NEUROGENIC
BLADDER
Dr Ashutosh Ojha
Mob-
9719713786(WhatsApp)
ashutosh8116@gmail.com
Outline of
the
presentation
Introduction
Applied physiology
Symptomatology
Types according to levels of
bladder dysfunction
Investigations
Treatment available
Why
understanding
of Bladder
15% of all population have some bladder dysfunction if
thoroughly investigated and worked upon.
People above 60 years have …50% bladder symptoms
Bladder dysfunction ..makes a patients ..smelling
…even untouchable …
Most of the dysfunction are treatable
Even good history and clinical examination can lead to
Diagnosis
Very few patients require sophisticated investigation
Hence..I PLEAD your valuable ATTENTION
Bladder
functions
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.
ANATOMY-UB
• 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
ANATOMY..BL 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)
3.Spinal micturition
centre
4. Peripheral nerves
1.Cortical micturition centre
2.Pontine micturition centre(PMC)
Sympathetic
(T11 –L2)
Parasympathetic
( S2,3,4)
(S2,3,4)
Control of micturition
Cortical
micturation
centre(CMC)
• Location: Paracentral lobule in the
medial aspect of the frontoparietal cortex
• Function: Inhibitory to PMC
• Dysfunction – loss of social
control of bladder
• The brain’s control of the PMC is
part of the social training that
children experience at age 2 - 4
years
Pontine
Micturition
Centre
(PMC)
• Also called Barrington’s nucleus
• Lateral region
• Function - continence, storage urine
stimulation results in a powerful
contraction of the urethral sphincter
• Medial region
• Function - micturition center
• stimulation results in decrease in
urethral pressure and silence of pelvic
floor EMG signal, followed by a rise in
detrusor pressure.
Sacral reflex or Sacral/Primitive
micturition centre (SMC/PMC)
1.Sacral parasympathetic nucleus
(SPN): S234- pelvic splanchnic
nerves (nervi erigentes) arise from
2.Somatic – Onufoid nuclei
Collection of external urethral
sphinter motoneurones
3. Levator Ani Motoneurones
Peripheral innervation
Stimulation Response
Parasympathetic
(S 2-4)
Excitatory to
detrusor, relaxes
sphincter -Helps void
Sympathetic
(T11- L2)
Inhibitory to detrusor,
↑trigone & Urethral
tone
Somatic ( S2 - 4) Excitatory to the
external sphincter
Micturition reflex
Internal sphincter –
no important role in micturition,
prevents leakage during filling and
prevents reflux of semen into bladder during
ejaculation
Sympathetic nerves –
no part in micturition
The Micturition Reflex
Sensation of bladder fullness via pelvic
and pudendal nerves to S 2,3,4
Periaqueductal gray matter
Medial Pontine micturition center
Frontal lobe decides social
appropriateness
Detrussor center (S 2,3,4) to pelvic nerves Onuf’s nucleus to pudendal nerves
RECIPROCAL ACTIVITY BETWEEN SPHINCTER & DETRUSOR
Micturition
On-off switch
Relay
center
Primitive
voiding
Cerebral
PMC
SMC
Symptomatology
Detrusor Hypereflexia
Detrusor Sphincter Dyssynergia
Resultant
• Poorly sustained hyperreflexic bladder
contraction (DH) and(DSD)
• Raised post voiding residual (PVR)
Exacerbation of symptoms
Extrapyramidal diseases
• Extrapyramidal features
• MSA, Parkinsons disease
• Autonomic dysfunction
• Cerebellar signs
Suprapontine
• Frontal lobe disorders
• Dementia, personality
change
• Aware about incontinence
unless extensive lesions
• Severe urgency, frequency &
urge incontinence without
dementia, socially aware
and embarrassed by
incontinence
• Urinary retention
Spinal Cord
• Signs of upper motor
neuron lesion in the
lower limbs (unless the
lesion is central
intramedullary and small)
• Erectile dysfunction in
men
• +/- Paraparesis
Brainstem
• Marked neurological
deficits dorsal and
discreet lesion defect
of bladder function
• MLF lesion
Internuclear
ophthalmoplegia
Neuropathy
• Long history of
neuropathic symptoms,
• Stocking glove
anesthesia
• Absent knee and ankle
jerks will be absent
• Small fiber sensory
impairment
demonstrable to the
level of the ankles
• Other features of
autonomic involvement
• Sexual dysfunction
• Bladder, sexual &
bowel dysfunction
• S 2, 3, 4 sensory loss
• Lax anal sphincter
• Bulbocavernosus (sacral
• reflexes) reflex lost
• +/- Foot deformities,
lower limb
abnormalities
• Cutaneous markers over
the back & sacrum
Cauda equina
Types according to
the level of bladder
dysfunction
a) Suprapontine/cortical lesion –
“Uninhibited /Cortical bladder”
Severe urgency, frequency & urge incontinence
with dementia – incontinent and inappropriate
voiding
without dementia- socially aware & embarrassed
by their incontinence.
