Early Brain Injury or Vasospasm? An Overview of Common Mechanisms

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.

The goal of this study is to review the common mechanisms of early brain injury and vasospasm.

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.

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.