Key result
Multiple mechanisms are involved in the pathogenesis of delayed insult after subarachnoid hemorrhage, suggesting that new therapies may need to target multiple pathways to prevent brain injury.
This review highlights the multifactorial pathogenesis of delayed cerebral ischemia after subarachnoid hemorrhage and emphasizes the need for multi-targeted therapeutic approaches.
Cautions against single-target therapies for delayed cerebral ischemia after subarachnoid hemorrhage; leaves open optimal multi-pathway combinations for prospective trials.
INTRODUCTION: Subarachnoid hemorrhage (SAH) patients often develop brain injury as a result of a number of delayed complications, resulting in significant morbidity and mortality. Many of these complications arise due to delayed cerebral ischemia, which occurs secondary to the hemorrhage. AREAS COVERED: The mechanisms of the delayed injury are reviewed, including angiographic vasospasm, cortical spreading ischemia, small arteriolar constriction, microthromboemboli, free radical injury and inflammation. Some current and prospective therapies for SAH are discussed, in the context of these complications. Statins have been particularly promising in experimental studies. EXPERT OPINION: Multiple mechanisms are involved in the pathogenesis of the delayed insult after SAH. New drugs may need to target multiple pathways to injury. Trials aiming to treat complications after SAH could benefit from taking into account the multifactorial pathogenesis of delayed insults.
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Wan et al. (2013) conducted a review in Subarachnoid hemorrhage (SAH). Statins and other prospective therapies was evaluated. Multiple mechanisms are involved in the pathogenesis of delayed insult after subarachnoid hemorrhage, suggesting that new therapies may need to target multiple pathways to prevent brain injury.
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