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Studies in subarachnoid hemorrhage (SAH) have traditionally focused on delayed secondary ischemic injury due to vasospasm, but more recently, attention has turned to early brain injury (EBI) in patients with poor-grade injury. The predictable and delayed nature of secondary brain injury makes SAH a unique illness. Large vessel arterial vasospasm occurs in approximately 70% of patients starting 3 to 5 days after the initial hemorrhage, peaking at 5 to 10 days, then slowly resolving over the following week or two.1 Delayed cerebral ischemia (DCI), defined as infarction, neurologic deterioration, or both from large vessel vasospasm occurs in about 20% of patients with SAH. Interventions and clinical investigation have long focused on DCI. Large trials have failed to improve long-term neurologic outcome despite ameliorating vasospasm.2 This has led to novel concepts of DCI pathophysiology, including microthrombosis, neuroinflammation, and cortical spreading depolarization (SD).1
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