This chapter explains the mechanisms leading to neuronal cell death and the most important neuroprotective strategies. Cerebral ischaemia and/or hypoxia may occur as a consequence of shock, respiratory failure, vascular stenosis or occlusion, vasospasm, neurotrauma or cardiac arrest. Ischaemic or traumatic challenges affect both inadequate delivery of oxygen and glucose, and impairment of mitochondrial function, leading to inadequate production of ATP. Two different types of cell death may occur following brain injury: necrosis and apoptosis. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral damage after brain injury. The proposed mechanisms of anaesthetic protection include reduction of cerebral metabolism and intracranial pressure (ICP), and suppression of seizures and sympathetic discharge. Hypoxia and ischaemia are recognized as important driving forces of erythropoietin expression in the brain, suggesting that erythropoietin is part of a self-regulating physiological protection mechanism to prevent neuronal injury.