Dr. Parag Moon
Dept. of Neurology,
Bladder divided into
◦ Detrusor (aka as “body” or “dome” of bladder)-
consists of smooth muscle
◦ Base-trigone and bladder neck, intimately
connected to pelvic floor.
Bladder outlet-two urethral sphincters
◦ Internal (smooth muscle) sphincter-bladder neck
and proximal urethra
◦ External (striated muscle) sphincter-membranous
Females-Less complex urinary sphincter
Cortical control areas
In frontal and cingulate gyri as well as
Provide inhibitory influence on micturition at
level of pons
Excitatory influence on external urinary
Allows voluntary control of micturition
Normal bladder evacuation can be delayed
until appropriate time and place to void are
Pontine micturition center (PMC, Barrington’s
nucleus or M-region)
Locus ceruleus, pontomesencephalic gray
matter, nucleus tegmentolateralis dorsalis.
Essential for coordination of micturition.
Modulates opposing effects of
parasympathetic and sympathetic nervous
systems on lower urinary tract.
From T11- L2 cord level
Synapse in inferior mesenteric and hypogastric
Continues via hypogastric nerves to α-adrenergic
receptors in bladder neck and proximal urethra,
β-adrenergic receptors in bladder fundus.
Also innervate parasympathetic ganglia in
Activation of thoracolumbar sympathetic
outflow-> norepinephrine release-> detrusor
relaxation and bladder neck (internal sphincter)
From detrusor nucleus (intermediolateral
column of gray matter) at S2–S4 cord level
Passes through pelvic nerves to cholinergic
parasympathetic neurons in ganglia in
Acetylcholine produces detrusor contraction
through M2 and M3 receptor
Proximal urethra-nitric oxide release->
urethral smooth muscle relaxation.
From pudendal (Onuf ’s) nucleus at S2–S4
Passes through pudendal nerve to external
Supraspinal Centers produce excitatory
influence on pudendal nucleus during bladder
filling stage to produce external urethral
sphincter and pelvic floor contraction to help
Three mixed nerves innervate urinary tract.
Pudendal nerves-somatic nervous system
Afferent information on state of bladder
filling-sensory fibers in dense suburothelial
and muscular plexuses.
Small myelinated Aδ fibers-distention and
Unmyelinated C fibers-painful stimuli.
Pelvic nerves-> sacral dorsal root ganglia->
◦ Damage to sensory fibers from bladder to spinal
◦ No bladder sensation, eventual loss of motor
◦ Damage to motor fibers from spinal cord to bladder
◦ Normal sensation, failure of motor function
◦ Injury to cortical regulation of bladder reflex
◦ Normal sensation and motor function, urge
incontinence, urinary frequency
◦ Damage to both motor and spinal fibers between
bladder and spinal cord
◦ Failure to generate bladder contraction, loss of
◦ Damage to spinal cord between sacrum and
◦ Poorly coordinated bladder function, loss of
Cortical lesions, such as intracranial bleed,
ischemic stroke, brain tumor, hydrocephalus.
Reduced awareness of bladder fullness and
low capacity bladder due to reduction of
inhibition of PMC by cortical and subcortical
No high bladder pressures developed.
Symptoms-urinary frequency, urgency, urge
Urodynamic testing- normal bladder
sensation and filling parameters, multiple
With an underlying neurologic-detrusor
With no known etiology-detrusor instability.
Urinary storage symptoms (frequency, urgency,
urge urinary incontinence)-57% to 83%
Voiding symptoms (poor force of stream,
hesitancy, incomplete emptying)-17% to 27%
Urodynamic-detrusor hyperreflexia and urethral
Striated urethral sphincter-poorly sustained
Symptoms of bladder outlet obstruction (BOO)-
should be confirmed by multichannel urodynamic
Degeneration of nucleus of Onuf
Denervation of external striated sphincter.
Sympathetic nerve atrophy-nonfunctional
bladder and an open bladder neck.
Urodynamic-detrusor hyperreflexia, few
individuals may have detrusor areflexia or
poorly sustained bladder contractions.
Bladder neck (internal sphincter)-open at
rest, with striated sphincter denervation.
