Primary brain injury occurs as a direct result of the initial insult. Secondary injury refers to progressive damage resulting from the body"s physiologic response to the initial insult. Ischemia is an important mechanism of brain injury that occurs when the blood supply is inadequate to meet metabolic needs. A lack of oxygen results in mitochondrial failure, atp depletion, and accumulation of intracellular calcium ions. Excessive release of excitatory amino acids, like glutamate, is thought to contribute to calcium overload during acute brain injury. Calcium overload is a critical event leading to cell dysfunction, membrane damage, and cell necrosis. Reperfusion injury occurs when blood flow is reintroduced to previously ischemic but viable cells. Free radicals are generated, which damage cell structures. Inflammatory cells are recruited to the area and may increase edema, block vessels, and contribute to free radical production. Autoregulation of cerebral blood flow achieves appropriate flow to meet metabolic needs despite changes in blood pressure and metabolism.