Int Urogynecol J (1993) 4:168-174
9 1993 The International Urogynecology Journal
Review Article
The Aging Bladder
A. E. Finkbeiner
University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
Abstract: Urinary bladder function changes with aging.
In the older population symptoms of increased diurnal
frequency, incontinence and/or retention are most
prevalent. Objective measurements of bladder function
in the aged reveal a high incidence of detrusor hyperac-
tivity and decrease in flow rates. Intrinsic changes of the
anatomy and neuropharmacology of the bladder associ-
ated with aging are noted in animal models and humans.
However, aging is also associated with central and
peripheral neurologic changes and diseases, as well as
anatomic and functional changes in the bladder outlet
which affect bladder function. At present it is difficult to
distinguish in the individual patient which of these
factors (extrinsic, intrinsic or both) are the etiology for
functional changes of the bladder with aging. For most
individuals, however, the major factors influencing
bladder changes with aging are extrinsic neurologic
diseases and/or changes in the bladder outlet.
Keywords: Aging; Bladder; Geriatrics; Urinary bladder
Introduction
Subjectively and objectively, it is clinically apparent
that alterations in both the storage and the evacuation
functions of the urinary bladder are commonly seen in
the aged population. Many studies have documented
the high incidence and prevalence of incontinence,
retention and increased diurnal frequency and urgency
in the aged. What is not so apparent, however, is the
etiology or etiologies for these changes.
Urinary bladder storage and evacuation functions are
Correspondence and offprint requests to: Dr Alex E. Finkbeiner,
Professor of Urology, University of Arkansas for Medical Sciences,
4301 West Markham, Little Rock, Arkansas 72205, USA.
International
Urogynecology
Journal
complex. Normal function is dependant upon intrinsic
bladder neuromuscular factors, as well as extrinsic
central and peripheral neurologic and neuromuscular
bladder outlet factors. Alteration of any of these intrin-
sic or extrinsic systems can result in alterations of
bladder function. In this review the effects of aging will
be addressed as they relate to each of these systems
involved in bladder function.
Urodynamics
Changes in bladder function associated with aging can
be objectively measured urodynamically. In studies on
rats [1-3] no age-related changes in bladder capacity or
bladder volume at micturition were noted; the average
plateau pressure significantly decreased and intravesical
pressure at micturition increased by greater than 100%
in old versus young rats.
Resnick and Yalla [4] concluded that bladder capa-
city, the ability to postpone voiding, urethral and
bladder compliance, uroftow rates and urethral length
and closing pressure (in women) all probably decline
with age. Brocklehurst and Dillane [5] found that
almost all aged non-incontinent women had abnormal
CMGs (desire to avoid, capacity and uninhibited
bladder contractions), and concluded that changes in
bladder function are part of the aging process.
In females Haylen et al. [6] found no significant
variation in either maximum or average flow rate with
respect to age or parity. However, in a study [7]
comparing healthy fertile versus healthy aged post-
menopausal females, an increased flow time with
decreased maximum and mean flow rates were found in
the aged women; they could not conclude, however,
whether the impaired flow was secondary to decreased
bladder contractility or a less compliant urethra
(estrogen deficiency). Malone-Lee [8] found decreased
The AgingBladder
maximum flow rate, decreased bladder capacity and
elevated residual volumes in elderly incontinent
women.
In healthy elderly males without overt neurologic
lesions, 33% complained of increased urinary fre-
quency, measured flow rates were decreased, maximum
intravesical pressure was elevated and detrusor hyper-
reflexia was found in over 50% of the patients studied
[9,10].
Several studies [1,6,8,11-13] have measured changes
in flow rates with aging in males. Both maximum and
average flow rates decline with age in men; the average
maximum flow rate of 18.5 ml/s at age 50 years declines
to an average maximum flow rate of 6.5 ml/s at age 80.
This decline appears to be progressive with time with
the maximum flow rate declining 1.0--2.9 ml/s/10 years
and the mean flow rate declining 0.6-1.6 ml/s/10 years in
men. Shimizu et al. [11] found that in elderly men the
normal flow curve declines and the obstructive flow
curve gradually increases with age.
While it is apparent that uroflow rates decline in men
with advancing age, it is not clear whether this is
secondary to outlet obstruction or whether older
bladders do not contract as efficiently.
