Pathophysiolo gy of

Urinar y Incontinence,
Voiding Dysfunction,
and Overactive Bladder
David D. Rahn, MD*, Shayzreen M. Roshanravan, MD

KEYWORDS
 Detrusor overactivity  Instability  Urinary stress incontinence
 Neuroanatomy  Neurophysiology

DEFINITIONS,TERMINOLOGY

Pelvic floor dysfunction may include problems of urine storage and evacuation, inad-
equate support of the pelvic viscera, colorectal/anal disorders, and acute or chronic
pelvic pain. When considering just the disorders of the lower urinary tract, there is
an abundance of terms describing the various symptoms and suspected etiologies
of these storage and evacuation problems; miscommunication and confusion may
result. The International Continence Society has attempted to standardize several
definitions based on patients’ symptoms to facilitate more effective communication
between physicians, patients, and researchers.1 These urinary disorders may be
divided into three categories: problems with storage, voiding, and postmicturition.
Among the storage symptoms, urinary incontinence is broadly defined as ‘‘the
complaint of any involuntary leakage of urine.’’ More specifically, stress urinary incon-
tinence is ‘‘involuntary leakage on effort or exertion, or on sneezing or coughing.’’
Urinary urgency is ‘‘the complaint of a sudden compelling desire to pass urine which
is difficult to defer’’ and urgency incontinence is ‘‘the complaint of involuntary leakage
accompanied by or immediately preceded by urgency.’’1,2 Taken together, overactive
bladder syndrome is ‘‘urgency, with or without urgency incontinence usually with
increased daytime frequency and nocturia.’’2
Voiding symptoms include problems with slow urinary stream, splitting or spraying,
intermittency or hesitancy with the urine flow, or straining to void. Postmicturition
symptoms include feelings of incomplete emptying and postmicturition dribble.
Although all of these labels may help characterize patients by their predominant

Division of Female Pelvic Medicine and Reconstructive Surgery, Department of Obstetrics and
Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard,
Dallas, TX 75390-9032, USA
* Corresponding author.
E-mail address: david.rahn@utsouthwestern.edu (D.D. Rahn).

Obstet Gynecol Clin N Am 36 (2009) 463–474

doi:10.1016/j.ogc.2009.08.012 obgyn.theclinics.com
0889-8545/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
464 Rahn & Roshanravan

symptoms, they do not provide insight into the degree to which symptoms bother
patients nor the etiology of these symptoms. This article presents a simplified expla-
nation of the mechanics of urine storage and emptying, establishing a framework to
understand how different physiologic and pathologic states may contribute to the
disorders mentioned earlier.

PHYSIOLOGIC NEUROANATOMY OF URINE STORAGE AND EVACUATION

The anatomy of the lower urinary tract is closely related to its function of storage and
evacuation of urine. The bladder remains relaxed during the storage phase and
contracts during the evacuation phase. The urethra acts in synchrony with the bladder
but has reciprocal actions: contracting during storage and relaxing during evacuation.
The coordinated function of this system depends on complex interactions between
the nervous system and the lower urinary tract anatomy.

Anatomy: Bladder
The urinary bladder is a muscular organ that consists of coarse bundles of smooth
muscle known as the detrusor muscle (Fig. 1). The bladder is lined by transitional
epithelium, which merges with the squamous epithelium of the urethra. Approximately
at the level of the ureteral orifices, the bladder can be divided into two parts: a body (or
dome) and a base. The base of the bladder includes the vesical trigone, which is
bounded by the two ureteral orifices and the internal urethral opening. An important
distinction between the dome and the base is the type of neurotransmitter receptor
that predominates (see Fig. 1). At the dome, beta-adrenergic and cholinergic recep-
tors predominate, whereas alpha-adrenergic receptors predominate at the base and
the proximal urethra. The primary cholinergic (muscarinic) receptor subtypes in the
human bladder are M2 and M3. Although there are more M2 receptors, the M3

