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THE MERCK MANUAL MEDICAL LIBRARY: The Merck Manual of Diagnosis and Therapy
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Introduction

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Trauma to the spine may produce injuries involving the spinal cord, vertebrae, or both. Occasionally, the spinal nerves are affected (see Peripheral Nervous System and Motor Unit Disorders: Symptoms and Signs). The anatomy of the spinal column is reviewed in another chapter (see Peripheral Nervous System and Motor Unit Disorders: Toxic Causes of NeuropathiesTables).

Etiology and Pathophysiology

Cord injury: During a typical year, there are about 11,000 spinal cord injuries in the US. Nearly 48% occur in motor vehicle collisions, and 23% result from falls. The remainder is attributed to violence (14%), sports (9%), and work-related accidents. About 80% of patients are male.

Spinal cord injuries occur when blunt physical force damages the vertebrae, ligaments, or disks of the spinal column, causing bruising, crushing, or tearing of spinal cord tissue, and when the spinal cord is penetrated (eg, by a gunshot or a knife wound). Such injuries can also produce vascular injury with resultant ischemia or hematoma (typically extradural), leading to further damage. All forms of injury can cause spinal cord edema, further decreasing blood flow and oxygenation. Damage may be mediated by excessive release of neurotransmitters from damaged cells, an inflammatory immune response with release of cytokines, accumulation of free radicals, and apoptosis.

Vertebral injury: Fractures may involve the vertebral body, lamina, and pedicles as well as the spinous, articular, articular, and transverse processes. Dislocations typically involve the facets. Subluxation involves ligament rupture without bony injury. In the neck, fractures of the posterior elements and dislocations can damage the vertebral arteries, causing a stroke-like syndrome.

Unstable vertebral injuries are those in which bony and ligamentous integrity is disrupted sufficiently that free movement can occur, potentially compressing the spinal cord or its vascular supply and resulting in marked worsening of neurologic function or pain. Such vertebral movement may occur even with a shift in patient position (eg, for ambulance transport, during initial evaluation). Stable fractures are able to resist such movement.

Specific injuries typically vary with mechanism of trauma. Flexion injuries can produce wedge fractures of the vertebral body or spinous process fractures. Greater flexion force may cause bilateral cervical cervical facet dislocation, or if the force occurs at the level of C1 or C2, odontoid fracture, atlantooccipital or atlantoaxial subluxation, or both fracture and subluxation. Rotational injury can cause unilateral facet dislocation. Extension injury most often causes posterior neural arch fracture. Compression injuries can cause burst fractures of vertebral bodies.

Cauda equina injury: The lower tip of the spinal cord (conus medullaris) is usually at the level of the L1 vertebra. Spinal nerves below this level comprise the cauda equina. Findings in spinal injuries below this level may mimic those of spinal cord injury, particularly conus medullaris syndrome.

Symptoms and Signs

The cardinal sign of cord injury is a discrete injury level in which neurologic function above the injury is intact, and function below the injury is absent or markedly diminished. Specific manifestations depend on the exact level (see Table 1: Spinal Trauma: Effects of Spinal Cord Injury by LocationTables) and whether cord injury is complete or partial. Priapism may occur in the acute phase of spinal cord injury.

Table 1

Effects of Spinal Cord Injury by Location

Location of Injury*

Possible Effects†

At or above C5

Respiratory paralysis and quadriplegia

Between C5 and C6

Paralysis of legs, wrists, and hands; weakened shoulder abduction and elbow flexion; loss of brachioradialis reflex

Between C6 and C7

Paralysis of legs, wrists, and hands, but shoulder movement and elbow flexion usually possible; loss of biceps jerk reflex

Between C7 and C8

Paralysis of legs and hands

At C8 to T1

With transverse lesions, Horner's syndrome (ptosis, miotic pupils, facial anhidrosis), paralysis of legs

Between T11 and T12

Paralysis of leg muscles above and below the knee

At T12 to L1

Paralysis below the knee

Cauda equina

Hyporeflexic or areflexic paresis of the lower extremities, usually pain and hyperesthesia in the distribution of the nerve roots, and usually loss of bowel and bladder control

At S3 to S5 or conus medullaris at L1

Complete loss of bowel and bladder control

*Abbreviations refer to vertebrae; the cord is shorter than the spine, so that moving down the spine, the cord segments and vertebral levels are increasingly out of alignment.

