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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.
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 urgency incontinence being especially common. More particularly, a unilateral cord lesion leads to a A central cord syndrome may lead to a lower motor neuron deficit and loss of pain and temperature appreciation, with sparing of posterior column functions. A radicular deficit may occur at the level of the injuryCor, if the cauda equina is involved, there may be evidence.
Treatment of the injury consists of immobilization andCif there is cord compressionCdecompressive laminectomy and fusion. Early treatment with high doses of corticosteroids (eg, methylprednisolone, 30 mg/kg by intravenous bolus, followed by 5.4 mg/kg/h for 23 hours) has been shown to improve Treatment with GM1 ganglioside for 3 or 4 weeks is an experimental approach that has also Anatomic realignment of the spinal cord by traction and other orthopedic procedures is Subsequent care of the residual neurologic deficitCparaplegia or quadriplegiaCrequires treatment of paraplegia or quadraplegia.