Acute traumatic spinal cord injury …

General Neurology

Updated 12.02.2023
Released 06.07.1999
Expires For CME 12.02.2026

Acute traumatic spinal cord injury

Authors: J Dedrick Jordan MD PhD, Vyas Viswanathan MD

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Editor: Randolph W Evans MD

Acute traumatic spinal cord injury

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Introduction

Overview

Acute traumatic spinal cord injury (TSCI) is a global epidemic in modern society. Yearly, there are 17,900 new cases of acute spinal cord injury in the United States of America alone, and over 2,966,000 people live with spinal cord injury. Motor vehicle accidents account for nearly half of all cases, followed by falls (16%), violence (including gunshot wounds) (12%), sports-related accidents (10%), and other causes (14%). Despite advances made in the understanding of the pathogenesis and improvements in the early recognition and treatment of coexisting complications, traumatic spinal cord injury remains a devastating event, often leading to permanent and severe disability. In this update, the authors provide an overview of the disease, including epidemiology, pathophysiology, clinical presentation, and management principles. Acute traumatic spinal cord injury (TSCI) is a global epidemic in modern society. Yearly, there are over 12,000 new cases of acute spinal cord injury in the United States of America alone, and over 260,000 people live with spinal cord injury. Motor vehicle accidents account for nearly half of all cases, followed by falls (16%), violence (including gunshot wounds) (12%), sports-related accidents (10%), and other causes (14%). Despite advances made in the understanding of the pathogenesis and improvements in the early recognition, and treatment of coexisting complications, TSCI remains a devastating event, often leading to permanent and severe disability. In this update, the authors provide an overview of the disease, including epidemiology, pathophysiology, clinical presentation, and management principles.

Key points

	• Most traumatic spinal cord injuries occur in association with impact to the vertebral column, resulting in direct compression or disruption of the spinal cord. Secondary injuries may ensue, resulting from ischemic and inflammatory processes, disrupted homeostasis, and apoptosis.
	• Prevention of the initial spinal cord injury remains the most effective method of managing this condition.
	There are no medical treatments that effectively treat or reverse acute spinal cord injury.
	• There is conflicting evidence of potential benefit of steroids in traumatic spinal cord injury with lack of clear outcome improvement. Their use is no longer endorsed by major society guidelines.
	• All traumatic spinal cord injuries require emergent neurosurgical (or orthopedic) consultation to evaluate the role of emergent surgical decompression.

Historical note and terminology

The earliest clinical account of spinal cord injury was given in the Edwin Smith Papyrus as "a disease that cannot be treated" (23). Hippocrates advocated several methods of reducing chronic spinal deformities, whereas Galen was able to localize cervical spinal cord injury by performing extensive vivisections. The biomechanical principle of immobilization was strongly advocated by Herbert Burrell, who also emphasized the need for spinal reduction (67). A gloomy prognosis for patients with spinal cord injury prevailed until the end of World War II. In 1944 Sir Ludwig Guttman founded the Spinal Injury Center at Stoke Mandeville Hospital in Aylesbury, England, the first center of its kind to focus on global care for patients with spinal cord injury. Subsequently, in the United States, the Veteran Administration initiated spinal cord injury services. These centers emphasized patient education, education to health care providers, prevention, early diagnosis, treatment of the injury and its complications, and physical and occupational health with rehabilitation facilities.

Clinical manifestations

Presentation and course

The clinical presentation of acute traumatic spinal cord injury depends on the degree of spinal cord injury and concurrent associated injuries. Nearly half of all traumatic spinal cord injuries involve the cervical cord. These patients will present with quadriparesis of variable degree or full quadriplegia.

The severity of the spinal cord injury is graded according to the American Spinal Injury Association (ASIA) grading scale.

The American Spinal Injury Association (ASIA) Impairment Scale, first issued in 1992, is an international classification of spinal cord injury based on neurologic deficits, including motor function and sensation, as well as bowel and bladder control from the S4 and S5 segments (01). Loss of function of these sacral segments constitutes a complete spinal cord injury. The ASIA scale has 5 different ratings, A to E, which correspond to complete spinal cord injury in ASIA A to no deficits detected in ASIA E. The specific criteria for each level of the grading scale are listed below.

ASIA A. "Complete" spinal cord injury, with no motor or sensory function preservation in the sacral segments S4 to S5 and no anal sphincter contraction or sensation.

ASIA B. "Incomplete" spinal cord injury, with sensory preservation but no motor function below the neurologic level, though with preservation of sacral segments S4 to S5.

ASIA C. "Incomplete" spinal cord injury, with motor function preservation in more than half of the key muscles below the neurologic level with a muscle grade of less than 3, which indicates the inability to move against gravity in a particular muscle group.

ASIA D. “Incomplete" spinal cord injury, with motor function preservation in at least half of the key muscles below the neurologic level with a muscle grade of 3 or more, indicating active muscle use against gravity in a particular muscle group.

ASIA E. "Normal" motor and sensory activity, with good strength throughout. It is possible to have spinal cord injury and neurologic deficits with completely normal motor and sensory scores.

The ASIA scale replaced the grading system developed by Frankel and colleagues in 1969, which proposed 5 categories of spinal cord injury based on the loss of neurologic function: (A) complete, (B) sensory function only, (C) useless motor function, (D) useful motor function, and (E) normal function. One of the main advantages of the ASIA scale over the Frankel scale is the ability to evaluate patients immediately, without trying to walk the patients.

In a complete cord injury (ASIA grade A), there is spared sensory level above the lesion, reduced sensation at the level of the lesion, and total loss of sensation at the next caudal level. Similarly, motor strength is spared above the lesion, but reduced at the level followed by complete paralysis (flaccid plegia) at the next myotome level. In the acute stage, reflexes are absent. In males, priapism may occur. The bulbocavernosus reflex is also absent, and urinary retention typically occurs as well.

Incomplete injuries (ASIA B through D) will present according to the degree of spinal cord injury and disruption of the various spinal cord tracts. Generally, sensation tends to be less disrupted than motor function. One plausible explanation is the fact that spinothalamic tracts are more peripheral and, therefore, less vulnerable to anterior-posterior compression/disruption.

In April 2019, the International Standards for Neurological Classification of Spinal Cord Injury was revised by ASIA and the International Spinal Cord Society. The 2 main changes included 1) changing the taxonomy for how comorbid nonspinal cord injury related weakness and 2) broadening the definition of zones of partial preservation (ZPP) (05).