†Priapism, reduced rectal tone, and changes in caudal reflexes may occur with injury at any level.

Vertebral injury, as with other fractures and dislocations, typically is painful, but patients who are distracted by other painful injuries (eg, long bone fractures) or whose level of consciousness is altered by intoxicants or head injury may not complain of pain.

Complete cord injury: Transection leads to immediate, complete, flaccid paralysis (including loss of anal sphincter tone), loss of all sensation and reflex activity, and autonomic dysfunction below the level of the injury.

High cervical injury (at or above C5) affects the muscles controlling respiration, causing respiratory insufficiency; ventilator dependence may occur, especially in patients with injuries at or above C3. Autonomic dysfunction from cervical injury can result in bradycardia and hypotension, termed neurogenic shock (see Shock and Fluid Resuscitation: Distributive shock); unlike in other forms of shock, the skin remains warm and dry. Arrhythmias and BP instability may develop. Pneumonia is a frequent cause of death in people with a high spinal cord injury, especially in those who are ventilator dependent.

Flaccid paralysis gradually changes over hours or days to spastic paralysis with increased deep tendon reflexes due to loss of descending inhibition. Later, if the lumbosacral cord is intact, flexor muscle spasms appear and autonomic reflexes return.

Partial cord injury: Partial motor and sensory loss occurs, and deep tendon reflexes may be exuberant. Motor and sensory loss may be permanent or temporary depending on the etiology; function may be lost briefly due to concussion or more lastingly due to a contusion or laceration. Sometimes, however, rapid swelling of the cord results in total neurologic dysfunction resembling complete cord injury. Termed spinal shock (not to be confused with neurogenic shock), symptoms resolve over one to several days; residual disability often remains.

Manifestations depend on which portion of the cord is involved; several discrete syndromes are recognized.

Brown-Séquard syndrome results from unilateral hemisection of the cord. Patients have ipsilateral spastic paralysis and loss of postural sense below the lesion, and contralateral loss of pain and temperature sensation.

Anterior cord syndrome results from direct injury to the anterior spinal cord or to the anterior spinal artery. Patients lose motor and pain sensation bilaterally below the lesion. Posterior cord function (vibration, proprioception) is intact.

Central cord syndrome usually occurs in patients with a narrowed spinal canal (congenital or degenerative) after a hyperextension injury. Motor function in the arms is impaired to a greater extent than that in the legs.If the posterior columns are affected, posture, vibration, and light touch are lost. If the spinothalamic tracts are affected, pain, temperature, and, often, light or deep touch are lost.Hemorrhage in the spinal cord from trauma (hematomyelia) is usually confined to the cervical central gray matter, resulting in signs of lower motor neuron damage (muscle weakness and wasting, fasciculations, and diminished tendon reflexes in the arms), which is usually permanent. Motor weakness is often proximal and accompanied by selective impairment of pain and temperature sensation.

Cauda equina lesions: Motor or sensory loss, or both, usually partial, occurs in the distal legs. Sensation is usually diminished in the perineal region (saddle anesthesia). Bowel and bladder dysfunction, either incontinence or retention, may occur. Men may have erectile dysfunction, and women diminished sexual response. Anal sphincter tone is lax, and bulbocavernosus and anal wink reflexes are abnormal. These findings may be similar to those of conus medullaris syndrome, a spinal cord injury.

Complications: Sequelae depend on the severity and level of the injury. Breathing may be impaired if the injury is at or above the C5 segment. Reduced mobility increases the risk of blood clots, UTIs, contractures, atelectasis and pneumonia, and pressure ulcers. Disabling spasticity may develop. Autonomic dysreflexia may occur in response to triggering events such as pain or pressure on the body. Chronic neurogenic pain may manifest as burning or stinging.

Diagnosis

Spinal cord injuries with trauma are not always obvious. Injury to the spine and spinal cord must be considered in patients with injuries that involve the head, pelvic fractures, penetrating injuries in the area of the spine, in most motor vehicle collisions, in any kind of major blunt injury, and in any injuries related to falling from heights or diving into water.

