Spinal cord injury (SCI) involves primary and secondary mechanisms of cellular damage. The primary injury results from mechanical forces (compression, distraction, laceration, transection) that disrupt neuronal axons, blood vessels, and cell membranes at the injury level. Secondary injury cascades begin within minutes and extend over weeks: ischemia from vascular disruption and vasospasm reduces oxygen delivery to vulnerable gray matter; excitotoxicity from excessive glutamate release activates NMDA and AMPA receptors, causing intracellular calcium overload and mitochondrial dysfunction; free radical generation and lipid peroxidation damage cell membranes; inflammatory mediators (TNF-alpha, IL-1beta) recruit neutrophils and macrophages that release proteolytic enzymes. Neurogenic shock occurs with injuries above T6 due to loss of sympathetic tone from the intermediolateral cell column, causing unopposed parasympathetic activity resulting in bradycardia, hypotension, and peripheral vasodilation. Spinal shock refers to the temporary loss of all reflex activity below the injury level, lasting hours to weeks, with areflexia giving way to hyperreflexia as upper motor neuron signs emerge.