Detrusor Function


  • Synonym: Automatic, hyperreflexic
  • Level of injury:
    • above the reflex voiding center in the sacral portion of the spinal cord (effectively at T12 or above)
  • Pathophysiology:
    • The person loses both the sensation that they need to void and voluntary, brain stem and cortical-derived coordinated control over the reflex voiding center.
    • When the bladder becomes sufficiently full for the stretch receptors in the detrusor muscle are activated, and an uncontrolled, spontaneous bladder contraction is stimulated through a simple reflex arc.
  • Relationship with the striated sphincter activity:
    • The reflex bladder contraction is generally out of phases with striated sphincter activity.
    • Bladder filling does not evoke a guarding reflex, the external sphincter does not respond.
    • At some volume the detrusor starts to contract, and at that time the sphincter contracts, the detrusor response slows and may stop briefly, only to resume as the sphincter contractions fades (DSD).
    • But it is really related more to improper phasing and sequencing of the reflex events in voiding than a true overt simultaneous antagonism between the two areas. Be that as it may very high sustained pressures can result from this discoordinate response.
    • In some cases the DSD is very short lived and the sphincter relaxes and permits reasonably normal voiding at normal pressures.
    • In others the sphincter is dominant and at the first detrusor response a very high level of sphincteric activity commences and reflex contractility of the bladder never actually develops.


  • Synonym: areflexic, acontractile
  • Level of injury:
    • lower motor neuron lumbosacral lesion with damage to the reflex voiding centers in the sacral portion of the spinal cord.
  • Pathophysiology
    • The bladder is decentralized, but not flaccid even though that term was formerly applied to lower motor neuron bladder dysfunction.
  • Relationship with the striated sphincter activity:
    • The proximal sphincter usually, but not always, escapes these injuries and functions quite normally during storage of urine. There is no neural pathway permit reflex voiding and to open the urethra.
    • There may be some external striated sphincter function as well, but that is also no longer linked to detrusor activity. The bladder fills and the individual detrusor muscle cells respond, and gradually develop pressure until Pdet overcomes fixed urethral resistance and leakage occurs. The same rules apply. If outlet resistance is high compliance will deteriorate, morphological changes will occur, incontinence will worsen and a grave risk to upper tract function will develop. These changes can be prevented by the early institution of intermittent catheterization and drug therapy to block the detrusor muscular response.

Other Comments

  • All neurogenic vesical dysfunction is an obstructive process. There is a lack of coordinate detrusor and sphincter activity.
  • The sphincter may contract against the contracting detrusor, or there may be no neural mechanism to open it when the bladder pressure rises as a result of an unchecked autonomous detrusor muscle response to volume.
  • The factors involved are the level of outlet resistance, and the time the detrusor is exposed to that resistance. Very high pressures as in some form of DSD may be only very brief, and not really dangerous. On the other hand a relatively benign looking situation where an areflexic detrusor faces a poor functional sphincter may give rise to sustained derusor pressures which are very dangerous.


Key Points of This Section
  • Neurogenic bladder dysfunction is an obstructive process.
  • Urodynamic testing is required to determine how severe the obstruction is.
  • These lesions with their associated dysfunction evolve over time and are not stable for months to years after injury.

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