Abstract

Intracerebral hemorrhage (ICH) accounts for 10% to 15% of all strokes. ICH continues to impart a considerable degree of morbidity and mortality, with 30-day mortality ranging from 44% to 50%.1–3 ICH remains a devastating disease, and current treatment options lag far behind those for ischemic stroke. There are no approved therapies, which improve outcome, and treatment remains mainly supportive. Despite the lack of available acute treatment options for ICH, the past decade of clinical and preclinical research has identified important concepts in its pathophysiology and how this information might be used in developing treatment. Recent clinical trials in ICH have identified important considerations in patient selection, which have informed current and future trials evaluating treatment for ICH, and preclinical work in ICH has identified new treatment targets. An understanding of the pathophysiology of the disease provides a starting point for identification of treatment targets. The pathophysiology of ICH begins with the predisposition of developing the disease, including genetics and risk factors that conspire to generate the initial hemorrhage. Once present, ICH causes both primary and secondary injury. The primary insult is attributable to disruption of adjacent tissue and mass effect.4 Secondary injury occurs with development of edema, free radical formation, inflammation, and direct cellular toxicity attributable to the deposited hematoma and subsequent degradation by-products. Each of these phases of disease provides a potential treatment target as shown in the Figure. The multiple steps along the path of disease also underscore the fact that successful treatment for ICH will most likely be multifaceted with different treatments at different time points. Figure. Treatment targets for intracerebral hemorrhage (ICH). A complete discussion of treatment targets for ICH is beyond the scope of this brief summary and has been reported recently.5 Ongoing clinical trials in ICH are outlined in …

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