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BLADDER DISORDERS 
MODERATOR –PROF. N.C.DWIVEDI(MD)(DM) 
BY-Anil kumar g (JR3)
Anatomy 
• The urinary bladder is a smooth muscle chamber 
composed of two main parts: 
– (1) the body, the major part, collects urine 
– (2) the neck, a funnel-shaped extension of the body, 
passing inferiorly and anteriorly into the urogenital 
triangle and connecting with the urethra
• On the posterior wall of the 
bladder, lying immediately above 
the bladder neck, is a small 
triangular area called the 
trigone. 
• The trigone can be identified by 
the fact that its mucosa, the 
inner lining of the bladder, is 
smooth, in contrast to the 
remaining bladder mucosa, 
which is folded to form rugae. 
• At the lowermost apex of the trigone, 
the bladder neck opens into the 
posterior urethra, and the two ureters 
enter the bladder at the uppermost 
angles of the trigone. 
• Each ureter, as it enters the bladder, 
courses obliquely through the detrusor 
muscle and then passes another 1 to 2 
centimeters beneath the bladder 
mucosa before emptying into the 
bladder
The bladder neck (posterior urethra) is 2 to 3 centimeters 
long, and its wall is composed of detrusor muscle interlaced 
with a large amount of elastic tissue. The muscle in this area is 
called the internal sphincter.
• Its natural tone normally keeps the bladder neck and posterior urethra empty 
of urine and, therefore, prevents emptying of the bladder until the pressure in 
the main part of the bladder rises above a critical threshold. 
• Beyond the posterior urethra, the urethra passes through the urogenital 
diaphragm, which contains a layer of muscle called the external sphincter of 
the bladder. 
• External sphincter muscle is a 
voluntary skeletal muscle, in contrast 
to the muscle of the bladder body and 
bladder neck, which is entirely smooth 
muscle. 
• The external sphincter muscle is under 
voluntary control of the nervous 
system and can be used to consciously 
prevent urination even when 
involuntary controls are attempting to 
empty the bladder.
Blood supply 
• The bladder is supplied by the superior and 
inferior vesical arteries which are branches of 
anterior trunk of internal iliac artery. 
• The veins that drain the bladder form a plexus on 
the infero-lateral surface before ending in the 
internal iliac vein. 
• Most of the lymph from the urinary bladder ends 
in the external iliac nodes.
Innervation of the Bladder 
• The principal nerve supply of the bladder is by way of the pelvic 
nerves, which connect with the spinal cord through the sacral 
plexus, mainly connecting with cord segments S-2 to S-4. 
• Coursing through the pelvic nerves are both sensory nerve fibers 
and motor nerve fibers. 
• The sensory fibers detect the degree of stretch in the bladder wall. 
Stretch signals from the posterior urethra are especially strong and 
are mainly responsible for initiating the reflexes that cause bladder 
emptying. 
• The motor nerves transmitted in the pelvic nerves are 
parasympathetic fibers. These terminate on ganglion cells located 
in the wall of the bladder. 
• Short postganglionic nerves then innervate the detrusor muscle.
• In addition to the pelvic nerves, two other types of innervation are 
important in bladder function. Most important are the skeletal 
motor fibers transmitted through the pudendal nerve to the 
external urethral sphincter. These are somatic nerve fibers that 
innervate and control the voluntary skeletal muscle of the 
sphincter. 
• 
• Also, the bladder receives sympathetic innervations from the 
sympathetic chain through the hypogastric nerves, connecting 
mainly with the L-1,L-2 segments of the spinal cord. 
• These sympathetic fibers stimulate mainly the blood vessels and 
have little to do with bladder contraction. 
• Some sensory nerve fibers also pass by way of the sympathetic 
nerves and may be important in the sensation of fullness and, in 
some instances, pain.
Innervation of the urinary bladder and its 
sphincters
Micturition Reflex 
• As the bladder fills, many superimposed 
micturition contractions begin to appear. They are 
the result of a stretch reflex initiated by sensory 
stretch receptors in the bladder wall, especially by 
the receptors in the posterior urethra when this 
area begins to fill with urine at the higher bladder 
pressures.
• Sensory signals from the bladder stretch receptors are 
conducted to the sacral segments of the cord through 
the pelvic nerves and then reflexively back again to the 
bladder through the parasympathetic nerve fibers by 
way of these same nerves.
• When the bladder is only partially filled, these 
micturition contractions usually relax spontaneously 
after a fraction of a minute, the detrusor muscles stop 
contracting, and pressure falls back to the baseline. 
• As the bladder continues to fill, the micturition reflexes 
become more frequent and cause greater contractions 
of the detrusor muscle. 
• Once a micturition reflex has occurred but has not 
succeeded in emptying the bladder, the nervous 
elements of this reflex usually remain in an inhibited 
state for a few minutes to 1 hour or more before 
another micturition reflex occurs. 
• As the bladder becomes more and more filled, 
micturition reflexes occur more and more often and 
more and more powerfully.
• Once the micturition reflex becomes powerful 
enough, it causes another reflex, which passes 
through the pudendal nerves to the external 
sphincter to inhibit it. 
• If this inhibition is more potent in the brain than 
the voluntary constrictor signals to the external 
sphincter, urination will occur. If not, urination 
will not occur until the bladder fills still further 
and the micturition reflex becomes more 
powerful.
Facilitation or Inhibition of 
Micturition by the Brain 
• The micturition reflex is a completely autonomic 
spinal cord reflex, but it can be inhibited or 
facilitated by centers in the brain. 
