Journal article
An introduction to the pathophysiology of aneurysmal subarachnoid hemorrhage.
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van Lieshout JH
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany. Jasper.vanLieshout@med.uni-duesseldorf.de.
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Dibué-Adjei M
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Cornelius JF
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Slotty PJ
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Schneider T
Institute for Neurophysiology, Medical Faculty, University of Cologne, Robert-Koch-Str. 39, 50931, Köln, Germany.
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Restin T
Zurich Centre for Integrative Human Physiology, Institute of Physiology, University of Zurich, Winterthurerstrasse 190, 8057, Zurich, Switzerland.
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Boogaarts HD
Department of Neurosurgery, Medical Faculty, Radboud University Nijmegen, Geert Grooteplein Zuid 10, 6525 GA, Nijmegen, the Netherlands.
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Steiger HJ
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Petridis AK
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Kamp MA
Department of Neurosurgery, Medical Faculty, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225, Düsseldorf, Germany.
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Published in:
- Neurosurgical review. - 2018
English
Pathophysiological processes following subarachnoid hemorrhage (SAH) present survivors of the initial bleeding with a high risk of morbidity and mortality during the course of the disease. As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important. However, a unifying theory for the pathophysiological changes following SAH has yet not been described. Some of these changes may be causally connected or present themselves as an epiphenomenon of an associated process. A causal connection between DCI and early brain injury (EBI) would mean that future therapies should address EBI more specifically. If the mechanisms following SAH display no causal pathophysiological connection but are rather evoked by the subarachnoid blood and its degradation production, multiple treatment strategies addressing the different pathophysiological mechanisms are required. The discrepancy between experimental and clinical SAH could be one reason for unsuccessful translational results.
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Language
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Open access status
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closed
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Identifiers
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Persistent URL
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https://sonar.ch/global/documents/47465
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