The document discusses the anatomy and physiology of the lower urinary tract. It describes the detrusor muscle, internal and external sphincters, and their innervation. It discusses the filling and voiding phases of the bladder and the roles of the parasympathetic, sympathetic, and somatic nervous systems. Various lesions involving the lower urinary tract are described, along with their associated clinical presentations.

1.  MODERATOR –DR. R. N. CHAURASIA
 SPEAKER- DR. ARUNAVA SARKAR

2.  Detrusor muscle:
 smooth muscle fibers arranged in spiral, longitudinal, and
circular bundles.
 the detrusor is innervated by sympathetic nervous system
fibers from the lumbar spinal cord and parasympathetic
fibers from the sacral spinal cord.

3.  External sphincter (sphincter urethrae):
 located at the bladder's distal inferior end in females and
inferior to the prostate (at the level of the membranous
urethra) in males
 is made of skeletal muscle,
 It is under voluntary control of the somatic nervous
system.
 It is innervated by pudendal nerves(S2,3,4)
 Internal sphincter muscle of urethra:
 It is located at the bladder's inferior end ,at the junction
of the urethra with the urinary bladder.
 a continuation of the detrusor muscle and is made of
smooth muscle,
 it is under involuntary or autonomic control

4. MALE FEMALE

5. PARASYMPATHETIC
CENTRE: S2-S4 in intermediolateral column
SUPPLY THROUGH: pelvic splanchnic nerves
END IN : GANGLIA IN BLADDER WALL
NEUROTRANSMITTER : ACh via M3
FUNCTION:
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 M2
and M3 on the detrusor smooth muscle cells initiates
Bladder detrusor contraction
Internal sphincter relaxation

6. SYMPATHETIC
CENTRE: T11-L2 intermediolateral column
SUPPLY THROUGH:
• sympathetic chain ganglia prevertebral ganglia
hypogastric and pelvic plexus inferior
mesentric ganglion post ganglionic fibres
FUNCTION:
• Via β3-adrenergic receptors -inhibition and
relaxation of the detrusor muscle.
• Through alpha-1 receptors causes Contraction
of internal sphincter
• Facilitate bladder storage and continence

7. SOMATIC
CENTRE: ONUF’S NUCLEUS in the
VENTRAL HORN of S2-S4
SUPPLY THROUGH: PUDENDAL NERVES
NT : Ach, NICOTINIC R.
FUNCTION : CONTROLS THE EXTERNAL
SPHINCTER

10.  AFFERENT ARC:
 Sensation of stretch arising from bladder wall travels through
the parasympathetic nerves to the center for micturition
 DETRUSOR CENTER OR SACRAL PARASYMPATHETIC NUCLEUS
 sacral segments S2-S4 of the spinal cord.
 EFFERENT ARC (PARASYMPATHATIC)
 travels through the pelvic nerves to the pelvic plexus; short
postganglionic fibers travel from the plexus to the detrusor
muscle.

11.  Dorsal Pontomesencephalic reticular formation micturition
center (located in the locus ceruleus, pontomesencephalic
gray matter, and nucleus tegmentolateralis dorsalis).
 The PMC makes connections with other brain centers to
control micturition, including the medial frontal cortex,
insular cortex, hypothalamus and periaqueductal gray (PAG).
 Pontine output is exitatory for voiding reflex.

12. CORTICAL CENTERS:
 Situated in
 Prefrontal lobe
 Paracentral lobule
 Cingulate gyrus
 Insula
 cortical input is inhibitory on micturition reflexes.

13. Subcortical centers:
 thalamic nuclei
 limbic system,
 Red nucleus
 Substantia nigra
 Hypothalamus
 Subthalamic nucleus.
Cerebellum :
 anterior vermis of the cerebellum
 fastigial nucleus are concerned with micturition.

