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Control of bladder
 

Control of bladder

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control of bladder

control of bladder

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    Control of bladder Control of bladder Presentation Transcript

    • CONTROL OF BLADDER
    • ANATOMY • Detrusor muscle: – is a layer of the urinary bladder wall made of smooth muscle fibers arranged in spiral, longitudinal, and circular bundles. – The smooth muscle of the bladder, the detrusor is innervated by sympathetic nervous system fibers from the lumbar spinal cord and parasympathetic fibers from the sacral spinal cord.
    • Urethral sphincters • External sphincter (sphincter urethrae): – located at the bladder's distal inferior end in females and inferior to the prostate (at the level of the membranous urethra) in males – It is a secondary sphincter to control the flow of urine through the urethra. – Unlike the internal sphincter muscle, the external sphincter is made of skeletal muscle, – It is under voluntary control of the somatic nervous system. – It is innervated by pudendal nerves • Internal sphincter muscle of urethra: – It is located at the bladder's inferior end and the urethra's proximal end at the junction of the urethra with the urinary bladder. – The internal sphincter is a continuation of the detrusor muscle and is made of smooth muscle, – it is under involuntary or autonomic control. – This is the primary muscle for prohibiting the release of urine.
    • • There are three layers of muscle that are known to control urine flow through the urethra; – an inner band of longitudinal smooth muscle – a middle band of circular smooth muscle – an external band of striated muscle called the rhabdosphincter. • The urethra is controlled by the sympathetic, parasympathetic, and somatic divisions of the peripheral nervous system. • The sympathetic innervation (nerve supply) comes from the sympathetic preganglionic neurons located in the upper lumbar spinal cord along the hypogastric nerve and terminates in the longitudinal and circular smooth muscle layers in the urethra. • The parasympathetic nerve supply comes from the parasympathetic preganglionic neurons in the sacral spinal cord and also terminates in the longitudinal and circular smooth muscle layers. • The somatic nerve supply arises from the urethral sphincter motor neurons in the ventral horn of the sacral spinal cord; better known as Onuf’s nucleus. The pudendal nerve that extends from Onuf’s nucleus, connects directly to the rhabdosphincter muscle to control micturation
    • PARASYMPATHETIC: CENTRE: S2-S4 in intermediolateral column SUPPLY THROUGH: pelvic splanchnic nerves END IN : GANGLIA IN BLADDER WALL NEUROTRANSMITTER : ACh VIA M2, M3 FUNCTION: Cholinergic preganglionic neurons within the intermediolateral sacral cord send axons to ganglionic cells within the pelvic plexus and the bladder wall. Postganglionic neurons within the bladder wall and pelvic plexus release acetylcholine, which activates cholinergic receptors M2 and M3 on the detrusor smooth muscle cells initiates Bladder detrusor contraction Internal sphincter relaxation
    • • SYMPATHETIC: CENTRE: T11-L2 intermediolateral column SUPPLY THROUGH: sympathetic chain ganglia-prevertebral gangliahypogastric and pelvic plexus –inferior mesentric ganglion –post ganglionic fibres FUNCTION: – innervate the bladder via short adrenergic neurons. – Via β-adrenergic receptors -inhibition and relaxation of the detrusor muscle. – Through alpha receptors causes Contraction of internal sphincter – Facilitate bladder storage and continence
    • • SOMATIC : CENTRE: ONUF’S NUCLEUS S2-S4 SUPPLY THROUGH: PUDENDAL NERVES FUNCTION : CONTROLS THE EXTERNAL SPHINCTER
    • BRADLEY’S LOOP • • • • LOOP 1 LOOP 2 LOOP 3 LOOP 4
    • LOOP 1- cerebral loop • involving the brainstem, cerebral cortex, and basal ganglia structures, which initiates and inhibits switching between filling and voiding states.
