Part of the reason for this lack of success likely stems from the fact that vasospasm occurs at multiple levels in the arterial and arteriolar circulation. Large artery narrowing seen in angiographically visible vessels only results in ischemic neurological symptoms in 50% of cases, and although there is a correlation between the severity of large artery spasm and symptomatic ischemia, there are patients with severe large artery spasm who never become symptomatic and others with quite modest spasm who not only develop symptoms but go on to develop infarction.206 Probably many factors contribute to the development of ischemia and infarction, including but not limited to distal microcirculatory failure, poor collateral anatomy, and genetic or physiological variations in cellular ischemic tolerance.207,208 DCI, especially that associated with arterial vasospasm, remains a major cause of death and disability in patients with aSAH. The management of aSAH-induced vasospasm is complex. Many significant advances in the understanding of aSAH-induced vasospasm and DCI have been made since Connolly et al Management of Aneurysmal Subarachnoid Hemorrhage 1723 publication of the previous version of these guidelines, which focused on prevention with oral nimodipine and maintenance of euvolemia, as well as treatment with triple-H therapy (hemodynamic augmentation therapy) and/or endovascular therapy with vasodilators and angioplasty balloons. 