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Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia
Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific res...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766617/ https://www.ncbi.nlm.nih.gov/pubmed/24058736 http://dx.doi.org/10.1155/2013/506584 |
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author | Carr, Kevin R. Zuckerman, Scott L. Mocco, J |
author_facet | Carr, Kevin R. Zuckerman, Scott L. Mocco, J |
author_sort | Carr, Kevin R. |
collection | PubMed |
description | Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets. |
format | Online Article Text |
id | pubmed-3766617 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-37666172013-09-22 Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia Carr, Kevin R. Zuckerman, Scott L. Mocco, J Neurol Res Int Review Article Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets. Hindawi Publishing Corporation 2013 2013-08-22 /pmc/articles/PMC3766617/ /pubmed/24058736 http://dx.doi.org/10.1155/2013/506584 Text en Copyright © 2013 Kevin R. Carr et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Carr, Kevin R. Zuckerman, Scott L. Mocco, J Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title | Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title_full | Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title_fullStr | Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title_full_unstemmed | Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title_short | Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia |
title_sort | inflammation, cerebral vasospasm, and evolving theories of delayed cerebral ischemia |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766617/ https://www.ncbi.nlm.nih.gov/pubmed/24058736 http://dx.doi.org/10.1155/2013/506584 |
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