 Central nervous system disorders are
frequent causes of urologic symptoms and
voiding dysfunction
 Appropriate recognition and timely
management relevant to neurological
conditions are important to avoid potentially
irreversible adverse outcomes.
Physiologic functions:
 Low pressure storage of adequate volumes of
urine
 periodic, voluntary expulsion of urine from the
bladder in a coordinated manner.
 coordinated activity mediated by the autonomic
and somatic nervous systems
 Disruption of neurotransmission at any level of the
neuraxis may result in significant alterations in urinary
function.
 hollow organ
 3 layers
 Compliance-dependent on the native
viscoelastic properties of the bladder wall.
 Low bladder compliance results in high urinary
storage pressure, which if unrecognized and
untreated, leads to upper urinary tract
deterioration and renal failure
 S2-4 segments of the spinal cord
 provides excitatory motor input to
the bladder.
 Cholinergic preganglionic neurons
within the intermediolateral
sacral cord send axons to
ganglionic cells within the pelvic
plexus and the bladder wall.
 Postganglionic neurons within the
bladder wall and pelvic plexus
release acetylcholine, which
activates cholinergic receptors on
the detrusor smooth muscle cells
and initiates bladder contraction
 originate in theT11-L2 spinal
segments,
 travel in the sympathetic chain
ganglia to the prevertebral ganglia in
the superior hypogastric and pelvic
plexuses
 innervate the bladder via short
adrenergic neurons.
 The bladder contains varying
expression of α- and β-adrenergic
receptors, and sympathetic
stimulation promotes storage of
urine
 Activation of β-adrenergic receptors within
the wall of the bladder provides inhibition
and relaxation of the detrusor muscle..
 bladder outlet
 α-Adrenergic receptors
predominate
 excitatory input to- results in
increased bladder outlet
closure force.
 internal urethral sphincter or
smooth muscle sphincter, has
a role in the maintenance of
continence and efficient
voiding
 Afferent (sensory) transmission of lower urinary
tract stimuli travels via the pelvic, hypogastric,
and pudendal nerves to the dorsal root ganglia
of the lumbosacral spinal cord.
 The pelvic nerve afferents monitor the volume
and the amplitude of bladder contraction viaAδ
and C fibers
 C fibres are also implicated in the transmission
of urgency and pain.
 The most proximal segment of the urethra in
consists primarily of smooth muscle, which is not
under voluntary control.
 Innervation of the proximal urethra is similar to that
of the bladder neck.
 At the level of the pelvic floor there is a sheet of
striated muscle extrinsic to the urethra, as well a
discrete layer of striated muscle within the wall of
the urethra.
 The extrinsic muscle consists of primarily fast-twitch
muscle fibers and is under voluntary control.
 The intrinsic muscle tissue, also called the intrinsic
sphincter or the rhabdosphincter, consists primary of
slow-twitch fibers and provides passive urinary
continence.
 Innervation of external sphincter and pelvic floor
musculature is primarily somatic from branches of the
pudendal nerve S3 and S4 segments .
 The anteromedial portion of the frontal lobes and
cingulate gyrus are involved in the voluntary initiation of
micturition and inhibition of reflex voiding activity.
 In general, cortical input is inhibitory on micturition
reflexes.
 remove the cortical inhibition, which results in increased
excitatory input to the brainstem, facilitation of the
micturition reflex
 urinary frequency and urgency.
 reflex can be localized to the
pontomesencephalic reticular formation.
 The pontine micturition center (PMC) or
Barrington’s nucleus, functions as a switch to
regulate bladder capacity and coordinate
bladder and external sphincter activity.
 stimulation of the PMC induces the sacral
parasympathetic neurons to fire, which results
in bladder contraction and reflex voiding
 Descending spinal efferent pathways from the
PMC to the sacral cord motor centers are
located in the reticulospinal tracts.
 The pons receives direct ascending input from
the bladder wall afferents, which travel through
the dorsal root ganglia and the posterior
columns of the spinal cord.
 Parasympathetic preganglionic neurons.
 Sympathetic preganglionic neurons.
 Somatic centers innervating the external sphincter
and pelvic floor musculature are localized atOnuf’s
nucleus within the anterior horn of the sacral cord at
the spinal cord level S2-4.
