Parkinsonism and Related Disorders 15 (2009) 81e87
www.elsevier.com/locate/parkreldis
Review
Urinary dysfunction in Parkinson’s disease: A review
Helen Blackett*, Richard Walker, Brian Wood
Northumbria Healthcare NHS Foundation Trust, Education Centre, Wansbeck General Hospital, Woodhorn Lane,
Ashington, Northumberland, NE63 9JJ, UK
Received 11 May 2007; received in revised form 22 October 2007; accepted 24 October 2007
Abstract
Urinary dysfunction, primarily in the form of detrusor overactivity, is highly prevalent amongst individuals with idiopathic Parkinson’s
disease (IPD). There has been increasing realisation of the importance of this and other non-motor features of the condition. The presentation
of, pathophysiology behind and management options for bladder dysfunction in IPD are discussed.
Crown Copyright Ó 2008 Published by Elsevier Ltd. All rights reserved.
Keywords: Parkinson’s disease; Parkinsonism; Urinary bladder; Autonomic; Anticholinergic
Contents
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Idiopathic Parkinson’s disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Prevalence of urinary dysfunction in IPD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Symptoms of urinary dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Control of the lower urinary tract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Mechanism of urinary dysfunction in IPD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.1. UD related to the disease process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.2. Pharmacological effects of antiparkinsonian medication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Bladder dysfunction in other conditions associated with parkinsonism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Management of bladder dysfunction in IPD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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1. Introduction
2. Background
Urinary dysfunction (UD), a manifestation of autonomic
failure, is common in idiopathic Parkinson’s disease (IPD).
It can significantly impact on an individual’s quality of life. Interest in this area is growing, although many questions remain
unanswered. This article reviews the prevalence, mechanism
and symptoms of urinary dysfunction in IPD.
IPD is the second most common neurodegenerative condition in the UK, with major medical and psychosocial implications. Both criteria for the diagnosis of IPD (UK Parkinson’s
Disease Society Brainbank Criteria), and tools for assessing resulting symptoms (Unified Parkinson’s Disease Rating Scale),
have primarily focused on the motor features of tremor, rigidity
and bradykinesia [1,2]. The recognition of the importance of
non-motor symptoms is illustrated by their incorporation into
more recently developed scales such as the SCOPA project in
* Corresponding author. Tel.: þ44 01670 529688; fax: þ44 01912 932709.
E-mail address: [email protected] (H. Blackett).
1353-8020/$ - see front matter Crown Copyright Ó 2008 Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.parkreldis.2007.10.016
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H. Blackett et al. / Parkinsonism and Related Disorders 15 (2009) 81e87
2004 and the Non-motor Screening Questionnaire in 2005 [3,4].
Urinary dysfunction is one of these non-motor symptoms.
3. Idiopathic Parkinson’s disease
IPD is a movement disorder associated with loss of dopaminergic neurons in the substantia nigra and the development of
Lewy bodies. A reduction in normal striatal dopamine levels
of 80% or more results in the cardinal symptoms of IPD,
namely bradykinesia, rigidity, rest tremor and postural instability [5]. These form the basis for the diagnosis of IPD as defined by the UK Parkinson’s Disease Society Brainbank
Criteria, the application of which helps distinguish IPD from
other forms of parkinsonism. For patients presenting with features suggestive of a parkinsonian syndrome, the differential
diagnosis includes cerebrovascular parkinsonism, drug-induced parkinsonism, progressive supranuclear palsy and multiple system atrophy (MSA). The features of the latter
diagnosis may include cerebellar and/or parkinsonian features
along with autonomic disturbance, urinary symptoms being
prominent from an early stage in many cases.
4. Prevalence of urinary dysfunction in IPD
Results from early studies suggested that urinary dysfunction
affects between 37% and 70% of individuals with IPD [6,7].
