Bladder dysfunctionDr behnaz ansari

Anatomic Considerations:�in the autonomic nervous system there arealways two efferent neurons serving thisalways two efferent neurons serving thisfunction, one (preganglionic) arising fromits nucleus in the brainstem or spinal cordand the other (postganglionic) arising fromspecialized nerve cells in peripheral ganglia

� The autonomic nervous system, from an anatomic point of view, isdivided into two parts: the craniosacral, or parasympathetic,and the thoracolumbar or sympatheticand the thoracolumbar, or sympathetic

� The systems differ architecturally in that the ganglion in thesympathetic nervous system is located in a contiguous andinterconnected, longitudinal chain (sympathetic chain) paravertebrally,whereas the parasympathetic ganglia are distributed in proximity to thestructures they innervate.

� Moreover, the main neurotransmitter of the postganglionic connectionto the end organ is norepinephrine in the case of the sympatheticnerves and acetylcholine for parasympathetic innervation. There areexceptions with regard to the sympathetic innervation of sweat glands(sudomotor), which are cholinergic.

The Parasym pathetic NervousSystem:�There are two divisions of the parasympathetic

nervous system: cranial and sacral The cranialnervous system: cranial and sacral. The cranialdivision originates in the visceral nuclei of themidbrain, pons, and medulla. These nuclei includethe Edinger-Westphal pupillary nucleus, superiorand inferior salivatory nuclei, dorsal motor nucleusof the vagus, and adjacent reticular nuclei.

� The preganglionic fibers from the Edinger-Westphal nucleustraverse the oculomotor nerve and synapse in the ciliaryganglion in the orbit; axons of the ciliary ganglion cellsinnervate the ciliary muscle and pupillary sphincter .

� The preganglionic fibers of the superior salivatory nucleusenter the facial nerve and, at a point near the geniculateganglion, form the greater superficial petrosal nerve, throughwhich they reach the sphenopalatine ganglion;postganglionic fibers from the cells of this ganglion innervatethe lacrimal gland .

� Other fibers originating in the saliva tory nuclei are carried in thefacial nerve and traverse the tympanic cavity as the chordatympani to eventually join the submandibular ganglion Cells oftympani to eventually join the submandibular ganglion. Cells ofthis ganglion innervate the submandibular and sublingualglands.

� Axons of the inferior saliva tory nerve cells enter theglossopharyngeal nerve and reach the otic ganglion through thetympanic plexus and lesser superficial petrosal nerve; cells ofthe otic ganglion send fibers to the parotid gland.

� Preganglionic fibers, derived from the dorsal motor nucleus ofthe vagus and adjacent visceral nuclei in the lateral reticularformation (mainly the nucleus ambiguus), enter the vagus nerveand terminate in ganglia situated in the walls of many thoracicand abdominal viscera.

�The sacral part of the parasympathetic systemoriginates in the lateral horn cells of the secondoriginates in the lateral horn cells of the second,third, and fourth sacral segments. Axons of thesesacral neurons, constituting the preganglionicfibers, traverse the sacral spinal nerve roots of thecauda equina and synapse in ganglia that lie withinthe walls of the distal colon, bladder, and otherpelvic organs

The Sympathetic NervousSystem:� The preganglionic neurons of the sympathetic division originate

in the intermediolateral cell column of the spinal gray matter,from the eighth cervical to the second lumbar segments.

� The axons of the nerve fibers originating in the intermediolateralcolumn are of small caliber and are myelinated; when grouped,they form the white comm unicating rami . These preganglionicfibers synapse with the cell bodies of the postganglionicneurons, which are collected into two large ganglionated chainsor cords, one on each side of the vertebral column(paravertebral ganglia), and several single prevertebral ganglia.These constitute the sympathetic ganglia.

�Axons of the sympathetic ganglion cells are also ofsmall caliber but are unmyelinatedsmall caliber but are unmyelinated.

�Most of the postganglionic fibers pass via graycommunicating rami to their adjacent spinal nervesof T5 to L2; they supply blood vessels, sweatglands, and hair follicles, and also form plexusesthat supply the heart, bronchi, kidneys, intestines,pancreas, bladder, and sex organs

� The sympathetic innervation of the adrenal medulla is uniquein that its secretory cells receive preganglionic fibers directly,via the splanchnic nerves. This is an exception to the rulethat organs innervated by the autonomic nervous systemreceive only postganglionic fibers.

