a) simulta-neously or (b) at different times. Possibility (b)seems to be more common.

• In publications it sometimes appears that mixedincontinence is assumed to include the symptomof stress incontinence, together with complaints ofurgency and frequency not related to the inconti-nence episodes. This is not mixed incontinence asdefined by the International Continence Societyand use of the term in this way should be avoided.

The sign corresponding to mixed incontinence is notclear.

The corresponding urodynamic observations includeseparate demonstration of urodynamic stress inconti-nence and detrusor overactivity incontinence in asingle urodynamic testing session.

• The picture becomes complicated if detrusor ove-

ractivity is provoked, e.g. by coughing, and leaka-ge ensues. Nevertheless it may reproduce possibi-lity (b).

• It is sometimes assumed that the observation ofurodynamic stress incontinence and (separately)detrusor overactivity reproduces the symptom ofmixed incontinence. This is not in conformitywith the definition.

• Clinical reports show that standard stress inconti-nence surgery can cure “mixed incontinence” butalso can lead to new symptoms of urgency. Howe-ver, as neither the symptom definitions used northeir urodynamic correlates are very clear, urody-namic objectification of symptomatic mixed uri-nary incontinence is difficult, and these reportsremain difficult to interpret.

Increased daytime frequency is the complaint bythe patient who considers that he/she voids too oftenby day.

This term is equivalent to the term pollakisuria, usedin many countries.

The corresponding sign is not clear.

The corresponding urodynamic observation might bedetrusor overactivity; alternatively a small bladdercapacity, with or without detrusor overactivity, mightaccount for the symptom. (Note however that blad-der capacity is a variable measurement, see sectionB.II, urge incontinence.) Increased diuresis, asshown by a bladder diary or voiding record, mightalso account for increased frequency.

2. FURTHER COMMENTS

Differentiation between urodynamic stress inconti-nence and detrusor overactivity incontinence issimple if clear detrusor overactivity can be demons-trated without physical activity and with the sensa-tion of urgency; or if leakage occurs on stress withno hint of any detrusor overactivity. However, inmany cases the correlation between symptoms andurodynamic observations is less clear.

Table 1 sets out for the main symptoms the principalcorresponding urodynamic observations. Note thatthis table does not imply that the cited urodynamicobservation is always made with the given symptom;urodynamic tests often reveal unexpected subtleties.For definitions and commentary see main text.

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1. STRESS URINARY INCONTINENCE

According to the standardised terminology of theInternational Continence Society, the symptom ofstress urinary incontinence is the complaint of invo-luntary leakage of urine on effort or exertion, or onsneezing or coughing. [4] Its relation to signs andurodynamic observations is considered in the intro-ductory section A.IV, Definitions and terminology.In this chapter we will also use the following urody-namically based definition of stress incontinence:Stress incontinence occurs when the bladder closuremechanism is competent (= continent) at rest, butbecomes incompetent under stress.

The key to the pathophysiology of stress incontinen-ce lies in understanding the impact of abdominal

pressure increase (“stress”) on the closure mecha-nism of the bladder outlet. Urodynamic measure-ments of the function of the bladder closure mecha-nism during stress are difficult, and most existingdata are reported with inadequate control of dataquality, or none at all. In considering any changesobserved in the bladder closure mechanism and pel-vic floor, or the impact of stress on these structures,the inherent limitations on measurement qualityshould be borne in mind. In general it is possible toverify stress incontinence urodynamically, but it isdifficult to exclude it urodynamically.

• Mixed urinary incontinence

This is discussed in section A.IV, Definitions and ter-minology.

2. NORMAL CONTINENCE MECHANISMS

The simple urodynamic rule for continence is that aslong as the urethral pressure is higher than the intra-vesical pressure, i.e. the urethral closure pressure ispositive, incontinence cannot occur. Active and pas-sive mechanisms play a role in maintaining conti-nence. Sustained tone of the circularly-arrangedsmooth and striated urogenital sphincter musclesprovides the resting closure pressure. The striatedmuscle within the proximal and mid-urethral regionsis generally referred to as the striated sphincter, theexternal urethral sphincter, or the rhabdosphincter. Incooperation with the circular smooth muscle, theexternal urethral sphincter mechanism as a wholecomprises nearly the proximal two-thirds of the ure-thra. [13] The requirement for equilibrium of forcessuggests that the longitudinal smooth muscle is alsoactive during urine storage (not during voiding, asoften suggested), so as to prevent tissue from beingsqueezed out from the high-pressure zone under thestriated sphincter; and that it forms an integral part ofthe closure mechanism, although it contributes to theclosure pressure only indirectly. [12] Any pressuresignal recorded in the striated sphincter is influencedby the surrounding abdominal contents and the pel-vic floor muscle. The fact that the striated sphincterand the periurethral skeletal muscle of the pelvicfloor differ histomorphologically and are physicallyseparate does not mean that that they do not worktogether mechanically; in fact, the periurethral skele-tal muscle of the pelvic floor seems to correspond tothe zone where urethral closure pressure is highest(see however Figure 1 for a different point of view).Thus one must assume a mechanical continuity bet-ween sphincter and surrounding pelvic floor so thatit is not possible to distinguish by urodynamic pres-

I. STRESS INCONTINENCE

B. MECHANISMS OF URINARYCONTINENCE AND

INCONTINENCE

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Table 1. Symptoms and corresponding urodynamic observa-tions

Symptom Urodynamic observation

Stress incontinence Urodynamic stress incontinence

Urge incontinence Detrusor overactivity incontinence withurgencyorUrethral relaxation incontinence with urgency

Mixed incontinence Urodynamic stress incontinence (USI) + detrusor overactivity incontinence (separately)Not recommended: USI + detrusor overactivity

Urgency Detrusor overactivity with sensationorother relevant urethral and/or vesical dysfunction (e.g. increased sensation)

Frequency Detrusor overactivityorother relevant urethral or vesical dysfunction (e.g. small bladder capacity or increased diuresis)

sure measurements between the individual contribu-tions of the sphincter and the pelvic floor muscle.[12]

Urinary continence is thought to be maintainedduring elevation of abdominal pressure by multiplemechanisms: the same sustained closure mechanismthat also acts during resting conditions; passive pres-sure transmission within the abdominal pressureregion;[13] and extra closure forces generated byactive contraction of the sphincter and the pelvicfloor. Because urethral pressure recording cannotidentify the origin of any pressure increase, andbecause published human data appear not to be ofhigh enough quality to exclude an artifactual “pres-sure” increase due to catheter movement within theurethra, or to the forces associated with bending oracceleration of the catheter, quantification of anyactive increase in urethral pressure is difficult.

