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Dr Pankaj Rathi
Outline of the
• Anatomy and physiology
• History taking
• Pathophysiology of
----Failure to Empty
----Failure to Store
• Reflex Neurogenic Bladder
• Autonomous Neurogenic
• 15% of all population have some bladder
dysfunction if thoroughly investigated
• People above 60 years have …50%
• Bladder dysfunction ..makes a
patients ..smelling even untouchable
• Most of the dysfunction are
• Even good history and clinical
examination can lead to Diagnosis
• Very few patients require sophisticated
• Hence..I PLEAD your valuable ATTENTION
Storage - at low pressure
until such time as it is
convenient and socially
acceptable to void ( 98% )
Voiding - initiated by
inhibition of the striated
sphincter and pelvic floor,
followed some seconds
later by a contraction of the
detrusor muscle.( 2 % )
Neurogenic bladder is most easily defined as a
failure of the bladder to function normally as a
result of neurologic insult to any component
of this control mechanism.
• Bladder is divided into the detrusor and the
base, which includes the trigone and bladder
• The bladder outlet
Internal (smooth muscle) sphincter in the
bladder neck and proximal urethra
The external (striated muscle) sphincter of
the membranous urethra.
• Spinal Cord segments
• Postganglionic --
Hypogastric and pelvic
nerves to the bladder.
• Causes relaxation of
• Promotes urinary
• Release noradrenaline
and provide excitatory
inputs to the bladder
neck and the urethra.
Parasympathetic Nerve supply
• Sacral spinal
• Stimulation causes
and inhibitory effect
• Initiates micturition .
Central Control of Micturition
• Cortical Centre
Medial Frontal lobe
Final control by directing micturition centres
to initiate or delay voiding, depending on the
• Pontine centre in the brainstem, which is
responsible for co-ordinating relaxation of the
external sphincter with bladder contractions
Pontine Micturition Centre
(PMC --Barrington’s nucleus or M-region)
• Essential for the coordination of micturition.
• In the bladder emptying stage, the PMC sends excitatory influence
> sacral spinal cord >detrusor contraction
• Simultaneously sending inhibitory influence > thoracolumbar cord >
internal urinary sphincter relaxation.
• Bladder storage phase, PMC inhibition > sacral spinal cord >
• Simultaneously sending excitatory influence > thoracolumbar cord >
internal urethral sphincter contraction.
• Sensation of bladder filling (100–200
• First urge to void (300–400 cc)
• Strong urge to void (400–500 cc)
• Normal bladder capacity(300–600cc)
History taking in Neurogenic
• Do they have sense of bladder filling ?
• Can they feel the urine passing ?
• Can they stop urine passing in midstream at will ?
• Does the bladder leak continually or suddenly
pass large volumes ?
• Is there any associated rectal disorder ?
• Is there any disorder of potency in male ?
• Is there any numbness in perineum ?
• Do you leak urine when you cough, laugh, lift
something or sneeze? How often?
• Do you ever leak urine when you have a
strong urge on the way to the bathroom? How
• How frequently do you empty your bladder
during the day?
• How many times do you get up to urinate
after going to sleep? Is it the urge to urinate
that wakes you?
• Do you wear pads that protect you from
leaking urine? How often do you have to
• Do you ever find urine on your pads or clothes
and were unaware of when the leakage
• Does it hurt when you urinate?
• Do you ever feel that you are unable to
completely empty your bladder
• Pelvic anatomy
• Neurological examination
• Mechanical issues such as prostate
enlargement or bladder prolapse
• Spinal cord
Classification of Neurogenic Bladder
(1) Lesions above the pontine micturition center (e.g., stroke or
brain tumor) producing an uninhibited bladder.
(2) Lesions between the pontine micturition center and sacral
spinal cord (e.g., traumatic spinal cord injury or multiple
sclerosis involving cervicothoracic spinal cord) producing an
upper motor neuron bladder.
(3) Sacral cord lesions that damage the detrusor nucleus but
spare the pudendal nucleus producing a mixed type A
(4) Sacral cord lesions that spare the detrusor nucleus but
damage the pudendal nucleus producing a mixed type B
(5) Lower motor neuron bladder from sacral cord or sacral nerve
FAILURE TO STORE
FAILURE TO STORE URINE
A 70-year-old woman is admitted to the neurology ICU
after a left-sided ischemic stroke.
On Examination , right-sided motor deficits, the patient is
unable to void.
A catheter is placed for bladder drainage.
The patient recovers some motor function, and her
bladder eventually regains the ability to empty; however,
the patient now complains of severe urgency and
frequency as well as new-onset urge incontinence.
Urodynamic testing demonstrates normal bladder
sensation and filling parameters; however, multiple
unstable contractions are noted during the filling phase.
The patient is able to generate normal bladder
pressures and empties the bladder to
Although she contracts the external sphincter in
an attempt to prevent leakage associated with
the unstable contractions, she is able to relax
the sphincter voluntarily to allow a normal
•How would you classify the type of neurogenic
bladder in this patient?
•How should this patient be managed?
Uninhibited Neurogenic Bladder
Cortical and subcortical structure damage.
