Ruptured intracranial aneurysms account for 85 percent of spontaneous subarachnoid hemorrhages (SAH). However, aneurysmal SAH is still a devastating event with high morbidity and mortality. The most common complications are aneurysm re-bleeding, hyponatremia, hydrocephalus, cerebral vasospasm (CV), delayed cerebral ischemia (DCI), and seizures. Although CV after aneurysmal SAH has been recognized for more than 70 years, its pathophysiological mechanism remains elusive and no effective treatment for CV currently exists. DCI following SAH is defined as the occurrence of neurological deficit, decreased level of consciousness, and/or cerebral infarction between 3 and 10 days after SAH. In recent decades, DCI was thought exclusively to be the consequence of CV and is the leading potentially treatable cause of morbidity and mortality in patients who experience the rupture of an intracranial aneurysm.

Many pathological processes have been proposed as possible mechanisms underlying delayed CV after SAH, including endothelial damage, smooth muscle contraction, changes in vascular responsiveness, and the inflammatory and/or immunological response of the vascular wall. Clinical trials have failed to provide consistent evidence that the reversal of CV with medications can improve patient outcomes. Moreover, effective medications that have improved SAH patient outcomes do not significantly reverse CV. Currently, the most critical aspect of CV after SAH is its failure to consistently respond to treatment and so only partial success has been achieved in both experimental studies and clinical trials. Therefore, the role of CV has shifted from the most significant determinant to one contributing factor, among other factors, to the process. Many alternative pathological theories regarding the development of DCI have been postulated, such as inflammation, spreading depolarization, and microthrombi. Early brain injury (EBI) following SAH was defined as acute pathophysiological events occurring within 72 hours of hemorrhage, including cerebral autoregulation and blood-brain barrier disruption, activation of inflammatory pathways, excitotoxicity, oxidative stress, and activation of apoptosis. EBI after SAH has recently been implicated as a promising new theory for the development of CV, DCI and other SAH-related complications.

The aim of this Special Issue is to develop a new nomenclature of CV, DCI and EBI after aneurysmal SAH to offer more precise diagnosis and therapeutic strategies to treat this devastating disease, and to investigate the roles and mechanisms of CV, EDI, and DCI after aneurysmal SAH. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• SAH-induced vasospasm, EBI, and DCI for the development of strategies to treat patients with aneurysmal SAH
• The mechanisms of CV, EBI, and DCI after aneurysmal SAH
• Therapeutic strategies for CV, EBI, and DCI after aneurysmal SAH
• The cross talk between EBI and CV after aneurysmal SAH
• The role of EBI and CV in the development of DCI after aneurysmal SAH
• The role of EBI on vasospasm and secondary brain injury after aneurysmal SAH
• Basic neuroscience research regarding the pathophysiological mechanism of SAH-induced primary and secondary brain damage
• A new nomenclature/definition of CV, DCI, and EBI after the aneurysmal SAH