Fig. 1. Urinary bladder. a, alpha adrenergic receptors; b, beta adrenergic; M, muscarinic

(cholinergic). (Courtesy of Lindsay Oksenberg, Dallas, TX)
 Pathophysiology of Lower Urinary Tract Dysfunction 465

receptors predominate in the mediation of detrusor contraction.3 The vesical neck is

that area of the bladder where the urethral lumen passes through the musculature
of the bladder base.4

Anatomy: Urethra
In women, the urethra is a complex 3 to 4 cm structure that extends from the bladder
to the external urethral opening (Fig. 2A, B). Surrounding the mucosal lining of the
urethra is a submucosal layer that contains a prominent vascular plexus. This plexus
is thought to contribute to the watertight closure of the urethral lumen. Adjacent to the
submucosal layer lie two layers of smooth muscle: a well-developed inner longitudinal
and a poorly defined outer circular layer. These smooth muscle layers are thought to
assist with constriction and opening of the urethral lumen. The most external layer of
the urethral wall consists of the striated urogenital sphincter muscles (see Fig. 2B).5,6
This complex consists of the sphincter urethrae and two strap like bands of muscle,
the urethrovaginal sphincter and compressor urethrae muscles (Fig. 3).7,8 The
sphincter urethrae surrounds the proximal region of the urethra. This muscle is an inte-
gral part of the urethral wall and its fibers are oriented in a circular fashion. The
compressor urethrae and urethrovaginal sphincter muscles arch over the ventral
surface of the urethra and are found just superior to the perineal membrane (see
Fig. 3).

Peripheral nervous system

Understanding the normal physiologic function of the lower urinary tract requires
a basic understanding of its peripheral innervation.9 The peripheral nervous system
has a somatic and an autonomic component. The somatic component innervates
skeletal or striated muscle, whereas the autonomic component innervates smooth
muscle, cardiac muscle, and glands. In the lower urinary tract, somatic nerves inner-
vate the muscles that comprise the striated urogenital sphincter complex. Autonomic
nerves supply the detrusor muscle of the bladder and smooth muscle of the urethra
(Fig. 4).

Fig. 2. Urethral anatomy. (A) Isolated urethral anatomy in cross section. Urethral coaptation
results in part from filling of the rich subepithelial vascular plexus. (B) Vesical neck and
urethral anatomy. (From Wai CY.Urinary incontinence. In: Schorge JO, Schaffer JI, Halvorson
LM, et al, editors. Williams Gynecology, 1st edition. New York: McGraw Hill Medical; 2008.
p. 517; with permission.) (Courtesy of Lindsay Oksenberg, Dallas, TX).
466 Rahn & Roshanravan

Fig. 3. Striated urogenital sphincter anatomy. With the perineal membrane removed or
reflected, one encounters the three component muscles of the striated urogenital sphincter.
(Courtesy of Lindsay Oksenberg, Dallas, Texas).

The autonomic nervous system is further divided into sympathetic and parasympa-
thetic divisions. Fibers arising from the intermediolateral gray column of the tenth
thoracic and first two lumbar spinal cord segments form the pelvic sympathetic
division. The pelvic parasympathetic division consists of fibers arising from the inter-
mediolateral cell columns of the second through fourth sacral cord segments. Auto-
nomic fibers that supply the pelvic viscera course in the superior and inferior
hypogastric plexuses (Fig. 5). The superior hypogastric plexus primarily contains
sympathetic fibers from the T10 to L2 cord segments and terminates by dividing
into right and left hypogastric nerves. The inferior hypogastric plexus, also known
as the pelvic plexus, is formed by visceral efferents from S2 to S4, which provide

Fig. 4. Peripheral nervous system innervation of the lower urinary tract. (Courtesy of Lindsay
Oksenberg, Dallas, TX).
 Pathophysiology of Lower Urinary Tract Dysfunction 467

Fig. 5. The pelvic plexus. (Courtesy of Lindsay Oksenberg, Dallas, TX).