Injury should also be considered in patients with altered sensorium, localized spinal tenderness, painful distracting injuries, or compatible neurologic deficits. Motor function is tested in all extremities. Sensation testing should involve both light touch (posterior column function), pinprick (anterior spinothalamic tract), and position sense. Identification of the sensory level is best done by testing from distal to proximal and by testing thoracic roots on the back to avoid being misled by the cervical cape. Priapism indicates spinal cord damage. Rectal tone may be decreased, and deep tendon reflexes may be exuberant or absent.

When spinal cord injury is suspected, the spine is immediately immobilized. Traditionally, plain x-rays are taken of any possibly injured areas. CT scans are obtained of abnormal areas and those areas for which clinical indicators suggest a high likelihood of injury. However, CT is being used increasingly as the primary imaging study for spinal trauma, because it has better diagnostic accuracy and, at many trauma centers, can be obtained rapidly. MRI helps identify the type and location of cord injury; it is the most accurate study for imaging the spinal cord and other soft tissues but may not be immediately available. Manifestations of injury may be characterized using the ASIA (American Spinal Injury Association) Impairment Scale or a similar instrument (see Table 2: Spinal Trauma: Spinal Injury Impairment Scale*Tables).

Table 2

Spinal Injury Impairment Scale*

Level

Impairment

A = Complete

No motor or sensory function, including in the sacral segments S4–S5

B = Incomplete

Sensory but not motor function is preserved below the neurologic level and includes the sacral segments S4—S5

C = Incomplete

Motor function is preserved below the neurologic level, and > 12 of key muscles below neurologic level have a muscle grade < 3

D = Incomplete

Motor function is preserved below the neurologic level, and at least 12 of key muscles below the neurologic level have a muscle grade > 3

E = Normal

Motor and sensory function are normal

*According to the American Spinal Injury Association.

Prognosis and Treatment

Transected or degenerated nerves in the cord do not recover, and functional damage is permanent. Compressed nerve tissue can recover its function. Return of a movement or sensation during the first week after injury heralds a favorable recovery. Dysfunction remaining after 6 mo is likely to be permanent.

Immediate care: An important goal is to prevent secondary injury to the spine or spinal cord. In unstable injuries, flexion or extension of the spine can contuse or transect the cord. Thus, when injured people are moved, inappropriate handling can precipitate paraplegia, quadriplegia, or even death from spinal injury. Patients who may have a spinal injury should have the spine immobilized immediately; the neck is held straight manually (in line stabilization) during endotracheal intubation. As soon as possible, the spine is fully immobilized on a firm, flat, padded backboard or similar surface to stabilize the position without excessive pressure. A rigid collar should be used to immobilize the cervical spine. Patients with thoracic or lumbar spine injuries can be carried prone or supine; those with cervical cord damage that could induce respiratory difficulties should be carried supine, with attention to maintaining a patent airway and avoiding chest constriction. Transfer to a trauma center is desirable.

Medical care should be directed at avoiding hypoxia and hypotension, both of which can further stress the injured cord. In cervical injuries higher than C5, intubation and respiratory support are usually needed.

Large doses of corticosteroids, started within 8 h after spinal cord injury, may improve the outcome in blunt injuries, but this finding has not been firmly established. Methylprednisolone Some Trade Names
MEDROL
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30 mg/kg IV over 1 h, followed by 5.4 mg/kg/h for the next 23 h is the recommended regimen. Injuries are treated with rest, analgesics, and muscle-relaxing drugs with or without surgery until swelling and local pain have subsided. Additional general treatment for trauma patients is discussed elsewhere (see Approach to the Trauma Patient: Evaluation and Treatment).

Unstable injuries are immobilized until bone and soft tissues have healed to ensure proper alignment; surgery with fusion and internal fixation is sometimes needed. Patients with incomplete cord injuries can have significant neurologic improvement after decompression. In contrast, in complete injury, return of useful neurologic function below the level of the injury is unlikely. Thus, surgery aims to stabilize the spine to allow early mobilization. The timing of surgery in incomplete lesions is debatable. Early surgery (eg, within 24 h) may have a better neurologic outcome and allows for earlier mobilization and rehabilitation. For complete injuries, surgery is sometimes done in the first few days, but it is not clear that this is necessary.

