neurology and implications in various disorders

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