Traumatic brain injury (TBI) and increased intracranial pressure (ICP) involve complex pathophysiological cascades causing both primary (mechanical) and secondary (biochemical) brain injury. Primary injury occurs at the moment of impact: coup injury (directly beneath the point of impact), contrecoup injury (opposite side from brain deceleration against the skull), diffuse axonal injury (DAI, widespread shearing of white matter tracts from rotational acceleration-deceleration, the most common cause of prolonged coma after TBI), and intracranial hemorrhage (epidural hematoma from middle meningeal artery rupture with classic lucid interval, subdural hematoma from bridging vein tears, subarachnoid hemorrhage, and intracerebral hemorrhage). Secondary injury evolves over hours to days and is the primary target of neurological nursing interventions. The ischemic cascade includes: excitotoxicity (glutamate release activates NMDA receptors causing massive calcium influx, triggering proteases, lipases, and endonucleases that destroy cellular structures), oxidative stress (free radical production overwhelms antioxidant defenses, causing lipid peroxidation of neuronal membranes), mitochondrial dysfunction (impaired ATP production and release of cytochrome c triggering apoptosis), neuroinflammation (microglial activation, blood-brain barrier disruption, and cerebral edema -- both vasogenic from BBB permeability and cytotoxic from cellular swelling),...