Trauma to the Spinal Cord

Epidemiology

There are 10,000 to 11,000 new cases of traumatic SCI in the United States each year. That number has increased slightly over the past two decades. The average age at injury has increased during that period from 28.7 years in 1973-1979 to 37.6 years in 2000-2003. There is substantial geographic variation in the incidence of SCI particularly in children, with the South and Midwest recording the highest frequency of these injuries. C5 is the most common level of SCI, whereas the most common level to produce paraplegia is T12.

For the general population, the causes of traumatic SCI have been motor vehicle accidents in about 50%, falls in 24%, violence including gunshot injuries in 11%, sports-related activities in 9%, and diverse other causes in 5%. Men are affected disproportionately more than women (80:20). Factors contributing to SCI during motor vehicle accidents include not wearing seat belts and alcohol/drug use.

In children, the overall incidence of SCI in the United States is estimated at 1.99 cases per 100,000 children. Boys are twice as likely as girls to suffer SCI: 2.79 cases/100,000 boys versus 1.15 cases per 100,000 girls. African-American children suffer the highest rate of injury (1.53 cases/100,000 children), whereas Asian-American children experience a significantly lower incidence than all other ethnic groups (0.36 cases/100,000 children). In children, the mechanisms of injury include motor vehicle accident, 56%; accidental fall, 14%; firearm injury, 9%; sports-related injury, 8%; and others, 13%.

Clinical Presentation

Patients presenting with possible SCI may be conscious or show impaired consciousness. The conscious patient typically complains of pain and loss of neurologic function or responds to inquiry about them. In these patients, neurologic evaluation discloses the level and density of the SCI. Inebriated, obtunded, or semiconscious patients may be unable to complain or respond appropriately to neurologic testing. This second group of patients should be examined with suspicion of SCI until proven otherwise. Impaired patients impose special requirements. They should be imaged thoroughly to ensure that all significant injuries are defined and must be handled especially carefully to ensure that they are protected against excess manipulation during the period of impairment. It is essential to determine the existence and extent of SCI at the earliest possible time because this will determine the appropriate management and outcome of this injury.

Local pain and tenderness may identify the level of anatomic injury. The level of anatomic injury, however, does not always correspond to the level of neurologic dysfunction. Severe injury to the T10-12 region may cause local spinal cord contusion, compression, and/or hematoma, whereas concurrent injury to the artery of Adamkiewicz causes infarction of an extensive segment of the spinal cord remote from the level of bone injury. Expanding compressive epidural hematoma may also produce a neurologic level far removed from the local injury.

Two major classifications have begun to standardize the evaluation and reporting of SCI to ensure adequate documentation of the extent of SCI: the Frankel classification and the more recent, more comprehensive impairment scale by the American Spinal Injury Association (ASIA). Radiologists should be familiar with the broad outlines of these classifications to communicate effectively with their colleagues ( Tables 12-1 and 12-2 ).

Acute SCI usually presents as an acute neurologic deficit. The deficit is designated complete when there is absence of sensory and motor function below the level of injury resulting in paraplegia or tetraplegia. The deficit is classified as incomplete when there is (partial) sparing or asymmetric involvement below the level of injury. Incomplete clinical presentations include specific syndromes such as central cord syndrome, mixed cord syndrome, anterior cord syndrome, and Brown-Séquard syndrome.

Months or years after the acute phase of the injury, SCI patients may show improvement, remain neurologically stable, or suffer new symptoms. New pain syndromes or spasms may suggest post-traumatic myelopathy from adhesions tethering or compressing the cord at the original site of injury or from cyst formation within (syringomyelia) or outside the spinal cord (arachnoid cyst). Scarring usually affects the cord at the site of the initial injury. Cysts and syringes may enlarge and extend away from the original injury for long distances, leading to signs and symptoms remote from the site of first injury.

Pathophysiology

Spinal cord trauma can be direct, indirect, or a combination of both depending on the causative mechanism. Direct trauma is caused by violence, principally penetrating knife wounds or missiles that pass into the spinal cord. Knives tend to injure the dorsolateral portion of the spinal cord, where the cord is least protected by bone. Knife injuries generally cause local edema and minimal hemorrhage confined to the level of injury. They usually are clinically incomplete. Occasionally, the penetrating implement may sever the spinal cord and cause complete SCI. Penetrating missiles may find their way into the spinal cord via the dorsolateral route or by exploding through the bony spine, causing shrapnel and/or bone fragments that lacerate the spinal cord. The explosion/laceration often creates a more severe and ragged SCI that extends far beyond the entry site. In this situation, the entry hole in the dura may be small, with minimal hemorrhage within the cord or within the subarachnoid, subdural, or epidural space around the cord. Chronically, extensive adhesions and gliosis in the medullary and perimedullary spaces may lead to cyst formation within the spinal cord, encystment of the subarachnoid space, and tethering of the spinal cord to the dural-bony canal at the level of injury. Concurrent vascular injury may cause ischemia and infarction of the spinal cord. Spinal subluxation and dislocation may produce additional compressive injuries to the spinal cord.

Indirect injury to the spinal cord is the more common injury and is due to compression and/or stretching of the spinal cord by fracture-dislocation, subluxation, ruptured discs and ligaments, and epidural hematomas. These injuries usually result from motor vehicle accidents, falls, sports injury, and so on. In some of these patients there may be no detectable bone abnormality (SCIWORA). Cervical fracture-dislocation is especially common at the C5-6 level, where it produces tetraplegia. Fracture-dislocation of the thoracic spine is more common in the lower thoracic spine (T11-12 level), where it causes paraplegia.

Pathology

Trauma to the spinal cord may cause contusion, hematoma, or a combination of both, resulting in cord swelling and/or interruption of fiber tracts. The spinal cord may also be compressed and flattened by a large epidural hematoma, buckled or swollen ligaments, herniated disc material, and/or retropulsed bone fragments. The cord may be lacerated or transected by bone fragments, subluxation, or dislocation of vertebrae. Complete transection is said to be rare, however, because some viable neuronal tissue is almost always visible at autopsy even when there appears to be absence of tissue radiographically. Depending on the extent of injury and the collateral circulation, areas of ischemia or infarction may extend far beyond the initial site of injury.

Chronic changes include atrophy, myelomalacia, cyst formation, cord tethering, and wallerian degeneration. These changes are related to resorption of hematoma, formation of perimedullary fibrous tissue, edema and swelling of the cord, accumulation of fluid within the spinal cord, and axonal death, in varying proportions. Acute spinal cord hematomas frequently lead to late spinal cord atrophy.

Fractures, subluxation, and dislocation can cause indirect injury to the spinal cord. Comminuted or burst fractures tend to compromise the spinal canal and compress the spinal cord. Subluxed and dislocated vertebrae behave in similar fashion.

The initial damage to the meninges depends on the form of injury. Knife injuries tend to produce a small hole in the dura. Exploding missiles may tear a large hole in the dura, whereas bone fragments cause varying degrees of laceration. Bleeding occurs in and around the meninges and may accumulate into large hematomas, which not uncommonly compress the spinal cord. In the chronic stage, the meninges may become scarred, sclerotic, or calcified with obliteration of the perimedullary space and formation of adhesions. The adhesions loculate the subarachnoid space to form secondary arachnoid cysts and/or tether the spinal cord to the bony wall of the spinal canal. Tethering itself may impede cerebrospinal fluid (CSF) pulsations around the cord and lead to hydrosyringomyelia of the spinal cord at the level of injury and for long distances above and below the injury.

Imaging