� This special arrangement can be explained by the fact thatcells of the adrenal medulla are the morphologic homologuesof the postganglionic sympathetic neurons and secreteepinephrine and norepinephrine (the postganglionictransmitters) directly into the bloodstream

�There are 3 cervical (superior, middle, andinferior or stellate) 11 thoracic and 4 to 6inferior, or stellate), 11 thoracic, and 4 to 6lumbar sympathetic ganglia. The headreceives its sympathetic innervation fromthe eighth cervical and first two thoraciccord segments.

� Postganglionic fibers from cells of the superior cervicalganglion follow the internal and external carotid arteries andinnervate the blood vessels and smooth muscle as well as theinnervate the blood vessels and smooth muscle, as well as thesweat, lacrimal, and salivary glands of the head. Includedamong these postganglionic fibers, issuing mainly from Tl, arethe pupillodilator fibers and those innervating the Muller muscleof the upper eyelid.

� The arm receives its postganglionic innervation from the inferiorcervical ganglion and uppermost thoracic ganglia (the twoare fused to form the stellate ganglion). The cardiac plexus andother thoracic sympathetic nerves are derived from the stellateganglion and the abdominal visceral plexuses, from the fifth tothe ninth or tenth thoracic ganglia

The Central Regulation of VisceralFunction:� Integration of autonomic function takes place at two

levels,the brainstem and the cerebrum. In the brainstem, themain visceral afferent nucleus is the nucleus tractussolitarius (NTS). The caudal NTS integrates these signalsand projects to a number of critical areas in thehypothalamus, amygdala, and insular cortex

� The supranuclear regulatory apparatus of the hypothalamusincludes three main cerebral structures: the frontal lobecortex, the insular cortex, and the amygdaloid and adjacentnuclei

�Sympathetic responses are most readilyobtained by stimulation of the posterior andobtained by stimulation of the posterior andlateral regions of the hypothalamus, andparasympathetic responses from theanterior regions.

Regulation of Bladder Function:� the main component of which is the large

detrusor (transitional type) muscle; a functionaldetrusor (transitional type) muscle; a functionalinternal sphincter composed of similar muscle;and the striated external sphincter or urogenitaldiaphragm. in the male, the internal sphincter alsoprevents the reflux of semen from the urethraduring ejaculation.

Micturation:� For micturition to occur, the sphincters must relax, allowing

the detrusor to expel urine from the bladder into the urethra.This is accomplished by a complex mechanism involvingmainly the parasympathetic nervous system (the sacralperipheral nerves derived from the second, third, and fourthsacral segments of the spinal cord and their somaticsensorimotor fibers) and, to a lesser extent, sympatheticfibers derived from the thorax. The vaguely localizablebrainstem "micturition centers,“ with their spinal andsuprasegmental connections, may contribute.

� The detrusor muscle receives motor innervation from nerve cellsin the intermediolateral columns of gray matter, mainly from thethird and also from the second and fourth sacral segments ofthird and also from the second and fourth sacral segments ofthe spinal cord (the "detrusor center"). These neurons giverise to preganglionic fibers that synapse in parasympatheticganglia within the bladder wall.

� There are also beta-adrenergic receptors in the dome of thebladder, which are activated by sympathetic fibers that arise inthe intermediolateral nerve cells of TlO, Tll, and T12 segments.These preganglionic fibers pass via inferior splanchnic nerves tothe inferior mesenteric ganglia ; pre- and postganglionicsympathetic axons are conveyed by the hypogastric nerve to thepelvic plexus.

� The internal sphincter and base of the bladder (trigone),consisting of smooth muscle, are also innervated to some extentby the sympathetic fibers of the hypogastric nerves; theirby the sympathetic fibers of the hypogastric nerves; theirreceptors are mainly of alpha-adrenergic type.

� The external urethral and anal sphincters are composed ofstriated muscle fibers. Their innervation, via the pudendalnerves, is derived from a densely packed group of somatomotorneurons (nucleus of Onuf) in the anterolateral horns of sacralsegments 2, 3, and 4. Cells in the ventrolateral part of Onuf'snucleus innervate the external urethral sphincter, and cells ofthe mediodorsal part innervate the anal sphincter. The musclefibers of the sphincters respond to the nicotinic effects of ACh.