In patients who have comorbid conditions that also cause weakness, the strength score was previously based on the presumed score if the comorbid condition did not exist and was marked with a “*”. With the new change, the strength score is documented as identified on testing with a “*” to indicate that an alternative cause of weakness may be present (05)

In cases of complete injury, where motor and sensory levels are absent in most the lowest sacral segments, zones of partial preservation were used to identify segments that may have partial sensory and motor levels involvement caudal to the area of injury. However, now zones of partial preservation will also include incomplete injuries that result in either absent sensory or motor function in the most caudal sacral segments (05).

In addition to complete and incomplete spinal cord injury, there are other clinical syndromes that may be seen in the setting of acute trauma. These include the following:

	• Central cord syndrome, which is characterized by disproportionately greater motor impairment in the upper extremities compared to lower extremities, with or without sensory impairment and with or without bladder dysfunction. This is typically described in the setting of mild trauma and concurrent cervical.
	• Brown-Sequard syndrome (Hemicord syndrome), which is characterized by a functional hemisection of the spinal cord that results in ipsilateral loss of motor function, ipsilateral loss of vibration, and proprioception and contralateral loss of temperature and pain sensation. Brown-Sequard syndrome may also be associated with Horner syndrome (ptosis, miosis, and anhidrosis) if there is coexisting cervical paravertebral sympathetic or inferior cervical ganglion injury. This pattern of injury has often been described in the setting of stabbing injury, disc herniation, hematoma, and tumors.
	• Anterior cord syndrome results in direct injury to the spinothalamic tract, thus resulting in loss of motor function and loss of sensation to pain, temperature, and light touch. Because the posterior column is preserved, these patients will have preserved proprioception and vibration. This pattern of injury may be seen with direct crush or compression injury.
	• Cervical cord neurapraxia is also known as transient quadriparesis. This phenomenon has been described in athletes. This is thought to reflect a “concussion” of the cervical spinal cord, with a mechanism of injury thought to be caused by axial loading of the cervical spine in a flexion or extension.
	• Conus medullaris syndrome is a consequence of injury to the conus and epiconus regions and is characterized by combined lower and upper motor neuron lesions with sphincter dysfunction.
	• Cauda equina syndrome is characterized by loss of function of the lumbar and sacral plexus nerves below the conus medullaris. It manifests with severe pain, saddle anesthesia (S3 to 5 dermatomes), bladder and bowel dysfunction, paraplegia in various degrees, absent Achilles tendon reflexes bilaterally, absent anal and bulbocavernosus reflexes, and sexual dysfunction.

Disruption of the autonomic pathways within and outside the spinal cord (craniosacral parasympathetic and cervicothoracic sympathetic outflow) may accompany the syndromes and lead to autonomic and visceral dysfunction. Furthermore, loss of diaphragm function (phrenic nerve) with ensuing respiratory difficulty or failure may occur.

Prognosis and complications

There are no therapeutic interventions with proven ability to reverse the consequences of the initial spinal cord injury and the resulting neurologic injury.

Early death following acute traumatic cord injury has historically been quoted as ranging from 5% to 25% (16; 68). A significant difference exists between recovery patterns of an incomplete and a complete spinal cord injury. Rate of motor score improvements is directly related to the initial severity and level of injury. With regards to neurologic recovery patterns in traumatic cervical spinal cord injury, only a small percentage of tetraplegics will have motor recovery below the first caudal segment from the neurologic level of injury (50). Most upper extremity recovery is expected during the first 6 months after injury. Motor strength improvement continues during the second year with lesser gains observed during the first year. According to Frankel, 11% of patients improve by at least 1 grade, but only 2.8% of patients improve to grade D (useful motor function) (31). Late conversion (30 days to 2.5 years post-injury) from complete to incomplete spinal cord injury following cervical injury occurs in 4% to 10% of patients. Patients who have this conversion within 1 to 3 months may have a better chance of motor recovery. Incomplete injuries have a much better prognosis; upper extremity motor recovery is almost twice as great as with quadriplegics. In summary, the greatest degrees of improvement are seen in those with incomplete injuries along with those without complicating medical comorbidities or initial complications.

Medical comorbidities are very common in the setting of acute spinal cord injury. Cardiovascular complications are well described and are directly related to disturbance of CNS-cardiac connections. At least 3 spinal cord elements involved in cardiovascular control have been identified. These are (1) descending vasomotor pathways, (2) sympathetic preganglionic neurons, and (3) spinal afferents (33). Injury to the cervical or high thoracic (above the T6 level) results in the loss of sympathetic nervous system (SNS) input to the heart and blood vessels and may lead to hypotension, bradycardia, autonomic dysreflexia, deep venous thrombosis (DVT), and long-term risk of coronary artery disease (CAD). Hypotension results from decreased compensatory vasoconstriction (mediated by input from the sympathetic nervous system) and decreased muscle activity and venous pooling. Symptoms can include light-headedness, dizziness, blurry vision, and/or fatigue. Bradycardia results from unopposed parasympathetic input to the heart from the vagus nerve. Autonomic dysreflexia (increase in blood pressure, headaches, flushing/sweating above the level of the injury, and bradycardia) results from interruption of sympathetic nervous system activity. Deep venous thrombosis occurs because of venous stasis secondary to muscle paralysis and a transient hypercoagulable state (32). Cardiopulmonary complications are the major cause of death in patients with acute spinal cord injury. The mortality rates are higher for cervical level injury, especially at the high cervical spinal cord. Mortality in acute spinal cord injury remains high, and 5% to 10% of patients die, even with advanced life support systems (38).

Lastly, increased incidence of coronary artery disease is related to the high incidence of metabolic syndrome in patients with spinal cord injury. Routine evaluation of cardiovascular risk factors should be performed, as well as appropriate modifications made (treatment of high blood pressure, treatment of high cholesterol, smoking cessation, etc.) (56).

Respiratory complications, including respiratory failure, pulmonary edema, pneumonia, and pulmonary emboli are considered the most frequent complications during the acute hospitalization after acute spinal cord injury (17; 85). The incidence of such complications are directly correlated with the level of spinal cord injury, with most common occurrence in higher cervical spinal cord injury (up to 84%). They may also occur in high thoracic spinal cord injuries.

