Spinal cord disease can result from diverse pathologic processes including trauma. Irrespective of the pathogenesis, it can lead to significant impairment of motor, sensory, or autonomic function.
This review focuses on the clinical description of common patterns of spinal cord involvement. Considerable differences exist in terms of clinical complications after traumatic and nontraumatic spinal cord injury (SCI). In this article, the general principles of management of traumatic SCI are emphasized. For specific nontraumatic neurologic diseases that affect the spinal cord, see Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and other articles listed in Differentials.
Trauma to the spinal cord typically leads to a combination of symptoms and signs resulting from immediate and delayed injury.
The initial mechanical trauma is secondary to traction and compression forces. Direct compression of neural elements by bone fragments, disc material, and ligaments damages both the central and peripheral nervous systems. Blood vessel damage also leads to ischemia. Rupture of axons and neural cell membranes also occurs. Microhemorrhages occur within minutes in the central gray matter and progress over the next few hours. Massive cord swelling happens within minutes. The cord fills the whole spinal canal at the injury level and leads to further secondary ischemia. Loss of autoregulation and spinal shock cause systemic hypotension and exacerbate ischemia.
Ischemia, toxic metabolic compounds, and electrolyte changes cause a secondary injury cascade. Hypoperfusion of gray matter extends to the surrounding white matter and alters the propagation of action potentials along the axons, contributing to spinal shock. Glutamate is a key element in the excitotoxicity. Massive release of glutamate leads to overstimulation of neighbor neurons and production of free radicals, which kill healthy neurons. Excitotoxic mechanisms kill neurons and oligodendrocytes, leading to demyelination. AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) glutamate receptors play a major role in oligodendrocyte damage. Additionally, recent evidence has shown that a wave of apoptosis further affects the oligodendrocytes up to 4 segments from the trauma site days and weeks after the initial trauma. Syringomyelia may develop as one outcome of this cascade.
Traumatic SCI accounts for an estimated annual incidence of approximately 40 cases per million population, or approximately 12,500 new cases each year, in the United States (published figures range from 28-55 cases per million people). This number excludes those who died at the scene of an accident. Currently, 240,000-337,000 patients with SCI are alive in the United States. 
SCI incidence is estimated at 15-40 cases per million population. In Australia, recent statistics report an age-adjusted rate of 14.5 cases per million population.
In 1927, Harvey Cushing described an 80% mortality rate for World War I soldiers with SCI in the first few weeks because of infections from bedsores and catheterization, with survival restricted to partial lesions. Today, in well-organized spinal cord centers, 94% of patients survive the initial hospitalization.
Recent statistics show the cost of the care of patients with C1-4 tetraplegia at approximately $1,048,259 in the first year and approximately $182,033 for each subsequent year.  Estimated lifetime costs for high tetraplegia are $4,651,158 for 25-year-old individuals and $2,556,197 for 50-year-old individuals. This amount does not include indirect costs such as loss of productivity, which vary with the educational background. Overall, lifetime costs range from $500,000 to $2 million, depending on the extent of injury and the location. Total direct costs for patients with SCI in the United States exceed $7 billion per year.
Life expectancy is greatly decreased, although major advances of medical management have markedly prolonged survival. Mortality rates are significantly higher during the first year after injury than during subsequent years. An Australian study found, among first-year survivors, overall 40-year survival rates were 47 and 62% for persons with tetraplegia and paraplegia, respectively. The most significant increases in mortality were seen in those with tetraplegia and American Spinal Injury Association Impairment Scale (AIS) grades A-C lesions, with SMRs between 5.4 and 9.0 for people <50 years, reducing with advancing attained age. 
In the past, renal failure was the leading cause of death after SCI. Currently, pneumonia, pulmonary emboli, and septicemia surpass renal failure. For further details of the epidemiology, please see information provided by the National Spinal Cord Injury Association.
Recent statistics show a rising incidence of SCI in African American people in the United States. Currently, about 24% of SCIs occur among blacks. 
According to the National Center for the Dissemination of Disability Research, from 1973-1978, 77.5% of the persons in the database were white people, 13.5% were black people, 5.7 % were Hispanic people, and 0.8% were Asian people. However, since 1990, only 59.1% were white people, while 27.6% were black people, 7.7% were Hispanic people, 0.4% were American Indian people, and 2.1% were Asian people.
Traumatic SCI is more common in young adult males, who are usually at a higher risk for motor vehicle accidents, violence, falls, and injury from recreational activities such as diving. Approximately 79% of spinal cord injuries occur among males. The male-to-female ratio in the United States is 4:1. 
The average age at injury has increased from 29 years during the 1970s to 42 years since 2010. 
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