Pathophysiology of Intracerebral Hemorrhage

Pathophysiology of Intracerebral Hemorrhage Intracerebral hemorrhage (ICH) is crucially important neurological emergency with high societal impact of >1 million deaths worldwide each year. The pathophysiology of intracerebral hemorrhage can be considered to occur in ≤2 conceptual phases. In the first phase, there is immediate cellular injury in the hemorrhage core because of the acute bleed and early hemorrhagic expansion. The final hemorrhagic volume after the period of hemorrhagic expansion and the location are of hemorrhage are strong predictors of outcome. Prevention of hemorrhagic expansion can be achieved, but doing so does not improve outcome. The second conceptual phase of brain hemorrhage is the persistent hematoma phase characterized by progressive damage to perihematomal tissue caused by mass effect, excitotoxic edema, and progressive neurotoxicity resulting from iron, thrombin, blood breakdown products, free radical formation, protease activation and inflammation, and hyperglycolysis. The evolutionary damage to the perihematomal tissue is complex and involves multiple mechanisms that are presumed to be linked to the presence of the mass of collected blood and progressive edema. Animal models demonstrate that persistence of the hematoma in brain tissue results in progressive brain edema, metabolic distress, and potentially other mechanisms, which result in long-term disability. We hypothesize that in humans, early removal of the hemorrhage from the parenchyma will result in avoidance or mitigation of these secondary insults and result in substantially enhanced neurological recovery.