Lesion evolution in cerebral ischemia

Byline: Tobias Back (2), Thomas Hemmen (2), Olaf G. Schuler (1) Keywords: brain ischemia; MRI; cardiac arrest; stroke; pathophysiology; cerebral ischemia Abstract: 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 (&gt 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. Author Affiliation: (1) Department of Neurology, Ludwig Maximilians University Munich, Marchioninistrasse 15, 81377, Munchen, Germany (2) Department of Neurology, Philipps University Marburg, R.-Bultmann-Str. 8, 35039, Marburg, Germany Article History: Registration Date: 01/01/2004 Received Date: 04/08/2003 Accepted Date: 15/01/2004