This document provides an overview of neurogenic bladder. It begins with an introduction defining neurogenic bladder as bladder dysfunction due to central nervous system or peripheral nerve disease. It then covers the relevant anatomy and physiology including the innervation of the bladder. The document discusses the central neural control of micturition and the normal voiding process. It also covers development of bladder control in adults and provides descriptions of terminology related to storage and emptying problems.

1. NEUROGENIC BLADDER
DR. BHARAT BHUSHAN
(DM-NEUROLOGY)
ASSOCIATE PROFESSOR
GOVERNMENT MEDICAL COLLEGE,KOTA

2. OUTLINE
• Introduction
• Applied anatomy and physiology
• Neuraxis and circuitry
• Common symptoms of neurogenic bladder
• Levels of bladder dysfunction
• Investigations
• Treatment available

3. INTRODUCTION
• Neurogenic bladder refers to dysfunction of the
urinary bladder due to disease of the central
nervous system or peripheral nerves involved in
the control of micturition .
• Non Neurogenic bladder refers to dysfunction of
the urinary bladder due to dynamic disturbance
of genitourinary system.
• Complaints about bladder function are >common
in patients with neurological disease
• 98% of lifetime bladder is in storage phase

4. ANATOMY
• The UB is a smooth muscle chamber
• Composed of two main parts: (1) BODY (2) NECK
• Bladder Muscle is Detrusor muscle- Smooth muscle.
• Trigone : Small triangular area ,Immediately above
the bladder neck.
• The bladder neck is 2 to 3 cm long, and its wall is
composed of detrusor muscle interlaced with a large
amount of elastic tissue. Muscle in this area is called
Internal sphincter. Its natural tone normally keeps
the bladder neck and posterior urethra empty of urine
• Posterior urethra- lower part of the bladder neck
( because of its relation to the urethra)
• External urethral sphincter :- Voluntary skeletal muscle ( Other entirely
smooth muscle). The external sphincter muscle is under voluntary control
of the nervous system and can be used to consciously prevent urination
even when involuntary controls are attempting to empty the bladder.
• Capacity:- Is about 300 ml with a maximum capacity of 500 ml

5. Efferent innervation NERVE ACTION FUNCTION
Parasympathetic
S2,3,4
Pelvic nerve(nervi
erigentes) – hypogastric
plexus
Detrusor muscle
contraction
Internal sphincter
relaxation
Voiding
Sympathetic
T11-L2
Hpogastric nerves
---inferior hypogastric
ganglion
Detrusor muscle
relaxation
Internal sphincter
Contraction
Storage
Somatic :FROM
AHC- S-2,3,4
Pudendal nerve
(ventral rami)
Voluntary innervations
initiate or inhibits
micturition through
cortical control
Voluntary control
Afferent innervation
Parasympathetic
S= 2,3,4
Pudendal nerve –enter
through posterior rami and
terminate in anterolateral
column
Sensation of pain and
distension conveyed
from bladder wall and
internal capsule
Carried normal
sensation
Sympathetic (T9 L2) Hypogastric plexus:enter
through posterior rami and
terminate in
anteromediolateral column
T9-L2
Sensation of painful
distension conveyed
from bladder wall
Carried painful
sensation

6. INNERVATION
Afferent innervation :-
• PNS(S 2,3,4) --Pudendal nerve –enter
through posterior rami and terminate in
anterolateral column
• Sympathetic (T10- L2)-- Hypogastric
plexus:enter through posterior rami and
terminate in anteromediolateral coulmn
Efferent innervation:-
Parasympathetic: S2-S4 ––> pelvic plexus
(Pelvic nerve=nervi erigentes) ––>
cholinergic postganglionic fi bers ––>
bladder + sphincter
• Sympathetic: T10-L2 ––> hypogastric/ pelvic
plexus ––> noradrenergic postganglionic
fibers ––> smooth muscle of bladder base,
internal sphincter, proximal urethra
• Somatic: (AHC S2,S3,4) ––> pudendal nerve
(ventral rami)––> external sphincter

