Neurogenic bladder Anatomy Physiology S/S Investigation & Treatment

1. Presented By :
Dr. Nukhaze Ali Asgher
AMTH,Lahore.
NEUROGENIC BLADDER

2. • 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.
INTRODUCTION

3. 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. 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

6. 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
• A-delta fibers – Micturition reflex,
stretch and fullness sensation
• C-fibers – Noxious sensation

7. • 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
NEURAXIS

8. 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)
Central neural control
PET studies Blok et al . Brain 1998

9. Innervations
1. Afferent
• Somatic: pudendal nerve
• Visceral: sympathetic and
parasympathetic
fibers (sensation of fullness)
2. 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

10. Central neural control
• Successful voiders –Rt Inferior frontal gyrus
Rt Ant cingulate gyrus
• Pontine micturition center- M region
• Unable to void – Mid cingulate gyrus Lat bilateral frontal
lobes
• Pontine storage center - L region PAG

11. 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

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

13.  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 open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.
Normal Voiding

14. • In child Controlled by it is 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
DEVELOPMENT IN CHILD

15. MICTURITION(VOIDING) REFLEX

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

17.  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.
Description of Terminology

18. 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
TYPE AND LOCALIZATION
OF BLADDER

19. UMN/LMN/SENSORY LESION

20. 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.

21. TYPE OF BLADDER

22. • 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
LOSS OF SUPRASPINAL CONTROL
(UNINHIBITED BLADDER):

23. • 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
SPINAL CORD LESION ABOVE SACRAL LEVEL
REFLEX NEUROGENIC BLADDER (AUTOMATIC)

24. • 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
SPINAL CORD LESION INVOLVING SACRAL LEVEL
AUTONOMOUS BLADDER:

25. • 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
LESION INVOLVING AFFERENT SENSORY NEURONS
SENSORY NEUROGENIC BLADDER

26. • 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
LESION INVOLVING EFFERENT MOTOR NEURONS
MOTOR PARALYTIC BLADDER:

27. • 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
CORTICAL LESION

28. 1. 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.
2. 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.

29. • 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.
Normal pressure hydrocephalus:

30. 3. 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.
4. 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

31. 5. 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

32.  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
Clinical evaluation - History:

33. • 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
Laboratory Studies

34. • 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
ASSESMENT OF LOWER URINARY
TRACT

35. • 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
INVESTIGATIONS

36. • 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
INVESTIGATIONS

37. • 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
TREATMENT:

38. • 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.
Non-invasive conservative treatment

39. • 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.
• 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
Generic Name-Oxybutynin,Tolterodine,Trospium chloride,propiverin.
Drugs for detrusor overactivity

40. • 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).
Drugs for detrusor underactivity

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

42. • 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 (e-g 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
Intermittent catheterization

43. • 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
TREATMENT