[An autopsy case of anoxic encephalopathy caused by transient upper airway obstruction].
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 bronchopneumonia. Postmortem examination revealed that, in addition to wide distribution of mild neuronal loss and astrocytosis in the cerebral and cerebellar gray matter, focal pseudolaminer necrosis of the IIIrd and IVth cortical layers was predominantly noticed in the calcarine cortex, pre- and postcentral gyri and transverse temporal cortex. However, the cortical architecture 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.
Yoshida
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Y
Department of Neuropathology, Hirosaki University, School of Medicine, Japan.
Honma
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Y
D000402:Airway Obstruction / Q000150:complications*; D001284:Atrophy; D002531:Cerebellum / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D005911:Gliosis / Q000473:pathology; D006801:Humans; D002534:Hypoxia, Brain / Q000209:etiology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D009474:Neurons / Q000473:pathology