This document summarizes the anatomy and physiology of the urinary bladder and urinary sphincters. It describes the neural pathways that control bladder filling and emptying from the cortical and subcortical areas down to the spinal cord and peripheral nerves. It then discusses various types of neurogenic bladder disorders that can result from lesions or injuries in different parts of the neural pathways.

1. Dr. Parag Moon
Senior Resident,
Dept. of Neurology,
GMC, Kota.

2.  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
urethra.
 Females-Less complex urinary sphincter
mechanism

3.  Cortical control areas
 In frontal and cingulate gyri as well as
subcortical areas
 Provide inhibitory influence on micturition at
level of pons
 Excitatory influence on external urinary
sphincter.
 Allows voluntary control of micturition
 Normal bladder evacuation can be delayed
until appropriate time and place to void are
chosen.

4.  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.

5.  In bladder emptying stage, PMC sends excitatory
influence ->sacral spinal cord ->detrusor
contraction
 Simultaneously sends inhibitory influence->
thoracolumbar cord->internal urinary sphincter
relaxation.
 In bladder storage phase, PMC inhibition->sacral
spinal cord supression-> detrusor relaxation
 Simultaneously sends excitatory influence-
>thoracolumbar cord->internal urethral
sphincter contraction.

6.  Ascending sensory information reaches
periaqueductal gray (PAG) matter->
hypothalamus and thalamus-> anterior
cingulate cortex, insula, prefrontal cortex.
 Inhibits PAG, which itself has excitatory input
to PMC.
 Hypothalamus has excitatory influence on
PAG.
 Conscious decision to void, prefrontal cortex
inhibition of PAG interrupted
 Simultaneously hypothalamus stimulates PAG.
 Result excitation of PMC.

7.  Spinal neurons regulating micturition
 Dorsal commissure, superficial dorsal horn,
parasympathetic nucleus.
 Interneurons send rostral projections
 Regulate spinal segmental reflexes.
 Glutamate-> excitatory transmitter
 Glycine and γ-aminobutyric acid (GABA)->
inhibitory neurotransmitters

8.  From T11- L2 cord level
 Synapse in inferior mesenteric and hypogastric
plexuses
 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
detrusor wall.
 Activation of thoracolumbar sympathetic
outflow-> norepinephrine release-> detrusor
relaxation and bladder neck (internal sphincter)
contraction

9.  From detrusor nucleus (intermediolateral
column of gray matter) at S2–S4 cord level
 Passes through pelvic nerves to cholinergic
parasympathetic neurons in ganglia in
detrusor.
 Acetylcholine produces detrusor contraction
through M2 and M3 receptor
 Proximal urethra-nitric oxide release->
urethral smooth muscle relaxation.

10.  From pudendal (Onuf ’s) nucleus at S2–S4
cord level
 Passes through pudendal nerve to external
sphincter.
 Supraspinal Centers produce excitatory
influence on pudendal nucleus during bladder
filling stage to produce external urethral
sphincter and pelvic floor contraction to help
maintain continence,

11.  Three mixed nerves innervate urinary tract.
 Hypogastric nerve-sympathetic
 Pelvic nerve-parasympathetic
 Pudendal nerves-somatic nervous system
innervation.

12.  Afferent information on state of bladder
filling-sensory fibers in dense suburothelial
and muscular plexuses.
 Small myelinated Aδ fibers-distention and
trigger micturition
 Unmyelinated C fibers-painful stimuli.
 Pelvic nerves-> sacral dorsal root ganglia->
PAG region.

14.  Bladder filling stage
 Supraspinal center inhibits PMC
 ↑↑thoracolumbar sympathetic outflow
 ↓↓sacral parasympathetic outflow to lower
urinary tract.
 ↑↑ pudendal nerve.
 Detrusor smooth muscle relaxation, bladder
neck smooth muscle contraction, external
urinary sphincter contraction.

15.  Bladder emptying phase
 Supraspinal centers’ inhibitory outflow to
PMC suppressed
 ↓↓thoracic sympathetic outflow
 ↑↑sacral parasympathetic outflow
 ↓↓pudendal nerve
 Detrusor smooth muscle contraction, bladder
neck smooth muscle relaxation, external
urinary sphincter relaxation.

