一過性気道閉塞による脳障害の1剖検例

AN AUTOPSY CASE OF ANOXIC ENCEPHALOPATHY CAUSED BY TRANSIENT UPPER AIR-WAY OBSTRUCTION

　抄録　短時間の気道閉塞が原因と考えられる中枢神経障害の1例について，組織学的病変分布を中心に報告する。症例は死亡時47歳男性，扁桃腺摘出後の喉頭痙攣により約6分間無酸素状態であった。この間脈拍は保たれていた。その後無言無動状態が2年5カ月続き死亡。剖検により，大脳および小脳を中心とする変性が広範に認められ，その中でも鳥距野，中心前・後回，横側頭回，前頭葉8領野の皮質は仮性層状壊死を呈した。アンモン角は保たれていた。有機水銀中毒症のそれによく類似しているこの分布は，無酸素血症により惹起されたと考えられ，酸素欠乏性脳症を解析する上で貴重な症例と考えられた。

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.