Spinal Cord Injury Autonomic Dysreflexia

Spinal cord injury (SCI) results from both primary and secondary mechanisms of cellular damage. The primary injury causes immediate tissue disruption, while secondary injury cascades begin within minutes and can extend over weeks. These secondary processes include ischemia caused by vascular disruption and vasospasm, which reduces oxygen delivery to the vulnerable gray matter. Additionally, excitotoxicity occurs due to excessive glutamate release, activating NMDA and AMPA receptors that lead to intracellular calcium overload and mitochondrial dysfunction. Free radical generation and lipid peroxidation further damage cell membranes. Inflammatory mediators such as TNF-alpha and IL-1beta recruit neutrophils and macrophages, which release proteolytic enzymes that exacerbate tissue injury. Understanding these underlying physiologic mechanisms is essential to connect them to measurable bedside cues and anticipate expected trend changes in patient status.