The transmission of abdominal pressure to the proxi-mal urethra is considered to be an important mecha-nism of continence. However, the term “transmis-sion” should not be taken literally in the sense thatthe pressure is generated somewhere else (e.g. in theupper abdomen) and transmitted to the proximal ure-thra. Much more realistic is the concept of an abdo-minal pressure region in all parts of which the abdo-minal pressure increases or decreases simultaneous-ly. For an increase in abdominal pressure to occur,the muscles which bound this region (the abdominaland pelvic muscle sheets and the diaphragm) mustdevelop tension. To generate this tension, musclecontraction must start before the abdominal pressureincreases measurably.

Simple mechanical considerations show that as longthe abdominal pressure increase affects the bladderand urethra similarly, the pressure balance maintai-ning continence is not altered and stress incontinen-ce cannot occur. Although this simplistic concept isvalid in principle, it is obviously not sufficient toexplain the mechanics of stress incontinence, as isclear from the failure of a variety of surgicalconcepts, which have attempted to elevate the blad-der neck back into the abdominal pressure region, soas to fully expose it to “abdominal pressure trans-mission”. [14]

Another possible mechanism for maintaining conti-nence is neurally-mediated urethral closure understress conditions. This concept is based on variousclinical observations combined with urodynamicmeasurements, including: (i) the fact that the urethralpressure rises prior to cough transmission, [15,16](ii) the fact that the increase in urethral pressureduring coughing exceeds the increase in bladder

pressure, [15,17-19] and (iii) the fact that bilateralpudendal nerve blockade reduces urethral closureforces during coughing. [20] However, recording oflocal urethral pressures under stress is subject to arti-facts caused by transducer movement along the ure-thral axis, or by interaction with the urethral wall dueto deformation or acceleration. In fact, Constantinouand coworkers [18] emphasized the directionality ofthe recorded signals, so making it clear that theywere not recording a closure pressure; therefore theinterpretation of the reported urodynamic observa-tions is questionable.

Nevertheless, despite these criticisms, the concept ofan active, neurally-mediated urethral closure mecha-nism operating under stress conditions may still becorrect. A recent study in rats using microtip trans-ducer catheters and nerve transection techniques hasshown that urethral contractile responses duringsneezing, which did not disappear after abdominalopening (and therefore cannot have been caused by“abdominal pressure transmission”) were suppressedby transection of somatic nerves innervating thestriated urethral sphincter and pelvic floor muscles.[21] These apparently active contractile responseswere most prominent in the middle third of the ure-thra, at the location of the striated sphincter and pel-vic floor muscles. At the bladder neck, on the contra-ry, the urethral pressure changes on sneezing werevery similar to those in the bladder, and were aboli-shed on opening the abdomen, suggesting that“abdominal pressure transmission” does play animportant role in bladder neck closure. This worksupports the view of Turner-Warwick that there are 2urethral closure mechanisms, a proximal and a distalone (Figure 1). [22,23] According to this view, theproximal mechanism relies on abdominal pressuretransmission to the bladder neck, which is maintai-ned closed by sustained smooth muscle contraction.The distal mechanism relies on changes in the pelvicfloor and striated sphincter, which have active aswell as passive components. Only if both mecha-nisms are faulty does the patient become stress-incontinent (Figure 1).

The “pressure” increase recorded in the urethra priorto any abdominal pressure increase has been termedthe “guarding reflex”. [18] However, contraction ofthe muscles surrounding the abdominal pressureregion is an essential part of any activity which isassociated with an abdominal pressure increase,irrespective of continence function. Muscle contrac-tion, as recorded for example in the striated sphinc-ter zone, may therefore precede the abdominal pres-sure increase.

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3. WHAT GOES WRONG? HOW ABNORMALITYLEADS TO INCONTINENCE

Differences in anatomy, direct physical insult fromchildbirthing events, and hormonal changes associa-ted with pregnancy, aging and menopause, leading toalterations in the distribution of neuronal receptors,have all been suggested as contributors to the preva-lence of incontinence in an aging female population.[24,25] DeLancey et al have also shown thatapproximately 60% of patients with prolapse butonly 30- 40% of incontinent females have a signifi-cant levator damage. [26]

Stress urinary incontinence is conventionally subdi-vided into two categories; (1) anatomic incontinence(type II incontinence or urethral hypermobility) and(2) intrinsic sphincter deficiency (type III inconti-nence, or a poorly functioning but better supportedurethral sphincter). [27,28] From the point of view ofour definition - that stress incontinence overcomes aclosure mechanism which is competent at rest - thenthis distinction seems to be either trivial or artificial.Obviously it takes less stress to overcome a weakurethral closure mechanism, and it is also obviousthat greater mobility indicates a weaker pelvic floorwhich will allow more deformation. The data show -as is to be expected - that sphincter function, as

represented by urethral closure pressure, is widelyoverlapping between continent and incontinentpatients. [5] There are no convincing data aboutmobility in normal or incontinent females, but itseems clear that stress urinary incontinence willalways be caused by some combination of these fac-tors. [29]

The dichotomy between intrinsic sphincter deficien-cy and urethral hypermobility is a modern reinter-pretation of the 2 continence mechanisms suggestedby Turner-Warwick [22] (see Figure 1). Impairmentof the proximal mechanism means that the bladderneck is open at rest, and thus is related to intrinsicsphincter deficiency (albeit in the proximal urethraonly). Impairment of the distal mechanism meansthat there is striated-sphincter/pelvic-floor weaknessor lack of muscle activity. Pelvic floor weaknessimplies hypermobility (at least in women). Impair-ment of both mechanisms seems to be a requirementfor incontinence. In women this implies a combina-tion of intrinsic sphincter deficiency and hypermobi-lity.

In spite of the preceding criticism, a low closurepressure may have prognostic value for surgery, assurgery primarily modifies the mobility by providingadditional suspension, but does not improve sphinc-ter function. It seems clear that in cases with a veryweak sphincter, - i.e. where it needs less “stress” andmobility to cause stress incontinence - surgery willbe less successful. Usually these cases show clinical-ly more severe stress incontinence. [30]

As stress incontinence appears to be caused bymechanical changes in active and passive tissues,and most urodynamic techniques measure mechani-cal parameters, the remainder of this section willfocus on the mechanics of continence and stressincontinence. Indeed, stress incontinence can be trea-ted successfully by modifying the mechanics of thebladder closure, either by improving active functionthrough muscle training or electrostimulation, or elseby adding a passive suspending structure such asTVT (tension-free vaginal tape), which alters mobi-lity and deformation of the bladder closure mecha-nism but does not normalize the physiologicalmechanics.

