Figure 1

The pathophysiology of brain injury after SAH may originate from 3 phenomena; transient global ischemia (due to increased intracranial pressure and decreased cerebral perfusion pressure), subarachnoid blood clot and acute hypertension. These may lead to a variety of secondary effects including brain edema, delayed large artery vasospasm, breakdown of the BBB, microcirculatory changes, thromboemboli, cortical spreading depression and delayed neuronal death due to apoptosis or other mechanisms. The end result is focal and scattered brain injury. The role of astrocytes is increasingly being recognized also. In the end, these processes have to cause neurological and neurobehavior deficits to be important and these will depend on what areas of the brain or networks in the brain are disrupted.