Pathobiology of ischaemic stroke: an integrated view

Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms...

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Bibliographic Details
Published in:Trends in Neurosciences 1999-09, Vol.22 (9), p.391-397
Main Authors: Dirnagl, Ulrich, Iadecola, Costantino, Moskowitz, Michael A.
Format: Article
Language:English
Subjects:
Acute-Phase Reaction - metabolism
Acute-Phase Reaction - physiopathology
Apoptosis
Biological and medical sciences
Brain
Brain - metabolism
Brain - physiopathology
Brain attack
Brain Ischemia - enzymology
Brain Ischemia - metabolism
Brain Ischemia - physiopathology
Cerebrovascular Disorders - enzymology
Cerebrovascular Disorders - metabolism
Cerebrovascular Disorders - physiopathology
Cyclooxygenase 2
Excitotoxicity
Humans
Inflammation
Isoenzymes - metabolism
Medical sciences
Membrane Proteins
Nerve Degeneration - metabolism
Nerve Degeneration - physiopathology
Neurology
Neurons
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Peri-infarct depolarizations
Prostaglandin-Endoperoxide Synthases - metabolism
Receptors, Glutamate - metabolism
Stroke
Treatment
Vascular diseases and vascular malformations of the nervous system
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Summary:Brain injury following transient or permanent focal cerebral ischaemia (stroke) develops from a complex series of pathophysiological events that evolve in time and space. In this article, the relevance of excitotoxicity, peri-infarct depolarizations, inflammation and apoptosis to delayed mechanisms of damage within the peri-infarct zone or ischaemic penumbra are discussed. While focusing on potentially new avenues of treatment, the issue of why many clinical stroke trials have so far proved disappointing is addressed. This article provides a framework that can be used to generate testable hypotheses and treatment strategies that are linked to the appearance of specific pathophysiological events within the ischaemic brain.
ISSN:0166-2236
1878-108X
DOI:10.1016/S0166-2236(99)01401-0