4. URODYNAMICS AND STRESS INCONTINENCE

The preceding discussion shows that our currentunderstanding of the pathophysiology and urodyna-mics of stress incontinence is limited. Therefore itappears reasonable to accept for the moment that the

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Figure 1. Concepts of female (in)continence mechanisms.On left in red, according to Turner-Warwick [22] the proxi-mal continence mechanism is formed by the smooth muscleof the bladder neck; the distal mechanism is formed by thestriated and smooth muscle of the mid-urethra, togetherwith (less certainly) the muscles of the pelvic floor (levatorani). On the right in blue, intrinsic sphincter deficiency(ISD) implies weakness of the smooth and striated musclesof the proximal and mid-urethra; hypermobility impliesweakness of the striated muscles of the pelvic floor.

diagnosis and treatment of stress urinary incontinen-ce should follow a pragmatic path based primarily onclinical experience rather than urodynamic measure-ments. Nevertheless, we should view this currentpractice critically, even though it seems to be reaso-nably successful. Diagnoses of stress incontinencethat rely on symptoms and signs alone, and the indi-cations for surgery drawn from them, are not basedon knowledge of the details of the pathophysiology.Correspondingly, treatment is not aimed at restora-tion of physiological function. Diagnostic imagingsuch as sonography offers some insight into thechanges that are introduced by surgery, e.g. by TVT.[31,32] The functional interpretation of these obser-vations is more speculative and descriptive than sys-tematic and scientific. However, the fact that thesefunctional interpretations are not supported byconsistent urodynamic data does not cast doubt onthe observations but rather emphasizes the problemswith current urodynamic measurement during stress.It is difficult to imagine that a catheter fixed outsidethe body could follow the remarkable deformationsobserved during Valsalva, [32] without the point ofmeasurement shifting or the urethra kinking andinfluencing the measurement.

Taking into account the preceding discussion, thefollowing questions will be addressed:

a) What is required for current routine practice?(Question 1)

All urodynamics should follow the principles of

good urodynamic practice. However, the idealisticaim of reproducing symptoms while making precisemeasurements in order to identify the underlyingcauses and to quantify the related pathophysiologicalprocesses, [33] is not yet fully applicable in stressincontinence. It is not difficult to support a sympto-matic diagnosis of stress incontinence urodynamical-ly, but it is not clear that such a confirmation is nee-ded. The additional capability of urodynamics toquantify parameters such as urethral pressure is alsonot of any clinical advantage as current treatment isnot quantitative, and does not need quantitativeinformation. Thus, invasive urodynamics is probablynot needed in the diagnosis of uncomplicated stressincontinence in a routine practice of high standardwhich includes, in addition to a careful dedicatedhistory and physical examination:

• a positive stress test;

• a voiding diary showing normal bladder capacity> 300 ml and no symptoms of urgency or urgeincontinence;

• a normal voiding function by diary and uroflow-metry, as documented by maximum flow rate,together with voided volume and post-void resi-dual urine volume. [33]

Urodynamics may however be helpful for prognosisand patient counselling. The evidence for theseviews is discussed in section D.I, Evaluation of thefemale patient.

b) What should be done urodynamically to improvecurrent clinical practice in diagnosing and treatingstress incontinence? (Question 2)

As the success rate in the treatment of uncomplica-ted stress incontinence seems to approach 100% [34]the focus of urodynamics should be on making surethat the stress incontinence is indeed uncomplicated,or on identifying the complicating factors. This isimportant for patients with previous surgery; withvoiding problems; with suspected obstruction orweak detrusor contraction; with reduced bladdercapacity; without a positive stress test; with urge ormixed urinary incontinence, particularly with sus-pected detrusor overactivity incontinence; or withsevere forms of stress incontinence. Carefully per-formed urodynamics can give information relevantto all of these aspects. Because these potential com-plicating factors, as well as the quality of urodyna-mics, differ greatly among patients and amongcentres, it is not surprising that no sound basis of evi-dence for the use of pre-operative urodynamics has

Question 1. What is required for current routinepractice?

Question 2. What should be done urodynami-cally to improve current clinicalpractice in diagnosing and treatingstress incontinence?

Question 3. What should be done urodynami-cally to further our understandingof the pathophysiology of stressincontinence and allow us to distin-guish different defects and combi-nations of defects that may lead todifferent forms of stress inconti-nence?

Question 4. What could be done urodynamical-ly to develop methods of repairingspecific defects and restoring phy-siological continence function?

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yet been established. Nevertheless, it is the commit-tee’s opinion that the knowledge provided by care-fully performed urodynamics is of advantage to anexperienced surgeon in all forms of complicatedstress incontinence.

c) What should be done urodynamically to furtherour understanding of the pathophysiology of stressincontinence, and allow us to distinguish differentdefects and combinations of defects, which maylead to different forms of stress incontinence?(Question 3)

According to our urodynamic definition, stressincontinence occurs when the bladder closuremechanism is competent (= continent) at rest, butbecomes incompetent under stress. At rest, we canmeasure the urethral closure function quite accurate-ly in terms of urethral closure pressure, keeping inmind that it depends on location within the urethra(among other factors) and can vary with time. Butthe measurements are not sufficient to characterizeincontinence under stress. Thus we would notexpect any single urodynamic parameter measured atrest to be specific or diagnostic for stress incontinen-ce, i.e. to be clearly different in women with andwithout stress incontinence. Clearly, as stress incon-tinence only occurs during stress, we should makemeasurements under stress, but this is difficult withcurrent techniques.

1. RESTING CONDITIONS

At rest, the biomechanics of the closure function of atubular structure such as the urethra is quite simple.It requires folding of the soft tissue tube and pressingof the inner lining by a concentric contraction. [12](The term “pressing” is preferable to the usual term“compressing,” which misleadingly may suggest thattissue is compressed to a smaller volume, while tis-sue in fact is incompressible. [12]) The best parame-ter to measure closure function is the pressure in thelumen as it just closes or opens. [35] Although tech-nically difficult, this is possible and there is no othermeaningful parameter available.

Urethral pressure recording requires a catheter to beplaced in the urethra, inevitably distending the ure-thra to the catheter’s diameter. Therefore the cathetershould be as thin as possible. Any catheter will havesome stiffness and weight which will deform the cur-ved, soft urethra. Therefore the catheter should be asflexible and light as possible. As the urethra hassignificant pressure gradients along its length, thelocation of the recorded pressure must be known.

For a urethral pressure profile (UPP), the pressurealong the urethra is recorded at rest during a givenperiod of time, typically about 40 seconds with awithdrawal speed of 1 mm/s, and thus combinesinformation about pressure, location and time varia-tion in a single graph. [1] From this graph the total(anatomic) urethral length, the functional length orcontinence zone, and the urethral closure pressurescan be obtained. One specific aspect of the UPP isthe maximum urethral closure pressure (MUCP),which is the highest pressure (relative to bladderpressure) generated along the functional length of theurethra. It usually corresponds to the striated sphinc-ter in the mid-urethra. [1] However, the profiledepends on multiple factors[36] such as age, positionof the patient, and filling volume. [37] Moreover,urethral pressure may vary with time in all locations,independently, synchronously, or even organized asperistaltic motility. Catheter movement and thedirection of movement influence the result, and theydepend on the catheter size, stiffness and surfacefriction. There are multiple other influences whichdepend on the method of pressure measurement. Theperfusion technique appears to mimic best the condi-tion for which urethral pressure is defined: a fluidpressure just opening the urethra. For such measure-ments it is possible to use small-diameter flexiblecatheters and low perfusion rates (about 1 ml/minunder resting conditions).

