This article is a brief summary of the 19 page article entitled “Traumatic Spinal Cord Injuries,” published as a Forensic Science Newsletter on January 15, 2017.
The earliest known reference to traumatic lesions of the spinal cord are found in the Edwin Smith Surgical Papyrus. During World War I, Riddoch, and later Head and Riddoch, gave what are now considered the classic descriptions of spinal transection in humans. World War II marked the turning point in the understanding and management of spinal injuries.
Mechanisms of Spinal Cord Injury
The usual circumstances of spinal cord injury, typically occurs in the following sequence: motor vehicular and motorcycle accidents, falls, gunshot or stab wounds, diving accidents, crushing industrial injuries, and birth injury. In the United States, the highest incidence of traumatic paraplegia is found in individuals involved in head-on collisions or those ejected from their vehicle. Although trauma may involve the spinal cord alone, the vertebral column is almost invariably injured at the same time. Not uncommonly, along with the spinal cord injury are associated injuries to the brain. The three types of traumatic lesions to the spinal cord are typically the result of fracture-dislocations, pure fractures, and pure dislocations, which are usually produced by vertical compression on the spinal column, to which either anteroflexion or retroflexion are added.
Anatomic Considerations: The commonest sites of spinal cord injury are at the levels of the upper cervical, the middle cervical and lower cervical, the lower thoracic, and the upper lumbar vertebrae.
Upper cervical: Injuries to the upper cervical vertebrae and the underlying spinal cord may occur through several mechanism, such as, compression (vertical loading), compression/flexion, compression/extension, tension, tension/extension, tension/flexion, torsion, horizontal shear, and lateral bending.
Middle and Lower cervical: These are injuries to the cervical vertebrae and spinal cord between C4-C8. They are the most common type of immediately nonfatal spinal injury.
Clinical Presentation of Cervical Injuries
Typically, in significant lesions occurring at the level of C4-C5 or above, the victim will experience loss of motor function at the time of the injury, manifested by tetraplegia, and paraplegia with lesions of the thoracic cord. Immediately following the spinal cord injury, there is complete loss of function below the level of injury.
Thoracic, Lumbar and Sacral Injuries
The thoracic vertebral column from T1-T10 has much more resistance to injury than does the cervical vertebrae and underlying spinal cord due to the added stability of the thoracic rib cage and costovertebral ligaments. T11-L5, are far more susceptible to injury due to increased flexibility in this region and the lack of lateral stability of the ribs. The most common traumatic injuries to the lower lumbar and sacral vertebrae are compression fractures.
Clinical Presentation of Cervical and Upper Thoracic Cord Injuries
Acutely, patients with cervical or upper thoracic cord injuries may develop neurogenic shock, which is caused by a loss of brainstem and higher center control of the sympathetic nervous system. A chronic complication of spinal cord injuries at or above T6 is autonomic dysreflexia, which is an uninhibited sympathetic response to noxious stimuli, which can lead to hypertension, headache, bradycardia, upper-body flushing and lower body vasoconstriction, piloerection, and sweating.
Pathophysiology of Spinal Cord Injury
The pathophysiology of spinal cord injury consists of multiple contiguous phases over distinct time periods, which can be categorized as immediate, acute, subacute, intermediate, and chronic.
Immediate Phase: Time of injury lasting approximately 2 hours. It is also referred to as the primary component. It is in this phase there is traumatic disruption of axons, blood vessels, cell membranes followed by the death of neurons and glia. It is believed the main pathological process is impaired perfusion at the cellular level leading to ischemia. Along with these morphologic changes other pathophysiologic processes are initiated, such as an inflammatory response and excitotoxicity. The acute, subacute, intermediate, and chronic phases collectively come under the broad classification of the secondary component.
Acute Phase: This phase last 2-48 hours. There is a continuation of the processes of the immediate phase, which include hemorrhage, edema, demyelination, the formation of cavities within the traumatized cord, along with axonal and neuronal necrosis, and a series of pathological changes which end with infarction. The inflammatory responses and excitotoxicity continue with evidence of ionic dysregulation, production of reactive oxygen species and reactive nitrogen species, enhanced BBB permeability, and cell death occurring either as necrosis or apoptosis.
Subacute Phase: This phase extends from 2 days-2 weeks. It is characterized by a robust phagocytic response and the development of an astrocytic scar.
Intermediate Phase: This phase extends from the 2 weeks-6 months. It is marked by further development of the astrocytic scar and restoration of the BBB.
Chronic Phase: This phase begins at the 6 month mark and is characterized by further development of the atrocytic scar, cysts and syrinxes within the traumatized cord, as well as wallerian degeneration and schwannosis.
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