[Pathological Review of Brain Damage After Aneurysmal Subarachnoid Hemorrhage]

Aneurysmal subarachnoid hemorrhage(SAH) causes brain injury and systemic complications, including cardiopulmonary dysfunction, which mutually affect each other. Post-SAH brain injury includes early brain injury(EBI) and delayed cerebral ischemia(DCI). EBI is a non-iatrogenic pathology occurring within 72 h of clinical SAH, primarily induced by increased intracranial pressure, subsequent transient global cerebral ischemia, and extravasated blood components. DCI typically develops between days 4 and 14 after clinical SAH because of erythrolysis(free hemoglobin) and EBI-mediated reactions. EBI and DCI share many pathologies, including large-artery spasm, microvascular spasm, microthrombosis, blood-brain barrier disruption, neuroinflammation, disturbance of venous outflow, and neuroelectric disturbances such as spreading depolarization and epileptic discharge. However, EBI and DCI differ not only in the timing of onset but also in their distribution, with EBI mainly occurring throughout the brain, while DCI occurs locally. Many substances, such as glutamic acid, cytokines, and matricellular proteins, mediate EBI and DCI pathologies. Further elucidation of EBI and DCI pathologies is essential for developing novel treatment strategies.