BASIC SCIENCE
Pathophysiology of urinary
incontinence
Arjun K Nambiar
Malcolm G Lucas
Abstract
Urinary incontinence is a condition with multi-factorial aetiology and a
complex pathophysiological basis. However, the underlying principles
are relatively simple. In this article we consider these pathophysiological
elements in separate sections to emphasise how they interact to effect a
change in lower urinary tract pressures during different phases of the
micturition cycle.
The interstitial cells have a key sensory role in the bladder, with much
research currently taking place to investigate their exact function. Neural
pathways, by comparison, are relatively well established and interactions
between the pontine micturition centre (PMC) in the brain stem and the
sacral micturition centre (SMC) in the sacral spinal cord, with voluntary
control from higher centres, provide neurological control of the lower uri-
nary tract. Depending on the level of a neurological deficit or injury,
certain recognizable patterns of bladder dysfunction can be identified.
Mechanical factors e the pelvic floor, striated sphincter muscles and
smooth muscles of the bladder and urethra e also play a major role in
maintaining normal continence.
Dysfunction of any of these elements can cause, to varying degrees, a
loss of urethral pressure, a rise in bladder pressure, or both. This imbal-
ance results in incontinence. An understanding of this principle, and the
pathophysiological mechanisms behind it, will help guide investigation
and treatment choices to best manage patients with this unfortunate
condition.
Keywords Bladder; lower urinary tract; neuro-urology; pathophysiology;
pelvic floor; pressure; urinary incontinence
Introduction
Urinary Incontinence (UI) is defined by the International Conti-
nence Society as the complaint of any involuntary leakage of
urine.1 There are a number of factors that may influence the
reported prevalence of UI, including sampling frame, response
rates, threshold definitions, types of UI and survey methods. But
broadly speaking the prevalence of UI in the general population
appears to be in the range of 30e60% in middle-aged and older
women, with the condition being twice as prevalent in women as
in men.2
The cause of UI can be multi-factorial, and understanding the
pathophysiological mechanisms requires an understanding of the
Arjun K Nambiar MBBS MRCS PG Cert (Clin Res) is a Clinical Research
Registrar in Urology at Morriston Hospital, ABM University LHB, UK.
Conflicts of interest: none declared.
Malcolm G Lucas FRCS (Urol) ChM is a Consultant Urologist at Morriston
Hospital, ABM University LHB, Hon. Senior Lecturer, Swansea
University, UK. Conflicts of interest: none declared.
SURGERY 32:6
relevant anatomy, physiology, neural control and biochemistry
of the lower urinary tract. In this article we will explore the
pathophysiological mechanisms underlying urinary incontinence
but also revisit the relevant normal anatomy and physiology, as
pertains to continence, before describing the abnormal.
Bladder wall physiology and neuromuscular control
The bladder wall and interstitial cells
The main purpose of the urinary bladder is to receive urine from
the kidneys and act as a compliant pouch to store that urine, until
such time as it is socially appropriate and convenient to void.
Structurally it is made up of interwoven fibres of detrusor muscle
that make up the body of the bladder, and specialized smooth
muscle fibres within the detrusor that arise from a distinct
embryological source. The muscle layers are lined internally by
an inner urothelium that acts as a protective layer. The bladder
urothelium is distensible along with the bladder muscle and
forms an effective bloodebladder barrier to prevent uraemia.3
Deep to the urothelium are found the interstitial cells, which
have recently been proposed to be the cells responsible for pace-
making activity in the bladder.4,5 Two types of interstitial cells
have been identified e the sub-urothelial interstitial cells (or
myofibroblasts) and the intra-detrusor interstitial cells. These
cells differ in molecular constitution and neurotransmitter
content, but M2 and M3 muscarinic receptor activity of sub-
urothelial interstitial cells have been found to correlate with
urgency scores in humans,6 and their position makes them
ideally situated to modify feedback mechanisms of ATP and
acetyl choline (ACh) between the urothelium and nerve end-
ings.7 The intra-detrusor interstitial cells can be spontaneously
active, so possibly have the pacemaker role, and they also
demonstrate cGMP activity.
Neurophysiology
The bladder and urethra are influenced by all three neural sys-
tems e sympathetic, parasympathetic and somatic (Figure 1).
They innervate the bladder through the pelvic plexus, formed by
contributions of the hypogastric (sympathetic) (T10-L2) and
pelvic (parasympathetic) (S2eS4) nerves as well as somatic
nerves. Sympathetic nerves release noradrenaline and innervate
the external urethral (rhabdo) sphincter, the excitatory a-adren-
ergic response resulting in an increase in muscular tone and
thereby outlet resistance. Being a striated muscle this external
sphincter is under a degree of voluntary control. There is also
evidence of a sympathetic reflex whereby bladder stretch results
in stimulation of b-adrenergic receptors in the detrusor that
enhance bladder relaxation and inhibit parasympathetic activity.
The parasympathetic nerves innervate the detrusor and via ACh
release stimulate detrusor contraction. Autonomic nerves are both
under higher control, mainly from the excitatory pontine micturi-
tion centre (PMC), located in the brain stem, which causes detrusor
contraction by parasympathetic excitation and simultaneous
external sphincter relaxation through sympathetic inhibition. The
PMC is normally under inhibitory influence from the frontal lobes
and cingulate gyrus via the peri-aqueductal grey (PAG), and these
centres are responsible for determining the socially acceptable and
convenient aspect of normal initiation of voiding.
The main control centres of bladder function are the pontine
micturition centre (PMC) mentioned above, and the sacral
279 2014 Elsevier Ltd. All rights reserved.
 BASIC SCIENCE