In a review on aging on the urinary tract Staskin [14]
cites several references to conclude that detrusor
instability has been shown to be related to aging, and
has been demonstrated in up to 50% of healthy elderly
men and women. Resnick and Yalla [4] agree that the
prevalence of uninhibited contractions probably
increases with age. Brocklehurst [15] concluded that the
aging of cortical neurons diminishes the central
inhibitory effects on the bladder, causing uninhibited
contractions and the symptoms of diurnal urgency,
frequency and incontinence. Ouslander et al. [16] state
that in men and women over age 65, detrusor instability
is the most common abnormal urodynamic finding,
being present in 37% of all patients and 43% of the
incontinent patients studied. Further, 34% of the
patients with detrusor hyperactivity also had elevated
residual volumes.
Comparing men with BPH to aged-matched control
women, Jones and Schoenberg [7] found detrusor
hyperreflexia in 11.1% of the women and 50% of the
men. In that there is no other readily available expla-
nation for the hyperreflexia in the women, and the fact
that some men have persistent hyperreflexia after treat-
ment of their BPH, this suggests that some hyper-
reftexia may be associated with the aging process.
Anderson et al. [6] noted that hyperreflexia is found
in 45% of patients with BPH and is seen commonly in
patients with CNS disease, and concludes that hyper-
reflexia seen in healthy men suggests incipient intra-
vesical obstruction or subclinical impairment of the
CNS as the cause of hyperreftexia.
In the incontinent elderly detrusor hyperreftexia or
unstable bladder was found in 80% of the women and
90% of the men, with significant age-related changes in
women but not in men [10]. In a survey of several
studies Leach and Yip [17] concluded that in the
169
incontinent elderly, the most common urodynamic find-
ing was detrusor instability, occurring in 10%-68% of
patients. Brocklehurst and Dillane [18] studied a group
of aged incontinent patients who all had abnormal
CMGs; 75% had large uninhibited bladder contractions
and many patients exhibited neurologic abnormalities.
Brown [19] found detrusor instability to be the major
cause of female incontinence, occurring in 30%-40% of
incontinent women. Resnick [20] states that detrusor
overactivity is the predominant cause (61%) and that
detrusor hyperactivity with impaired contractile
function is the second most common (33%) cause of
incontinence in the institutionalized elderly. Castleden
et al. [21] evaluated 100 elderly incontinent patients
urodynamically. Sixteen percent had normal studies,
68% exhibited uninhibited detrusor contractions, 11%
atonic bladders and 5 % irritable bladders. In an attempt
to correlate other conditions such as dementia, CVA
and diabetes, no specific associations could be identi-
fied. There was, further, no correlation between mental
test scores and any urodynamic measurement in the
patients with unstable bladders.
Ouslander et al. [16] evaluated men and women over
age 65 years. Incontinence was found in 81% women
and 60% men. Twenty percent of the patients without
incontinence and urodynamic abnormalities; 20% had
neurologic findings and these findings did not correlate
with whether or not the patient was incontinent;
detrusor instability was found in 37% of all the patients
and 43% of the incontinent patients, with 34% of the
patients with detrusor instability having elevated residu-
als; 5% had a contractile bladders but 34% had residuals
greater than 100 cc; 62% of the men had abnormal
prostates; 31% of the women had vaginal mucosal
atrophy and one-third of the women had abnormal
urethral profiles.
Several authors [1,4,22] concluded that aging per se is
not the cause of uninhibited contractions, but they are
secondary to neurologic disease and/or bladder outlet
obstruction commonly seen in the aged and, given
uninhibited contractions with or without overt neuro-
logic disease or outlet obstruction, one cannot differen-
tiate whether the contractions are incidental to normal
aging, consequent to outlet abnormality or due to
neurologic disease.
Intrinsic Anatomic and Histochemical
Changes of the Bladder
Various studies have looked at intrinsic anatomic and
histochemical changes of the bladder in aging.
Endothelium
Bronklehurst [15] noted that leakiness of the endothe-
lium increases with advancing age but is of uncertain
significance.
170
Elastin
Cortivo et al. [23] found that an increase in elastin occurs
in normal individuals as a result of the aging process.
Submucosa
Levy and Wright [24] looked at the morphologic
changes of the bladder mucosa with aging, and noted
that collagen fibers separate and no longer form fasci-
cles, and that this process is acclerated in the presence of
obstruction. Further, deposits of electron-dense parti-
cles are found within intercollagenous channels, and the
smooth muscle of the submucosa disappears with age.
