The role of immune inflammation in aneurysmal subarachnoid hemorrhage

Exp Neurol. 2021 Feb:336:113535. doi: 10.1016/j.expneurol.2020.113535. Epub 2020 Nov 27.

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating disease, which mainly caused by the rupture of an intracranial aneurysm. Clinical trials have demonstrated that cerebral vasospasm (CVS) is not the sole contributor to delayed cerebral ischemia (DCI) and poor outcomes in patients with aSAH. Currently, accumulating evidence suggests that early brain injury (EBI), which occurs within 72 h after the onset of aSAH, lays the foundation for subsequent pathophysiological changes and poor outcomes of patients. The pathological mechanisms of EBI mainly include increased intracranial pressure, oxidative stress, neuroinflammation, blood-brain barrier (BBB) disruption, cerebral edema and cell death. Among them, the brain immune inflammatory responses involve a variety of immune cells and active substances, which play an important role in EBI after aSAH and may be related to DCI and long-term outcomes. Thus, attention should be paid to strategies targeting cerebral immune inflammatory responses. In this review, we discuss the role of immune inflammatory responses in the occurrence and development of aSAH, as well as some inflammatory biomarkers related to CVS, DCI, and aSAH outcomes. In addition, we also summarize the potential therapeutic drugs that target cerebral immune inflammatory responses for patients with aSAH in current research.

Keywords: Delayed cerebral ischemia; Early brain injury; Immunity; Microglia; Neuroinflammation; Subarachnoid hemorrhage; Vasospasm.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Biomarkers
  • Humans
  • Inflammation / immunology*
  • Inflammation / pathology
  • Subarachnoid Hemorrhage / immunology*
  • Subarachnoid Hemorrhage / pathology

Substances

  • Biomarkers