The diagram shows a composite of pathophysiological events occurring after SCI, including the acute (e.g., edema and hemorrhage), subacute (e.g., inflammation), and chronic (e.g., cavitation) phases. The primary and secondary injury mechanisms involve edema, hemorrhage, inflammation, apoptosis, necrosis, excitotoxicity, lipid peroxidation, electrolyte imbalance, ischemia/vasospasm, and blood vessel occlusion. Oligodendrocytes and neurons die, resulting in axonal demyelination and disruption of synaptic transmission. In the subacute and chronic phases, a fluid-filled lentiform-shaped cavity or cyst forms in the center of the cord, with surrounding hypertrophic astrocytes and macrophages. These and other cells secrete extracellular matrix and inhibitory molecules, such as chondroitin sulfate proteoglycans (CSPG), which compose the glial scar, resulting in a physical and chemical barrier to regeneration.