Ischemia exerts a variety of harmful effects on the cerebral structures, results in damage that is pathologically characterized by the presence of tissue necrosis (i.e., infarction). This chapter reviews the cerebral pathological changes that occur at the level of the brain parenchyma in patients with clinical strokes, and also describes the different mechanisms of vessel and heart disease that underlie brain infarcts. Large brain infarcts are produced by occlusion of the major arteries or branches of these arteries. The extent of the brain infarct resulting from occlusion of these arteries is determined by the functional efficacy of collateral circulation via leptomeningeal arteries, the circle of Willis, or the ophthalmic artery. The chapter discusses the forms of ischemic brain injury that are not characterized by the presence of tissue pan necrosis (i.e., infarct) such as incomplete infarction and white matter changes. The effect of ischemia on the white matter can be acute, severe, and localized, leading to small areas of necrosis (lacunar infarction). Data from animal models that helps us to understand the morphological physiopathology of brain ischemia is presented. Incomplete infarction is characterized by the occurrence of damage selectively limited to some cells or cellular components while the remaining ones are spared.

Neuropathology of ischemic brain injury / J. Ogata, H. Yamanishi, L. Pantoni (HANDBOOK OF CLINICAL NEUROLOGY). - In: Stroke / [a cura di] M. Fisher. - [s.l] : Elsevier, 2008. - ISBN 9780444520036. - pp. 93-116 [10.1016/S0072-9752(08)01905-2]

Neuropathology of ischemic brain injury

L. Pantoni
Ultimo
2008

Abstract

Ischemia exerts a variety of harmful effects on the cerebral structures, results in damage that is pathologically characterized by the presence of tissue necrosis (i.e., infarction). This chapter reviews the cerebral pathological changes that occur at the level of the brain parenchyma in patients with clinical strokes, and also describes the different mechanisms of vessel and heart disease that underlie brain infarcts. Large brain infarcts are produced by occlusion of the major arteries or branches of these arteries. The extent of the brain infarct resulting from occlusion of these arteries is determined by the functional efficacy of collateral circulation via leptomeningeal arteries, the circle of Willis, or the ophthalmic artery. The chapter discusses the forms of ischemic brain injury that are not characterized by the presence of tissue pan necrosis (i.e., infarct) such as incomplete infarction and white matter changes. The effect of ischemia on the white matter can be acute, severe, and localized, leading to small areas of necrosis (lacunar infarction). Data from animal models that helps us to understand the morphological physiopathology of brain ischemia is presented. Incomplete infarction is characterized by the occurrence of damage selectively limited to some cells or cellular components while the remaining ones are spared.
brain; brain infarction; brain ischemia; carotid arteries; cerebral amyloid angiopathy; cerebral arteries; humans; medicine (all); neurology; neurology (clinical)
Settore MED/26 - Neurologia
2008
Book Part (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/573212
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