Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.

Primary Injury

Primary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.

Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or violent dislocations), resulting in localized bleeding and swelling. More severe trauma can lead to laceration or transection, where the spinal cord is partially torn or completely severed. Another mechanism, distraction, results from excessive stretching of the cord, typically in high-speed accidents or falls.

Beyond structural damage, primary injury causes direct cellular destruction. Neurons and supporting cells (such as astrocytes, oligodendrocytes, and microglia) are damaged, disrupting the spinal cord’s microenvironment. Axonal shearing further worsens injury, as long nerve fibers in pathways such as the corticospinal and spinothalamic tracts are stretched or severed, impairing motor and sensory transmission.

Vascular disruption is another critical component. Rupture of blood vessels leads to hemorrhage and ischemia, depriving surrounding tissue of oxygen and nutrients, causing additional cell failure.

Secondary Injury

These combined effects—cell destruction, axonal damage, swelling, and hemorrhage—initiate the secondary injury phase. This delayed cascade develops over hours to days, amplifying damage through inflammation, oxidative stress, and progressive cell death.