Neurogenic Bladder

1. NEUROGENIC LOWER URINARY
TRACT DYSFUNCTION

2. • INTRODUCTION
• CLASSIFICATIONS
• CAUSES
• EVALUATION
• APPROACH
• SPECIFIC NEUROLOGICAL DISORDERS
• TREATMENT

3. INTRODUCTION
• Attracting considerable interest in
neurorehabilitation practice
• importance of this problem to patients’ health
and quality of life is now recognized
• Bladder symptoms are common and
distressing but also potentially amenable to
treatment.

4. THE BLADDER IN HEALTH AND
NEUROLOGICAL DISEASE
• two roles: storage of urine and voiding at
appropriate times
• a complex neural control system acts like a
switching circuit to maintain a reciprocal
relationship between the reservoir function of
the bladder and sphincteric function of the
urethra

5. • PMC controls this system and it in turn
receives input from higher centers,
particularly the medial aspects of the frontal
lobes.
• Disruption of the spino-bulbo-spinal
micturition pathway results in impaired
storage and voiding.

6. Efferent pathways of the lower
urinary tract

7. Storage Dysfunction
• results from lesions affecting the spinal or
suprapontine micturition pathways
• resultsin symptoms such as frequency,
urgency, and urgency incontinence

8. Voiding Dysfunction
• typically seen in patients with spinal cord
lesions
• symptoms such as hesitancy, straining, slow
and interrupted stream, or urinary retention

9. Detrusor Sphincter Dyssynergia
• characterized by simultaneous contraction of
the external urethral sphincter and detrusor
• loss of coordinated activity
• void within minutes of having supposedly
emptied their bladder (double voiding)

10. CLASSIFICATIONS
• Several classification systems have been
proposed to better distinguish types of
neurogenic LUTD
• Bradley loop classification - Described in 1982,
organizes the types of neurogenic bladder by
level of injury to different “loops” in the
neurologic control mechanism

11. • Current classifications have been based on
• Neurourologic - Bors-Comarr, Hald and
Bradley, Gibbons
• Functional - Wein
• Urodynamic – Lapides, Krane and Siroky,
Chancellor and Blaivas
• Combination of bladder and urethral function
based on urodynamics - International
Continence Society

12. Neuro-Urologic Classifications
• Bors and Comarr Classification (1971)
–SENSORY NEURON LESION
–MOTOR NEURON LESION
–LMN NEURON LESION
–MIXED LESION
• Gibbons classification (1976)
–Suprasacral
–Sacral: Motor / sensory / Mixed

13. Urodynamic Classifications
• Lapides classification (1970)
– Sensory neurogenic bladder
– Motor paralytic bladder
– Autonomous neurogenic bladder
– Uninhibited neurogenic bladder
– Reflex neurogenic bladder

14. KRANE AND SIROKI (1979)
• DETRUSOR HYPER REFLEXIA
- COORDINATED SPHINCTERS
- NONRELAXING STRIATED SPHINCTER
- DENERVATED STRIATED SPHINCTER
- NON RELAXING SMOOTH MUSCLE
SPHINCTER
DETRUSOR AREFLEXIA
- COORDINATED SPHINCTER
- NON RELAXING STRIATED SPHINCTER
- DENERVATED STRIATED SPHINCTER
- NON RELAXING SMOOTH MUSCLE SPHINCTER

15. INTERNATIONAL CONTINENCE
SOCIETY CLASSIFICATION
• DETRUSOR - NORMAL
-OVERACTIVE
- UNDERACTIVE
• SPHINCTER - NORMAL
- OVERACTIVE
- UNDERACTIVE
• SENSATION - NORMAL
- OVERACTIVE
- UNDERACTIVE

16. CAUSES OF NEUROGENIC LOWER
URINARY TRACT DYSFUNCTION

17. Incontinence In The
Neurologicalpatient
• Multifactorial
• Neurological lesion affecting bladder control -
detrusor overactivity
• Behavioural and cognitive impairment -
memory loss, apraxia, visuospatial
disorientation, language dysfunction, loss of
social inhibitions

18. • Urological causes - bladder outlet
obstruction, urinary tract infection, genuine
stress incontinence
• Functional incontinence - reduced mobility,
poor toilet access
• Medication-induced

