ANATOMY OF BLADDER
The lower part of the bladder neck
is also called the posterior
urethra because of its relation
to the urethra
The smooth muscle of the bladder
is called the detrusor muscle
The bladder neck (posterior
urethra) is a 2 to 3 cm long,
and its wall is composed of
detrusor muscle interlaced
with a large amount of elastic
The muscle in this area is
called the internal sphincter
Beyond the posterior urethra,
the urethra passes through the
urogenital diaphragm, which
contain a layer of muscle called
the external sphincter of the
Tonicaly contracted normaly
The bladder outlet: trigone, ureterovesical junction, bladder neck, and
α-Adr receptors predominate in this area, and stimulation of
postganglionic α-adr receptors provides excitatory input to bladder outlet
that results in increased bladder outlet closure force.
Proximal/internal (smooth muscle sphincter)‐formed by circular
smooth muscle fibers at bladder neck and proximal prostatic urethra.
Distal/external (striated sphincter)‐
‐‐Slow twitch fibers responsible for baseline tonic activity
‐‐Fast twitch responsible for voluntary contractions
Parasympathetic innervation (pelvic nerve) mediates-
Detrusor muscle contraction (ACh, M3 muscarinic receptors)
Relaxation of IUS (NO)
Sympathetic innervation (hypogastric nerve) mediates-
Relaxation of detrusor β3-adrenoceptors).
contraction of IUS (NA α1-adrenoceptors)
Arises from the spinal motoneurones of Onuf’s nucleus(S2–S4).
During storage, pudendal nerve keeps the striated urethral sphincter closed.
Preganglionic neurons (PGNs) of
Parasympathetic----Sacral segment. Iintermediate grey matter (laminae
V–VII) of spinal cord.
Sympathetic ---- Lumbar segment. Iintermediate grey matter (laminae V–
VII) of spinal cord.
Parasympathetic PGNs send dendrites into the dorsal commissure and
into the lateral funiculus and lateral dorsal horn of the spinal cord and
exhibit an extensive axon collateral system that is distributed bilaterally in
The somatic motor neurons that innervate the EUS are located in the
ventral horn (lamina IX) in Onuf's nucleus.
Interneurons in the lumbo-sacral spinal cord that are involved in LUT
function are located in the dorsal commissure, the superficial dorsal horn
and the parasympathetic nucleus.
Some of these interneurons send long projections to the
brain, whereas others make local connections in the spinal
cord and participate in segmental spinal reflexes.
In the brain, some neurons are specific for micturition:
The neurons of Barrington's nucleus (also called the pontine
micturition centre (PMC)
The periaqueductal grey (PAG),
Cell groups in the caudal and preoptic hypothalamus.
The neurons of several parts of the cerebral cortex, in particular the
medial frontal cortex.
Physiology of micturition
As the bladder fills with urine, the wall stretches, impulse are initiated by stretch
receptors in the bladder wall causing sensory signals to convey to the dorsal nerve
root S2,3,4 segments of spinal cord through pelvic nerves and then back to the
urinary bladder through parasympathetic fibres in the same nerve.
During this reflex sympathetic effrents are reflexly inhibited.
FRONTAL LOBE: Inhibitory
-Distention of bladder produces low-level
bladder afferent firing.
-This in turn stimulates the symp outflow
to outlet and pudendal outflow to EUS.
-These responses occur by spinal reflex
pathways and represent “guarding
reflexes,” which promote continence.
-Sympathetic firing also inhibits detrusor
muscle and transmission in bladder
At the initiation of micturition, intense
vesical aff activity activates
spinobulbospinal reflex pathway, then,
• Activation PMC via PAG, which inhibits
pudendal outflow to EUS and sympathetic
outflow to detrusor, and later it stimulates
parasympathetic outflow to detrusor and
urethra leading to voiding.
Neuroanatomy of bladder control
Antero medial frontal lobes involved in voluntary initiation and
inhibition of micturition, delay of reflex voiding.