The commonly used catheter-mounted microtrans-ducers record a signal produced by interaction withthe urethral wall. The sensing surface area of thetransducer is small and only a minimal force is nee-ded to yield a significant apparent pressure (1 gram

weight acting on 1 mm2 results in an apparent pres-sure of 100 cm H2O). It is well documented that

signals recorded with catheter-mounted microtrans-ducers are directionally different, and thus cannotrepresent just urethral pressure. [38] They depend onthe urethral deformation caused by the catheter’slack of flexibility and weight. For the urethra (andalso for the anal canal) it is misleading to interpretsuch directional differences in terms of local “direc-tional pressure” or any contribution to closure func-tion. The directional differences exist only with thespecific catheter in the urethra. In fact it is probablyeasiest to interpret the directional interactions if arigid, thick catheter is used, [12,35,39,40] the exactopposite of the conditions best suited to making ure-thral pressure measurements.

The maximum urethral closure pressure alone does

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not provide any information about the integrity of thebladder neck or proximal urethra (i.e. the proximalcontinence mechanism), and it can be highly variableas a result of involuntary contractions of the smoothand striated muscles of the urethral sphincter, per-haps provoked by the irritative nature of the catheteritself. The size, stiffness and type of catheter, rate ofperfusion, patient position, and bladder volume, allhave an effect on the pressure readings. A study byWang and coworkers showed that the pressure mea-sured by the perfusion method was 24.5 cm H2O

higher on average than that measured with a micro-tip catheter. However, pressure profiles measuredwith the two types of catheter had similar reproduci-bility. [41] Culligan and coworkers compared an 8 Fmicrotip catheter with a 10 F fibre-optic catheter andfound that the urethral pressures measured with thelarger catheter were significantly greater, by 14 cmH2O on average, but they found no differences bet-ween the values of the leak point pressures (seebelow) measured with the two catheters. [42]

Balloon catheters, either water-filled as used inearly studies [43,44], or air-filled, as recently re-developed under the name T-doc, have a limited spa-tial resolution along the length of the urethra, deter-mined by the size of the balloon. The resolutionappears however to be better than 5 mm for T-docs.These balloons should not have any directionalityand record a true pressure (which may not be equalto the urethral pressure because of their finite diame-ter and potential for overinflation). Air- and water-filled balloons measure pressure from different refe-rence levels, and this has to be allowed for. A furtherpossibility is to measure urethral pressure with amicrotransducer enclosed in a balloon. [45]

2. WHAT HAPPENS TO THE URETHRAL CLOSUREMECHANISM DURING STRESS?

The perfusion technique has a limited temporal reso-lution and is reliable only at rest, not during condi-tions of rapidly varying stress. Other techniques havebetter temporal resolution, but that does not meanthat they show fewer artifacts, only different arti-facts. In practice, it seems to be impossible to recorda precise local pressure in a mobile urethra duringstress, using a catheter. All aspects of urethra/cathe-

ter interaction increase under stress, and the site ofpressure recording is difficult to determine becauseof the potential for uncontrollable shifting of thecatheter during stress. Shifts of up to 8 mm havebeen reported at the bladder neck during coughing.[46] In theory, it should be possible to determine thisshift by using multiple transducers along the catheterover the whole profile length, [47] but multiple-transducer catheters are of rather large diameter andquite rigid, and therefore yield directional forcesignals rather than urethral pressures.

• Urethral stress profile

A large number of publications deal with a greatvariety of methods for measuring and analyzing theso-called stress profile, i.e. a recording of a urethralpressure profile while the patient coughs at regularintervals.

The profile is a sequential presentation of time-varying local pressures, subject to the same limita-tions as discussed above, which are aggravated byadditional problems. A popular form of quantifica-tion of the stress profile is the “pressure transmissionratio.” (Note: as discussed above, pressure transmis-sion is a misleading term.) Most published stressprofiles show obvious artifacts. For example, onewould expect a gradient in the response to cough inthe midurethra, where both the abdominal pressureand the cough response fall to zero outside the abdo-minal pressure region. Nevertheless, many stressprofiles show pressure spikes in the most distal ure-thra, even outside the functional urethral length(Figure 2)

Usually the response to cough is measured in the ure-thra and in the bladder and the transmission ratio iscalculated by dividing the amplitude of the urethralpressure increase by the intravesical increase,expressing the result as a percentage. The typicaltransmission profile, which is the transmission ratioplotted against position in the urethra (expressed as apercentage of the urethral length), shows a declinefrom 100% pressure transmission at the bladder neckto 70% in the proximal urethra, followed by anincrease to 85% or higher in the mid- or distal ure-thra. [48] This is often interpreted as evidence for anactive contraction of sphincter and/or pelvic floorcontraction during stress, but it can also be explainedjust by shifting of the catheter (Figure 3). [49] Inpractice it seems to be impossible to identify the ori-gin of a higher or lower transmission ratio, andsophisticated interpretations are therefore questio-nable.

To summarise, urethral pressure recording in aresting patient is possible but quite difficult. Evenwith standardized methodology there is a varietyof potential artifacts which should be consideredcritically when interpreting the results.

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• Can we measure the “stress”?

Leak-point pressures: The ‘abdominal’ or ‘Valsalva’leak-point pressure (LPP), as defined by Internatio-nal Continence Society, is the intravesical pressure atwhich urine leakage occurs due to increased abdomi-nal pressure in the absence of a detrusor contraction.

[4] The procedure is a dynamic evaluation of theseverity of sphincteric dysfunction, and as such hasbeen considered by many to reflect the pathophysio-logical mechanism associated with stress incontinen-ce. Further, it avoids the complex artifacts of urethralpressure recordings. A low pressure reading mayidentify a subgroup of patients with a severelydeficient sphincteric mechanism who may benefitfrom a videourodynamic evaluation. [50] This proce-dure requires only basic urodynamic equipment: oneintravesical pressure catheter and one abdominalpressure catheter (placed in either the vagina or rec-

In summary: In practice it is impossible to use acatheter to measure a strictly local, artifact-freeurethral pressure under stress.

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Figure 2. Example of a stress urethral pressure profile. Thetop trace shows the bladder responses to a series of coughs(spikes). The middle trace shows the corresponding ure-thral responses, recorded while the measuring catheter isslowly withdrawn out of the bladder, through the urethra,and into the atmosphere. Responses are seen even in themost distal part of the urethra (red arrows). The bottomtrace shows the difference between the middle and toptraces.