• Urgency at low bladder volume (Detrusor
• Sudden uncontrollable evacuation
• No residual urine and little risk of infection
• No high bladder pressures developed that can lead
to upper urinary tract damage
• Safe Bladder
• PMC is intact .
Causes of Uninhibited Bladder
• Lesion affecting IInd frontal gyrus and pathway
leading from it down to pontine micturition
• Frontal lobe Tumors
• Parasagital meningioma
• Anterior communicating artery aneurysms ,
• NPH ,
• Parkinsons disease
TREATMENT OF FAILURE TO STORE
• Unstable bladder contractions
• Urge incontinent episode
• Drugs to block parasympathetic activation of
• Oxybutynin, tolterodine, trospium,
darifenacin, and solifenacin
Upper motor neuron neurogenic bladder
(REFLEX NEUROGENIC BLADDER)
A 35-year-old man with a history of a complete T2
spinal cord injury is referred for urinary
incontinence . He does not use a catheter and
voids into a diaper.
• Serum creatinine level --2.5 mg/dL
• Renal ultrasonography : Bilateral hydronephrosis
with some bilateral renal cortical thinning.
• Urodynamic testing : Poorly compliant bladder
with baseline storage pressures rising above 40
cm H2O after only 100 mL of fluid is instilled.
• Unstable contractions against a closed bladder
• The procedure is stopped early because the
patient complains of facial flushing, headache,
and sweating. At this time, the patient’s blood
pressure is 240/120 mm Hg and heart rate is
• How does this patient’s spinal cord injury
contribute to his clinical picture, and how
should this patient be managed ?
Upper motor neuron neurogenic bladder
• Bladder fullness is not appreciated and
intravesical pressure rises may only be indicated
by profuse sweating , pallor, flexor spasms and
rise in BP
• Reflex emptying of bladder may occur without
• Bladder is small and contracted and capable of
holding maximal volume of 250 ml
• The spinal cord damage renders the bladder and
• Bladder hypertonicity >high storage pressures
> upper urinary tract at risk for reflux and
eventual loss of renal function.
• Instability and reflex incontinence
• Patient is often unaware of any of these
Goals of Therapy
• Protecting upper urinary tracts from sustained
high filling and voiding pressures (>40cm )
• Achieving regular bladder emptying, avoiding
stasis and bladder overdistension and
minimising postvoiding residual volumes to
less than 100mls (ideally <50mls)
• Preventing and treating complications.
• Maintaining continence and avoiding
frequency and urgency
• Clean intermittent self-catheterisation (CISC)
every 4-6 hours
• Anticholinergic medication
Oxybutynin hydrochloride (5mg tds)
Tolterodine (1-2mg bd)
• Cystoscopic placement of an intraurethral
• BTX injection into the external sphincter to
provide a “medical sphincterotomy
Botulinum toxin (BTX)
• Multiple detrusor injections (200 U or 300 U) were
performed cystoscopically, resulting in a significant
improvement in incontinent episodes when compared
with placebo and a durable response lasting up to the
end of the 24-week study
• Other possible side effects include detrusor areflexia,
urinary retention, increased residual urinary volume,
and erectile dysfunction
Botox Detrusor Hyperreflexia Study Team. J Urol
Int. braz j urol. vol.33 no.2 Rio de
Janeiro Mar./Apr. 2007
March 2, 2000
N Engl J Med 2000; 342:665
incontinence grade in 62%
of patients with
detrusor overactivity as
compared with 21% of
patients in the placebo
• Eur Urol 2005;48: 650–5.
Sacral nerve neuromodulation
Significantly decreased urge incontinent episodes from
8.8 to 2.3 episodes per day as well as reduced pad
usage from a mean of 4.7 to 0.82 pads daily in patients
with urge incontinence refractory to conservative
Improvements in urinary urge incontinence,
urgency/frequency, or retention were sustained over
time, with 59% of patients reporting more than a 50%
reduction in pad usage 3 years after initial implantation
Urol 2000; 163:1849–54.
FAILURE TO EMPTY
A 45-year-old woman with insulin-dependent diabetes since
childhood is referred for urinary incontinence .
On examination :
No history of urinary retention but states that she has had dribbling
urinary incontinence that is not associated with an urge to void.
Urine examination : Normal
Postvoid residual volume 1500 mL of urine
The patient states that she had no urge to void at that time.
Video urodynamics demonstrate that the patient has a large
capacity,poorly sensitive bladder and impaired bladder contractility.
• A 23-year-old man presents to the emergency department with
complaints of groin pain and urinary retention.
• He has a history of multiple sexually transmitted diseases, including
herpes simplex, gonorrhea, and chlamydia.
• He has been unable to void for 18 hours despite a strong urge to void.
• Physical examination reveals an active herpetic infection with multiple
vesicular lesions at the base of the penile shaft. A catheter is placed with
return of 1 L of clear urine.
• Cystoscopy reveals no obstructive lesions and a normal-appearing bladder
• Urodynamic testing demonstrates normal sensation and capacity, but the
patient is unable to generate any voiding contractions.
How would you classify the type of neurogenic
bladder in each of these patients?