14.  From the pontomesencephalic micturition center,
efferents to the spinal cord descend by way of
the reticulospinal tracts (located medially and
anteriorly in the anterior funiculus) to the detrusor
motor neurons in the intermediolateral cell
columns of the sacral gray matter (S2–S4).
 Efferents from the cortical and subcortical
micturition centers descend by way of the
pyramidal tracts to the pudendal nuclei (Onuf’s
nucleus) in the sacral spinal cord (S2–S4).
 The pudendal nerves, whose motor neurons are
located in the ventral horns of sacral segments
S2–S4, innervate the striated muscle around the
urethra

15.  Onuf’s nucleus
 It is a distinct group of neurons located in the ventral part
(laminae IX) of the anterior horn of the sacral region ( S1 to
S3 mainly in S2 )of the spinal cord.
 It contains motor neurons, and is the origin of the pudendal
nerve.
 The neurons of Onuf’s nucleus are responsible for
controlling external sphincter muscles of the anus and
urethra.

17.  The filling phase of the bladder is maintained by
sympathetic control .
 The emptying phase of the bladder is controlled by
the parasympathetic system.

18. During the storage of urine,
distention of the bladder produces
low-level vesical afferent firing
stimulates the sympathetic
outflow in the hypogastric nerve
to the bladder outlet (the
bladder base and the urethra)
Sympathetic firing also inhibits
contraction of the detrusor
muscle and modulates
neurotransmission in bladder
ganglia leading to receptive
dialatation of bladder
Stimulates the pudendal
outflow to the external
urethral sphincter.
External sphincter
constricts

19. Intense bladder-afferent firing in the pelvic
nerve activates spinobulbospinal reflex
pathways that pass through the pontine
micturition centre which is under continious
cortical inhibition.
This stimulates the
parasympathetic outflow
to the bladder and to
the urethral smooth
muscle
Inhibits pudendal
outflow to the
urethral outlet
Inhibits the
sympathetic
outflow to
urethral outlet.
If 1. afferent signals from the bladder are sufficiently
strong
2. voiding is safe
3. voiding socially appropriate
Then cortical inhibition decreases.

22. Classification
Neuroanatomic
Bors and Comar 1971
Bradely 1986 (Loop system)
Hald and Bradely 1982
Urodynamic
 Krane and Siroky 1979
Lapides 1970

23.  Supraspinal lesion
 Suprasacral spinal lesion
 Infrasacral lesion
 Peripheral autonomic neuropathy
 Muscular lesion

26.  A 45 year old women with IDDM since childhood
has h/o recurrent bladder infection.Her
diabetes is poorly controlled and she suffers
from bilateral lower extremity diabetic
neuropathy. She denies a history of urinary
retention but states that she has had dribbling
urinary incontinence that is not associated with
an urge to void.
 Urinalysis --- no abnormalities.
 USG PVRU--- 1500 mL.
 Video urodynamics --- a large capacity, poorly
sensitive bladder and impaired bladder
contractility.

27.  Found with lesions that involve the posterior roots or
posterior root ganglia of the sacral nerves, or the
posterior columns of the spinal cord.
 Occur in tabes dorsalis, diabetes mellitus
 Bladder sensation is absent, and there is no desire to
void.
 There is painless urinary retention, distention,
dribbling,overflow incontinance .
 Large amount of residual urine.
 Patient can void voluntarily (motor intact).
 Complicated by UTI.

28.  A 23-year-old man presents to the emergency
department with complaints of groin pain and urinary
retention. He has a history of multiple sexually
transmitted diseases. He has been unable to void for 18
hours despite a strong urge to void.
 Physical examination----an active herpetic infection
with multiple vesicular lesions at the base of the penile
shaft.
 A catheter is placed with return of 1 L of clear urine.
 Cystoscopy--- no obstructive lesion
 Urodynamic testing----normal sensation and capacity,
but the patient is unable to generate any voiding
contractions.

29.  Develops in lesions involving the efferent motor fibers to
the detrusor or the detrusor motor neurons in the sacral
spinal cord.
 Occurs in lumbar spinal stenosis, lumbosacral meningo-
myelocele, or following radical hysterectomy or
abdominoperineal resection,Herpes zoster infection.
 Painful urinary retention,as sensation is intact &
impaired bladder emptying.
 The bladder distends and decompensates.
 Residual urine is markedly increased.
 The bulbocavernosus and superficial anal reflexes are
usually absent , but sacral and bladder sensation are
present

30.  A 45-year-old man presented urinary retention with no
sensation of need to void and continuous dribbling with
not able to void voluntarily after recently undergoing an
abdominoperineal resection for rectal cancer. He has no
past history of urinary retention or infection, urethral
stricture disease, or benign prostatic hypertrophy. A
catheter was placed with return of 600 mL of urine.
During that time, the patient was comfortable and had
no sensation of needing to void.
 Cystoscopy -- normal
 Urodynamic test---a normal capacity, compliant bladder.
The patient is unable to sense filling at any volume and
is also unable to generate any voiding contraction.

