Spinal cord injury is a devastating medical condition that can lead to permanent sensory, motor, and autonomic impairments. The severity and extent of neurological deficits depend on several factors such as the level of injury, the extent of spinal cord damage (complete or incomplete), and the presence of secondary complications. Primary spinal cord injuries are the result of direct damage to the spinal cord. Secondary spinal cord injuries refer to the cascade of pathological processes that occur following the initial insult, such as ischemia, hypoxia, inflammation, excitotoxicity, oxidative stress, reactive gliosis, and apoptosis and necrosis. There are three distinct phases of spinal cord injury. The acute phase lasts up to a few days and is driven by ischemia, hypoxia, vasogenic edema, and neuronal excitotoxicity. This is followed by the subacute phase, which ranges from days to weeks and is characterized by mitochondrial phosphorylation, increased reactive oxygen species production, and neuroinflammation. Lastly, the chronic phase can last for months to years after injury and is caused by acute axonal degeneration, axonal remodeling, Wallerian degeneration, and glial scar formation. The extent of primary and secondary spinal cord injury and the progression through the acute, subacute, and chronic phases will dictate the severity of neurological deficits and impairments. Targeted therapeutic interventions may help minimize tissue damage and promote functional recovery in individuals who have suffered spinal cord injuries.