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Spinal cord injury may be
During a typical year, there are about 11,000 spinal cord injuries in the US.
The most common causes of spinal cord injuries are
The remainder of spinal cord injuries are attributed to assault (14%), sports (9%), and work-related accidents. About 80% of patients are male.
In the elderly, falls are the most common cause. Osteoporotic bones and degenerative joint disease may increase the risk of cord injury at lower impact velocities due to angulations formed by the degenerated joints, osteophytes impinging on the cord, and brittle bone allowing for easy fracture through critical structures.
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 cause 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 injuries may be
In the neck, fractures of the posterior elements and dislocations can damage the vertebral arteries, causing a syndrome resembling a brain stem stroke.
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 pain and potential worsening of neurologic function. 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 cause wedge fractures of the vertebral body or spinous process fractures. Greater flexion force may cause bilateral facet dislocation, or if the force occurs at the level of C1 or C2, odontoid fracture, atlanto-occipital 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.
The cardinal sign of spinal 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. Muscle strength is assessed using the standard 0 to 5 scale. Specific manifestations depend on the exact level (see Table: Effects of Spinal Cord Injury by Location) and whether cord injury is complete or incomplete. Priapism may occur in the acute phase of spinal cord injury.
In addition to motor and sensory function, upper motor neuron signs are an important finding in cord injury. These signs include increased deep tendon reflexes and muscle tone, a plantar extensor response (upgoing toe), clonus (most commonly found at the ankle by rapidly flexing the foot upward), and a Hoffman reflex (a positive response is flexion of the terminal phalanx of the thumb after flicking the nail of the middle finger).
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.
Effects of Spinal Cord Injury by Location
Complete cord injury 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 cord injury can result in bradycardia and hypotension, termed neurogenic shock; unlike in other forms of shock, the skin remains warm and dry. Arrhythmias and blood pressure 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.
Incomplete motor and sensory loss occurs, and deep tendon reflexes may be hyperactive. 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, which is 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 position 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 resulting 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.
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.
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.
Spinal injuries resulting from trauma are not always obvious. Injury to the spine and spinal cord must be considered in patients with
In elderly patients, spinal cord injury must also be considered after minor falls.
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.
Traditionally, plain x-rays are taken of any possibly injured areas. CT is done of areas that appear abnormal on x-rays and areas at risk of injury based on clinical findings. 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: Spinal Injury Impairment Scale*).
Spinal Injury Impairment Scale*
If a fracture passes through the transverse foramen of a cervical vertebrae, a vascular study is usually warranted (typically, CT angiography) to rule out a dissection.
Transected or degenerated nerves in the cord usually do not recover, and functional damage is often 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; however, ASIA grade may improve by one grade for up to one year after injury. Some new research demonstrates return of some function in previous complete spinal cord injuries with spinal cord stimulation.
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 due to 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, have long been used in attempt to improve the outcome in blunt injuries, but this finding has not been firmly established and is no longer standard treatment.
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 provided as necessary.
Unstable injuries are immobilized until bone and soft tissues have healed in 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.
Early surgery allows for earlier mobilization and rehabilitation. Recent studies suggest that the optimal timing of decompression surgery for incomplete cord injuries is within 24 h of injury. For complete injuries, surgery is sometimes done in the first few days, but it is not clear that this timing affects outcome.
Nursing care includes preventing urinary and pulmonary infections and pressure ulcers—eg, by turning the immobile patient every 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.
Drugs effectively control spasticity in some patients. Drugs such as baclofen 5 mg po tid (maximum, 80 mg during a 24-h period) and tizanidine 4 mg po tid (maximum, 36 mg during a 24-h period) are typically used for spasticity occurring after spinal cord injury. Intrathecal baclofen 50 to 100 mcg once/day may be considered in patients in whom oral drugs are ineffective.
Rehabilitation is needed to help people recover as fully as possible. 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.
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 and minimize scar tissue formation in the injured cord are under study. Such treatments include injections of autologous, incubated macrophages; human-derived embryonic stem cell oligodendrocytes; neural stem cells; and trophic factors. Stem cell research is under study; many animal studies have shown promising results and there have been several phase I and II human clinical trials.
Implantation of an epidural stimulator is another treatment modality under investigation to improve voluntary movement after spinal cord injury. During epidural stimulation, electrical pulses are delivered to the surface of the spinal cord below the injury.
Suspect spinal cord injuries in patients who have a high-risk injury mechanism (including minor falls in the elderly), an altered sensorium, neurologic deficits suggesting cord injury, or localized spinal tenderness.
To ensure recognition of incomplete spinal cord injuries, test motor function and sensory function (including light touch, pinprick, and position sensation) and check for disproportionate weakness in the upper extremities.
Immediately immobilize the spine in patients at risk.
Arrange for immediate CT or, if available, MRI.
Arrange for surgery within 24 h of injury if patients have incomplete cord injuries.
Treat irreversible spinal cord injury with multimodal rehabilitation and drugs that control spasticity.
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