b) Pontine lesion –
“ Reflex / Automatic bladder”
DH,
Arreflexia in pts with INO
c) Spinal (subpontine/suprasacral)
“ Spastic Bladder”
Disorders of storage and emptying
DSD (true only if above T6 level), DH
d) Sacral and subsacral lesions
I) Afferent fibres involved only –
“Atonic /Areflexic bladder”
Overflow incontinence
Straining for micturition
No DSD, no DH
II) Both afferent and efferent involved –
“Autonomous bladder”
Small capacity , acting of its own. No DSD/DH
UMN-
SPASTIC
LMN-
FLACCID
AREFLEXIC
Cerebral
PMC
SMC
Causes of various levels of dysfunction
a) Suprapontine and Pontine Causes
• Stroke
• Tumors
• Dementia (AD,FTD)
Spinal causes (subpontine/suprasacral)
Sacral and Subsacral causes
Management-
Investigations
• Noninvasive bladder investigations-
• Post void residual volume –
• In without catheterization,Ultrasound (
N is <100ml)
• Uroflowmetry-
• Voided volume ( >100ml)
• Maximal flow, maximal and average flow
rate (M > 20ml/sec and F > 15ml/sec)
Cystometry-
• Measure detrusor
pressure (Intravesical
pressure & Rectal
pressure)
• Bladder infused till 400 to 600ml –
Pressure shouldnot rise to >15cm water
(Stable bladder)
• Neurogenic detrusor overactivity –
Involutary detrusor contraction during
filling phase
• Voiding phase – Detrusor pressure
• M<50cm of
water
F < 30cm water
Sphincter EMG –
Reinnervation with prolonged duration of
MUAPs
Neuroimaging –MRI
Cauda equina & conus lesions, spinal,
supra pontine and pontine lesions
Treatment - Detrusor overactivity
• Anticholinergics
- Oxybutynin, Tolterodine
- M3 blockers- Darifenacin
• Tricyclic antidepressants
- Imipramine
• Desmopressin intranasally – once in 24 hrs
• Botulinum toxin A
• Intravesical capsaicin –
instilled with a balloon catheter
Neurogenic Detrusor overactivity
Treatment
Only Urinary Retention
(If residual volume > 100ml)
• Clean intermittent self
catheterisation (CISC)
• Permanent indwelling
catheter
Detrusor overactivity &
Retention
• Anticholinergic drugs
• CISC
Treatment
• External device – condom catheter
• Sacral nerve stimulators – for DI
• Nerve root stimulators – S 2,3,4 for voiding
assisting defecation
• Surgery – Augmentation cystoplasty, artificial
sphincter, urinary diversion with stoma
collection bag
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
•Thank you
References
• Harrisons’ Principles of Internal Medicine
• Victor Adam Neurology
• Adam Atlas of Anatomy
• The whole presentation made to help PG Intenal
Med/ Surgery / Neurology and UG students …
Comments requested at
• Mob-+919719713786(WhatsApp Only)
• Email- ashutosh8116@gmail.com
• Reader ,Internal Medicine …..

