Spinal Cord Injuries
- Author: Lawrence S Chin, MD, FACS; Chief Editor: Brian H Kopell, MD more...
Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or permanent, in the cord’s normal motor, sensory, or autonomic function. Patients with SCI usually have permanent and often devastating neurologic deficits and disability. The most important aspect of clinical care for the SCI patient is preventing complications related to disability. Supportive care has shown to decrease complications related to mobility. Further, in the future our increasing fund of knowledge of the brain-computer interface might mitigate some of the disabilities associated with SCI.
Signs and symptoms
The extent of injury is defined by the American Spinal Injury Association (ASIA) Impairment Scale (modified from the Frankel classification), using the following categories[3, 4] :
A = Complete: No sensory or motor function is preserved in sacral segments S4-S5 
B = Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5
C = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade of less than 3
D = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade that is greater than or equal to 3
E = Normal: Sensory and motor functions are normal
Definitions of complete and incomplete spinal cord injury, as based on the above ASIA definition, with sacral-sparing, are as follows[3, 4, 5] :
Complete: Absence of sensory and motor functions in the lowest sacral segments
Incomplete: Preservation of sensory or motor function below the level of injury, including the lowest sacral segments
Signs of respiratory dysfunction include the following:
Loss of ventilatory muscle function from denervation and/or associated chest wall injury
Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion
Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs
A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction, as follows:
With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent
With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective
With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak
With lower cord injuries, respiratory function improves
With injuries at T11, respiratory dysfunction is minimal; vital capacity is essentially normal, and cough is strong
See Clinical Presentation for more detail.
The following laboratory studies can be helpful in the evaluation of spinal cord injury:
Arterial blood gas (ABG) measurements - May be useful to evaluate adequacy of oxygenation and ventilation
Lactate levels - To monitor perfusion status; can be helpful in the presence of shock
Hemoglobin and/or hematocrit levels - May be measured initially and monitored serially to detect or monitor sources of blood loss
Urinalysis - Can be performed to detect any associated genitourinary injury
Imaging techniques in spinal cord injury include the following:
Plain radiography - Radiographs are only as good as the first and last vertebrae seen, therefore, radiographs must adequately depict all vertebrae
Computed tomography (CT) scanning - Reserved for delineating bony abnormalities or fracture; can be used when plain radiography is inadequate or fails to visualize segments of the axial skeleton
Magnetic resonance imaging (MRI) - Used for suspected spinal cord lesions, ligamentous injuries, and other soft-tissue injuries or pathology
See Workup for more detail.
Emergency department care
Airway management - The cervical spine must be maintained in neutral alignment at all times; clearing of oral secretions and/or debris is essential to maintaining airway patency and preventing aspiration
Hypotension - Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury; a diligent search for occult sources of hemorrhage must be made
Neurogenic shock - Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 L is the initial treatment of choice; maintain adequate oxygenation and perfusion of the injured spinal cord; supplemental oxygenation and/or mechanical ventilation may be required [6, 7]
Head injuries - Amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, or a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning
Ileus - Placement of a nasogastric (NG) tube is essential; antiemetics should be used aggressively
Pressure sores - To prevent pressure sores, turn the patient every 1-2 hours, pad all extensor surfaces, undress the patient to remove belts and back pocket keys or wallets, and remove the spine board as soon as possible
Treatment of pulmonary complications and/or injury in patients with spinal cord injury includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax.
Emergent decompression of the spinal cord is suggested in the setting of acute spinal cord injury with progressive neurologic deterioration, facet dislocation, or bilateral locked facets. The procedure is also suggested in the setting of spinal nerve impingement with progressive radiculopathy, in patients with extradural lesions such as epidural hematomas or abscesses, and in the setting of the cauda equina syndrome.
Spinal cord injury (SCI) is an insult to the spinal cord resulting in a change, either temporary or permanent, in its normal motor, sensory, or autonomic function. Patients with spinal cord injury usually have permanent and often devastating neurologic deficits and disability. According to the National Institutes of Health (NIH), "among neurological disorders, the cost to society of automotive SCI is exceeded only by the cost of mental retardation."