• These centers include 
– (1) strong facilitative and inhibitory centers in the 
brain stem, located mainly in the pons, and 
– (2) several centers located in the cerebral cortex that 
are mainly inhibitory but can become excitatory
• The micturition reflex is the basic cause of micturition, but 
the higher centers normally exert final control of 
micturition as follows: 
– 1. The higher centers keep the micturition reflex partially 
inhibited, except when micturition is desired. 
– 2. The higher centers can prevent micturition, even if the 
micturition reflex occurs, by continual tonic contraction 
of the external urethral sphincter until a convenient time 
presents itself. 
– 3. When it is time to urinate, the cortical centers can 
facilitate the sacral micturition centers to help initiate a 
micturition reflex and at the same time inhibit the 
external urethral sphincter so that urination can occur.
• cortical activation with 
bladder filling, brain activity 
increased with increasing 
bladder volume in the 
periaqueductal gray- PAG 
matter in the midline pons, 
in the mid–cingulate 
cortex, and bilaterally in 
the frontal lobe area. 
• Inhibition of micturition 
was related to activation 
of parietal cortex, 
cerebellum, putamen. 
and supplementary 
motor area 
• insular, posterior 
parietal, and prefrontal 
activation during urinary 
storage.
Abnormalities of Micturition
Irritative Voiding Symptoms 
• Urgency 
– is the sudden desire to void 
– in inflammatory conditions such as cystitis or in hyperreflexic neuropathic 
conditions such as neurogenic bladders resulting from upper motor neuron 
lesions. 
• Dysuria 
– painful urination 
– associated with inflammation. 
– The pain is typically referred to the tip of the penis in men or to the urethra in 
women. 
• Frequency 
– is the increased number of voids during the daytime, and 
– nocturia is nocturnal frequency. 
– Adults normally void five or six times a day and once at most during the 
nighttime hours. 
– Increased frequency may result from increased urinary output or decreased 
functional bladder capacity
Obstructive Voiding Symptoms 
• Hesitancy 
– is a delay in the initiation of micturition. 
– results from the increased time required for the bladder to attain the high 
pressure necessary to exceed that of the urethra in the obstructed setting. 
• Decreased force of stream results from the high resistance the bladder faces 
and is often associated with a decrease in caliber of the stream. 
• Intermittency is the interruption of the urinary stream 
• Postvoid dribbling the uncontrolled release of the terminal few drops of 
urine. 
• Obstructive symptoms are most commonly due to benign prostatic 
hyperplasia, urethral stricture, or neurogenic bladder disorders, prostatic or 
urethral carcinoma and foreign body are other causes.
Incontinence 
• Urinary incontinence is the involuntary loss of urine. 
• Total incontinence, patients lose urine at all times and in all 
positions. 
• Stress incontinence is the loss of urine associated with activities 
that result in an increase in intra-abdominal pressure (coughing, 
sneezing, lifting, exercising). 
• Uncontrolled loss of urine preceded by a strong urge to void is 
known as urge incontinence. 
• Chronic urinary retention may result in overflow incontinence. 
• The evaluation and treatment vary with each of the categories.
Uncontrolled Contraction of the 
Bladder Muscle 
Normal bladder Patients with 
urge 
incontinence 
Patients with 
urge or 
frequency 
Urethral resistance Uncontrolled bladder 
muscle contractions 
23
Bladder sphincter dyssynergia (detrusor sphincter dysynergia 
(DSD), neurogenic detrusor overactivity (NDO) 
• It is a consequence of a neurological pathology such as 
spinal injury or multiple sclerosis that disrupts central 
nervous system regulation of the micturition reflex 
resulting in dys-coordination of the bladder 
musculature and the external urethral sphincter. 
• Instead of the urethral muscle relaxing completely 
during voiding, it dys-synergically contracts causing the 
flow to be interrupted and the bladder pressure to rise. 
• On cystography there is an irregular appearance of the 
bladder outline due to muscular contraction against 
the unrelaxed bladder sphincter.
Symptoms 
• Symptomatically, people with this condition 
generally experience daytime and night time 
wetting, urinary retention, and often have a 
history of urinary tract and bladder infections. 
Constipation and encopresis are often associated 
with this condition. 
Diagnosis 
• Strictly DSD can only be diagnosed from an CMG 
trace
Neurologic disorders causing urinary 
disturbences: 
With regard to the neurologic diseases that cause 
bladder dysfunction, 
• multiple sclerosis, usually with urinary urgency, is 
by far the most common. 
• degenerative diseases (Parkinson disease and 
multiple system atrophy) for 14 percent, 
• spinal cord disorders account for 12 percent of 
cases, 
• and frontal lobe lesions for 9 percent.
Complete destruction of the cord below T12 
– conus lesions 
– trauma, myelodysplasias, tumor, venous angioma, and necrotizing myelitis. 
– bladder is paralyzed for voluntary and reflexactivity 
– no awareness of the state of fullness; 
– voluntary initiation of micturition is impossible; 
– the tonus of the detrusor muscle is abolished and the bladder distends as 
urine accumulates until there is overflow incontinence; 
– voiding is possible only by the Crede´ maneuver, i.e.,lower abdominal 
compression and abdominal straining. 
• Usually the anal sphincter and colon are similarly affected, and there is 
“saddle” anesthesia and abolition of the bulbocavernosus and anal 
reflexes as well as the tendon reflexes in the legs. 
• The cystometrogram shows low pressure and no emptying contractions. 
• Management: catherisation & anticholinergics
Disease of the sacral motor neurons in the spinal 
gray matter 
– autonomic bladder , autonomous bladder 
– the anterior sacral roots, or peripheral nerves innervating the 
bladder 
– lumbosacral meningomyelocele and the tethered cord 
syndrome. 