Ennervation of the bladder

Pre-frontal
cortex

Pontine
micturition
centre

Inferior
T10 mesenteric Hypogastric
T11 ganglion nerve
T12
L1
L2

Sacral S2
Pelvic
micturition S3
S4
plexus
centre

Pudendal Levator
nerve ani
External
sphincter

Afferent via pudendal

and pelvic nerves

Figure 1

micturition centre (SMC). The SMC is located at S2eS4 spinal
levels and communicates with the PMC via spinothalamic tracts.
It also has afferent inputs via the pelvic nerves as well as motor
output via parasympathetic nerves. The clinical effects of
neurological lesions affecting bladder function can largely be
determined by assessing whether the main lesion affects the
pathway above the PMC, between PMC and SMC, or involves the
SMC and lower pathways.
The normal filling and voiding cycle
The bladder performs a number of physiological functions, but
basically it serves to store a convenient amount of urine without
significant rise in pressure until such time as it is socially
acceptable to void, and without itself being damaged by the toxic
substances present in the urine it holds. To be able to do this it
has some inherent properties and features.
 Compliance e the net-like arrangement of detrusor fibres
and the poor electrical coupling between the muscle cells
results in the visco-elasticity of the bladder and absence of
tetanic contractions that are seen in other smooth muscles
of the gastrointestinal tract and uterus.8
 Protective urothelium e which forms the effective bloode
bladder barrier alluded to earlier, and protects the inner
layers of the bladder wall from the toxic effects of prolonged
contact with urine.
 Co-ordinated neuronal control e resulting in synchronous
activation of smooth muscles and relaxation of striated
muscles causing detrusor contraction, bladder neck open-
ing and funnelling, and sphincter relaxation to effect void-
ing. Neural switches are reset at the end of the void to revert
to baseline striated muscle tone (contracted sphincter) and
relaxed smooth muscle (bladder neck and wall).