After a suspected SCI, the goals are to establish the diagnosis and initiate treatment to prevent further neurologic injury from either mechanical instability secondary to injury from the deleterious effects of cardiovascular instability or respiratory insufficiency.
SCI terminology and classification
The International Standards for Neurological and Functional Classification of Spinal Cord Injury (ISNCSCI) is a widely accepted system describing the level and extent of injury based on a systematic motor and sensory examination of neurologic function.[3, 4] The following terminology has developed around the classification of spinal cord injuries:
Tetraplegia (replaces the term quadriplegia): Injury to the spinal cord in the cervical region, with associated loss of muscle strength in all 4 extremities
Paraplegia: Injury in the spinal cord in the thoracic, lumbar, or sacral segments, including the cauda equina and conus medullaris
The percentage of spinal cord injuries as classified by the American Spinal Injury Association (ASIA) is as follows:
Incomplete tetraplegia: 29.5%
Complete paraplegia: 27.9%
Incomplete paraplegia: 21.3%
Complete tetraplegia: 18.5%
The most common neurologic level of injury is C5. In paraplegia, T12 and L1 are the most common level. The following image depicts the ASIA classification by neurologic level.
See also Hypercalcemia and Spinal Cord Injury, Spinal Cord Injury and Aging, Rehabilitation of Persons With Spinal Cord Injuries, Central Cord Syndrome, Brown-Sequard Syndrome, and Cauda Equina and Conus Medullaris Syndromes.
Historical information in SCI classification
In 1982, ASIA first published standards for neurologic classification of patients with spinal injury, followed by further refinements to definitions of neurologic levels, identification of key muscles and sensory points corresponding to specific neurologic levels, and validation of the Frankel scale. In 1992, the International Medical Society of Paraplegia (IMSOP) adopted these guidelines to create true international standards, followed by further refinements. A standardized ASIA method for classifying spinal cord injury (SCI) by neurologic level was developed (see the image above).
The spinal cord is divided into 31 segments, each with a pair of anterior (motor) and dorsal (sensory) spinal nerve roots. On each side, the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neuroforamina. The spinal cord extends from the base of the skull and terminates near the lower margin of the L1 vertebral body. Thereafter, the spinal canal contains the lumbar, sacral, and coccygeal spinal nerves that comprise the cauda equina. As a result, injuries below L1 are not considered spinal cord injuries (SCIs), because they involve the segmental spinal nerves and/or cauda equina. Spinal injuries proximal to L1, above the termination of the spinal cord, often involve a combination of spinal cord lesions and segmental root or spinal nerve injuries.
The spinal cord itself is organized into a series of tracts or neuropathways that carry motor (descending) and sensory (ascending) information. These tracts are organized somatotopically within the spinal cord. The corticospinal tracts are descending motor pathways located anteriorly within the spinal cord. Axons extend from the cerebral cortex in the brain as far as the corresponding segment, where they form synapses with motor neurons in the anterior (ventral) horn. They decussate (cross over) in the medulla before entering the spinal cord.
The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and vibration information to the sensory cortex. They do not decussate until they reach the medulla. The lateral spinothalamic tracts transmit pain and temperature sensation. These tracts usually decussate within 3 segments of their origin as they ascend. The anterior spinothalamic tract transmits light touch. Autonomic function traverses within the anterior interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1, whereas parasympathetic system pathways exit between S2 and S4.
Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensation. Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation. Anterior cord injury causes paralysis and incomplete loss of light touch sensation.
Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous system fibers exit from the spinal cord between C7 and L1. The parasympathetic system nerves exit between S2 and S4. Therefore, progressively higher spinal cord lesions or injury causes increasing degrees of autonomic dysfunction.
The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature sensation, and autonomic dysfunction. The posterior spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in the neck and descend from the base of the skull. Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow.
The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. For example, a lower cervical spine fracture may result in disruption of the vertebral artery that ascends through the affected vertebra. The resulting vascular injury may cause an ischemic high cervical cord injury. At any given level of the spinal cord, the central part is a watershed area. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome.
Spinal cord injury (SCI), as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the spinal cord injury.
Spinal cord injury can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage:
Destruction from direct trauma
Compression by bone fragments, hematoma, or disk material
Ischemia from damage or impingement on the spinal arteries
Edema could ensue subsequent to any of these types of damage.
Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of sympathetic nervous system control in acute spinal cord injury. Hypothermia is also characteristic. This condition does not usually occur with spinal cord injury below the level of T6 but is more common in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance, with the associated vascular dilatation. Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.
Shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. That is, spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions.
An initial increase in blood pressure due to the release of catecholamines, followed by hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. These symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [MSR]).
Primary vs secondary SCIs
Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary spinal cord injury. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.
Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas or abscesses cause acute cord compression and injury. Spinal cord compression from metastatic disease is a common oncologic emergency.
Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary spinal cord injury without spinal fracture or dislocation. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in spinal cord injury without radiologic abnormality (SCIWORA).
SCIWORA was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or computed tomography (CT) scanning evidence of fracture or dislocation. However with the advent of magnetic resonance imaging (MRI), the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury. SCIWORA should now be more correctly renamed as "spinal cord injury without neuroimaging abnormality" and recognize that its prognosis is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury.[9, 10, 11]
Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or hypoxic effects compound the extent of spinal cord injury.
Complete vs incomplete spinal cord syndrome
One of the goals of the physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete. In most clinical scenarios, physicians should use a best-fit model to classify the spinal cord injury syndrome.
A complete cord syndrome is characterized clinically as complete loss of motor and sensory function below the level of the traumatic lesion. Incomplete cord syndromes have variable neurologic findings with partial loss of sensory and/or motor function below the level of injury; these include the anterior cord syndrome, the Brown-Séquard syndrome, and the central cord syndrome.
Anterior cord syndrome involves a lesion causing variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception.
Brown-Séquard syndrome, which is often associated with a hemisection lesion of the cord, involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.
Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities, with sacral sensory sparing. The pattern of motor weakness shows greater distal involvement in the affected extremity than proximal muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in the upper extremities (eg, sensation of burning in the hands or arms), are common.
Other cord syndromes
The conus medullaris syndrome, cauda equina syndrome, and spinal cord concussion are briefly discussed below.
Conus medullaris syndrome is a sacral cord injury, with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs, whereas the sacral segments occasionally may show preserved reflexes (eg, bulbocavernosus and micturition reflexes). Motor and sensory loss in the lower limbs is variable.
Cauda equina syndrome involves injury to the lumbosacral nerve roots in the spinal canal and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true spinal cord injury, the affected limbs are areflexic. Cauda equina syndrome is usually caused by a central lumbar disk herniation.
A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage.
Since 2005, the most common causes of spinal cord injury (SCI) remain: (1) motor vehicle accidents (40.4%); (2) falls (27.9%), most common in those aged 45 y or older. Older females with osteoporosis have a propensity for vertebral fractures from falls with associated SCI; (3) interpersonal violence (primarily gunshot wounds) (15.0%), which is the most common cause in some US urban settings. Among patients who had suffered an assault, spinal cord injury from a penetrating injury tended to be worse than that from a blunt injury ; (4) and sports (8.0%), in which diving is the most common cause). Spinal cord injury (SCI) due to trauma has major functional, medical, and financial effects on the injured person, as well as an important effect on the individual's psychosocial well-being.[14, 15, 16]
Other causes of spinal cord injury include the following:
Iatrogenic injuries, especially after spinal injections and epidural catheter placement
Vertebral fractures secondary to osteoporosis
Injuries often associated with traumatic spinal cord injury also include bone fractures (29.3%), loss of consciousness (17.8%), and traumatic brain injury affecting emotional/cognitive functioning (11.5%).
The rate of alcohol intoxication among individuals who sustain spinal cord injuries is 17-49%.
The incidence of spinal cord injury in the United States is approximately 40 cases per million population, or about 12,000 patients, per year based on data in the National Spinal Cord Injury database. However, this estimate is based on older data from the 1990s as there has not been any new overall incidence studies completed. Estimates from various studies suggest that the number of people in the United States alive in 2010 with spinal cord injury was about 265,000 persons (range, 232,000-316,000).
Spinal cord injuries occur most frequently in July and least commonly in February. The most common day on which these injuries occur is Saturday. Spinal cord injuries also occur more frequently during daylight hours, which may be due to the increased frequency of motor vehicle accidents and of diving and other recreational sporting accidents during the day.