17.  Neurogenic bladder affects
 40–90%-multiple sclerosis,
 37–72% -Parkinsonism
 15%-stroke
 70–84%-spinal cord injury
 61%-spina bifida
 Other causes-autonomic neuropathy, pelvic
surgery sequelae, cauda equina syndrome

18.  Sensory
◦ Damage to sensory fibers from bladder to spinal
cord
◦ No bladder sensation, eventual loss of motor
function
 Motor
◦ Damage to motor fibers from spinal cord to bladder
◦ Normal sensation, failure of motor function
 Uninhibited
◦ Injury to cortical regulation of bladder reflex
◦ Normal sensation and motor function, urge
incontinence, urinary frequency

19.  Autonomous
◦ Damage to both motor and spinal fibers between
bladder and spinal cord
◦ Failure to generate bladder contraction, loss of
bladder sensation
 Reflex
◦ Damage to spinal cord between sacrum and
brainstem
◦ Poorly coordinated bladder function, loss of
sensation, incontinence

20.  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
structure damage.
 No high bladder pressures developed.
 Symptoms-urinary frequency, urgency, urge
urinary incontinence.

21.  Urodynamic testing- normal bladder
sensation and filling parameters, multiple
unstable contractions
 With an underlying neurologic-detrusor
hyperreflexia
 With no known etiology-detrusor instability.
 Detrusor overactivity,

22.  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
sphincter bradykinesia.
 Striated urethral sphincter-poorly sustained
contraction.
 Symptoms of bladder outlet obstruction (BOO)-
should be confirmed by multichannel urodynamic
studies.

23.  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.

24.  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
hyperreflexia
 Activation of prejunctional M1 receptors
which facilitates acetylcholine release,

25.  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
activities-normal.
 After spinal shock, bladder function returns.
detrusor activity increases in reflex excitability to
an overactive state—detrusor hyperreflexia.

26.  Hypertrophy of detrusor muscle
 If detrusor pressure exceeds internal/external
urinary sphincter pressure-incontinence
 Symptoms -Urgency, frequency, hesitancy,
interupted stream, urge incontinence.

27.  Spinal cord lesions (above sixth thoracic
vertebrae)
 Urodynamic-detrusor hyperreflexia, striated
sphincter dyssynergia, smooth sphincter
dyssynergia.
 Autonomic dysreflexia-exaggerated sympathetic
response to any stimuli below level of lesion.
 Inciting event-instrumentation of urinary bladder
or rectum.
 Sweating, headache, hypertension, and reflex
bradycardia

28.  Acute management of autonomic dysreflexia-
decompress rectum or bladder.
 Parenteral ganglionic or adrenergic blocking
agents, such as chlorpromazine, may be
used.
 Oral blocking agents, including terazosin,
may be used prophylactically
 Spinal anesthetic before instrumentation.

29.  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
anticholinergic medications.

30.  detrusor overactivity of the bladder
 noted in 50% to 90% of patients with MS and
detrusor
 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

31.  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

32.  Anti cholinergic- oxybutynin, tolterodine,
trospium, darifenacin, solifenacin
 Botulinum toxin A injection
 Intravesical capsaicin injection
 Sacral rhizotomy

33.  Detrusor hyperactivity with impaired bladder
contractility (DHIC)
 Frequent but weak involuntary detrusor
contractions
 Incontinence despite incomplete bladder
emptying
 Associated with bladder trabeculation, slow
bladder contraction velocity, elevated urinary
residual volume after voiding attempts.
 Seen in nursing home residents

34.  Pelvic trauma, low myelomeningocele,
surgery
 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.

35.  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.

36.  Herpetic infection, trauma, pelvic surgery,
lumbar spinal stenosis, lumbosacral
meningomyelocoele
 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
emptying

37.  Indwelling catheter
 Intermittent clean catheterization
 Bethanechol
 Sacral stimulation
 Bladder muscle augmentation

39. Thank You

40.  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