However, many of these studies may have overestimated the
prevalence of UD since they were published prior to the recognition of MSA as a separate disease entity. In addition, many
studies recruited patients with symptomatic bladder dysfunction
from tertiary referral centres. The use of non-validated questionnaires and the inclusion of patients with other forms of ‘parkinsonism’ such as cerebrovascular parkinsonism may have led to
further bias. More recent studies, using accepted diagnostic
criteria for IPD, have found the prevalence of UD to be between
27% and 39% [8,9]. When compared to a control group the
relative risk of bladder symptoms in IPD is 2-fold [10].
5. Symptoms of urinary dysfunction
UD in IPD is most frequently caused by urinary storage problems, rather than voiding dysfunction, and is manifest as an ‘overactive bladder’. This is a symptom complex defined by the
International Continence Society as ‘urgency, with or without
urge incontinence, usually with frequency and nocturia’ [11].
The most prevailing urinary symptom in IPD is ‘nocturia’ (up
to 86%), followed by ‘urgency’ (33e71%) and ‘frequency’
(16e68%) [8,9,12]. These may lead to urinary incontinence,
which may be in part functional if immobility or poor manual
dexterity complicates the situation. Since many patients with
IPD have a disturbed sleep pattern and nocturnal polyuria, the
actual prevalence of definite nocturia may be overestimated [13].
systems. During bladder filling (the urinary storage phase)
the efferent sympathetic nervous system, via hypogastric
nerves originating in the lumbar spinal cord, is active. This
allows compliance and distension of the bladder muscle to
accommodate urine, as well as maintaining closure of the internal urethral sphincter [14]. Importantly, it also inhibits
parasympathetic stimulation of the bladder [15]. Efferent
parasympathetic innervation to the bladder, originating in
S2eS4 segments of the spinal cord and acting via pelvic
splanchnic nerves, has the opposite effect, that is to say
contraction of the detrusor muscle, relaxation of the urethral
smooth muscle and facilitation of voiding [16]. The central
nervous system ensures that micturition occurs under voluntary control, at a time and place that is socially acceptable.
Functional brain imaging has been used to confirm those
cortical and brainstem areas that are involved in the control
of micturition. Two micturition centres exist in the pons,
namely the pontine micturition centre [17,18] and the pontine
storage centre [17]. The former is the more important of
the two areas and facilitates the urinary reflex. The role of
the pontine storage centre is less well understood [19], but it
has connections with the somatic nerves that cause closure of
the external urethral sphincter. Other cortical areas of note
include the periaqueductal grey area [17,18,20], the right prefrontal cortex [17,18,20]and the right anterior cingulate gyrus
[20]. The periaqueductal grey area receives afferent information from the bladder concerning degree of bladder fullness,
as well as from the hypothalamus and other higher cortical
centres. It may act as a relay centre, facilitating voiding through
connections with the pontine micturition centre [21].
Input from higher cortical areas such as the prefrontal cortex and the anterior cingulate gyrus ensure that voiding takes
place at a time that is socially acceptable.
Not only is the autonomic nervous system central to efferent bladder control, but it also forms the afferent components.
Pain and temperature receptors, and mechanoreceptors located
in the urinary system relay information to the brain via sympathetic and parasympathetic nerves.
In addition to the somatic and autonomic nervous system
control of the bladder, the dopaminergic system is also required for normal micturition control. Dopaminergic neurons,
originating in a region of the midbrain known as the ventral
tegmental area, project to the pontine micturition centre. Stimulation of D1 receptors is inhibitory, whereas D2 stimulation is
facilitatory [22].
The process of bladder control is highly complex and is
dependent on the integrity of large areas of the cerebral and
extra-cerebral nervous systems. It is therefore not surprising
that IPD, and the ensuing damage to multiple areas of both
the peripheral and central nervous systems, should cause
bladder dysfunction.