Nursing care includes preventing urinary and pulmonary infections and pressure ulcers—eg, by turning the immobile patient q 2 h (on a Stryker frame when necessary). Deep venous thrombosis prophylaxis is required. An inferior vena cava filter could be considered in immobile patients.

Long-term care: Drugs effectively control spasticity in some patients. Oral agents such as baclofen Some Trade Names
LIORESAL
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5 mg po tid (maximum, 80 mg during a 24-h period) and tizanidine Some Trade Names
ZANAFLEX
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4 mg po tid (maximum, 36 mg during a 24-h period) are typically used for spasticity occurring after spinal cord injury. Intrathecal baclofen Some Trade Names
LIORESAL
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50 to 100 μg once/day may be considered in patients in whom oral drugs are ineffective.

Rehabilitation is needed to help people recover as fully as possible (see Rehabilitation: Rehabilitation For Other Disorders). Rehabilitation, best provided through a team approach, combines physical therapies, skill-building activities, and counseling to meet social and emotional needs. The rehabilitation team is best directed by a physician with training and expertise in rehabilitation (physiatrist); it usually includes nurses, social workers, nutritionists, psychologists, physical and occupational therapists, recreational therapists, and vocational counselors (see also Rehabilitation).

Physical therapy focuses on exercises for muscle strengthening, passive stretch exercises to prevent contractures, and appropriate use of assistive devices such as braces, a walker, or a wheelchair that may be needed to improve mobility. Strategies for controlling spasticity, autonomic dysreflexia, and neurogenic pain are taught. Occupational therapy focuses on redeveloping fine motor skills. Bladder and bowel management programs teach toileting techniques, which may require intermittent catheterization. A bowel regimen, involving timed stimulation with laxatives, is often needed.

Vocational rehabilitation involves assessing both fine and gross motor skills, as well as cognitive capabilities, to determine the likelihood for meaningful employment. The vocational specialist then helps identify possible work sites and determines need for assistive equipment and workplace modifications. Recreation therapists use a similar approach in identifying and facilitating participation in hobbies, athletics, and other activities.

Emotional care aims to combat the depersonalization and the almost unavoidable depression that occur after losing control of the body. Emotional care is fundamental to the success of all other components of rehabilitation and must be accompanied by efforts to educate the patient and encourage active involvement of family and friends.

Treatments to promote nerve regeneration are under study. Such treatments include injections of autologous, incubated macrophages; epidural administration of BA-210, an experimental drug that may be neuroprotective and stimulate nerve growth; and oral administration of HP-184 for treatment of chronic spinal cord injury. Also, one trial aims to determine optimal timing of surgery. Stem cell research is in its infancy; some early animal studies have shown promising results.

Spinal Cord Injury in Children

Although children < 10 yr have the lowest rate of spinal cord injuries, such injuries are not rare.In children < 8 yr, cervical spine injuries occur most commonly above C4; in those > 8 yr, injuries at C5 to C8 are more common. Of increasing importance has been the recognition of Spinal Cord Injury Without evidence Of Radiologic Abnormality (SCIWORA). This type of injury occurs almost exclusively in children and is related to direct spinal cord traction, spinal cord concussion, and vascular injury.

Spinal cord injury should be suspected in any child that has been in a motor vehicle collision, has fallen from a height 3 m, or has had a submersion injury. SCIWORA is suspected in children who have even transient symptoms of neurologic dysfunction or lancinating pains down the spine or extremities and a mechanism of injury compatible with spinal cord injury.

Treatment is similar to that in adults, with immobilization and attention to the adequacy of oxygenation, ventilation, and circulation. Treatment may also include high-dose corticosteroids (same weight-based dose as for adults). Children with significant spinal cord trauma should be transferred to a pediatric trauma center as soon as possible.

Last full review/revision April 2007 by J. Brad Bellotte, MD; James E. Wilberger, MD

Content last modified April 2007

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