– a lower motor neuron paralysis of the bladder. 
– sacral and bladder sensation are intact. 
• Various causes pertain in cauda equina disease, the 
most frequent being compression by epidural tumor or 
disc, neoplastic meningitis, and radiculitis from herpes 
or cytomegalovirus. 
• a hysterical patient can suppress motor function and 
suffer a similar distention of the bladder.
Interruption of sensory afferent fibers 
– atonic bladder 
– as in diabetes and tabes dorsalis (tabetic bladder). 
– motor nerve fibers unaffected 
• Although a flaccid (atonic) paralysis of the bladder may be 
purely motor or sensory, as described above, in most clinical 
situations there is interruption of both afferent and efferent 
innervation, as in cauda equina compression or severe 
polyneuropathy. 
• Neuropathies affecting mainly the small fibers are the ones 
usually implicated (diabetes, amyloid, etc.), but urinary 
retention also occurs in certain acute neuropathies such as 
Guillain-Barre´ syndrome. 
• Treatment includes intermittent self catheterisation
Upper spinal cord lesions, above T12 
– reflex neurogenic (spastic) bladder, automatic bladder 
– multiple sclerosis and traumatic myelopathy, which are the 
commonest causes; myelitis, spondylosis, arteriovenous 
malformation (AVM), syringomyelia, and tropical spastic 
paraparesis 
– If the cord lesion is of sudden onset, the detrusor muscle suffers 
the effects of spinal shock. At this stage, urine accumulates and 
distends the bladder to the point of overflow. 
– As the effects of spinal shock subside, the detrusor usually 
becomes reflexly overactive (detrusor hyperreflexia), and since 
the patient is unable to inhibit the detrusor and control the 
external sphincter, urgency, precipitant micturition, and 
incontinence result. 
– Incomplete lesions result in varying degress of urgency in voiding.
• With slowly evolving processes involving the upper cord, such as 
multiple sclerosis, the bladder spasticity and urgency worsen with 
time and incontinence becomes more frequent. 
• In addition, initiation of voluntary micturition is impaired and 
bladder capacity is reduced. 
• Bladder sensation depends on the extent of involvement of sensory 
tracts. 
• Bulbocavernosus and anal reflexes are preserved. 
• The cystometrogram shows uninhibited contractions of the 
detrusor muscle in response to small volumes of fluid.
• Some patients can still control urination in this 
condition by stimulating the skin (scratching or 
tickling) in the genital region, which sometimes 
elicits a micturition reflex. 
• Management: 
– Decompress the rectum or bladder - reverses the 
effects of unopposed sympathetic outflow. 
– Terazosin/ spinal anesthetic may be used as 
prophylaxis.
Mixed type of neurogenic bladder. 
• In diseases such as multiple sclerosis, subacute 
combined degeneration, tethered cord, and 
syphilitic meningomyelitis, bladder function may be 
deranged from lesions at multiple levels, i.e., spinal 
roots, sacral neurons or their fibers of exit, and 
higher spinal segments. 
• The resultant picture is a combination of sensory, 
motor, and spastic types of bladder paralysis.
• Stretch injury of the bladder wall, as occurs with anatomic 
obstruction at the bladder neck and occasionally with voluntary 
retention of urine, as in hysteria. 
• Repeated overdistention of the bladder wall often results in 
varying degrees of decompensation of the detrusor muscle and 
permanent atonia or hypotonia, although the evidence for this 
mechanism is uncertain. 
• The bladder wall becomes fibrotic and bladder capacity is greatly 
increased. 
• Emptying contractions are inadequate, and there is a large 
residual volume even after the Crede´ maneuver and strong 
contraction of the abdominal muscles. 
• As with motor and sensory paralyses, the patient is subject to 
cystitis, ureteral reflux, hydronephrosis and pyelonephritis, and 
calculus formation.
• Frontal lobe incontinence 
Often the patient, because of his confused mental 
state, ignores the desire to void and the subsequent 
incontinence. There is also a supranuclear type of 
hyperactivity of the detrusor and precipitant 
evacuation. 
• Nocturnal enuresis 
or urinary incontinence during sleep, due presumably 
to a delay in acquiring inhibition of micturition.
Urodynamic Studies 
1.Noninvasive Bladder 
Investigations 
voiding diary may be kept by either 
the patient or the caregiver of the 
approximate amount drunk, 
frequency of micturition, and 
episodes of incontinence, recorded 
over the course of several days. 
This gives a useful indication of the 
severity of the bladder complaints 
on which management decisions 
can be based.
a.Urinary flowmetry: 
• noninvasive investigation, valuable 
particularly when combined with an 
ultrasound measurement of the 
postmicturition residual volume. 
• It as a base of the collecting system is a 
spinning disk, and flow of urine onto this disk 
tends to slow its speed of rotation, which a 
servomotor holds constant. 
• Urine flow is derived from measurement of 
the power necessary to maintain rotation 
speed, and the machine usually produces a 
graphic printout, together with an analysis, 
for the time taken to reach maximal flow, 
maximum and average flow rates, and the 
voided volume 
A, Urinary flow meter. The side of the uroflow transducer 
has been cut away to show the disk at the base of the 
funnel, which rotates as urine passes into the collecting 
vessel. B, Typical (normal) printout from the uroflowmeter. 
A total of 290 mL was voided (upper trace), with a 
maximum flow rate of 30 mL per second (lower trace). 
b.simple ultrasound 
machines are now available 
that require little operator 
training and make it easy to 
determine whether the 
postmicturition residual is 
negligible or in excess of 100 
mL
Investigations Requiring 
Catheterization 
• Cystometry, the registration of bladder 
pressure, can be performed during filling 
and voiding . 