7. Mechanism of urinary dysfunction in IPD
6. Control of the lower urinary tract
The neurological control of the bladder is highly complex,
involving coordination of the somatic and autonomic nervous
There is no consensus on the association of UD with other
disease variables such as disease stage or duration. Some
studies have shown a correlation between these variables and
H. Blackett et al. / Parkinsonism and Related Disorders 15 (2009) 81e87
degree of bladder dysfunction [8,12], whereas others have not
[9,10]. There have been suggestions that UD in IPD is related
to patient age, rather than the disease itself [23], although the
author’s study population (including controls) were drawn
from a group symptomatic of UD. There is no documentation
concerning symptom burden in the two groups, such that the
‘controls’ may have had the more prominent urinary symptoms. The results of this study are in contradiction to other
control-matched studies involving questionnaire assessments
in men [24] and urodynamic evaluations in women [25]. It
is of note that in some cases bladder symptoms may be the
result of co-existent disease processes, such as urinary tract
infection, diabetes or benign prostatic hypertrophy. However,
UD in IPD is not explained solely by bladder outflow obstruction. Studies have got round the concerns regarding coexisting
prostatic disease in men with IPD by studying female patients
only. Women with IPD symptomatic of UD have been shown
to have a lower bladder capacity and a higher rate of detrusor
overactivity at lower bladder volumes than those without [25].
The mechanism by which IPD influences micturition
should be separated into two broad groups:
1. UD related to the disease process
2. Pharmacological effects of antiparkinsonian medication.
7.1. UD related to the disease process
The effect of IPD on the bladder typically leads to detrusor
overactivity, which is a urodynamic diagnosis referring to an
involuntary rise in detrusor pressure during filling of the bladder [11], but less commonly may lead to detrusor underactivity
or detrusoresphincter pseudo-dyssynergia. The latter finding,
more prevalent in individuals with MSA, describes the situation in which there is loss of the normal coordination between
the detrusor muscle and the external urethral sphincter, leading
to detrusor muscle contraction against a closed sphincter and
vice-versa.
Some studies have suggested impaired relaxation or bradykinesia of the external urethral sphincter may exist in IPD
[26]. The resultant voiding dysfunction resembles bladder outflow obstruction, such as that caused by prostatic enlargement.
Most evidence, however, indicates that urine storage phase
abnormalities are more prevalent than voiding phase changes,
implying that bradykinesia of the external urethral sphincter is
not the leading mechanism behind UD in IPD.
Dopaminergic mechanisms are thought to play a central
role in normal micturition control and dysfunction of these
may lead to detrusor overactivity. Dopaminergic neurons
have both inhibitory and stimulatory effects on micturition acting via D1 and D2 receptors respectively. Such neurons are of
particular abundance in the substantia nigra pars compacta
(SNC) and the ventral tegmental area (VTA) of the midbrain.
The most widely accepted theory is that the basal ganglia inhibits the micturition reflex in the ‘normal’ situation via D1 receptors, and that cell depletion in the SNC in IPD, results in loss of this
D1-mediated inhibition and consequently detrusor overactivity.
83
Further evidence for the SNC exerting an influence on micturition
comes from studies on cats, demonstrating inhibition of the micturition reflex following electrical stimulation of the SNC [27,28]. In
addition, in vivo microdialysis measuring striatal dopamine levels
in cats during the normal micturition cycle, confirmed striatal dopamine levels to be significantly increased during the urinary storage phase when compared to the voiding phase [29]. Studies on
marmosets with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridipine
(MPTP)-induced parkinsonism have demonstrated detrusor overactivity [30].
Winge et al. [31] demonstrated loss of nigrostriatal dopaminergic neurons on single photon emission computed tomography (SPECT) imaging amongst IPD patients with lower
urinary tract symptoms. The severity of urinary dysfunction
correlated with the relative degeneration of the caudate
nucleus, a part of the basal ganglia which receives dopaminerich innervation from the SNC and VTA.
Electrical stimulation of the VTA in cats has been shown to
result in both inhibitory and stimulatory effects on micturition
[28], the latter being mediated via D2 receptors. Since the
SNC has an inhibitory effect on micturition and the VTA is
heterogeneous in function, the overall net dopaminergic output
from these areas is likely to be inhibitory. While there is loss
of both inhibitory and stimulatory neurons in IPD it is possible
that with disproportionately more damage to the former,
detrusor overactivity arises.
