NEUROGENIC BLADDER

dr. Selly Marisdina, Sp.S

OVERVIEW

• The urinary bladder is optimally designed for

the storage and expulsion of urine
• Urine storage and emptying functions are
governed by a complex physiologic process
that involves several brain regions, various
leveles of the spinal cord, the smooth muscles
of the bladder and bladder neck, and the
striated external urethral sphincter.
• Neuro-urologic Coordination of Lower Urinary
Tract Function
– Cortex and brain stem : cortical pathways
controlling micturition, Pontine and
medullary reflex activity
– Spinal cord afferent and efferent pathways:
Thoracolumbar sympathetic pathways
– Peripheral pathways: Peripheral
parasympathetic pathways, Pudendal nerve
afferent and efferent function
– Bladder and urethral sphincter: Intrinsic
detrusor muscle function, Bladder neck
competence and ability to relax, Resistance
to flow throug the prostatic urethra, Distal
urethral sphincter continence and relaxation
during micturition, Pelvic floor function.
Cerebral Cortex
Inhibition and facilitation of the micturition reflex.
Tonic activity of the cerebral cortex and midbrain
are inhibitory signals to the detrusor muscle to
prevent the bladder from emptying (contracting)
until a socially acceptable time and place to urinate
is available.
Superiomedial portion of the frontal lobes and the
corpus callosum : the areas of major detrusor
innervation
• Pontine Micturition Center
– In the rostral brain stem
– Coordinate micturition reflex.
– Sacral reflex arc: sacral micturition center.
– When the neural pathways between the pontine and
sacral micturition center are intact, micturition is
achieved by activation of the micturion reflex, resulting
in a coordinated series of events consisting of
relaxation of the striated urethral musculature, detrusor
contraction, and opening of the bladder neck an urethra.
– Neurologic lesions that interrupt these pontine-sacral
pathways: uncoordinate micturition in the form of
DESD
• Spinal cord
– Innervation of the lower urinary tract is derived from three
sets of peripheral nerves:
• The sacral parasympathetic (pelvic nerve)
• Thoracolumbar sympathetic (hypogastric nerve and
sympathetic chain)
• Sacral somatic (pudendal nerve)
– The bony vertebral levels T11-L1 (nerve levels S2-4):
• the center for micturition control.
• Trauma to this level: detrusor areflexia
• Lesion above the sacral micturition center: bladder
with reflex activity but lacking volitional control
(detrusor hyperreflexia)
• Neurogenic bladder: a malfunctioning urinary bladder due
to neurologic dysfuncion or insult emanating from internal
or external trauma, disease, or injury.
• Common neurologic disorders associated with lower
urinary tract dysfunction include multiple sclerosis,
cerebral vascular accidents, myelodysplasia, Parkinson’s
disease, spinal cord injury, herniated discs, and diabetes
mellitus.
NEUROPHYSIOLOGY
• Control of the bladder and urethra is exercised through the
central and peripheral neurvous systems.
Afferent Innervation:
those passing in the pelvic nerve to the sacral spinal
cord (S2-4), small-diameter fibers that are linked with
tension receptors in the bladder wall.
Afferent pathways from striated muscle sphincters and
from the urethra, which transmit sensations of warm,
cold, pain, and passage of urine, travel in the pudendal
nerve to the sacral cord (S2-4).
• Peripheral innervation
– Thoracolumbar Sympathetic nerves:
• The cell bodies of the sympathetic nerves: intermedial
lateral cell column of the T10-L2
• Promote the storage of urine by two mechanisms
(mediated by alpha adrenoceptors)
– During filling: direct sympathetic stimulation of
alpha-adrenoceptors  manintains closure of the
vesical neck and proximal urethra.
– Relaxation of the body of the detrusor:
accomplished via a sympathetic beta-
adrenoceptor.
• Urinary accomodation occurs and the micturition
reflex is inhibited
– Sacral Parasympathetic nerves
• Pelvic nerve: primary parasympathetic nerve involved in
micturition.
• Primary neurotransmitter at both the preganglionic and
postganglionic synapse: acetylcholine
• Stimulate the detrusor to contract.
• The nucleus of the pelvic nerve: in the intermedial cell
column of the S2-4
– Somatic nerves
• Pedundal nerve: primary innervation of the striated
muscles of the pelvic floor and rhabdosphincter
• Cell bodies of teh pedundal nerve originate in
Onufrowicz’s nucleus in the anterior horn of S2-4.
• Regulates the actions of the muscles under voluntary
control.
