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Neurology in Practice

THE BARE ESSENTIALS

Uro-Neurology
Jalesh N Panicker,1 Clare J Fowler2

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

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

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

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

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Neurology in Practice

▶ Videourodynamics uses fluoroscopic x-ray dysfunction and increasing cognitive impairment


monitoring during urodynamics and allows tend to be related.
demonstration of vesicoureteral reflux and any
structural abnormalities of the bladder and ▶ Patients may have detrusor overactivity as a
bladder neck. result of the underlying neurodegenerative
changes affecting the suprapontine centres
responsible for bladder control
The need for a complete urodynamic study in
▶ Cognitive and behavioural problems, urologi-
every patient with neurogenic bladder symptoms
cal/urogynaecological causes, immobility and
is the subject of debate. Patients with spinal cord
cholinesterase inhibitors may contribute to
injury, spina bifida and possibly advanced MS
incontinence
should undergo urodynamic studies because of
▶ On the other hand, incontinence, urinary tract
their higher risk of upper tract involvement and
infections and several of the antimuscarinic
renal impairment, although ultrasound of the
medications used for treating detrusor overac-
upper tract is a less invasive method for monitor-
tivity may worsen cognitive and behavioural
ing structural changes. In early MS, urodynamics
problems.
should be carried out only in those whose urinary
symptoms are refractory to conservative treat-
ment or who are bothered by their symptoms and Stroke
wish to undergo further interventions. More than 50% of stroke patients have urinary
The pattern of bladder symptoms, and results incontinence during the acute phase. Risk factors
of these various tests, depend on the level of the for incontinence include lesion size, concomi-
neurological lesion (table 1). tant illnesses such as diabetes and increasing
age. Lesions in the anteromedial frontal lobe and
putamen are more commonly associated with
CAUSES OF NEUROGENIC LOWER URINARY incontinence. The burden of white matter hyper-
TRACT DYSFUNCTION intensities causing leukoariaosis is as powerful a
Dementia risk factor for urinary incontinence as damage in
Incontinence is often a prominent symptom and specific regions. Incontinence is independently
it tends to occur early in normal pressure hydro- associated with the severity of neurological dis-
cephalus, dementia with Lewy bodies, vascu- ability and institutionalisation.
lar dementia and frontotemporal dementia but
later on in the course of Alzheimer’s disease
Parkinson’s disease and multiple system atrophy
and Parkinson’s disease with dementia. Bladder
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
Figure 4 Uroflowmetry, a non-invasive test for voiding functions, demonstrating urinary
disease and lower limb pyramidal dysfunction.
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 Infrasacral lesion (eg, conus
Parkinson’s disease) (eg, myelopathy) medullaris, cauda equina)
Symptoms: Urgency, frequency, urgency Urgency, frequency, urgency incontinence, hesitancy, Hesitancy, retention
History and bladder diary incontinence retention
Bladder scan: No postvoid residual urine ±Raised postvoid residual urine Postvoid residual urine >100 ml
Postvoid residual urine
Uroflowmetry Normal flow Interrupted flow Poor/absent flow
Urodynamics Detrusor overactivity Detrusor overactivity,detrusor–sphincter Detrusor underactivity, sphincter
dyssynergia insufficiency

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Neurology in Practice

Most commonly, patients report storage symp-


toms such as urgency and frequency. Voiding Box 1 Non-urological causes for urinary
symptoms depend on the degree of spinal cord retention
involvement. Bladder dysfunction is also common
in acute disseminated encephalomyelitis and may
persist after the other neurological impairments Neurological causes
▶ Detrusor external sphincter dyssynergia
have resolved.
(eg, due to myelopathy)
▶ Detrusor underactivity: loss of voluntary
Spinal cord injury voiding (lesion of conus medullaris or
Patients may initially be in retention during the spinal roots), multiple system atrophy, pure
acute stage of spinal shock but they then develop autonomic failure, radical pelvic surgery
the typical pattern of detrusor–sphincter dyssyn- ▶ Meningitis retention syndrome
ergia and detrusor overactivity as spinal reflexes Non-neurological causes
return. ▶ Primary disorder of urethral sphincter
relaxation (Fowler’s syndrome)
▶ Dysfunctional voiding (behavioural)
Spina bifida
▶ Medications: anticholinergics, opiates
More than 90% of children with spina bifida
▶ Primary detrusor muscle failure
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- Box 2 Fowler’s syndrome (primary disorder
ety of fi ndings: detrusor overactivity, detrusor of urethral sphincter relaxation)
underactivity or low bladder compliance with
ineffective contractions. The bladder outlet
may show detrusor–sphincter dyssynergia or it
Clinical features
▶ Young women, aged 15–30 years
may be incompetent with a static or fi xed distal
▶ Chronic urinary retention, no urge, bladder
sphincter. Young patients with normal bladder
function can develop lower urinary tract dys-
volume >1000 ml
▶ No evidence of urological or neurological
function later on in life as a result of spinal cord
tethering and bladder symptoms should be reg-
disease
▶ Straining does not improve bladder emptying
ularly reviewed.
▶ Pain with clean intermittent self-catheterisation,
particularly when removing catheter
Cauda equina syndrome ▶ Many have polycystic ovaries and are hirsute,
Lower motor neuron disturbance affecting the obese with acne, have menstrual irregularities
sacral nerve roots can result in voiding dysfunc- and infertility
tion and chronic urinary retention due to reduced ▶ Several patients are taking opiates, most
or absent detrusor contractions. Patients may often for back pain, musculoskeletal pain or
notice reduced sensation of bladder fi lling, inabil- endometriosis, which may cause persistence
ity to initiate micturition voluntarily and eventu- of retention and worsening bladder emptying
ally bladder distension to the point of overflow Investigations
incontinence. However, some patients may occa- ▶ Raised maximum urethral pressure
sionally have detrusor overactivity. ▶ Increased urethral sphincter volume on
ultrasound
▶ Concentric needle EMG of the urethral sphincter
URINARY RETENTION
demonstrating characteristic findings of
Iatrogenic causes from medications are often
complex repetitive discharges and decelerating
missed—opiates, medications with anticholin-
bursts
ergic properties (eg, antipsychotic drugs, antide-
Treatment
pressants and anticholinergic respiratory agents),
▶ The only effective treatment to restore voiding
α-adrenoceptor agonists, benzodiazepines,
is sacral neuromodulation
non-steroidal anti-inflammatory drugs and cal-
cium channel antagonists may all cause urinary
retention. MANAGEMENT
Neurologists are sometimes referred patients The goals are to achieve continence, improve
in urinary retention after a urological evaluation quality of life, prevent urinary tract infections
has excluded a ‘structural’ lesion obstructing the and preserve upper urinary tract function.
lower urinary tract. Once history, examination
and relevant investigations such as spinal MRI,
clinical neurophysiology and perhaps lumbar Voiding dysfunction
puncture have excluded a neurological cause, var- Before starting treatment, the postvoid residual
ious functional disorders need to be considered volume should be measured; in patients with
(box 1 and 2). impaired voiding, more than 100 ml is likely to

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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).

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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.

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Neurology in Practice

Further reading Box 3 Red flags that suggest referral to a


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

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