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Neurogenic bladder
Neurogenic bladder
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Urinary bladder

  1. 1. Dr. Parag Moon Senior Resident, Dept. of Neurology, GMC, Kota.
  2. 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. 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. 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. 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. 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. 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. 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. 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. 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. 11.  Three mixed nerves innervate urinary tract.  Hypogastric nerve-sympathetic  Pelvic nerve-parasympathetic  Pudendal nerves-somatic nervous system innervation.
  12. 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.
  13. 13.  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.
  14. 14.  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.
  15. 15.  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
  16. 16.  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
  17. 17.  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
  18. 18.  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.
  19. 19.  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,
  20. 20.  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.
  21. 21.  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.
  22. 22.  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,
  23. 23.  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.
  24. 24.  Hypertrophy of detrusor muscle  If detrusor pressure exceeds internal/external urinary sphincter pressure-incontinence  Symptoms -Urgency, frequency, hesitancy, interupted stream, urge incontinence.
  25. 25.  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
  26. 26.  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.
  27. 27.  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.
  28. 28.  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
  29. 29.  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
  30. 30.  Anti cholinergic- oxybutynin, tolterodine, trospium, darifenacin, solifenacin  Botulinum toxin A injection  Intravesical capsaicin injection  Sacral rhizotomy
  31. 31.  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
  32. 32.  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.
  33. 33.  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.
  34. 34.  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
  35. 35.  Indwelling catheter  Intermittent clean catheterization  Bethanechol  Sacral stimulation  Bladder muscle augmentation
  36. 36. Thank You
  37. 37.  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