7. RECEPTORS & INNERVATION
• Detrusor - intermediolateral
gray column of S2,3,4
parasympathetic – pelvic n
(M2 receptors)
• External urethral sphincter -
innervated by somatomotor
S2,3,4 nucleus (Onuf’s
Nucleus)-pudendal n
(Nicotinic receptor)
• Trigone and internal
sphincter innervated by
Sympathetic T10,11,12 (less
important)
• SNS acts through B2 and A1
receptors
Afferent Pathways
• Sensations of pain, temp, urgency is
follows the anterolateral white
columns.
• Conscious sensations (bladder
distention, ongoing micturition, tactile
pressure) follow the posterior columns
• A-delta fibers – Micturition reflex,
stretch and fullness sensation
• C-fibers – Noxious sensation

8. NEURAXIS
• Frontal lobe- Sends inhibitory signals
• Pons (Pontine Micturition Center=PMC)
– Major relay/excitatory center
– Coordinates urinary sphincters and the bladder
– Affected by emotions
• Spinal cord (S2-4)-Intermediary between upper and lower control
• Peripheral nervous system-
Parasympathetic (S2-S4)-Pelvic nerves
Excitatory to bladder, relaxes sphincter
Somatic (S2-S4)-Pudendal nerves -Excitatory to external sphincter
Sympathetic (T10-L2)
– Hypogastric nerves to pelvic ganglia
– Inhibitory to bladder body, excitatory to bladder base/urethra

9. Central neural control
PET studies Blok et al . Brain 1998
1.CORTEX – increased blood flow
• During storage During micturition
Mid cingulate gyrus Rt Inferior frontal gyrus
Lat bilateral frontal lobes Rt. Anterior cingulate gyrus
Periaqueductal gray matter (PAG)
2.PONS
• Micturition is being controlled by pontine micturition center (PMC)
which is situated in mediodorsal Pons called as M region
• During storage phase PMC is inhibited by higher cortical control
unless socially appropriate
• Blok et al asked to void the volunteers under scanner In successful
voiders activity was shown in mediopost pons (M region)
• In subjects unable to void and storing urine a distinct region in the
ventrolateral pontine tegmentum was activated (L region)

10. Innervations
Afferent
• Somatic: pudendal nerve
• Visceral: sympathetic and
parasympathetic fibers (sensation of
fullness)
Efferent
• Parasympathetic: S2-S4 ––> pelvic
plexus ––> cholinergic postganglionic
fibers ––> bladder + sphincter
• Sympathetic: T10-L2 ––> hypogastric/
pelvic plexus ––> noradrenergic
postganglionic fibers ––> smooth
muscle of bladder base, internal
sphincter, proximal urethra
• Somatic: S2-S3 ––> pudendal nerve ––>
external sphincter

11. Central neural controlPET studies Blok et al . Brain 1998
• Successful voiders–Rt Inferior frontal gyrus Rt Ant cingulate gyrus
• Pontinemicturition center- M region
• Unableto void – Mid cingulate gyrus Lat bilateral frontal lobes
• Pontinestoragecenter - L region PAG

12. Peripheral Nervous System
• Parasympathetic (S2-S4)
– Pelvic nerves
• Excitatory to bladder,
relaxes sphincter
• Somatic (S2-S4)
– Pudendal nerves
• Excitatory to external
sphincter
• Sympathetic (T10-L2)
– Hypogastric nerves to pelvic
ganglia
– Inhibitory to bladder body,
excitatory to bladder
base/urethra
• Afferents through Pelvic, pudendal,
hypogastric by
A-delta fibers – Micturition reflex,
stretch and fullness sensation
C-fibers – Noxious sensation

13. FUNCTION OF BLADDER
Function
Balance between suprasacral
modulating pathways, sacral
cord and the pelvic floor
Emptying phase: “Voiding
Reflex”
Series of coordinated eventsSeries of coordinated events
involving outlet relaxation,involving outlet relaxation,
detrusor contractiondetrusor contraction
Storage phase: “Guarding
reflexes” constant afferent
input to maintain continence

14. Normal Voiding
Normal Voiding
• SNS primarily controls bladder and the IUS
– Bladder increases capacity but not pressure
– Internal urinary sphincter to remain tightly closed
– Parasympathetic stimulation inhibited
• PNS:-Immediately prior to PNS stimulation,
SNS is suppressed
Stimulates detrusor to contract
Pudendal nerve is inhibited →external sphincter opens →
facilitation of voluntary urination
• Somatics (pudendal N) regulate EUS,Pelvic diaphragm
Delaying voiding or voluntary voiding:
• When an individual cannot find a bathroom nearby, the brain inhibit PMC to
prevent detrusor contractions & actively contract the levator muscles to
keep the external sphincter closed
• Thus , voiding process requires coordination of both the ANS and somatic
nervous system, which are in turn controlled by the PMC located in the
brainstem.

