Subarachnoid hemorrhage: epidemiology, risk factors, pathogenesis, and clinical therapies

Subarachnoid hemorrhage (SAH) is an extremely lethal cerebrovascular emergency that can lead to severe long term neurological deficits. Modern research evidence indicates that the incidence of SAH varies significantly across different regions and populations, and this variation is determined by the interaction between non-modifiable factors (such as age, gender, family history, and genetic susceptibility) and modifiable factors (such as hypertension, smoking, drug use, and metabolic disorders). Advancements in vascular biology and genomics further suggest that extracellular matrix instability, endothelial dysfunction, chronic inflammation, and population-specific genetic variations play crucial roles in aneurysm formation and rupture. After aneurysm rupture, SAH triggers a biphasic injury cascade. Early brain injury (EBI) occurs within minutes to hours, manifesting as a sudden increase in intracranial pressure, systemic hypoperfusion, blood brain barrier disruption, neuroinflammation, cerebral edema, and metabolic failure. These early disturbances create favorable conditions for delayed cerebral ischemia (DCI), which occurs several days later due to microvascular dysfunction, impaired neurovascular coupling, cortical spreading depolarization, and progressive immunometabolic changes. Understanding this mechanistic continuum is of great significance for early detection and selection of treatment targets. Recent advancements in neuroimaging, biomarker development, and multimodal monitoring have improved diagnostic accuracy, while current management measures include rapid aneurysm fixation, optimized intensive care, and emerging neuroprotective strategies. Despite these advancements, treatment outcomes remain suboptimal, highlighting the need for further improvements in risk stratification, mechanism-based interventions, and population specific preventive measures. This review synthesizes the latest knowledge on the epidemiology, risk factors, pathogenesis, and clinical management of SAH to support a more comprehensive research and care framework.