    • LOOP 1 • • • • FRONTAL CORTEX BASAL GANGLIA THALAMIC NUCLEI CEREBELLUM PONTOMESENCEPHALIC RETICULAR FORMATION
    • • INTERRUPTION OF THIS LOOP OCCURS IN • • • • • • CVA BRAIN TUMOUR HEAD INJURY MULTIPLE SCLEROSIS PARKINSONS DISEASE INTERRUPTION OF THIS LOOP RESULTS IN UNINHIBITED BLADDER
    • LOOP 2- Cord loop • From brainstem structures to the conus medullaris), which coordinates detrusor and sphincter contract ion and relaxation.
    • LOOP 2 • BRAIN STEM MICTURITION CENTRE RETICULOSPINAL TRACT LATERAL AND POSTERIOR COLUMN DETRUSOR
    • • THIS LOOP IN AFFECTED IN • • • • • SP CORD TRAUMA MULTIPLE SCLEROSIS SPINAL CORD TUMOUR ARACHNOIDITIS PARTIAL INTERRUPTION RESULTS IN DETRUSOR HYPER REFLEXIA UNABLE TO GENERATE VOLUNTARY VOIDING
    • LOOP-3 Detrusor reflex loop • detrusor afferents to pudendal motor neurons, which causes sphincter relaxation when the detrusor is active.
    • LOOP-3 • DETRUSOR MUSCLE CONTRACTION • AFFERENTS TO PUDENTAL MOTOR NEURONS • INHIBITION OF INTERNAL SPINCTER • SPINCTER RELAXATION
    • LOOP-4 Urethral reflex loop • from urethral afferents to pudendal motor neurons), which maintains the sphincter tone when the detrusor is inactive.
    • LOOP 4 • PUDENTAL MOTOR NUCLEI • INTERNEURONS • DETRUSOR & EXT SPHINCTER
    • LOOP -5 Corticospinal pathways • from motor cortex to pudendal motor neurons, which are concerned with the voluntary control of the sphincters and pelvic floor.
    • Neurotransmitors • The sympathetic storage reflex or pelvic-to-hypo-gastric reflex is initiated when the bladder swells. Stretch receptors cause postganglionic neurons to release norepinephrine (NE). NE causes the bladder to relax and the urethra to contract, thus preventing urine loss. • The somatic storage reflex or the pelvic-to-pudendal or guarding reflex is initiated when one laughs, sneezes, or coughs, which causes increased bladder pressure. Glutamate is the primary excitatory transmitter for the reflex. Glutamate activates NMDA and AMPA receptors which produce action potentials. These action potentials activate the release of acetylcholine causing the rhabdosphincter muscle fibers to contract. When the guarding reflex does not function normally, SUI occurs
    • SPINAL REFLEX ARC • AFFERENT ARC: – Sensation of stretch arising from bladder wall travels through the parasympathetic nerves to the center for micturition • DETRUSOR CENTER OR SACRAL PARASYMPATHETIC NUCLEUS – sacral segments S2,S4 of the spinal cord. • EFFERENT ARC (PARASYMPATHATIC) – travels through the pelvic nerves to the pelvic plexus; short postganglionic fibers travel from the plexus to the detrusor muscle.
    • HIGHER CENTERS • CORTICAL CENTERS: – Situated in • Medial frontal lobe • Cingulate gyrus • Corpus collosum • cortical input is inhibitory on micturition reflexes.
    • • Subcortical centers: – thalamic nuclei – limbic system, – Red nucleus – Substantia nigra – Hypothalamus – Subthalamic nucleus. • Cerebellum : – anterior vermis of the cerebellum – fastigial nucleus are concerned with micturition.
    • • Lesions resulting from tumors, aneurysms, or cerebrovascular disease remove the cortical inhibition, which results in increased excitatory input to the brainstem, facilitation of the micturition reflex, and the clinical appearance of urinary frequency and urgency. • Descending fibers in the corticospinal tracts emanate from the cortical region to innervate sacral parasympathetic neurons and the motor nucleus controlling voluntary sphincter function
    • PONTINE MICTURITION CENTERS (Barrington's nucleus): – pontomesencephalic reticular formation micturition center (located in the locus ceruleus, pontomesencephalic gray matter, and nucleus tegmentolateralis dorsalis). – collection of cell bodies located in the rostral pons in the brainstem involved in the supraspinal regulation of micturition (urination). – The PMC makes connections with other brain centers to control micturition, including the medial frontal cortex, insular cortex, hypothalamus and periaqueductal gray (PAG). – The PAG in particular acts a relay station for ascending bladder information from the spinal cord and incoming signals from higher brain areas.
