In this we will discuss about the Innervation of Urinary bladder & various types of bladder pathology associated

1. NERVE SUPPLY AND TYPS OF
BLADDER
• DR. TARUN KUMAR

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

3. • The bladder is the most anterior element of the
pelvic viscera. Situated in the pelvic cavity when
empty, but expands superiorly into the
abdominal cavity when full.
• The urinary bladder is abdominal at birth,
positioned at the extraperitoneal area of the
lower abdominal wall.
• Around the 5th or 6th year of age the bladder
gradually descends into the area of the true
(minor) pelvis.
INTRODUCTION

4. • Urinary bladder functions as a storage organ that
can empty to completion at appropriate time and
place.
• Problems related to bladder are often obvious
like enuresis, incontinence or may not be
apparent like recurrent UTIs, day time urgency
frequency syndrome.
• Early intervention may prevent renal damage
from retrograde effects of high bladder pressures.

5. ANATOMY
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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

6. • Ureterovesical Junction :
• As the ureter approaches the bladder, 2 to 3 cm from the bladder, a
fibromuscular sheath (of Waldeyer) extends longitudinally over the
ureter and follows it to the trigone.
• The ureter pierces the bladder wall obliquely, travels 1.5 to 2 cm,
and terminates at the ureteral orifice. As it passes through a hiatus
in the detrusor (intramural ureter), it is compressed and narrows
considerably.
• The intravesical portion of the ureter lies beneath the urothelium, it
is backed by a strong plate of detrusor muscle. With bladder filling,
this arrangement is thought to result in passive occlusion of the
ureter, like a flap valve

7. • This anatomic arrangement helps prevent reflux during bladder
filling by fixing and applying tension to the ureteral orifice. As the
bladder fills, its lateral wall telescopes outward on the ureter,
thereby increasing intravesical ureteral length.
• Vesicoureteral reflux is thought to result from insufficient
submucosal ureteral length and poor detrusor backing.
• Chronic increases in intravesical pressure resulting from bladder
outlet obstruction can cause herniation of the bladder mucosa
through the weakest point of the hiatus above the ureter and
produce a “Hutch diverticulum” and reflux.

8. INNERVATION
Afferent innervation :-
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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

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

10. RECEPTORS & INNERVATION
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• 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 B3 and A1
receptors
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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

11. NEURAXIS
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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

12. • Afferents to Spinal cord : sphincter relaxation
• Afferents to Pons : Contraction of detrusor
• Spinal center: Reflex ill-sustained contractions of
detrusor leads to incomplete evacuation
• Pontine center: Coordinating center. Synchronization
and maintenance of sustained contractions to
complete evacuation.
• Cortical Center: Controls pontine center till a suitable
socially acceptable situation for micturition is available.

13. 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

14. Normal Voiding
Normal Voiding
• SNS primarily controls bladder and the IUS
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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:
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• 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. 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 nerves
Detrussor center (S 2,3,4) to pelvic nerves
Micturition

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

17. DEVELOPMENT
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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
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1-2 yrs: conscious
sensation of bladder
fullness develops
3yrs: Ability to initiate or
inhibit voiding voluntarily
develops
4yrs: 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 efferent
Mechanism
Ganglia
Perineal
stimulation

18. • 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
Bladder Disorders

19. 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
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Non compliant bladder -Irritable bladder
Inadequate sphincter tone during filling
• Emptying Problem: Failure to empty completely, on command, efficiently at
low pressures
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Failure of neurological control of bladder -Bladder muscle failure
Failure of sphincter relaxation during voiding
• Storage symptoms
Frequency
Urgency
Urge incontinence
Nocturia
Voiding symptoms:
Hesitency
Slow stream
Straining to void
Terminal dribbling
Feeling of incomplete emptying.

20. 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
Urgency: extreme desire to void
Urinary incontinence: Involuntary loss of urine that is
objectively demonstrable & is a social or hygenic
problem
Nocturia : Interruption of sleep by urge to void

21. Description of Terminology
• Overflow incontinence: Involuntary passage of urine at a greater than
normal bladder capacity. Due to impaired detrusor contractility OR
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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
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

22. TYPE AND LOCALIZATION OF
BLADDER
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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

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

24. 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.

25. CORTICAL BLADDER (UNINHIBITED BLADDER):
Physiologic: Newborns and infants – periodic
complete evacuation.
Pathologic:
• Lesion in paracentral lobule (cerebral palsy,
multiple sclerosis, trauma, infarcts)
• Uncontrolled evacuation in socially unacceptable
situations.
• Since pontine arc is intact evacuation is complete,
no residual urine and coordination is good, no
detrusor sphincter dyssynergia.
• No VUR, “Safe bladder.”
• Associated with dementia (frontal lobe).

26. UMN/ AUTOMATIC /HYPERREFLEXIC
BLADDER
• 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. AUTONOMOUS BLADDER:
• Combined involvement of both sensory and motor
limbs (Cauda equina lesions, spina bifida)
• Local vesical plexus takes over the control and
functions as autonomous bladder
• Continuous dribbling
• Incomplete evacuation
• High residual volumes

28. SENSORY NEUROGENIC BLADDER
• Afferent sensory limb is lost
• No bladder sensation
• Overflow incontinence
• Can void with straining in a
timetablefashion, but emptying is
incomplete.
• Bulbocavernosus & anal reflexes absent
• Causes: Tabes dorsalis Neuropathies
mainly small fibers: DM, Amyloidosis

29. MOTOR PARALYTIC BLADDER:
• Lesion involving Efferent motor limb
• Bladder tone flaccid, sensation intact
• Painful retention of urine or impaired
bladder emptying
• 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,GBS.

30. • Lesion in at/below spinal level (anterior horn
cell, nerve)
• No spinal reflex – areflexic, huge capacity
bladder
• Overflow incontinence
• High residual volume - infections
LMN/AREFLEXIC BLADDER

31. Diabetic cystopathy:
• 10 or more years after the onset of DM
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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
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- long-term indwelling catheterization, or urinary diversion.

32. 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

33. 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

34. 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

35. INVESTIGATIONS
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• 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

36. TREATMENT:
• Non-invasive conservative treatment
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– Behavior therapy
– 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

37. NON-INVASIVE CONSERVATIVE TREATMENT
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• 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.

38. Drugs for detrusor overactivity
• Anticholinergic are the most useful medications available for neurogenic
detrusor overactivity.
GENERIC NAME
Oxybutynin
DOSE (mg)
2.5-5
Tolterodine ( selective) 2
FREQUENCY
tds
bd
• Trospium chloride 20 bd
• Propiverin
• Solifenacin
• Darifenacin
25-150 tds

39. • Beta-3 receptor Agonist :
Mirabegron (25-50mg OD)
Virabegron ( FDA approved 2020)
• Combination Therapy :Combination therapy with an
anti-muscarinic and a beta-3 adrenoceptor agonist for OAB
refractory to monotherapy with either anti-muscarinics or
beta-3 adrenoceptor agonists can be considered.

40. Drugs for detrusor underactivity
• Cholinergic drugs, such as bethanechol chloride and
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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).

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

42. Intermittent catheterization
• Intermittent self- or third-party catheterization is the gold
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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

43. GUIDELINES FOR CATHETERIZATION
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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.

44. OTHER 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. Bladder outlet resistance can be
reduced without completely losing the
closure function of the urethra
• The laser technique is advantageous
Sphincterotomy

45. TAKE HOME MESSAGE
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• 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