the parasympathetic component by way of the pelvic nerves. The lateral extensions of
the superior hypogastric plexus, the hypogastric nerves and rami from the sacral
portion of the sympathetic chain, contribute the sympathetic component to the pelvic
plexus. The pelvic plexus divides into three portions according to the course and
distribution of its fibers: the middle rectal plexus, uterovaginal plexus (or
Frankenhauser’s ganglion), and vesical plexus (see Fig. 5).10
The somatic component of the peripheral nervous system that is relevant to lower
urinary tract function takes origin from Onuf’s somatic nucleus (Fig. 6). Onuf’s nucleus,
located in the ventral horn of the gray matter of S2 through S4, contains the neuronal
cell bodies of the fibers that supply the striated urogenital sphincter complex. The ure-
throvaginal sphincter and compressor urethrae are innervated by the perineal branch
of the pudendal nerve. The sphincter urethrae are variably innervated by somatic effer-
ents that travel in the pelvic nerves.

Neurophysiology
Normal voiding function requires higher cortical areas of the brain, which allow for
voluntary control over the primitive autonomic reflex arcs found within the sacral spinal
cord. This central coordination of micturition largely occurs in the pontine micturition
center. The parietal lobes and thalamus receive and coordinate the bladder detrusor
afferent stimuli, whereas the frontal lobes and basal ganglia modulate with inhibitory
signals. There is also peripheral coordination that occurs in the sacral micturition
center (S2–4). Precise knowledge of the neural pathways involved in voiding remains
controversial; the concepts presented here represent a summary of the major
pathways.
Urine storage depends predominantly on sympathetic neural activity. During
storage, bladder distention results in afferent input from sensory neurons located in
468 Rahn & Roshanravan

Fig. 6. Onuf’s somatic nucleus. (Courtesy of Lindsay Oksenberg, Dallas, TX).

the bladder wall. This leads to activation of urethral motor neurons in Onuf’s nucleus,
which results in contraction of the striated urogenital sphincter muscles by way of the
pudendal nerve. Simultaneously, activation of the spinal sympathetic reflex (T11–L2)
by way of the hypogastric nerves results in alpha-adrenergic contraction of urethral
smooth muscle with increased tone at the vesical neck and inhibition of parasympa-
thetic transmission, which inhibits detrusor contraction.11 The net effect is that urethral
pressure remains greater than detrusor pressure, facilitating storage (Fig. 7). When
there are increases in abdominal pressure, a fascial and muscular urethral support
hammock compresses the urethra to help maintain continence12; this is also accom-
plished when the pelvic muscles are contracted.
Voiding is largely a parasympathetic event. This begins with efferent impulses from
the pontine micturition center, which results in inhibition of somatic fibers in Onuf’s
nucleus and voluntary relaxation of the striated urogenital sphincter muscles. These
efferent impulses also result in preganglionic sympathetic inhibition with opening of
the vesical neck and parasympathetic stimulation, which results in detrusor musca-
rinic contraction. The net result is relaxation of the striated urogenital sphincter
complex causing decreased urethral pressure, followed almost immediately by detru-
sor contraction and voiding (Fig. 8).

NEUROGENIC CAUSES OF URINE STORAGE AND EVACUATION DYSFUNCTION

Voluntary control of the micturition reflex is mediated by connections between the

frontal cerebral cortex and the pons. Voluntary control of the striated urogenital
sphincter muscles is through the corticospinal pathway connecting the frontal cortex
with Onuf’s somatic nucleus. Disruption of these neural pathways can result in
dysfunctional storage and voiding patterns.
Lesions in the cortical centers of the brain can result in urge incontinence, enuresis,
and urethral spasm. Patients may be unaware of their incontinence. Patients suffering
from stroke, Alzheimer disease, multi-infarct dementia, other dementias, Parkinson
 Pathophysiology of Lower Urinary Tract Dysfunction 469

Fig. 7. Urine storage. Bladder distention from filling leads to alpha-adrenergic contraction of
the urethral smooth muscle and increased tone at the vesical neck (T11-L2 spinal sympa-
thetic reflex); activation of urethral motor neurons in Onuf’s nucleus with contraction of
striated urogenital sphincter muscles (by way of the pudendal nerve); and inhibited para-
sympathetic transmission with decreased detrusor pressure. a, alpha adrenergic receptors;
b, beta adrenergic; M, muscarinic (cholinergic). (Courtesy of Lindsay Oksenberg, Dallas, TX).