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 BASIC SCIENCE
Figure 2 The inner lining of the urethra.
We have already seen that the bladder is controlled mainly by
the SMC, PMC and higher centres (frontal lobes, cingulate gyrus
and basal ganglia) through inter-linked neural pathways
involving the peri-aqueductal grey (PAG). Neural circuits con-
trolling bladder function mature with age. In infancy, the bladder
is controlled largely by reflex activity through the PMC and SMC.
PMC inputs are predominantly excitatory to the SMC, and
bladder filling sensations are also transmitted rapidly through
afferent pathways in the spinal reflex arc to efferent neurons that
cause bladder emptying. Hence the reflex bladder of infancy.
With maturing of neural circuitry higher centres exert an inhib-
itory effect on these reflex pathways resulting in voluntary con-
trol over micturition.
During the normal filling phase the bladder fills with urine
due to its compliant property. Afferent signals pass from the
bladder to the SMC and PMC, gradually reaching a threshold that
brings bladder sensation to consciousness. Bladder afferent ac-
tivity also causes reflex sympathetic firing through the pudendal
nerve (the guarding reflex) through a spinal reflex arc and hence
promotes continence by increasing rhabdosphincter tone. Once
voluntary signals pass from higher centres to the PMC, loss of
inhibition of PMC to SMC signals occur. This stimulates para-
sympathetic excitation and simultaneous excitation of inhibitory
inter-neurons that synapse with sympathetic motor neurons of
Onufs nucleus (in the SMC).
Sympathetic inhibition results in relaxation of the urethral
sphincter and hence entry of a small amount of urine into the ure-
thra. This stimulates further reflex bladder contractions via spinal
reflex and somatic/supraspinal mechanisms. Parasympathetic
excitation occurs simultaneously, augmenting sphincter relaxation
and bladder smooth muscle contraction resulting in exponential
increase in bladder pressure and expulsion of urine.
Despite the complexity of the physiological mechanisms,
normal filling and voiding cycles work remarkably well in most
people. However, as with any body system, things can go wrong.
Urinary incontinence is largely due to a pressure imbalance be-
tween the urethra and bladder e when the bladder pressure
exceeds urethral pressure there will be a tendency for urine to
SURGERY 32:6
leak through. This is the normal situation during voiding, but at
any other time will result in incontinence. Hence based on the
pathophysiological mechanisms urinary incontinence can be
divided into: those abnormalities resulting in loss of urethral
pressure; those abnormalities resulting in high bladder pressures;
and mixed bladder and urethral dysfunction.
Abnormalities causing a loss of urethral pressure
The urethra and sphincter
Smooth muscles from the bladder trigone continue down into the
proximal urethra and form a circumferential ring at the internal
meatus.9
The vesical neck refers to an area at the bladder base where
the urethral lumen passes through the thick muscle of the
bladder base and where the detrusor surrounds the trigonal ring
and internal urinary meatus.9 The functional importance of this
area lies in its sympathetic innervation e selective damage to
this nerve supply results in the vesical neck remaining open at
rest, which can result in poorer outcomes following stress in-
continence surgery.9
The inner lining of the urethra e the mucosa (urothelium) is
folded in longitudinal layers allowing for considerable distensi-
bility and also provides space for a rich sub-mucosal plexus that
may act as a cushion to promote co-aptation by way of special-
ized arteriovenous anastomosis9,10 (Figure 2).
The muscular layers of the urethra are considerably different
in males and females:
In males e at the commencement of the membranous urethra
there is a layer of circular striated fibres anteriorly in a horse-
shoe configuration that forms the rhabdosphincter. External to
these fibres lie the striated fibres of the pelvic floor, and hence
the fixity of the membranous urethra. The penile urethra has
very little muscular tissue and hence plays a minimal role in
continence apart from the passive resistance provided by its
length.
In the female urethra the urethral smooth muscle, contin-
uous with the smooth muscle from the bladder trigone, lies
281 2014 Elsevier Ltd. All rights reserved.
 BASIC SCIENCE

Figure 3 (a) The levator ani muscles from below after the vulvar structures and perineal membrane have been removed showing the arcus tendineus
levator ani, external anal sphincter, puboanal muscle, perineal body uniting the two ends of the puboperineal muscle, iliococcygeal muscle and
puborectal muscle. The urethra and vagina have been transected just above the hymenal ring. (b) The levator ani muscle seen from above looking over
the sacral promontory showing the pubovaginal muscle. The urethra, vagina and rectum have been resected just above the pelvic floor. From reference 10
with kind permission.

