Neurology in Practice
THE BARE ESSENTIALS
1
Locum Consultant Neurologist
in Uro-Neurology, Department
of Uro-Neurology, The National
Hospital for Neurology and
Neurosurgery, UCL Institute of
Neurology, London, UK
2
Professor of Uro-Neurology,
Department of Uro-Neurology,
The National Hospital for
Neurology and Neurosurgery,
UCL Institute of Neurology,
London, UK
Correspondence to
Dr J N Panicker, Department
of Uro-Neurology, The National
Hospital for Neurology and
Neurosurgery, UCL Institute
of Neurology, London WC1N
3BG, UK;
j.panicker@ion.ucl.ac.uk
178
Uro-Neurology
Jalesh N Panicker,1 Clare J Fowler2
Neurogenic lower urinary tract dysfunction—the
so-called neurogenic bladder—can result from
many neurological conditions. The importance
of this problem to patient health and quality of
life is now better recognised, particularly as these
days many of the symptoms can be treated.
THE LOWER URINARY TRACT AND ITS
NEUROLOGICAL CONTROL
Optimal patient management requires an under-
standing of the physiology of the lower urinary
tract, and its derangement in neurological dis-
ease. The lower urinary tract consists of the blad-
der and urethra and has just two roles: storage of
urine and voiding at appropriate times. To regu-
late this, a complex neural control system acts
like a switching circuit to maintain a reciprocal
relationship between the reservoir (storage) func-
tion of the bladder and the continence (voiding)
function of the urethra (figure 1). The pontine
micturition centre is responsible for switching
between the ‘storage’ phase and ‘voiding’ phase.
It in turn receives input from other centres, par-
ticularly the periaqueductal grey of the midbrain,
hypothalamus and cortical areas such as the pre-
frontal cortex.
Storage phase
▶ In health, the bladder is in the storage phase for
99.8% of the time, achieved by inhibition of
parasympathetic activity and so relaxation of
the detrusor muscle of the bladder wall. This
results in ‘bladder compliance’ so that intra-
vesical pressure remains below 10 cm H 2O.
▶ Simultaneously, sympathetic and pudendal
nerve mediated tonic contraction of the ure-
thral sphincters ensures continence.
▶ Functional imaging suggests that the pon-
tine micturition centre is tonically inhib-
ited during bladder filling by signals arising
from the periaqueductal grey. Other areas
that show ‘activation’ during bladder fill-
ing include the anterior cingulate gyrus and
right insula.
Voiding phase
▶ When it is consciously deemed appropriate
to void, the periaqueductal grey no longer
exerts tonic inhibition on the pontine mic-
turition centre. This results in relaxation
of the pelvic floor muscles as well as the
external and internal urethral sphincters,
along with parasympathetic mediated detru-
sor contraction.
▶ Intact neural pathways between the bladder
and the pontine micturition centre are essen-
tial for the coordinated activity between the
detrusor and urethral sphincters.
▶ The prefrontal cortex is responsible for com-
plex cognitive and socially appropriate behav-
iours, including voiding.
NEUROGENIC BLADDER DYSFUNCTION
Storage phase dysfunction most commonly
results from lesions of the spinal or suprapontine
pathways controlling micturition. This results in
involuntary spontaneous or induced contractions
of the detrusor muscle (detrusor overactivity)
which can be identified during the fi lling phase in
urodynamic studies (figure 2).
Voiding phase dysfunction usually results from
lesions of the spinal or infrasacral pathways.
In myelopathy, this is due to simultaneous con-
traction of the external urethral sphincter and
detrusor muscle—detrusor–sphincter dyssyner-
gia—which can result in both incomplete bladder
emptying and abnormally high pressures in the
bladder. Impaired detrusor contractions due to
reduced parasympathetic drive from the descend-
ing bulbospinal pathways may also contribute to
incomplete bladder emptying. In lesions affect-
ing the infrasacral pathway, such as of the cauda
equina (or occasionally a peripheral neuropathy),
voiding dysfunction results from poorly sustained
detrusor contractions and possibly non-relaxing
sphincters.
COMPLICATIONS ARISING FROM THE
NEUROGENIC BLADDER
▶ Detrusor overactivity and reduced bladder
wall compliance result in raised intravesical
pressure which can in turn lead to structural
changes in the bladder wall such as trabecula-
tions and diverticuli.
▶ The upper urinary tract (kidney and ureter)
can also show changes such as vesicoureteric
reflux and hydronephrosis, predisposing to
renal impairment and even end stage renal
disease.
▶ For reasons that are unclear, upper urinary
tract damage and renal failure are surprisingly
unusual in multiple sclerosis (MS).
2010;10:178–185. doi:10.1136/jnnp.2010.213892
 Neurology in Practice