Other complications may include pressure ulcers (bedside sores) related to immobility. Gastrointestinal complications such as gastric stress ulceration particularly in the acute setting and paralytic ileus may also occur. Temperature control disturbance, particularly in high cervical spinal cord injury, can also pose a problem, as affected patients lack vasomotor control and, therefore, are not able to sweat below the lesion. Depression and adjustment disorders are also common following acute spinal cord injury. Therefore, a multidisciplinary approach in preventing and addressing potential complications are followed in such subset of patients.

Clinical vignette

A 33-year-old man was involved in a rollover motor vehicle accident. He was an unrestrained passenger in the backseat of a car. He had loss of consciousness for some time, but he eventually regained consciousness and was able to crawl from the vehicle. Paramedics immobilized him in a cervical collar, and he was transported to an emergency facility via life flight. He was neurologically intact. Plain x-rays of the cervical spine showed dislocation of C7 over T1.

Cervical spine (swimmer’s view) (x-ray)

Plain x-ray of lateral cervical spine (swimmer’s view) showing the C7/T1 region. There are inherent difficulties in visualization of this part of the spine, but this view is essential and should be included in the initial screenin...

CT scan of this level revealed a facet injury with jumped facets and significant canal compromise.

Acute traumatic spinal cord injury (CT)

(A) CT scan sagittal reconstruction is useful, especially at the cervicothoracic junction to measure the canal encroachment and the bony injury. (B) CT of cervical spine demonstrates the dislocation at C7 and T1 with overriding fa...

A 3-dimensional CT was helpful in visualization of the spinal column.

Traumatic spinal cord injury (3D CT)

Three-dimensional CT is a recent addition to neuroimaging and provides a circumferential view of the bony architecture. (Contributed by Dr. Prasad Vannemreddy.)

MRI disclosed severe spinal cord compression and a disrupted intervertebral disc.

Traumatic spinal cord injury (MRI)

T2-weighted MRI images show fresh blood collection and they differentiate cord edema from contusions and hemorrhages. This information is useful in prognostication. (Contributed by Dr. Prasad Vannemreddy.)

Cervical spine traction was applied using Gardner Wells tongs. Closed reduction was not attempted. Emergency surgical decompression of the spinal canal with excision of fractured C7 body, open reduction, placement of bone graft, and internal fixation using screws and plates were performed.

Comment. Motor vehicle accidents account for more than half of cervical spinal cord injuries. Seat belt restraints are useful in reducing the severity of the overall injury (45). External immobilization of the spine is indicated for all persons in motor vehicle accidents until a spinal injury is ruled out. Once a patient can be evaluated medically in a hospital, routine radiographic evaluation should include careful screening of C1, C2, C7, and T1 visualization; open mouth view for odontoid and swimmer’s view for C7/T1 (53). Radiographic evaluation of the cervical spine is not complete without adequate visualization of the spine from C1 through T1. The trauma series of CT scanning for spinal trauma is helpful with 1 mm to 3 mm sections and multiplanar reconstruction to visualize posterior element fractures. MRI scan is essential to detect soft tissue injuries and the spinal cord damage that allows prognostication (69). Older age and MRI findings consistent with spinal cord edema or hemorrhage predicted worse outcome (82).

Biological basis

Etiology and pathogenesis

Spinal cord injury can be due to more than one of the following components: mechanical insult, biochemical derangement, hemodynamic alteration, and/or the premorbid condition of the patient. Direct tissue destruction, motion stress to the damaged cord accentuating existing damage to the neural tissue, and compression injury constitute the mechanical insult. Spinal cord injury occurs in 2 stages, the primary trauma and the secondary cascade of events that result in tissue death and dysfunction (63). In the primary phase, physical injury directly results in hemorrhage and neuronal dysfunction that progresses to cell death. The mechanical insult consists of direct tissue destruction, motion stress to the damaged cord accentuating existing damage to the neural tissue, and compression injury. This physical injury produces the initial neural dysfunction. Over a period, in the secondary phase, changes in the microvasculature, sluggish axoplasmic flow, and alterations in signaling cascade result in further tissue loss and impaired function. The spinal cord becomes swollen and necrotic with changes in the microvasculature and sluggish axoplasmic flow. Progressive gray matter necrosis ensues, with fragmentation of white matter. The amount of tissue disruption is proportional to the severity of the injury. With time, a cascade of events known as secondary injury ensues. Presently, the physical tissue disruption is not amenable to any treatment. However, the secondary phase, which previously had been refractory to treatment, is now emerging as a target for therapeutic intervention.

Spinal cord injury can be due to more than one of the following components: mechanical insult, biochemical derangement, hemodynamic alteration, or premorbid condition of the patient. Direct tissue destruction, motion stress to the damaged cord accentuating existing damage to the neural tissue, and compression injury constitute the mechanical insult. This physical injury produces the initial neural dysfunction. Over a period, the spinal cord becomes swollen and necrotic with changes in the microvasculature and sluggish axoplasmic flow. Progressive gray matter necrosis ensues, with fragmentation of white matter. The amount of tissue disruption is proportional to the severity of the injury; with time, a cascade of events known as secondary injury ensues. The physical tissue disruption is not amenable to any treatment at the present time. It is the secondary injury, which is thought to be refractory to treatment that now seems to respond to therapeutic intervention.

From a primary injury standpoint, the spinal cord may recover to a certain extent, but secondary pathological processes related to biochemical and hemodynamic derangements occur independently. A massive assimilation of lysosomes and a release of hydrolases, along with mitochondrial alterations with a decreased cytochrome oxidase activity, have been observed. The ionic channels show decreased activity. Within 6 hours to 8 hours, a breakdown of neuromembranes and neurofilaments occurs with a release of lipid peroxidase and hydrolytic destruction (11). This is described as the key step in the initiation of the secondary injury cascade, and some medical management strategies of acute spinal cord injury have focused around these cellular events and time window. Some investigations have suggested a programmed cell death (apoptosis) mediated by capsase-3 protease in spinal cord injury (24). Apoptotic cell death contributes to tissue damage at the site of injury, and prevention of this process results in neurologic recovery after spinal cord injury (52). Research in genetic control and biochemical markers of apoptotic cell death has identified a gene encoding a protein in round worms (44) and in the mammalian homologs of cell death mechanisms (58). Further research showed that caspase-1 (ICE) and caspase-3 (CPP-32) were expressed in oligodendrocytes, and their inhibition prevented apoptotic cell death (43).