31.  It is one without external innervation.
 Seen with lesions of sacral spinal cord, conus
medullaris and cauda equina. , S2-S4 motor or
sensory roots, or the peripheral nerves, and with
congenital anomalies such as spina bifida.
 It occurs with sacral myelomeningocele and
tumors of the conus medullaris–cauda equina
region .
 Bladder sensation is absent.
 There is no reflex or voluntary control of the
bladder.
 Contractions occur as the result of stimulation of
the intrinsic neural plexuses within the bladder
wall.

32. Urinary retention because the tone of the
detrusor muscle is abolished  large residual
urine  overflow incontinence.
The bladder capacity may greatly increase,
and its walls may become fibrotic.
There is associated saddle anesthesia with
absence of the bulbocavernosus and superficial
anal reflexes.
Anal sphincter control is often similarly
affected.

33.  A 70-year-old woman is admitted to the neurology
service after a left-sided ischemic stroke. In addition to
right-sided motor deficits, the patient is unable to void.
A catheter is placed for bladder drainage. The patient
recovers some motor function, and her bladder
eventually regains the ability to empty; however, the
patient now complains of severe urgency and frequency
as well as new-onset urge incontinence.
 Cystoscopy –normal
 Urodynamic test---normal bladder sensation and filling
parameters; multiple unstable contractions are noted
during the filling phase. The patient is able to generate
normal bladder pressures and empties the bladder to
completion.

34.  There is a loss of the cortical inhibition of
reflex voiding.
 Bladder tone remains normal.
 Bladder distention causes contraction in
response to the stretch reflex.
 There is frequency, urgency, and urge
incontinence that are not associated with
dysuria.
 Hesitancy may precede urgency.
 Bladder sensation is usually normal.
 There is no residual urine.

35.  A 35-year-old man with a history of a complete T2 spinal
cord injury has urgency ,frequency and poor urinary
stream.He does not use a catheter and voids into a
diaper.
 Serum creatinine -- is 2.5 mg/dL.
 USG – B/L hydronephrosis with B/L renal cortical
thinning.
 Urodynamic test-- a poorly compliant bladder with
baseline storage pressures rising above 40 cm H2O after
only 100 mL of fluid is instilled. The urodynamic study
also demonstrates unstable contractions against a closed
bladder outlet. The procedure is stopped early because
the patient complains of facial flushing, headache, and
sweating. At this time, the patient’s blood pressure is
240/120 mm Hg and heart rate is 40 bpm.

36.  Lesions above the level of the sacral bladder
center and below the level of the PMC.
 Interruption of both the descending autonomic tracts to
the bladder and the ascending sensory pathways above
the sacral segments of the cord.
 UMN CUT OFF but LMN INTACT.
 Detrusor spinter synergia lost results in obstructed
voiding, an 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.
 Bulbocavernosus and superficial anal reflexes
intact.

37.  Detrusor becomes overactive, so there is urinary
frequency, urgency, urge incontinence (the
patient is unable to inhibit the detrusor reflex).
 Contractions occur spontaneously or may be
provoked by coughing or changing posture.(stress
incontinence)
 Inability to initiate micturition voluntarily.
 Small volumes of urine stimulate uninhibited
detrusor muscle contraction; the bladder capacity
is reduced but residual urine may be increased .
 With lesions above the splanchnic out flow (T6 or
above), bladder fullness may induce a “mass reflex”
with paroxysmal HTN, headaches, diaphoresis, and
bradycardia.