Figure 1 Innervation of the lower urinary tract. (A) Sympathetic fibres (blue) originate in the T11–L2 segments of the spinal cord and run through
the inferior mesenteric ganglia (inferior mesenteric plexus, IMP) and the hypogastric nerve (HGN) or through the paravertebral chain to join the pelvic
nerves at the base of the bladder and the urethra. Parasympathetic preganglionic fibres (green) arise from the S2–S4 spinal segments and travel in
sacral roots and pelvic nerves (PEL) to ganglia in the pelvic plexus (PP) and in the bladder wall; this is where the postganglionic nerves that supply
parasympathetic innervation to the bladder arise. Somatic motor nerves (yellow) that supply the striated muscles of the external urethral sphincter
arise from S2–S4 motor neurons and pass through the pudendal nerves. L1, first lumbar root; S1, first sacral root; SHP, superior hypogastric plexus; SN,
sciatic nerve; T9, ninth thoracic root. (B) Efferent pathways and neurotransmitter mechanisms that regulate the lower urinary tract. Parasympathetic
postganglionic axons in the pelvic nerve release acetylcholine (ACh) which produces bladder contraction by stimulating M3 muscarinic receptors in the
bladder wall smooth muscle. Sympathetic postganglionic neurons release noradrenaline (NA) which activates β3 adrenergic receptors to relax bladder
wall smooth muscle and activate α1 adrenergic receptors to contract urethral smooth muscle. Somatic axons in the pudendal nerve also release ACh
which produces contraction of the external sphincter striated muscle by activating nicotinic cholinergic receptors. Reproduced with permission from
Fowler et al (Nat Rev Neurosci 2008;9:453–66).

▶ On the other hand, patients with spinal cord
injury are prone to upper tract damage and
renal disease, and have five times the age stan-
dardised risk for renal failure compared with
the general adult population.
▶ Similarly, the risk is higher in adults with spina
bifida, who have an eight times risk for devel-
oping renal failure, and this may be a leading
cause of death.
▶ Risk of renal failure is highest in patients who
have raised intravesical pressure due to detru-
sor overactivity, low bladder compliance and a
competent bladder neck.
▶ Patients are prone to various genitourinary
tract infections such as cystitis, pyelonephri-
tis and epididymo-orchitis and also to bladder
stones.
DIAGNOSTIC EVALUATION
History
As ever, history taking is the cornerstone of evalu-
ation and should assess both the storage and void-
ing phases of micturition.
▶ Patients with storage dysfunction complain of
frequency of micturition, nocturia, urgency
and urgency incontinence.
▶ Patients with voiding dysfunction complain
of hesitancy, straining for micturition, slow
and interrupted stream or may be in urinary
retention. Unfortunately, the history of void-
ing function is often unreliable as more than
50% of patients may be unaware of incomplete
bladder emptying. The history should there-
fore be supplemented by a bladder scans (see
below).
▶ The bladder diary records the time and vol-
ume of each voiding, urinary output and epi-
sodes of incontinence and urgency, and is an
extension of the history (figure 3).
Screening for urinary tract infections
Combined rapid tests of urine, using reagent strips
for urinalysis (‘dipstick’ test), is advisable for
patients presenting with new bladder symptoms
or at follow-up if there are unexplained changes in
bladder symptoms. The negative predictive value
for excluding urinary tract infection is 98% but

2010;10:178–185. doi:10.1136/jnnp.2010.213892 179

 Neurology in Practice

Figure 2 Filling cystometry demonstrating detrusor overactivity. Red trace (Pabd), intra-abdominal pressure recorded by the rectal catheter; dark
blue trace (Pves), intravesical pressure recorded by the bladder catheter; pink trace (Pdet), subtracted detrusor pressure (Pves−Pabd). Green traces
represent volume infused during the test (Vinf) and volume voided (Vura) while the orange trace represents urinary flow (Qura). Black arrows indicate
detrusor overactivity and black arrowhead indicates incontinence.

