ArticleSaudi journal of anaesthesia2013
Early brain injury and subarachnoid hemorrhage: Where are we at present?
Article in Saudi journal of anaesthesia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Effect of isolated intracranial hypertension on cerebral perfusion within the phase of primary disturbances after subarachnoid hemorrhage in rats.Frontiers in cellular neuroscience · 2023Article
- Decreased Expression of CIRP Induced by Therapeutic Hypothermia Correlates with Reduced Early Brain Injury after Subarachnoid Hemorrhage.Journal of clinical medicine · 2022Article
- Neuroprotective Effects of Early Brain Injury after Subarachnoid Hemorrhage in Rats by Calcium Channel Mediating Hydrogen Sulfide.Cellular and molecular neurobiology · 2021Article
- Atorvastatin ameliorates early brain injury through inhibition of apoptosis and ER stress in a rat model of subarachnoid hemorrhage.Bioscience reports · 2018Article
- Recombinant human brain-derived neurotrophic factor prevents neuronal apoptosis in a novel in vitro model of subarachnoid hemorrhage.Neuropsychiatric disease and treatment · 2017Article
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Authors and funding
4 authors.
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Abstract
The current era has adopted many new innovations in nearly every aspect of management of subarachnoid hemorrhage (SAH); however, the neurological outcome has still not changed significantly. These major therapeutic advances mainly addressed the two most important sequels of the SAH-vasospasm and re-bleed. Thus, there is a possibility of some different pathophysiological mechanism that would be responsible for causing poor outcome in these patients. In this article, we have tried to compile the current role of this different yet potentially treatable pathophysiological mechanism in post-SAH patients. The main pathophysiological mechanism for the development of early brain injury (EBI) is the apoptotic pathways. The macro-mechanism includes increased intracranial pressure, disruption of the blood-brain barrier, and finally global ischemia. Most of the treatment strategies are still in the experimental phase. Although the role of EBI following SAH is now well established, the treatment modalities for human patients are yet to be testified.
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