Traumatic injury to the spinal cord leads to mechanical stresses on the spinal cord vasculature causing tearing of the vessels. The blood supply to the spinal cord consists of the anterior median longitudinal artery and the posterolateral longitudinal arteries (intrinsic arteries) and a series of arteries arising from outside the vertebral column (extrinsic arteries). Rupture of the blood vessels results in intraparenchymal hemorrhage, which is initially localized to the highly vascularized and most vulnerable central gray matter. The hemorrhage extends to the dorsal columns in the rostral and caudal segments, resulting in damage not only at the site of injury but also to nearby healthy tissue. Damage to the vasculature of the spinal cord results in the breakdown of the blood-spinal cord barrier at the site of injury and along the axis of the spinal cord. Altered barrier permeability leaves the spinal cord vulnerable to the toxic effects of inflammatory cells. Posttraumatic inflammation, characterized by leukocytes and macrophages, is thought to contribute to secondary pathogenesis through myelin vesiculation, lipid peroxidation, and the production of toxic molecules that damages healthy tissue.

Epidemiology

Incidence and prevalence. In the United States, nearly 296,000 people live with traumatic spinal cord injury, with traumatic spinal cord injury affecting over 172,900 new patients per year in the United States alone, translating into approximately 260,000 people living with spinal cord injury in the United States being affected every year (47; 60).

Between 1973 and 2016, spinal cord injuries account for the loss of 1 million years of healthy life in the United States, with a national morbidity and mortality burden surpassing that of multiple sclerosis, Parkinson disease, and HIV/AIDS (41).

Worldwide, the incidence of spinal cord injury is nearly 1 million per year, with over 27 million prevalent cases. However, the incidence varies greatly depending on regions with high income. Western Europe, North America, Pacific Asia, and North America have over double the age-standardized incident cases compared to Latin America, Southeast Asia, and many regions of Africa.

Globally, the rate of spinal cord injury has remained nearly constant over the last 2 decades (35), though more people are living with disease given the population growth during this time period.

Age and gender. Traumatic spinal cord injury has historically been a disease of young adults. Over the last few decades, the mean age of individuals with spinal cord injury in the United States has risen from just over 28 years old in the 1970s to 40 years old in 1993 to 50 years old in 2012 (47). This also varies internationally. Hagen and colleagues summarize age at ictus for multiple countries (40).

In the United States, men account for nearly 80% of new spinal cord injury cases (60). Globally, males have a higher incidence of spinal cord injury in their 20s and 30s compared to females, though by 50 years of age, both genders have similar incidence of injury (35).

Mechanism. Traumatic spinal cord injury has historically been a disease of young adults. In the 1970s, the average age at injury was just over 28 years old, with most cases occurring between 16 and 30 years old. However, and in the past 3 decades, the average age of spinal cord injury has now increased to 40 years of age. The vast majority of these patients (80.9%) are male; two thirds of them are Caucasian, 27% are African, 7.9% are Hispanic, and 2% are Asian (59). A tendency toward greater incidence during warmer months and during weekends has also been correlated (50). Blumer and Quine provide an international comparison of the prevalence of spinal cord injury (10).

Falls and motor vehicle accidents are the most common cause of spinal cord injury in many countries and account for two thirds of cases in America (40; 35; 60). In the United States, acts of violence accounted for nearly a quarter of spinal cord injuries in the 1990s but has since declined to 13%.

In Western Europe and Canada, spinal cord injury related to assault is much rarer than in the United States (34). On the other hand, in North Africa and the Middle East, conflict and terrorism are the unfortunate leading causes of spinal cord injury (35).

Since 2005, the most common cause of spinal cord injury has been motor vehicle accidents (41.3%). This has held true for several decades. This is followed by falls (27.3%), acts of violence (primarily gunshot wounds) (15%), sport accidents (10%), and miscellaneous (10% to 15%). Acts of violence as a cause of spinal cord injury peaked in the 1990s at nearly 25%, but it has since declined to its current level. Worldwide, the etiology and incidence differ. For example, in Western Europe and Canada, spinal cord injury related to assault is much rarer compared to the United States of America, whereas in areas of active conflicts, trauma and shrapnel wounds are the leading cause of traumatic spinal cord injury (34).Traumatic spinal cord injury affects over 12,000 new patients per year in the United States alone, translating into approximately 260,000 people living with spinal cord injury in the United States (59).

Traumatic spinal cord injury affects over 12,000 new patients per year in the United States alone, translating into approximately 260,000 people living with spinal cord injury in the United States (59). Traumatic spinal cord injury has historically been a disease of young adults. In the 1970s, the average age at injury was just over 28 years old, with most cases occurring between 16 and 30 years old. However, and in the past 3 decades, the average age of spinal cord injury has now increased to 40 years old. The vast majority of these patients (80.9%) are male; two thirds of them are Caucasian, 27% are African, 7.9% are Hispanic, and 2% are Asian (59). A tendency toward greater incidence during warmer months and during weekends has also been correlated (50). Blumer and Quine provide an international comparison of the prevalence of spinal cord injury (10).

Since 2005, the most common cause of spinal cord injury has been motor vehicle accidents (41.3%). This has held true for several decades. This is followed by falls (27.3%), acts of violence (15%), primarily gunshot wounds, sport accidents (10%), and miscellaneous (10% to 15%). Acts of violence as a cause of spinal cord injury peaked in the 1990s at nearly 25%, but it has since declined to its current level. Worldwide, the etiology and incidence differ. For example, in Western Europe and Canada, spinal cord injury related to assault is much rarer compared to the United States of America, whereas in areas of active conflicts, trauma and shrapnel wounds are the leading cause of traumatic spinal cord injury (34).

Prevention

No effective treatment cure for spinal cord injury is currently available; hence, prevention remains the most effective means of management. Motor vehicle accidents, falls, and violence are the major causes of spinal cord injury in the United States, and policy change targeting these issues can help decrease the incidence of spinal cord injury. Both can be reduced by vigilant law enforcement and avoidance of areas that are more prone or known to harbor violence. The use of seat belt restraints, air bags, and traffic rules have resulted in a reduction in the rate of catastrophic injury in the United States (45; 76). Education of the public regarding injury prevention is a continuing challenge, and the Think First Foundation, an award winning national brain and spinal cord injury prevention program founded jointly by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons, is an effective educational tool in this regard.

