The Pathophysiology of Intracerebral Hemorrhage Formation and Expansion

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Abstract
Intracerebral hemorrhage is a devastating disease. Despite its clinical importance, the pathophysiology of intracerebral hemorrhage is not well understood. Hematoma expansion occurs in a large subset of patients and is a predictor of poor outcomes. Since hematoma growth provides a potential opportunity for therapeutic intervention, a thorough understanding of its biological mechanisms is of key importance. After vessel rupture, an initial hematoma forms. Following this initial phase, accumulating evidence suggests that the mass effect causes secondary vessel rupture, which contributes to the hematoma and may trigger an avalanche of further vessel ruptures. The circumstances under which this occurs and to what extent secondary hemorrhage contributes to final hematoma volume remain unknown, however. To address these questions, a translational approach seems most suitable. Current experimental models include intracranial injections of collagenase or autologous blood. Each has individual strengths and weaknesses in its ability to simulate human intracerebral hemorrhage. The ultimate goal for improved understanding and modeling of the pathophysiology of hematoma expansion is to identify new treatment approaches.

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