Diagram showing neural circuits controlling continence and micturition, Diagram showing neural circu

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This lecture was conducted during the Nephrology
Unit Grand Ground by Medical Student rotated
under Nephrology Division under the supervision
and administration of Prof. Jamal Al Wakeel, Head
of Nephrology Unit, Department of Medicine and
Dr. Abdulkareem Al Suwaida, Chairman of
Department of Medicine. Nephrology Division is
not responsible for the content of the
presentation for it is intended for learning and
/or education purpose only.
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(No Transcript)
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Normal Micturition

• Presented by
• Rinda Mousa
• Medical Student
• July 2008

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Diagram showing neural circuits controlling
continence and micturition                     
                                                  
   
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• Central coordination of micturition occurs in the
  pontine micturition center.
• The parietal lobes and thalamus
  receive and coordinate detrusor afferent stimuli
  while the frontal lobes and basal ganglia provide
  modulation with inhibitory signals.
• Peripheral coordination occurs in the sacral
  micturition center at cord levels S2-S4.
• 1-Sympathetic efferents from spinal
  levels T11-L2 via the hypogastric nerve mediate
  alpha-adrenergic contraction of the urethral
  smooth muscle and relaxation of bladder smooth
  muscle (detrusor) to allow urine storage during
  bladder filling.
• 2- Sphincter closure is augmented
  by striated sphincter muscle contraction with
  cholinergic somatic stimulation from cord levels
  S2-S4 via the pudendal nerve .
• 3- A fascial and muscular urethral
  support "hammock" compresses the urethra when
  there is increased abdominal pressure or when the
  pelvic muscles are contracted

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Diagram showing neural circuits controlling
continence and micturition                     
                                                  
   
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• When detrusor afferent stimuli indicate the need
  to void, parasympathetic activation via the
  pelvic nerve from the sacral micturition center.
  This, in turn, causes muscarinic contraction of
  the detrusor muscle and preganglionic inhibition
  of sympathetics, leading to urethral relaxation .
• In addition, a variety of neurotransmitter
  systems in the urothelial lining of the bladder
  and in bladder interstitial cells likely play a
  role in mediating bladder contraction and
  relaxation via afferent signaling .

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• Urine storage reflexes.
• Distension of the bladder produces low level
  vesical afferent firing, which in turn stimulates
• (1) the sympathetic outflow to the
  bladder outlet (base and urethra) .
• (2) pudendal outflow to the external
  urethral sphincter.
• These responses occur by spinal reflex pathways
  and represent "guarding reflexes," which promote
  continence.
• Sympathetic firing also inhibits detrusor muscle
  and modulates transmission in bladder ganglia.
• A region in the rostral pons (the pontine
  storage center, or "L" region) increases external
  urethral sphincter activity.

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Diagram showing neural circuits controlling
continence and micturition                     
                                                  
   
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• (B) Voiding reflexes.
• Intense bladder afferent firing activates
  spinobulbospinal reflex pathways passing through
  the pontine micturition center, which stimulate
• 1-the parasympathetic outflow to the
  bladder and internal sphincter smooth muscle
• 2-inhibit the sympathetic and pudendal
  outflow to the urethral outlet.
• Ascending afferent input from the spinal cord may
  pass through relay neurons in the periaqueductal
  gray (PAG) before reaching the pontine
  micturition center.

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Diagram showing neural circuits controlling
continence and micturition                     
                                                  
   
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Normal voiding physiology (Panel A) and
involuntary detrusor contraction commonly
associated with symptoms of urge incontinence and
overactive bladder (Panel B)
                                                  
        
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Patterns of neurogenic detrusor-sphincter
dysfunction
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The large circles represent the detrusor and the
small circles the urinary sphincter. Dotted lines
represent normal function, thin lines decreased
function (hypo- or areflexia), and thick lines
increased function (hyperreflexia). Suprapontine
lesions typically result in detrusor
hyper-reflexia (uninhibited contractions) with
normal sphincter function. Suprasacral lesions
typically result in both detrusor and sphincter
hyperreflexia, with detrusor-sphincter
dyssynergia. Lumbosacral lesions may result in
several patterns, including (1) detrusor
hyperreflexia with sphincter hyporeflexia/areflexi
a, or (2) impaired detrusor contractility with
sphincter hyperreflexia. Complete subsacral conus
lesions typically result in both detrusor and
sphincter hyporeflexia. Subsacral cauda equina
and peripheral nerves lesions result in detrusor
hyporeflexia with intact sphincter function if
the pelvic nerve plexus is damaged but the
pudendal nerve is intact, and in normal detrusor
function with sphincter hyporeflexia if the
pudendal nerve is damaged but the pelvic nerve is
intact. In rare instances, epiconal lesions may
result in normal detrusor function with sphincter
hyperreflexia, but impaired detrusor function
with sphincter hyperreflexia is most common.
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• Overflow incontinence
• is a term used to describe the dribbling
  and/or continuous leakage associated with
  incomplete bladder emptying, due to impaired
  detrusor contractility and/or bladder outlet
  obstruction.
• Neurogenic bladder is a nonspecific term used to
  refer to conditions ranging from areflexic
  noncontractile bladder to detrusor overactivity
  (Urge incontinence).
• Painful bladder syndrome/interstitial cystitis
  (PBS/IC)
• is a disorder characterized by bladder pain
  of variable severity, due to urothelial
  abnormalities altered bladder epithelial
  expression of HLA Class I and II antigens,
  decreased expression of uroplakin , and altered
  integrity of the glycosaminoglycan (GAG) layer .
  It is likely that neurologic upregulation with
  central sensitization and increased activation of
  bladder sensory neurons during normal bladder
  filling . It is also possible that the increase
  in visceral (bladder) sensitivity is secondary to
  a primary somatic injury (bowel and other pelvic
  organs) that has sensitized central pathways that
  overlap with afferents from the bladder.

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• Age-related
  change.
• The prevalence of involuntarydetrusor
  overactivity increases with aging. Detrusor
  overactivity has been found in 21 percent of
  healthy, continent..
• The ability to postpone voiding decreases, and
  the total capacity of the bladder may diminish.
• Urinary flow rate decreases in both older men and
  women, probably due to an age-related decrease in
  detrusor contractility .
• Low estrogen levels after menopause result in
  atrophy of the superficial and intermediate
  layers of the urethral mucosal epithelium with
  subsequent atrophic urethritis, diminished
  urethral mucosal seal, loss of compliance, and
  irritation.
• Most older men have benign prostatic hyperplasia.
  Approximately one-half develop prostate
  hypertrophy with the potential for bladder outlet
  obstruction and voiding symptoms.
• The diurnal pattern of fluid excretion may shift
  towards increased volume of urine excreted later
  in the day. Possible causes include peripheral
  edema due to comorbid diseases and medications .

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• Thank you