The elusive nature of events that sustain cerebral vasospasm after subarachnoid hemorrhage resulting from a ruptured aneurysm presents major challenges in designing effective therapies for this frequently devastating condition. Protracted cerebral artery constriction entails several dynamic components in intracellular signaling events initiated by endothelial factors, products of hemolysate, and numerous kinases, as well as increased intracellular Ca(2+). The rationale for potential treatment modalities and their efficacy are discussed in this brief review.