Kitta et al. hypothesised that brain activation patterns (measured using positron emission tomography (PET)) in response
to bladder filling would be different in patients with IPD when
compared to healthy volunteers [32]. In contrast to healthy
volunteers neither the pons nor the anterior cingulate cortex
(ACC) was activated during bladder filling in their study population of 10 patients with IPD. However, lack of activation of
the pons has previously been demonstrated during voluntary
inhibition of micturition [33], and may therefore have resulted
from patients attempting to avoid urinary incontinence during
the investigation. The most prominent activation during detrusor overactivity in the IPD group was found in large portions
of the cerebellum, and to a lesser extent in the supplementary
motor area. In contrast to these findings, Herzog et al. [34],
through combining urodynamic and PET investigations on
11 IPD patients who had previously undergone implantation
of a subthalamic deep brain stimulator, demonstrated increased activity in the lateral frontal cortex and ACC of the
brain when the bladder was full and subthalamic deep brain
stimulation (STN-DBS) ‘off’. The level of activity in these
areas was reduced when STN-DBS was ‘on’, but increased
regional cerebral blood flow was still apparent in the ACC.
7.2. Pharmacological effects of antiparkinsonian
medication
Levodopa has been shown to both aggravate and alleviate
bladder symptoms in IPD [35,36]. Questionnaire-based assessments of UD have not shown a correlation between severity of
bladder symptoms and dose of levodopa [8,9]. However, while
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H. Blackett et al. / Parkinsonism and Related Disorders 15 (2009) 81e87
studies using urodynamics have given conflicting results, they
do confirm that levodopa has an effect on the bladder.
Studies have looked at the effect of levodopa on the bladder
in both early and late stage disease. Brusa et al. showed levodopa worsened detrusor overactivity in patients with early
stage disease through a central rather than peripheral action
[37]. In patients with advanced disease, who are troubled by
‘wearing off’ phenomena, levodopa worsened detrusor overactivity during bladder filling, but facilitated voiding by exerting
a relatively greater effect on detrusor contractility compared to
external sphincter closure [38].
Winge et al. demonstrated that IPD patients with more troublesome bladder symptoms had significantly higher bladder capacity
when medicated, than after a period off treatment, while patients
without bladder symptoms had no difference [39]. Furthermore,
an increase in bladder capacity of 30% and 87% has been demonstrated in IPD patients with detrusor overactivity following
administration of levodopa and apomorphine respectively [40].
The dopamine D1 and D2 receptor agonist apomorphine
(used as a parenteral agent in later disease) improves voiding
efficiency as measured by an increase in urine flow rate and
reduction in post-void residual urine volume (PVR), but has
an unpredictable effect on the detrusor muscle e either reducing or aggravating detrusor overactivity [41]. Aranda et al.
suggested apomorphine may improve detrusor overactivity
through D1 receptor stimulation [40]. Further support for the
theory that D1 stimulation improves bladder function comes
from animal studies. Pergolide, a D1 and D2 receptor agonist,
which has a higher affinity for D1 receptors than levodopa, has
been shown to improve bladder function in parkinsonian monkeys [30] as well as in patients with IPD [42]. Kuno et al. [43],
in their case report of three female patients with IPD, describe
a reduction in the frequency of nocturia following the substitution of pergolide for bromocriptine. For two of these patients,
there was also an improvement in irritative urinary symptoms.
However the use of pergolide is restricted by reports suggesting
a link between pergolide and cardiac valve abnormalities [44].
The selective D2 agonist bromocriptine, has been shown to
be of no value in the treatment of detrusor overactivity in
patients without a diagnosis of IPD [45]. We are unaware of
studies of bladder dysfunction related to other anti-parkinsonian agents. The effects of dopaminergic treatment on bladder
control and urodynamic parameters are unpredictable in the
individual patient, although most patients experience significant changes, whichever medication is used.