Racial, sexual, age-related differences in incidence
A significant trend over time has been observed in the racial distribution of persons with spinal cord injury. Since 2005, 66.5% are white, 26.8% are black, 8.3% are Hispanic, and 2.0% are Asian.
Males are approximately 4 times more likely than females to have spinal cord injuries. Overall, males account for 80.7% of reported injuries in the national database.
Since 2005, the average age at injury is 40.7 years, reflecting the rise in the median age of the general population in the United States. About 50% of spinal cord injuries occur between the ages of 16 and 30 years, 3.5% occur in children aged 15 years or younger, and about 11.5% in those older than 60 years (11.5%). Greater mortality is reported in older patients with spinal cord injury.
Pediatric SCI data
The pediatric data parallels that of the adult data on spinal cord injuries. Using information from the Kids' Inpatient Database (KID) and the National Trauma Database (NTDB), Vitale and colleagues found that, with regard to the annual pediatric incidence rate a significantly greater incidence of spinal cord injuries was found in black children (1.53 cases per 100,000 children) than in Native American children (1.0 case per 100,000 children) and Hispanic children (0.87 case per 100,000 children), and the frequency in Asian children was significantly lower than that in all other races (0.36 per 100,000 children). In addition, the likelihood that boys would suffer spinal cord injuries (2.79 cases per 100,000)was found to be more than twice that of girls (1.15 cases per 100,000).
The overall incidence of pediatric SCI is 1.99 cases per 100,000 US children. As estimated from the above data, 1455 children are admitted to US hospitals annually for treatment of spinal cord injuries.
Vitale et al also looked at the major causative factors of pediatric cases, reporting the following incidences , again paralleling adult data:
Motor vehicle accidents - 56%
Accidental falls - 14%
Firearm injuries - 9%
Sports injuries - 7%
Among children in the study, 67.7% of those injured in a motor vehicle accident were not wearing a seatbelt. Alcohol and drugs were found to have played a role in 30% of all pediatric cases of spinal cord injuries.
Other epidemiologic data
Marital, educational, and employment status of patients with spinal cord injuries are discussed below.
Single persons sustain spinal cord injuries more commonly than do married persons. Research has indicated that among persons with spinal cord injuries whose injury is approximately 15 years old, one third will remain single 20 years postinjury. The marriage rate after SCI is annually about 59% below that of persons in the general population of comparable gender, age, and marital status.
Marriage is more likely if the patient is a college graduate, previously divorced, paraplegic (not tetraplegic), ambulatory, living in a private residence, and independent in the performance of activities of daily living (ADL).
The divorce rate annually among individuals with spinal cord injury within the first 3 years following injury is approximately 2.5 times that of the general population, whereas the rate of marriages contracted after the injury is about 1.7 times that of the general population.
The divorce rate in those who were married at the time of their injury is higher if the patient is younger, female, black, without children, nonambulatory, and previously divorced. The divorce rate among those who were married after the spinal cord injury is higher if the individual is male, has less than a college education, has a thoracic level injury, and was previously divorced.
The rate of injury differs according to educational status, as follows:
Less than a high school degree: 39.8%
High school degree: 49.9%
Associate degree: 1.6%
Bachelors degree: 5.9%
Masters or doctorate degree: 2.1%
Other degree: 0.7%.
Patients with spinal cord injury classified as American Spinal Injury Association (ASIA) level D are more likely to be employed than individuals with ASIA levels A, B, and C (see Neurologic level and extent of injury under Clinical). Persons employed tend to work full-time. Individuals who return to work within 1 year of injury tend to return to the same job. Those individuals who return to work after 1 year of injury tend to work for a different employer at a different job requiring retraining.
The likelihood of employment after injury is greater in patients who are younger, male, and white and who have more formal education, higher reported intelligence quotient (IQ), greater functional capacity, and less severe injury. Patients with greater functional capacity, less severe injury, history of employment at the time of injury, greater motivation to return to work, nonviolent injury, and ability to drive are more likely to return to work, especially after more elapsed time following injury.
