Increasing body of experimental and clinical data indicates that early brain injury after initial bleeding largely contributes to unfavorable outcome after subarachnoid hemorrhage (SAH). This review presents molecular mechanisms underlying brain injury at its early stages after SAH. PubMed was searched using term 'subarachnoid hemorrhage' and key words referring to molecular and cellular pathomechanisms of SAH-induced early brain injury. The authors reviewed intracranial phenomena and molecular agents that contribute to the early development of pathological sequelae of SAH in cerebral and vascular tissues, including cerebral ischemia and its interactions with injurious blood components, blood-brain barrier disruption, brain edema and apoptosis. It is believed that detailed knowledge of molecular signaling pathways after SAH will serve to improve therapeutic interventions. The most promising approach is the protection of neurovascular unit including anti-apoptosis therapy.