Background and Purpose-Brain edema is a life-threatening consequence of stroke and leads to an extension of the affected tissue. The space-occupying effect due to brain edema can be quantified in rat stroke models with the use of MRI. The present study was performed to test 2 hypotheses: (1) Can quantification of the space-occupying effect due to brain edema serve as a noninvasive measure for brain water content? (2) Does morphometric assessment of brain swelling allow determination of true infarct size on MRI after correction for the space-occupying effect of edema? Methods-Thirty rats were subjected to permanent suture middle cerebral artery occlusion. MRI was performed after 6 or 24 hours, and hemispheric swelling was assessed morphometrically. Interobserver and intraobserver agreements were determined for MRI measurements. In study I, the space-occupying effect due to brain edema was correlated with the absolute brain water content by the wet/dry method. In study II, lesion volumes corrected and uncorrected for edema were calculated on MRI and on TTC staining and compared. Results-Interobserver and intraobserver agreements for MRI measurements were excellent (rՆ0.97). Brain water content and hemispheric swelling correlated well after 6 and 24 hours (rՆ0.95). Corrected lesion volumes correlated with rϭ0.78 between TTC staining and MRI. Without edema correction, lesion volumes were overestimated by 20.3% after 6 hours and by 29.6% after 24 hours of ischemia. Conclusions-Morphometric assessment of hemispheric swelling on MRI can determine the increase in absolute brain water content noninvasively and can also provide ischemic lesion volumes corrected for brain edema.

Cell injury leads to exposure of intracellular material and is associated with increased permeability of vessels in the vicinity of the damage. Here, we demonstrate that natural extracellular RNA as well as artificial RNA (poly- I IntroductionBrain homeostasis is maintained by the blood-brain barrier (BBB), which forms a mechanical and functional threshold between the central nervous system and the systemic circulation. The barrier is relatively impermeable to ions, many amino acids, small peptides, and proteins, and thus contributes to the maintenance of a specific neural tissue environment. In vertebrates, the BBB exists at the level of the endothelial cells that form brain capillaries 1 in order to regulate and limit the degree of trans-and paracellular flux. 2 The tight barrier properties of the BBB result from the absence of fenestrations, the low number of pinocytotic vesicles, and the presence of tight intercellular junctions between endothelial cells with extremely high electrical resistance. 3 Pathologic conditions associated with brain tumors, head injury, or ischemic stroke are accompanied by endothelial-cell dysfunction, leading to increased permeability across the BBB, which might lead to the development of vasogenic cerebral edema. 4,5 Vascular endothelial growth factor (VEGF) as a hypoxia/ischemia inducible protein in vitro and in vivo is one of the strongest natural permeability factors 6 and a likely candidate for the development of ischemia-and tumor-induced vasogenic brain edema. 7-9 VEGF stimulates endothelial-cell growth and migration in vitro 10,11 and angiogenesis in vivo. 6,12 VEGF was originally described as a potent vascular permeability factor responsible for the accumulation of plasma protein-rich fluid in the ascites of patients with tumors. 13 Structurally, VEGF exists as a dimeric glycoprotein of molecular weight (Mr) 34 000 to 42 000 and is related to the platelet-derived growth factor family of molecules. 14 Although VEGF is the product of a single gene, 6 differentially spliced isoforms between 121 and 206 amino acid residues exist in humans 15,16 that exhibit similar functional activities. Different isoforms are distinguished by their affinity for heparin: although VEGF 121 does not bind heparin, VEGF 165 has moderate affininity for heparin, whereas VEGF 189 and VEGF 206 bind heparin with high affinity. 17 VEGF exerts its multiple actions by ligation with tyrosine kinase receptors, VEGFreceptor 1 (VEGF-R1), as well as VEGF-R2, [18][19][20] which are expressed on vascular endothelial cells. A third member, VEGF-R3 is expressed on lymphatic endothelial cells. 21 During pathologic conditions of the brain associated with tumor burden, stroke, or head injury, nucleic acids might be released by damaged cells. RNA-proteolipid complexes were detected in the circulation of patients with cancer and were suggested to represent a specific secretory product of cancer cells. 22 Accordingly, circulating RNA is present in blood plasma of patients with tumors. 23 The presence of specific types ...

TCCS is a noninvasive bedside method that provides rapid and reliable data regarding stroke subtype and mechanism immediately after onset. Window failure is a serious limitation of this method.