Patients with a complete spinal cord injury (SCI) have a less than 5% chance of recovery. If complete paralysis persists at 72 hours after injury, recovery is essentially zero. In the early 1900s, the mortality rate 1 year after injury in patients with complete lesions approached 100%. Much of the improvement since then can be attributed to the introduction of antibiotics to treat pneumonia and urinary tract infection (UTI).
The prognosis is much better for the incomplete cord syndromes.
If some sensory function is preserved, the chance that the patient will eventually be able walk is greater than 50%.
Ultimately, 90% of patients with spinal cord injury return to their homes and regain independence.
Providing an accurate prognosis for the patient with an acute SCI usually is not possible in the emergency department (ED) and is best avoided.
Life expectancy and mortality
Approximately 10-20% of patients who have sustained a spinal cord injury do not survive to reach acute hospitalization, whereas about 3% of patients die during acute hospitalization.
Originally the leading cause of death in patients with spinal cord injury who survived their initial injury was renal failure, but, currently, the leading causes of death are pneumonia, pulmonary embolism, or septicemia. Heart disease,[20, 21] subsequent trauma, suicide, and alcohol-related deaths are also major causes of death in these patients.[22, 23] In persons with spinal cord injury, the suicide rate is higher among individuals who are younger than 25 years.
Among patients with incomplete paraplegia, the leading causes of death are cancer and suicide (1:1 ratio), whereas among persons with complete paraplegia, the leading cause of death is suicide, followed by heart disease.
Life expectancies for patients with spinal cord injury continues to increase but are still below the general population. Patients aged 20 years at the time they sustain these injuries have a life expectancy of approximately 35.7 years (patients with high tetraplegia [C1-C4]), 40 years (patients with low tetraplegia [C5-C8]), or 45.2 years (patients with paraplegia). Individuals aged 60 years at the time of injury have a life expectancy of approximately 7.7 years (patients with high tetraplegia), 9.9 years (patients with low tetraplegia), and 12.8 years (patients with paraplegia).
A 2006 study by Strauss and colleagues reported that among patients with spinal cord injury, during the critical first 2 years following injury, a 40% decline in mortality occurred between 1973 and 2004. During that same 31-year period, there had been only a small, statistically insignificant reduction in mortality in the post 2-year period for these patients.
Studies have found that patients with spinal cord injury who suffer from pain have less life satisfaction than do patients in whom pain is well controlled; this may also affect the patients' general outlook on life.[25, 26]
Patients younger than 65 years with muscle grade of 3 or greater in the myotome L3 and S1, and light touch sensation in the dermatome L3 and S1 within 15 days of injury (all within American Spinal Injury Association [ASIA] impairment scale D), are more likely to be independent indoor walkers within a year of injury. Rehabilitation goals in this group should therefore be geared toward functional capacity and within expected independent walking.
Brain-computer interface for SCI
SCI can leave patients with severe or complete permanent paralysis. Brain-computer interface (BCI) can potentially restore or substitute for motor behaviors in patients with a high-cervical SCI. Recent studies have shown that patients with SCI are able to control virtual keyboards, a computer cursor, and a limb prosthetic device using BCI technologies. The BCI outputs are accomplished by acquiring neurophysiological signals associated with a motor process in the cerebral cortex, analyzing these signals in real time, and subsequently translating them into commands for a limb prosthesis. These are promising findings; in the future, BCI may provide a permanent solution for restoration of motor functions in SCI patients.
Walking assistance systems
In 2014, the FDA approved a wearable, motorized device to help individuals with paraplegia due to an SCI sit, stand, and walk with assistance from a companion.[1, 2] The device, which is intended for patients with SCIs at levels T7-L5 and for those with level T4-T6 injuries when used only in rehabilitation institutions, consists of the following:
Fitted metal brace that supports the legs and part of the upper body
Motors that provide movement to the hips, knees, and ankles
Computer and power supply worn on the back
Before using the device, caregivers and patients are required to undergo extensive training.
As part of inpatient therapy, patients with spinal cord injury (SCI) should receive a comprehensive program of physical and occupational therapy.
Many spinal cord injuries result from incidents involving drunk driving, assaults, and alcohol or drug abuse. Spinal cord injuries from industrial hazards, such as equipment failures or inadequate safety precautions, are potentially preventable causes. Unfenced, shallow, or empty swimming pools are known hazards.
