Background
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.
Pathophysiology
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.
Epidemiology
Frequency
Traumatic SCI accounts for an estimated annual incidence of approximately 54 cases per million population, or approximately 17,810 new cases each year, in the United States. This number excludes those who died at the scene of an accident. The current (2020) estimated number of people with SCI living in the United States is 294,000, with a range from 250,000 to 368,000 persons. [1]
Globally, SCI incidence is estimated at 15–40 cases per million population. In Australia, statistics report an age-adjusted rate of 14.5 cases per million population.
In 2018, the prevalence rate of people with a disability of all ages in the United States was 12.6%, or 40,585,700 people. Among the six types of disablities identified in the US Census Bureau's American Community Survey (ACS), the highest prevalence rate was for "Ambulatory Disabilty" at 6.8%. [2]
Mortality/Morbidity
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.
Statistics show the cost of the care of patients with C1-4 tetraplegia at approximately $1,149,629 in the first year and approximately $199,637 for each subsequent year. [1] Estimated lifetime costs for high tetraplegia are $5,100,941 for 25-year-old individuals and $2,803,391 for 50-year-old individuals. This amount does not include indirect costs such as loss of productivity, which vary with the educational background. 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 greater 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. [3]
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.
Race
Statistics show a rising incidence of SCI in African American people in the United States. In 2020, about 24% of SCIs occured among blacks. [1]
According to data from the 2018 American Community Survey (ACS), among working-age people in the United States, 10.4% of whites; 13.3% of Blacks; 17% of Native Americans; 4.3% of Asians; and 9.7% persons of some other race reported a disability. [2]
Sex
Traumatic SCI is more common in young adult males, who are usually at a greater risk for motor vehicle accidents, violence, falls, and injury from recreational activities such as diving. Approximately 78% of new spinal cord injuries occur among males. The male-to-female ratio in the United States is 4:1. [1]
Age
The average age at injury has increased from 29 years during the 1970s to 43 years since 2015. [1]
Prognosis
Spinal trauma and other spinal cord diseases often cause severe physical impairment secondary to motor, sensory, and autonomic impairment.
Overall, life expectancy is greatly decreased, although major advances of medical management have markedly prolonged survival. [1]
The ability to predict clinical outcome after SCI based on early examination is limited. The most important predictor of improved outcome is retention of sacral sensation (S4-5), especially pinprick, 72 hours to 1 week after injury. In general, most individuals regain one level of motor function, mostly within the first 6 months, although further improvement can be observed years later. Age is also a prognostic factor. In central cord syndrome, 91% of patients younger than 50 years regain ambulation, whereas only 41% of people older than 50 years develop a similar outcome.
Transient or chronic reactive mild or severe depression is very common after SCI. In the case of trauma, younger patients often have greater functional improvement from acute spinal injury. The suicide rate among individuals with SCI is nearly 5 times higher than in the general population and is lower for men than for women. In 1998, Hartkopp et al also observed a 2 times higher suicide rate in marginally disabled persons compared to more severely affected individuals. [23]
Patient Education
Education is an essential element for efficient rehabilitation and for prevention of the multiple complications following SCI. Multiple Web sites and written literature are available for the education of the patient and family.
For more details about available programs, please see the following:
For excellent patient education resources, see eMedicineHealth's patient education article Bladder Control Problems.
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A T1-weighted MRI that depicts a lesion with high signal enhancement inside the cervical spinal cord. This type of signal enhancement is consistent with blood and is most commonly observed secondary to cord trauma.