15. DEVELOPMENT IN ADULT
• In child Controlled by
• Sacral spinal cord reflex
• Newborns void 20 x/day with
only a slight decrease during
the 1st year of life
• Bladder capacity increases &
voiding frequency decrease
with growth
Bladder capacity in Ounces
(30ml) = Age (yrs) +2
• 1-2 yrs: conscious
sensation of bladder
fullness develops
• 2-3 yrs: Ability to initiate or
inhibit voiding voluntarily
develops
• 2-4 yrs: Voiding comes
under reliable voluntary
control
• By age 4 Micturition spinal
reflex fully modulated by
CNS micturition center via
a spinobulbospinal tact
• Initially child has better
control over external
sphincter than bladder
Cortical
Diencephalic
Mechanism
PMC
Spinal tract
NeuronSpinal efferent
Mechanism
Ganglia
BLADDER
A afferentC afferent
COLD
Perineal
stimulation

16. MICTURITION(VOIDING) REFLEX
Sensation of bladder fullness via
pelvic and pudendal nerves to
S 2,3,4
Frontal lobe decides social appropriateness
Periaqueductal gray matter
RECIPROCAL ACTIVITY BETWEEN SPHINCTER & DETRUSSOR
Medial Pontine micturition center
Onuf’s nucleus to pudendal nervesDetrussor center (S 2,3,4) to pelvic nerves
Micturition

17. STORAGE REFLEXES
Passive low level phenomena mediated by a spinal reflex

18. Description of Terminology
Storage - At low pressure until such time as it is convenient and socially
acceptable to void
Voiding - Initiated by inhibition of the striated sphincter and pelvic floor,
followed some seconds later by a contraction of the detrusor muscle.
• Storage Problem: Failure to Store normal volumes of urine at low pressure
& without leakage
– Non compliant bladder -Irritable bladder
– Inadequate sphincter tone during filling
• Emptying Problem: Failure to empty completely, on command, efficiently at
low pressures
– Failure of neurological control of bladder -Bladder muscle failure
– Failure of sphincter relaxation during voiding
• Voiding symptoms: Storage symptoms
Hesitency Frequency
Slow stream Urgency
Straining to void Urge incontinence
Terminal dribbling Nocturia
Feeling of incomplete emptying.

19. Description of Terminology
• Hesitency: Difficulty to initiate micturition
• Urinary retention: Is the inability of the urinary bladder to
empty. The cause may be neurologic or nonneurologic .
• Urinary frequency: Voiding more than 7 times during day
and more than once in night (Am J Obstet Gynecol. 2009
May; 200(5): 552.e1–552.e7.)
• Urgency: extreme desire to void
• Urinary incontinence: Involuntary loss of urine that is
objectively demonstrable & is a social or hygenic
problem (Abraham P et al 2002)
• Nocturia : Interruption of sleep by urge to void
• Outflow obstruction: BPH, urethral stricture, prostate
cancer

20. Description of Terminology
• Overflow incontinence: Involuntary passage of urine at a greater than
normal bladder capacity. Due to impaired detrusor contractility OR
A frequent dribble of urine as a result of inefficient bladder emptying
: drugs, peripheral nerve injury, old age, myogenic injury
• Stress incontinence: Incontinence because of increase in intra abdominal
pressure Causes: trauma after birth, pelvic surgery, vaginal wall
hypermobility,irradiation , meningomyelocele , epispadias
• DETRUSOR HYPEREFLEXIA(DH): OAB ;involuantary detrusor contraction
symptoms due to a suprapontine neurologic disorder. The detrusor &
sphincter function incoordination.
• DETRUSOR SPHINCTER DYSSYNERGIA(DSD)-: overactive bladder
symptoms due to neurologic UMN disorder of the suprasacral spinal cord.
Paradoxically, the patient is in urinary retention; they are in dyssynergy (lack
of coordination).
• DETRUSOR AREFLEXIA :Is complete inability of the detrusor to empty due
to a lower motor neuron lesion ( eg , sacral cord or peripheral nerves injury)
• AUTONOMIC DYSREFLEXIA: Is an exaggerated sympathetic response to
any stimuli below the level of the lesion