Hand L. FDA OKs device to help people with some spinal injuries walk. Medscape Medical News. June 26, 2014. [Full Text].
FDA news release. FDA allows marketing of first wearable, motorized device that helps people with certain spinal cord injuries to walk. US Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm402970.htm. Accessed: June 29, 2014.
American Spinal Injury Association. International Standards for Neurological Classifications of Spinal Cord Injury. revised ed. Chicago, Ill: American Spinal Injury Association; 2000. 1-23.
Ditunno JF Jr, Young W, Donovan WH, Creasey G. The international standards booklet for neurological and functional classification of spinal cord injury. American Spinal Injury Association. Paraplegia. 1994 Feb. 32(2):70-80. [Medline].
Waters RL, Adkins RH, Yakura JS. Definition of complete spinal cord injury. Paraplegia. 1991 Nov. 29(9):573-81. [Medline].
Wuermser LA, Ho CH, Chiodo AE, Priebe MM, Kirshblum SC, Scelza WM. Spinal cord injury medicine. 2. Acute care management of traumatic and nontraumatic injury. Arch Phys Med Rehabil. 2007 Mar. 88(3 Suppl 1):S55-61. [Medline].
Congress of Neurologic Surgeons. Blood pressure management after acute spinal cord injury. Neurosurgery. 2002 Mar. 50(3 Suppl):S58-62. [Medline].
Westgren N, Levi R. Quality of life and traumatic spinal cord injury. Arch Phys Med Rehabil. 1998 Nov. 79(11):1433-9. [Medline].
Kriss VM, Kriss TC. SCIWORA (spinal cord injury without radiographic abnormality) in infants and children. Clin Pediatr (Phila). 1996 Mar. 35(3):119-24. [Medline].
Pang D. Spinal cord injury without radiographic abnormality in children, 2 decades later. Neurosurgery. 2004 Dec. 55(6):1325-42; discussion 1342-3. [Medline].
Yucesoy K, Yuksel KZ. SCIWORA in MRI era. Clin Neurol Neurosurg. 2008 May. 110(5):429-33. [Medline].
Rhee P, Kuncir EJ, Johnson L, Brown C, Velmahos G, Martin M, et al. Cervical spine injury is highly dependent on the mechanism of injury following blunt and penetrating assault. J Trauma. 2006 Nov. 61(5):1166-70. [Medline].
National Spinal Cord Injury Statistical Center (NSCIS). Spinal cord injury facts and figures at a glance. February 2011. [Full Text].
Krause JS, Sternberg M, Lottes S, Maides J. Mortality after spinal cord injury: an 11-year prospective study. Arch Phys Med Rehabil. 1997 Aug. 78(8):815-21. [Medline].
DeVivo MJ. Epidemiology of traumatic spinal cord injury. Kirshblum S, Campagnolo DI, DeLisa JA, eds. Spinal Cord Medicine. Baltimore, Md: Lippincott Williams & Wilkins; 2002. 69-81.
Go BK, DeVivo MJ, Richards JS. The epidemiology of spinal cord injury. Stover SL, DeLisa JA, Whiteneck GG, eds. Spinal Cord Injury. Gaithersburg, Md: Aspen; 1995. 21-55.
Avery JD, Avery JA. Malignant spinal cord compression: a hospice emergency. Home Healthc Nurse. 2008 Sep. 26(8):457-61; quiz 462-3. [Medline].
Vitale MG, Goss JM, Matsumoto H, Roye DP Jr. Epidemiology of pediatric spinal cord injury in the United States: years 1997 and 2000. J Pediatr Orthop. 2006 Nov-Dec. 26(6):745-9. [Medline].
Krause JS. Years to employment after spinal cord injury. Arch Phys Med Rehabil. 2003 Sep. 84(9):1282-9. [Medline].
Morse LR, Stolzmann K, Nguyen HP, Jain NB, Zayac C, Gagnon DR, et al. Association between mobility mode and C-reactive protein levels in men with chronic spinal cord injury. Arch Phys Med Rehabil. 2008 Apr. 89(4):726-31. [Medline]. [Full Text].
Furlan JC, Fehlings MG. Cardiovascular complications after acute spinal cord injury: pathophysiology, diagnosis, and management. Neurosurg Focus. 2008. 25(5):E13. [Medline].