19. Transient Causes of Urinary Incontinence “DIAPPERS”
• D - delirium
• I - infection (asymp. UTI does not cause UI)
• A - atrophic urethritis or vaginitis
• P - pharmaceuticals
• P - psychologic factors (depression, etc)
• E - endocrine disorders, excess urine output
• R - restricted mobility
• S - stool impaction
NEJM 1989;320:1

20. Suprapontine causes
• Stroke
• Traumatic brain injury
• Degeneration: Parkinson disease, Alzheimer
disease, dementia with Lewy bodies
• Hydrocephalus, normal pressure
hydrocephalus
• Cerebral palsy
• Neoplasm

21. Infrapontine–suprasacral causes
• Demyelination: multiple sclerosis, transverse
myelitis, NMOSD
• Trauma - SCI
• Vascular: arteriovenous malformations, spinal
cord infarction
• Neoplasm: metastasis, primary
• Hereditary: hereditary spastic paraparesis
• Infections: tropical spastic paraparesis (HTLV-
I)

22. Infrasacral causes
• Spina bifida
• Intervertebral disk prolapse
• Arachnoiditis
• Diabetes mellitus
• Pelvic surgery and nerve injury

23. EVALUATION

24. History-taking
• History-taking forms the cornerstone of evaluation
• should assess both the storage and voiding phases of
micturition
• important also to enquire about bowel,
gynaecological and sexual functions as they often
coexist
• Medication history should be reviewed – opiates,
anticholinergic properties (eg, antipsychotic drugs,
antidepressant ) and α-adrenoceptor agonists

25. • storage dysfunction - frequency for
micturition, nocturia, urgency and urgency
incontinence.
• Urgency, frequency and nocturia, with or
without incontinence - called the overactive
bladder syndrome, urge syndrome or urgency-
frequency syndrome

26. • voiding dysfunction - hesitancy for micturition,
a slow and interrupted urinary stream, the
need to strain to pass urine, and double
voiding, complete urinary retention
• functional incontinence - inability to reach
the toilet in a timely manner due to their
neurological deficits or to poor toilet
accessibility

27. Bladder Diary
• supplements the history taking
• records the frequency for micturition,
volumes voided, episodes of incontinence,
and fluid intake over the course of a few days
• provides a realtime objective patient-reported
measure of LUT symptoms, which might not
be obtained through history taking or
questionnaires

29. Physical Examination
• critical in deciding whether a patient’s
urogenital complaints are neurological in
origin
• bladder disturbances generally have been
shown to correlate with lower limb deficits
• Exceptions - lesions of the conus medullaris
and cauda equina, where findings may be
confined to saddle anesthesia and absence of
sacral cord mediated reflexes such as the anal
reflex or bulbocavernosus reflex

30. Physical Examination
• CNS – e/o paraparesis, impaired DTR in lower limbs,
peripheral neuropathy, assess urogenital sensations,
sacral cord mediated reflexes (bulbocavernosus
reflex, anal reflex),
• inspection of the lumbosacral spine
• L/E – bladder distention, suprapubic tenderness in
overflow incontinence
• P/R – prostate, impacted stool, anal sphincter tone
and squeeze response
• Functional assessment of mobility to go to toilet and
dexterity to remove clothes

32. Laboratory evaluation
• Urine routine , Urine culture and sensitivity –
screening for UTI’s
• RFT’s, Uric acid
• Serum electrolytes
• Input-Output chart

33. Bladder Scan - PVR
• extent of incomplete bladder emptying cannot
be predicted from history or clinical
examination
• pertinent to estimate the PVR
• Ultrasonography - portable bladder scanner
• Catheterization - “in-out” catheterization,
especially in patients who perform
intermittent self-catheterization

35. • Done within 5 min of intentional voiding
• >100ml is significant
• single measurement often not representative and if
possible, a series of measurements should be made
over the course of 1 or 2 weeks
• raised PVR volume – voiding dysfunction, however, it
cannot be used to discern whether this is caused by
poor detrusor contractility or by obstruction, for
which urodynamics would be required

36. Ultrasound Scan
• patients known to be at risk of upper tract
disease
• performed periodically (at least every 6
months) to evaluate for evidence of damage
such as upper urinary tract dilatation or renal
scarring.
• also detect complications of neurogenic
bladder dysfunction such as bladder stones.