Figure 3. Schematic diagram of measured values of pres-sure transmission ratio (full circles) along the length of theurethra, based on traces similar to those in Figure 2. [49]Part of the urethral response may be due to a shift of themeasuring catheter within the urethra on each cough. Cor-rection for an assumed shift of 5 mm alters the values tothose shown by open circles, revealing that the dip in pres-sure transmission ratio at around 20% of functional lengthmay be an artifact of the catheter shift.

tum). As the patient performs a progressively stron-ger Valsalva manoeuvre, the leak point pressure cor-responds to the lowest intravesical pressure thatresults in a loss of urine. However, the Valsalva leakpoint pressure has a significant percentage of falsenegative results, up to 40% as reported by Pescherset al. [51]

Accurate and reproducible leak point pressures aredifficult to obtain because of the many independentvariables affecting the test results: catheter size,bladder volume and patient position. Another limi-ting factor among older patients may be that they areunable to generate adequate abdominal pressures tocause a leakage of urine under test circumstances. Ifthis occurs, greater abdominal pressures can be gene-rated with a cough leak point pressure. Kuo hasrecently compared the Valsalva and cough leak pointpressures, using videourodynamic examinations. Heconcluded that the value of the leak point pressurerequired to make a diagnosis of intrinsic sphincterdeficiency (ISD) was lower for Valsalva than forcough. [52]

A cough, in contrast to a Valsalva manoeuvre, maycause greater muscular contraction within the pelvicfloor, resulting in decreased vesical neck mobility.For this and other reasons, cough-induced leak pointpressures are usually higher than those obtained witha Valsalva manoeuvre.

Since there is no standardized protocol for the test,discrepancies are inevitable. Madjar et al. retrospec-tively investigated aspects of the Valsalva leak pointpressure in 264 female patients who afterwardsunderwent anti-incontinence surgery. [53] They loo-ked at the relationship between “VLPP(tot)” (measu-red from true zero of pressure, see Figure 4), and“∆VLPP” (the increase in pves over the pre-Valsalvabaseline). As is obvious from the figure, if a fixedvalue of 60 cm H2O is used as a cutoff to differen-tiate intrinsic sphincter deficiency from urethralhypermobility, ∆VLPP is much more likely to sug-gest intrinsic sphincter deficiency than VLPP(tot) (in67% versus 40% of patients). However, neither para-meter strongly predicted the outcome of anti-inconti-nence surgery. (See section I.3 for further discus-sion.) (Figure 4)

The commonly quoted reference of 60 cm H2O orless for the diagnosis of intrinsic sphincter deficien-cy has not been consistently utilized either in studyprotocols or in prospective studies proving that thispressure can accurately make the diagnosis. [54]Patients with a leak point pressure greater than 90 cm

H2O are conventionally not considered to havesignificant intrinsic sphincter deficiency, as suchhigh pressures are usually associated with urethralhypermobility. It has been reported that, in clinicalpractice, leak point pressure values in the range of60–90 cm H2O are usually judged individuallyaccording to the severity and duration of the patient’ssymptoms, as well as accompanying co-factors. [55]As discussed above, however, all stress-incontinentpatients have some combination of hypermobilityand intrinsic sphincter deficiency.

Other factors that can affect leak point pressure rea-dings include the presence of the catheter itself aswell as its diameter. Maniam and Goldman examinedpatients with a positive cough stress test and a nega-tive Valsalva leak point pressure for leakage of urine,and found that more than 50% of these women losturine on repeating the Valsalva leak point pressureafter removing the catheter. [56] This suggests butdoes not prove that the catheter could mask urineloss. Studies of voiding flow rates with and withouta catheter are sometimes taken to indicate the effectof the catheter itself. For example, Baseman et aldetermined in a study of 21 continent women thatflow rates with a small (6 F) catheter in the urethrawere significantly lower than those in free-flow stu-dies, by 6.4–7.4 ml/s. [57] However, there are other

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Figure 4. Measurement of Valsalva leak point pressure(VLPP). The VLPP is the intravesical pressure at which lea-kage occurs on Valsalva; it may be measured from the truezero of pressure (VLPP(tot), blue arrow), or from the base-line intravesical pressure just before the Valsalva (∆∆VLPP,black arrow). In fact neither corresponds to the originaldescription,[143] which used the value of intravesical pres-sure prior to bladder filling as the baseline (red arrow). Forwomen in the standing position, ∆∆VLPP is much smallerthan VLPP(tot), by about 33 cm H2O on average. [53]

possible reasons for such a difference, and it is notclear that a catheter will necessarily inhibit stressurine leakage, or falsely elevate the pressure requiredfor leakage to occur. Faerber and Vashi [58] reportedthat Valsalva leak point pressure measurement madeat a bladder volume of 250-300 ml correlated bestwith the fluoroscopic observation of type III stressincontinence with an open bladder neck at rest (i.e. afailure of the proximal continence mechanism).

Höfner and coworkers [59] have suggested perfor-ming a cough leak point pressure combined withmeasurement of the actual volume of urine loss,using a standard uroflowmeter with a modified fun-nel. They report significant differences in the timedelay measured between the cough pressure spikeand the urine loss. They interpret this by assumingthat immediate leakage indicates stress incontinenceand delayed leakage potentially indicates urge incon-tinence, or detrusor overactivity incontinence trigge-red by the cough. Although not yet confirmed, theseresults show clearly the difference between obser-ving leakage with the naked eye and measuring lea-kage objectively. Furthermore, the authors found thatthe leakage volume, but not the measured leak pointpressures, were associated with the clinical degree ofstress incontinence.

d)What could be done urodynamically to developmethods of repairing specific defects and restoringphysiological continence function? (Question 4)

We need the abdominal pressure to understand detru-

sor contraction, i.e. to determine detrusor pressure.The current technique is well suited to this purposeand provides good results if the established standardsare followed. [33] The situation is different when wetry to understand the impact of stress on the bladderclosure mechanism. “Stress” is always associatedwith an increase in abdominal pressure and its effecton the pelvic floor and bladder outlet, but the abdo-minal pressure is not specifically related to the stresswhich causes incontinence.

The pelvic floor is the anatomical structure whichprovides closure to the abdominal region betweenthe pelvic bones. It is a three-dimensional structure,i.e. it has a considerable thickness, which is penetra-ted by the urethral, vaginal, and anal canals. We canexpect a gradient in the abdominal pressure, from itsfull value to zero across the thickness of the pelvicfloor. This gradient must affect measurements suchas the urethral pressure profile, which are performedacross the thickness of the pelvic floor.

