Neuropathology of Spinal Cord Injury

The term ‘spinal cord injury’ refers to damage to the spinal cord resulting from trauma (e.g. a car crash) or from disease or degeneration (e.g. cancer) (WHO 2013a). Up to 90 % of these cases are due to traumatic causes (WHO 2013a). Therefore, neuropathology of traumatic spinal cord injury is focused below. Pathophysiology of traumatic spinal cord injury involves two main phases (Nakamura et al. 2003). These are the primary spinal cord injury following the trauma, and the secondary injury that are mediated by the inflammatory response to the primary spinal cord injury.

Primary Injury After Traumatic Spinal Cord Injury

Neuropathology of the initial spinal cord injury can be categorized as acute impact or compression (Kraus 1996). Acute impact injury is a concussion of the spinal cord. These inertial forces disrupt the blood-spinal cord barrier (BSCB). This type of injury initiates a cascade of events focused on the gray matter and results in haemorrhagic necrosis. The initiating event is a hypoperfusion of the gray matter. The primary events also involve massive ionic influx referred to as traumatic depolarization. Increases in intracellular calcium and reperfusion injury play key roles in cellular injury and occur early after injury. The extent of necrosis is contingent on the amount of initial force of trauma but also involves concomitant compression, perfusion pressures, and blood flow. The major inflammatory neurotransmitters released from the damaged tissue are excitatory amino acids, which may explain the neuropathology of diffuse axonal injury in traumatic spinal cord injury. Spinal cord compression occurs when a mass impinges on the spinal cord causing increased parenchymal pressure. This occurs in the white matter, whereas gray matter structures are preserved. Rapid or a critical degree of compression will result in the collapse of the venous side of the microvasculature, resulting in vasogenic edema. Vasogenic edema exacerbates parenchymal pressure, and may lead to rapid progression of spinal cord dysfunction (Kraus 1996). The expression of high levels of glucose transporter 1 was observed in capillaries from acutely injured the spinal cord, which occurs in association with compromised blood-spinal cord barrier function. Vascular endothelial growth factor also plays a role in neuronal tissue disruption and increases the permeability of the blood-spinal cord barrier via the synthesis and release of nitric oxide. Figure 8.1 depicts the neuropathology of the primary injury after traumatic spinal cord injury.

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