Background: Subarachnoid hemorrhage (SAH) following rupture of an intracranial is associated
with high mortality and morbidity. The late deterioration of the patient’s neurological status or late cognitive
dysfunctions even after secure clipping or decent endovascular treatment which is defined as delayed
ischemic neurological deficits recently has been attributed to vasospasm. Due to the failure of specific anti–
vasospastic agents in clinical trials researchers focused to explore new pathological mechanisms to be responsible
for the delayed deterioration of the patients suffering from SAH. Early brain injury (EBI), as a
new term in the SAH research area has been the focus of scientist for the past couple of years.
Objective: The goal of this study is to review the common mechanisms of early brain injury and vasospasm.
Results: The acute events following SAH, such as increased intracranial pressure and decreased cerebral
blood flow, causing global cerebral ischemia initiate a cascade of pathological changes including
inflammation, lipid peroxidation, cell death and blood brain barrier disruption.
Conclusion: The more insight we gain into the EBI we realize that there are a bunch of common
mechanisms between EBI and vasospasm. In the SAH management, a therapy targeting these early injuries
may also reduce the later developing pathological neurological complications.