No effective treatment for spinal cord injury is currently available; hence, prevention remains the most effective means of management. Motor vehicle accidents and violence are the 2 major causes of spinal cord injury in the United States, and both can be reduced by vigilant law enforcement and avoidance of areas that are more prone or known to harbor violence. Interestingly, the use of seat belt restraints, air bags, and traffic rules have resulted in a reduction in the rate of catastrophic injury in the United States, although the design of a completely safe seat belt restraint has yet to be developed (45; 76). Education of the public regarding injury prevention is a continuing challenge, and the Think First Foundation, an award winning national brain and spinal cord injury prevention program founded jointly by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons, is an effective educational tool in this regard.

Management

The primary assessment of the patient with trauma or suspected acute spinal cord injury in the field should follow the standard ABCD prioritization protocol scheme: airway, breathing, circulation, and disability (neurologic status).

Once in the emergency department or acute care setting, prioritization of any other concurrent life-threatening injuries such as acute systemic hemorrhage or airway compromise should be triaged and addressed accordingly. Occasionally, stabilization of other life-threatening emergencies may take precedence of the initial evaluation or management of acute spinal cord injury, according to the clinical evaluation of the acute care provider.

In the initial acute setting, vital signs including heart rate monitoring, pulse oximetry, temperature, respiratory status, and blood pressure are all standard of care evaluation/monitoring.

Routine screening of all trauma victims for spinal cord injury is essential, and special imaging may be obtained as appropriate. Immobilization of the spine must be continued until a serious spinal instability is ruled out. The mainstay of spinal cord injury care has been medical, rather than surgical.

Clinical trials focused on the medical management of spinal cord injury have attempted to study the efficacy of substances such as steroids (methylprednisolone), ganglioside GM-1, nimodipine, thyrotropin-releasing factor, and glutamate receptor antagonism, to name just a few (42).

The use of steroids (methylprednisolone) in the treatment of spinal cord injury has been one of the most controversial topics, with a significant amount of research having been conducted on their efficacy and safety. The largest study to examine the role of methylprednisolone in spinal cord injury was the National Acute Spinal Cord Injury Study (NASCIS). This landmark series of 3 studies examined high-dose methylprednisolone versus low-dose methylprednisolone, high-dose methylprednisolone versus placebo (naloxone, an opioid antagonist), and finally, the timing of the dose of methylprednisolone relative to the timing of the initial injury. It was determined that there may be some initial benefit to patients receiving methylprednisolone in the earliest time points relative to the onset of injury (30 mg/kg bolus followed by infusion of 5.4 mg/kg per hour), for 24 hours if administered within 3 hours of injury or for 48 hours if initiated 3 hours to 8 hours after injury (11; 12). However, these initial benefits to patients, although seen at 6 weeks and 6 months post injury, were not seen at 1 year postinjury. High doses of steroids were also associated with a significantly higher incidence of severe pneumonia, sepsis, and death. The 2013 society guidelines endorsed by the American Associated of Neurological Surgeons, as well as the Congress of Neurological Surgeons, advise that the use of glucocorticoids in the acute spinal cord injury is no longer recommended (46). The Canadian Association of Emergency Physicians concur, however, that the treatment with glucocorticoids is a treatment option and not a standard. The American Academy of Emergency Medicine endorses similar statement. Hence, use of steroids in the setting of acute spinal cord injury no longer constitutes standard of care. It is notable, however, that most clinicians that administer steroids for spinal cord injury predominantly do so for fear of litigation (22).

The controversy about steroids is also likely not settled for good. The NASCIS III trial compared 3 treatment groups: methylprednisolone administered for 48 hours, methylprednisone administered for 24 hours, and tirilazad mesylate administered for 48 hours. For patients treated within 3 hours, there was no difference in outcomes among treatment groups at 1 year. For patients treated between 3 to 8 hours, 48 hours of methylprednisolone was associated with a greater motor but not functional recovery, compared with other treatments. Patients who received the longer duration infusion of methylprednisolone had more severe sepsis and severe pneumonia compared with the shorter duration of infusion; mortality was similar in all treatment groups.

Significant advances have been made in the management of spinal column injury, though the impact of surgical correction of the spinal fractures on outcome from the cord injury remains elusive (21; 78). However, indications for surgery may include spinal instability (radiologically proven by dynamic views of spine or clinically indicated by painful movements of spine), progressive neurologic deficits with extrinsic spinal cord compression, compound spinal injuries with or without neurologic dysfunction, and deterioration of existing neurologic function.

Surgery is performed with the intent of decompressing the spinal cord in patients with neurologic deficit and ongoing spinal cord compression, and realigning the spinal column to restore spinal stability to facilitate early patient mobilization and eventual rehabilitation (83).

Several classification systems have been proposed to help assess whether a patient with traumatic spinal cord injury requires surgery, though no single system has gained widespread use because each has disadvantages. To overcome the deficiencies of classification, the Spine Trauma Study Group has developed 2 classification systems for spinal trauma (83).

The first classification system is the Subaxial Cervical Spine Injury Classification (Table 1). The Spine Trauma Study Group recommends that patients with a subaxial cervical spine injury score of less than 4 be treated non-operatively, and those with a score greater than 4 should be treated operatively. Patients with a score of exactly 4 can be managed with or without surgery at the discretion of the management team.

Table 1. The Subaxial Cervical Spine Injury Classification System

Injury variable	Weighted severity points
Morphology
No abnormality Compression Distraction Rotation/Translation	0 1 3 4
Disco-ligamentous complex integrity
Intact Indeterminate Disrupted	0 1 2
Neurologic status
Intact Root injury Complete cord injury Incomplete cord injury Cord compression with neurodeficit	0 1 2 3 1
(83)

The second classification system is the Thoracolumbar Spine Injury Classification (Table 3). The Spine Trauma Study Group recommends that patients with thoracolumbar spine injury scores of less than 4 be treated non-operatively, and those with a score greater than 4 should be treated operatively. Patients with a score of exactly 4 can be managed with or without surgery at the discretion of the management team.

