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Neurocritical Care
Published in: Neurocritical Care 2/2017

01-04-2017 | Review Article

Mechanisms of Global Cerebral Edema Formation in Aneurysmal Subarachnoid Hemorrhage

Authors: Erik G. Hayman, Aaron Wessell, Volodymyr Gerzanich, Kevin N. Sheth, J. Marc Simard

Published in: Neurocritical Care | Issue 2/2017

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Abstract

A growing body of clinical literature emphasizes the impact of cerebral edema in early brain injury following aneurysmal subarachnoid hemorrhage (aSAH). Aneurysm rupture itself initiates global cerebral edema in up to two thirds of cases. Although cerebral edema is not a universal feature of aSAH, it portends a poor clinical course, with quantitative analysis revealing a direct correlation between cerebral edema and poor outcome, including mortality and cognitive deficits. Mechanistically, global cerebral edema has been linked to global ischemia at the time of aneurysm rupture, dysfunction of autoregulation, blood breakdown products, neuroinflammation, and hyponatremia/endocrine abnormalities. At a molecular level, several culprits have been identified, including aquaporin-4, matrix metalloproteinase-9, SUR1-TRPM4 cation channels, vascular endothelial growth factor, bradykinin, and others. Here, we review these cellular and molecular mechanisms of global cerebral edema formation in aSAH. Given the importance of edema to the outcome of patients with aSAH and its status as a highly modifiable pathological process, a better understanding of cerebral edema in aSAH promises to hasten the development of medical therapies to improve outcomes in this frequently devastating disease.
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Metadata
Title
Mechanisms of Global Cerebral Edema Formation in Aneurysmal Subarachnoid Hemorrhage
Authors
Erik G. Hayman
Aaron Wessell
Volodymyr Gerzanich
Kevin N. Sheth
J. Marc Simard
Publication date
01-04-2017
Publisher
Springer US
Published in
Neurocritical Care / Issue 2/2017
Print ISSN: 1541-6933
Electronic ISSN: 1556-0961
DOI
https://doi.org/10.1007/s12028-016-0354-7

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