• Detrusor pressure is derived by subtraction 
of the abdominal pressure (measured using 
a rectal line) from the intravesical pressure 
(measured using a vesical line). The 
efficiency of the subtraction usually is 
checked at the beginning of cystometry by 
asking the subject to cough. 
• This produces an increase in abdominal 
pressure and hence in intravesical pressure, 
but no increase in detrusor pressure. 
Cystometry during bladder filling. The bladder was filled (top trace) at 50 mL per minute (Vinfus) to a total of 
300 mL. Detrusor pressure (Pdet) is derived by subtracting pressure in the rectum (Pabd) from the measured 
intravesical pressure (Pves). At the beginning of the trace, these two values can be seen to be subtracting 
effectively because on coughing there is an abrupt increase in intravesical pressure but no increase in detrusor 
pressure. The detrusor pressure did not exceed 10 cm H2O, which is normal.
VIDEOCYSTOMETRY : 
When cystometry is carried out using a contrast filling medium and the 
procedure is visualized radiographically, the technique is known as 
videocystometry. 
CATHETER-MOUNTED TRANSDUCER: 
 Urethral pressure profile is measured using a catheter-mounted 
transducer that is drawn slowly through the urethra by a motorized 
armature. 
 The test is called static if no additional maneuver such as coughing or 
straining is performed. 
 If intravesical pressure is measured simultaneously while the patient 
coughs repeatedly during withdrawal of the catheter, the 
transmission of the cough impulse in the urethra and bladder can be 
measured and expressed as a ratio—the transmission pressure ratio. 
 measurements of the urethral pressure profile and parameters 
derived from it would be useful in assessing genuine stress 
incontinence
Neurophysiological Investigations 
Electromyography: 
To assess the extent of relaxation of the urethral 
sphincter during voiding. 
Interruption of the neural pathways between the 
pons and the sacral cord results in loss of 
coordination of sphincter and detrusor muscle 
activity, a condition known as detrusor-sphincter 
dyssynergia. 
Neuroimaging: MRI
Therapy of Disordered Micturition 
Goals in treatment: 
• Preservation of upper urinary tract 
• Maintain adequate bladder capacity with good 
compliance 
• Promote low-pressure micturition 
• Avoid bladder over-distension 
• Prevent urinary tract infection 
• Minimize use of Foley catheter 
• Choose therapy that minimizes patient risks while 
maximizing social, emotional, and vocational 
acceptability
MANAGEMENT OF BLADDER 
DISORDERS 
1.Detrusor Overactivity: 
Antimuscarinic medications are the mainstay of 
treatment
• main side effect is dry mouth, with less common 
effects of blurred vision, drowsiness, and 
constipation. Darifenacin and solifenacin are newer 
anticholinergics, with greater specificity for the M3 
receptor. 
• Botulinum A toxin (BoNT/A): 
introduced in the treatment of bladder overactivity by 
injection into the detrusor smooth muscle under 
cystoscopic guidance.
Normal N-M 
transmission 
Mechanism of Action 
Botulinum toxin
Desmopressin spray: 
• First introduced to treat DI, 
• Widely prescribed for children with nocturnal enuresis, 
• patients with MS and nighttime frequency also have 
used it. 
• Disabled patients and their caregivers, the difficulties 
of the patient having to get up to go to the toilet 
several times in the night can be considerable. 
• One or two nasal puffs of desmopressin from a 
metered-dose spray administered on retiring reduces 
urine output for the following 6 to 8 hours and may 
significantly lessen nighttime urinary frequency. 
• An oral preparation of desmopressin is now available. 
• Used once in 24 hours 
• Not be given to the elderly, in whom its use may 
precipitate congestive heart failure.
2.Incomplete Bladder Emptying or Urinary 
Retention 
Sterile intermittent catheterization 
• Most patients are advised initially to perform 
the technique at least twice a day 
• Although bacteriuria is noted in 50% of 
patients doing clean intermittent self-catheterization, 
the incidence of symptomatic 
urinary tract infections fortunately is low .
• In spinal cord disease, a combination 
of intermittent self-catheterization 
and an oral anticholinergic deals 
effectively with both aspects of 
bladder malfunction. 
• In a borderline significant residual 
volume, starting an anticholinergic 
may have the effect of increasing it . 
• This should be suspected if the 
medication has some initial beneficial 
effect for several days that then 
disappears. 
• This combined approach works well 
in patients with spinal cord disease 
such as MS, provided that the patient 
is not too severely disabled. recommended management of neurological 
incontinence. CISC, clean intermittent self-catheterization; 
PVR, postvoid residual
Permanent Indwelling Catheters: 
• When the patient is no longer able to perform self-catheterization, 
or when urge incontinence and 
frequency are unmanageable. 
• No longer weight-bearing and is chair-bound. 
• Suprapubic catheter is a better long-term 
alternative to an indwelling urethral catheter and 
often is the method of choice in managing 
incontinence in patients for whom other means are 
no longer effective.
The bladder symptoms in multiple sclerosis (MS) become increasingly difficult to manage with 
progression of spinal cord disease. This diagram summarizes the various measures that may be 
effective at each stage. BoNT/A, botulinum toxin A; CBME, cannabis-based medicinal extract, 
CISC, clean intermittent self-catheterization; DDAVP, trademark for preparation of 
desmopressin; IDC, indwelling catheter
External Device: 
Urge incontinence is the main problem and the bladder 
empties completely, some men are able to wear an 
external device attached around the penis. 