Subthalamic deep brain stimulation (STN-DBS) has been
shown to produce a significant improvement in bladder capacity and first desire to void in a population of 16 patients with
IPD who underwent urodynamic investigations off medication,
with the STN-DBS both on and off [46]. These results are in
keeping with more recent studies [34].
often occur at an earlier stage in the disease course when
compared to IPD, and precede, or are the presenting feature,
in around 60% of patients [48]. Urinary incontinence is significantly more common in MSA than IPD, occurring in 60e
73% of patients [46,48,49], compared to between 15% and
33% of patients with IPD [48,49]. Post-void residual urine
volumes of more than 100 ml are commonly seen and have
been demonstrated in about half of patients with MSA
[47,49]. This is in contrast to IPD where significant postvoid residual urine volumes are rarely seen [48]. Similarly,
detrusoresphincter-dyssynergia is more common, being demonstrated in 45% of patients in one study of 121 patients with
MSA [47]. The severity and high prevalence of UD in MSA
when compared to IPD can be explained when one considers
the neuropathology of the former. Vast areas of the nervous
system responsible for bladder control are affected, in addition to those dopaminergic mechanisms central to UD in
IPD. This includes, among others, atrophy of those regions
from which neurons supplying the bladder and internal and
external sphincters arise [50].
The literature concerning bladder dysfunction in other conditions associated with parkinsonism is limited. Sakakibara
et al. [51] confirmed bladder symptoms were prevalent among
nine subjects with progressive supranuclear palsy (PSP) they
studied, with a variety of findings being demonstrated on
urodynamics, including detrusor overactivity and detrusore
sphincter dyssynergia. The same authors have also looked at
urinary disturbances in corticobasal degeneration (CBD)
[52]. Urinary symptoms were significantly more common in
those individuals with CBD when compared with controls,
and had an association with increasing duration of disease.
As with the PSP population, a number of findings were elicited
on urodynamics including detrusor overactivity, reduced bladder capacity and detrusor underactivity. The numbers of subjects in this study (n ¼ 10) makes application of their results
to the general population difficult. The gait disturbance seen
in patients with normal pressure hydrocephalus (NPH) may
resemble that of Parkinson’s disease. Urinary incontinence
forms part of the ‘classical triad’ of symptoms pertaining to
this condition. Despite this, few studies of bladder dysfunction
in NPH have been undertaken. Urodynamic investigations
have demonstrated detrusor overactivity, which improves
following implantation of a ventriculoperitoneal shunt [53].
However, this is based on only four individuals with NPH,
and there is little in the way of corroborating evidence from
further studies.
Clearly bladder dysfunction and parkinsonism are not
limited solely to those individuals with idiopathic Parkinson’s
disease. Further research concerning the association of urinary
abnormalities and these conditions is necessary.
9. Management of bladder dysfunction in IPD
8. Bladder dysfunction in other conditions associated
with parkinsonism
Autonomic symptoms, including UD, are prominent in
MSA, affecting up to 96% of patients [47]. Urinary symptoms
The drug treatment of choice for detrusor overactivity is
anticholinergic medication. To our knowledge, no randomised
controlled studies of this class of drug in the treatment of UD
in PD have been conducted. Most data available for their
H. Blackett et al. / Parkinsonism and Related Disorders 15 (2009) 81e87
efficacy and tolerability come from studies of detrusor overactivity in patients with urinary dysfunction from another cause.
However, anticholinergics were the first widely accepted treatment for the symptoms of parkinsonism, possibly being used
in this context in ancient Indian medicine [54]. Concerns
regarding potential adverse drug effects (both short-term and
potentially long-term), such as falls and cognitive decline,
have restricted their use among those managing IPD.
Bennett et al. [55] studied the effect of long acting oxybutynin on 39 patients with detrusor overactivity resulting from
a neurogenic cause. Seven IPD patients were included in their
sample population. Following 1 week of treatment they demonstrated a significant reduction in the number of voids over
24 h, frequency of nocturia and incontinence, with no serious
adverse effects, although the results were not broken down by
disease process.
