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Physiology of micturition and
Neuroanatomy of bladder
MODERATOR:
• Dr Sanjai Singh
Assisstant prof
DEPT OF PMR
KGMU
PRESENTED BY:
• Dr Joe Antony
JR1
DEPT OF PMR
KGMU
Contents
1) INTRODUCTION
2) ANATOMY OF BLADDER, URETHRAL SPHINCTER & URETHRA
3) INNERVATION OF BLADDER
4) CONTROL OF MICTURITION
5) MECHANISM OF MICTURITION
6) VOIDING PHYSIOLOGY
7) GERIATRIC VOIDING PHYSIOLOGY
8) PAEDIATRIC VOIDING PHYSIOLOGY
9) CLASSIFICATION OF NEUROGENIC BLADDER
10) VOIDING DYSFUNCTION IN NEUROGENIC DISORDERS
INTRODUCTION
Micturition is process of passing urine. This is
primarily reflex phenomena which is mostly
integrated in spinal cord which is further
influenced by activation of higher centres
Urine formation starts in kidney
Urine flows down to bladder through ureter
Urinary bladder stores urine up to critical
volume & empty it at appropriate time following
suitable rise in pressure & critical volume.
BLADDER GROSS ANATOMY:-
It is hollow muscular distensible organ
in pelvis just above & behind pubic
bone.
Empty bladder-tetrahedral in
shape Full bladder -ovoid
It has:-
1) Apex
2) Neck
3) 3 surfaces-
Superior &right and left inferolateral
BLADDER
Anatomically it is divided into:-
DETRUSOR- composed of
smooth m/s bundle that
crisscross & interlace each other.
At bladder neck muscle fibre assume circular
arrangement which allow them to act as
functional sphincter .
TRIGONE:- located at inferior base of bladder.
Extends from urethral orifice to bladder neck.
Normal bladder capacity 400-500ml
URETHRAL SPHINCTER
• INTERNAL SPHINCTER:-
– It is consider as functional
sphincter because there is a
progressive increase in tone
with bladder filling so,that
the urethral pressure is
greater than intravesical
pressure.
• EXTERNAL SPHINCTER :-
– Is under voluntary control.
– The striated m/s fibre has
proportion of slow twitch
fibre with capacity for steady
tonic compression of
urethra.
FUNCTION OF URETHRAL SPHINCTER
External sphincter closed most of the time.
Sensation of filling bladder felt at volume of about 150 ml.
Sensation to pass urine is felt at 150-250ml
.
At 400ml sensation to pass urine become uncomfortable.
At 700ml it become very painful leading to loss of control.
URETHRA
.
Urethra contains inner longitudinal &outer semicircular layer of smooth m/s.
Circular m/s layer exerts a sphinctric effect along entire length.
FEMALE URETHRA is 3-4 cm
MALE URETHRA is 18-20cm
It has-
• Prostatic part (3cm)
• Membranous part (1.5)
• Penile part (15cm)
INNERVATION OF BLADDER
PARASYMPATHETIC FIBERS originates
from DETRUSOR nucleus located in
intermediolatral gray
matter of sacral cord S2, S3 ,S4 to reach bladder
via pelvic nerve
Cholinergic receptors( M2>M3)
Contraction of bladder
(They are mainly distributed in the body of
bladder ,TRIGONE, bladder neck & urethra.)
SYMPATHETIC FIBERS originates in
intermediolateral gray column from T11 toL2
& reach bladder via hypogastric nerve.
Alpha receptor concentrated in
TRIGONE, bladder neck, urethra leading
to maintenance of continence by
contracting bladder neck.
beta receptor concentrated in body of
bladder leading to its relaxation which
enhance storage.
SENSORY /AFFERENT FIBERS:PELVIC NERVE
It has 2 types:-
Small myelinated A delta:- Respond in graded fashion to
bladder distension which is needed for normal voiding.
Unmyelinated C fibers:- They do not respond to bladder
distension. Only activated by chemical or cold temperature
irritating bladder wall.
INNERVATION OF URETHRAL SPHINCTER
INTERNAL SPHINCTER:-
innervated by sympathetic & parasympathetic nerve
therefore it is under autonomic control.
EXTERNAL SPHINCTER:- somatic fibers originated from
S2 ,S3, S4 innervate bladder & external sphincter via
pudendal nerve.
INNERVATION OF BLADDER &URETHRAL SPHINCTER
CONTROL OF MICTURITION
•Micturition reflex controlled by brain stem.