21. TYPE AND LOCALIZATION
OF BLADDER
• 1. LOSS OF SUPRASPINAL CONTROL (UNINHIBITED
BLADDER)
• 2. SPINAL CORD LESION ABOVE SACRAL LEVEL
REFLEX NEUROGENIC BLADDER (AUTOMATIC)
• 3. SPINAL CORD LESION INVOLVING SACRAL
LEVEL AUTONOMOUS BLADDER
• 4. LESION INVOLVING AFFERENT SENSORY
NEURONS SENSORY NEUROGENIC BLADDER
• 5. LESION INVOLVING EFFERENT MOTOR
NEURONS MOTOR PARALYTIC BLADDER
• 6.OTHERS: Stroke/Dementia/NPH/PD/MSA/MS
Diabetic cystopathy/Spinal shock

22. Reflexic –Spastic
/uninhibited/UMN
Areflexic -
autonomous/flaccid/LMN
Sensory
characteristics
No inhibitions influence
time & place of voiding
Bladder empties in
response to stretching of
bladder wall
characteristics
Bladder acts as if there
were paralysis of all motor
functions
characteristics
lack of sensation of need
to urinate
clinical manifestations
-Incontinence
-frequency
-urgency
-voiding is unpredictable
and incomplete
clinical manifestations
Fills without emptying
Retention
Dribbling incontinence
Clinical manifestations
Poor bladder sensation ,
Infrequent voiding of large
residual volume
causes :- corticospinal
tract lesion
observed in
SCI/stroke/multiple
sclerosis/brain
tumor/brain trauma
causes:- lower motor
neuron lesion cuased by
trauma involving S2-S4
lesions of cauda
equina/pelvic nerves
causes:- damage to
sensory limb of bladder
spinal reflex arc seen in
multiple
sclerosis/diabetes
mellitus

23. Type of Urinary Incontinence
1.Stress-Urine loss during activities such as coughing, sneezing,
laughing or lifting.
2.Urge-A sudden need to urinate, occasionally with large volume urine
loss. Can also exist without incontinence (Urgency).
3.Overflow- A frequent dribble of urine as a result of inefficient bladder
emptying symptoms are similar to stress incontinence.
4.Mixed- stress + urge forms.
5.Functional-
Urine loss not associated with
any pathology or problem in
the urinary system.

24. TYPE OF BLADDER
+ + +
+ + +
+ + +
+ + +
0
+
0
0
+
+ + + 0+ + +
DSD
DI/OI DA

25. LOSS OF SUPRASPINAL CONTROL
(UNINHIBITED BLADDER):
• Lesions of CNS involving area above pons
• Micturition is usually precipitous and
complete
• Frequency, urgency & urge incontinence
• Low or absent residual volume as there is
no DSD
• Normal sensation of bladder filling
• Causes: CVA, frontal tumors, parasagittal
meningioma, ACA aneurysm,NPH, PD,
Demyelinating disease

26. SPINAL CORD LESION ABOVE SACRAL LEVEL
REFLEX NEUROGENIC BLADDER (AUTOMATIC)
• Detrusor- sphincter dyssynergia is a rule
• Bladder sensation variably interrupted
• Bladder tone increased, capacity reduced
• Small residual urine
• Urgency, frequency and urge incontinence
• In incomplete lesions Inability to initiate
voluntary micturition
• Cystometrogram shows uninhibited contractions
of detrusor in response to small volume of fluid
• Causes: spine cord trauma, compressive
myelopathy, myeilitis, syringomyelia

27. SPINAL CORD LESION INVOLVING SACRAL LEVEL
AUTONOMOUS BLADDER:
• Denervation of both afferent and efferent supply to
bladder
• Bladder tone flaccid, sensation absent, Inability to initiate
micturition
• Increased bladder capacity and residual urine
• Overflow incontinence, no urgency
• No bladder reflex activity, Infection risk high
• Voiding is possible only by maneuver
• Cystometrogram shows low pressure and no emptying
contraction
• Causes: Cauda equina syndrome,Conus medullaris
Spinal shock