37. • Bladder/detrusor wall thickness and
ultrasound estimated bladder weight are
being investigated as noninvasive alternatives
to assess neurogenic LUT dysfunction
• but are not yet established diagnostic options

38. Urodynamic Studies
• examine the function of the lower urinary
tract
• divided into noninvasive investigations and
those requiring urethral catheterization

39. Noninvasive Bladder Investigations
Uroflowmetry
• is a valuable, noninvasive investigation to
detect voiding dysfunction
• combined with an ultrasound measurement of
the PVR
• should be done before any treatment and can
be used to monitor treatment outcomes
• important that the patient performs the test
with a comfortably full bladder, containing if
possible a volume of at least 150 mL

40. • privacy is essential and a spurious result may
be obtained if the subject is not fully relaxed
• significant neurogenic bladder disorder is
unlikely if a patient has good bladder capacity
and normal urine flow rate, and empties to
completion

43. Disadvantage
• flow rate and PVR volume depend on both
detrusor function and bladder outlet
resistance
• uroflowmetry is unable to discriminate
between the underlying mechanisms

44. INVESTIGATIONS REQUIRING
CATHETERIZATION

45. Cystometry
• evaluates the pressure–volume relationship
during nonphysiological filling of the bladder
and during voiding
• detrusor overactivity - main abnormality
sought during filling cystometry
• characterized by involuntary detrusor
contractions, which may be spontaneous or
provoked

46. Urodynamics Lab

48. Filling cystometry demonstrating
detrusor overactivity

49. Videocystometry
• cystometry is carried out using a contrast
filling medium and the procedure visualized
radiographically
• gives additional information about
morphological changes that are consequent to
neurogenic bladder dysfunction in the
presence of vesicoureteric reflux
• opportunity to inspect the outflow tract
during voiding is of great value in patients
with suspected obstruction

50. • valuable in demonstrating the underlying
pathophysiology of a patient’s urinary tract
• provides information about the safety and
efficiency of bladder filling and emptying
• valuable for assessing risk factors for upper
urinary tract damage and planning
management
• helpful in identifying concomitant urological
conditions such as bladder outflow
obstruction or stress incontinence

51. Indications
• spinal cord injury, spina bifida, and advanced
MS should undergo complete urodynamic
study
• significant risk of upper tract involvement and
renal impairment
• Valuable for demonstrating the underlying
pathophysiology of LUTD, detecting risk
factors for upper urinary tract damage(high
detrusor pressures) and planning
management

52. • Other conditions such as early MS, stroke, and
PD - some authors have recommended to
restrict the initial evaluation to noninvasive
tests
• risk for upper urinary tract damage is less

53. Urethral pressure profile
• measured using a catheter mounted
transducer that is run slowly through the
urethra by a motorized armature
• can be performed in men or women
• found to be helpful in the assessment of
women with obstructed voiding or urinary
retention, some of whom have abnormally
high urethral pressures

54. Overactive bladder
Pdet
cmH2O
0
50
100
150
Pves
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150
Pabd
cmH2O
0
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100
150
Qura
ml/s
0
5
10
15
Uro - Voiding Cystometry#1
20 s 00:00 00:40 01:20 02:00 02:40 03:20 04:00
75
leak2
82
ST c CC
CB1
VB
MP
MF
VE

55. Sphincter Dyssynergia
Pdet
cmH2O
0
30
60
90
120
150
180
210
Pves
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Pabd
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ml/s
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EMG
uV
0
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Uro - Voiding Cystometry#2
10 s 09:04 09:24 09:44 10:04 10:24
MP MF VE

56. URONEUROPHYSIOLOGY

57. Pelvic floor Electromyography
• first introduced for assessing the extent of
relaxation of the urethral sphincter during
voiding, with the aim of recognizing detrusor–
sphincter dyssynergia
• now rarely recorded
• technically difficult to obtain a good quality
EMG signal from urethral sphincter

58. • evaluation of men with suspected
dysfunctional voiding
• Recording electrical silence from the urethral
sphincter during voiding would exonerate the
external sphincter as the cause of voiding
dysfunction

59. Sphincter EMG
• demonstrate changes of reinnervation in the
urethral or anal sphincter in neurogenic
disorders
• Diagnosis of MSA - anterior horn cells in the
Onuf nucleus are selectively lost, results in
changes in the sphincter muscles that can be
identified by EMG

61. • Evaluation of Suspected Cauda Equina Lesions
- investigating innervation of the sacral
second, third, and fourth nerve roots
• Investigation of Urinary Retention in Young
Women - Fowler syndrome ,characteristic
abnormality on urethral sphincter EMG,
consisting of complex repetitive discharges,
akin to the “sound of helicopters” and
decelerating bursts, akin to the “sound of
underwater recording of whales.”