Figure 3 Bladder diary

over 24 h demonstrating
daytime and night-time
frequency, low volume
voids and incontinence,
in a patient with detrusor
overactivity.

the positive predictive value for confi rming infec- Urodynamics

tion is only 50%.
Measurement of postvoid residual urine
Because the extent of incomplete bladder empty-
ing cannot be predicted from the history or clini-
Urodynamic tests assess detrusor and bladder
outlet function.
▶ Uroflowmetry is a non-invasive assessment of
voiding (figure 4).
▶ Filling cystometry and pressure–flow studies

cal examination, it is often important to estimate
postvoid residual urine by ultrasonography, most
commonly using a portable bladder scanner, or by
‘in–out’ catheterisation.
Ultrasonography is helpful to exclude compli-
cations such as bladder stones and should be per-
formed periodically to assess the integrity of the
upper urinary tract in patients known to be at
risk of damage.
are more invasive tests that measure pressure–
volume relationships during bladder fi lling
and voiding (figure 2).
▶ Urodynamic evaluation also helps to identify
concomitant local disorders that may contribute
to lower urinary tract dysfunction such as bladder
outlet obstruction due to prostate enlargement
in men and stress incontinence in women, and
their relative contribution to bladder symptoms.

180 2010;10:178–185. doi:10.1136/jnnp.2010.213892


▶ Videourodynamics uses fluoroscopic x-ray
monitoring during urodynamics and allows
demonstration of vesicoureteral reflux and any
structural abnormalities of the bladder and
bladder neck.
The need for a complete urodynamic study in
every patient with neurogenic bladder symptoms
is the subject of debate. Patients with spinal cord
injury, spina bifida and possibly advanced MS
should undergo urodynamic studies because of
their higher risk of upper tract involvement and
renal impairment, although ultrasound of the
upper tract is a less invasive method for monitor-
ing structural changes. In early MS, urodynamics
should be carried out only in those whose urinary
symptoms are refractory to conservative treat-
ment or who are bothered by their symptoms and
wish to undergo further interventions.
The pattern of bladder symptoms, and results
of these various tests, depend on the level of the
neurological lesion (table 1).
CAUSES OF NEUROGENIC LOWER URINARY
TRACT DYSFUNCTION
Dementia
Incontinence is often a prominent symptom and
it tends to occur early in normal pressure hydro-
cephalus, dementia with Lewy bodies, vascu-
lar dementia and frontotemporal dementia but
later on in the course of Alzheimer’s disease
and Parkinson’s disease with dementia. Bladder
Figure 4 Uroflowmetry, a non-invasive test for voiding functions, demonstrating urinary
flow with a normal bell shaped curve and a maximum flow rate of 21 ml/s.
Table 1 Diagnostic evaluation of neurogenic bladder dysfunction
Suprapontine lesion (eg, stroke, Infrapontine suprasacral lesion
Parkinson’s disease) (eg, myelopathy)
Symptoms: Urgency, frequency, urgency Urgency, frequency, urgency incontinence, hesitancy,
History and bladder diary incontinence retention
Bladder scan: No postvoid residual urine ±Raised postvoid residual urine
Postvoid residual urine
Uroflowmetry Normal flow Interrupted flow
Urodynamics Detrusor overactivity Detrusor overactivity,detrusor–sphincter
dyssynergia
2010;10:178–185. doi:10.1136/jnnp.2010.213892
Neurology in Practice
dysfunction and increasing cognitive impairment
tend to be related.
▶ Patients may have detrusor overactivity as a
result of the underlying neurodegenerative
changes affecting the suprapontine centres
responsible for bladder control
▶ Cognitive and behavioural problems, urologi-
cal/urogynaecological causes, immobility and
cholinesterase inhibitors may contribute to
incontinence
▶ On the other hand, incontinence, urinary tract
infections and several of the antimuscarinic
medications used for treating detrusor overac-
tivity may worsen cognitive and behavioural
problems.
Stroke
More than 50% of stroke patients have urinary
incontinence during the acute phase. Risk factors
for incontinence include lesion size, concomi-
tant illnesses such as diabetes and increasing
age. Lesions in the anteromedial frontal lobe and
putamen are more commonly associated with
incontinence. The burden of white matter hyper-
intensities causing leukoariaosis is as powerful a
risk factor for urinary incontinence as damage in
specific regions. Incontinence is independently
associated with the severity of neurological dis-
ability and institutionalisation.
Parkinson’s disease and multiple system atrophy
The severity of lower urinary tract dysfunction
in Parkinson’s disease is correlated with the stage
of the disease, suggesting a relationship between
dopamine loss and bladder dysfunction. Urgency
and frequency are the commonest symptoms,
resulting from detrusor overactivity.
Bladder symptoms in multiple system atrophy
often precede other clinical manifestations; in
the early stages, incontinence usually arises from