38.  Acute elevation in BP coupled with bradycardia occuring
usually with lesions at T6 or above.

39. Irritating stimulus below
the level of spinal cord
injury, such as an overfull
bladder
The stimulus sends nerve
impulses to the cord, where
they travel upward until they
are blocked by the lesion at
the level of injury.
Since the impulses cannot
reach the brain, a reflex is
activated that increases
activity of the sympathetic
system
spasms and a narrowing of
the blood vessels (splanchnic
& peripheral)
BP rise
On sensing this rise in BP
by baroreceptors brain
starts parasympathetic
response
Blocked at the level of lesion
leading to bradycardia &
vasodialation. above the level
(fushing, sweating, pupil
constriction)

40.  Anterior regions of the frontal lobes are critical for
bladder control. Among patients with disturbed bladder
control, various frontal lobe disturbances have been
reported, including
 intracranial tumors,
 damage after rupture of an aneurysm,
 penetrating brain wounds, and
 prefrontal lobotomy (leucotomy).
 The typical picture of frontal lobe incontinence is of a
patient with severe urgency and frequency of
micturition and urge incontinence but without
dementia; the patient is socially aware and embarrassed
by the incontinence.

41.  Patients with NPH present with a gradually
progressive disorder. The classic triad
consists of the following:
 Abnormal gait: Earliest feature and most
responsive to treatment; bradykinetic,
broad-based and shuffling gait
 Urinary incontinence: Urinary frequency,
urgency, or incontinence
 Dementia: Prominent memory loss and
bradyphrenia; forgetfulness, decreased
attention, inertia.

42.  The cause of urinary incontinence in dementia is
probably multifactorial.
 Not all incontinent older adults are cognitively
impaired, and not all cognitively impaired older
adults are incontinent.
 In a study of patients with progressive cognitiv
decline, incontinence was observed to occur in more
advanced stages of Alzheimer disease, whereas it
could occur earlier on in the course of patients with
dementia with Lewy bodies.

43.  Small vessel disease of the white matter
(leukoaraiaosis) is associated with urgency,
incontinence .
 it is increasingly becoming clear that this is an
important cause of incontinence in the functionally
independent elderly (Tadic et al., 2010).

47.  Bladder symptoms in Parkinson disease (PD)
correlate with neurological disability (Araki and Kuno,
2000) and stage of disease.
 It appears that bladder dysfunction does not occur
until some years after the onset of motor symptoms
and that the dysfunction is correlated with the
extent of dopamine depletion (Sakakibara et al., 2001c).
(Braak et al., 2004),

48.  38 to 71% of PD patients report lower urinary tract
symptoms (LUTS) (Andersen, 1985; Berger et al., 1987).
 Nocturia (56.7%) is the most common symptom,
followed by urinary urgency and these together are
the commonest nonmotor symptoms in PD.
 The most common abnormality in urodynamic studies is
detrusor overactivity (Araki et al., 2000b).
 It is thought that neuronal loss in the substantia nigra
would disinhibit the normal effect of basal ganglia on
the micturition reflex, resulting in detrusor
overactivity.

49.  MSA must be suspected if bladder symptoms dominate
the clinical picture at onset of a parkinsonism condition.
 As many as 41% of MSA patients present with LUTS and
97% have LUTS during the disease course (Sakakibara et al.,
2001d, 2010, 2011; Sammour et al., 2009). These include -------
 Daytime frequency (45% of women, 43% of men), night-
time frequency (65%, 69%), urinary urgency (64% of
men), urgency incontinence (66% of women, 75% of
men,) (Saunders,2006).
 The bladder affection in MSA is much earlier and more
disabling as compared to PD. Patients with MSA are
more likely to have a high (>100 mL )PVR and detrusor–
sphincter dyssynergia.

50.  Voiding difficulty is a rare but recognized
symptom of a posterior fossa tumor and has
been reported in series of patients with
brainstem disorders (Fowler, 1999).
 In an analysis of urinary symptoms of 39
patients who had had brainstem strokes,
lesions that resulted in micturition
disturbance usually were dorsally situated
.(Sakakibara et al., 1996)

51.  Spinal cord disorders are the most common
cause of neurogenic bladder dysfunction.

52.  Initially after acute spinal cord injury, there usually is a
phase of neuronal shock of variable duration characterized
clinically by complete urinary retention, with urodynamics
demonstrating an acontractile detrusor.
 Gradually over the course of weeks, new reflexes emerge
to reinitiate bladder emptying and cause detrusor
contractions in response to low filling volumes.
 The neurophysiology of this recovery has been studied in
cats and it has been proposed that after spinal injury, C
fibers emerge as the major afferents, forming a spinal
segmental reflex that results in automatic voiding.