62. Pudendal Somatosensory Evoked
Potentials.
• recorded from the scalp following electrical
stimulation of the dorsal nerve of penis or
clitoral nerve
• abnormal when a spinal cord lesion is the
cause of sacral sensory loss or neurogenic
detrusor overactivity

63. Pudendal Nerve Terminal Motor
Latency (PNTML).
• only test of motor conduction for the pelvic floor
• stimulated either per rectally or vaginally using the St
Mark electrode, records from the external anal
sphincter
• Prolongation was initially considered evidence for
pudendal nerve damage
• This test has not proved contributory in the
investigation of patients with suspected pudendal
neuralgia.

64. Penilo-Cavernosus Reflex.
• formally known as the “bulbo cavernosus” reflex
• assesses the sacral root afferent and efferent
pathways
• dorsal nerve of penis (or clitoris) is electrically
stimulated and recordings are made from the bulbo
cavernosus muscle
• of value in patients with bladder dysfunction
suspected to be secondary to cauda equina damage
or damage to the lower motor neuron pathway

65. APPROACH TO NEUROGENIC
LOWER URINARY TRACT
DYSFUNCTION

66. • Lesions of the nervous system result in
characteristic patterns of bladder dysfunction,
depending upon the level of the lesions in the
neurological axis
• storage function - affected following
suprapontine or infrapontine/suprasacral
lesions
• voiding function - affected by infrapontine
lesions

67. Suprapontine lesions
• detrusor overactivity and storage dysfunction
• Patients present with urgency, frequency,
nocturia and urgency incontinence
(collectively known as overactive bladder
symptoms)

68. Infrasacral lesions
• reduced detrusor contractility and voiding
dysfunction, nonrelaxing urethral sphincters
• patients present with hesitancy, slow and
interrupted stream, feeling of incomplete
emptying, and are often in retention

69. Infrapontine–suprasacral lesions
• resulting in both storage and voiding
dysfunction
• detrusor overactivity and detrusor sphincter
dyssynergia (simultaneous contraction of the
external urethral sphincter and detrusor
muscle)
• results in incomplete bladder emptying and
abnormally high bladder pressures

70. Patterns of LUTD following
neurological disease

71. Diagnostic Findings in Patients with
Suspected Neurogenic Bladder
Dysfunction

72. Detrusor Overactivity
• Different mechanisms
• Suprapontine - Damage to the suprapontine
neural circuitry results in removal of the tonic
inhibition of the PMC, spontaneous
involuntary detrusor contractions occur
• spinal cord lesions - due to the emergence of
a segmental reflex at the level of the sacral
cord, mediated by capsaicin-sensitive C-fibre
afferents, which drive involuntary detrusor
contractions

73. Risk of upper urinary tract
complications
• Detrusor overactivity in combination with DSD
- result in high intravesical pressures
• morphological changes in the bladder wall -
trabeculations and (pseudo-)diverticula
• Increased risk of upper urinary tract
complications such as vesico-uretero-renal
reflux, hydronephrosis, renal impairment, and
eventually ESRD

74. • SCI or spina bifida have a substantially higher
risk of developing renal failure compared with
the general adult population
• low in patients with slowly progressive non-
traumatic neurological disorders, such as MS
and IPD
• Duration of MS and severity of disability are
risk factors for upper urinary tract
complications

75. LUTD IN SPECIFIC NEUROLOGICAL
DISORDERS

76. Dementia
• Incontinence is often a prominent symptom
• occur at variable times during the natural
history of dementia
• early in NPH, DLB, vascular dementia, and FTD
• late in the course of Alzheimer’s disease or
Parkinson’s disease with dementia
• also from cognitive and behavioural problems,
urological causes, and immobility

77. • treatment of incontinence can exacerbate the
dementia
• Antimuscarinic medications (detrusor
overactivity), can block central muscarinic M1
receptors, resulting in altered cognition
• mitigated by using medications with low
selectivity for the M1 receptor, such as
darifenacin or restricted permeability across
the bloodbrain barrier, such as trospium
chloride.

