Subarachnoid hemorrhage (SAH) is a critical emergency in neurology, often associated with poor prognosis. Clinical studies have found that early brain injury (EBI) is widespread among SAH patients and may be a significant cause of poor outcomes. Preclinical research has made progress in understanding the mechanisms of EBI, with microglia being a major cellular component involved. The neuroinflammation in EBI is primarily driven by M1-type microglia, which participate in the disruption of the blood-brain barrier and neuronal death; additionally, M2-phenotype microglia exhibit functions that alleviate cerebral edema and improve neurological damage. Therefore, elucidating the polarization of microglia after SAH and their involvement in EBI pathways is of great significance for intervening in the neuroinflammatory response to SAH.