Facilitatory area and area of
coordination present in pons
•Inhibitory area present in
midbrain
•Posterior hypothalamus facilitatory areafor
micturition
•Cortex has voluntary inhibitory control on
micturition
MICTURITION REFLEX
Filling of bladder
Stimulates stretch receptor (A delta
fibers) present in wall of bladder
Center for spinal reflex is sacral S2,3
&4 segment of spinal cord
Stimulate motor fibre of
parasympathetic system causing
contraction of detrusor muscle
leading to MICTURATION
VOIDING PHYSIOLOGY
FILLING PHASE
There is little rise in bladder pressure
Intravesical pressure is maintained by sympathetic stimulation
beta receptor, alpha receptor- increase in urethral sphincter tone
Full intravesical pressure (0-6cm of H2O &it should not be>15 cm of H2O
Filling continued leading to steady progressive rise in intravesical pressure
EMPTYING PHASE
Cessation of urethral sphincter pressure & funneling of bladder neck
No reflex inhibition to sacral micturation centre from sphincter
Detrusor contraction
Urethral sphincter kept open throughout micturition & no rise in
intravesical pressure during voiding
GERIATRIC VOIDING PHYSIOLOGY
The Kidney undergoes age related changes in which there is :-
1) decrease in Glomerular blood flow & renal blood
flow 2). decrease in concentrating ability
There is increase urgency with increase daytime frequency
&nocturia ,incontinence & incomplete emptying in absence
of identified cause.
Urodynamic studies shows that older adults have involuntary
bladder contraction during filling which leads to these symptoms.
PEDIATRIC VOIDING PHYSIOLOGY
In newborn sacral micturition reflex is primarily responsible for voiding.
There is little inhibition of micturition reflex from the cerebral cortex.
Neonates & infants have involuntary reflex voiding occur at 50-100ml.
At 1yr childshows awareness of bladder evacuation & can begin to delay
urination for a brief period by contracting sphincter
voluntary.
5yrs 90% children voluntary control of micturition.
CLASSIFICATION
OF
NEUROGENIC
BLADDER
CLASSIFICATION OF NEUROGENIC BLADDER
VOIDING DYSFUNCTION IN
NEUROLOGICAL DISORDERS
• Supra pontine lesions
• Supra sacral/ Pontine lesions
• Sacral spinal cord lesions
• Infra sacral lesions
Supra pontine lesions
• Lesions- CVA,degenerative diseases, hydrocephalus,
IC neoplasms,TBI, Parkinsons disease, Multiple
sclerosis
• Inability to initiate voiding, inappropriate timing,
detrusor overactivity incontinence
• Normal detrussor- sphincter synergy
PARKINSON’S DISEASE
•Delayed relaxation of sphincter
•Delay in urine flow on attempted voiding
•If pontine micturition center is also affected, urinary retention
and overflow incontinence ( acontractile bladder)
Multiple sclerosis
•In this 90% pt. develop urinary manifestation.
•White matter of spinal cord also involved to
a varying degree
•Presents with variable features
SURASACRAL SPINAL CORD/PONTINE
LESION
Traumatic SCI - m/c suprasacral lesion affecting voiding.
Other cause are:- transverse myelitis,
primary or metastatic tumour etc.
Initial period of spinal shock - Areflexia of somatic
system below level of injury- detrusor areflexia – urinary
retention
• Initial reflex return ( such as bulbo cavernous reflex) in 1-3 days
• Recovery of bladder function follows recovery of skeletal muscle reflexes
• Spinal shock is not an all or nothing phenomenon
• Beginning of involuntary bladder contractions- can be considered as ‘Out
of spinal shock’- Usually 6-8 weeks
– BCR
– ICE WATER TEST
•Detrusor areflexia - Uninhibited bladder contraction
become stronger leading to postvoidal residual
volume decrease.
•PVR reaches lowest by 12 weeks of injury
•After that, expected finding will be, detrusor
overactivity with significant detrussor-sphincter-
dyssenergia, resulting in significant PVR ( high
pressure bladder)
SACRAL LESION
•LESION ARE:
1. spinal trauma,
2. herniated lumbar disc,
3. primary or metastatic tumour
4. lumbar stenosis,
5. intervertebral disc protrusion & prolapse
leading to cauda equina syndrome.
Damage to sacral cord or root
Acontractile bladder usually with
impaired sphincter activity (decreased
compliance may or may not be seen)
In partial injury
Areflexia with decrease bladder
compliance- progressive increase in
vesical pressure
PERIPHERAL LESION
M/c lesion is peripheral neuropathy secondary to DM.