78. Stroke
• More than 50% of stroke patients may have
urinary incontinencen during the acute phase
• Approximately 70% of survivors of
hemispheric strokes suffer transient urinary
incontinence.
• Risk factors for incontinence include lesion
diameter, presence of comorbid illnesses such
as diabetes, and age

79. • Incontinence is significantly associated with severe
neurological disability, institutionalization and
increased mortality
• Lesions in the anteromedial frontal lobe,
paraventricular white matter, and putamen are more
commonly associated with bladder symptoms
• small-vessel disease of the white matter - associated
with urgency incontinence, important cause of
incontinence in functionally independent people
older than 60 years

80. PD
• LUTS are common in Parkinson disease - Thirty-eight
to 71%
• correlation between bladder dysfunction,
neurological disability and Hoehn and Yahr stage
• suggesting a relationship between dopaminergic
degeneration and bladder dysfunction
• bladder dysfunction does not occur until some years
after the onset of motor symptoms

81. • Storage symptoms are the most common
• Nocturia (56.7%) is the most common
symptom, followed by urinary urgency and
these together are the commonest nonmotor
symptoms in PD

82. • nocturnal polyuria (NP) - significant cause of
nocturia
• related to loss of circadian rhythm in PD
• NP does not improve with anti-muscarinics
directed to help OAB symptoms
• Other causes - prostatic enlargement, pelvic
floor weakness, stress incontinence, and
bradykinesia of pelvic floor muscles causing
“pseudo-dyssynergia”

83. Multiple System Atrophy
• bladder symptoms dominate the clinical
picture at onset
• 41% of present with LUTS and 97% have LUTS
during the disease course
• incontinence usually arises from detrusor
overactivity and external sphincter weakness
• more likely to have a high (>100 mL) PVR,
DSD, an open bladder neck at the start of
bladder filling on videocystometrogram, and a
neurogenic EMG of the anal sphincter

84. Spinal Cord Lesions
• most common cause of neurogenic bladder
dysfunction
• acute SCI there is initially a phase of spinal
shock - detrusor is hypocontractile /
acontractile and associated with complete
urinary retention
• duration of this phase varies - about 6 weeks

85. • Gradually over the course of weeks, new
reflexes emerge to reinitiate bladder
emptying and cause detrusor contractions in
response to low filling volumes
• C fibers emerge as the major afferents,
forming a spinal segmental reflex
• abnormally overactive, small-capacity bladder

86. Multiple sclerosis
• LUTS are common in MS - 75%
• strong association - recognized between bladder
symptoms and the presence of clinical spinal cord
involvement
• Most commonly, patients report storage symptoms
such as urgency and frequency, and voiding
symptoms depending upon spinal cord involvement
• 90 % percent of patients have bladder symptoms if
the duration is greater than 10 years and symptoms
occur on average 6 years into the illness

87. Spinal cord injury
• initially in urinary retention during the spinal shock
• develop symptoms as spinal reflexes return
• DSD and DO are the hallmarks of spinal cord injury
• Sustained high intravesical pressures can ensue,
increasing the risk of upper urinary tract damage
• Autonomic dysrefl exia can occur after lesions at or
above the T6 spinal cord level, triggered by urinary
tract infections (UTIs)

88. Videocystometrogram spinal cord
injury

89. Spina bifida
• more than 90% of children with spina bifida
have bladder dysfunction
• Symptoms generally start in infancy or
childhood
• Videourodynamic studies have demonstrated
a variety of findings: there may be detrusor
overactivity, detrusor underactivity, or low
compliance with ineffective contractions

90. • Bladder outlet may show detrusor sphincter
dyssynergia, or may be incompetent with a
static or fixed distal sphincter
• The incidence of upper urinary tract damage
tends to increase with age
• Adults with spina bifida have eight times the
age-standardized risk of renal failure
compared to the adult population

91. Cauda Equina Lesions
• Damageto the cauda equina leaves the
detrusor decentralized, rather than
denervated
• postganglionic parasympathetic innervation is
unaffected
• bladder dysfunction after a cauda equina
lesion is unpredictable, even detrusor
overactivity has been described

