Traumatic injury to the spinal cord can result in devastating loss of neurologic functions. Deficits may vary, from minimal observable disruption of a patient’s abilities to complete paralysis with ventilator dependence, complete requirement for personal care, and inability to engage in meaningful activity. Spinal cord injury (SCI) has been suggested to lead to death in up to 75% of injured patients if forensic reports of pre-hospital mortality are included. This severity had changed very little in millennia, with similar mortality described in medical writings of ancient Greece, military encounters in the 19th century, and the modern United States as recent as the 1970s. Fortunately, the understanding of SCI epidemiology, pathophysiology, and treatment has increased to such an extent that advances in pre-hospital care, pharmacological treatment, surgical management, and regenerative medicine have made survival more routine and neurologic recovery a possibility, if not a reality.

Throughout the United States and developed countries around the globe, SCI identification and reporting have become more standardized. The National SCI Database routinely collects information from SCI Model Systems which represent a sample of trauma centers around the United States. The United States reports the highest rate of SCI per year with 40 injuries occurring per million of the population. This translates into approximately 12,000 new injuries per year. This figure is even higher among American military personnel and is estimated in the range of 400 per million. The global point prevalence of patients living with SCI is also highest in the United States at 906 per million, or 273,000 individuals. The mean age at the time of SCI has increased from approximately 29 years in 1979 to approximately 42 years of age currently. Over 80% of SCI patients are male and approximately 67% are Caucasian. Patients of lower socioeconomic status may also be at elevated risk of SCI, which is largely attributed to higher rates of drug and alcohol use, as well as risk taking behavior. These patients are most often injured by high-energy mechanisms with motor vehicle collision causing 36% of SCI in the United States and up to 60% globally. Falls, violence, and sports-related injury are the next most common causes of SCI. The cervical spine is injured in up to 60% of cases. Incomplete tetraplegia is the most common neurologic presentation and is observed in over 40% of patients.

Elderly individuals comprise a second group of SCI and are injured more frequently by low-energy falls. These patients often have underlying cervical spinal stenosis and perhaps even subtle myelopathy, the presence of which predicts that a SCI will be more severe than if no underlying spinal cord dysfunction were present.

Demographic characteristics among SCI populations vary between geographic regions and have been changing over time. Canada, for example, has reported fewer injuries from violence than from sports injuries. The proportion of African-American SCI patients has increased in the United States over the past three decades while the proportion of Caucasian patients has decreased. African-American patients are also more likely to be readmitted to a hospital in the 10 years following SCI. Just over half of patients report being employed at the time of injury and only half report being married at the time of SCI. Considering also that SCI often prevents future employment and other social engagements, and can lead to an average lifetime cost of $5 million, a strong argument can be made that SCI occurs in an “at-risk” population which only becomes more disadvantaged following injury. Future research into psychosocial and economic prevention must be undertaken to improve these aspects of outcome.

The spinal cord is comprised anatomically of axonal tracts, cell bodies, supportive glial cells, and vasculature. An understanding of these key components is critical to the pathophysiology of SCI as well as potential treatment strategies. Spinal cord tracts are partitioned according to the specific function transmitted either from the spinal cord to the brain, or from the cerebral cortex distally. The dorsal columns convey proprioception and vibration
sense. Since these tracts decussate in the brain stem, the dorsal columns convey sensation from the ipsilateral side of the body. The spinothalamic tracts convey light touch, pain, and temperature sense and travel anterolateral to the grey matter cell bodies of the anterior horn. The spinothalamic tracts cross in the spinal cord below the vertebral level and therefore provide sensation from the opposite side of the body. The lateral corticospinal motor tracts cross in the pyramids of the brain stem and travel lateral to the dorsal horn grey matter. A unilateral injury to the lateral corticospinal tract would therefore cause an ipsilateral loss of motor function. The corticospinal tracts are arranged somatotopically, with the axons supplying the cervical spine located most medially and those for the thoracic, lumbar, and sacral segments located more laterally. The grey matter of the spinal cord contains the neuronal cell bodies. Support, immune function, and myelin are supplied by astrocytes, microglia, and oligodendrocytes, respectively. Spinal cord perfusion is provided by the anterior spinal artery, paired posterior spinal arteries, and radicular arteries. While the anterior spinal artery is often depicted as a single contiguous structure, there may be sizable amounts of anatomic variation in patients, with some individuals thought to have multiple noncontiguous anterior spinal arteries or various configurations of collateral spinal blood supply. The transverse intramedullary arterioles are the branches most vulnerable to injury and can lead to ischemia of the spinal cord if compromised.

Spinal cord injury occurs as a result of a twofold process of initial direct damage and secondary physiologic damage. Direct damage results from the impact of displaced fracture fragments, dislocations, disk herniations, and external penetrating objects as well as from traction to the spinal cord that occurs secondary to blunt force trauma. Only rarely does frank transection of the spinal cord occur from injury (Fig. 6.1). Direct injury disrupts cell bodies, axons, myelin, and the intrinsic spinal vasculature. Secondary injury results from the physiological response to the damaged tissue. Within the first few hours of injury, the blood–spinal cord barrier is disrupted and allows for ingress of pro-inflammatory cells which induce interleukins, prostaglandins, and free radicals. Capillary permeability increases as a result, leading to spinal cord edema. Inflammation and edema further compress vascular structures, leading to thrombosis and ischemia. Stimulation of neural tissue leads to a supraphysiologic release of neurotransmitters and endogenous opioids, in turn leading to a supraphysiologic release of calcium. This process, known as excitotoxicity, induces both neural necrosis and programmed cell death through characteristic signal transduction pathways. Within the first few days of injury, migration of macrophages and regenerative cells leads to removal of cellular and myelin debris, resulting in spinal cord cavitation and gliosis or scarring. The sum total of these secondary effects is often propagation of the initial injury and prevention of meaningful neural regeneration.

Limiting the severity of initial and secondary damage in SCI requires rapid identification of injury and initiation of treatment. The adoption of the Advanced Trauma Life Support program and regional coordination of emergency responders has led to a streamlined method for the identification of patients with presumed neurologic injury at the site of trauma and transportation to appropriate trauma centers. Improved pre-hospital care has significantly changed the probability of surviving occipitocervical and other injuries that routinely would have been fatal even a few decades ago.

Upon arrival to a trauma center and after the airway, breathing, and circulation have been secured, a patient should be objectively assessed for neurologic functions and deficits. Physical examination findings should be correlated with available spinal imaging to identify the injury or injuries that may be responsible for apparent examination findings. Injuries that range from disk herniation to complete disruption of the spinal column (Fig. 6.2) can result in trauma to the spinal cord. Once one spinal injury is identified, the entire spinal column from occiput to sacrum must be examined radiographically.