Ischemic Stroke: Pathogenesis

Ischemic Stroke: Pathogenesis
Small artery occlusion
Acute infarction (<20mm diameter) of basal or brainstem penetrating arteries Large artery atherosclerosis Atherosclerotic plaque 1, diameter of intro- or extracranial vessel ,50%, 50% stenosis Authors: Andrea Kuczynski Reviewers: Cardio aortic embolism Other Unknown Sina Marzoughi Usama Malik Andrew M Demchuk* Clot forms in the heart, travels to the brain * MD at time of publication 4, 02 and glucose in infarct location 4, CBF I` lactate Note: the pathophysiology and exact mechanism is not well known. 1 Glucose metabolism in penumbra 4, Anaerobic metabolism Peri-infarct depression-like depolarization ATP Activate biochemical pathways (see downstream effects of excitotoxicity) Dysfunction of Nair ATPase pump on neurons Astrocytes release Glu Astrocyte death -* Microglia clear debris Release TNFa, IFy, IL-1p H2O influx with Na' I` Na', Ca' influx, K± outflux Excitotoxicity t Volume of infarct Edema Activate mGluR Inflammation Abbreviations: ATP: adenosine triphosphate BA: basilar artery BBB: blood brain barrier CBF: cerebral blood flow Glu: glutamate ICA: internal carotid artery MCA: middle cerebral artery mGluR: metabotropic Glu receptors 02: oxygen Depolarization Ca2+ influx Compress vessels and tissues Neurons release Glu Breakdown BBB Activate catabolic proteases, lipases, nucleases Oxidative and nitrosative injury Secondary inflammation Legend: Necrosis Pathophysiology Mechanism Weakness, slurred speech, visual field losses, autonomic dysfunction (see Ischemic Stroke: Impairment by Localization stroke slide)