The simplest and least obtrusive is a self-sealing latex 
condom sheath, which can be put on each night or kept in 
place for up to 3 days. 
Sacral Nerve Stimulators 
• An extradural sacral nerve stimulator can be highly 
effective in lessening detrusor overactivity that is 
resistant to anticholinergic medication. 
• It seems highly likely that the mechanism of action of 
this device is stimulation in the presacral region of the 
pelvic afferents, which are known to have an inhibitory 
effect on the detrusor.
• Surgery : 
• range from minimally invasive procedures, (TVT, 
TOT) to increase bladder outflow resistance, or 
implantation of an artificial urethral sphincter, to 
the surgical techniques of increasing bladder 
capacity by cystoplasty or urinary diversion into a 
conduit or catheterizable reservoir
REFERENCES 
• Neurology in Clinical Practice e-dition, 5th 
Edition Bradley, Daroff, Fenichel & Jankovic. 
• ADAMS AND VICTOR’S PRINCIPLES OF 
NEUROLOGY Eighth Edition.

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Bladder disorders(neurogenic)

  • 1. BLADDER DISORDERS MODERATOR –PROF. N.C.DWIVEDI(MD)(DM) BY-Anil kumar g (JR3)
  • 2. Anatomy • The urinary bladder is a smooth muscle chamber composed of two main parts: – (1) the body, the major part, collects urine – (2) the neck, a funnel-shaped extension of the body, passing inferiorly and anteriorly into the urogenital triangle and connecting with the urethra
  • 3. • On the posterior wall of the bladder, lying immediately above the bladder neck, is a small triangular area called the trigone. • The trigone can be identified by the fact that its mucosa, the inner lining of the bladder, is smooth, in contrast to the remaining bladder mucosa, which is folded to form rugae. • At the lowermost apex of the trigone, the bladder neck opens into the posterior urethra, and the two ureters enter the bladder at the uppermost angles of the trigone. • Each ureter, as it enters the bladder, courses obliquely through the detrusor muscle and then passes another 1 to 2 centimeters beneath the bladder mucosa before emptying into the bladder
  • 4. The bladder neck (posterior urethra) is 2 to 3 centimeters long, and its wall is composed of detrusor muscle interlaced with a large amount of elastic tissue. The muscle in this area is called the internal sphincter.
  • 5. • Its natural tone normally keeps the bladder neck and posterior urethra empty of urine and, therefore, prevents emptying of the bladder until the pressure in the main part of the bladder rises above a critical threshold. • Beyond the posterior urethra, the urethra passes through the urogenital diaphragm, which contains a layer of muscle called the external sphincter of the bladder. • External sphincter muscle is a voluntary skeletal muscle, in contrast to the muscle of the bladder body and bladder neck, which is entirely smooth muscle. • The external sphincter muscle is under voluntary control of the nervous system and can be used to consciously prevent urination even when involuntary controls are attempting to empty the bladder.
  • 6. Blood supply • The bladder is supplied by the superior and inferior vesical arteries which are branches of anterior trunk of internal iliac artery. • The veins that drain the bladder form a plexus on the infero-lateral surface before ending in the internal iliac vein. • Most of the lymph from the urinary bladder ends in the external iliac nodes.
  • 7. Innervation of the Bladder • The principal nerve supply of the bladder is by way of the pelvic nerves, which connect with the spinal cord through the sacral plexus, mainly connecting with cord segments S-2 to S-4. • Coursing through the pelvic nerves are both sensory nerve fibers and motor nerve fibers. • The sensory fibers detect the degree of stretch in the bladder wall. Stretch signals from the posterior urethra are especially strong and are mainly responsible for initiating the reflexes that cause bladder emptying. • The motor nerves transmitted in the pelvic nerves are parasympathetic fibers. These terminate on ganglion cells located in the wall of the bladder. • Short postganglionic nerves then innervate the detrusor muscle.
  • 8. • In addition to the pelvic nerves, two other types of innervation are important in bladder function. Most important are the skeletal motor fibers transmitted through the pudendal nerve to the external urethral sphincter. These are somatic nerve fibers that innervate and control the voluntary skeletal muscle of the sphincter. • • Also, the bladder receives sympathetic innervations from the sympathetic chain through the hypogastric nerves, connecting mainly with the L-1,L-2 segments of the spinal cord. • These sympathetic fibers stimulate mainly the blood vessels and have little to do with bladder contraction. • Some sensory nerve fibers also pass by way of the sympathetic nerves and may be important in the sensation of fullness and, in some instances, pain.
  • 9. Innervation of the urinary bladder and its sphincters
  • 10. Micturition Reflex • As the bladder fills, many superimposed micturition contractions begin to appear. They are the result of a stretch reflex initiated by sensory stretch receptors in the bladder wall, especially by the receptors in the posterior urethra when this area begins to fill with urine at the higher bladder pressures.
  • 11. • Sensory signals from the bladder stretch receptors are conducted to the sacral segments of the cord through the pelvic nerves and then reflexively back again to the bladder through the parasympathetic nerve fibers by way of these same nerves.
  • 12.
  • 13. • When the bladder is only partially filled, these micturition contractions usually relax spontaneously after a fraction of a minute, the detrusor muscles stop contracting, and pressure falls back to the baseline. • As the bladder continues to fill, the micturition reflexes become more frequent and cause greater contractions of the detrusor muscle. • Once a micturition reflex has occurred but has not succeeded in emptying the bladder, the nervous elements of this reflex usually remain in an inhibited state for a few minutes to 1 hour or more before another micturition reflex occurs. • As the bladder becomes more and more filled, micturition reflexes occur more and more often and more and more powerfully.