 Descending input toOnuf’s nucleus is derived from
the lateral corticospinal tract
 Efferent somatic stimulation of the external
sphincter begins atS Onuf’s nucleus and
travels thro the pudendal nerves ,innervates
the sphincter and the pelvic floor.
 The central sensorimotor pathways concerned with
micturition and sphincter control can therefore be
summarized as follows
1. The cerebral loop -initiates and inhibits switching between
filling and voiding states
2.Corticospinal pathways - with the voluntary control of the
sphincters and pelvic floor.
3.The cord loop - coordinates detrusor and sphincter
contraction and relaxation.
3
.
4.The urethral reflex loop –maintains the
sphincter tone when the detrusor is inactive.
5.The detrusor reflex loop -causes sphincter
relaxation when the detrusor is active.
 lesions above the level of the sacral bladder center and
below the level of the PMC.
 occurs in conditions causing quadriplegia or paraplegia
MS.
 Loss of the normal inhibition from higher centers results
in detrusor contraction
 urinary frequency, urgency
 The bladder capacity is reduced but residual urine may
be increased
 Simultaneous contraction of the sphincter and
the detrusor during voiding
 results in obstructed voiding, interrupted urinary
stream, incomplete emptying, and high
intravesical pressures because the sphincter
fails to relax correctly
 Upper urinary tract dilatation and kidney
damage may develop subsequently.
 seen with complete lesions below theT12 segment that involve
the conus medullaris and cauda equina.
 occurs with sacral myelomeningocele and tumors of the conus
medullaris–cauda equina region.
 initial shock phase of spinal cord injury.
 The bladder is paralyzed, and there is no awareness of the state
of fullness.
 there is urinary retention because the tone of the detrusor
muscle is abolished and the bladder distends as urine
accumulates.
 Motor paralytic bladder
lesions involving the efferent motor fibers to the
detrusor
painful urinary retention
 Sensory paralytic bladder
tabes dorsalis, syringomyelia, or diabetes mellitus.
caused by the impairment of the afferent pathways
bladder physiology.pptx

bladder physiology.pptx

  • 2.
     Central nervoussystem disorders are frequent causes of urologic symptoms and voiding dysfunction  Appropriate recognition and timely management relevant to neurological conditions are important to avoid potentially irreversible adverse outcomes.
  • 3.
    Physiologic functions:  Lowpressure storage of adequate volumes of urine  periodic, voluntary expulsion of urine from the bladder in a coordinated manner.  coordinated activity mediated by the autonomic and somatic nervous systems  Disruption of neurotransmission at any level of the neuraxis may result in significant alterations in urinary function.
  • 4.
     hollow organ 3 layers  Compliance-dependent on the native viscoelastic properties of the bladder wall.  Low bladder compliance results in high urinary storage pressure, which if unrecognized and untreated, leads to upper urinary tract deterioration and renal failure
  • 5.
     S2-4 segmentsof the spinal cord  provides excitatory motor input to the bladder.  Cholinergic preganglionic neurons within the intermediolateral sacral cord send axons to ganglionic cells within the pelvic plexus and the bladder wall.  Postganglionic neurons within the bladder wall and pelvic plexus release acetylcholine, which activates cholinergic receptors on the detrusor smooth muscle cells and initiates bladder contraction
  • 6.
     originate intheT11-L2 spinal segments,  travel in the sympathetic chain ganglia to the prevertebral ganglia in the superior hypogastric and pelvic plexuses  innervate the bladder via short adrenergic neurons.  The bladder contains varying expression of α- and β-adrenergic receptors, and sympathetic stimulation promotes storage of urine
  • 7.
     Activation ofβ-adrenergic receptors within the wall of the bladder provides inhibition and relaxation of the detrusor muscle..
  • 8.
     bladder outlet α-Adrenergic receptors predominate  excitatory input to- results in increased bladder outlet closure force.  internal urethral sphincter or smooth muscle sphincter, has a role in the maintenance of continence and efficient voiding
  • 9.
