Edema formation in the hyperacute phase of ischemic stroke

Abstract

Vasogenic brain edema occurs much earlier than expected following permanent MCAO and leads to MLS and mechanical compression of adjacent brain structures. Since compression effects can impair rCBF, early edema formation can significantly contribute to infarct formation and thus represents a promising target for neuroprotection.

Potential of Early [ 18 F]-2-Fluoro-2-Deoxy-D-Glucose Positron Emission Tomography for Identifying Hypoperfusion and Predicting Fate of Tissue in a Rat Embolic Stroke Model

“…20 -22 We have recently characterized early cortical rCBF dynamics in this model by real-time imaging using Laser Speckle Contrast Imaging. 23 Moreover, this model easily allows remote vessel occlusion within MRI 12,24 and, as we show here, PET scanners.…”

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

“…On the other hand, oxygen and glucose supply is reduced due to microvascular constriction in response to the depolarization (Dreier et al, 1998;Strong et al, 2007;Luckl et al, 2009). Early formation of vasogenic edema within the first 3 hours is another factor contributing to progressively disturbed tissue perfusion in the penumbra due to mechanical compression of adjacent microvessels and veins in hemispheric experimental stroke in rats (Walberer et al, 2008;Gerriets et al, 2009). CSD alters bloodbrain barrier permeability even in healthy tissue by activating brain matrix metalloproteinases, in particular matrix metalloproteinases-9 (Gursoy-Ozdemir et al, 2004).…”

Neuroprotective effects of erythropoietin pretreatment in a rodent model of transient middle cerebral artery occlusion

“…22 Particularly, focal ischemia followed by reperfusion leads to severe damage to the BBB integrity, allowing water and macromolecules to cross into brain tissue as early as 20-45 minutes following permanent middle cerebral artery (MCA) occlusion. 15 The detrimental edema further reduces focal blood flow, and induces cell necrosis and apoptosis. 37 Furthermore, widespread interactions among BBB disruption, edema formation, and lower blood flow become a vicious cycle, which accelerates brain damage.…”