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I.はじめに
急性一酸化炭素中毒(以下,急性CO中毒と記す)は,近年増加の傾向にあり,20歳台に多くその半数が自殺を目的とし,そのほとんどが都市ガス吸入による急性CO中毒であるという18)。その臨床経過には,非間歇型・間歇型があり,それぞれの経過に対応する脳病変として,非間歇型では淡蒼球の対称性壊死と大脳皮質の壊死,間歇型では大脳白質の病変,即ちGrinker7)のいうCO—Leukoencephalopathyがその特徴とされて来た。なかでも大脳白質の病変は,間歇型の病理学的基盤とも考えられていた。これに対して,白木ら23,24)は,CO中毒における急性期から遷延期にかけての脳病変の主座は,間歇型・非間歇型にかかわらず大脳白質にあるとしており,急性CO中毒の本質的な病変については,まだ議論の余地をを残している。ここに報告する症例は,臨床経過は非間歇型であるが,脳の病変は従来間歇型で報告されて来た所見に一致するものである。さらに高松ら25)がかつて純粋なCOガスを用いて猫で行なつた実験的CO中毒(すべて非間歇型)の脳の病変に一致しており,本例は急性CO中毒の本質的な病変について示唆に富む症例と考え,報告する。
A report was made on a case of acute carbon monoxide poisoning (uninterrupted form) with ex-tensive necrosis in cerebral white matter.
History: A 26-year-old female attempted suicide with city gas after taking bromvalerylurea (10 gm). She was admitted to the medical clinic in an un-conscious state, having been asphyxiated overnight. She remained unconscious for several days, then developed apallic syndrome. Her mental state did not vary during her hospitalization. In the course of the hospital stay, she sometimes developed fever, and rales were heared in both lungs. She died on the 116th day after admission.
Post Mortem Findings: At necropsy, extensive bilateral bronchopneumonia was found as the im-mediate cause of death. The brain weighed 1050 gm. and it was normal on inspection. On coronal sectioning of the formalin fixed brain, a moderate hydrocephalus was seen which was pronounced especially in the anterior and it was noted that white matter was friable and crumly.
Microscopic examination revealed severe spongy appearance of necrosis most prominent in the frontallobe and extending into the occipital region, and multiple irregular foci of demyelination were seen throughout the central white matter. The peri-vascular spaces were widened and fibrosed in part, with scattered round-cell infiltrates. The arcuate fibers were preserved throughout. Numerous fat-granule cells and many droplets of sudan positive material were seen in the same area but reactive glial fibrosis and astrocytic proliferation were minimal. Axis cylinders were disrupted and thinned out in some areas. The cerebral cortex and basalganglia showed minimal neuronal damage with cell shrinkage and ischemic change throughout.
It was considered from the review of clinical and experimental cases that primary lesion in CO-poisoning was in the cerebral white matter. As to the pathogenesis, it might be postulated that histotoxic action on the tissue brought about de-myelination of the cerebral white matter.
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