Human cerebral infarct: a proposed histopathologic classification based on 137 cases
We studied the microscopic features of 137 cases of human cerebral infarct. In each case, the age of the lesion was determined by measuring the time elapsed between initial clinical presentation and date of surgery or death. Multiple microscopic variables were analyzed on hematoxylin and eosin-stain...
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Veröffentlicht in: | Acta neuropathologica 2004-12, Vol.108 (6), p.524-530 |
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Sprache: | eng |
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Zusammenfassung: | We studied the microscopic features of 137 cases of human cerebral infarct. In each case, the age of the lesion was determined by measuring the time elapsed between initial clinical presentation and date of surgery or death. Multiple microscopic variables were analyzed on hematoxylin and eosin-stained sections. There were 104 (76%) male and 33 (24%) female patients with a median age of 64 years. The location of the infarcts included 129 cerebral, 5 cerebellar, and 1 each in the pons, midbrain and medulla. The age of the lesions ranged from 1 day to 53 years. All lesions were single and varied from lacunes to large infarcts in the distribution of one or more cerebral arteries. Key histologic features of the proposed classification are as follows: (1) phase of acute neuronal injury (11 cases studied), age 1-2 days, characterized by the presence of neuronal changes, and spongiosis of the neuropil and absence of neuronal ferrugination, chronic inflammation, macrophages, neo-vascularization and cavitation; (2) phase of organization subdivided into: (a) phase of acute inflammation (31 cases), age 3-37 days, characterized by coagulative necrosis, and frequent acute inflammation, and (b) phase of chronic inflammation (57 cases), age 10 days-53 years, characterized by the presence or absence of coagulative necrosis, neuronal injury, red neurons, macrophages, mononuclear inflammatory cells, perivascular cuffing, cavitation, gliosis, spheroids; absence of neutrophils; and (3) phase of resorption (38 cases), age 26 days-23 years, characterized by absence of an inflammatory response. Neuronophagia is not a feature of cerebral infarcts. |
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ISSN: | 0001-6322 1432-0533 |
DOI: | 10.1007/s00401-004-0918-z |