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Abstract
Non-traumatic subarachnoid hemorrhage (SAH) represents about 5 to 6% of the overall incidence of stroke and is associated with high morbidity and mortality. Despite the substantial research and clinical efforts, delayed cerebral ischemia (DCI) is still the major complication after SAH and represents an important factor for severe neurological deficits. Cerebral vasospasm (VSP) has been recognised for a long time as an important underlying pathophysiologic cause of DCI, but it is now clearer that the mechanisms underlying DCI are multifactorial. Among other pathomechanisms proposed, ischemia-producing cortical spreading depolarizations (CSDs) are likely to be involved in DCI development. Understanding the plethora of different pathophysiological derangements after SAH is very important for the development of new therapies, in order to abolish secondary ischemic brain injuries early-on and improve patients’ outcome. In this review, we strive to summarise the mechanisms and therapeutic developments of DCI.
Keywords: Cerebral vasospasm, cortical spreading depolarization, delayed cerebral ischemia, spreading ischemia, subarachnoid hemorrhage, treatment, Spontaneous subarachnoid hemorrhage (SAH), DCI, CSF, CSDs
Current Neurovascular Research
Title:Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: From Vascular Spasm to Cortical Spreading Depolarizations
Volume: 9 Issue: 4
Author(s): Zelong Zheng, Renan Sanchez-Porras, Edgar Santos, Andreas W. Unterberg and Oliver W. Sakowitz
Affiliation:
Keywords: Cerebral vasospasm, cortical spreading depolarization, delayed cerebral ischemia, spreading ischemia, subarachnoid hemorrhage, treatment, Spontaneous subarachnoid hemorrhage (SAH), DCI, CSF, CSDs
Abstract: Non-traumatic subarachnoid hemorrhage (SAH) represents about 5 to 6% of the overall incidence of stroke and is associated with high morbidity and mortality. Despite the substantial research and clinical efforts, delayed cerebral ischemia (DCI) is still the major complication after SAH and represents an important factor for severe neurological deficits. Cerebral vasospasm (VSP) has been recognised for a long time as an important underlying pathophysiologic cause of DCI, but it is now clearer that the mechanisms underlying DCI are multifactorial. Among other pathomechanisms proposed, ischemia-producing cortical spreading depolarizations (CSDs) are likely to be involved in DCI development. Understanding the plethora of different pathophysiological derangements after SAH is very important for the development of new therapies, in order to abolish secondary ischemic brain injuries early-on and improve patients’ outcome. In this review, we strive to summarise the mechanisms and therapeutic developments of DCI.
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Cite this article as:
Zheng Zelong, Sanchez-Porras Renan, Santos Edgar, W. Unterberg Andreas and W. Sakowitz Oliver, Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: From Vascular Spasm to Cortical Spreading Depolarizations, Current Neurovascular Research 2012; 9 (4) . https://dx.doi.org/10.2174/156720212803530663
DOI https://dx.doi.org/10.2174/156720212803530663 |
Print ISSN 1567-2026 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5739 |
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