Turner AP, Bombardier CH, Rimmele CT. A typology of alcohol use patterns among persons with recent traumatic brain injury or spinal cord injury: implications for treatment matching. Arch Phys Med Rehabil. 2003 Mar. 84(3):358-64. [Medline].
Frisbie JH, Tun CG. Drinking and spinal cord injury. J Am Paraplegia Soc. 1984 Oct. 7(4):71-3. [Medline].
Strauss DJ, Devivo MJ, Paculdo DR, Shavelle RM. Trends in life expectancy after spinal cord injury. Arch Phys Med Rehabil. 2006 Aug. 87(8):1079-85. [Medline].
Budh CN, Osteråker AL. Life satisfaction in individuals with a spinal cord injury and pain. Clin Rehabil. 2007 Jan. 21(1):89-96. [Medline].
Widerström-Noga E, Biering-Sørensen F, Bryce T, Cardenas DD, Finnerup NB, Jensen MP, et al. The international spinal cord injury pain basic data set. Spinal Cord. 2008 Dec. 46(12):818-23. [Medline].
van Middendorp JJ, Hosman AJ, Donders AR, Pouw MH, Ditunno JF Jr, Curt A, et al. A clinical prediction rule for ambulation outcomes after traumatic spinal cord injury: a longitudinal cohort study. Lancet. 2011 Mar 19. 377(9770):1004-10. [Medline].
Wolpaw JR, McFarland DJ. Control of a two-dimensional movement signal by a noninvasive brain-computer interface in humans. Proc Natl Acad Sci U S A. 2004 Dec 21. 101(51):17849-54. [Medline].
Birbaumer N, Ghanayim N, Hinterberger T, Iversen I, Kotchoubey B, Kubler A. A spelling device for the paralysed. Nature. 1999 Mar 25. 398(6725):297-8. [Medline].
Pfurtscheller G, Muller GR, Pfurtscheller J, Gerner HJ, Rupp R. Thought'--control of functional electrical stimulation to restore hand grasp in a patient with tetraplegia. Neurosci Lett. 2003 Nov 6. 351(1):33-6. [Medline].
Harris MB, Sethi RK. The initial assessment and management of the multiple-trauma patient with an associated spine injury. Spine. 2006 May 15. 31(11 Suppl):S9-15; discussion S36. [Medline].
Ho CH, Wuermser LA, Priebe MM, Chiodo AE, Scelza WM, Kirshblum SC. Spinal cord injury medicine. 1. Epidemiology and classification. Arch Phys Med Rehabil. 2007 Mar. 88(3 Suppl 1):S49-54. [Medline].
Claydon VE, Krassioukov AV. Orthostatic hypotension and autonomic pathways after spinal cord injury. J Neurotrauma. 2006 Dec. 23(12):1713-25. [Medline].
Brown CV, Antevil JL, Sise MJ, Sack DI. Spiral computed tomography for the diagnosis of cervical, thoracic, and lumbar spine fractures: its time has come. J Trauma. 2005 May. 58(5):890-5; discussion 895-6. [Medline].
Grogan EL, Morris JA Jr, Dittus RS, et al. Cervical spine evaluation in urban trauma centers: lowering institutional costs and complications through helical CT scan. J Am Coll Surg. 2005 Feb. 200(2):160-5. [Medline].
Keenen TL, Antony J, Benson DR. Non-contiguous spinal fractures. J Trauma. 1990 Apr. 30(4):489-91. [Medline].
Powell JN, Waddell JP, Tucker WS, Transfeldt EE. Multiple-level noncontiguous spinal fractures. J Trauma. 1989 Aug. 29(8):1146-50; discussion 1150-1. [Medline].
Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000 Jul 13. 343(2):94-9. [Medline].
Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. 2003 Dec 25. 349(26):2510-8. [Medline].
Stiell IG, Wells GA, Vandemheen KL. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001 Oct 17. 286(15):1841-8. [Medline].
Acheson MB, Livingston RR, Richardson ML, Stimac GK. High-resolution CT scanning in the evaluation of cervical spine fractures: comparison with plain film examinations. AJR Am J Roentgenol. 1987 Jun. 148(6):1179-85. [Medline].