  • 14. • Once the micturition reflex becomes powerful enough, it causes another reflex, which passes through the pudendal nerves to the external sphincter to inhibit it. • If this inhibition is more potent in the brain than the voluntary constrictor signals to the external sphincter, urination will occur. If not, urination will not occur until the bladder fills still further and the micturition reflex becomes more powerful.
  • 15. Facilitation or Inhibition of Micturition by the Brain • The micturition reflex is a completely autonomic spinal cord reflex, but it can be inhibited or facilitated by centers in the brain. • These centers include – (1) strong facilitative and inhibitory centers in the brain stem, located mainly in the pons, and – (2) several centers located in the cerebral cortex that are mainly inhibitory but can become excitatory
  • 16. • The micturition reflex is the basic cause of micturition, but the higher centers normally exert final control of micturition as follows: – 1. The higher centers keep the micturition reflex partially inhibited, except when micturition is desired. – 2. The higher centers can prevent micturition, even if the micturition reflex occurs, by continual tonic contraction of the external urethral sphincter until a convenient time presents itself. – 3. When it is time to urinate, the cortical centers can facilitate the sacral micturition centers to help initiate a micturition reflex and at the same time inhibit the external urethral sphincter so that urination can occur.
  • 17. • cortical activation with bladder filling, brain activity increased with increasing bladder volume in the periaqueductal gray- PAG matter in the midline pons, in the mid–cingulate cortex, and bilaterally in the frontal lobe area. • Inhibition of micturition was related to activation of parietal cortex, cerebellum, putamen. and supplementary motor area • insular, posterior parietal, and prefrontal activation during urinary storage.
  • 18.
  • 20. Irritative Voiding Symptoms • Urgency – is the sudden desire to void – in inflammatory conditions such as cystitis or in hyperreflexic neuropathic conditions such as neurogenic bladders resulting from upper motor neuron lesions. • Dysuria – painful urination – associated with inflammation. – The pain is typically referred to the tip of the penis in men or to the urethra in women. • Frequency – is the increased number of voids during the daytime, and – nocturia is nocturnal frequency. – Adults normally void five or six times a day and once at most during the nighttime hours. – Increased frequency may result from increased urinary output or decreased functional bladder capacity
  • 21. Obstructive Voiding Symptoms • Hesitancy – is a delay in the initiation of micturition. – results from the increased time required for the bladder to attain the high pressure necessary to exceed that of the urethra in the obstructed setting. • Decreased force of stream results from the high resistance the bladder faces and is often associated with a decrease in caliber of the stream. • Intermittency is the interruption of the urinary stream • Postvoid dribbling the uncontrolled release of the terminal few drops of urine. • Obstructive symptoms are most commonly due to benign prostatic hyperplasia, urethral stricture, or neurogenic bladder disorders, prostatic or urethral carcinoma and foreign body are other causes.
  • 22. Incontinence • Urinary incontinence is the involuntary loss of urine. • Total incontinence, patients lose urine at all times and in all positions. • Stress incontinence is the loss of urine associated with activities that result in an increase in intra-abdominal pressure (coughing, sneezing, lifting, exercising). • Uncontrolled loss of urine preceded by a strong urge to void is known as urge incontinence. • Chronic urinary retention may result in overflow incontinence. • The evaluation and treatment vary with each of the categories.
  • 23. Uncontrolled Contraction of the Bladder Muscle Normal bladder Patients with urge incontinence Patients with urge or frequency Urethral resistance Uncontrolled bladder muscle contractions 23
  • 24. Bladder sphincter dyssynergia (detrusor sphincter dysynergia (DSD), neurogenic detrusor overactivity (NDO) • It is a consequence of a neurological pathology such as spinal injury or multiple sclerosis that disrupts central nervous system regulation of the micturition reflex resulting in dys-coordination of the bladder musculature and the external urethral sphincter. • Instead of the urethral muscle relaxing completely during voiding, it dys-synergically contracts causing the flow to be interrupted and the bladder pressure to rise. • On cystography there is an irregular appearance of the bladder outline due to muscular contraction against the unrelaxed bladder sphincter.
  • 25.
  • 26. Symptoms • Symptomatically, people with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition. Diagnosis • Strictly DSD can only be diagnosed from an CMG trace
  • 27. Neurologic disorders causing urinary disturbences: With regard to the neurologic diseases that cause bladder dysfunction, • multiple sclerosis, usually with urinary urgency, is by far the most common. • degenerative diseases (Parkinson disease and multiple system atrophy) for 14 percent, • spinal cord disorders account for 12 percent of cases, • and frontal lobe lesions for 9 percent.
  • 28. Complete destruction of the cord below T12 – conus lesions – trauma, myelodysplasias, tumor, venous angioma, and necrotizing myelitis. – bladder is paralyzed for voluntary and reflexactivity – no awareness of the state of fullness; – voluntary initiation of micturition is impossible; – the tonus of the detrusor muscle is abolished and the bladder distends as urine accumulates until there is overflow incontinence; – voiding is possible only by the Crede´ maneuver, i.e.,lower abdominal compression and abdominal straining. • Usually the anal sphincter and colon are similarly affected, and there is “saddle” anesthesia and abolition of the bulbocavernosus and anal reflexes as well as the tendon reflexes in the legs. • The cystometrogram shows low pressure and no emptying contractions. • Management: catherisation & anticholinergics
  • 29. Disease of the sacral motor neurons in the spinal gray matter – autonomic bladder , autonomous bladder – the anterior sacral roots, or peripheral nerves innervating the bladder – lumbosacral meningomyelocele and the tethered cord syndrome. – a lower motor neuron paralysis of the bladder. – sacral and bladder sensation are intact. • Various causes pertain in cauda equina disease, the most frequent being compression by epidural tumor or disc, neoplastic meningitis, and radiculitis from herpes or cytomegalovirus. • a hysterical patient can suppress motor function and suffer a similar distention of the bladder.