Table 2. The Thoracolumbar Spine Injury Classification System

Injury variable	Weighted severity points
Morphology
No abnormality Compression Rotation/Translation Distraction	0 1 3 4
Posterior ligamentous complex integrity
Intact Indeterminate Disrupted	0 2 3
Neurologic status
Intact Root injury	0 2
Conus, cord injury
Complete cord injury Incomplete cord injury Cauda equina	2 3 3

Although experimental and clinical data are still accumulating in the area of surgical treatment following traumatic spinal cord injury, it appears that rapid surgical or traction decompression of the spinal cord in the early time period following spinal cord injury may improve functional outcomes (19; 09; 15; 78; 74; 61). A multicenter, international, prospective cohort study, Surgical Timing in Acute Spinal Cord Injury Study (STASCIS), was conducted between 2002 and 2009 to compare the effectiveness of early (less than 24 hours post-injury) versus late (24 hours or greater post injury) surgery (27). The results of the STASCIS study showed that the odds of at least a 2-grade ASIA Impairment Scale (AIS) improvement were 2.8 times higher at 6-month follow-up among patients who had early surgery. The study also showed no statistically significant difference in complications between the early and late surgical group. Also, a retrospective study that included patients with acute traumatic spinal cord injury between 2000 and 2011 suggested decreased costs and length of stay for acute care with early surgery after acute traumatic spinal cord injury, especially when performed within 24 hours of injury (54). There is more evidence to suggest that early surgical interventions should be considered to improve neurologic recovery, decrease health care costs, and potentially decrease complication rates.

Closed or open reduction with disc or bone fragments within the spinal canal can sometimes result in neurologic dysfunction, and continuous monitoring for new deficits is mandatory when the patient is on traction and during surgery (37). Delayed neurologic deterioration in complete spinal cord injury is not rare, and attempts have been made to specifically identify the temporal subgroups that are at a higher risk of delayed deterioration. It has been shown that early deterioration is typically related to traction and immobilization, whereas delayed deterioration (after 24 hours) is associated with sustained hypotension in patients with fracture dislocations.

Late sequelae of spinal cord injury, including posttraumatic syrinx or cyst formation and malunited spinal fractures, also require attention. There was no significant difference observed between early and late surgery for the spinal column injury, especially in the cervical region (74). In a study, Kerwin and colleagues concluded that reasonable compliance with an early spinal fracture fixation protocol produced some outcome improvements in non-neurologic outcome (49). Early spine stabilization reduced length of hospital stay in all patients. Patients with thoracic spine trauma and a spinal cord injury had the greatest benefit in reduction of morbidity, HLOS and ICULOS from early stabilization. Global stabilization of the patient is desirable, and optimum information should be obtained regarding the injuries to the spinal column and the spinal cord before surgical intervention. The clinical characteristics of chronic pain in spinal cord injury patients are controversial. Rogano and colleagues (66) prospectively evaluated 81 patients with chronic pain due to spinal cord lesions. The mean pain intensity according to the visual analogue scale was 9.4. The pain intensity was not associated with the magnitude of the spinal lesion, location of the lesion, occurrence of myofascial pain syndrome, or onset of pain. In about 38% of the patients, pharmacological and rehabilitative procedures were effective. Dorsal root entry zone lesion was effective for the treatment of transitional pain in patients with complete section of the spinal cord; spinal cord stimulation was effective for patients with partial lesions of the spinal cord; and intrathecal opioid infusion was effective for both conditions. Because of the high prevalence and the refractory nature of pain following spinal cord injury, it is important to increase the understanding of what factors aggravate different types of pain. This information is related to pain generating mechanisms and may, thus, be useful in the diagnosis and management of these difficult pain conditions. Widerstrom-Noga and Turk conducted a study to identify variables that exacerbate chronic pain associated with spinal cord injury (80). A principal components analysis detected 5 sets of factors that were reported to magnify pain: negative mood, prolonged afferent activity (bowel, bladder, somatic), weather, voluntary physical activity, and transient somatic afferent activity. Negative mood and prolonged afferent activity were frequently and significantly associated with both pain characteristics and psychosocial issues.

With integrated spinal care programs, the average stay for tetraplegics in spinal cord injury centers is 2 to 3 months and 1 to 2 months for a paraplegic.

Cardiovascular complications due to spinal cord injury, including acute hypotension, should be treated with intravenous fluids and, if needed, vasopressors. Hypotension may ensue from systemic causes and blood loss as well as from loss of autoregulation due to the spinal cord injury itself. Based on a study by Vale and colleagues, augmentation of mean arterial pressure to at least 85 mm Hg has become common practice, even though other studies have demonstrated variable results (75).

Long-term hypotension should be treated with oral fluid intake and salt tablets, pseudoephedrine, then fludrocortisone, and finally midodrine. Other medications include desmopressin (DDAVP), erythropoietin, and octreotide. Atropine is the drug of choice for the treatment of bradycardia, but it is rarely used in the rehabilitation setting. Phenylephrine and dopamine can also be used (65).

Given that the most common cause of death for patients with spinal cord injury is of pulmonary origin, specific attention needs to be paid to pulmonary support. Patients with high cervical cord injury may either require intubation from the beginning, or can fatigue during the initial period. Weakened cough and intercostal muscles contribute to possible respiratory failure. Oftentimes, severe lung collapse and atelectasis with mucus plugging is a recurrent clinical problem.

Spinal cord injury and spinal cord rehabilitation provide comprehensive rehabilitation care to reach the patient's functional goals in an acute inpatient, subacute, home, or outpatient rehabilitation setting. Spinal cord injury and spinal cord medical specialists are trained specifically on the evaluation and management of the unique medical and surgical conditions of patients suffering from spinal cord injury. These medical specialists are trained in the care and rehabilitation of persons with spinal cord dysfunction resulting from traumatic or nontraumatic spinal cord injuries, and they work in coordination, both in clinical care and in research, with a variety of other medical and surgical specialists for the care and optimum functional recovery for patients with spinal cord injury. A multidisciplinary approach is warranted to achieve a long-term satisfactory outcome, with initiation of a rehabilitation program at the time of admission. The team should be comprised of physicians, nurses, physiatrists, and allied health care personnel including rehabilitation nurses, nurse clinicians, physical, occupational, recreational, and educational therapists, rehabilitation technicians, psychologists, social service specialists, vocational rehabilitation counselors, sexuality and reproduction counselors, dietitians, peer counselors, driver education personnel, and administrative personnel (29).

