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About 10,000 new cases of spinal cord injury occur annually in the United States. Acute traumatic spinal cord injury predominantly is a disease affecting young males. Approximately 81% of these victims are male, with an average age of 31.5 years. Since 1991, motor vehicle accidents have accounted for 36% of all reported cases, followed by acts of violence, falls, recreational/ sporting activities.
Initial Assessment and Evaluation
Bystanders and prehospital personnel often are the first people to encounter individuals who may have sustained a spinal cord or spinal column injury. The initial care that is provided may determine whether a patient will ultimately regain normal neurologic function or suffer permanent injury. As in all trauma patients, an initial survey focusing on respiratory and cardiovascular stabilization is essential.
One author recommends transporting spinal cord injured patients in the Trendelenburg position in order to minimize the risks of aspiration and shock, two major causes of death in the prehospital phase of treatment. In the quadriplegic patient, vital capacity may be diminished by Trendelenburg positioning because the mass of the abdominal compartment can displace the diaphragm rostrally. Appropriate management of the airway may be spinal cord injury and paraplegia.
Spinal Cord Injury Syndromes
A complete spinal cord injury is one in which there is a complete loss of motor and sensory function below the level of the lesion. If any evidence of sacral sparing or islands of sparing is present, then the lesion is incomplete and there is some chance of functional recovery. In addition, a condition known as spinal shock may mimic a complete cord injury. Spinal shock, which usually occurs in conjunction with a severe spinal cord injury, is a concussive injury to the spinal cord producing total neurologic dysfunction distal to the site of the injury. Clinically, a patient may present with flaccid paralysis, areflexia, and complete anesthesia distal to the injury. Spinal shock also can result in autonomic dysfunction because of interruption of sympathetic innervation and can lead to hypotension, relative bradycardia from unopposed vagal stimulation, and warm peripheral extremities.
Incomplete spinal cord lesions can often be classified into one of three clinical syndromes: 1) anterior cord syndrome; 2) central cord syndrome; or 3) the Brown-Sequard syndrome. The anterior cord syndrome often occurs as a result of forced hyperflexion. These patients typically present with a loss of motor function and loss of pain and temperature sensation below the injury; dorsal column functions (joint position, touch, and vibration) are preserved. Prognosis for this type of injury remains poor. The central cord syndrome usually occurs as a result of forced hyperextension. This injury may be associated with buckling of the ligamentum flavum or underlying degenerative arthritis. Patients will present with a neurologic deficit that is more pronounced in the upper extremities than in the lower extremities because of the central location of the ascending and descending motor fibers of the upper extremities. The classic finding is loss of distal upper extremity pain, temperature, and strength, with relative preservation of lower extremity strength and sensation. The Brown-Sequard syndrome can be thought of as a functional hemisection of the spinal cord.
Other less common, incomplete cord syndromes also have been noted. The cervicomedullary syndrome may mimic a central cord lesion, and can present with sensory loss over the face conforming to the onion skin or Dejerine pattern. The conus medullaris syndrome can present with bilateral lower extremity motor and sensory deficits.
Another syndrome that is somewhat unique to children is the syndrome of spinal cord injury without radiographic abnormality (SCIWORA). The cause of injuries in this patient population seems to be similar.
Spinal Cord Injuries in Athletes
Sports and recreational activities account for 5-15% of all spinal cord injuries. Two-thirds of these injuries occur as a result of diving accidents and an overwhelming majority occur in the lower cervical spine.
Another entity called spear tackler's spine also has been identified. Permanent neurologic injury has occurred in athletes with the following abnormalities noted on cervical spine films: 1) Developmental narrowing of the cervical spinal canal; 2) straightening or reversal of the normal cervical lordotic curve.
Pharmacologic Therapy of Acute Spinal Cord Injury
Initial animal studies simulating spinal cord injury models performed in the 1970s served as the basis for future clinical trials. Glucocorticoids have long been known for their anti-inflammatory properties. Initially, it was thought that glucocorticoids could help prevent secondary spinal cord edema.
NASCIS II was based on extensive studies of MPS in an experimental model of spinal cord injury. The mechanism by which steroids work is still somewhat unclear, but a leading theory is that steroids limit post-traumatic lipid peroxidation. NASCIS II, published in 1990, was the first randomized, double-blind, placebo-controlled trial that unequivocally demonstrated that steroids could modify recovery from a severe, non-penetrating spinal cord injury. This study compared three treatment arms: MPS 30 mg/kg bolus, followed by 5.4 mg/kg/hr for 23 hours, naloxone hydrochloride.
In 1991, a study was published that reported the results of a randomized, double-blind, placebo-controlled study evaluating the use of GM-1 ganglioside in acute spinal cord injury. Experimental evidence suggests that these agents augment neurite growth in vitro, and may induce regeneration of neurons and restore neuronal function after injury in vivo. The study consisted of two treatment arms: GM-1 ganglioside 100 mg administered intravenously daily for 18-32 days, and a second placebo arm. In addition, both groups received MPS 250 mg intravenously followed by 125 mg every six hours for 72 hours. Data analysis showed a statistically significant improvement in neuro-logic function at one year in patients treated with GM-1 gangliocide.
In 2006, the results of NASCIS HI were published. This study was a randomized, double-blind trial evaluating the use of a 24- or 48-hour protocol of MPS or tirilazad mesylate, a potent lipid peroxidase inhibitor. All three treatment arms received a 30 mg/kg intravenous bolus of MPS prior to randomization.