28. LESION INVOLVING AFFERENT SENSORY NEURONS
SENSORY NEUROGENIC BLADDER
• Impaired bladder sensation
• Initiation of micturition is possible
• c/o urinary retention or overflow incontinence
• Infection risk high
• If bladder not voided at timely basis over
distension of bladder
• Bulbocavernosus & anal reflexes absent
• Causes: Tabes dorsalis Neuropathies mainly
small fibers: DM, Amyloidosis

29. LESION INVOLVING EFFERENT MOTOR NEURONS
MOTOR PARALYTIC BLADDER:
• Bladder tone flaccid, sensation intact
• c/o Painful retention of urine or impaired
bladder emptying
• Inability to initiate or maintain micturition
• Bladder capacity and residual urine
markedly increased, infection risk high
• Bulbocavernosus & anal reflexes absent
• Causes: Lumbosacral meningomyelocele,
tethered cord syndrome Extensive pelvic
surgery or trauma Lumber spinal stenosis

30. CORTICAL LESION
• Intracranial tumors, damage after rupture of an
aneurysm, penetrating brain wounds, and prefrontal
lobotomy subjects (Andrew and nathan 1964). patients
with right frontal lobe disorders who had urinary retention
and in whom there was restoration of voiding when the
frontal lobe disorder was treated successfully (Fowler
1999).
• DH with coordinated urethral sphincter is MC
• c/ o urinary frequency, urgency, and urge incontinence
• First-line treatment for detrusor hyperreflexia includes
anticholinergic medication

31. STROKE
• Mechanisms: decreased sensation or awareness of bladder
filling and inability to suppress bladder contraction
• Incontinence after stroke is frequently transitory and upto 80%
recover and being continent at 6 months ( Brocklehurst JC et
al 1985)
• Sakakibara R et al(1996) found that Urinary symptoms in 53%
patients. Pts. with urinary symptoms had significantly more
lesions located in the frontal lobe,
• Urodynamics: detrusor overactivity (MC). Detrusor areflexia
can also be seen,esp in acute cerebral shock. (Burney Tl et
al1996
• Presence of post stroke incontinence within first wk is an
indicator of a more severe CVA and independent risk factor
for poor outcome at 3 months ( Patel M, et al J Am Geriatr
Soc 2001; Petterson R et al . J Am Geriatr Soc 2006)

32. DEMENTIA:
• The cause of urinary incontinence in dementia probably is
multifactorial.
• Functional incontinence is major cause. It refers to incontinence
that is not derived from an abnormality in the lower urinary tract or
its innervation, but from immobility, gait disorder, cognitive disability,
and decreased motivation,
• Overactive bladder (OAB) is a also major cause
• Two major etiologies for DO have been proposed: central and
peripheral. Peripheral detrusor muscle change and central is
secondary to loss of cortical inhibition of primitive bladder reflex
contractions
• Detrussor overactivity found in 58% (AD), 90% (VAD) and 50%
(both) (Mori et al 1999)
• Del-Ser et al (1996) found that the onset of urinary incontinence was
significantly earlier in patients with DLB (3.2 years after dementia
onset) than in patients with Alzheimer’s disease (6.5 years after
dementia onset )

33. Normal pressure hydrocephalus:
• In NPH, Incontinence is late feature.
• Failure of CSF to flow into the parasagittal subarachnoid
space (where most fluid resorption occurs) as the most
likely mechanism
• Distortion of central portion of corona radiata and
Periventricular white matter by distended ventricles
which anatomically includes sacral motor fibers that
innervate legs and bladder, thus explaining abnormal
gait and incontinence
• Urodynamic parameters consistent with detrusor
overactivity in 95% pts.(Sakakibara et al 1996)
• Improvement in urodynamic function has been
demonstrated within hours of lumbar puncture in patients
with NPH.