The longer acting anticholinergic tolterodine XL (extended
release) has been shown to be more efficacious and better
tolerated when compared to short acting oxybutynin [56].
However, more recently solifenacin succinate has been shown
to have a superior effect on urinary symptoms compared with
tolterodine XL, although limited data are presented regarding
its adverse effects [57]. Solifenacin and darifenacin have
emerged as alternatives to the traditional anticholinergic
drugs. Whereas the older anticholinergics such as oxybutynin
acted on several subtypes of the muscarinic receptor, present
not only in the bladder, but also in the heart, central nervous
system, gut and salivary glands, these newer agents act specifically on the M3 receptors present in the bladder. A recent review of the pharmacotherapy for overactive bladder concluded
that while M3 selective muscarinic agents may not be more
efficacious in treating resultant bladder symptoms, they had
superior tolerability, with no significant cardiac or central
nervous system adverse effects [58]. Darifenacin had no significant impact on cognitive tests performed on a population
of 129 normal volunteers aged over 65 years [59].
Trospium chloride is a non-selective anticholinergic agent
that, due to its low lipid solubility, does not cross the
bloodebrain barrier. One 12 month study compared trospium
chloride with immediate release oxybutynin in 358 patients
with detrusor overactivity of any cause [60]. They concluded
that trospium was as efficacious as oxybutynin, but had
a more favourable adverse effect profile.
Several studies have confirmed that anticholinergics may
impair mental functioning in IPD. Cooper et al. [61] carried
out a randomised, controlled, single-blinded trial of 82 newly
diagnosed IPD patients, assigned to receive levodopa, bromocriptine or the anticholinergic benzhexol. They demonstrated
deterioration in cognition as measured by the Wechsler
Memory Scale in those receiving benzhexol, while the scores
for this test were enhanced in those receiving levodopa. It is
however noteworthy that benzhexol was designed to act on
the central nervous system, and is therefore more likely to
result in adverse cognitive effects than tolterodine, which
has a more peripheral mechanism of action.
Since anticholinergic treatment may cause retention of
urine it is important to measure post-void residual urine
85
volumes both prior to, and during, its administration. Despite
its restrictions, anticholinergic medication, when appropriately
monitored, remains a valid treatment option for UD in IPD.
The riskebenefit profile for a particular individual must be
considered in each case.
In those individuals with persisting urinary symptoms related to possible detrusor overactivity or bladder outlet obstruction, referral to a urologist for further investigation may be
necessary. The latter, when combined with large post-void
residual urine volumes, can be managed with intermittent or indwelling long-term catheterisation. There have been suggestions that patients with IPD have a poor outcome with high
rates of urinary incontinence following transurethral prostatectomy [62]. This is more likely to occur if lack of voluntary
sphincter control is present pre-operatively. It is possible that
the high incidence of post-prostatectomy UI among individuals
with IPD reported in earlier studies reflects the inclusion of
patients with MSA, amongst whom high rates of urinary incontinence exist. More recent evidence looking at IPD patients undergoing radical prostatectomy for prostate cancer showed
76% of patients remained continent of urine 1 year postoperatively [63], although their exclusion of patients with autonomic symptoms and the different nature of the surgery does
not make this data comparable. Furthermore, the authors do
not comment on the rate of urinary incontinence in their nonIPD population undergoing surgery.
10. Conclusions
Urinary dysfunction, primarily in the form of detrusor overactivity, is highly prevalent amongst individuals with IPD.
This may arise from direct effects of the disease, as a result
of Parkinson’s disease treatment or indirectly (for example
as a result of impaired mobility). The most widely accepted
mechanism by which IPD exerts its effect on the bladder is
through cell depletion in the substantia nigra resulting in
loss of the normal D1-mediated inhibition of micturition.
The mainstay of treatment for detrusor overactivity is anticholinergic medication. One must take into account the riskebenefit ratio for an individual when prescribing such medication,
and be alert to potential adverse effects. Referral to a urologist
may be appropriate for further investigation and management.
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