detrusor overactivity but incomplete bladder emp-
tying and urinary retention become the predomi-
nant problems as the disease progresses. An open
bladder neck on videourodynamics is often seen
in men with multiple system atrophy.
MS and other demyelinating disorders
Problems with micturition are very common in
MS, generally correlating with the severity of the
disease and lower limb pyramidal dysfunction.
Infrasacral lesion (eg, conus
medullaris, cauda equina)
Hesitancy, retention
Postvoid residual urine >100 ml
Poor/absent flow
Detrusor underactivity, sphincter
insufficiency
181
 Neurology in Practice
Most commonly, patients report storage symp-
toms such as urgency and frequency. Voiding
symptoms depend on the degree of spinal cord
involvement. Bladder dysfunction is also common
in acute disseminated encephalomyelitis and may
persist after the other neurological impairments
have resolved.
Spinal cord injury
Patients may initially be in retention during the
acute stage of spinal shock but they then develop
the typical pattern of detrusor–sphincter dyssyn-
ergia and detrusor overactivity as spinal reflexes
return.
Spina bifida
More than 90% of children with spina bifida
have bladder dysfunction, through deficits in
the somatic as well as the autonomic innerva-
tion of the bladder. Symptoms generally start in
infancy or childhood but occasionally in adult-
hood. Urodynamic studies demonstrate a vari-
ety of fi ndings: detrusor overactivity, detrusor
underactivity or low bladder compliance with
ineffective contractions. The bladder outlet
may show detrusor–sphincter dyssynergia or it
may be incompetent with a static or fi xed distal
sphincter. Young patients with normal bladder
function can develop lower urinary tract dys-
function later on in life as a result of spinal cord
tethering and bladder symptoms should be reg-
ularly reviewed.
Cauda equina syndrome
Lower motor neuron disturbance affecting the
sacral nerve roots can result in voiding dysfunc-
tion and chronic urinary retention due to reduced
or absent detrusor contractions. Patients may
notice reduced sensation of bladder fi lling, inabil-
ity to initiate micturition voluntarily and eventu-
ally bladder distension to the point of overflow
incontinence. However, some patients may occa-
sionally have detrusor overactivity.
URINARY RETENTION
Iatrogenic causes from medications are often
missed—opiates, medications with anticholin-
ergic properties (eg, antipsychotic drugs, antide-
pressants and anticholinergic respiratory agents),
α-adrenoceptor agonists, benzodiazepines,
non-steroidal anti-inflammatory drugs and cal-
cium channel antagonists may all cause urinary
retention.
Neurologists are sometimes referred patients
in urinary retention after a urological evaluation
has excluded a ‘structural’ lesion obstructing the
lower urinary tract. Once history, examination
and relevant investigations such as spinal MRI,
clinical neurophysiology and perhaps lumbar
puncture have excluded a neurological cause, var-
ious functional disorders need to be considered
(box 1 and 2).
182
Box 1 Non-urological causes for urinary
retention
Neurological causes
▶ Detrusor external sphincter dyssynergia
(eg, due to myelopathy)
▶ Detrusor underactivity: loss of voluntary
voiding (lesion of conus medullaris or
spinal roots), multiple system atrophy, pure
autonomic failure, radical pelvic surgery
▶ Meningitis retention syndrome
Non-neurological causes
▶ Primary disorder of urethral sphincter
relaxation (Fowler’s syndrome)
▶ Dysfunctional voiding (behavioural)
▶ Medications: anticholinergics, opiates
▶ Primary detrusor muscle failure
Box 2 Fowler’s syndrome (primary disorder
of urethral sphincter relaxation)
Clinical features
▶ Young women, aged 15–30 years
▶ Chronic urinary retention, no urge, bladder
volume >1000 ml
▶ No evidence of urological or neurological
disease
▶ Straining does not improve bladder emptying
▶ Pain with clean intermittent self-catheterisation,
particularly when removing catheter
▶ Many have polycystic ovaries and are hirsute,
obese with acne, have menstrual irregularities
and infertility
▶ Several patients are taking opiates, most
often for back pain, musculoskeletal pain or
endometriosis, which may cause persistence
of retention and worsening bladder emptying
Investigations
▶ Raised maximum urethral pressure
▶ Increased urethral sphincter volume on
ultrasound
▶ Concentric needle EMG of the urethral sphincter
demonstrating characteristic findings of
complex repetitive discharges and decelerating
bursts
Treatment
▶ The only effective treatment to restore voiding
is sacral neuromodulation
MANAGEMENT
The goals are to achieve continence, improve
quality of life, prevent urinary tract infections
and preserve upper urinary tract function.
Voiding dysfunction
Before starting treatment, the postvoid residual
volume should be measured; in patients with
impaired voiding, more than 100 ml is likely to
2010;10:178–185. doi:10.1136/jnnp.2010.213892
 Neurology in Practice

