Cerebral vasospasm (cVSP) consists of the vasoconstriction of large and small intracranial vessels which can lead to cerebral hypoperfusion, and in extreme cases, delayed ischemic deficits with stroke. While most commonly observed after aneurysmal subarachnoid hemorrhage (aSAH), cVSP can also occur after traumatic brain injury (TBI) as we have described in detail in this review. For the past decades, the research attention has focused on cVSP because of its association with delayed cerebral ischemia, which is the largest contributor of morbidity and mortality after aSAH. New discoveries in the cVSP pathophysiology involving multifactorial complex cascades and pathways pose new targets for therapeutic interventions in the prevention and treatment of cVSP. The goal of this review is to demonstrate the commonalities and differences in epidemiology and pathophysiology of both aSAH and TBI-associated cVSP, and highlight the more recently discovered pathways of cVSP. Finally, the latest cVSP surveillance methods and treatment options are illustrated.