Connecting the Early Brain Injury of Aneurysmal Subarachnoid Hemorrhage to Clinical Practice

Aneurysmal subarachnoid hemorrhage (SAH) is a devastating neurological disease that has a mortality rate as high as 67% in some series. Traditional research and treatment has focused on addressing the delayed events of cerebral vasospasm following SAH. However, the physiological and cellular events of early brain injury (EBI) make significant contributions to patient outcomes and may even be a more significant factor than delayed cerebral vasospasm. FBI is the result of physiological derangements such as increased intracranial pressure (ICP), decreased cerebral blood flow (CBF), and global cerebral ischemia, which results in blood brain barrier dysfunction, inflammation, and oxidative cascades that lead to neuronal cell death. The consequence of these events to the patient is often death or significant neurological disability. The link between EBI and outcome has come under intense focus with recent studies failing to show improved outcomes following significant inhibition of cerebral vasospasm, and research into the inhibition of FBI cascades is being perused as an effective means of treating SAH patients.