They suggest that such submucosal changes may cause
changes in compliance, alter muscle function and affect
nerve conduction.
Protein
Johnson et al. [25] found no change in the amount of
protein in rat bladders with aging, while others noted an
18% reduction [26] and a 25% reduction [27] in protein
in aging bladders.
Muscle Cells
Two studies [28,29] found that the size of human
detrusor smooth muscle cells does not vary with age.
Phospholipids
Wheeler et al. [27] noted a 40% reduction in the
percentage of phospholipid content and a 69% increase
in the cholesterol/phospholipid ratio, indicative of a
more rigid lipid bilayer in the aged rat bladder.
Collagen
The average percentage of collagen in human bladders
based on autopsy specimens is 57.4% (+ 9%) of dry
weight of insoluble protein [14,30,31]. The collagen
content is 10% higher in females and 3% lower in males
above the age of 50. The differences between males and
females seem to increase in direct proportion to age.
Females develop a significant increase in bladder
collagen compared to males; this difference may be
explained by the parallel development of detrusor
muscle mass (and hence, a lower collagen/muscle ratio)
in males due to a high frequency of outlet obstruction.
The deposition of collagen in female bladders may result
in a proportional decrease in detrusor contractility.
A.E. Finkbeiner
Contractile Function
Based on the finding of no change in the maximum
contractile response of the bladder to the non-specific
muscle stimulant KC1 with age, it is suggested there is no
change in the ability or capacity of the bladder to
contract with aging [1,26,32].
Intrinsic Neuropharmacologic Changes of the
Bladder
Several investigators have tried to determine whether
intrinsic changes occur in the bladder with aging, rela-
tive to neuroreceptor density or affinity and/or response
to pharmacologic agents. Animal studies relating to the
cholinergic innervation of the bladder have produced
conflicting results. Studies on female rats showed a
lower maximum response to ACh without a decrease in
intravesical pressure in aged compared to adult rats, and
it was concluded that the response of the bladder to
ACh is reduced by aging [33].
Alternatively, other studies on isolated whole rat
bladder preparations found that the contractile re-
sponse to bethanechol [3], and other cholinergic
agonists [25] did not change with age, and there were no
age-related alterations in cholinergic muscarinic
receptor recognition sites in the aged rat bladder, i.e.
there was no difference in either the number of binding
sites or the affinity of the receptors [34].
Still other studies indicate that there is an increased
responsiveness to cholinergic agents of the bladder with
aging.
Two studies [35,36] found an age-related increase in
the maximum contractile response to ACh and an
increased number of muscarinic cholinergic receptors.
Ordway et al. [37] noted no age-related changes in the
bladder body, but an age-related increase in maximum
response to ACh and bethanechol in the bladder base
(but not to oxotremorine or pilocarpine). No change in
receptor affinity was noted in either region. They
concluded that the age-related increase in response was
regionally specific and only to certain muscarinic agents.
Ordway et al. [26] also noted an age-related increase
in the number of muscarinic receptors in the bladder
body, but this increase was proportional to bladder
growth, and hence constant per amount of bladder
tissue. Further, no age-related changes in maximum
contractions were elicited by muscarinic agonists in the
bladder body. However, in the bladder base there was
an age-related increase in the maximum contractions
elicited by the muscarinic agonists ACh, bethanechol
and oxotremorine. Further, the total number of muscar-
inic receptors in the base decrease with age, but the
density per mg protein remained constant because of an
age-related decrease in the percentage of protein. Thus,
an inverse relationship between function and receptor
number may indicate that changes in responsiveness
result from post-receptor alterations, such as change in
The AgingBladder
the coupling of the activated receptor to contractile
elements.
A study in humans [28] of varying ages with normal
urodynamics and no bladder trabeculation found a
linear reduction in the amount of acetylcholinesterase-
positive nerves observed with increasing age (light
microscopy) as well as a reduction in the amount of
nerves/mm~ of detrusor (electron microscopy). They
concluded that there is a real reduction in the number of
nerve axons in the bladder with age.
Conflicting findings have been noted regarding the
changes in adrenergic function of the bladder with age.
