Ischemic injuries of the brain. Morphologic evolution.
A variety of ischemic mechanisms, including those secondary to an arterial occlusion and those of transient cardiac arrest, injured the brain in a diverse but predictable manner. Analyses of the topographic distribution of the lesions and evaluation of the cellular responses allowed prediction of the approximate age and most likely cause of the ischemic injury. Infarcts, caused by arterial occlusions, involved the corresponding arterial territory and were either pale or hemorrhagic, depending on whether the ischemic territory was reperfused. The hemorrhage of venous infarcts was more extensive than that of arterial infarcts. An extreme instance of nonocclusive global brain ischemia resulted from massive increases in intracranial pressure, as may happen after closed head injuries, with or without intracranial bleeding. Transient global ischemia caused by a cardiac arrest, for example, resulted in multifocal lesions that involved all brain components.
D001921:Brain / Q000378:metabolism / Q000473:pathology*; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000473:pathology; D002560:Cerebrovascular Circulation; D006323:Heart Arrest / Q000150:complications; D006801:Humans; D000860:Hypoxia / Q000473:pathology; D007427:Intracranial Pressure; D002546:Ischemic Attack, Transient / Q000473:pathology; D010101:Oxygen Consumption