SENSORY NEUROGENIC BLADDER
• Case 1 demonstrates lack of bladder sensation
that has led to overfilling of the bladder.
• Poor bladder sensation
• Bladder get distended without triggering a
reflex bladder contraction.
• Patient is unaware that the bladder is
• Over time, detrusor failure and urinary
• Dribbling incontinance of sufficientely large
volume that patient claim that they have
• Residual urine measured in liters with high
• Voiding possible with considerable starining
but evacuation is incomplete .
MOTOR NEUROGENIC BLADDER
• Case 2 demonstartes normal sensation of bladder filling but is
unable to generate detrusor pressure sufficient to empty the
• Hallmark of the motor Neurogenic bladder, a result of insult or
injury to the efferent nerve supply to the detrusor muscle.
• Patient’s sensation remains intact, this is solely a motor deficit.
• Possible etiologies of injury to the efferent nerves to the bladder
include herpetic infection, trauma, and iatrogenic injury due to
MOTOR NEUROGENIC BLADDER
• Hallmark of the motor
Neurogenic bladder, a result of
insult or injury to the efferent
nerve supply to the detrusor
• Patient’s sensation remains
intact, this is solely a motor
• Possible etiologies of injury to the
efferent nerves to the bladder
include herpetic infection,
trauma, and iatrogenic injury due
to pelvic surgery
TREATMENT OF FAILURE TO EMPTY
• The mainstay of therapy catheter drainage
• Sacral nerve root neuromodulation ( Interstim
• Early studies demonstrated improvement in
urinary flow from virtually no flow to a mean
maximal flow rate of 13.9 mL/sec.12
• In addition, postvoid residual volumes improved
from 7 8 % of total voided volume to 5 % to 10
% of total voided volume.
J Urol 1 9 9 8;15 9 :14 7 6–8
AUTONOMOUS NEUROGENIC BLADDER
• A 45-year-old man is referred for urinary retention after recently
undergoing an abdominoperineal resection for rectal cancer.
• No significant past history of urinary symptoms
• A catheter was placed intraoperatively without difficulty, but the
patient was unable to void after the catheter was removed.
• After 12 hours, the catheter was replaced, with return of 600 mL of
• During that time, the patient was comfortable and had no sensation
of needing to void.
• Urodynamic testing demonstrates a normal capacity, compliant
bladder. The patient is unable to sense filling at any volume and is
also unable to generate any voiding contraction.
• Damage to motor and
in cauda equina or
• Not able to feel
sensation of bladder
filling and unable to
Autonomous bladder ( Subsacral
• Cauda Equina lesions , pelvic surgery , pelvic malignant
disease , spina bifida and high lumbar disc lesions
• Continual driblling incontinance
• Considerable residual urine and high infection risk
• Large atonic bladder
• Can be associated perineal numbness and loss of sexual
No high bladder storage pressure
• Clean intermittent catheterization
• Indwelling catheters
• Sacral nerve root neuromodulation.
• Filling cystometrogram
• Micturition cystometrogram
• Four channel recording of abdominal pressure
( Rectal catheter ) , total bladder pressure ( via
bladder catheter ) , substracted true
intravesical( detrusor ) pressure and flow rate
• Empty bladder pressure –1 cm H20
• Vesical sensation felt at 100-150 ml ( 6 cm
• Bladder distended 400 to 600 ml , rhythmical
contraction accompanied by sense of urgency
Summary of European Association of Urology
(EAU) Guidelines on Neuro-Urology
EUROPEAN UROLOGY 69 (2016) 324–333
• For neurogenic detrusor overactivity, antimuscarinic
therapy is the recommended first-line medical
• Alternative routes of administration (ie, transdermal
or intravesical) of antimuscarinic agents may be
used. 2 A
• Outcomes for neurogenic detrusor overactivity may
be maximized by considering a combination of
antimuscarinic agents. 3 B
• To decrease bladder outlet resistance, a-blockers could be
prescribed. 1b A
• For underactive detrusor, no parasympathicomimetics
should be prescribed. 1a A
• In neurogenic stress urinary incontinence, drug treatment
should not be prescribed. 4 A
• Botulinum toxin injection in the detrusor is the most
effective minimally invasive treatment to reduce
neurogenic detrusor overactivity. 1a A
• Sphincterotomy is a treatment option for detrusor
sphincter dyssynergia. 3 A
Take Home message
• Neurological evaluation is important to diagnose type of
• Urodynamic studies are important to diagnose detrusor
hyperreflexia (DH), detrusor sphincter dyssynergia (DSD),
detrusor areflexia and organic outlet obstruction
• For DH, anticholinergics are primary T/t.
• For DSD, anticholinergics with α - blocker may be tried
along with CIC
• For detrusor areflexia best therapy is CIC
• Long term use of indwelling urinary catheter to be avoided
• Harrisons’ Principles of Internal Medicine
• Victor Adam Neurology
• John Pattern : Neurological differential diagnosis
• Bickerstaff : Neurological examination in Clinical
• Bradley : Neurology in clinical practice
• Neurogenic BladderAdvances in Urology
Volume 2012, Article ID 816274, 16 pages