Ouslander et al. [16] found no significant age-related
changes in the affinity to alpha-adrenergic agents in the
base or body of the bladder in rats, but in the body (but
not the base) there was an age-related increase in
maximum contraction elicited by phenylephrine, norep-
hinephrine and clonidine (increase of alphaa adrenergic
activation with age). They concluded there was age-
related increase in the maximal response to alpha1
adrenergic agonists in the body of the bladder but not
the base.
Other studies [3,35] found no age-related changes in
the contractile response of the rat bladder to phenyleph-
rine. Johnson et al. [25] found that in rats the only
age-related changes in the bladder were a progressive
decrease in monoamine oxidase activity in both the
body and base, and a decrease in norepinephrine
concentration in older rats. The differences were small,
however, and probably insignificant. They conclude
that the cholinergic and adrenergic neurochemistry
remains stable with age.
Some studies indicate that estrogen can alter the
neurochemistry of the bladder. In immature rabbits
estrogen induced a marked increase in the response to
alpha-adrenergic, muscarinic cholinergic and purinergic
agonists in the bladder body, but with no significant
alterations in the bladder base. No changes were noted
in beta-adrenergic receptor density [38].
Other agents have been evaluated and no age-related
changes in the response of the bladder in rats to
stimulation by isoproterenol, substance P, histamine,
oxytocin, PG2 alpha and seratonin were found [3,35].
Extrinsic Neurologic Factors
The major extrinsic factor affecting bladder function is
neurologic. Studies of neurologic changes with aging
have been conducted on non-urinary organs, particular
the cardiac and central nervous systems.
There is considerable evidence from human and
animal studies that the adrenergic nervous system con-
trol of cardiac function is altered by aging, particularly a
reduction in beta-adrenergic responses in the cardiac
and peripheral vascular systems [39,40].
Several studies in humans and animals indicate there
are alterations in the alpha- and beta-adrenergic and
dopamine receptors in various parts of the brain with
171
aging. This is generally characterized by an age-related
decrease in number without a change in affinity of the
receptors [39,41,42].
Two excellent reviews [43,44] address the issue of
changes in central neurotransmitters and neuro-
receptors with aging. Alterations in responsiveness to
hormones and neurotransmitters with aging do occur,
and appear to be due to changes at both the receptor
and post-receptor levels. At present no definite con-
clusions can be made to localize particular post-receptor
alterations responsible for age-related changes in
responsiveness.
Cognitive disorders such as acute confusional states,
dementia and depression occur in the aged population,
and have been implicated as etiologies for bladder
disorders, particularly incontinence [15,21,45]. In such
alterations of consciousness the patient may not recog-
nize a micturition urge or be capable of voiding in a
socially acceptable place or manner. Castleden et al.
[21] did mental scores and urodynamics on an aged
incontinent population and found no correlation
between the mental test score and any urodynamic
measurement in those patients with unstable bladders.
In that bladder function is so dependent upon neuro-
logic control, it can be expected that bladder function
may be altered by various neurologic diseases.
Although not confined to the aged population, many of
the following are commonly seen in the aged.
Lesions confined to the brain generally will not alter
the sensory or voluntary motor function of the bladder,
but commonly cause loss of the inhibitory reflex,
causing uninhibited bladder contractions characterized
by increased diurnal urgency and frequency with or
without urge incontinence. Such lesions associated with
uninhibited bladder contractions include cerebral
vascular accidents [4,14,15,17], Parkinson's disease
[4,14,17], Alzheimer's disease [ 4 ] , demyelinating
diseases such as multiple sclerosis [17], cerebral ataxia
[17], and normal pressure hydrocephalus [14].
Increased nocturnal frequency is the most common
urinary symptoms in the elderly in both sexes, and it
increases in severity with age, being present in 31% of
women aged 45-64 years, and 61% of the elderly. It is
associated with cerebral deterioration secondary to
atherosclerosis or cerebral senescence [19].
In one study of non-incontinent aged females [5] 40%
had cerebral neurologic disorders such as CVAs or
Parkinsonism, and most of these patients with abnormal
urodynamic findings had a history of hemiplegia.
It has been reported that a significant number of
incontinent elderly have upper motor neurologic dis-
ease [4]. Brocklehurst and Dillane [18] reported that
83% of the incontinent elderly have some CNS disease,
50% of women with incontinence have had a CVA, 25%
suffer from cerebral arteriosclerosis and a large number
have dementia. When a series of incontinent aged
women were compared to continent aged women, a
much higher percentage of the incontinent women had
decreased intellectual capacity and an increased
incidence of bilateral hyperreflexia of their lower
172
extremities. Proof was not offered, however, that these
neurologic diseases were the sole cause of incontinence.
