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AN AUTOPSY CASE OF ANOXIC ENCEPHALOPATHY CAUSED BY TRANSIENT UPPER AIR-WAY OBSTRUCTION Yasuji Yoshida 1 , Yoshiaki Honma 2 1Department of Neuropathology, Institute for Neurological Science, Hirosaki University, School of Medicine 2Department of Neurology, Sado General Hospital pp.1211-1216
Published Date 1989/12/1
DOI https://doi.org/10.11477/mf.1406206445
  • Abstract
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We reported the pathological findings of an autopsy case of anoxic encephalopathy, with special reference to the topography of degenerative changes in the nervous system. A 47 year-old man, who had an episode of sudden upper air-way obstruction although his radial artery pulsation was maintained, and then suffered from akinetic mutism and myoclonus for 2 years and 5 months, died of broncopneumonia. Postmortem examina-tion revealed that, in addition to wide distribution of mild neuronal loss and astrocytosis in the cerebral and cerebellar gray matter, focal pseudo-laminer necrosis of the Erd and Nth cortical layers was predominantly noticed in the calcarine cortex, pre- and postcentral gyri and transverse temporal cortex. However, the cortical architec-ture of the Ammon's horn, arterial boundary zones and depths and sides of sulci was not involved. This topography of neuronal degeneration was considered to correspond with those of methyl-mercury intoxication. However, his history and neurological examination before the episode denied the intoxication. Conclusively, the characteristic distribution of the brain damage in this case are resulted from the episode of pure anoxic anoxia, suggesting that the anoxic encephalopathy would make up a different involvement pattern of the brain from those of ischemic encephalopathy.


Copyright © 1989, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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