Other cause are:- Chronic alcoholism,
• herpes zoster,
• GB syndrome,pelvic surgery.
there is decrease bladder sensation, bladder
overdistension and increased PVRs
• Thank you

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neuroantomy of bladder

  • 1. Physiology of micturition and Neuroanatomy of bladder MODERATOR: • Dr Sanjai Singh Assisstant prof DEPT OF PMR KGMU PRESENTED BY: • Dr Joe Antony JR1 DEPT OF PMR KGMU
  • 2. Contents 1) INTRODUCTION 2) ANATOMY OF BLADDER, URETHRAL SPHINCTER & URETHRA 3) INNERVATION OF BLADDER 4) CONTROL OF MICTURITION 5) MECHANISM OF MICTURITION 6) VOIDING PHYSIOLOGY 7) GERIATRIC VOIDING PHYSIOLOGY 8) PAEDIATRIC VOIDING PHYSIOLOGY 9) CLASSIFICATION OF NEUROGENIC BLADDER 10) VOIDING DYSFUNCTION IN NEUROGENIC DISORDERS
  • 3. INTRODUCTION Micturition is process of passing urine. This is primarily reflex phenomena which is mostly integrated in spinal cord which is further influenced by activation of higher centres Urine formation starts in kidney Urine flows down to bladder through ureter Urinary bladder stores urine up to critical volume & empty it at appropriate time following suitable rise in pressure & critical volume.
  • 4. BLADDER GROSS ANATOMY:- It is hollow muscular distensible organ in pelvis just above & behind pubic bone. Empty bladder-tetrahedral in shape Full bladder -ovoid It has:- 1) Apex 2) Neck 3) 3 surfaces- Superior &right and left inferolateral
  • 5. BLADDER Anatomically it is divided into:- DETRUSOR- composed of smooth m/s bundle that crisscross & interlace each other. At bladder neck muscle fibre assume circular arrangement which allow them to act as functional sphincter . TRIGONE:- located at inferior base of bladder. Extends from urethral orifice to bladder neck. Normal bladder capacity 400-500ml
  • 6. URETHRAL SPHINCTER • INTERNAL SPHINCTER:- – It is consider as functional sphincter because there is a progressive increase in tone with bladder filling so,that the urethral pressure is greater than intravesical pressure. • EXTERNAL SPHINCTER :- – Is under voluntary control. – The striated m/s fibre has proportion of slow twitch fibre with capacity for steady tonic compression of urethra.
  • 7. FUNCTION OF URETHRAL SPHINCTER External sphincter closed most of the time. Sensation of filling bladder felt at volume of about 150 ml. Sensation to pass urine is felt at 150-250ml . At 400ml sensation to pass urine become uncomfortable. At 700ml it become very painful leading to loss of control.
  • 8. URETHRA . Urethra contains inner longitudinal &outer semicircular layer of smooth m/s. Circular m/s layer exerts a sphinctric effect along entire length. FEMALE URETHRA is 3-4 cm MALE URETHRA is 18-20cm It has- • Prostatic part (3cm) • Membranous part (1.5) • Penile part (15cm)
  • 9. INNERVATION OF BLADDER PARASYMPATHETIC FIBERS originates from DETRUSOR nucleus located in intermediolatral gray matter of sacral cord S2, S3 ,S4 to reach bladder via pelvic nerve Cholinergic receptors( M2>M3) Contraction of bladder (They are mainly distributed in the body of bladder ,TRIGONE, bladder neck & urethra.)
  • 10. SYMPATHETIC FIBERS originates in intermediolateral gray column from T11 toL2 & reach bladder via hypogastric nerve. Alpha receptor concentrated in TRIGONE, bladder neck, urethra leading to maintenance of continence by contracting bladder neck. beta receptor concentrated in body of bladder leading to its relaxation which enhance storage.
  • 11. SENSORY /AFFERENT FIBERS:PELVIC NERVE It has 2 types:- Small myelinated A delta:- Respond in graded fashion to bladder distension which is needed for normal voiding. Unmyelinated C fibers:- They do not respond to bladder distension. Only activated by chemical or cold temperature irritating bladder wall.
  • 12. INNERVATION OF URETHRAL SPHINCTER INTERNAL SPHINCTER:- innervated by sympathetic & parasympathetic nerve therefore it is under autonomic control. EXTERNAL SPHINCTER:- somatic fibers originated from S2 ,S3, S4 innervate bladder & external sphincter via pudendal nerve.
