Abstract
Cerebral vasospasm research has been focused on investigating the mechanisms of prolonged delayed vasoconstriction of cerebral arteries following subarachnoid hemorrhage (SAH). However, it has been clarified that induction of significant vasodilation of such arteries does not lead to better overall outcomes in SAH patients. On the other hand, early brain injury, such as cortical spreading depression, early cortical depolarization waves, and impairment of neurovascular coupling, is seen acutely after SAH and may play a significant role in early impairment of brain function following SAH. These results clearly indicate that it is time to reconsider what causes this early brain damage and dictates patient outcome following SAH; classical delayed cerebral vasospasm following SAH might be an epiphenomenon. It is of utmost importance to investigate whether early brain injury and delayed cerebral vasospasm correlate with each other following SAH or are independent. Recent results of cerebral vasospasm research indicates future directions, and such investigations would lead to better outcome for SAH patients.
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