     Afferent (sensory)transmission of lower urinary tract stimuli travels via the pelvic, hypogastric, and pudendal nerves to the dorsal root ganglia of the lumbosacral spinal cord.  The pelvic nerve afferents monitor the volume and the amplitude of bladder contraction viaAδ and C fibers  C fibres are also implicated in the transmission of urgency and pain.
  • 10.
     The mostproximal segment of the urethra in consists primarily of smooth muscle, which is not under voluntary control.  Innervation of the proximal urethra is similar to that of the bladder neck.  At the level of the pelvic floor there is a sheet of striated muscle extrinsic to the urethra, as well a discrete layer of striated muscle within the wall of the urethra.
  • 11.
     The extrinsicmuscle consists of primarily fast-twitch muscle fibers and is under voluntary control.  The intrinsic muscle tissue, also called the intrinsic sphincter or the rhabdosphincter, consists primary of slow-twitch fibers and provides passive urinary continence.  Innervation of external sphincter and pelvic floor musculature is primarily somatic from branches of the pudendal nerve S3 and S4 segments .
  • 12.
     The anteromedialportion of the frontal lobes and cingulate gyrus are involved in the voluntary initiation of micturition and inhibition of reflex voiding activity.  In general, cortical input is inhibitory on micturition reflexes.  remove the cortical inhibition, which results in increased excitatory input to the brainstem, facilitation of the micturition reflex  urinary frequency and urgency.
  • 13.
     reflex canbe localized to the pontomesencephalic reticular formation.  The pontine micturition center (PMC) or Barrington’s nucleus, functions as a switch to regulate bladder capacity and coordinate bladder and external sphincter activity.  stimulation of the PMC induces the sacral parasympathetic neurons to fire, which results in bladder contraction and reflex voiding
  • 14.
     Descending spinalefferent pathways from the PMC to the sacral cord motor centers are located in the reticulospinal tracts.  The pons receives direct ascending input from the bladder wall afferents, which travel through the dorsal root ganglia and the posterior columns of the spinal cord.
  • 15.
     Parasympathetic preganglionicneurons.  Sympathetic preganglionic neurons.  Somatic centers innervating the external sphincter and pelvic floor musculature are localized atOnuf’s nucleus within the anterior horn of the sacral cord at the spinal cord level S2-4.  Descending input toOnuf’s nucleus is derived from the lateral corticospinal tract
  • 16.
     Efferent somaticstimulation of the external sphincter begins atS Onuf’s nucleus and travels thro the pudendal nerves ,innervates the sphincter and the pelvic floor.
  • 17.
     The centralsensorimotor pathways concerned with micturition and sphincter control can therefore be summarized as follows 1. The cerebral loop -initiates and inhibits switching between filling and voiding states 2.Corticospinal pathways - with the voluntary control of the sphincters and pelvic floor. 3.The cord loop - coordinates detrusor and sphincter contraction and relaxation. 3 .
  • 18.
    4.The urethral reflexloop –maintains the sphincter tone when the detrusor is inactive. 5.The detrusor reflex loop -causes sphincter relaxation when the detrusor is active.
  • 20.
     lesions abovethe level of the sacral bladder center and below the level of the PMC.  occurs in conditions causing quadriplegia or paraplegia MS.  Loss of the normal inhibition from higher centers results in detrusor contraction  urinary frequency, urgency  The bladder capacity is reduced but residual urine may be increased
  • 21.
     Simultaneous contractionof the sphincter and the detrusor during voiding  results in obstructed voiding, interrupted urinary stream, incomplete emptying, and high intravesical pressures because the sphincter fails to relax correctly  Upper urinary tract dilatation and kidney damage may develop subsequently.
  • 22.
     seen withcomplete lesions below theT12 segment that involve the conus medullaris and cauda equina.  occurs with sacral myelomeningocele and tumors of the conus medullaris–cauda equina region.  initial shock phase of spinal cord injury.  The bladder is paralyzed, and there is no awareness of the state of fullness.  there is urinary retention because the tone of the detrusor muscle is abolished and the bladder distends as urine accumulates.
  • 23.
     Motor paralyticbladder lesions involving the efferent motor fibers to the detrusor painful urinary retention  Sensory paralytic bladder tabes dorsalis, syringomyelia, or diabetes mellitus. caused by the impairment of the afferent pathways