inside the striated urogenital sphincter muscle and consists of
inner longitudinal (shortens and funnels urethra during voiding)
and thin outer circular (constricting) layer. The outer layer is
formed by the striated urogenital sphincter, which runs circum-
ferentially in the upper two-thirds but distally extends to encircle
the vagina as the urethrovaginal sphincter, or along the inferior
pubic ramus as the compressore urethra9 (Figure 3a). Therefore
in the proximal segment the striated muscle probably constricts
the urethra, while in the distal segment it compresses the urethra
antero-posteriorly. Compressive forces usually need to be exerted
against a firm surface to be effective, and in the case of urethral
compression this firm structure is the pelvic floor.
Urethral pressure, or urethral tone, is maintained mainly by
two factors e muscular tone of the sphincter (which is largely
under neural control) and co-aptive forces of the urethral lumen.
Co-aptive forces can be hampered by any condition that results in
loss of the rich sub-mucosal plexus of the urethra and can pre-
dispose to, if not cause, urinary incontinence. Hormonal in-
fluences play a large role here and especially in women oestrogen
deficiency, such as post-menopause, can result in dryness of the
mucosa and loss of urethral co-aptation resulting in loss of ure-
thral closure pressure and stress urinary incontinence (SUI).
Muscular tone of the sphincter is maintained at rest by sym-
pathetic activity through the pudendal nerve. Damage to the motor
part of the pudendal nerve therefore can result in loss of sphincter
tone and SUI. Vaginal delivery, especially instrument-assisted, can
predispose to this type of injury which explains the preponderance
of SUI in post-partum females. Motor neuropathies can also have a
similar effect, as can trauma and pelvic surgery.
The pelvic floor
The pelvic floor forms the base, or floor, of the abdominal cavity
and has to withstand the variable pressures that can be exerted
on it from above. It consists of several components lying between
the pelvic peritoneum and the vulvar skin: from inside to outside
the peritoneum, viscera and endopelvic fascia, the levator ani
muscles, perineal membrane and external genital muscles.9
Broadly speaking, these can be grouped together into a
muscular component, a connective tissue and fascial component,
and a visceral component. The visceral and fascial (endopelvic
fascia) components are inextricably linked in so much as the
fascial component can have no mechanical effect without being
anchored to the viscera, hence these two layers are sometimes
known, together, as the viscero-fascial layer. This layer consists