Fig. 8. Urine evacuation. Efferent impulses from the pontine micturition center cause inhibi-
tion of somatic fibers in Onuf’s nucleus with voluntary relaxation of the striated urogenital
sphincter muscles; preganglionic sympathetic inhibition with relaxation at the vesical neck;
and parasympathetic stimulation with detrusor muscle contraction. a, alpha adrenergic
receptors; M, muscarinic (cholinergic). (Courtesy of Lindsay Oksenberg, Dallas, Texas).
470 Rahn & Roshanravan

disease, or multiple sclerosis with suprapontine lesions may experience involuntary

detrusor contractions, which occur in synchrony with relaxation of the urethra. These
contractions can result in neurogenic detrusor overactivity with urgency/frequency
and urgency incontinence.
High spinal cord or upper motor neuron lesions can also result in neurogenic detru-
sor overactivity. However, the detrusor contractions are not synchronized with urethral
relaxation, resulting in detrusor-sphincter dyssynergia where patients can also have
urinary retention. This dyssynergia can be seen with acute spinal cord trauma, cervical
or lumbar stenosis, disc herniation, or chronic conditions involving the spinal cord,
such as multiple sclerosis.
Lastly, lower motor neuron lesions, as seen with injury to the peripheral nervous
system, may result in reduced contraction of the detrusor muscle. This may manifest
as overflow incontinence. In developed countries, the most common cause of periph-
eral neuropathy is diabetes. Injury to the pelvic plexus can be seen with resection
surgery, such as radical hysterectomy or rectal surgery. In these cases, parasympa-
thetic innervation is mainly affected.

MUSCULAR CAUSES OF URINE STORAGE AND EVACUATION DYSFUNCTION

The detrusor muscle’s functional ability to contract appropriately may be altered as

a result of aging, atrophy, trauma, or decreased muscular innervation. The smooth
muscle contractions of the detrusor require several interacting biochemical pathways
to raise intracellular calcium levels; these include adenosine triphosphate (ATP) phos-
phorylation, protein kinases, and potassium and calcium channels. Alterations in any
of these pathways may result in inappropriate contractions or loss in contractility.13,14
Studies have demonstrated that women who have detrusor overactivity have struc-
tural changes in their bladder walls at the tissue and cellular levels. Electron micros-
copy examining the ultrastructural anatomy of detrusor cells suggests that patients
who have overactivity have an abnormal number of intercellular connections used
for communication between smooth muscle cells, which may facilitate the generation
of inappropriate detrusor contractions.15 At a light microscopic level, overactive
bladder tissue has demonstrated increases in elastin, collagen, and segments of
denervated muscle.16

STRESS URINARY INCONTINENCE

Theories regarding the maintenance of urinary continence during increases in intra-

abdominal pressure involve concepts of pressure transmission, anatomic support,
and urethral integrity. Most simply, continence during these times of physical stress
requires anatomic urethral support and urethral integrity. Ideal support requires intact
and healthy (1) ligaments along the lateral aspects of the urethra, termed the puboure-
thral ligaments; (2) anterior vaginal wall and its lateral fascial condensation; (3) arcus
tendinous fascia pelvis; and (4) levator ani muscles. Collectively, this support provides
a firm backboard against which the urethra is supported during increases in intra-
abdominal pressure. With the loss of this support, downward forces, such as from
a cough, sneeze, or laugh, are not countered as they should be; the urethra funnels
at the urethrovaginal junction; the urethra becomes more patent and has a reduced
closing pressure; and continence is lost (Fig. 9).17
Mechanical closure/integrity of the urethra is also necessary to prevent stress
urinary incontinence. This closure/integrity requires mucosal surface coaptation and
intact viscoelastic properties of the urethral epithelium, a healthy underlying urethral
vascular plexus, and contraction of the surrounding musculature (see Fig. 2). Defects
 Pathophysiology of Lower Urinary Tract Dysfunction 471

