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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
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Delayed Cerebral Ischemia after Subarachnoid Hemorrhage
Asad Ikram1, Muhammad Ali Javaid1, Santiago Ortega-Gutierrez2
1Department of Neurology, University of New Mexico, MSC10-5620, 1, Albuquerque, NM 87131, USA.
Summary
Delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (aSAH) involves more than just large artery vasospasm. Microvascular dysfunction and brain inflammation also contribute to DCI, necessitating new diagnostic and treatment strategies.
Area of Science:
- Neuroscience
- Neurology
- Critical Care Medicine
Background:
- Delayed cerebral ischemia (DCI) is a significant complication of aneurysmal subarachnoid hemorrhage (aSAH), leading to increased mortality and morbidity.
- Traditionally, large cerebral artery vasospasm was considered the primary cause of DCI.
- Emerging evidence suggests other factors play a crucial role in DCI development.
Purpose of the Study:
- To review and synthesize current literature on factors contributing to DCI in aSAH.
- To explore mechanisms beyond large cerebral artery vasospasm implicated in DCI.
- To highlight the need for improved diagnostic and therapeutic approaches for DCI.
Main Methods:
- Comprehensive literature search of PubMed database.
- Inclusion of articles discussing DCI in aSAH, focusing on various contributing factors.
- Analysis of factors including microvascular spasm, micro-thrombosis, cerebrovascular dysregulation, and cortical spreading depolarization.
Main Results:
- DCI in aSAH is multifactorial, involving not only large artery vasospasm but also microvascular spasm, micro-thrombosis, cerebrovascular dysregulation, and cortical spreading depolarization.
- These factors contribute to brain parenchymal inflammation, early brain injury, and subsequent DCI.
- The interplay of these mechanisms challenges the traditional view of DCI pathogenesis.
Conclusions:
- DCI following aSAH is a complex process influenced by multiple pathophysiological mechanisms.
- Refinement of diagnostic tools for early DCI detection is crucial.
- Development of novel interventions targeting these multifactorial causes is essential, though their clinical efficacy in aSAH patients requires further investigation.