Future hope for recovery following spinal cord injury may lie at least partially in spinal cord stimulation, neuroprotective medication, cell transplantation, gene therapy, or even modulation of the inflammatory immune response following spinal cord injury.

The use of spinal cord stimulation to treat spinal cord injury has been an important development. In a landmark paper in Nature, Wagner and colleagues describe the use of epidural stimulation to enable functional motor and task-specific sensory in patients with severe spinal cord injury (77). By using patterned electrical stimulation, the group describe restoration of voluntary gait in 3 individuals with chronic cervical cord injury who had either partial or complete absence of motor or sensory function in their legs 6 years after their injury. Although previous animal models found benefit with constant epidural stimulation, in humans, persistent stimulation can impair functional recovery by impairing proprioceptive circuitry (30). Motor neuron activation maps were created using electromyography data, neuraxial imaging, and computational modeling, and the investigators identified optimal electrode placement for motor recruitment. By using patterned stimulation, the study participants were able to walk on a treadmill for as long as a kilometer without exhausting the muscles or impairing the gait injury (77). The combination of a 4 to 5 times per week rehabilitation program over 5 months with the epidural stimulation promoted further functional recovery. Prior to study enrollment, the patients had participated in extensive standard rehabilitation without significant improvements. Fascinatingly, after treatment with this experimental protocol, patients recovered some voluntary leg movements even without the stimulation. Two other research groups have found similar functional motor improvement with an extensive multimodal rehabilitation regimen combined with epidural electrical stimulation (03; 36). This paper opened the gates to a level of recovery after spinal cord injury that was not previously thought possible and will be the focus of ongoing research and clinical trials.

Riluzole is a sodium and calcium channel blocker that is being investigated for its role in improving functional recovery following spinal cord injury. Though its mechanism of action is being studied, riluzole may confer a neuroprotective role in spinal cord injury by decreasing excitotoxicity through glutamergic inhibition. Animal studies demonstrate therapeutic benefits of riluzole by decreasing tissue injury, nocioception, spasticity, and improving motor function (70). Data for riluzole use in spinal cord injury are sparse. The largest human trial in riluzole use in spinal recovery is from a multicenter, double-blind, randomized phase 3 trial comparing riluzole to placebo in patients undergoing surgical decompression for degenerative cervical myelopathy, the most common nontraumatic cause of spinal cord injury (25). Three hundred patients with moderate to severe degenerative cervical myelopathy undergoing surgical decompression were randomized to riluzole (n=147) versus placebo (n=153). Although both groups demonstrated improvement in motor and sensory recover and pain at 6 months, there was no difference between the 2 treatment arms. However, at 1 year, patients in the riluzole arm showed an improvement in neck pain scoring scales compared to placebo, though this was not a primary endpoint. It is not known if the effect size of cervical myelopathy surgery masks any benefits seen with riluzole (25). Only 2 small human trials comparing riluzole to placebo in spinal cord injury have been performed. In a randomized controlled trial with 60 patients (30 in each arm), riluzole showed improvement in pain scores and functional motor and sensory recovery at 6 months compared to placebo. A dose of 50 mg twice per day was used for 8 weeks (57). The second study, a phase I study of 36 patients matched to study-eligible registry controls, primarily assessed the safety and feasibility of prescribing 50 mg riluzole to spinal cord injury patients within 12 hours of injury. Patients with ASIA A to C spinal cord injury were prescribed riluzole 50 mg twice per day. Despite not being powered for efficacy, they found that the riluzole group had improved motor scores compared to the matched-control cohort, particularly in those with ASIA B level injury (39). Still further research needs to be performed to identify the most effective dose, duration of treatment, appropriate time to first dose, and the patients most likely to benefit. Currently, there is a phase IIb/III multicenter, randomized controlled trial comparing riluzole to placebo in acute spinal cord injury that is active; however, results have not yet been published (26).

Advances have been made in experimental transplantation of myelinating cells regeneration (14; 28; 18) and bone marrow stromal cells (64; 72; 73; 86) into humans to help promote the spinal cord, with some promising initial findings in the recovery of patients with spinal cord injury. Experimental enhancement of spontaneous plasticity is currently being explored as a useful tool to promote further recovery after adult central nervous system injury (79). The identification of the genes controlling apoptosis appears to be another promising step in this direction. Another important aspect of the treatment that has attracted attention is rehabilitation. Studies have been conducted to assess the effects of early rehabilitation on the ultimate outcomes in spinal cord injury. Rehabilitation should always begin as early as possible to take advantage of “the more robust plasticity” occurring after insult. It has been shown that rehabilitation, if instituted early, improves physical functional independence for ASIA motor score and contributes to good physical activities of daily living (71; 13).

Brown and colleagues also focus on restorative neurology, which is characterized as evaluating the damaged nervous system setup of the injured patient and, afterwards, attempting to salvage functioning inputs and outputs by fully utilizing them (13). Restorative neurology should not replace current rehabilitation techniques; rather, it should accompany it. Medications that abolish spasticity should not be used until an assessment is made of whether the patient retains the ability to modulate spasticity volitionally. The first step is to augment appropriate inputs and outputs with techniques such as transcutaneous stimulation.

The next step is to reduce focal maladaptive outputs. Botulinum toxin, neurolytic agents, and neurotomies can reduce the effect of pathological outputs and lead to expression of latent function, muscles that were previously “inhibited by reciprocal mechanisms.” In addition, techniques such as cooling and elimination of nociceptive stimuli can eliminate inappropriate inputs. Finally, some surgical intervention used to reroute nerves and functional tendons can lead to greater functionality. Restorative neurology in spinal cord injury patients may lead to a much greater quality of life.

Arija-Blazquez and colleagues used electromyostimulation in men with acute spinal cord injury to observe subsequent effects on muscle and bone (04). Eight men who were 8 weeks out from injury were randomized into intervention or control groups. The intervention group underwent 14 weeks of therapy, 47 minutes a day for 5 days a week. The quadriceps femoris (QF) muscle was targeted. The results showed that the intervention group had a statistically significant increase in quadriceps femoris muscle size compared to the control group. Bone loss, however, was similar in both groups. The study shows that muscle growth can continue even after complete spinal cord injury.