contribute to bladder dysfunction. A single mea- ▶ Caffeine reduction may reduce urgency and
surement is not representative and, when pos- frequency in people who drink plenty of cof-
sible, several should be made over 1–2 weeks. fee and tea.
Complete bladder emptying is important for ▶ Bladder retraining, whereby patients void by
avoiding recurrent urinary tract infections, the clock and voluntarily ‘hold on’ for increas-
maintaining upper urinary tract function and ingly longer periods, aims to restore the nor-
optimising the management of storage symp- mal pattern of micturition.
toms. As there are no effective medications for ▶ Pelvic floor exercises and neuromuscular stim-
improving voiding, catheterisation is usually the ulation may have a role, if voiding dysfunc-
best option. tion has been excluded, for ameliorating mild
Clean intermittent self-catheterisation is preferred symptoms.
as it avoids the long term complications asso-
ciated with a permanent indwelling catheter. Antimuscarinic medications competitively inhibit
However, the patient’s cognitive state, moti- acetylcholine at muscarinic receptors and improve
vation, manual dexterity and visual acuity are urgency, frequency and incontinence; their effect
important factors to consider. Frequency of cath- is by relaxing the detrusor muscle. Since the intro-
eterisation depends on the postvoid residual vol- duction of oxybutynin, several newer agents have
ume, detrusor pressure and fluid intake. been marketed (table 2) but the only significant
Reflex voiding using trigger techniques, and difference between them is their adverse effect
Credé’s manoeuvre (non-forceful, smooth even profi le.
pressure from the umbilicus towards the pubis), Adverse effects resulting from the non-specific
are usually not recommended as they may result anticholinergic action include dry mouth, blurred
in high detrusor pressures and incomplete bladder vision for near objects, tachycardia and consti-
emptying during voiding. pation. These drugs can also block central mus-
Suprapubic vibration using a mechanical ‘buzzer’ carinic M1 receptors and cause impairment in
has been demonstrated to be effective in MS cognition and consciousness in susceptible indi-
patients with incomplete bladder emptying and viduals; this might be mitigated by medications
detrusor overactivity, but its effect is limited. with low selectivity for the M1 receptor such as
α-Blockers relax the internal urethral sphincter darifenacin or restricted permeability across the
in men and there is evidence that they improve blood–brain barrier such as trospium.
bladder emptying and reduce postvoid residual Postvoid residual urine may increase following
volumes. However, this is not consistently seen in treatment and should be monitored by repeat blad-
clinical practice unless there is concomitant blad- der scans, especially if initial beneficial effects are
der outlet obstruction. short lasting. In many patients, there may also be
Botulinum toxin injections into the external ure- underlying voiding dysfunction and often it is the
thral sphincter may improve bladder emptying judicious combination of antimuscarinic medica-
in patients with spinal cord injury and significant tion with clean intermittent self-catheterisation
voiding dysfunction. which provides the most effective management
for neurogenic bladder dysfunction (figure 5).
Storage dysfunction Desmopressin, a synthetic analogue of arginine
Non-pharmacological measures are generally effec- vasopressin, temporarily decreases urine produc-
tive in the early stages when symptoms are mild. tion and volume determined detrusor overactivity
by promoting water reabsorption at the distal and
▶ Fluid intake of around 1–2 l a day, although collecting tubules of the kidney. It is useful for the
this should be individualised and it is often treatment of frequency or nocturia in conditions
helpful to assess fluid balance by means of a such as MS and spina bifida, providing symptom
bladder diary. free periods of up to 6 h. It is also helpful in man-
aging nocturnal polyuria which may be seen in
Parkinson’s disease and dysautonomia. However,
it should be prescribed with caution in patients
Table 2 Antimuscarinic medications available in the UK (presented alphabetically) over the age of 65 years or with dependant leg
Generic name Trade name Daily dose (mg) Frequency oedema, and should not be used more than once in
24 h for fear of hyponatraemia and heart failure.
Darifenacin Emselex 7.5–15 od
Botulinum toxin type A injected into the detrusor
Fesoterodine Toviaz 4–8 od
muscle under cystoscopic guidance appears to be
Oxybutynin immediate release Ditropan, cystrin 2.5–20 bd–qds
Oxybutynin ER Lyrinel XL 5–20 od
a highly promising, although as yet unlicensed,
Oxybutynin transdermal Kentera 36 mg (3.9 mg/24 h) One patch twice weekly
treatment for intractable detrusor overactivity.
Propantheline Pro-banthine 15–120 tds (1 h before food) Although patients often have to perform clean
Propiverine Detrunorm 15–60 od–qds intermittent self-catheterisation afterwards,
Solifenacin Vesicare 5–10 od the effect lasts 9–13 months and it significantly
Tolterodine immediate release Detrusitol 2–4 bd improves storage symptoms and quality of life.
Tolterodine extended release Detrusitol XL 4 od Patients have fewer urinary tract infections and
Trospium Regurin 20–40 bd (before food) reduced urethral leakage when using an indwell-
bd, twice daily; od, once daily; qds, four times daily; tds, three times daily. ing catheter (catheter bypassing).