92. Peripheral neuropathy
• LMN disturbance in patients with
polyradiculopathy or peripheral neuropathy
results in reduced or absent detrusor
contractions
• Patients have reduced sensation of bladder
fullness, inability to initiate micturition
voluntarily and bladder distension to the point
of overflow incontinence

93. Diabetic Neuropathy
• onset of the bladder dysfunction is insidious, with
progressive loss of bladder sensation and
impairment of bladder emptying over years,
eventually culminating in chronic low pressure
urinary retention
• Urodynamics - impaired detrusor contractility,
reduced urine flow, increased postmicturition
residual volume, and reduced bladder sensation
• vesical afferent and efferent fibers are involved,
causing reduced awareness of bladder filling and
decreased bladder contractility

94. Fowler’s syndrome
• young woman in complete urinary retention, no
underlying urological or neurological disease, a
diagnosis of Fowler’s syndrome should be considered
• primary disorder of urethral sphincter relaxation
• results in an inhibition of detrusor contractions
• Urethral sphincter electromyography (EMG) shows a
characteristic pattern of activity and the urethral
pressures are usually raised
• respond particularly favorably to sacral
neuromodulation

95. TREATMENT

96. Principles Of Management
• goals of management are to achieve urinary
continence, improve quality of life, prevent UTIs, and
preserve upper urinary tract function
• should address both voiding and storage dysfunction
• determined by the severity of symptoms and risk of
developing upper urinary tract damage
• multidisciplinary approach between neurology,
urology, and primary care is essential

97. General Measures
• Nonpharmacological measures - effective in
the early stages when symptoms are mild
• fluid intake of around 1 to 2 liters a day
• Caffeine reduction
• Bladder retraining - patients void by the clock
and voluntarily “hold on” for increasingly
longer periods, aims to restore the normal
pattern of micturition
• Pelvic floor exercises and neuromuscular
stimulation

98. MANAGEMENT OF STORAGE
DYSFUNCTION

99. Physical treatments
• Behavioural therapy - incontinence is associated with
cognitive deficits, and motor deficits
• correcting faulty habits such as frequent voiding
• Timed voiding - separating toilet visits by fixed
intervals of time
• Habit retraining - identifying the natural voiding
pattern of a patient and the development of an
individualised toileting schedule
• Verbal prompts and positive reinforcement
• Pelvic floor exercises

100. Anti-Muscarinic Medications
• mainstay of treatment for detrusor
overactivity
• Detrusor relaxation, lower intravesical
pressures, and reduced storage symptoms
• M3 - widely distributed throughout the
detrusor, urothelium, and suburothelium
• M2 receptor is functionally the most relevant
subtype in the bladder

101. Adverse events
• nonspecific anticholinergic - dry mouth,
blurred vision for near objects, tachycardia,
and constipation
• block central M1 receptors and cause
impairment of cognition and consciousness
• mitigated by medications which have low
selectivity for the M1 receptor, such as
Darifenacin, or restricted permeability across
the blood brain barrier, such as Trospium

102. Commonly used antimuscarinic
drugs

103. • Measurement of the PVR should be done
before antimuscarinic treatment is started
• judicious combination of anti muscarinic
treatment plus intermittent self-
cathetersation provides the most effective
management for neurogenic LUT dysfunction

104. • Desmopressin - reduces urine production and
volume-determined detrusor overactivity
• Nocturia, nocturnal polyuria
• β3-Adrenoceptor agonists – mirabegron
• does not cause anticholinergic s/e and
cognitive impairment

105. Intradetrusor Botulinum toxin
• revolutionised the management of neurogenic
overactive bladder
• type A that is generally used for urological
indications
• several different preparations, only
onabotulinumtoxinA is licensed for treatment of
detrusor overactivity incontinence
• highly effective, safe, and well tolerated
• 20 to 30 injections are made into the bladder wall,
requiring a cystoscopy, effect lasts 8 to 11 months

106. Neuromodulation
• Electrical stimulation of peripheral nerves
such as the sacral nerve roots, tibial nerve,
pudendal nerve, and dorsal genital nerves
• overall quality of the evidence is low
• mechanism of action is uncertain, modulation
of sacral afferent nerves and spinal cord-
mediated reflexes through inhibitory
interneurons is key