Neurogenic bladder UG & PG

  • 1.
  • 2.
    Outline of the presentation Introduction Applied physiology Symptomatology Typesaccording to levels of bladder dysfunction Investigations Treatment available
  • 3.
    Why understanding of Bladder 15% ofall population have some bladder dysfunction if thoroughly investigated and worked upon. People above 60 years have …50% bladder symptoms Bladder dysfunction ..makes a patients ..smelling …even untouchable … Most of the dysfunction are treatable Even good history and clinical examination can lead to Diagnosis Very few patients require sophisticated investigation Hence..I PLEAD your valuable ATTENTION
  • 4.
    Bladder functions Storage - atlow 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.
  • 5.
    ANATOMY-UB • External urethralsphincter :- 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.
    ANATOMY..BL Neck • Thebladder 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)
  • 7.
    3.Spinal micturition centre 4. Peripheralnerves 1.Cortical micturition centre 2.Pontine micturition centre(PMC) Sympathetic (T11 –L2) Parasympathetic ( S2,3,4) (S2,3,4) Control of micturition
  • 8.
    Cortical micturation centre(CMC) • Location: Paracentrallobule in the medial aspect of the frontoparietal cortex • Function: Inhibitory to PMC • Dysfunction – loss of social control of bladder • The brain’s control of the PMC is part of the social training that children experience at age 2 - 4 years
  • 9.
    Pontine Micturition Centre (PMC) • Also calledBarrington’s nucleus • Lateral region • Function - continence, storage urine stimulation results in a powerful contraction of the urethral sphincter • Medial region • Function - micturition center • stimulation results in decrease in urethral pressure and silence of pelvic floor EMG signal, followed by a rise in detrusor pressure.
  • 10.
    Sacral reflex orSacral/Primitive micturition centre (SMC/PMC) 1.Sacral parasympathetic nucleus (SPN): S234- pelvic splanchnic nerves (nervi erigentes) arise from 2.Somatic – Onufoid nuclei Collection of external urethral sphinter motoneurones 3. Levator Ani Motoneurones
  • 11.
  • 12.
    Stimulation Response Parasympathetic (S 2-4) Excitatoryto detrusor, relaxes sphincter -Helps void Sympathetic (T11- L2) Inhibitory to detrusor, ↑trigone & Urethral tone Somatic ( S2 - 4) Excitatory to the external sphincter
  • 13.
    Micturition reflex Internal sphincter– no important role in micturition, prevents leakage during filling and prevents reflux of semen into bladder during ejaculation Sympathetic nerves – no part in micturition
  • 14.
    The Micturition Reflex Sensationof bladder fullness via pelvic and pudendal nerves to S 2,3,4 Periaqueductal gray matter Medial Pontine micturition center Frontal lobe decides social appropriateness Detrussor center (S 2,3,4) to pelvic nerves Onuf’s nucleus to pudendal nerves RECIPROCAL ACTIVITY BETWEEN SPHINCTER & DETRUSOR Micturition
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
    Resultant • Poorly sustainedhyperreflexic bladder contraction (DH) and(DSD) • Raised post voiding residual (PVR) Exacerbation of symptoms
  • 21.
    Extrapyramidal diseases • Extrapyramidalfeatures • MSA, Parkinsons disease • Autonomic dysfunction • Cerebellar signs Suprapontine • Frontal lobe disorders • Dementia, personality change • Aware about incontinence unless extensive lesions • Severe urgency, frequency & urge incontinence without dementia, socially aware and embarrassed by incontinence • Urinary retention
  • 22.
    Spinal Cord • Signsof upper motor neuron lesion in the lower limbs (unless the lesion is central intramedullary and small) • Erectile dysfunction in men • +/- Paraparesis Brainstem • Marked neurological deficits dorsal and discreet lesion defect of bladder function • MLF lesion Internuclear ophthalmoplegia
  • 23.