Sends inhibitory signals to detrusor
To avoid voiding till an appropriate location is found
Has connection with pons; and corticospinal fibres synapse with motor
nuclei controlling striated sphincter
Pontine micturition centre
At pontomesencephalic reticular formation (barrington nucleus)
Dorsomedial tegmental region – center for micturiton ( M-region )
Ventrolateral pontine tegmentum - center for storage (L-region)
Affected by emotions, some people may experience incontinence when
they are excited or scared
Pontine Micturition Center
Bladder filling detrusor muscle
stretch receptors signal to the
pons Frontal lobe
Perception of this signal (bladder
fullness) as a sudden desire to go
to the bathroom
Normally, the brain sends an
inhibitory signal to the Pons to
inhibit the bladder from
contracting until a bathroom is
Urge to urinate disappears
When urination appropriate,
brain sends excitatory signals to
the Pons, allowing voiding.
Somatic (S2‐S4), Pudendal nerves(Excitatory to external sphincter)
Parasympathetic (S2‐S4) (Excitatory to bladder)
--Hypogastric nerves to pelvic ganglia
--Inhibitory to bladder body, excitatory to bladder base/urethra
Neurogenic bladder dysfunction
This has been classified by Lapides into :
1. Uninhibited bladder
2. Reflex neurogenic bladder
3. Sensory paralytic bladder
4. Motor paralytic bladder
5. Autonomous bladder
Dysfunctions in Neurological Disorders
Spinal or Suprasacral lesions
At or distal to Sacral lesion
Urgency: “the complaint of a sudden compelling desire to void, which
is difficult to defer”
Nocturia: when he/she wakes at night one or more times to void.
Frequency: 8->8 void/24 hour
Incontinence: inability to hold urine
Urge incontinence: sudden, intense urge to urinate followed by an
involuntary loss of urine.
Hesitancy: difficulty in begining a urination reflex.
Straining to void
Loss of cortical inhibition of
P Normal + Var
Interruption of descending
autonomic tract and ascending
sensory pathway leading to reflex
and involuntary micturition
+ + ++
cauda or N
Interrutption of sensory and motor
supply leading to loss of reflex
and volutary control
No + +++
Interruption of sensory supply A
No + +++
Interruption of motor supply P Reduced
No + +++
Mixed type A bladder: that damage the detrusor nucleus but spare the
Renders the detrusor flaccid (also referred to as detrusor areflexia), while the
intact pudendal nucleus is spastic producing a hypertonic EUS.
The bladder is large and has low pressure, so the spastic EUS produces
Mixed type B bladder: that spare the detrusor n. but damage the pudendal n.
Flaccid EUS and spastic bladder.
The bladder capacity is low but vesicular pressures are usually not elevated
since there is little outflow resistance.
SUPRAPONTINE LESIONS :
Decreased descend inhibitory input to pons.
Coordinated activity of the sphincter and the
Urgency, frequency, nocturia, and
occasionally urge incontinence.
Filling upto a normal threshold of 300‐350ml
Bladder emptying too quickly and too often,
with relatively low volumes of urine.
CVA, Brain tumors, Hydrocephalus.
SPINAL CORD INJURY
(1) above spinal segment T6,
(2) below T6 to the sacral cord
(3) distal to the sacral cord (cauda equina).
Bladder contractility and reflex contraction are dependent on an intact
sacral cord and sacral reflex arcs, with injury to the sacral segments of the
spinal cord resulting in detrusor areflexia and fixed EUS tone.
Initially, flaccid muscle paralysis and absent somatic activity as well as
suppressed autonomic activity below the lesion.
Absence of sensation and motor function, loss of voluntary control and
The bladder is acontractile and areflexic.
But, b/c of preservation of EUS tone, urinary incontinence is usually
secondary to poor emptying and overflow incontinence.
Suprasacral cord injury (UMN)
Detrusor overactivity, smooth sphincter synergy (if below T6), and striated
The dyssynergic striated sphincter causes a functional obstruction with
poor bladder emptying and high detrusor pressure.
Smooth sphincter dyssynergy is present with lesions above T6.
Functionally, the m/c problem in patients with suprasacral SCI is
failure of both filling/storage (because of detrusor overactivity) and
emptying (because of striated or smooth sphincter dyssynergia, or
Lesions above the T6 sympathetic outflow tract, response to specific stimuli
can cause a massive disordered autonomic discharge.
Pounding headache, hypertension, bradycardia, and flushing with sweating
above the zone of the lesion.
The stimulus for autonomic dysreflexia is most often distention or
manipulation of the bladder or rectum.
An areflexic bladder with an open bladder neck, inconsistent.