107. Percutaneous tibial nerve
stimulation (PTNS)
• safe and effective minimally invasive treatment -
mild or moderate overactive bladder symptoms
• typical treatment course consists of stimulating the
nerve through a fine gauge stainless steel needle
using a fixed frequency electrical signal, once weekly
for 30 minutes, over an 8–12-week period
• effect is fairly short lived
• Transcutaneous tibial nerve stimulation (TTNS) is an
alternative that can be done at home

108. Sacral Neuromodulation
• extra dural sacral nerve stimulator
• mainstay of treatment in Fowler syndrome
• highly effective in detrusor overactivity refractory to
anti-muscarinic medications
• does not increase the PVR volume and its effect is
not temporally limited
• early bilateral SNM during the phase of spinal shock
seems to prevent the subsequent development of
neurogenic detrusor overactivity and urinary
incontinence in patients with complete SCI
• progressive neurological disease are not candidates

109. Surgery

110. • best solution for long-term bladder
management
• however, does not apply to patients with
progressive neurological disease causing
incontinence

111. Nerve Root Stimulators
• patients who have suffered a complete spinal
cord transection, but in whom the caudal
section of the cord and its roots are intact
• stimulating electrodes are placed around the
lower sacral roots (S2 to S4)
• activated by an external switching device.
• applied intrathecally to the anterior roots, the
posterior roots are cut at the same time

112. Permanent Indwelling Catheters
• patient is no longer able to perform self-
catheterization
• incontinence is refractory to management
• indwelling Foley catheter
• major problems is catheter bypassing, occurs
when strong detrusor contractions produce a
rapid urine flow that cannot drain sufficiently
quickly

113. • common response - to use a wider caliber
catheter
• with the effect that the bladder closure
mechanism becomes progressively stretched
and destroyed
• detrusor contraction may be of sufficient
intensity to extrude the 10- or 20-mL balloon
of the catheter from the bladder, causing
further damage to the bladder neck and
resulting in a totally incompetent outlet

114. • Bladder stones and recurrent infections are
also more likely
• preferred alternative - suprapubic catheter
• better long-term alternative to a urethral
catheter
• preserves urethral integrity, and helps to
promote perineal hygiene and sexual
functions

115. MANAGEMENT OF VOIDING
DYSFUNCTION

116. Intermittent catheterisation
• best time to begin intermittent
catheterisation
• PVR volume - related to the overall bladder
capacity, consistently more than 100 mL has
been advocated if the patient is
symptomatic/or more than one-third of
bladder capacity
• risk of upper urinary tract damage
• Catheterisation four to six times per 24 h is
recommended to manage complete urinary

117. Other interventions
• Triggered reflex voiding - provoking a bladder
contraction through stimulation of sacral and lumbar
dermatomes (eg, suprapubic tapping and thigh
scratching)
• most successful in patients with a suprasacral spinal
cord lesion
• Bladder expression using Valsalva or Crede
manoeuvres (manual compression of the lower
abdomen) is not usually recommended because
these could be associated with a rise in intravesical
pressures

118. Algorithm for the management of
neurogenic LUTD

119. Management of lower neurologic
LUTDS

120. Stepwise Approach to Neurogenic
Bladder Dysfunction
• treatment options offered to a patient should
reflect the severity of bladder dysfunction,
which generally parallels the extent of
neurological disease
• beyond a certain point, incontinence may
become refractory to all treatment options
• at this stage a long-term indwelling catheter
should be offered.

121. Stepwise approach

122. Early Referral To A Urology
Service
• Symptoms refractory to treatment
• Recurrent urinary tract infections
• Suspicion of concomitant pathologies such as
bladder outlet obstruction due to prostate
enlargement, stress incontinence
• Renal impairment
• Demonstrated hydronephrosis

123. • Presence of haematuria
• Pain suspected to be originating from the
urinary tract
• Consideration of suprapubic catheterization
• Consideration of urological procedures such
as intradetrusor injections of botulinum toxin
A or surgeries such as augmentation
cystoplasty or urinary diversion

124. REFERENCES
• Panicker JN, Fowler CJ, Kessler TM. Lower
urinary tract dysfunction in the neurological
patient: clinical assessment and management.
Lancet Neurol. 2015 Jul;14(7)
• Panicker JN, De Sèze M, Fowler CJ. Neurogenic
lower urinary tract dysfunction. Handb Clin
Neurol. 2013
• Bradley’s Neurology in Clinical Practice 7th