Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage
Delayed cerebral ischaemia has been described as the single most important cause of morbidity and mortality in patients who survive the initial aneurysmal subarachnoid haemorrhage. Our understanding of the pathophysiology of delayed cerebral ischaemia is meagre at best and the calcium channel blocke...
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2015
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pubmed-47520282016-03-01 Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage Flynn, Liam Andrews, Peter Review Delayed cerebral ischaemia has been described as the single most important cause of morbidity and mortality in patients who survive the initial aneurysmal subarachnoid haemorrhage. Our understanding of the pathophysiology of delayed cerebral ischaemia is meagre at best and the calcium channel blocker nimodipine remains the only intervention to consistently improve functional outcome after aneurysmal subarachnoid haemorrhage. There is substantial evidence to support cerebral vessel narrowing as a causative factor in delayed cerebral ischaemia, but contemporary research demonstrating improvements in vessel narrowing has failed to show improved functional outcomes. This has encouraged researchers to investigate other potential causes of delayed cerebral ischaemia, such as early brain injury, microthrombosis, and cortical spreading depolarisation. Adherence to a common definition of delayed cerebral ischaemia is needed in order to allow easier assessment of studies using multiple different terms. Furthermore, improved recognition of delayed cerebral ischaemia would not only allow for faster treatment but also better assessment of interventions. Finally, understanding nimodipine’s mechanism of action may allow us to develop similar agents with improved efficacy. F1000Research 2015-11-02 /pmc/articles/PMC4752028/ /pubmed/26937276 http://dx.doi.org/10.12688/f1000research.6635.1 Text en Copyright: © 2015 Flynn L and Andrews P http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Flynn, Liam Andrews, Peter |
spellingShingle |
Flynn, Liam Andrews, Peter Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
author_facet |
Flynn, Liam Andrews, Peter |
author_sort |
Flynn, Liam |
title |
Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
title_short |
Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
title_full |
Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
title_fullStr |
Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
title_full_unstemmed |
Advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
title_sort |
advances in the understanding of delayed cerebral ischaemia after aneurysmal subarachnoid haemorrhage |
description |
Delayed cerebral ischaemia has been described as the single most important cause of morbidity and mortality in patients who survive the initial aneurysmal subarachnoid haemorrhage. Our understanding of the pathophysiology of delayed cerebral ischaemia is meagre at best and the calcium channel blocker nimodipine remains the only intervention to consistently improve functional outcome after aneurysmal subarachnoid haemorrhage. There is substantial evidence to support cerebral vessel narrowing as a causative factor in delayed cerebral ischaemia, but contemporary research demonstrating improvements in vessel narrowing has failed to show improved functional outcomes. This has encouraged researchers to investigate other potential causes of delayed cerebral ischaemia, such as early brain injury, microthrombosis, and cortical spreading depolarisation. Adherence to a common definition of delayed cerebral ischaemia is needed in order to allow easier assessment of studies using multiple different terms. Furthermore, improved recognition of delayed cerebral ischaemia would not only allow for faster treatment but also better assessment of interventions. Finally, understanding nimodipine’s mechanism of action may allow us to develop similar agents with improved efficacy. |
publisher |
F1000Research |
publishDate |
2015 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4752028/ |
_version_ |
1613537967336325120 |