There is a fixed EUS, with 10% to 15% of patients having detrusor–striated
Patients usually suffer from incontinence as a result of filling pressures
overcoming the low fixed sphincter pressures and transient increases in
intra-abdominal pressure (stress incontinence).
DISEASED AT OR DISTAL TO SACRAL SPINAL CORD
SACRAL SPINAL CORD INJURY
Over time, decreased bladder compliance and elevated storage pressure
The bladder outlet is classically described as a competent but non-
relaxing smooth sphincter with a fixed EUS not responsive to voluntary
Sensory examination of
Anterior abdominal wall: thoracic
Lower extremities: lumbar lumbar nerve roots.
The anterior portions of the scrotum and labia majora derive
innervation from the thoracolumbar spinal cord.
The sacral nerve roots innervate the posterior portion.
Saddle area of the perineum evaluate the afferent limb of pudendal n.
Basic motor and muscular tone—specifically, the tibialis anterior,
gastrocnemius, and toe extensors, innervated by the lower lumbar and
upper sacral nerves.
P/R to evaluate the external anal sphincter is important for evaluation of
the pelvic floor musculature.
Voluntary contraction of the external anal sphincter confirms
innervation of the pelvic floor and integrity of the corticospinal tract.
Preserved sphincter tone in the absence of voluntary contraction is
consistent with a suprasacral lesion, whereas diminished tone is
consistent with a sacral or peripheral nerve abnormality.
Neurological examination: to evaluate the integrity of sensorimotor
pathway known as the segmental reflex arcs
Cystoscopy : detrusor overactivity as trabeculation and diverticula, urethral
strictures and prostatic obstruction.
Voiding cystourethrogram: vesicoureteric reflux morpholgic changes
Urodyanamic testing: Non invasive
Assesment of PVR and urolflowmetry
No absolute volume above which PVR is
universally considered to be abnormal.
(<100ml), ideally <50 ml.
PVR indicates poor bladder contractility or
BOO or both,
Uroflowmetry: provides the data on the
rate of urinary flow over time from the
A low flow rate indicates poor bladder
contractility or BOO or both.
Normal uroflow rate : 25ml/sec
Obstructed : < 5ml/sec
Reliable only when voided volumes is
Evaluate the compliance of bladder
during filling and voiding.
Detrusor pressure is measured.
At 50 and 100 ml/min.
1st sensation: 100 ml
Full: b/w 400 and 600 ml
• Low detrusor pressures at initiation
• Normal bladder sensations
• No detrusor contraction during filling
• Rapid rise in detrusor pressure just prior to voiding
• Voiding at detrusor pressure below 40 cm in males & 20 cm in females.
3 Voiding States
Low detrusor pressure and high flow rate (unobstructed)
High detrusor pressure and low flow rate (obstructed)
Low detrusor pressure with low flow rate (poor detrusor contractility).
Sphincter EMG is used to record bioelectric potentials generated by the
striated sphincter complex during bladder filling, storage, and micturition.
It provides information on voluntary control of the pelvic floor
musculature and coordination between the detrusor and pelvic floor.
During bladder filling, EMG activity should gradually increase and reach a
maximum before voiding.
This so-called guarding reflex is also present during the Valsalva
maneuver, coughing, or other maneuvers that increase abdominal
Failure to store urine
Management of detrusor overactivity or impaired
Timed voiding and pelvic floor exercises
Timed voiding and pelvic floor exercises
Decreased fluid intake
Avoidance of dietary irritants such as caffeine, bowel regulation and
avoidance of constipation and timed voiding.
Bladder retraining and pelvic floor muscle exercises
Anticholinergic: Oxybutynin (5mg TDS), Flavoxate, tolterodine.
By blockage of muscarinic Ach receptors to inhibit unstable detrusor
Cathter induced bladder spasm,
Beta agonist: Mirabegron
Activation of beta-3 adrenargic receptors relaxes the detrusor smooth muscle
during the storage phase.
Alpha blocker: BOO. Phenoxybenzammine (10-20 mg BD), prazocin (0.5-2 mg BD
Tricyclic antidepressant: imipramine
Anticholinergic and sympathetic action
Decrease bladder contractality and increase sphincter resistance
Botulinum toxin A: (blocks NMJ presynaptic vesicle fusion, which prevent Ach
release. Ideopathic or neurogenic detrusor overactivity (200 U) and decreased
bladder compliance(100 U).
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