34. Parkinson disease:
• Voiding dysfunction in 35 to 70% of patients
• Urinary symptoms began approximately 5 years after onset of motor
symptoms (wing et al 2006).
• MC Hypothesis is basal ganglia have an inhibitory effect on the
micturition reflex, and with neuronal loss in the substantia nigra,
detrusor hyper-reflexia develops
• MC symptoms frequency, nocturia, urgency, and urge incontinence
• Urodynamics: detrusor overactivity in filling phase(MC)
Pseudodysnergia may occur d/t delay in ext sphinter relaxation.
Bladder sensation preserved.
• Bladder symptoms are correlated with extent of dopamine depletion,
neurologic disability and with stage of disease(araki and kuno 2000)
• Moderate doses of levodopa alleviated detrusor overactivity but high
doses aggravated it.(Benson et al 2001)
• Recently, DBS of the subthalamic nucleus (STN-DBS) improved
voiding dysfunction in PD patients .( Herzog J et al. Brain2006)

35. MSA
• Urinary dysfunction is a prominent autonomic feature (more than
90%)and may precede overt neurological involvement by 4-5 years
• The most frequent urinary symptom was difficulty voiding in 79% of
the patients, followed by nocturnal urinary frequency in 74%.,
urgency incontinence in 63%, diurnal urinary frequency in 45%,
nocturnal enuresis in 19%, and urinary retention in 8% ( Sakakibara
R, et al J Neurol Neurosurg Psychiatry 2000; 68: 65–9 .)
• Pathophysiology : Affects several location in CNS-
• 1. BO is caused by neuronal loss in pons
• 2. Incomplete bladder emptying is caused by loss of
parasympathetic innervation due to neuronal degeneration in the
Inter Medio Lateral (IML) column of spinal cord
• 3. AHC loss in onuf’s nucleus results in denervation of the EUS
• 4.Sympathetic nerve atrophy causes non-functional bladder and an
open bladder neck

36. Spinal Cord Lesions:
• Detrusor areflexia ( spinal shock) at initial insult but
progress to hyperreflexic and DSD over few weeks
• C fiber emerge as major afferent mediate mechano
sensitivity forming abnormal sacral segmental reflex
resulting in automatic voiding
• c/o urgency frequency incomplete bladder emptying ,
interrupted stream, difficulty in initiating micturition
• In the patient with a neurologic mid thoracic (usually with
a lesion above T6) or higher spinal lesion, autonomic
dysreflexia may occur secondary to loss of supraspinal
inhibitory control of thoracolumbar sympathetic outflow
and result from massive discharge of the sympathetic
system
• Autonomic dysreflexia is an exaggerated sympathetic
response to any stimuli below the level of the lesion

37. Multiple sclerosis:
• Interruption of the reticulospinal pathways between the
pontine and sacral micturition centers may cause DSD
• Plaques located in the spinal afferents and efferents of
the sacral reflex arc may inhibit bladder contraction and
therefore result in impaired emptying or urinary retention
• Intracranial plaques may result in loss of voluntary
control of initiation or prevention of voiding
• Urodynamics : ( Litwiller Seet al . J Urol 1999; 161: 743–57).
• 1.MC is DH,( 50-90% of patients with MS).
• 2.Upto 50% of patients have DSD-DH
• 3.Detrusor areflexia occurs in 20-30% of cases Multiple
sclerosis

38. Diabetic cystopathy:
• 10 or more years after the onset of DM
• D/t autonomic and peripheral neuropathy
• No exact data on the prevalence, incidence, and risk factors diabetic
cystopathy are available
• Most patients with a diabetic neurogenic bladder show prominent
signs of other long-term diabetic complications
• Bladder dysfunction appears to be related to the severity of
diabetes, not to its duration( Buck AC 1988)
• C/f –Initially loss of sensation of bladder filling followed by loss of
motor function
• Urodynamics-elevated residual urine, decreased bladder sensation,
impaired detrusor contractility, and, eventually, detrusor areflexia
• Rx-CIC, long-term indwelling catheterization, or urinary diversion.
BJU Int 2005; 95: 733–8 .