Griffiths et al. [46] studied a geriatric age group with
incontinence and found that the presence of urge
incontinence was strongly associated with depressed
perfusion of the cerebral cortex and midbrain, as deter-
mined by SPECT scans.
In a contrary conclusion, Castleden et al. [21] found
that urinary incontinence in most elderly residents was
not associated with immobility or cerebral disease, in
that only 38% of elderly incontinent patients had
clinically detectable neurologic lesions.
The effects of lesions of the spinal cord cephalad to
the sacral reflex arc on the bladder vary with the extent
and degree of the lesion. The sensory limb and/or
voluntary motor function may or may not be impaired
completely or incompletely, and hence the patient's
urinary symptoms may vary. A nearly constant finding,
however, is detrusor hyperreflexia with or without
detrusor-sphincter dyssynergia. Such diseases of the
cord that may alter bladder function include cervical
spondylosis, cervical radiculopathy, spondylosis, spinal
stenosis, osteoarthritis, syringomyelia, tethered cord,
spinal cord injury, transverse myelitis, multiple sclero-
sis, vascular diseases such as spinal artery syndrome,
disc disease and osteoarthritis [4,14,17,47].
Lesions of the sacral cord and/or peripheral nerves
generally result in varying degrees of motor and sensory
impairment, with resultant urinary symptoms of loss of
urge, retention symptoms and/or overflow inconti-
nence. Such lesions include peripheral neuropathies
secondary to diabetes mellitus, hypothyroidism,
uremia, tabes dorsalis, peripheral vascular disease and
vitamin B12 deficiency, and may also be seen after
radical pelvic surgery for malignant tumors of the
rectum, prostate or uterus [14,15,17,47].
Chun et al.[3] concluded that age-related differences
in micturition are related primarily to changes in neuro-
nal innervation and control of micturition, rather than
in the contractility of the bladder.
Changes in Renal Function
Changes in urinary frequency may be associated with
changes in urinary volume. In one study [1] a 93%
increase in urinary output was noted in 22-24-month-
old rats compared to rats 5-7 months old. In humans,
age-related changes in glomerular filtration rate, renal
blood flow and renal tubular function with loss of
concentrating ability has been documented [14]. The
resultant increased volume due to physiologic renal
changes can account for diurnal increased frequency.
These symptoms can be further exaggerated if the
patient has diabetes mellitus and/or is taking a diuretic.
Increasing nocturia may also be associated with the
night-time mobilization of peripheral edema secondary
to cardiac failure and/or peripheral vascular disease
[14,15].
A.E. Finkbeiner
Outlet Obstructions
Anatomic outlet obstruction is rare in females but
commonly seen in older males, secondary to BPH,
carcinoma of the prostate and/or urethral strictures.
Changes in the bladder are commonly seen secondary to
outlet obstruction.
Surgically induced vesicle-neck obstruction in dogs
resulted in a 300% increase in the ratio of bladder to
total body weight [31]. In rabbits [48] obstruction of the
outlet results first in marked dilitation of the bladder,
followed by thickening of the bladder wall. Temporary
submucosal edema is observed, followed by increased
connective tissue deposition followed by increased
muscle mass. Both cellular hyperplasia and hypertrophy
occurs within 30 days, with a resultant fivefold increase
in muscle cell volume and a threefold increase in muscle
cell number.
In humans, Mayo and Hinman [23] found decreased
muscle contractility and dilatation if intracellular
spaces with collagen formation induced by chronic
outlet obstruction. Gilpin et al [29] found that in
human obstructed and trabeculated bladders the
smooth muscle cells undergo compensatory hyper-
trophy, with an increase in mean cell length and
infiltration of the connective tissue in the detrusor cell
bundles. Susset [31] also found that the bladder in
patients with BPH revealed markedly thickened walls,
with an abnormal increase in both muscle and colla-
gen. Cortivo et al. [23] found no change in the collagen
content of the bladder with obstruction, but did note
an increase in bladder elastin (particularly polar amino
acids) with aging.
