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AN AUTOPSY CASE OF ACUTE CARBON MONOXIDE POISONING (UNINTERRUPTED FORM) WITH EXTENSIVE NECROSIS IN CEREBRAL WHITE MATTER Yoshio Mitsuyama 1,2 , Isao Takamatsu 3 1Department of Neuropsychiatry, Faculty of Medicine, Kyushu University 3Wakahisa Mental Hospital pp.1111-1118
Published Date 1974/11/1
DOI https://doi.org/10.11477/mf.1406203625
  • Abstract
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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.


Copyright © 1974, 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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