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.
Export Options
About this article
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 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Glaucoma and Aging
Current Aging Science Family History and Preclinical Atherosclerosis
Current Hypertension Reviews Editorial (Oxidative Stress in the Vascular Wall: A Useful Physiological Process or a Therapeutic Target in Vascular Disease?)
Recent Patents on Cardiovascular Drug Discovery Involvement of Orexigenic Peptides in the Mechanism of Gastric Mucosal Integrity and Healing of Chronic Gastric Ulcers
Current Pharmaceutical Design Vascular Endothelium: Functioning in Norm, Changes in Atherosclerosis and Current Dietary Approaches to Improve Endothelial Function
Mini-Reviews in Medicinal Chemistry Is there a Relationship between Endothelial Dysfunction of the Brachial Artery, Carotid Intima-Media Thickness and Soluble Receptors of Tumor Necrosis Factor-Alpha?
Vascular Disease Prevention (Discontinued) Assessment of Endothelial Function by Positron Emission Tomography
Current Cardiology Reviews The Molecular Genetics of Migraine: Toward the Identification of Responsible Genes
Current Genomics L-Arginine Analogs – Inactive Markers or Active Agents in Atherogenesis?
Cardiovascular & Hematological Agents in Medicinal Chemistry Nimodipine Reappraised: An Old Drug With a Future
Current Neuropharmacology Bacterial Conjunctivitis in Childhood: Etiology, Clinical Manifestations, Diagnosis, and Management
Recent Patents on Inflammation & Allergy Drug Discovery Endothelial Dysfunction and Platelet Hyperaggregation in Type 2 Diabetes Mellitus: The Era of Novel Anti-diabetic Agents
Current Medicinal Chemistry Biologics for Extraintestinal Manifestations of IBD
Current Drug Targets Brain Perfusion In Sepsis
Current Vascular Pharmacology Clinical Implications of COX-1 and / or COX-2 Inhibition for the Distal Gastrointestinal Tract
Current Pharmaceutical Design Endothelial Function Assessment in Complicated Hypertension
Current Pharmaceutical Design Static Cerebral Blood Flow Autoregulation in Humans
Current Hypertension Reviews Brainstem Neuropeptides and Vagal Protection of the Gastric Mucosal Against Injury: Role of Prostaglandins, Nitric Oxide and Calcitonin-Gene Related Peptide in Capsaicin Afferents
Current Medicinal Chemistry Anabolic Androgenic Steroid (AAS) Related Deaths: Autoptic, Histopathological and Toxicological Findings
Current Neuropharmacology Human Papilloma Virus Vaccine Associated Uveitis
Current Drug Safety