Abstract
The etiology of brain infarction is clearly multifactorial, and it is generally accepted that numerous interacting mechanisms determine the ultimate fate of brain tissue subjected to critical focal ischemia — whether it turns into frank necrosis, remains morphologically intact but functionless, or resumes normal physiologic activities after a while. Moreover, there is little doubt that the clinical signs and symptoms of ischemic stroke cannot be related to the ischemic focus alone. Much of the resulting deficit, e.g., the often severely disabling “organic brain syndrome”, must be attributed rather to secondary deactivation of structurally unaltered tissue suddenly deprived of its established neuronal input.
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© 1987 ECSC, EEC, EAEC, Brussels-Luxembourg
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Pawlik, G. et al. (1987). Brain Glucose Metabolism and Blood Flow in Ischemic Stroke. In: Heiss, WD., Pawlik, G., Herholz, K., Wienhard, K. (eds) Clinical efficacy of positron emission tomography. Developments in Nuclear Medicine, vol 12. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3345-3_4
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DOI: https://doi.org/10.1007/978-94-009-3345-3_4
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