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 BASIC SCIENCE

mainly of parametrium (attaching the uterus to the pelvic side Abnormalities causing high bladder pressures
wall) and paracolpium (attaching the vagina to the pelvic side
Bladder pressure is a function of compliance, and compliance, as
wall and ischial spine). These layers are made up of connective
we have already seen, is a result of the unique structural
tissue that, like most connective tissues, will stretch if exposed to
composition of the bladder coupled with effective neural control.
prolonged and repeated stress. In normal healthy individuals
Biochemical signalling pathways in the bladder wall are a
these forces are usually absorbed by the muscular components of
subject of intense study at the moment and we still do not yet
the pelvic floor e the levator ani and perineal membrane.
have all the answers. It is thought that interstitial cells may play
The levator ani is a complex of three muscles arising almost
a key role in bladder sensitivity through muscarinic, adren-
circumferentially from the pelvic wall, starting from the pubic arch
ergic, neurokinin, nitric oxide and cGMP pathways. If these
in front and continuing along ridges of dense connective tissue
cells do in fact play a role in bladder pacemaker activity then
called the arcus tendineus fascia pelvis (ATFP) and arcus tendi-
they could well be the key to understanding the entity we
neus levator ani (ATLA) (Figure 3b). The levator ani along with its
currently refer to as idiopathic detrusor overactivity (IDO).
fascial coverings is often referred to as the pelvic diaphragm, and
This results in involuntary spasm of bladder muscle resulting in
the opening in the diaphragm through which the urethra and
transient, sometimes sustained and intense, rises in bladder
vagina pass is called the urogenital hiatus. The hiatus therefore is
pressure that can occasionally overcome urethral closure
bounded anteriorly by the pubic symphysis, laterally by the le-
pressure and result in incontinence (urgency urinary inconti-
vator ani muscles and posteriorly by the perineal body and
nence or UUI).
external anal sphincter. Normal baseline activity of the levator ani
These originate from afferent pathways, but detrusor over-
keeps the hiatus closed and compresses the vagina and urethra
activity can also result from neurogenic overactivity e loss of
against the pubic bone. This, by extension, results in no or little
inhibition from supra-sacral centres resulting in reflex spasms of
tension on the ligamentous supports of the pelvic organs. In case
parasympathetic activity. Due to the complexity of neural control
of damage to the pelvic floor the ligaments have to bear the strain
and the different patterns of neurological disease the effects on
of holding the pelvic organs in place between the high pressure of
bladder function can be vastly varied, but neurogenic detrusor
the abdominal cavity and low external atmospheric pressure. In
overactivity (NDO) is a well-recognized phenomenon that results
such a situation it is only a matter of time before the ligaments
in increased efferent firing parasympathetic neurons to the
become overloaded and are over-stretched, leading to pelvic organ
bladder resulting in detrusor spasms and high bladder pressures.
prolapse and predisposing to stress urinary incontinence.
Due to the more persistent nature of the parasympathetic activity
The ligamentous support of the paraurethral tissue, the para-
in NDO there is a tendency for these patients to have high resting
colpium, attaches to the arcus tendineus fascia pelvis (ATFP) that
bladder pressures that can endanger kidney function.
in turn attaches to the pubic bone and ischial spine, and also to
Depending on the level of the lesion the effect on bladder
the levator ani muscle itself. Therefore it follows that any defect in
function can vary immensely, however keeping in mind our
the ATFP or levator ani can result in both a loss of urethral sup-
earlier discussion on neuromuscular control certain patterns of
port and a loss of the base upon which the urethra is compressed
dysfunction can be identified (Figure 4).
to maintain continence during a rise in intra-abdominal pressure.
 Disease of the frontal lobe/cingulate gyrus leads to a loss
Another factor we must consider when talking about urethral
of inhibition of the PMC and results in a regression to an
pressure is that it is not constant even during the filling phase. The
infant bladder whereby voiding occurs without any re-
urethra must be able to withstand transient rises in intra-
gard for social circumstance or convenience. e.g. cerebro-
abdominal pressure (IAP) (and hence bladder pressure) to main-
vascular accidents (stroke), Parkinsons disease, cerebral
tain continence and this is achieved through the physical system
trauma or severe epilepsy.
discussed in the anatomy of the pelvic floor e the paraurethral
 Lesions below the brain stem but above the conus can result
supports in the lower third of the urethra keep it relatively fixed
in a loss of co-ordination between the detrusor and sphincter
while the upper third is relatively mobile. During a transient rise in
(referred to as detrusor-sphinctre dyssynergia), but almost
IAP the urethra is compressed against the pelvic floor muscles and
inevitably neurogenic detrusor overactivity due to a hyper-
effectively closed off. Pelvic floor weakness or distortion of pelvic
reflexic bladder. e.g. multiple sclerosis, cord lesions
anatomy as a result of pelvic organ prolapse can upset this
(paraplegics)
mechanism and hence cause SUI. Prolonged third stages of labour,
 Lesions of the sacral spinal cord can lead to a flaccid pa-
assisted delivery and perineal tears all predispose to pelvic floor
ralysis of the bladder with sensory loss (referred to as an
weakness post-partum and therefore increase the risk of SUI.
areflexic or non-contractile bladder) and possibly a loss of
In men the common causes of pudendal nerve damage,
compliance. The extent of this can vary, as the bladder is
sphincter weakness and pelvic floor weakness are neuropathic or
not completely denervated because the post-ganglionic
surgical, with radical prostectomy being the most common sur-
parasympathetic neurons synapse in the bladder wall
gical cause. The nature of the surgery necessitates removal of the
and hence may still retain some activity. e.g. spina bifida,
pre-prostatic and prostatic urethra along with the proximal cir-
prolapsed inter-vertebral disc.
cular sphincter. As a result continence is maintained by mainly
 Lesions of the peripheral nerves or nerve roots can cause a
the rhabdosphincter, and often neuropathic damage during sur-
mixed picture depending on the nerve roots involved.
gery can result in sphincter weakness. The degree of incontinence
These can be very difficult to diagnose and extremely high
varies depending on the degree of residual sphincter function but
risk bladders can be missed due to a lack of overt symp-
it is not uncommon for these men to have very poor urethral
toms. e.g. cauda equina injury.
closure pressures and consequently severe SUI.