2010;10:178–185. doi:10.1136/jnnp.2010.213892 183

 Neurology in Practice

Sacral neuromodulation and posterior tibial nerve

stimulation can help manage neurogenic detru-
sor overactivity. The exact mechanism of action
remains unclear.
Surgical options such as augmentation cystoplasty
or urinary diversion are guided by discussions in
the setting of a multidisciplinary team, consider-
ing the degree of disability of the patient.

APPLIANCES AND EQUIPMENT

A range of continence aids such as penile sheaths
and disposable body worn pads may be helpful for
containing incontinence when other measures are
unsatisfactory. Men should be assessed and fitted
with external drainage systems if needed, and be
reviewed periodically. When appropriate, reuse-
able products such as pants and bed pads should
also be offered, as well as the full range of toilet-
ing equipment such as hand held urinals, aids and
portable commodes.

URINE INFECTION
▶ Urine should not be routinely tested unless
there are symptoms suggesting infection;
asymptomatic bacteriuria alone in a patient
performing clean intermittent self-catheteri-
sation is not an indication for antibiotics.
▶ Antibiotics should be limited to symptomatic
urinary tract infections.
▶ Unrestricted use of prophylactic antibiotics
can lead to drug resistance; however, in indi-
Figure 5 Algorithm for the management of neurogenic bladder dysfunction. viduals with proven recurrent urinary tract
Reproduced with permission from the BMJ Publishing Group (J Neurol Neurosurg infections in whom no urological structural
Psychiatry 2009;80:470–7). CISC, clean intermittent self-catheterisation; PVR, postvoid abnormality has been identified and whose
residual volume; UTI, urinary tract infection. intermittent catheterisation technique cannot

Figure 6 Stepwise approach to neurogenic bladder dysfunction management with progressing disability.

