Study of the pathophysiology of cerebrovascular hemorrhage: closing of arteries due to atherosclerosis, arterial thrombosis, and embolism; decrease in perfusion due to hypotension or reduced cardiac output; disruption of autoregulation mechanisms leading to regional hypoperfusion. Consequences include lack of oxygen and glucose supply, ATP depletion, dysfunction of Na+/K+ pump, cell swelling, glutamate release and excitotoxicity, lactic acid increase, oxidative stress, neuroinflammation, reperfusion injury, necrosis and apoptosis