Aneurysmal subarachnoid hemorrhage (aSAH) is one of the most devastating form of stroke. Many physiopathology mechanisms ensue after cerebral aneurysm rupture with blood silting up in the subarachnoid space, including hydrocephalus, cell apoptosis, blood-brain barrier dysfunction, macrovascular vasospasm, microthrombosis and cortical spreading depolarization which interact with each other and work throughout the damage process. Recently, clinical trials gradually pay more attention to two phases of injury after aSAH: the early phase known as early brain injury (EBI) and the delayed phase, delayed cerebral ischemia (DCI). These two phases are main processes accounting for neural injury and are thought to be closely linked with the outcomes of the patients. This review makes a brief summary on the mechanism of cerebral injury after aSAH, mostly on EBI and DCI.