� According to Ruch, the descending pathways from themidbrain tegmentum are inhibitory and those from thepontine tegmentum and posterior hypothalamus arefacilitatory. The pathway that descends with thecorticospinal tract from the motor cortex is inhibitory. Thusthe net effect of lesions in the brain and spinal cord on themicturition reflex, at least in animals, may be either inhibitoryor facilitatory.

Neurogenic BladdergDysfunction

� The storage function of the bladder is affected followingsuprapontine or infrapontine/suprasacral lesions. This results ininvoluntary spontaneous or induced contractions of the detrusorinvoluntary spontaneous or induced contractions of the detrusormuscle (detrusor overactivity), which can be identified duringthe filling phase of urodynamics.

� The voiding function of the bladder can be affected byinfrapontine lesions. Following spinal cord damage, there issimultaneous contraction of the external urethral sphincter anddetrusor muscle, detrusor-sphincter dyssynergia, whichresults in incomplete bladder emptying and abnormally highbladder pressures.

� Following lesions of the conus medullaris or cauda equina,voiding dysfunction can be due to poorly non-relaxingurethral sphincters and sustained detrusor contractions .

Cortical Lesions:� Among patients with disturbed bladder control, various frontal

lobe disturbances have been reported: intracranial tumors,damage after rupture of an aneurysm, penetrating brainwounds, and prefrontal lobotomy (leukotomy). The typicalclinical picture of frontal lobe incontinence is a patient withsevere urgency and frequency of micturition and urgeincontinence but without dementia; the patient is Micturition isnormally coordinated, indicating that the disturbance is in thehigher control of these processes. Urinary retention also hasbeen described in patients with brain lesions.

�A much less common cause of dementia is normal-pressure hydrocephalus where incontinence is apressure hydrocephalus, where incontinence is acardinal feature. Improvement in urodynamicfunction has been demonstrated within hours oflumbar puncture (LP) in patients with this disorder.

Basal Ganglia Lesions:� Bladder symptoms in Parkinson disease (PD) correlate with

neurological disability (Araki and Kuno, 2000) and stage ofdisease; both findings appear to support a link betweendopaminergic degeneration and symptoms of urinarydysfunction.

� The most frequent complaints are of nighttime frequency,urgency, and difficulty voiding (Sakakibara et al., 2001a), andthe most common abnormality in urodynamic studies isdetrusor overactivity (Araki et al., 2000).

� In a patient with severe urinary symptoms but mildparkinsonism a diagnosis of multiple systemparkinsonism, a diagnosis of multiple systematrophy (MSA) should be considered. The onset ofurogenital symptoms in MSA may precede overtneurological involvement; ED and bladdersymptoms begin on average 4 to 5 years beforediagnosis and 2 years before more specificneurological symptoms appear.

� It is thought that detrusor overactivity is caused by neuronalloss in the pontine region, whereas incomplete bladderemptying is caused by loss of parasympathetic innervation ofthe detrusor after neuronal degeneration in theintermediolateral cell columns of the spinal cord. In addition,anterior horn cell loss in the Onuf nucleus results indenervation of the urethral sphincter so that the patient has acombination of detrusor overactivity, incomplete bladderemptying, and a weak sphincter

Brainstem Lesions:� Voiding difficulty is a rare but recognized symptom of a

posterior fossa tumor and has been reported in series ofpatients with brainstem disorders (Fowler, 1999).

� The proximity in the dorsal pons between the pontinemicturition center and medial longitudinal fasciculus meansthat a disorder of eye movements, such as an internuclearophthalmoplegia (INO), is highly likely in patients with apontine disorder causing a voiding difficulty.

Spinal Cord Lesions:�Spinal cord disorders are the most common cause

for neurogenic bladder dysfunction Transspinalfor neurogenic bladder dysfunction. Transspinalpathways connect the pontine micturition centersto the sacral cord. Intact connections arenecessary to effect the reciprocal activity of thedetrusor and sphincter needed to switch betweenstorage and voiding. After disconnection from thepons, this synergistic activity is lost, resulting indetrusor-sphincter dyssynergia.

� Initially after acute SCI, there usually is a phase ofneuronal shock of variable durationneuronal shock of variable duration,characterized clinically by complete urinaryretention and urodynamics demonstrating anacontractile detrusor. Gradually over the course ofweeks, new reflexes emerge to drive bladderemptying and cause detrusor contractions inresponse to low filling volumes.