    • Course from higher centres • From the pontomesencephalic micturition center, efferents to the spinal cord descend by way of the reticulospinal tracts (located medially and anteriorly in the anterior funiculus) to the detrusor motor neurons in the intermediolateral cell columns of the sacral gray matter (S2–S4). • Efferents from the cortical and subcortical micturition centers descend by way of the pyramidal tracts to the pudendal nuclei (Onuf’s nucleus) in the sacral spinal cord (S2–S4). • The pudendal nerves, whose motor neurons are located in the ventral horns of sacral segments S2–S4, innervate the striated muscle around the urethra
    • • Onuf’s nucleus – It is a distinct group of neurons located in the ventral part (laminae IX) of the anterior horn of the sacral region of the spinal cord . It extends from S1 to S3 mainly in S2 – It is involved in the maintenance of micturition and defecatory continence, as well as muscular contraction during orgasm. – It contains motor neurons, and is the origin of the pudendal nerve. – The neurons of Onuf’s nucleus are responsible for controlling external sphincter muscles of the anus and urethra. – The dorsomedial subnucleus innervates the the ventrolateral subgroup connects to the urethral striated sphincter (vonluntary sphincter) and rectal striated sphincter – Onuf’s nucleus controlled the ischiocavernosus and bulbocavernosus muscles which function in penile erection and ejaculation in males. – Neurotransmitters in Onuf's nucleus – The motoneurons in Onuf’s nucleus contain a dense array of serotonin and norepinephrine receptors and transmitters and are activated by glutamate. When the 5-HT and NE receptors are stimulated, the guarding reflex occurs to prevent voiding of the bladder caused by unexpected abdominal pressure sneezing, coughing etc.
    • • REGULATION OF MICTURITION: – Micturition is a spino-bulbo-spinal reflex. In response to stretch, afferent impulses are carried to the sacral spinal cord. – Sacral cord projections to the PAG are relayed to the pontine micturition center (Barrington's nucleus) – The pontine micturition center is under the control of centers in the forebrain. – During bladder filling, neurons within the PMC are turned off. – at a critical level of bladder distention, the afferent activity arising from mechanoreceptors in the bladder wall switches the PMC on and enhances its activity. – neurons in the PMC send descending excitatory projections to spinal parasympathetic preganglionic neurons innervating the bladder and inhibitory interneurons regulating Onuf's nucleus. – This activation results in relaxation of the urethra and contraction of the bladder due to stimulation of parasympathetic and inhibition of sympathetic outflow to the bladder, and the removal of somatic activation of the external urethral sphincter. This pattern of activity can also be elicited through the conscious desire to void
    • • There is a curious preservation of the Onuf nucleus neurons in amyotrophic lateral sclerosis. • The internal uretheral sphincter at the neck of the bladder receives its innervation from the intermediolateral column at the T12-L1 level, via the sympathetic prevertebral plexus and the hypogastric nerve
    • • In the infant, bladder function is purely reflex, but with cortical maturation and the completion of myelination inhibitory control over this reflex develops, as well as voluntary regulation of the external sphincter. • Normal micturition requires intact autonomic and spinal pathways, and cerebral inhibition and control of the external sphincter must be normal
    • • Forebrain lesions may cause loss of voluntary bladder control, but do not affect the spino-bulbo-spinal reflex mechanisms. • Disruption of the bulbospinal pathway from the pontine micturition center to the sacral cord, and lesions affecting the afferent and efferent connections between the bladder and the conus medullaris may cause severe disturbances in bladder function. • The term neurogenic bladder refers to bladder dysfunction caused by disease of the nervous system. • Symptoms of bladder dysfunction are often among the earliest manifestations of nervous system disease. • Frequency, urgency, precipitate micturition, massive or dribbling incontinence, difficulty in initiating urination, urinary retention, and loss of bladder sensation may occur. • One practical classification of neurogenic bladder dysfunction is based on urodynamic criteria and includes the following types: – – – – – uninhibited, Reflex autonomous, sensory paralytic motor paralytic.