  • 30. Interruption of sensory afferent fibers – atonic bladder – as in diabetes and tabes dorsalis (tabetic bladder). – motor nerve fibers unaffected • Although a flaccid (atonic) paralysis of the bladder may be purely motor or sensory, as described above, in most clinical situations there is interruption of both afferent and efferent innervation, as in cauda equina compression or severe polyneuropathy. • Neuropathies affecting mainly the small fibers are the ones usually implicated (diabetes, amyloid, etc.), but urinary retention also occurs in certain acute neuropathies such as Guillain-Barre´ syndrome. • Treatment includes intermittent self catheterisation
  • 31. Upper spinal cord lesions, above T12 – reflex neurogenic (spastic) bladder, automatic bladder – multiple sclerosis and traumatic myelopathy, which are the commonest causes; myelitis, spondylosis, arteriovenous malformation (AVM), syringomyelia, and tropical spastic paraparesis – If the cord lesion is of sudden onset, the detrusor muscle suffers the effects of spinal shock. At this stage, urine accumulates and distends the bladder to the point of overflow. – As the effects of spinal shock subside, the detrusor usually becomes reflexly overactive (detrusor hyperreflexia), and since the patient is unable to inhibit the detrusor and control the external sphincter, urgency, precipitant micturition, and incontinence result. – Incomplete lesions result in varying degress of urgency in voiding.
  • 32. • With slowly evolving processes involving the upper cord, such as multiple sclerosis, the bladder spasticity and urgency worsen with time and incontinence becomes more frequent. • In addition, initiation of voluntary micturition is impaired and bladder capacity is reduced. • Bladder sensation depends on the extent of involvement of sensory tracts. • Bulbocavernosus and anal reflexes are preserved. • The cystometrogram shows uninhibited contractions of the detrusor muscle in response to small volumes of fluid.
  • 33. • Some patients can still control urination in this condition by stimulating the skin (scratching or tickling) in the genital region, which sometimes elicits a micturition reflex. • Management: – Decompress the rectum or bladder - reverses the effects of unopposed sympathetic outflow. – Terazosin/ spinal anesthetic may be used as prophylaxis.
  • 34. Mixed type of neurogenic bladder. • In diseases such as multiple sclerosis, subacute combined degeneration, tethered cord, and syphilitic meningomyelitis, bladder function may be deranged from lesions at multiple levels, i.e., spinal roots, sacral neurons or their fibers of exit, and higher spinal segments. • The resultant picture is a combination of sensory, motor, and spastic types of bladder paralysis.
  • 35. • Stretch injury of the bladder wall, as occurs with anatomic obstruction at the bladder neck and occasionally with voluntary retention of urine, as in hysteria. • Repeated overdistention of the bladder wall often results in varying degrees of decompensation of the detrusor muscle and permanent atonia or hypotonia, although the evidence for this mechanism is uncertain. • The bladder wall becomes fibrotic and bladder capacity is greatly increased. • Emptying contractions are inadequate, and there is a large residual volume even after the Crede´ maneuver and strong contraction of the abdominal muscles. • As with motor and sensory paralyses, the patient is subject to cystitis, ureteral reflux, hydronephrosis and pyelonephritis, and calculus formation.
  • 36. • Frontal lobe incontinence Often the patient, because of his confused mental state, ignores the desire to void and the subsequent incontinence. There is also a supranuclear type of hyperactivity of the detrusor and precipitant evacuation. • Nocturnal enuresis or urinary incontinence during sleep, due presumably to a delay in acquiring inhibition of micturition.
  • 37. Urodynamic Studies 1.Noninvasive Bladder Investigations voiding diary may be kept by either the patient or the caregiver of the approximate amount drunk, frequency of micturition, and episodes of incontinence, recorded over the course of several days. This gives a useful indication of the severity of the bladder complaints on which management decisions can be based.
  • 38. a.Urinary flowmetry: • noninvasive investigation, valuable particularly when combined with an ultrasound measurement of the postmicturition residual volume. • It as a base of the collecting system is a spinning disk, and flow of urine onto this disk tends to slow its speed of rotation, which a servomotor holds constant. • Urine flow is derived from measurement of the power necessary to maintain rotation speed, and the machine usually produces a graphic printout, together with an analysis, for the time taken to reach maximal flow, maximum and average flow rates, and the voided volume A, Urinary flow meter. The side of the uroflow transducer has been cut away to show the disk at the base of the funnel, which rotates as urine passes into the collecting vessel. B, Typical (normal) printout from the uroflowmeter. A total of 290 mL was voided (upper trace), with a maximum flow rate of 30 mL per second (lower trace). b.simple ultrasound machines are now available that require little operator training and make it easy to determine whether the postmicturition residual is negligible or in excess of 100 mL
  • 39. Investigations Requiring Catheterization • Cystometry, the registration of bladder pressure, can be performed during filling and voiding . • Detrusor pressure is derived by subtraction of the abdominal pressure (measured using a rectal line) from the intravesical pressure (measured using a vesical line). The efficiency of the subtraction usually is checked at the beginning of cystometry by asking the subject to cough. • This produces an increase in abdominal pressure and hence in intravesical pressure, but no increase in detrusor pressure. Cystometry during bladder filling. The bladder was filled (top trace) at 50 mL per minute (Vinfus) to a total of 300 mL. Detrusor pressure (Pdet) is derived by subtracting pressure in the rectum (Pabd) from the measured intravesical pressure (Pves). At the beginning of the trace, these two values can be seen to be subtracting effectively because on coughing there is an abrupt increase in intravesical pressure but no increase in detrusor pressure. The detrusor pressure did not exceed 10 cm H2O, which is normal.