 URINE STORAGE
– Bladder fills with urine  its walls begin to stretch and it assumes a spherical
shape  the thickness of the bladder wall diminshes and the detrusor muscle
stretches with filling.
– Since the ureter is fixed by its attachment to the trigone and Waldeyer’s
sheath, its intramural portion is stretcehed  the lumen becomes longer and
narrower  increasing the resistance to flow  prevent vesicoureteral reflux.
– Behavior of the bladder : a combination of active and passive forces.
• Passive properties of the bladder: elastin, collagen, and smooth muscle
• Active forces: contractile elements of smooth muscle
– Urethral pressure remains greater than intravesical pressure  maintain
urinary continence
– If the urethral pressure is abnormally low or if the intravesical pressure is
abnormally high  urinary incontinence.
– The difference between intravesical and intraurethral pressure: urethral
closure pressure.
 Common cause of storage problem
 Detrusor Hyperreflexia
urge incontinence and low residual volume.
The more common causes are multiple sclerosis,
cerebrovascular diseases, normal pressure
hydrocephalus, Parkinson disease, spinal cord
trauma, and trauma or tumor affecting the frontal
lobes of the brain.
 Sphincter incontinence
detrusor function is normal and stress incontinence
is due solely to deficient activation of the external
urethral sphincter.
the most common type of bladder emptying disorder
in women, occurs mainly after hysterectomy and in
multiparous women with uterine prolapse.
 MICTURITION REFLEX
– The storage phase of the urinary bladder can be switched to the
voiding phase either involuntarily (reflexively) or voluntarily.
– Involuntary reflex voiding occurs in an infant when the
volume of urine exceeds the voiding threshold.
– When the bladder is filled to capacity  the stretch receptors
within the bladder wall signal the sacral cord  sends a message
back to the bladder indicating that it is time to empty the bladder
 the pudendal nerve causes relaxation of the levator ani so that
the pelvic floor muscle relaxes The pudendal nerve also
signals the external sphincter to open The sympathetic nerves
send a message to the internal sphincter to relax and open,
resulting in a lower urethral resistance.
 When the urethral sphincters relax and open the parasympathetic nerves
trigger contraction of the detrusor  the pressure generated by the
bladder overcomes the urethral pressure, resulting in urinary flow.
 Newborn infants: repetitious cycle of bladder filling and emptying occurs
in newborn infants.
 The bladder empties as soon as it fills because the brain of an infant has
not matured enough to regulate the urinary system.
 Because urination is unregulated by the infant's brain, predicting when the
infant will urinate is difficult.
 As the infant brain develops, the PMC also matures and gradually
assumes voiding control.
 childhood (usually at age 3-4 years) this primitive voiding reflex
becomes suppressed and the brain dominates bladder function.
 Primitive voiding reflex may reappear in people with spinal cord injuries.
 Senility: the voluntary control may be lost in senility or following a
cetebrovascular accident, with a consequent regression to reflex
micturition.
• Alteration of Micturition Reflexes
– Spinal Cord injury, transverse myelitis, multiple sclerosis, and
myelodysplasia  interup “long-routed micturition reflex” 
uncoordinated micturition.
– Suprapontine neurologic lesions (cerebrovascular accident,
tumor, Parkionons’s disease, and normal pressure hydrocephalus
 loss of control over the micturition reflex without DESD.
DELAYING VOIDING OR VOLUNTARY
VOIDING
 Bladder function is automatic but completely governed by the brain 
makes the final decision on whether or not to void.
 The normal function of urination : an individual has the ability to stop
and start urination on command.
 The healthy adult:
 aware of bladder filling and can willfully initiate or delay voiding.
the PMC functions as an on-off switch that is activated by stretch
receptors in the bladder wall and is, in turn, modulated by
inhibitory and excitatory neurologic influences from the brain.
 When the bladder is full, the stretch receptors are activated.
 The individual perceives the activation of the stretch receptors as the
bladder being full, which signals a need to void.
 When an individual cannot find a bathroom nearby, the brain
bombards the PMC with a multitude of inhibitory signals to prevent
detrusor contractions  actively contract the levator muscles to keep
the external sphincter closed or initiate distracting techniques to
suppress urination.
 NEUROLOGIC LESION ASSOCIATED
NEUROGENIC BLADDER
• Suprasacral spinal cord lesions (traumatic spinal cord injury, multiple
sclerosis, transverse myelitis) : detrusor hyperreflexia and detrusor-
external sphincter dyssynergia (DESD).