Fig. 9. Stress urinary incontinence: the pressure-transmission theory. (From Wai CY. Urinary
incontinence. In: Schorge JO, Schaffer JI, Halvorson LM, et al, editors. Williams Gynecology.
1st edition. New York: McGraw Hill Medical; 2008. p. 518; with permission.)

in any of these components may contribute to stress incontinence by way of ‘‘intrinsic

sphincter deficiency.’’12 Possible etiologies of such defects include prior retropubic
surgery with denervation or scarring of the urethra and supporting tissue, prior pelvic
radiotherapy, hypoestrogenism, diabetic neuropathy, and other degenerative
neuronal diseases. Childbirth and associated trauma can physically disrupt the
musculature of the urogenital sphincter or its supportive fascia or muscles (levator
ani) or may cause nerve damage with immediate or delayed stress urinary
incontinence.

COMORBID CONDITIONS AND OTHER FACTORS AFFECTING URINE STORAGE

AND EVACUATION

Urinary incontinence often reflects multidimensional and multiple impairments.

Besides requiring intact micturition physiology (including the lower urinary tract,
pelvic, and neurologic components described earlier), continence depends on an
intact functional ability to toilet oneself. Several medical conditions and pharmaco-
logic agents can negatively impact this ability. One pneumonic designed to highlight
these potentially reversible or transient contributors to urinary incontinence is
DIAPPERS: Dementia/delirium, Infection, Atrophic vaginitis, Psychological, Pharma-
cologic, Endocrine, Restricted mobility, and Stool impaction.18
Continence requires the cognitive ability to recognize and react appropriately to the
sensation of a full bladder, motivation to maintain dryness, sufficient mobility and
manual dexterity, and ready access to toilet facilities. Patients who have dementia
or significant psychological impairments often do not have this necessary cognitive
ability or motivation for maintenance of continence, and women who have severe
physical handicaps or restricted mobility may simply not have time to reach the toilet,
especially in the setting of urinary urgency/overactive bladder.
Urinary tract infections cause inflammation of the bladder mucosa. Sensory afferent
activity increases with this inflammation, which contributes to an overactive bladder.
Similarly, estrogen deficiency may lead to atrophic vaginitis and urethritis with
increased local irritation and a greater risk of urinary tract infection and overactive
bladder. Topical estrogen may ameliorate symptoms and infections should be treated
before other incontinence interventions are considered.3
472
Table 1
Medications that may contribute to voiding dysfunction

Medication Examples Mechanism Effect

Alcohol Beer, wine, Diuretic effect, Polyuria, frequency
liquor sedation,
immobility
Alpha-adrenergic Decongestants, IUS contraction Urinary retention
agonist diet pills
Alpha-adrenergic Prazosin, terazosin, IUS relaxation Urinary leakage
blockers doxazosin
Anticholinergic Inhibit bladder Urinary retention or
agents contraction, functional
sedation, fecal incontinence
impaction
Antihistamines Diphenhydramine,
scopolamine,
dimenhydrinate
Antipsychotics Thioridazine,
chlorpromazine,
haloperidol
Antiparkinsonians Trihexyphenidyl,
benztropine
mesylate
Skeletal muscle Orphenadrine,
relaxants cyclobenzaprine
Tricyclic Amitriptyline,
antidepressants imipramine,
nortriptyline,
doxepin
Miscellaneous Dicyclomine,
disopyramide
Angiotensin- Enalapril, captopril, Chronic cough Urinary leakage
converting lisinopril, losartan
enzyme
inhibitors
Calcium-channel Nifedipine, Relaxes bladder, Urinary retention,
blockers nicardipine, fluid retention nocturnal diuresis
isradipine,
felodipine
Cyclooxygenase-2 Celecoxib Fluid retention Nocturnal diuresis
selective NSAID
Diuretics Caffeine, HCTZ, Increases urinary Polyuria
furosemide, frequency,
bumetanide, urgency
acetazolamide,
spironolactone
Narcotic analgesics Opiates Relaxes bladder, Urinary retention and/
fecal impaction, or functional
sedation incontinence
Thiazolidinediones Rosiglitazone, Fluid retention Nocturnal diuresis
pioglitazone,
troglitazone

