Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) that is mediated 
by effects of transient cerebral ischaemia during bleeding plus effects of the 
subarachnoid blood. Secondary effects of SAH include increased intracranial 
pressure, destruction of brain tissue by intracerebral haemorrhage, brain shift, 
and herniation, all of which contribute to pathology. Many patients survive 
these phenomena, but deteriorate days later from delayed cerebral ischaemia 
(DCI), which causes poor outcome or death in up to 30% of patients with SAH. DCI 
is thought to be caused by the combined effects of angiographic vasospasm, 
arteriolar constriction and thrombosis, cortical spreading ischaemia, and 
processes triggered by EBI. Treatment for DCI includes prophylactic 
administration of nimodipine, and current neurointensive care. Prompt 
recognition of DCI and immediate treatment by means of induced hypertension and 
balloon or pharmacological angioplasty are considered important by many 
physicians, although the evidence to support such approaches is limited. This 
Review summarizes the pathophysiology of DCI after SAH and discusses established 
treatments for this condition. Novel strategies--including drugs such as 
statins, sodium nitrite, albumin, dantrolene, cilostazol, and intracranial 
delivery of nimodipine or magnesium--are also discussed.