Cerebral vasospasm is the most common and most dangerous complication of subarachnoid hemorrhage (SAH). If it can not be diagnosed and treated early, it will result in delayed cerebral ischemia and delayed ischemic neurological deficits, and seriously affect the outcomes of patients. SAH can cause oxidative stress and inflammation, causing vasospasm, and leading to brain tissue damage. Numerous studies have shown that the concentrations and activities of numerous metabolites will change in these pathological physiological processes. Identification of the changes of location, time and trend of these markers has important clinical significance for investigating the mechanism of cerebral vasospasm after SAH and seeking better therapeutic targets. This article reviews the molecular markers of cerebral vasospasm after SAH.
Key words:
Subarachnoid Hemorrhage; Vasospasm, Intracranial; Biological Markers