![]() ![]() Like the parietal cortex, the posterior colliculus, subserving auditory reflexes, has a high metabolic rate and is particularly vulnerable to processes that interfere with neuronal energy metabolism. The well-defined foci of pallor, with hemorrhage, affecting the posterior collicular nucleus bilaterally, and the nucleus of the lateral lemniscus resemble those of ischemic lesions. ![]() Note also the necrosis of the nucleus of the lateral lemniscus. In most cases, the cause of brain infarction is incidental and/or attributable to invasive sampling techniques such as blood or marrow collection in which emboli gain access to the venous or arterial systems.ĭepicts a bilaterally symmetrical lesion of acute necrosis of the posterior colliculus. The hippocampus is relatively spared from the ischemia. , there is little, if any, evidence of inflammatory infiltrate at the margin of the lesion, indicating that the infarction is less than 24 hours old. In ischemic brain lesions, the typical morphologic criteria of neuronal necrosis may take more than 24 hours of survival to manifest in hematoxylin and eosin sections. Note the pallor signifying early necrosis of the affected region (arrows) that involves much of the thalamus, hypothalamus, cerebral peduncle, and optic tract unilaterally. The hippocampal dentate gyrus is identified by a white arrow in The fibrin and fat embolus is enlarged in Identifies the infarctive effects of acute vascular occlusion by an arterial embolus (arrowhead). In NTP studies, infarcts are diagnosed as necrosis, and the term “malacia” is reserved for gross lesions in the brain. ![]() This section focuses on the morphology of brain necrosis caused by differing processes and the nature of the responses. ![]()
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