Pharmacologic agents may improve rehabilitation in spinal cord injury (20). There is evidence that GM-1 ganglioside, clonidine, and cyproheptadine improved walking in patients with incomplete spinal cord injury when used in combination with physical therapy. However, the evidence is preliminary, and more studies need to be performed on drugs for the rehabilitation process.

Additionally, a number of noninvasive pharmacologic neuroprotective treatments, including therapeutic hypothermia, NSAID, electrical stimulation, autologous macrophages, thyrotropin-releasing hormone, neuronal growth factor, and neuroprotective agents (such as riluzole, minocycline, basic fibroblast growth factors) have been tried on animal models with the hope of reducing secondary damage and maximizing the spared neurologic tissues. However, none of these approaches have yet been successfully translated to humans (51) and are currently not recommended by society guidelines (81).

These trials were reported to reduce apoptosis, vasogenic edema, and tissue damage. There are some obvious gaps to fill in order to translate to humans (eg, the time window to initiate the treatment or the optimal dose of medicine).

Therapeutic hypothermia has been shown to reduce inflammatory cell infiltration and vasogenic edema, and it stabilizes the blood brain barrier (55). Despite this, hypothermia may have some serious side effects, including increasing risk of infection, coagulopathy, cardiovascular side effects (such as bradycardia, cardiac arrhythmias), and risk of deep venous thrombosis. Although hypothermia has been accepted as standard of care in select post-cardiac arrest patients, further randomized controlled trials are needed to prove the efficacy of hypothermia for neurologic protection after spinal cord injury. Currently, a clinical trial assessing the efficacy of hypothermia in the setting of acute cervical SCI is enrolling (NCT02991690), although prior randomized clinical trials of hypothermia in the setting of acute traumatic brain injury was found to be ineffective (02).

Stem cell transplantation may seem as an attractive approach for acute spinal cord injury. The rationale for stem cells transplantation and neurologic improvement stem from the different mechanism of actions of these multipotent cells. This includes trophic support cell replacement, immune modulation, and remyelination. Generally, stromal or mesenchymal cells are isolated from various tissues, such as bone marrow, cartilage, and fat, and they are delivered as either intrathecal, intraparenchymal, or intravenous infusion (07). However, the quality of current available studies are widely heterogeneous, with mixed therapeutic efficacy. A large 2013 systemic meta-analysis of all preclinical studies determined that the overall preclinical results are encouraging (62). Although this is promising, one needs to be cautious in how to extrapolate such therapeutic implications in clinical practice, given the lack of any large randomized controlled trials on the use of stem cells in acute traumatic spinal cord injury and lack of current FDA control.

Valproic acid has also been used in rats after acute spinal cord injury with observable benefits (87), with increased levels of histone acetylation recovery and decreased macrophage numbers in rats receiving valproic acid with spinal cord injury compared to a control group with spinal cord injury. Effects of sulforaphane, a derivative of broccoli, have shown to decrease morbidity in mice after spinal cord injury. The mice were administered sulforaphane (SF) 10 minutes and 72 hours after contusion spinal cord injury. Sulforaphane treatment upregulated antioxidant response at injury site, decreased levels of inflammatory cytokines, and enhanced motor function in limbs. Sulforaphane should be considered for therapy in humans with spinal cord injury (08). Some pharmacologic agents, namely opioids, should be avoided after acute spinal cord injury. Opioids can act synergistically with spinal cord injury to increase development of subsequent pain and risk of infection, as well as attenuate locomotor recovery (84).

Interestingly, even mood can influence the rehabilitation of spinal cord injury patients (48). Patients who coped better after injury tended to show better outcomes with functionality. Studies show that rehabilitation is an exciting field for research in spinal cord injury and these patients, in combination with a team of caring specialists, can accomplish a lot to restore function post-injury, unlike previous mindsets that painted spinal cord injury as unalterable.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

J Dedrick Jordan MD PhD

Dr. Jordan of LSU Health Shreveport has no relevant financial relationships to disclose.
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Vyas Viswanathan MD

Dr. Viswanathan of Duke University had no relevant financial relationships to disclose.
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Editor

Randolph W Evans MD

Dr. Evans of Baylor College of Medicine received honorariums from Abbvie, Amgen, Biohaven, Impel, Lilly, and Teva for speaking engagements.
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Former Authors

Marc-Alain Babi MD
Katharina M Busl MD MS
Anil Nanda MD, Ajay Jawahar MD, Prasad Vannemreddy MD, Ibrahim Ali Omeis MD, Bartley Mitchell MD, Parveen Athar MD, Courtney M Preston MD, Osman Athar, Marc Alain Babi MD, and Katharina M Busl MD MS

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male>female, >2:1
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: athletes

ICD & OMIM codes

ICD-9: Fracture of vertebral column without mention of spinal cord injury: 805.00-805.9

Fracture of vertebral column with spinal cord injury: 806.00-806.9

Spinal cord injury without evidence of spinal bone injury: 952.00-952.9

Other paralytic syndromes: 344.00-344.9

Unspecified disease of the spinal cord: 336.9
ICD-10: Fracture of neck (cervical vertebrae, cervical spine, other parts of neck): S12-S12.9

Injury of nerves and spinal cord at neck level: S14-S14.6

Other paralytic syndromes: G83

Disease of spinal cord, unspecified: G95.9

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Acute traumatic spinal cord injury

Associated Disorders

Paraparesis
Paraplegia
Posttraumatic spinal instability
Posttraumatic syringomyelia
Spinal fractures and dislocations
- Spinal injury
- Spinal instability
- Tetraparesis
- Tetraplegia

Differential Diagnosis

ankylosing spondylosis
congenital or acquired spinal canal stenosis
ossification of posterior longitudinal ligament or yellow ligament
spina bifida occulta
intraspinal cysts
- Chiari malformations
- craniocervical junction abnormalities
- tethered spinal cord syndrome

Also Relevant

Radiation myelopathy
Sleep disorders associated with neuromuscular and spinal cord disorders
Spasticity
Treatment of neurotrauma with neurotrophic factors
Vascular disorders of the spinal cord

Clinical Categories

General Neurology

Patient Handouts

Web References

Clinical Trials

NIH: Spinal Injury

Acute traumatic spinal cord injury

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Table 1. The Subaxial Cervical Spine Injury Classification System

Table 2. The Thoracolumbar Spine Injury Classification System

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Questions or Comment?

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