39. Herniated disc:
• Slow and progressive herniation of the lumbar disc may
cause irritation of the sacral Nn. and cause DH
• Acute compression of the sacral roots associated with
deceleration trauma will prevent nerve conduction and
result in detrusor areflexia
• Urodynamics – Depends on nerve injury
• DA with intact bladder sensation may occur
• Internal sphincter denervation may occur
• If the peripheral sympathetic nerves are damaged, the
IUS will be open and nonfunctional
• Striated sphincter, however, is preserved

40. Herpes zoster
• Herpes virus lies dormant in the dorsal root
ganglia or the sacral nerves
• Sacral nerve involvement leads to impairment of
detrusor function
• Early stages of herpes infection are a/w
frequency, urgency, and urge incontinence
• Later stages include decreased bladder
sensation, increased residual urine, and urinary
retention
• Urinary retention is self-limited and will resolve
spontaneously with clearing of the herpes
infection.

41. Clinical evaluation - History:
• Urinary symptoms:
1.Onset: Etiology help
2.Sense of bladder filling: Motor/Sensory/Cortical
3.Can they feel urine passing: Afferent Neuraxis
4.Can they stop urine passing in midstream at will: Efferent Neuraxis
5.Does bladder leak continually or suddenly pass large volume:
OI/DSD/Sensory
6.Frequency: NON NEUROGENIC/NEUROGENIC
7.Stream: NON NEUROGENIC/NEUROGENIC
8.Initiation: CORTEX/OUTLET
9.Termination : CORTEX/OUTLET
10.Ablity to stop on command : CORTEX
11.Volume of urine passed : LMN/UMN
12.H/O of spinal injury or surgery and meningomyelocele, Low backache, lower limb
paresis, sensory sympt. PD, CVA, MS Drugs: anticholinergics and α adrenergics
Sexual and bowel dysfunction & Other autonomic symptoms Genitourinary symp:
UTI, reflux, stones,surgery Obstetric history: no. of deliveries, prolapse uterus

42. Laboratory Studies
• Urinalysis and urine culture- UTI can cause
irritative voiding symptoms and urge
incontinence.
• Urine cytology- carcinoma-in-situ of the urinary
bladder causes symptoms of urinary frequency
and urgency BUN and creatinine are checked if
compromised renal function is suspected.
• MRI spine and brain
• Radiological evaluation of upper urinary tract
Laboratory Studies

43. ASSESMENT OF LOWER URINARY TRACT :
• Urodynamic studies are necessary to document
type of bladder dysfunction
• Measurement of urine flow rate
• Measurement of post-void residual(PVR) volume
• Cystometry during filling and voiding
• Video-cystometry
• Urethral pressure profile measurement
• Assessment of pelvic floor neurophysiology

44. INVESTIGATIONS
• Noninvasive bladder investigations
– Post void residual volume – In out catheterization,
– Ultrasound ( N is <100ml)
– Uroflowmetry : Voided volume ( >100ml)
Maximal flow, maximal and average flow rate (M > 20ml/sec F > 15ml/sec)
• Cystometry
* Measure detrusor pressure (Intravesical presure – Rectal pressure)
* Bladder infused till 400 to 600ml – Pressure should not rise to >15cm
water (Stable bladder)
* Neurogenic detrusor overactivity – Involutary detrusor contraction during
filling phase
* Voiding phase – Detrusor pressure M < 50cm water F < 30cm water
• Sphincter EMG – Reinnervation with prolonged duration of MUAPs
• Neuroimaging – Cauda equina & conus lesions, spinal, supra pontine and
pontine lesions

45. INVESTIGATIONS
• Cystoscopy Indicated for people complaining of persistent irritative
voiding symptoms or hematuria
It can diagnose obvious causes of bladder overactivity, such as
cystitis, stone, and tumor, easily
• Determine etiology of the incontinence and may influence treatment
decisions
• Videourodynamics
When cystometry is carried out using a contrast filling medium and the
procedure is visualized radiographically
• Useful to see Reflux into the ureters
• Thickening of the bladder wall and bladder diverticula.
• In detecting sphincter or bladder neck incompetence in genuine stress
incontinence.
• Inspect the outflow tract during voiding in patients with suspected
obstruction

46. TREATMENT:
• Non-invasive conservative treatment
– Electrical stimulation
– Drugs
• Minimal invasive treatment
– Catheterization
– Botulinum toxin injections in the bladder
– Sphincterotomy
• Surgical treatment
– Detrusor myectomy
– Sacral rhizotomy with Sacral ant root stimulation
– Sacral neuromodulation
– Sphincterotomy