5. WHAT URODYNAMIC TESTS SHOULD BEDONE IN FUTURE?

a) Imaging

Imaging, although not usually considered part ofurodynamics, is developing so rapidly that it willsoon have adequate spatial and dynamic resolution toprovide quantitative mechanical information com-plementary to that given by pressure measurements.Sonography and MRI are particularly promising.Investigation of local pelvic-floor deformations andmobility in three dimensions would be very interes-ting, because the strength of the pelvic floor deter-mines not only its own mobility and deformation, butthat of all structures resting on it. Without any defor-mation of the pelvic floor under stress nothing elsecan move.

The speed of deformation occurring under stress islikely to be higher than can be observed with thenaked eye. In practice the eye is supplemented by animaging system with its own time constant, whichslows down observation. The usual X-ray imageintensifier systems are obviously slower than the

To summarise, the current urodynamic parametersand the currently available techniques do not offerthe clinically relevant information needed for aknowledge-based (i.e. detailed and specific)approach, to the diagnosis and treatment of indi-vidual pathophysiology in a patient with stressincontinence. In summary, despite problems with standardiza-

tion, with current equipment it should be possibleto measure the intravesical and abdominal pressu-re at the time of leakage under stress, and to iden-tify and hence correct artifacts. However, we donot know of any systematic research into thevarious aspects of the leak point pressure. In addi-tion, it is important to ask what potential informa-tion could be gleaned from this parameter. It isobvious that any leak point pressure depends on amultiplicity of factors, and that it is a measure ofSUI severity, as it reflects the critical level of“stress” needed to produce leakage. It is unclearhowever whether a quantification of the severityof incontinence by a leak point pressure is moreuseful than a traditional clinical grading. It can beexpected that, when it has been adequately eva-luated, the recently developed urethral retro-pres-sure URP [60] will perform at best similarly to theleak point pressure and UPP.

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naked eye. Thus, it is likely that the true extent ofdeformation is not yet known. Sonography shouldprovide a better dynamic resolution.

The combination of a defined pressure in an intra-urethral balloon with imaging of how the urethra isdistended by that pressure can provide additionalinformation about bladder outlet structure and func-tion. [61,62]

b) Urethral pressure

As the urethral pressure is the key to understandingwhat happens to the closure mechanism under stresswe must develop new methods to measure it thatavoid the artifacts we have described, or at leastallow us to identify and correct the artifacts. Thereare in principle two possibilities, either to detect andmeasure the movement of the catheter, or else tomake the catheter so thin and flexible that it does notmove or interfere with the measurement. To avoidmovement, some form of intravesical or intra-ure-thral fixation may be unavoidable. On the otherhand, a thin, flexible catheter could incorporate thevery small transducers that are available throughnanotechnology. In any case, it will be necessary tomake specifically local pressure recordings in orderto understand closure function under stress. Globalmeasurements of compound parameters such as aleak point pressure cannot provide the informationthat is needed.

c) Measurement of stress

In principle we could try to measure the “stress”itself, but not by such a crude and unspecific measu-re as abdominal pressure. It is not possible to evenbegin such a program without a detailed and realisticbiomechanical model of the function of the urethralsphincter and the pelvic floor, so as to identify anddefine the pathophysiologically relevant parametersthat should be measured, such as (physical) stressand strain, deformation and acceleration. It is diffi-cult to develop such a biomechanical model of conti-nence function and the specific biomechanicalchanges which lead to stress incontinence. Yet onlywith a proper model will we be able to understandthe limits and potential of mechanical urodynamicparameters, define better parameters, develop newways and methods of measurement, and test the newparameters.

d) Vaginal pressure profile and abdominal pressureregion

The abdominal pressure region is a suitable urody-

namic term for the region which includes all of thelower urinary tract except the distal urethra, togetherwith the surrounding intra-abdominal tissues, all ofwhich are subject to the same abdominal pressure.Across the thickness of the pelvic floor, the pressurefalls from the abdominal pressure inside to zero(atmospheric) outside. In the urethra and the rectumthe sphincters provide a clear demarcation of theabdominal pressure region, but as there is no sphinc-ter in the vagina the demarcation is less clear. Thevaginal pressure profile should provide informationabout it.

e) Elements of a biomechanical model and measu-rements to test it

Some essential elements of a biomechanical modeland the urodynamics of stress incontinence havebeen outlined by Ashton-Miller and DeLancey. [26]Increasing tension and stretch of the pelvic floorduring an abdominal pressure increase affect the ure-thral sphincter also. The anatomical/biomechanicaldetails of the penetration of the urethra through thepelvic floor are key to understanding how continen-ce is maintained as abdominal pressure increases,how stress incontinence occurs, and how it can becured surgically. Such hypotheses as the vaginalhammock theory [63] could be tested by makingvaginal as well as urethral pressure profile recor-dings. Since there is necessarily a pressure gradientacross an effectively supporting hammock, theremust be a difference, during stress and perhaps alsoat rest, between the abdominal and urethral and vagi-nal pressures measured at the same anatomical level,with the vaginal pressure being the lowest.

Similar recordings could be used to test otherconcepts, such as that of independent proximal anddistal continence mechanisms, one relatively passiveand one clearly active, which react differently tochanges in abdominal pressure.

Of course, in making such measurements all thelimitations of pressure recordings during stressapply, but if we have a “catheter-free” pressurerecording method for the urethra we can use thesame technique in the vagina. Simultaneous recor-ding of intravesical and abdominal pressures toge-ther with multiple local pressures in the urethra andin the vagina should be possible - without interferen-ce from catheter-shift and directional artifacts - andthis will be a very important step in the understan-ding of the behavior of the urinary tract under stress.

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6. STRESS INCONTINENCE: CONCLUSION ANDRECOMMENDATIONS

1. INTRODUCTIONa) Urodynamic tests conventionally performed

Urge incontinence is one of the symptoms of theoveractive bladder symptom complex (see sectionA.IV, definitions and terminology). [64] To identifyit a history is needed, but to objectively establish theunderlying mechanism of incontinence requires tes-ting. This is particularly important because symp-toms are not specific for the underlying dysfunction(see Tables 6-9, section C.IV). To reproduce thesymptom during urodynamic testing, it is oftennecessary to perform manoeuvres to provoke detru-sor overactivity and leakage, since only about 50%of detrusor overactivity is revealed during slow,supine filling cystometry. [65] Although the urody-namic observation corresponding to urge incontinen-ce is “detrusor overactivity incontinence” [64] (seeFigure 5) in fact, however, when examining patientswith urge incontinence, many investigators havebeen satisfied with the observation of involuntarycontractions (detrusor overactivity) only, rather thanactual leakage. This has led to some confusion(Figure 5).