– Inappropriate contraction of the striated urethral musculature
during involuntary destrusor contractions  the bladder is
contracting against a closed sphincter, the resulting high detrusor
pressure can cause vesicoureteral reflux or ureteral obstruction.
• Lumbosaccral lesions (myelodysplasia, cauda equina injury): detrusor
areflexia and low bladder compliance.
• Neurologic lesions above the spinal cord (stroke and Parkinson’s
disease): lower risk for developing urologic complications unless benign
prostatic hyperthropy, long-term treatment with an indwelling vesical
catheter can develop urolithiasis, infection, low bladder compliance,
and even bladder cancer
Brain lesion
 Lesions of the brain above the pons destroy the master control center,
causing a complete loss of voiding control.
 The voiding reflexes of the lower urinary tract—the primitive voiding
reflex—remain intact.
 urge incontinence, or spastic bladder (medically termed detrusor
hyperreflexia or overactivity).
 The bladder empties too quickly and too often, with relatively low quantities,
and storing urine in the bladder is difficult rush to the bathroom and even
leak urine before reaching their destination, maywake up frequently at night
to void.
 Typical examples of a brain lesion are stroke, brain tumor, or Parkinson
disease. Hydrocephalus, cerebral palsy, and Shy-Drager syndrome.
Shy-Drager syndrome is a rare condition that also causes the bladder
neck to remain open
• Spinal cord lesion
– spastic bladder or overactive bladder.
– The bladder empties too quickly and too frequently.
– If both the bladder and external sphincter become
spastic at the same time an overwhelming desire
to urinate but only a small amount of urine may
dribble out.
– The medical term: detrusor-sphincter dyssynergia
(the bladder and the external sphincter are not in
synergy)
– the bladder is trying to force out urine, the external
sphincter is tightening to prevent urine from
leaving.
– spinal cord injuries, Multiple sclerosis (MS),
myelomeningocele.
• Sacral cord injury
– prevent the bladder from emptying.
– If a sensory neurogenic bladder is present, the affected individual may
not be able to sense when the bladder is full.
– Detrusor areflexia: motor neurogenic bladder  the individual will
sense the bladder is full and the detrusor may not contract  difficulty
eliminating urine and experience overflow incontinence; the bladder
gradually overdistends until the urine spills out.
– Typical causes: a sacral cord tumor, herniated disc, and injuries that
crush the pelvis, after a lumbar laminectomy, radical hysterectomy, or
abdominoperineal resection, tethered cord syndrome (a neurologic
condition in which the tip of the sacral cord is stuck near the sacrum
and cannot stretch as the child grows taller)
– Ischemic changes of the sacral cord associated with the tethering cause
the manifestation of dysfunctional voiding symptoms.
• Peripheral nerve injury
– Diabetes mellitus and AIDS
– urinary retention.
– destroy the nerves to the bladder may lead to
silent, painless distention of the bladder.
– chronic diabetes: lose the sensation of bladder
filling first, before the bladder decompensates
difficulty urinating, hypocontractile bladder.
– Other diseases: poliomyelitis, Guillain-Barré
syndrome, severe herpes in the genitoanal area,
pernicious anemia, and neurosyphilis (tabes
dorsalis).
Nonneurogenic Bladder Dysfunction
– Infravesical obstruction
• benign prostatic hyperplasia,
• manifests itself clinically with urinary urgency, pollakiuria,
nocturia, urinary retention, and overflow incontinence.
– Dysfunction of the external urethral sphincter,
– Enuresis
• is defined as bedwetting, by day or night, in individuals over the
age of 4 years, in the absence of any demonstrable causative
lesion.
• not a neurogenic disturbance.
• The important differential diagnoses include organic
neurological and urological causes of bedwetting, including
epilepsy, spina bifida occulta, and malformations of the
urogenital tract.
• A 24-hour EEG recording is indicated in some cases.
DIAGNOSTIC TEST
Laboratory Studies
Urinalysis and urine culture: Urinary tract infection
Urine cytology
Carcinoma-in-situ of the urinary bladder causes
symptoms of urinary frequency and urgency.
Irritative voiding symptoms out of proportion to
the overall clinical picture and/or hematuria
warrant urine cytology and cystoscopy.
Chem 7 profile
Blood urea nitrogen (BUN) and creatinine (Cr)
are checked if compromised renal function is
suspected.
 Other Tests
 Voiding diary
A voiding diary is a daily record of the patient's bladder
activity. It is an objective documentation of the patient's
voiding pattern, incontinent episodes, and inciting events
associated with urinary incontinence.
 Pad test
This is an objective test that documents the urine loss.