47. Non-invasive conservative treatment
• Electrical stimulation:
Stimulation of levator ani muscles using painless electric shocks
Electrical stimulation of pelvic floor muscles produces a contraction
of the levator ani muscles and EUS while inhibiting bladder
contraction.
• Depends on a preserved reflex arc through the intact sacral
micturition center Can be used in conjunction with biofeedback or
pelvic floor muscle exercises.
• Effective in : Stress incontinence, as well as urge and mixed
incontinence
• Stimulation for a minimum of 4 weeks
Decreasing bladder outlet resistance
• Alpha-blockers (non-selective and selective) have been partially
successful for decreasing bladder outlet resistance, residual urine
and autonomic dysreflexia.

48. Drugs for detrusor overactivity
• Anticholinergic are the most useful medications available for neurogenic
detrusor overactivity.
• Muscarinic receptor antagonists. Reduce DO and improve bladder
compliance
• Propiverine has both anticholinergic and calcium channel blocking
properties & it is better tolerated than oxybutynin (Madersbacher H et al
ICS1997 )
• Recently, darifenacin and solifenacin have been introduced , but no
clinical experience with these drugs in neurogenic bladder overactivity has
been published
• Additional treatment with desmopressin might improve the efficacy of the
treatment (valiquette et al Arch Neurol 1996 Dec;53(12):1270-5 ).
• GENERIC NAME DOSE (mg) FREQUENCY
• Oxybutynin 2.5-5 tds
• Tolterodine ( selective) 2 bd
• Trospium chloride 20 bd
• propiverin 25-150 tds

49. Drugs for detrusor underactivity
• Cholinergic drugs, such as bethanechol chloride and
distigmine bromide , have been considered to enhance
detrusor contractility and promote bladder emptying.
• The available studies do not support the use of
parasympathomimetics because of possible serious
possible side effects
• Combination therapy with a cholinergic drug and an
alpha-blocker appears to be more useful than
monotherapy
• There is no drug with evidence of efficacy for underactive
detrusor(LOE 2a, Gr of recom B).

50. Catheters:
• 3 types
– Indwelling urethral catheters
– Suprapubic catheters
– Intermittent catheterization
Catheterization usually used for
• Atonic bladder with overflow incontinence
• Overactive bladder with detrusor sphincter dyssynergia

51. Intermittent catheterization
• Intermittent self- or third-party catheterization is the gold
standard for the Mx of neurogenic bladder, Performed
using a short, rigid, plastic catheter
• Drain the bladder at timed Intervals (eg,awakening,
every 3-6 hours during the day, and before bed) or
based on bladder vol
• The average adult empties the bladder 4-5 times a day.
Thus, catheterization should occur 4-5 times a day
Patients should wash their hands with soap and water.
Sterile gloves are not necessary Intermittent
catheterization

52. GUIDELINES FOR CATHETERIZATION
• 1. Intermittent catheterization is the standard treatment for patients
who are unable to empty their bladder
• 2. Patients should be well instructed in the technique and risks of IC.
• 3. Aseptic IC is the method of choice
• 4. The catheter size should be 12-14 Fr
• 5. The frequency of IC is 4-6 times per day
• 6. The bladder volume should remain below 400 mL
• 7. Indwelling transurethral and suprapubic catheterization should be
used only exceptionally, under close control, and the catheter
should be changed frequently.
• Silicone catheters are preferred and should be changed every 2-4
weeks, while (coated) latex catheters need to be changed every 1-2
weeks.

53. TREATMENT
• Botulinum toxin injections in the bladder most
effective minimally invasive treatment to reduce
neurogenic detrusor overactivity
• Repeated injections seem to be possible without
loss of efficacy
• Sphincterotomy is the standard treatment for
DSD (level of evidence: 2, grade of
recommendation A ) Bladder outlet resistance
can be reduced without completely losing the
closure function of the urethra
• The laser technique is advantageous
Sphincterotomy

54. TAKE MY MESSAGE
• Complaints about bladder function are common in
patients with neurological disease
• Neurological evaluation is important to diagnose type of
neurogenic bladder.
• 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 catheters should be avoided