Lesion evolution in cerebral ischemia

Abstract

There is sound evidence from histopathological and magnetic resonance imaging (MRI) studies that focal ischemic brain lesions tend to increase in size over time. Considerable lesion growth was observed in models of animal stroke as well as in patients presenting with hemispheric stroke. In focal cerebral ischemia, lesions predominantly enlarge early within 12 hours after onset. Ischemic injury is caused by complete necrosis in most of the affected tissue. By contrast, in global cerebral ischemia as seen after cardiac arrest, lesions appear late (>12 h) in selectively vulnerable brain regions such as the hippocampus, and neurons are damaged by apoptotic cell death. The high and regionally distinct vulnerability of the brain explains why prolonged periods of global ischemia result in widespread loss of energy metabolites combined with diffuse brain edema and global damage. Postulated mechanisms involved in lesion growth include among others excitotoxicity, periinfarct depolarizations, lactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling. Research in the field faces two main challenges. First,maturation phenomena of injury may require special imaging techniques to detect early ischemic changes. Second, the dynamic nature of the changes underlines the need to conduct longitudinal studies with a variety of imaging techniques (e. g., metabolic imaging, diffusion/perfusion MRI, positron emission tomography) that require a differentiated interpretation of the alterations observed.

Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity

“…Since alcohol circulates freely through the whole brain, rather than selectively to these regions, it seemed most likely that damage to hippocampus and entorhinal cortex by ethanol reflects differential susceptibility of these neuronal populations to ethanolinduced damage, similar to ischemia-induced neuronal cell loss (Back et al, 2004).…”

Plasma Antioxidant Activity as a Marker for a Favourable Outcome in Acute Ischemic Stroke

“…In the periphery of the ischemic area, where perfusion takes place, a lesser ischemia develops. The blood flow is reduced 20-40% of normal flow (Back et al, 2004Belayeev et al, 1997Hossman, 1994). In this area, which is potentially salvageable, called penumbra, the degree of ischemia and timing of reperfusion determine the outcome for individual cells.…”

Cholesterol depletion inhibits synaptic transmission and synaptic plasticity in rat hippocampus

“…The hippocampus is involved in learning and memory processes (Bliss and Lomo, 1973) and appears to be a very vulnerable region in several neurodegenerative diseases (Back et al, 2004). For this purpose, we focused on the role exerted by cholesterol on the primary neurotransmitter receptors involved in synaptic transmission and plasticity by using electrophysiological recordings of hippocampal brain slices treated with methyl-β-cyclodextrin (MβCD), a molecule that dissolves the hydrophobic core of lipid rafts (Kilsdonk et al, 1995).…”