    • Uninhibited neurogenic bladder • there is a loss of the cortical inhibition of reflex voiding, • while bladder tone remains normal. • Bladder distention causes contraction in response to the stretch reflex. • There is frequency, urgency, and incontinence that are not associated with dysuria. • Hesitancy may precede urgency. • Bladder sensation is usually normal. • There is no residual urine.
    • Reflex neurogenic bladder/SPASTIC/hyperreflexic • lesions above the level of the sacral bladder center and below the level of the pontomesencephalic micturition center. • occurs with severe myelopathy or extensive brain lesions causing interruption of both the descending autonomic tracts to the bladder and the ascending sensory pathways above the sacral segments of the cord. • UMN CUT OFF LMN INTACT • associated with quadriplegia or paraplegia and in advanced cases of multiple sclerosis • Detrusor spinter synergia lost results in obstructed voiding, an interrupted urinary stream, incomplete emptying, and high intravesical pressures because the sphincter fails to relax correctly . • Upper urinary tract dilatation and kidney damage may develop subsequently.
    • • Loss of the normal inhibition from higher centers results in detrusor contraction during bladder filling. • contractions occur spontaneously or may be provoked by coughing or changing posture.(stress incontinence) • detrusor becomes overactive, so there is urinary frequency, urgency, urge incontinence (the patient is unable to inhibit the detrusor reflex), • inability to initiate micturition voluntarily. • Small volumes of urine stimulate uninhibited detrusor muscle contraction; the bladder capacity is reduced but residual urine may be increased (increased postmicturit ion residual volume). • bulbocavernosus and superficial anal reflexes are preserved. • With lesions above the splanchnic out flow, bladder fullness may induce a “mass reflex” with paroxysmal hypertension, headaches, diaphoresis, and bradycardia.
    • Autonomous/FLACID neurogenic bladder • is one without external innervation. • seen with complete lesions below the T12 segment that involve the conus medullaris and cauda equina. , S2-S4 motor or sensory roots, or the peripheral nerves, and with congenital anomalies such as spina bifida. • It occurs with sacral myelomeningocele and tumors of the conus medullaris–cauda equina region • There is destruction of the parasympathetic supply. • Sensation is absent • There is no reflex or voluntary control of the bladder; • contractions occur as the result of stimulation of the intrinsic neural plexuses within the bladder wall. • The amount of residual urine is large, but the bladder capacity is not greatly increased
    • • urinary retention because the tone of the detrusor muscle is abolished • the bladder distends as urine accumulates. Inability to initiate micturition, • overflow incontinence, and increased residual urine develop . • There is associated saddle anesthesia with absence of the bulbocavernosus and superficial anal reflexes. • Anal sphincter control is often similarly affected. • The bladder capacity may greatly increase, and • its walls may become fibrotic. • A large residual urine volume may therefore occur because of incomplete detrusor contractions.
    • Motor paralytic bladder • develops when the motor nerve supply to the bladder is interrupted. • The bladder distends and decompensates, • but sensation is normal. • The residual urine and bladder capacity vary. • Occurs in lumbar spinal stenosis, lumbosacral meningomyelocele, or following radical hysterectomy or abdominop erineal resect ion. • In most of these cases, pat ients suffer from painful urinary retention or imp aired bladder emptying. • Residual urine is markedly increased. • The bulbocavernosus and sup erficial anal reflexes are usually absent , but sacral and bladder sensation are present .
    • Sensory paralytic bladder • occur in tabes dorsalis, syringomyelia, or diabetes mellitus • is found with lesions that involve the posterior roots or posterior root ganglia of the sacral nerves, or the posterior columns of the spinal cord. • Sensation is absent, and there is no desire to void. He can void voluntarily (motor intact) • There may be distention, dribbling, and difficulty both in initiating micturition and in emptying the bladder. • There is a large amount of residual urine • Urinary retention, overflow incontinence, or urinary tract infection may be early symptoms. • The bulbocavernosus and superficial anal reflexes may be absent , decreased, or present .