184 2010;10:178–185. doi:10.1136/jnnp.2010.213892


Further reading
▶ Abrams P, Cardozo L, Fall M, et al.; Standardisation Sub-committee of the
International Continence Society. The standardisation of terminology of lower
urinary tract function: report from the Standardisation Sub-committee of the
International Continence Society. Neurourol Urodyn 2002;21:167–78.
▶ Beck RO, Betts CD, Fowler CJ. Genitourinary dysfunction in multiple
system atrophy: clinical features and treatment in 62 cases. J Urol
1994;151:1336–41.
▶ Chapple CR, Khullar V, Gabriel Z, et al. The effects of antimuscarinic
treatments in overactive bladder: an update of a systematic review and
meta-analysis. Eur Urol 2008;54:543–62.
▶ DasGupta R, Fowler CJ. The management of female voiding dysfunction:
Fowler’s syndrome—a contemporary update. Curr Opin Urol
2003;13:293–9.
▶ DasGupta R, Kavia RB, Fowler CJ. Cerebral mechanisms and voiding
function. BJU Int 2007;99:731–4.
▶ de Sèze M, Ruffion A, Denys P, et al.; GENULF. The neurogenic bladder in
multiple sclerosis: review of the literature and proposal of management
guidelines. Mult Scler 2007;13:915–28.
▶ Fowler CJ, Griffiths D, de Groat WC. The neural control of micturition. Nat
Rev Neurosci 2008;9:453–66.
▶ Fowler CJ, Panicker JN, Drake M, et al. A UK consensus on the management
of the bladder in multiple sclerosis. J Neurol Neurosurg Psychiatry
2009;80:470–7.
▶ Kalsi V, Gonzales G, Popat R, et al. Botulinum injections for the treatment of
bladder symptoms of multiple sclerosis. Ann Neurol 2007;62:452–7.
▶ Verhamme KM, Sturkenboom MC, Stricker BH, et al. Drug-induced
urinary retention: incidence, management and prevention. Drug Saf
2008;31:373–88.
be improved, it is reasonable to start pro-
phylactic low dose antibiotics; this decision
should be taken in consultation with a urol-
ogy specialist team.
▶ The value of cranberry juice in preventing uri-
nary tract infections is debatable.
STEPWISE APPROACH TO A PATIENT WITH
NEUROGENIC BLADDER DYSFUNCTION
The treatment options should reflect the sever-
ity of the symptoms which generally parallel
the extent of the neurological disease (figure 6).
However, beyond a certain point, the symptoms
may become refractory to all treatments and it is
at this stage that a long term indwelling cathe-
ter should be offered. This should be a suprapu-
bic rather than a urethral catheter because of the
impact of the latter on urethral integrity, peri-
neal hygiene and sexuality. Intermittent bladder
2010;10:178–185. doi:10.1136/jnnp.2010.213892
Neurology in Practice
Box 3 Red flags that suggest referral to a
specialist urology/urogynaecology service
▶ Haematuria
▶ Renal impairment
▶ Recurrent urinary tract infections
▶ Bladder stones
▶ Pain thought to be arising from the urinary
tract
▶ Suspicion of concomitant local pathologies such
as bladder outlet obstruction due to prostate
enlargement in men, stress incontinence in
women
▶ Symptoms refractory to treatment
▶ Consideration for intradetrusor injections of
botulinum toxin A
▶ Long term suprapubic catheterisation planned
▶ Consideration for surgery such as augmentation
cystoplasty or urinary diversion
drainage with a catheter valve, as opposed to
continuous drainage into a leg bag, depends on
whether the bladder has a reasonable capacity to
store urine.
Although most patients can be managed along
these lines, there are specific situations where spe-
cialist urology or urogynaecology services should
be involved (box 3).
CONCLUSIONS
▶ Lower urinary tract dysfunction is common
in many neurological diseases and should be
medically manageable in most individuals.
▶ Evaluation requires assessment of storage dys-
function, voiding dysfunction, upper urinary
tract integrity and infection.
▶ Postvoid residual urine greater than 100 ml
suggests significant voiding dysfunction and
clean intermittent self-catheterisation is the
treatment of choice.
▶ Antimuscarinic medications are the main-
stay of treatment for the symptoms of storage
dysfunction.
Acknowledgements This article was reviewed by Jan van Gijn,
Utrecht, The Netherlands.
Provenance and peer review Commissioned; externally peer
reviewed.
Competing interests CJF is the recipient of unrestricted educa-
tional grants from Allergan and has also acted as a consultant for
Allergan and Medtronic.
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