�Because bladder innervation arises more caudallythan innervation of the lower limbs any form ofthan innervation of the lower limbs, any form ofspinal cord disease that causes bladderdysfunction is likely to produce clinical signs in thelower limbs as well, unless the lesion is limited tothe conus. This rule is sufficiently reliable to be ofgreat value in determining whether a patient has aneurogenic bladder caused by spinal cord disease.

Spinal Cord Injury:�After SCI, bladder dysfunction can be of such

severity as to cause ureteric refluxseverity as to cause ureteric reflux,hydronephrosis, and eventual upper urinary tractdamage. Before the introduction of moderntreatments, renal failure was a common cause ofdeath after SCI.

Multiple Sclerosis:�The pathophysiological consequences of

progressive MS affecting the spinal cord for theprogressive MS affecting the spinal cord for thebladder are similar to those of SCI.

�70% of a self-selected group of patients with MSresponding to a questionnaire classified the impactbladder symptoms had on their life as “high” or“moderate” (Hemmett et al., 2004).

� The most common urinary symptom is urgency; all series ofurodynamic studies in patients with MS have shown that thisis due to detrusor overactivity. Hesitancy of micturition maybe a symptom patients volunteer or admit on directquestioning, but the more disabled may find themselvesunable to initiate micturition voluntarily, emptying theirbladders only with an involuntary hyperreflexiccontraction and an interrupted urinary flow.

� A particular problem in MS is that neurological symptomsmay deteriorate acutely when the patient has an infectionand pyrexia, including urinary tract infection (UTI).

Conus and Cauda EquinaLesions:� Impairment of bladder, bowel, and sexual function

is particularly difficult for patients to bearis particularly difficult for patients to bearpsychologically when they are otherwise ambulantand mobile. Although a number of series havereported the urodynamic changes that can occurafter a cauda equina lesion, no analysis has beenperformed to assess the effect of a cauda equinalesion on quality of life.

Disturbances of PeripheralInnervation:�Diabetic Neuropathy:�Urodynamic studies demonstrate impaired�Urodynamic studies demonstrate impaired

detrusor contractility, reduced urine flow, increasedpostmicturition residual volume, and reducedbladder sensation. It seems likely that vesicalafferent and efferent fibers are involved, causingreduced awareness of bladder filling anddecreased bladder contractility.

� Amyloid Neuropathy:� Lower urinary tract symptoms generally appear early on and

are present in 50% of patients within the first 3 years of thedisease. Patients most often complain of difficulty in bladderemptying and incontinence (Andrade, 2009).

� Immune-Mediated Neuropathies:� Approximately one-fourth of patients with Guillain-Barré

syndrome have bladder symptoms. These symptoms usuallyoccur in those patients with more severe neuropathy andappear after limb weakness is established. Both detrusorareflexia and bladder overactivity have been described.

�Autoimmune AutonomicGanglionopathyGanglionopathy

�Pure Autonomic Failure�Myotonic Dystrophy

Urinary Retention in YoungWomen Fowler syndrome :�Urinary retention or symptoms of obstructed

voiding in young women in the absence of overtvoiding in young women in the absence of overtneurological disease have long puzzled urologistsand neurologists alike, and in the absence of anyconvincing organic cause, the condition was oncesaid to be “hysterical.” The typical clinical picture isthat of a young woman in the age range of 20 to 30years who presents with retention and a bladdercapacity greater than 1 L.

� MRI of the brain, spinal cord, and cauda equina are normal. Thelack of sacral anesthesia makes a cauda equina lesionimprobableimprobable.

� An association between this syndrome and polycystic ovarieswas described in the original description of the syndrome.

� In some young women with urinary retention, concentric needleelectrode examination of the striated muscle of the urethralsphincter reveals complex repetitive discharges and myotonia-like activity, decelerating bursts.

� it could until recently only be managed symptomatically.However, it is now known that these patients respondparticularly favorably to sacral neuromodulation.

Diagnostic Evaluation:�History�Bladder Diary�Bladder Diary�Physical Examination�Screening for Urinary Tract Infections�Bladder Scan�Ultrasound Scan�Urodynamic Studies

Urodynamic Studies:�Urodynamic studies examine the function of the

lower urinary tract Included in this aspect oflower urinary tract. Included in this aspect ofevaluation are measurements of urine flow rateand residual volume, cystometry during both fillingand voiding, videocystometry, and urethralpressure profilometry.

