By activation of endothelial EPO receptors, the circulating EPO may appose inflammatory pathways in cerebral arteries and attenuate vasospasm induced by SAH. In vivo studies have found that systemic administration of EPO (i.p. 1000units/kg) immediately after SAH can improve survival and motor functions [Buemi 2000]. The systemic delivery of EPO has the advantage that it is universally available to the capillary endothelium in the whole brain, in contrast to intraventricular injection, which is highly localized and not practical in clinical settings [Brines 2000]. Because the concentration of EPO in CSF is independent of the serum level and the extent of BBB disruption in patients suffering from aneurysmal SAH, the EPO in CSF is predominantly produced by the brain in order to match its need [Springborg 2003]. Therefore, an early activation of endothelial EPO-R may be a potential therapeutic strategy, which in fact has been proved by a reduction of S100 protein in CSF (a marker of brain damage) and restoration of cerebral autoregulation (for at least 48 hours) after systemic administration of recombinant human EPO [Springborg 2002]. Therefore, 90,000 Iuof epoetin beta will be use to achieve the maximal effects on CBF and autoregulation in these SAH patients to be studied.