What is the pathogenesis of neurogenic bladder caused by a spinal cord injury (SCI)?

Updated: Dec 24, 2020
  • Author: Bradley C Gill, MD, MS; Chief Editor: Edward David Kim, MD, FACS  more...
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When an individual sustains a spinal cord injury (eg, from a diving accident or motor vehicle injury), the initial neurologic response is spinal shock. During this spinal shock phase, the affected individual experiences flaccid paralysis below the level of injury, and the somatic reflex activity is either depressed or absent.

The anal and bulbocavernosus reflex typically is absent. The autonomic activity is depressed, and the individual experiences urinary retention and constipation. Urodynamic findings are consistent with areflexic detrusor and rectum. The internal and external urethral sphincter activities, however, are normal.

The spinal shock phase typically lasts 6-12 weeks but may persist longer in some cases. During this time, the urinary bladder must be drained with CIC or indwelling urethral catheter.

When the spinal shock phase wears off, bladder function returns but the detrusor activity increases in reflex excitability to an overactive state (ie, detrusor hyperreflexia). Depending on the level of the lesion, detrusor sphincter dyssynergia–detrusor hyperreflexia (DSD-DH) may develop. Thus, these patients must be monitored for leaking between CIC, and periodic urodynamic testing must be performed for this alteration in detrusor behavior. During urodynamic studies, intravesical instillation of cold saline may indicate return of reflex activity or help better characterize the lesion.

Realizing that suprasacral lesions exhibit detrusor areflexia at initial insult but progress to hyperreflexic state over time is important. Conversely, sacral cord lesions are associated with areflexic bladders that may become hypertonic over time.

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