Clinical meaning
Spinal cord injury involves primary mechanical damage (compression, laceration, distraction, or transection) followed by secondary injury cascades that extend damage over hours to weeks. Primary injury disrupts axons, blood vessels, and cell membranes. Secondary injury begins within minutes: hemorrhage in the central gray matter (hemorrhagic necrosis), ischemia from vasospasm and thrombosis of spinal cord microvasculature, excitotoxicity (glutamate release), calcium influx causing protease activation and mitochondrial failure, free radical lipid peroxidation, and inflammatory cell infiltration. Wallerian degeneration of disrupted axons proceeds over days to weeks. Neurogenic shock (distinct from spinal shock) occurs with injuries above T6: loss of sympathetic outflow causes vasodilation, hypotension, and bradycardia with preserved or warm extremities. Spinal shock is the transient loss of all neurological function below the injury level — return of the bulbocavernosus reflex signals its resolution and allows accurate prognosis of injury completeness (ASIA classification).