II. URGE INCONTINENCE

A plausible biomechanical model, based on currentknowledge is a prerequisite for deeper understan-ding of the pathophysiology of stress incontinence.New types of measurements will be required to testand refine it. Only after that, when the pathophy-siology of stress incontinence is understood inmuch more detail, will new therapies and new sur-gical approaches, aimed at re-establishing normalphysiological conditions, suggest themselves.

• Recommendations for research

1 Development of new methods of measuringurethral, vaginal and rectal pressure or force,free of artifacts due to distortion by and shift ofthe catheter.

2 Integration of new pressure or force measure-ments with advanced (high-speed) imagingtechniques, so as to develop a new and morecomplete biomechanical model of normal andabnormal pelvic and bladder outlet mechanics.

3 Integrated approaches to the study of urinaryand faecal (anal) incontinence.

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Figure 5. Detrusor overactivity (DO). In this example there is phasic detrusor overactivity (red arrows), which ultimately leadsto leakage; this is detrusor overactivity incontinence (DOI, purple arrow).

Filling cystometry with various provocativemanoeuvres is the basic test in urge incontinenceand other manifestations of overactive bladder.Conventionally, it is intended to identify or rule outdetrusor overactivity and/or detrusor overactivityincontinence, as well as to test subjects’ bladder-filling sensations. In addition it is desirable to ruleout urodynamic stress incontinence as an explana-tion of the subject’s symptoms.

Ambulatory urodynamics may be performed in aneffort to capture more realistic or more physiologicalobservations, especially of incontinence episodes.Monitoring is usually continued for a period of about3-4 hours.

Other supplementary tests may be done to check forpossible alternative or coexisting pathology:

1. Coughing and Valsalva manoeuvres, sometimesincluding abdominal leak point pressure measure-ment or video observations, are usually done toreveal or rule out possible urodynamic stressincontinence. They may also provoke detrusoroveractivity.

2. Urethral pressure measurements may be perfor-med to identify a poorly functioning urethralsphincter (intrinsic sphincter deficiency), a pos-sible contributor to both urodynamic stress incon-tinence [1] and urethral relaxation incontinence.[66]

3. Voiding studies may be done to confirm or rule outbladder outlet obstruction, a possible contributorto detrusor overactivity, especially in men.

Many technical aspects of these tests were discussedin detail at the previous consultation;[1] others aredealt with in sections B.I (Stress incontinence) andD.I (Evaluation of the female patient) of this currentchapter.

b) Mechanisms of continence and (urge) inconti-nence

1. DETRUSOR OVERACTIVITY

It seems clear that, if there is never any involuntarydetrusor contraction, there can be no detrusor ove-ractivity incontinence or urge incontinence (with thecaveat that urethral sphincter relaxation withoutdetectable detrusor contraction may sometimes beresponsible [4,67]). However, the converse is notnecessarily true: some individuals show involuntarycontractions (detrusor overactivity) during urodyna-mic testing but do not suffer from urge incontinence(see Figure 6 and Table 3 in section C.II, Normal

values). (Similarly, sphincter relaxation can occur innormal volunteers also. [68]) Detrusor overactivity isa urodynamic observation, not a condition and not adiagnosis. It may be associated with any of the ove-ractive bladder complex of symptoms, with orwithout urge incontinence, or with no symptoms atall (see Table 8 in section C.IV and Figure 6). There-fore the mechanism of continence is not just theabsence of detrusor overactivity. There is some evi-dence (a) that good sphincter function helps to pre-vent urge incontinence in the face of detrusor ove-ractivity, [66,69] (b) that abnormality of bladder sen-sation may play a role, [66,70,71], (c) that the cha-racteristics of the detrusor contraction itself may dif-fer in those who suffer more or less severely fromurge incontinence, [72] and (d) more generally thatmany different factors interact to determine whetheror not a given subject will suffer from urge inconti-nence, and how severe it will be (Figure 6).

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Figure 6. Relations among the overactive bladder complex ofsymptoms (OAB), urge incontinence (urge UI), detrusor ove-ractivity (DO), and neurological disease. Detrusor overactivity(red circle) may be neurogenic (overlap with green circle) ornon-neurogenic. It is observed in some healthy, symptom-freesubjects (overlap with yellow circle). Many individuals withDO have overactive bladder symptoms (overlap with bluecircle). Urge incontinence (hatched circle) is one of the ove-ractive bladder symptoms and so falls entirely within the bluecircle. As shown by its overlaps, urge incontinence may occurwith or without detrusor overactivity, and with or without neu-rological disease, but it does not occur in normal subjects (yel-low circle). Not shown on this diagram are some subjects whopresent with OAB symptoms that have a behavioural basis(e.g. excessive fluid intake) and are urologically normal.

Nevertheless, detrusor overactivity is at the heart ofurge incontinence, and it is essential to define it andto try to identify its causes. Detrusor overactivity isthe observation of an involuntary increase in detrusorpressure during urodynamic testing. To generate ameasurable pressure increase requires a coordinatedcontraction of the greater part of the bladder since, ifpart of the bladder is non-contracting (and thereforerelaxed and extensible), the contracting part canshorten without a detectable increase in pressure. Infact, local contractions of the bladder wall are ubi-quitous, in bladder strips, excised bladders and intactbladders in situ. [73,74] Thus small-scale detrusoroveractivity is normal, and it must result in smallpressure fluctuations (which however are not usuallymeasurable in awake, moving and breathinghumans). Therefore, to place any particular numeri-cal limit on the amplitude of pressure changes thatmight be regarded as normal or abnormal (e.g. 15 cmH2O [75]) would be entirely arbitrary.

There is no reason to believe that detrusor overacti-vity has a single cause. The lower urinary tract is adeceptively simple organ system that is controlled byvery extensive tracts of the central nervous system.Dysfunction at any level from the cerebral cortex tothe end organs may lead to detrusor overactivity andurge incontinence. [76,77] Detrusor overactivity iscommon in neurological conditions such as multiplesclerosis, spinal cord injury, and stroke. [76] Urgeincontinence becomes more common in old age, [78]where it is associated with cognitive impairment andregionally impaired cerebral perfusion. [71] Thusurge incontinence and its underlying mechanismdetrusor overactivity may sometimes have a neuro-pathic origin. The types of neuropathy in questionare associated with suprasacral lesions, which arebelieved to interfere with voluntary control of themicturition reflex by the cerebral cortex. Detrusoroveractivity of this sort often involves abnormalityof urethral function (e.g. detrusor-sphincter dyssy-nergia) as well as detrusor function. Of course,patients with a neurological lesion may sometimesshow detrusor overactivity that is non-neurogenic.

2. CAUSES OF DETRUSOR OVERACTIVITY

In spite of the important role of neurological lesions,many patients with detrusor overactivity and urgeincontinence have no detectable neurological abnor-mality. Some have co-existent urethral obstruction,and it is often claimed that the detrusor overactivityis a consequence of this mechanical outflow obstruc-tion, or of changes in the bladder secondary to it.

