Spinal Shock  


  • After a significant SCI or trauma to the spinal cord, or roots
  • A period for decreased excitability of spinal cord segments with a suppression of autonomic activity as well as somatic reflex activity (flaccid muscle paralysis) at or below the level of injury

Pathophysiologic Mechanism

  • Clinical course of spinal shock
    • Lasting for 1 week - 1 year, with a typical duration of 6-12 weeks in complete suprasacral spinal cord lesions [McGuire 1985]
    • Lasting a shorter period of time in incomplete lesions and even only a few days in some patients.
    • Surgical manipulation of the spinal cord, and spinal roots is associated with similar clinical picture, but less severe, in both children and adults.
  • Actual pathophysiologic mechanism: poorly understood
  • Urinary bladder:
    • Acontractile and areflexic
    • Smooth contour bladder radiologically, with no evidence of trabeculation
  • Bladder neck:
    • Generally closed and competent except some cases of sympathetic thoracolumbar injury and after prior transurethral resection, or after spinal cord infraction involving the lower throracic cord segments [Sullivan 1992]
  • Striated sphincter:
    • No guarding reflex
    • No voluntary control [Fam 1988]
    • Maximum urethral closure pressure:
      • Lower than normal but still maintained (some sphincter tone exists, but Crede voiding is easy during spinal shock after a prior transurethral prostatic resection which suggests most sphincteric activity is not skeletal muscle driven)
  • Somatic reflexes:
    • The most peripheral somatic reflexes of the sacral cord segments (anal reflex or bulbocavernosus reflex) may never disappear.
  • Overall clinical manifestation of the lower urinary system:
    • Urinary retention
    • Urinary incontinence generally does not occur except for overflow incontinence.
  • For more information, also refer here

Recovery from the Spinal Shock

  • Pathophysiology:
    • For more details, please refer to these
    • For more information, please refer to this case example
  • First clinical manifestation
    • Signs for recovery:
      • Spontaneous voiding but incomplete emptying
      • Involuntary voiding or leakage between catheterizations (CIC)
      • These urinary tract functional changes are associated temporarily with recovery of lower extremity deep tendon reflexes.
    • Urodynamical view:
      • Initially poorly sustained bladder contractions
      • Only low-pressure contractions
  • Further changes
    • Strength and duration of such involuntary contractions increase
    • Involuntary voiding with incomplete bladder emptying
    • Ultimately detrusor hyperreflexia, with DSD, or detrusor areflexia with a fixed sphincter evolve.
Key Points of This Section
  • Overall clinical manifestation during the spinal shock period is urinary retention. Therefore, proper urinary drainage should be accomplished.
  • During the recovery from spinal shock, every attempt should be made to preserve as low a bladder storage pressure as possible.
  • Treatment of uninhibited reflex contractility of the bladder at this stage will not impair ultimate recovery of bladder function should the neural injury permit that. On the other hand prevention of reflex contractility and incontinence, and a high bladder pressure, is much easier done at this stage than later when reflex pathways are well established. Our general rule is: do not let reflex contractility be reestablished if it can be prevented. Use intermittent catheterization and medical therapy as soon as feasible after injury.


  • McGuire EJ, Savastano JA. Urodynamics and management of the neuropathic bladder in spinal cord injury patients. J Am Paraplegia Soc 8 (1985), pp. 28–32.
  • Sullivan M, Yalla SV: Spinal cord injury and other forms of myeloneuropathies. Probl Urol 1992;6:643–658.
  • Fam B, Yalla SV: Vesicourethral dysfunction in spinal cord injury and its management. Semin Neurol 1988;8:150–156.

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