Abbreviations: HCTZ, hydrochlorothiazide; IUS, internal urethral sphincter; NSAID, nonsteroidal

antiinflammatory drug. From Wai CY. Urinary incontinence. In: Schorge JO, Schaffer JI, Halvorson
LM, et al, editors. Williams Gynecology. 1st edition. New York: McGraw Hill Medical; 2008. p. 521;
with permission.
 Pathophysiology of Lower Urinary Tract Dysfunction 473

Although incontinence should not be viewed as a normal consequence of aging,

there are several physiologic changes that occur in the lower urinary tract with aging
that may predispose one to incontinence, overactive bladder, or other voiding difficul-
ties. First, the prevalence of involuntary detrusor contractions increases with aging,
with detrusor overactivity being found in 21% of healthy, continent, community-
dwelling elderly.19 Total bladder capacity may diminish and the ability to postpone
voiding decreases, leading to urinary frequency. Meanwhile, urinary flow rate
decreases in older men and women likely because of an age-related decrease in de-
trusor contractility.20 In women, postmenopausal decrease in estrogen levels results
in atrophy of the urethral mucosal seal, loss of compliance, and bladder irritation,
which may predispose to stress and urgency urinary incontinence. Age-related
changes in renal filtration rate and alterations in diurnal levels of antidiuretic hormone
and atrial natriuretic factor shift the diurnal pattern of fluid excretion toward increased
volume of urine excreted later in the day.21 Comorbid conditions, such as congestive
heart failure, hypothyroidism, venous insufficiency, and the effects of certain medica-
tions all contribute to peripheral edema leading to urinary frequency and nocturia
when a patient is supine.
Diabetes mellitus can lead to osmotic diuresis and polyuria when there is poor
glucose control. Polydipsia from diabetes insipidus or excessive intake of caffeine
or alcohol can also lead to polyuria/urinary frequency. Similarly, abnormalities of argi-
nine vasopressin with its impaired secretion or action may cause polyuria and noctu-
ria; these carefully selected patients may benefit from desmopressin therapy.3
Finally, stool impaction resulting from poor bowel habits and constipation can
contribute to overactive bladder symptoms, perhaps from local irritation or direct
compression against the bladder wall.
As alluded to earlier, there are many medications that may cause or worsen urinary
incontinence or other forms of voiding dysfunction. This dysfunction occurs through
changes in rate of urine production, the integrity of the sympathetic and parasympa-
thetic nervous systems, and cognition. It is important to note patients’ use of diuretics,
anticholinergic medications, alcohol, psychotropic medications, narcotics, alpha
agonists or antagonists, beta mimetics, or calcium channel blockers (see Table 1).

SUMMARY

The coordinated function of the lower urinary tract system depends on the normal and
complex interactions between the nervous system and the lower urinary tract
anatomy. A thorough understanding of these components and their interactions is
essential to properly diagnose and manage lower urinary tract dysfunction.

ACKNOWLEDGMENTS

The authors thank Ms. Lindsay Oksenberg, medical illustrator, University of Texas
Southwestern Office of Medical Education, for use of the many illustrations demon-
strating lower urinary tract neurophysiology.

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