53.  The abnormally overactive, small-capacity bladder
leads to experience urgency and frequency.
However, patients with complete transection of the
cord may not complain of urinary urgency.
 Detrusor overactivity is severe, incontinence is
highly likely.
 Detrusor–sphincter dyssynergia, contributes to
incomplete bladder emptying. This difficulty may
exacerbate the symptoms of the overactive bladder.

54.  After SCI, bladder dysfunction can be of such
severity as to cause ureteric reflux,
hydronephrosis, and eventual upper urinary
tract damage.

55.  In 4 % of patient bladder involvement is initial presenting symptom.
 Bladder dysfunction is present in >90% of MS patients, and in a third
of patients, dysfunction results in weekly or more frequent episodes
of incontinence.
 During normal reflex voiding, relaxation of the bladder sphincter (α-
adrenergic innervation) is coordinated with contraction of the
detrusor muscle in the bladder wall (muscarinic cholinergic
innervation).
 Detrusor hyperreflexia, due to impairment of suprasegmental
inhibition, causes urinary frequency, urgency, nocturia, and
uncontrolled bladder emptying.
 Detrusor sphincter dyssynergia, due to loss of synchronization
between detrusor and sphincter muscles, causes difficulty in
initiating and/or stopping the urinary stream, producing hesitancy,
urinary retention, overflow incontinence, and recurrent infection.

56.  Damage to the cauda equina leaves the
detrusor decentralized, rather than
denervated, because the postganglionic
parasympathetic innervation is unaffected.
This distinction may explain why the bladder
dysfunction after a cauda equina lesion is
unpredictable and why even detrusor
overactivity has been described (Podnar,
2014).

57. CONUS MEDULLARIS CAUDA EQUINA
LESION LIMITED TO TERMINAL
SPINAL CORD AND
INTRAMEDULLARY
INVOLVES MULTIPLE
NERVE ROOTS AND
EXTRAMEDULLARY
SPONTANEOUS PAIN NOT COMMON AND NOT
SEVERE,IN PERINEUM OR
THIGHS
SEVERE PROMINENT
RADICULAR
ASYMMETRICAL PAIN IN
DISTRIBUTION OF SACRAL
NERVES
SENSORY DEFICIT SADDLE BILATERAL
SYMMETRIC,DISSOCIATION
OF SENSATION
SADDLE ASYMMETRIC,NO
DISSOCIATION OF
SENSATION
MOTOR DEFICIT SYMMETRIC NOT
MARKED,FASCICULATION
MAY PRESENT
ASYMMETRIC
,MARKED,NO
FASCICULATION.
REFLEX LOSS ACHILLES ABSENT PATELLAR AND ACHILLES
MAY ABSCENT
BLADDER /BOWEL EARLY AND MARKED LATE AND LESS MARKED.

58.  Diabetic Neuropathy- The onset of the bladder
dysfunction is insidious with progressive loss of
bladder sensation and impairment of bladder
emptying over years, eventually culminating in
chronic low pressure urinary retention (Hill et al.,
2008).
 Vesical afferent and efferent fibers are involved,
causing reduced awareness of bladder filling and
decreased bladder detrusor contractility.

59.  Amyloid Neuropathy-Autonomic manifestations are
common and these include erectile dysfunction,
orthostatic hypotension, bladder dysfunction, distal
anhydrosis and abnormal pupils.
 LUTS generally appear early and are present in 50%
of patients within the first 3 years of the disease.
 Patients most often complain of difficulty in bladder
emptying and incontinence (Andrade,2009)

60.  Approximately a quarter of all patients have
bladder symptoms.
 These symptoms usually occur in the patients with
more severe neuropathy and appear after limb
weakness is established.
 Both detrusor areflexia and bladder overactivity
have been described.

