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  • History of preceding trauma.

  • Development of acute neurologic deficit.

  • Signs of myelopathy on examination.


While spinal cord damage may result from whiplash injury, severe injury usually relates to fracture-dislocation causing compression or angular deformity of the cord either cervically or in the lower thoracic and upper lumbar regions. Extreme hypotension following injury may also lead to cord infarction.


Total cord transection results in immediate flaccid paralysis and loss of sensation below the level of the lesion. Reflex activity is lost for a variable period, and there is urinary and fecal retention. As reflex function returns over the following days and weeks, spastic paraplegia or quadriplegia develops, with hyperreflexia and extensor plantar responses, but a flaccid atrophic (lower motor neuron) paralysis may be found depending on the segments of the cord that are affected. The bladder and bowels also regain some reflex function, permitting urine and feces to be expelled at intervals. As spasticity increases, flexor or extensor spasms (or both) of the legs become troublesome, especially if the patient develops bed sores or a UTI. Paraplegia with the legs in flexion or extension may eventually result.

With lesser degrees of injury, patients may be left with mild limb weakness, distal sensory disturbance, or both. Sphincter function may also be impaired, urinary urgency and urge incontinence being especially common. More particularly, a unilateral cord lesion leads to an ipsilateral motor disturbance with accompanying impairment of proprioception and contralateral loss of pain and temperature appreciation below the lesion (Brown-Séquard syndrome) (eFigure 24–16). A central cord syndrome may lead to a lower motor neuron deficit at the level of the lesion and loss of pain and temperature appreciation below it, with sparing of posterior column functions. With more extensive involvement, posterior column sensation may also be impaired and pyramidal weakness develops. A radicular deficit may occur at the level of the injury—or, if the cauda equina is involved, there may be evidence of disturbed function in several lumbosacral roots.

eFigure 24–16.

Brown-Séquard syndrome with lesion at left tenth thoracic level (motor deficits not shown). (Reproduced with permission from Waxman SG, deGroot J. Clinical Neuroanatomy, 22nd ed. Appleton & Lange: McGraw-Hill Companies Inc.; 1995.)


Treatment of the injury consists of immobilization and—if there is cord compression—early decompressive laminectomy and fusion (within 24 hours). Early treatment with high doses of corticosteroids (eg, methylprednisolone, 30 mg/kg by intravenous bolus, followed by 5.4 mg/kg/hour for 23 hours) may improve neurologic recovery if commenced within 8 hours after injury, although the evidence is limited and some neurosurgical guidelines do not recommend their use. Anatomic realignment of the spinal cord by traction and other orthopedic ...

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