Bracken MB, Shepard MJ, Hellenbrand KG, et al. Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. J Neurosurg. 1985 Nov. 63(5):704-13. [Medline].
Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997 May 28. 277(20):1597-604. [Medline].
Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev. 2002. CD001046. [Medline].
Nesathurai S. Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma. 1998 Dec. 45(6):1088-93. [Medline].
Hurlbert RJ, Hamilton MG. Methylprednisolone for acute spinal cord injury: 5-year practice reversal. Can J Neurol Sci. 2008 Mar. 35(1):41-5. [Medline].
Sansam KA. Controversies in the management of traumatic spinal cord injury. Clin Med. 2006 Mar-Apr. 6(2):202-4. [Medline].
Hadley MN, Walters BC, Grabb PA, et al. Pharmacological therapy after acute spinal cord injury. Neurosurgery. 2002. 50 Suppl:63-72.
Eck JC, Nachtigall D, Humphreys SC, Hodges SD. Questionnaire survey of spine surgeons on the use of methylprednisolone for acute spinal cord injury. Spine. 2006 Apr 20. 31(9):E250-3. [Medline].
Anderson P. New CNS/AANS Guidelines Discourage Steroids in Spinal Injury. Medscape Medical News. Mar 28 2013. Available at http://www.medscape.com/viewarticle/781669. Accessed: April 7 2013.
Hadley MN, Walters BC. Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries. Neurosurgery. Mar 2013;72(Suppl 2):1-259. Available at http://journals.lww.com/neurosurgery/toc/2013/03002. Accessed: Apr 9 2013.
Geisler FH, Dorsey FC, Coleman WP. Recovery of motor function after spinal-cord injury--a randomized, placebo-controlled trial with GM-1 ganglioside. N Engl J Med. 1991 Jun 27. 324(26):1829-38. [Medline].
Bagnall AM, Jones L, Duffy S, Riemsma RP. Spinal fixation surgery for acute traumatic spinal cord injury. Cochrane Database Syst Rev. 2008 Jan 23. CD004725. [Medline].
Gaebler C, Maier R, Kutscha-Lissberg F, Mrkonjic L, Vecsei V. Results of spinal cord decompression and thoracolumbar pedicle stabilisation in relation to the time of operation. Spinal Cord. 1999 Jan. 37(1):33-9. [Medline].
Mirza SK, Krengel WF 3rd, Chapman JR, Anderson PA, Bailey JC, Grady MS. Early versus delayed surgery for acute cervical spinal cord injury. Clin Orthop Relat Res. 1999 Feb. (359):104-14. [Medline].
Vaccaro AR, Daugherty RJ, Sheehan TP, et al. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine. 1997 Nov 15. 22(22):2609-13. [Medline].
Lyrica (pregabalin) [package insert]. New York, NY: Pfizer. June 2012. Available at [Full Text].
Sanin L, Parsons B, et al. Weekly Assessments of Pain and Sleep During a 17-week, Double-blind, Placebo-controlled Trial of Pregabalin for the Treatment of Chronic Neuropathic Pain After Spinal Cord Injury. American Academy of Neurology 64th Annual Meeting. Emerging Science Poster #005. Presented April 25, 2012. New Orleans, LA.
Annual Report for the Model Spinal Cord Injury Care Systems. December 2007;
Fehlings MG, Perrin RG. The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence. Injury. 2005 Jul. 36 Suppl 2:B13-26. [Medline].
Fisher CG, Noonan VK, Dvorak MF. Changing face of spine trauma care in North America. Spine (Phila Pa 1976). 2006 May 15. 31(11 Suppl):S2-8; discussion S36. [Medline].
Goodman A. Pregabalin Rapidly Relieves Neuropathic Pain in Spinal Cord Injury. Medscape Medical News. Available at http://www.medscape.com/viewarticle/804197. Accessed: May 18, 2013.
Hurlbert RJ. Strategies of medical intervention in the management of acute spinal cord injury. Spine (Phila Pa 1976). 2006 May 15. 31(11 Suppl):S16-21; discussion S36. [Medline].
Parsons B, Emir B. Examining the time-to-improvement of pain in patients with chronic neuropathic pain due to spinal cord injury. J Pain. April 2013. 14(4, Supplement):S60.