NONINVASIVE BLADDERINVESTIGATIONS:� A commonly used design for a flow meter consists of a

commode or urinal into which the patient passes urine asnaturally as possible. In the base of the collecting system is aspinning disc. The urinary flow is calculated based upon thepower necessary to maintain the rotation speed.

� A graphic printout of the urinary flow is obtained, and timetaken to reach maximum flow, maximum and average flowrates, and voided volume are analyzed . It is important thatthe patient performs the test with a comfortably full bladdercontaining, if possible, a volume of at least 150 mL.

INVESTIGATIONS REQUIRINGCATHETERIZATION:� Cystometry evaluates the pressure/volume relationship during

nonphysiological filling of the bladder and during voiding. The detrusorpressure is derived by subtraction of the abdominal pressure (measuredpressure is derived by subtraction of the abdominal pressure (measuredusing a catheter in the rectum) from the intravesical pressure(measured using a catheter in the bladder). The rate of filling isrecorded by the machine, which pumps sterile water or saline throughthe catheter in the bladder.

� For speed and convenience, most laboratories use filling rates ofbetween 50 and 100 mL/min. This nonphysiological rapid filling doesmean that the full bladder capacity can be reached usually within 7 or 8minutes. The first sensation of bladder filling may be reported at around100 mL, and full capacity is reached between 400 and 600 mL. Inhealthy persons, the bladder expands to contain this amount of fluidwithout an increase of pressure more than 15 cm H2O.

�When bladder filling has been completed,the patient voids into the flow meter withthe patient voids into the flow meter, withthe bladder and rectal lines still in place.Valuable information can be obtained bymeasuring detrusor pressure and urine flowsimultaneously.

Electromyography:� EMG has been used to demonstrate changes of

reinnervation in the urethral or anal sphincter in a fewneurogenic disorders.

� Lesions of the cauda equina� Isolated urinary retention in young woman� anterior horn cells� in the Onuf nucleus are selectively lost in MSA, and this

results in changes in the sphincter muscles that can beidentified by EMG.

Management of NeurogenicBladder Dysfunction:� Voiding Dysfunction:� Intermittent self-catheterization Reflex voiding using trigger techniques

and the Credé maneuver (nonforceful smooth even pressure appliedand the Credé maneuver (nonforceful, smooth, even pressure appliedfrom the umbilicus toward the pubis) are usually not recommended, asthey may result in high detrusor pressure and incomplete bladderemptying during voiding (Fowler et al., 2009).

� Suprapubic vibration using a mechanical “buzzer” has beendemonstrated to be effective in patients with MS with incompletebladder emptying and detrusor overactivity, but its effect is limited(Prasad et al., 2003).

� Alpha-blockers relax the internal urethral sphincter in menbladder outletobstruction.

� Botulinum toxin injections

Storage Dysfunction:� Antimuscarinic Medications� DesmopressinDesmopressin� Cannabinoids� Botulinum Toxin� Vanilloids� Sacral Neuromodulation� Nerve Root Stimulators� Surgery

Case report:

� A 66-year-old woman suffered from severe stress incontinencewhich had gradually developed into continuous urinaryincontinenceincontinence.

� Video-urodynamic studies at the first presentation demonstratedan a contractile detrusor without bladder sensation (bladdersensation at first desire to void >600 mL) in cystometry andactivity in the external-sphincter electromyography with a needleelectrode.

� On standing up, almost all of her urine leaked without postvoidresidual urine, with a Valsalva leak point pressure of less than45 cm H2O, indicating an intrinsic sphincter deficiency (Fig. 1).There were no neurological abnormalities including touch, painsensations and motor weakness, and the patella tendon reflexand Achilles tendon reflex were normal.

� Two years later, the patient suddenly experienced syncope,and thus visited the emergency room. She underwent atracheotomy because of bilateral paralysis of the vocal cords

� Three years later, she had difficulty in using her hands and alsoexperienced gait difficulty. She was hospitalized because shecould no longer carry out intermittent self catheterization andcould no longer carry out intermittent self-catheterization andalso had a urinary tract infection.

� A neurological examination revealed a weakness of theextensor and flexor muscle of the neck, and disproportionateantecollis, and orthostatic hypotension (blood pressure onsupine position: 140/80 mmHg, on standing up: 100/70 mmHg).The Jaw reflex, Patella tendon reflex and Achilles tendon reflexwas brisk, and rigidity and akinesia were noted. Cerebellarataxia including a positive finger-nose test and knee-toe testwas noted.

What guess?g