However, this may not necessarily be so:[79] anotherpossibility is that prostatic enlargement by itself mayalter afferent signals to the brain, precipitating detru-sor overactivity. Other patients may have subtleabnormalities of the neurological control system thatcannot be recognized with current urodynamic tech-niques. Even when there is no evident neurologicalbasis for this condition, it can often be triggered byfactors that apparently act at the cortical level, suchas the proximity of a toilet, the sound of runningwater, or hand-washing. [80] Thus there is evidencethat the brain is involved in urge incontinence. Yetthe afferent signals reaching the brain, cortical pro-cessing of these signals, and the influence of theemotions on bladder function remain almost entirelyuninvestigated. Bladder sensation – one manifesta-tion of the afferent signals – is studied in a most rudi-mentary way. It is unlikely that any abnormalitiesinvolving these factors, if they existed at all, wouldbe recognized by current techniques.

Detrusor overactivity is a fairly frequent observationin apparently healthy, symptom-free volunteers.Thirty years ago, idiopathic detrusor overactivitywas regarded as being like red hair, unusual (preva-lence 10%) but not abnormal, and the original term“unstable bladder” was invented precisely because itdid not suggest any particular underlying abnormali-ty. [22] Two decades later it was claimed that “Anybladder contraction during filling is abnormal.”[81]In fact, the average proportion of healthy subjectswith detrusor overactivity on filling cystometry is11%, and it is much greater – about 45% - whenobservations are made during ambulatory monito-ring (see Tables 3 and 4 in section C.II, Normalvalues). Thus detrusor overactivity may sometimesbe normal. For this reason it would be helpful to usedescriptive terminology that does not imply patholo-gy, for example “phasic detrusor contraction(s)” ins-tead of “detrusor instability” or “detrusor overactivi-ty”. [82]

The observation of detrusor overactivity in apparent-ly normal, symptom-free subjects has been referredto as “overdiagnosis.” In contrast, detrusor overacti-vity is quite frequently not observed during urodyna-mic examination of patients who indubitably sufferfrom urge incontinence [83] (see discussion of sensi-tivity and specificity in section C.IV). This has beenreferred to as “underdiagnosis”. Ambulatory testing,like other aggressive provocative manoeuvres wasintended to reduce “underdiagnosis,” but it alsoincreases “overdiagnosis.” In fact the terms “over-”and “underdiagnosis” are inappropriate because

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detrusor overactivity is not a diagnosable condition,but a urodynamic observation that may or may not bemade in any particular case, [84] depending in parton the method of measurement. [79] If it is related toneuropathy or to symptoms such as urge incontinen-ce, urgency, frequency, or nocturia, the observationis suggestive of abnormality. If not, it presumablyreflects normal behavior.

An essential characteristic of detrusor overactivity isthat it is involuntary. Even in humans it is sometimesdifficult to establish whether a particular detrusorcontraction or voiding episode is voluntary or invo-luntary, for example if there is a language barrier ora communication disorder. In animals it is particular-ly difficult to construct reliable models of detrusoroveractivity and urge incontinence.

Even if detrusor overactivity begins involuntarily, itmay be possible to voluntarily suppress it, or at leastto contract the urethral sphincter voluntarily so as toprevent leakage until the contraction subsides. Suchcharacteristics of patient behavior may be clinicallyjust as important as the presence or absence of detru-sor overactivity. [85-87]

3. SENSATIONS AND CYSTOMETRIC VOLUMES

Sensations are an important part of the observationsmade during cystometry. The normal sensations ofbladder filling form a continuum from first sensationof bladder filling, through first desire to void, tostrong desire to void. During cystometry most inves-tigators note the bladder volumes at which the nor-mal sensations occur (or they note the absence ofsuch sensations). It is usually believed that thevolumes tend to be smaller – that is, sensation isincreased - in the overactive bladder syndrome.

The sensation of urgency – the sudden and compel-ling desire to void that is difficult to inhibit [4] – isabnormal. It seems to be dichotomous – either pre-sent or absent – in contrast to the continuum of nor-mal cystometric sensations. It is part of the definitionof urge incontinence, but may also be an independentsymptom or an independent urodynamic observa-tion. The sensation of urgency during cystometry isoften but not always associated with the presence ofdetrusor overactivity. Ideally the sensation of urgen-cy, if it is reported as a symptom, should be reprodu-ced during urodynamic testing.

When detrusor overactivity is observed, the qualityof the accompanying sensation (if any) may be animportant observation. [69,72,83,88]

Maximum cystometric capacity is nearly always

noted. Clearly a very large capacity suggests at theleast reduced sensation, since, with normal sensa-tion, discomfort limits the volume that can be infu-sed into the bladder. The meaning of the maximumcystometric capacity is not always the same, becausethe criteria for stopping filling are different in diffe-rent situations. In near-normal individuals, strongsensation (discomfort) is usually the limiting factor.If detrusor overactivity, or overt detrusor overactivi-ty incontinence, occurs, then this will usually limitfurther bladder filling, particularly if accompaniedby urgency. If compliance is low (see section “com-pliance” below), then the constantly rising detrusorpressure may persuade the investigator not to conti-nue filling; alternatively overflow incontinence mayoccur and filling be discontinued for that reason. Ifsensation is reduced and compliance is normal, andthere is little or no detrusor overactivity, then thebladder may be filled almost indefinitely and thepatience of the investigator and the subject may bethe limiting factor.

During filling cystometry, the volumes correspon-ding to the various sensations and to maximum capa-city should in principle represent the volume ofliquid actually in the bladder. [4] Frequently howe-ver the volume infused into the bladder is recorded.The difference between these two volumes is thevolume of urine produced by the subject It may besubstantial if low filling rates are employed.

2. REPRODUCIBILITY AND FUNDAMENTAL REA-SONS FOR VARIABILITY OF FILLING CYSTO-METRY

Data on the variability of cystometric parameters aregiven in section C.I, Reproducibility of filling cysto-metry and ambulatory monitoring.

• Reproducibility and voluntary control

The lower urinary tract is controlled by numerouslayers of the nervous system. The lower layers (per-ipheral, spinal and supraspinal up to and includingthe periaqueductal gray), constitute the voidingreflex and can work together automatically, but thetopmost layers – the emotional or limbic nervoussystem [89] and the cortex – integrate reflex beha-vior into the social life of the individual. Their pur-pose is to prevent the automatic operation of thereflex and allow voiding only when it is both safeand appropriate to do so. They are able both toadvance and delay the moment of reflex voiding. Bydesign, therefore, the upper layers of the control sys-tem introduce variability into the function of the

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lower tract, and this variability depends on consciousdecision-making (to void or not to void) and on theunconscious operation of the emotional nervous sys-tem (safe to void or not safe?) (Figure 7).

The var

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