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Discussion Starter #1 (Edited)
The detruser muscle is supplied by parasympathetic nerves from S2-S4 via pelvic splanchnic nerves these fibers cause detruser contraction and relaxation of the internal urethral sphincter (voiding). While sympathetic fibers from T11-L2 work the contrary retaining urine. Pudendal nerve supplies somatic voluntary control of the external urethral sphincter.
There's a bladder contraction reflex arc (just like the skeletal muscle reflex arc) that sends afferents and receive efferents to and from the sacral spinal cord. The higher cortical and spinal cord levels sends inhibitory impulses to the sacral centers.

Lower Motor Neuron Damage

  • Autonomous Neurogenic Bladder = Sacral spinal centers damaged
  • Motor Neurogenic Bladder = Efferents damage
  • Sensory Neurogenic Bladder = Afferents damage (no stretch sensation conveyed to spinal cord)
All of the three cause distended bladder with overflow incontinence and dribbling and predisposition to infection. The autonomous variety may show some spinal cord lesions on MRI.

Upper Motor Neuron Damage

  • Automatic Neurogenic Bladder = is loss of brain stem control over the spinal centers and leads to retention. Damage at any level above the conus medularis causes what's called Spastic bladder in which manual stimulation results in a reflex forceful contraction of the detruser muscle.
  • Uninhibited Neurogenic Bladder = is no cortical control over the brain stem centers. Voiding mechanics is normal but uninhibited at misappropriate times and places. example children before toilet training and frontal lobe lesions.
 
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