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 BASIC SCIENCE

Causes of bladder and urethral dysfunction

Bladder/urethral dysfunction Risk Examples
category

Reflex bladder CVA

Pre-frontal cortex Cortical injury
Co-ordinated sphincter relaxation Low Cerebral trauma
Complete emptying Epilepsy
Peri-aqueductal grey Parkinsons
Pontine micturition
centre (PMC)

Supra-sacral injury Reflex bladder Cord injury

Detrusor sphincter dyssynergia (DSD) High Transverse myelitis
Poor emptying/high pressure MS

Sacral injury Non-contractile bladder Spina bifida

Poor emptying High Prolapsed disc
SUI
Sacral micturition
Poor compliance
centre (SMC)

Nerve root injury Mixed picture Cauda equina injury

Varies depending on root involvement Variable Peripheral neuropathy

Figure 4

Neurological lesions are very often incomplete and patterns
vary depending on the underlying disease, therefore the pattern
of bladder involvement can also vary dramatically with combi-
nations of the above three pictures. It is also not uncommon for
patients with no overt symptoms of bladder dysfunction to have
significant underlying bladder pathology that may pose a risk to
the upper tracts due to very high storage pressures or reflux.
Conditions that commonly result in high risk bladders are
congenital cord injuries and spina bifida, spinal cord injuries
(paraplegia, tetraplegia) and cauda equina injuries. Neurological
diseases that cause relatively low risk bladders include MS, CVA
and Parkinsons disease.
Mixed bladder and urethral dysfunction
It is not uncommon for high bladder pressures and low urethral
pressures to co-exist, resulting in a mixed picture of incontinence
that is more difficult to evaluate. As we have already discussed,
stimulation of the urethra by flow of urine into its proximal
segment can lead to reflex stimulation of the bladder. Therefore
in patients with low urethral pressures this constant reflex
stimulation can cause bladder overactivity and detrusor spasms.
In this situation treating the main cause (low urethral pressure)
may be all that is required to resolve (or at least significantly
improve) the situation. Indeed it has been demonstrated that
treatment of SUI through surgery often improves or even cures
symptoms of IDO.3
On the other hand all the aforementioned causes of high
bladder pressures could simply occur simultaneously with
causes of low urethral pressure, compounding the problem.
These cases can be difficult to evaluate and require careful
investigation before deciding on the appropriate strategy to fix
the problem.
The pathophysiology of urinary incontinence involves the
interplay of anatomic, biochemical, neurological and even
endocrine factors. These interactions are highly complex, but the
end result simply involves an alteration in the balance of bladder
versus urethral pressures. Therefore the investigation and treat-
ment pathways of lower urinary tract dysfunction follow this
basic principle e to identify the pressure imbalance and try to
correct it. Urodynamic evaluation can give a snapshot of varia-
tions in pressure during a given filling and voiding cycle. This
coupled with a careful history and examination can very often
provide adequate evidence of the dysfunction in an individual
patient. Intervention can then be planned to either reduce
bladder pressure or augment urethral pressure to try and restore
the balance. A
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