61.  Although myotonic activity has not been found in the
sphincter or pelvic floor of patients with myotonic
dystrophy, bladder symptoms may be prominent and
difficult to treat, presumably because bladder
smooth muscle is involved.
 With advancing disease, megacolon and fecal
incontinence also may become intractable problems

63. Storage dysfunction Voiding dysfunction
Frequency for micturition,
Nocturia,
Urgency and urgency incontinence
Urgency, frequency and nocturia,
with or without incontinence, is
called the overactive bladder
syndrome
Hesitancy for micturition,
Slow and interrupted urinary stream,
the Need to strain to pass urine, and
Double voiding

64.  1- Screening for Urinary tract infection.
 2-USG-PVRU
 3-Uroflowmetry
 4- Cystometry: evaluates the pressure–volume
relationship during nonphysiological filling of the
bladder and during voiding.
 5-Videocystometry-When cystometry is carried out
using a contrast filling medium and the procedure
visualized radiographically.
 6-Electromyography.

65.  7- Pudendal Nerve Terminal Motor Latency
(PNTML).
 8- Pudendal Somatosensory Evoked
Potentials.

69. MANAGEMENT

70.  Maintaining a bladder diary
 Restricted fluid intake
 Bladder retraining-whereby patients void by the
clock and voluntarily “hold on” for increasingly
longer periods, aims to restore the normal pattern
of micturition.
 Pelvic floor exercises and neuromuscular stimulation

71. Anti-Muscarinic Medications
 Detrusor overactivity is a major cause of
incontinence in patients with neurogenic
bladder disorders. The sensation of urgency
is experienced as the detrusor muscle begins
to contract, and if the pressure continues to
rise, the patient senses impending
micturition. Anti-muscarinic medications are
the mainstay of treatment for detrusor
overactivity.

73. DESMOPRESSIN
Action-temporarily reduces urine
production and volume-determined
detrusor overactivity by promoting water
re-absorption at the distal and collecting
tubules of the kidney.
 Useful in treatment of urinary frequency or nocturia
in patients with MS, providing symptom relief for up to
6 hours (Bosma et al.,2005).
 Caution in patients--
 over the age of 65 or with dependent leg edema,
 and should not be used more than once in 24 hours for
fear of fluid overload and hyponatremia.

74.  Botulinum toxin type A injected into the detrusor
muscle under cystoscopic guidance has been shown
to improve detrusor overactivity, symptoms of an
overactive bladder related to this, and quality of
life.
 Dose-200-300 U/cycle
 Repeating dose no sooner than 3 months
 The effect lasts 8 to 11 months, at which point the
patient is eligible for further injections (Kalsi et
al.,2007).

75.  Sacral Neuromodulation
 Percutaneous Tibial Nerve Stimulation

77.  This device was pioneered by Professor Giles Brindley.
 In patients who have suffered a complete spinal cord
transection,but in whom the caudal section of the cord
and its roots are intact, the implantation of a nerve
root stimulator may be considered.
 The principle on which they work is that the
stimulating electrodes are placed around the lower
sacral roots (S2 to S4) and activated by an external
switching device. The stimulating electrodes are
usually applied intrathecally to the anterior roots.

78.  Beta-3-Receptor Agonists. The recent
licensing of an oral beta-3-receptor agonist,
mirabegron 25 mg OD, offers a new
approach to the management of the
overactive bladder.
 Cannabinoids.
 Vanilloids.

79.  when the patient is no longer able to
perform self-catheterization, or when
incontinence is refractory to management.
 an indwelling Foley catheter
 a suprapubic catheter.

81.  The mainstay of therapy for failure to empty is
catheter drainage. This can be accomplished by
using
 1.an indwelling urethral catheter,
 2.placement of a suprapubic catheter, or
 3.clean intermittent self catheterization
 The concept of clean intermittent catheterization
was introduced by Lapides and colleagues8 in the
early 1970s and dramatically changed the
management.

82.  Botulinum toxin injections into the external urethral
sphincter may improve bladder emptying in patients
with spinal cord injury who have significant voiding
dysfunction (Naumann et al., 2008).
 Suprapubic vibration using a mechanical “buzzer” has
been demonstrated to be effective in patients with MS
with incomplete bladder emptying and detrusor
overactivity; however, its effect is limited (Prasad et al.,
2003).
 Bethanechol is a cholinergic agonist that has been
approved by the U.S. Food and Drug Administration for
use in patients with atonic bladders.

83.  Early diagnosis and management is key to
preserve and restore bladder function.
 Management should be step wise and
personalised.