Intravesical methylene blue test or oral phenazopyridine or
Urised (which contains methylene blue) may be used.
Methylene blue turns the urine color blue; phenazopyridine
turns the urine color orange.
Patients should resume their usual physical activities while
wearing a perineal pad. If the pads turn to orange or blue, the
patient is experiencing urine loss. If the pads remain white,
moisture most likely is a normal vaginal fluid.
 Diagnostic Procedures
 Postvoid residual urine
The postvoid residual urine (PVR) measurement is a part of basic
evaluation for urinary incontinence. If the PVR is high, the bladder
may be contractile or the bladder outlet may be obstructed. Both of
these conditions will cause urinary retention with overflow
incontinence.
 Uroflow rate
Uroflow rate is a useful screening test used mainly to evaluate
bladder outlet obstruction. Uroflow rate is volume of urine voided
per unit of time.
Low uroflow rate may reflect urethral obstruction, a weak detrusor,
or a combination of both. This test alone cannot distinguish an
obstruction from a contractile detrusor.
 Filling cystometrogram
A filling cystometrogram (CMG) assesses the bladder capacity,
compliance, and the presence of phasic contractions (detrusor
instability). Most commonly, liquid filling medium is used.
An average adult bladder holds approximately 50-500 mL of urine.
During the test, provocative maneuvers help to unveil bladder
instability.
– Voiding cystometrogram (pressure-flow study)
• Pressure-flow study simultaneously records the voiding detrusor
pressure and the rate of urinary flow. This is the only test able to
assess bladder contractility and the extent of a bladder outlet
obstruction.
• Pressure-flow studies can be combined with voiding cystogram
and videourodynamic study for complicated cases of incontinence.
– Cystogram
• A static cystogram (anteroposterior and lateral) helps to confirm
the presence of stress incontinence, the degree of urethral motion,
and the presence of a cystocele. Intrinsic sphincter deficiency will
be evident by an open bladder neck. The presence of a
vesicovaginal fistula or bladder diverticulum also may be noted.
• A voiding cystogram can assess bladder neck and urethral function
(internal and external sphincter) during filling and voiding phases.
A voiding cystogram can identify a urethral diverticulum, urethral
obstruction, and vesicoureteral reflux.
 Electromyography
 Electromyography (EMG) helps to ascertain the presence of coordinated
or uncoordinated voiding. Failure of urethral relaxation during bladder
contraction results in uncoordinated voiding (detrusor sphincter
dyssynergia). EMG allows accurate diagnosis of detrusor sphincter
dyssynergia common in spinal cord injuries.
 Cystoscopy
 The role of cystoscopy in the evaluation of neurogenic bladder is to
allow discovery of bladder lesions (eg, bladder cancer, bladder stone)
that would remain undiagnosed by urodynamics alone.
 General agreement is that cystoscopy is indicated for patients
complaining of persistent irritative voiding symptoms or hematuria. The
physician can diagnose obvious causes of bladder overactivity, such as
cystitis, stone, and tumor, easily. This information is important in
determining the etiology of the incontinence and may influence treatment
decisions.
 Videourodynamics
 Videourodynamics is the criterion standard for evaluation of a patient
with incontinence. Videourodynamics combines the radiographic
findings of voiding cystourethrogram (VCUG) and multichannel
urodynamics.
 Videourodynamics enables documentation of lower urinary tract
anatomy, such as vesicoureteral reflux and bladder diverticulum, as well
as the functional pressure-flow relationship between the bladder and the
urethra.
 Treatment and Management
• Medical Care
• Absorbent products
• Urethral occlusive devices
• Catheters
• Indwelling urethral catheters
• Suprapubic catheters
• Intermittent catheterization
• Surgical care
Medications Used to Treat Neurogenic
Bladder
• Estrogen derivatives
• Conjugated estrogen (Premarin)
• Anticholinergic drugs
• Propantheline bromide (Pro Banthine)
• Dicyclomine hydrochloride (Bentyl)
• Hyoscyamine sulfate (Levsin/SL, Levsin, Levsinex,
Cystospaz M, Levbid)
• Antispasmodic drugs
• Solifenacin succinate (VESIcare)
• Darifenacin (Enablex)
• Oxybutynin chloride (Ditropan IR, Ditropan XL)
• Tolterodine L-tartrate (Detrol and Detrol LA)
• Trospium (Sanctura)
• Fesoterodine (Toviaz)
• Tricyclic antidepressant drugs
• Imipramine hydrochloride (Tofranil)
• Amitriptyline hydrochloride (Elavil)