Detrusor-sphincter dyssynergia (DSD)-
simultaneous detrusor and urinary sphincter
contractions produce high pressures in
bladder (up to 80–90 cm H2O)
Leads to vesicoureteral reflux
Lesions above T10 level
Detrusor overactivity, or detrusor
Activation of prejunctional M1 receptors
which facilitates acetylcholine release,
Spinal Cord Lesions
In acute lesion-spinal shock.
Anal and bulbocavernosus reflex typically absent.
Urinary retention and constipation.
Urodynamic-areflexic detrusor and rectum.
Internal and external urethral sphincter
After spinal shock, bladder function returns.
detrusor activity increases in reflex excitability to
an overactive state—detrusor hyperreflexia.
Spinal cord lesions (above sixth thoracic
Urodynamic-detrusor hyperreflexia, striated
sphincter dyssynergia, smooth sphincter
Autonomic dysreflexia-exaggerated sympathetic
response to any stimuli below level of lesion.
Inciting event-instrumentation of urinary bladder
Sweating, headache, hypertension, and reflex
Acute management of autonomic dysreflexia-
decompress rectum or bladder.
Parenteral ganglionic or adrenergic blocking
agents, such as chlorpromazine, may be
Oral blocking agents, including terazosin,
may be used prophylactically
Spinal anesthetic before instrumentation.
Spinal cord lesions (below T6)
Urodynamic-detrusor hyperreflexia, striated
sphincter dyssynergia, and smooth sphincter
dyssynergia but no autonomic dysreflexia.
Incomplete bladder emptying secondary to
detrusor sphincter dyssynergia, or loss of
facilitatory input from higher centers.
Cornerstone of treatment involves CIC and
detrusor overactivity of the bladder
noted in 50% to 90% of patients with MS and
areflexia in 20% to 30% of patients with MS
often noted during the
first 10 years following MS diagnosis and
tends to increase
as the patient’s level of disability worsens
Urinary incontinence is a common symptom
Urodynamic-detrusor overactivity, poor
bladder compliance, a fixed, obstructing
outlet that may be incompetent as well.
Risk of upper urinary tract damage
Detrusor hyperactivity with impaired bladder
Frequent but weak involuntary detrusor
Incontinence despite incomplete bladder
Associated with bladder trabeculation, slow
bladder contraction velocity, elevated urinary
residual volume after voiding attempts.
Seen in nursing home residents
Pelvic trauma, low myelomeningocele,
Both afferent and efferent neural connections
to bladder are lost
Failure to generate bladder contraction, loss
of bladder sensation
Urodynamic-normal capacity, compliant
bladder, nable to sense filling at any volume,
nable to generate any voiding contraction.
Tabes dorsalis, diabetes, syringomyelia
Poor bladder sensation
Allows bladder to distend without triggering a
reflex bladder contraction.
Gradual stretching of detrusor muscle-
detrusor failure, atonia
Urodynamics-large capacity, poorly sensitive
bladder and impaired bladder contractility
Painless urinary retention, overflow
incontinence and increased risk of UTI.
Herpetic infection, trauma, pelvic surgery,
lumbar spinal stenosis, lumbosacral
Normal sensation of bladder filling but is
unable to generate detrusor pressure
sufficient to empty bladder.
Urodynamic -normal sensation and capacity,
no generation of voiding contractions.
Painful urinary retention or impaired bladder
Neuroanatomy, neurophysiology and
neuropharmacology of urinary bladder;
Continuum 2013;pg 7-20
Swaiman’s pediatric neurology: disorders of
micturition and defecation; pg 2157-2170.
Neurogenic Bladder; Peter T., Peter M.;
Advances in Urology;Volume 2012, Article ID
816274, 16 pages
The Epidemiology and Pathophysiology of
Neurogenic Bladder; David Ginsberg; Am J
Manag Care. 2013;19:S191-S196
Parece que tem um bloqueador de anúncios ativo. Ao listar o SlideShare no seu bloqueador de anúncios, está a apoiar a nossa comunidade de criadores de conteúdo.
Atualizámos a nossa política de privacidade.
Atualizámos a nossa política de privacidade de modo a estarmos em conformidade com os regulamentos de privacidade em constante mutação a nível mundial e para lhe fornecer uma visão sobre as formas limitadas de utilização dos seus dados.
Pode ler os detalhes abaixo. Ao aceitar, está a concordar com a política de privacidade atualizada.