E1-Badawi et al. [49] correlated bladder structure and
urodynamic patterns in geriatric patients without overt
neurologic deficits. Long sarcolemmal bands were the
main feature of the aging detrusor per se. The
obstructed detrusor was characterized by branching
hypertrophic muscle cells with marked fibroelastosis;
detrusor hyperactivity by protrusion of the cellular
junctions; the non-obstructed bladder with impaired
contractility by an enwrapped cell pattern; and pro-
found smooth muscle/axonal degeneration was noted in
the bladder with impaired contractility (whether
detrusor hypertrophy or obstruction is present or
absent).
In both males and females Gosling et al. [50] noted a
significant decrease in the amount of muscle per mm 2 of
bladder tissue in patients with outlet obstruction due to
infiltration of the detrusor muscle bundles by connective
tissue. It was also noted that the amount of nerves/mm2
of muscle decreased in obstructed versus control
bladders.
Brocklehurst [51] evaluated post-mortem bladder
changes in women aged 75-102 years. The majority of
the bladders exhibited marked trabeculation due to
detrusor hypertrophy and loss of the supporting elastic
tissue, causing cellules and diverticulae. He attributed
these age-related changes to either CNS diseases caus-
The Aging Bladder
ing uninhibited contractions, or to outlet obstruction
due to fibrosis secondary to chronic infection.
Brocklehurst [15] noted that in males with outlet
obstruction the bladder hypertrophies with trabecu-
lation and ultimately diverticulae, and in aged and
incontinent females similar findings are present, sug-
gesting that areas of weakness develop in the interstices
of the detrusor. Since there was no anatomic
obstruction demonstrated in these females, it is felt that
these findings result from uninhibited contractions
against a closed neck, resulting in functional outlet
obstruction.
Up to 50% of males with BPH have detrusor hyper-
reflexia. The associated irritative symptoms of BPH
may be secondary to uninhibited bladder contractions
(motor response) or bladder hypersensitivity (sensory
response). Changes in the threshold level of the neuro-
muscular responses of the bladder to stretch may be the
mechanism for uninhibited contraction. Relief of
obstruction will improve the uninhibited contractions
and irritative symptoms in 50%-75% of patients
[6,7,14,19].
In conclusion, separating the effect of age per se from
secondary effects (outlet obstruction and neurologic
disease) is difficult [1], and age-related changes are
mostly changes in neuronal innervation, central control
of micturition or outlet obstruction rather than changes
in the contractility of the bladder [3].
Outlet Relaxation
Decreased outlet resistance can result in stress inconti-
nence. In the aging mouse there is loss of smooth muscle
and increased collagen in the urethra [15].
An age relationship of maximum urethral closure
pressure exists in women, with a steady decline as they
become older. Although this age-related decline is seen
in both continent and incontinent women, it is felt
to be a factor in the etiology of incontinence in the
aged [52]. Estrogen deficiency has been implicated in
changes of the submucosal vascular supply and
muscular bulk of the urethra, which contribute to
urethral closure pressure, and exogenous estrogen can
improve the symptoms associated with outlet relaxation
[14].
An etiology of stress incontinence secondary to exter-
nal urinary sphincter dysfunction may be attributed to
the fact that in aging skeletal muscle there is a decrease
in muscle volume, with replacement by adipose connec-
tive tissue, which is more marked in women than in men
[19].
McGuire et al. [53] identified detrusor instability in
27% of women with stress incontinence. Since the
majority had cessation of the hyperreflexia postopera-
tively, it is suggested that the detrusor instability is
associated with the outlet disease and not an intrinsic
bladder change.
173
Miscellaneous Factors Affecting Changes in
Bladder Function in the Aged
Factors possibly solely or in part causing urinary inconti-
nence and/or retention include psychologic [15], com-
munication problems [21], ambulation problems
secondary to neurologic or skeletal diseases [15,21],
environmental changes such as being institutionalized,
with enforced immobility, loss of independence and
need for nursing assistance [15], retention for fecal
impaction [15], incontinence from bacteriuria [15],
nocturnal frequency from change in sleep patterns [15],
post-prostatectomy incontinence [17], or urinary
retention after anesthetic and/or major surgery [47].
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EDITORIAL COMMENT: The terms detrusor hyperactivity,
detrusor hyperreflexia, detrusor instability and uninhibited
contractions are used in this article. The author has intention-
ally not redefined them to correspond to established termino-
logy to distinguish the terms. Rather the terms used are as they
appear in the original articles.