  • 40. VIDEOCYSTOMETRY : When cystometry is carried out using a contrast filling medium and the procedure is visualized radiographically, the technique is known as videocystometry. CATHETER-MOUNTED TRANSDUCER:  Urethral pressure profile is measured using a catheter-mounted transducer that is drawn slowly through the urethra by a motorized armature.  The test is called static if no additional maneuver such as coughing or straining is performed.  If intravesical pressure is measured simultaneously while the patient coughs repeatedly during withdrawal of the catheter, the transmission of the cough impulse in the urethra and bladder can be measured and expressed as a ratio—the transmission pressure ratio.  measurements of the urethral pressure profile and parameters derived from it would be useful in assessing genuine stress incontinence
  • 41. Neurophysiological Investigations Electromyography: To assess the extent of relaxation of the urethral sphincter during voiding. Interruption of the neural pathways between the pons and the sacral cord results in loss of coordination of sphincter and detrusor muscle activity, a condition known as detrusor-sphincter dyssynergia. Neuroimaging: MRI
  • 42. Therapy of Disordered Micturition Goals in treatment: • Preservation of upper urinary tract • Maintain adequate bladder capacity with good compliance • Promote low-pressure micturition • Avoid bladder over-distension • Prevent urinary tract infection • Minimize use of Foley catheter • Choose therapy that minimizes patient risks while maximizing social, emotional, and vocational acceptability
  • 43. MANAGEMENT OF BLADDER DISORDERS 1.Detrusor Overactivity: Antimuscarinic medications are the mainstay of treatment
  • 44. • main side effect is dry mouth, with less common effects of blurred vision, drowsiness, and constipation. Darifenacin and solifenacin are newer anticholinergics, with greater specificity for the M3 receptor. • Botulinum A toxin (BoNT/A): introduced in the treatment of bladder overactivity by injection into the detrusor smooth muscle under cystoscopic guidance.
  • 45. Normal N-M transmission Mechanism of Action Botulinum toxin
  • 46. Desmopressin spray: • First introduced to treat DI, • Widely prescribed for children with nocturnal enuresis, • patients with MS and nighttime frequency also have used it. • Disabled patients and their caregivers, the difficulties of the patient having to get up to go to the toilet several times in the night can be considerable. • One or two nasal puffs of desmopressin from a metered-dose spray administered on retiring reduces urine output for the following 6 to 8 hours and may significantly lessen nighttime urinary frequency. • An oral preparation of desmopressin is now available. • Used once in 24 hours • Not be given to the elderly, in whom its use may precipitate congestive heart failure.
  • 47. 2.Incomplete Bladder Emptying or Urinary Retention Sterile intermittent catheterization • Most patients are advised initially to perform the technique at least twice a day • Although bacteriuria is noted in 50% of patients doing clean intermittent self-catheterization, the incidence of symptomatic urinary tract infections fortunately is low .
  • 48. • In spinal cord disease, a combination of intermittent self-catheterization and an oral anticholinergic deals effectively with both aspects of bladder malfunction. • In a borderline significant residual volume, starting an anticholinergic may have the effect of increasing it . • This should be suspected if the medication has some initial beneficial effect for several days that then disappears. • This combined approach works well in patients with spinal cord disease such as MS, provided that the patient is not too severely disabled. recommended management of neurological incontinence. CISC, clean intermittent self-catheterization; PVR, postvoid residual
  • 49. Permanent Indwelling Catheters: • When the patient is no longer able to perform self-catheterization, or when urge incontinence and frequency are unmanageable. • No longer weight-bearing and is chair-bound. • Suprapubic catheter is a better long-term alternative to an indwelling urethral catheter and often is the method of choice in managing incontinence in patients for whom other means are no longer effective.
  • 50. The bladder symptoms in multiple sclerosis (MS) become increasingly difficult to manage with progression of spinal cord disease. This diagram summarizes the various measures that may be effective at each stage. BoNT/A, botulinum toxin A; CBME, cannabis-based medicinal extract, CISC, clean intermittent self-catheterization; DDAVP, trademark for preparation of desmopressin; IDC, indwelling catheter
  • 51. External Device: Urge incontinence is the main problem and the bladder empties completely, some men are able to wear an external device attached around the penis. The simplest and least obtrusive is a self-sealing latex condom sheath, which can be put on each night or kept in place for up to 3 days. Sacral Nerve Stimulators • An extradural sacral nerve stimulator can be highly effective in lessening detrusor overactivity that is resistant to anticholinergic medication. • It seems highly likely that the mechanism of action of this device is stimulation in the presacral region of the pelvic afferents, which are known to have an inhibitory effect on the detrusor.
  • 52. • Surgery : • range from minimally invasive procedures, (TVT, TOT) to increase bladder outflow resistance, or implantation of an artificial urethral sphincter, to the surgical techniques of increasing bladder capacity by cystoplasty or urinary diversion into a conduit or catheterizable reservoir
  • 53. REFERENCES • Neurology in Clinical Practice e-dition, 5th Edition Bradley, Daroff, Fenichel & Jankovic. • ADAMS AND VICTOR’S PRINCIPLES OF NEUROLOGY Eighth Edition.