    Neuropathy • Long historyof neuropathic symptoms, • Stocking glove anesthesia • Absent knee and ankle jerks will be absent • Small fiber sensory impairment demonstrable to the level of the ankles • Other features of autonomic involvement • Sexual dysfunction • Bladder, sexual & bowel dysfunction • S 2, 3, 4 sensory loss • Lax anal sphincter • Bulbocavernosus (sacral • reflexes) reflex lost • +/- Foot deformities, lower limb abnormalities • Cutaneous markers over the back & sacrum Cauda equina
  • 24.
    Types according to thelevel of bladder dysfunction
  • 26.
    a) Suprapontine/cortical lesion– “Uninhibited /Cortical bladder” Severe urgency, frequency & urge incontinence with dementia – incontinent and inappropriate voiding without dementia- socially aware & embarrassed by their incontinence.
  • 27.
    b) Pontine lesion– “ Reflex / Automatic bladder” DH, Arreflexia in pts with INO c) Spinal (subpontine/suprasacral) “ Spastic Bladder” Disorders of storage and emptying DSD (true only if above T6 level), DH
  • 28.
    d) Sacral andsubsacral lesions I) Afferent fibres involved only – “Atonic /Areflexic bladder” Overflow incontinence Straining for micturition No DSD, no DH II) Both afferent and efferent involved – “Autonomous bladder” Small capacity , acting of its own. No DSD/DH
  • 29.
  • 30.
    Causes of variouslevels of dysfunction a) Suprapontine and Pontine Causes • Stroke • Tumors • Dementia (AD,FTD)
  • 31.
  • 32.
  • 33.
    Management- Investigations • Noninvasive bladderinvestigations- • Post void residual volume – • In without catheterization,Ultrasound ( N is <100ml) • Uroflowmetry- • Voided volume ( >100ml) • Maximal flow, maximal and average flow rate (M > 20ml/sec and F > 15ml/sec)
  • 34.
    Cystometry- • Measure detrusor pressure(Intravesical pressure & Rectal pressure) • Bladder infused till 400 to 600ml – Pressure shouldnot rise to >15cm water (Stable bladder) • Neurogenic detrusor overactivity – Involutary detrusor contraction during filling phase • Voiding phase – Detrusor pressure • M<50cm of water F < 30cm water
  • 35.
    Sphincter EMG – Reinnervationwith prolonged duration of MUAPs Neuroimaging –MRI Cauda equina & conus lesions, spinal, supra pontine and pontine lesions
  • 36.
    Treatment - Detrusoroveractivity • Anticholinergics - Oxybutynin, Tolterodine - M3 blockers- Darifenacin • Tricyclic antidepressants - Imipramine • Desmopressin intranasally – once in 24 hrs • Botulinum toxin A • Intravesical capsaicin – instilled with a balloon catheter
  • 37.
  • 38.
    Treatment Only Urinary Retention (Ifresidual volume > 100ml) • Clean intermittent self catheterisation (CISC) • Permanent indwelling catheter Detrusor overactivity & Retention • Anticholinergic drugs • CISC
  • 39.
    Treatment • External device– condom catheter • Sacral nerve stimulators – for DI • Nerve root stimulators – S 2,3,4 for voiding assisting defecation • Surgery – Augmentation cystoplasty, artificial sphincter, urinary diversion with stoma collection bag
  • 40.
    TAKE MY MESSAGE • • • • • • • Complaintsabout 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
  • 41.
  • 42.
    References • Harrisons’ Principlesof Internal Medicine • Victor Adam Neurology • Adam Atlas of Anatomy • The whole presentation made to help PG Intenal Med/ Surgery / Neurology and UG students …
  • 43.
    Comments requested at •Mob-+919719713786(WhatsApp Only) • Email- ashutosh8116@gmail.com • Reader ,Internal Medicine …..