Notes on Bladder Reflexes (Jan 29)

In an atonic bladder, reflex contractions of the detrusor muscle are typically absent or significantly reduced

This condition is also referred to as a ‘flaccid’ or ‘areflexic’ bladder because:

1. The detrusor muscle is the smooth muscle that makes up most of the bladder wall and is responsible for bladder contraction during voiding.
2. The detrusor muscle is primarily controlled by parasympathetic (pelvic splanchnic) nerves from spinal cord segments S2-S4.
3. Damage to S2-S4 nuclei or to peripheral nerve fibers can impair parasympathetic outflow to the detrusor muscle, resulting in a loss/reduction of tone and normal spinal reflexes that cause detrusor contraction. Other causes of atonic bladder include:
   1. Diabetic neuropathy
   2. Compression of the conus medullaris or cauda equina, e.g. by tumours, trauma, disc herniation, or epidural abscesses
   3. Myelodysplasia involves developmental defects of the spinal cord
   4. Venous angioma can compress nearby nerves or blood vessels
   5. Necrotizing myelitis involves inflammation and necrosis (death) of spinal cord tissue
   6. GBS attacks the peripheral nerves, which may include those that control bladder function
   7. Amyloidosis involves the deposition of amyloid proteins in various tissues, including the nerves
4. As a result, the bladder cannot empty effectively, which leads to:
   1. Urinary retention
   2. Bladder distension
   3. Overflow incontinence (vesical pressure > sphincter pressure)
   4. Increased post-void residual volume

Top-down view of the neural control of micturition

• Cortex
  • The dorsal anterior cingulate cortex (ACCx) and supplementary motor area (SMA):
    • generate the sensation of urgency, and
    • help postone micturition
  • Bladder filling is monitored:
    • consciously by the insular cortex
    • unconsciously by the parahippocampal area
  • The medial prefontal lobe inhibits the periaqueductal gray (PAG) to raise the initiation threshold for voiding.
• Brainstem
  • The periaqueductal gray (PAG) activates the pontine micturition center (PMC) to initiate voiding when the bladder reaches a set point volume
  • The PMC facilitates voiding by:
    • activating sympathetic neurons (T10-L2), which reach the bladder via the hypogastric nerve
    • inhibiting parasympathetic neurons (S2-S4), which form the pelvic splanchnic nerves that innervate the detrusor muscle and (in males) internal urinary sphincter (IUS).
    • inhibiting somatic motor neurons (S2-S4, “Onuf’s nucleus”), which travel in the pudendal nerve and regulate tone of the external urinary sphincter (EUS).
• Spinal cord
  • Motor
    • Sympathetic nerve at T10-L2 provide tonic stimulation of the IUS in males, and inhibit detrusor contraction
    • Parasympathetics from S2-S4 provide tonic stimulation to the detrusor muscle
    • Onuf’s nucleus at S2-S4 provides tone to the EUS
  • Sensory
    • Afferents carrying pain and temperature synapse at different levels, depending on their origin in the bladder:
      • Afferents from the fundus travel with sympathetics and synapse at T10-L2
      • Afferents from the neck of the bladder travel with parasympathetics and synapse at S2-S4
    • Fullness of the bladder is sensed by mechanoreceptors in the bladder wall
      • Afferents synapse at S2-S4 parasympathetics, allowing reflex contraction of the detrusor
      • Fibers also ascend to the cortex via the spinothalamic (‘regular’ fullness) and posterior column-medial lemniscus (‘very’ full) pathways.
• Urine flow and urethra
  • The sensation of urine flow through the urethra promotes sphincter relaxation and detrusor contraction
  • When flow stops, the urethral sphincters contract, which triggers detrusor relaxation through the urethral reflex

Effects of lesions

• Bilateral medial frontal micturition centers (medial surface of superior frontal gyrus):
  • reflex activation of pontine and spinal micturition centers when the bladder is full
  • urine flow (sphincter tone) and bladder emptying (detrusor contractility) are normal, but may not be under voluntary control
  • individuals may or may not be aware of incontinence, depending on whether or not the insular cortex is affected
  • Common causes: hydrocephalus, parasagittal meningioma, bifrontal glioblastoma, traumatic brain injury, neurodegeneration
• Below the PMC and above the conus medullaris at S2-S4:
  • initially, the bladder is flaccid and acontractile/atonic
    • bladder distension can activate bladder contraction through the sacral reflex
    • however, the spino-ponto-spinal reflex is lost, sphincters remain contracted during bladder contraction
    • discoordination of bladder and sphincter tone is called ‘detrusor-sphincter dyssnergia’
    • this can be associated with spinal shock, which results in an areflexic bladder with urinary retention because the detrusor muscle is unresponsive
  • over time, the bladder becomes spastic/hyperreflexic
    • This pathway is mediated by unmyelinated C-fiber afferents, which become more excitable
    • in addition to bladder sphincter dyssnergia, spontaneous, involuntary bladder contractions cause spasms at low urine volumes, which:
      • increase intravesical pressure
      • perpetuate inefficient voiding
      • increase urinary frequency
      • may produce a sense of urgency when the detrusor contracts