  • 13. INNERVATION OF BLADDER &URETHRAL SPHINCTER
  • 14. CONTROL OF MICTURITION •Micturition reflex controlled by brain stem. Facilitatory area and area of coordination present in pons •Inhibitory area present in midbrain •Posterior hypothalamus facilitatory areafor micturition •Cortex has voluntary inhibitory control on micturition
  • 15. MICTURITION REFLEX Filling of bladder Stimulates stretch receptor (A delta fibers) present in wall of bladder Center for spinal reflex is sacral S2,3 &4 segment of spinal cord Stimulate motor fibre of parasympathetic system causing contraction of detrusor muscle leading to MICTURATION
  • 16. VOIDING PHYSIOLOGY FILLING PHASE There is little rise in bladder pressure Intravesical pressure is maintained by sympathetic stimulation beta receptor, alpha receptor- increase in urethral sphincter tone Full intravesical pressure (0-6cm of H2O &it should not be>15 cm of H2O Filling continued leading to steady progressive rise in intravesical pressure
  • 17. EMPTYING PHASE Cessation of urethral sphincter pressure & funneling of bladder neck No reflex inhibition to sacral micturation centre from sphincter Detrusor contraction Urethral sphincter kept open throughout micturition & no rise in intravesical pressure during voiding
  • 18. GERIATRIC VOIDING PHYSIOLOGY The Kidney undergoes age related changes in which there is :- 1) decrease in Glomerular blood flow & renal blood flow 2). decrease in concentrating ability There is increase urgency with increase daytime frequency &nocturia ,incontinence & incomplete emptying in absence of identified cause. Urodynamic studies shows that older adults have involuntary bladder contraction during filling which leads to these symptoms.
  • 19. PEDIATRIC VOIDING PHYSIOLOGY In newborn sacral micturition reflex is primarily responsible for voiding. There is little inhibition of micturition reflex from the cerebral cortex. Neonates & infants have involuntary reflex voiding occur at 50-100ml. At 1yr childshows awareness of bladder evacuation & can begin to delay urination for a brief period by contracting sphincter voluntary. 5yrs 90% children voluntary control of micturition.
  • 22. VOIDING DYSFUNCTION IN NEUROLOGICAL DISORDERS • Supra pontine lesions • Supra sacral/ Pontine lesions • Sacral spinal cord lesions • Infra sacral lesions
  • 23. Supra pontine lesions • Lesions- CVA,degenerative diseases, hydrocephalus, IC neoplasms,TBI, Parkinsons disease, Multiple sclerosis • Inability to initiate voiding, inappropriate timing, detrusor overactivity incontinence • Normal detrussor- sphincter synergy
  • 24. PARKINSON’S DISEASE •Delayed relaxation of sphincter •Delay in urine flow on attempted voiding •If pontine micturition center is also affected, urinary retention and overflow incontinence ( acontractile bladder)
  • 25. Multiple sclerosis •In this 90% pt. develop urinary manifestation. •White matter of spinal cord also involved to a varying degree •Presents with variable features
  • 26. SURASACRAL SPINAL CORD/PONTINE LESION Traumatic SCI - m/c suprasacral lesion affecting voiding. Other cause are:- transverse myelitis, primary or metastatic tumour etc. Initial period of spinal shock - Areflexia of somatic system below level of injury- detrusor areflexia – urinary retention
  • 27. • Initial reflex return ( such as bulbo cavernous reflex) in 1-3 days • Recovery of bladder function follows recovery of skeletal muscle reflexes • Spinal shock is not an all or nothing phenomenon • Beginning of involuntary bladder contractions- can be considered as ‘Out of spinal shock’- Usually 6-8 weeks – BCR – ICE WATER TEST
  • 28. •Detrusor areflexia - Uninhibited bladder contraction become stronger leading to postvoidal residual volume decrease. •PVR reaches lowest by 12 weeks of injury •After that, expected finding will be, detrusor overactivity with significant detrussor-sphincter- dyssenergia, resulting in significant PVR ( high pressure bladder)
  • 29. SACRAL LESION •LESION ARE: 1. spinal trauma, 2. herniated lumbar disc, 3. primary or metastatic tumour 4. lumbar stenosis, 5. intervertebral disc protrusion & prolapse leading to cauda equina syndrome.
  • 30. Damage to sacral cord or root Acontractile bladder usually with impaired sphincter activity (decreased compliance may or may not be seen) In partial injury Areflexia with decrease bladder compliance- progressive increase in vesical pressure
  • 31. PERIPHERAL LESION M/c lesion is peripheral neuropathy secondary to DM. Other cause are:- Chronic alcoholism, • herpes zoster, • GB syndrome,pelvic surgery. there is decrease bladder sensation, bladder overdistension and increased PVRs